COURT FILE NO.: CV-00000327/18

DATE: 20230501

ONTARIO

SUPERIOR COURT OF JUSTICE

BETWEEN:

WILLIAM JOHNSON, JENNIFER JOHNSON and ROBERTA JOHNSON

Plaintiffs

– and –

LAKERIDGE HEALTH CORPORATION, DR. MORRIS NEALE GINSBURG, DR. SHENIF LADAK, DR. DAVID CRISP, DR. ROSE-ANNE VIEIRA, DR. GEOFFREY DONSKY, JOHN DOE AND JANE DOE

Defendants

Paul Harte, Maria Damiano and Jan Marin, for the Plaintiffs

Darryl Cruz and Bonnie Greenaway, for the Defendant, Dr. Rose-Anne Vieira

HEARD: November 21, 22, 25, 28, and December 1, 2022

REASONS FOR DECISION

J. dI LUCA J.:

Overview

[1] On October 30, 2012, the plaintiff, William Johnson, suffered a life-altering stroke. He had been admitted to hospital following an initial stroke that occurred on or about October 17, 2012. He was put on antiplatelet therapy to prevent secondary stroke. When he was discharged from hospital on October 23, 2012, the defendant Dr. Rose-Anne Vieira, failed to review a critical imaging report.

[2] Mr. Johnson claims that had Dr. Vieira reviewed this imaging report, he would not have been discharged and would have been given anticoagulation instead of antiplatelet therapy to prevent a secondary stroke.

[3] While Mr. Johnson was given anticoagulation therapy prior to his second stroke, he nonetheless suffered the second stroke. He argues that the delay in starting that therapy, which occurred as a result of Dr. Vieira’s failure to review the imaging report, caused the secondary stroke.

[4] Dr. Vieira admits that she was negligent in failing to review the critical imaging report before discharging Mr. Johnson. However, she submits that the plaintiffs have failed to prove causation.

[5] Damages have been agreed upon. As such, the sole issue in this trial is causation.[^1] Through the efforts of skilled counsel, this trial was conducted in an efficient yet comprehensive fashion, and included a detailed agreed statement of fact, joint document book and very helpful opening and closing submissions.

[6] Two experts testified on the issue of causation. Dr. Louis Caplan, a world-renowned expert in stroke and professor at Harvard University, testified on behalf of the plaintiffs. Dr. David Gladstone, a leading Canadian expert in stroke, testified on behalf of the defendant. The expert evidence reveals the existence of a debate in the medical community around the comparative efficacy of anticoagulation therapy versus antiplatelet therapy in the prevention of secondary strokes stemming from vertebral artery dissections.

[7] In what follows, I will review the legal framework for the determination of causation. I will then review the background evidence provided through the Agreed Statement of Facts. I will then turn to a review of the expert evidence, followed lastly by my assessment of that evidence through the legal framework.

The Legal Framework

The Test for Causation

[8] A successful action in negligence requires that the plaintiff prove four elements: (1) that the defendant owed a duty of care to the plaintiff; (2) that the defendant’s behaviour breached the standard of care; (3) that the plaintiff sustained damage; and, (4) that the damage was caused, in fact and in law, by the defendant’s breach, see Mustapha v. Culligan of Canada Ltd., 2008 SCC 27, [2008] 2 S.C.R. 114, at para. 3.

[9] The test for causation was set out by the Supreme Court of Canada in Clements v. Clements, 2012 SCC 32, [2012] 2 S.C.R. 181, at paras. 8-9, as follows:

The plaintiff must show on a balance of probabilities that “but for” the defendant’s negligent act, the injury would not have occurred. Inherent in the phrase “but for” is the requirement that the defendant’s negligence was necessary to bring about the injury – in other words that the injury would not have occurred without the defendant’s negligence. This is a factual inquiry. If the plaintiff does not establish this on a balance of probabilities, having regard to all of the evidence, her action against the defendant fails. [Emphasis in original]

The “but for” test for causation must be applied in a robust common sense fashion. There is no need for scientific evidence of the precise contribution the defendant’s negligence made to the injury.[^2]

[10] Causation relates to both “general” and “specific” causation. In most cases, general causation is not an issue. It is obvious. In other cases, general causation is not obvious and must be established on the evidence, either directly or by inference, see Baghbanbashi et al. v. Hassle Free Clinic et al., 2014 ONSC 5934 at para. 9, and Rothwell v. Raes, 1990 CanLII 6610 (ONCA), at paras. 4 and 8.

[11] The defendant’s act or omission need not be the only cause of the plaintiff’s injury. It is sufficient if the defendant’s act or omission is a cause of the plaintiff’s injury, see Blackwater v. Plint, 2005 SCC 58, at para. 78. An act or omission will be “a cause” of the plaintiff’s injury where it either caused or contributed in some not insubstantial or immaterial manner to the injury, see Uribe v. Tsandelis, 2021 ONCA 377 at para. 35, and Donleavy v. Ultramar Ltd., 2019 ONCA 687, at para. 72.

[12] In medical malpractice cases, strict scientific proof of causation is often elusive or unavailable due to the negligent acts of the defendants. As a result, the courts are required to take a “robust and pragmatic” approach to the fact-finding component of causation, see Benhaim v. St-Germain, 2016 SCC 48, at para. 54, and Estate of Mary Fleury et al. v. Olayiwola A. Kassim, 2022 ONSC 2464, at para. 109. In the absence of evidence to the contrary, proof of causation may be established by way of inference, even when positive or scientific proof has not been adduced, see Snell v. Farrell, 1990 CanLII 70 (SCC), [1990] 2 S.C.R. 311.

[13] That said, the “robust and pragmatic” approach is not a substitute for factual evidence of causation, see Aristorenas v. Comcare Health Services (2006), 2006 CanLII 33850 (ON CA), 83 O.R. (3d) 282 (C.A.), at paras. 54, 63-64, and Fowlow v. Southlake Regional Health Centre, 2014 ONCA 193, at paras. 5, 10.

[14] Where the issue of causation relates to delayed medical diagnosis and treatment, the “but for” analysis requires the plaintiff to prove on a balance of probabilities that the delay “caused or contributed to the unfavourable outcome”, see White v. St. Joseph’s Hospital, 2019 ONCA 312 at para. 25, and Salter v. Hirst, 2011 ONCA 609, at para. 16. A mere loss of chance of a better outcome is not a sufficient basis upon which to find causation, see Cottrelle v. Gerrard (2003), 2003 CanLII 50091 (ON CA), 67 O.R. (3d) 737 (C.A.) at paras. 25-26, Laferriere v. Lawson, 1991 CanLII 87 (SCC), [1991] 1 S.C.R. 541 at pp. 608-9 and St-Jean v. Mercier, 2002 SCC 15, at para. 106. Ultimately, the plaintiff must establish that but for the breach of the standard of care, the outcome would probably have been avoided.

[15] A common analytical approach to the causation analysis involves a three-part inquiry based on the following questions: (1) what likely happened; (2) what would likely have happened had the defendant not breached the standard of care; and, (3) where should fault be allocated, see Sacks v. Ross, 2017 ONCA 773, at para. 47. In this case, the third question is not necessary as there is only one alleged tortfeasor.

Assessing Competing and Contradictory Expert Evidence

[16] In Sit v. Trillium Health Centre, 2020 ONSC 2458, at paras. 120-125, Trimble J. set out the following analytical framework for the assessment of competing and contradictory expert evidence:

[120] In evaluating the evidence of competing experts and deciding which expert’s opinion to accept over another’s, the court must evaluate the expert as any other witness as described above. In addition, however, the court must apply the following three-step process:

[121] Step 1: Qualifications and Impartiality - at this stage, the court should consider the qualifications of each expert witness, examine the experts’ training and experience, and consider their level of competence in the field in which they were qualified to give an opinion: Vescio (Litigation guardian of) v. Garfield, [2007] O.J. No. 2624 (S.C.), at para. 102.

[122] The court must also consider whether the expert was impartial, or whether he or she appeared to unreasonably favour the party who called him or her as a witness. An expert’s lack of independence and impartiality goes not only to the admissibility of the expert’s evidence, but also to the weight to be given to that evidence once it is admitted: White Burgess, Langille, Inman v. Abbott and Haliburton Co., 2015 SCC 23, [2015] 2 S.C.R. 182, at para. 45.

[123] Step 2: Assessment of Evidentiary Basis for the Opinion - at this stage, the court must examine the facts and assumptions upon which the expert relied on to form their opinion: D.M. Drugs Ltd. (c.o.b. Harris Guardian Drugs) v. Bywater (c.o.b. Parkview Hotel), 2013 ONCA 356, at paras. 40, 48.

[124] Step 3: Examining the Whole of the Opinion - at this stage, the court must examine and evaluate the opinion itself, as a whole. Did the expert consider all relevant information and give it appropriate emphasis in reaching the conclusion?: D.M. Drugs Ltd., at paras. 40, 48.

[125] In assessing the weight of competing experts’ opinions, like any other evidence, the trier of fact is entitled to accept or reject any part or all of the evidence in order to determine how much weight to give any expert’s evidence: Biddersingh, at para. 66. The court, however, must accept or reject an expert’s opinion on a given issue as a whole. The court is not entitled to pick and choose among various aspects or portions of the expert’s opinion on a given issue and fashion a new opinion from those aspects or portions that the court prefers from each experts’ opinion. Generally, the court does not have the expertise to determine whether the expert is right or wrong in their opinion: Cornell, at para. 1; ter Neuzen, at para. 51. Where the court does this, it would, in effect, assume the role of the expert.

[17] An expert’s opinion may be based to varying degrees on statistical evidence. In assessing the expert’s opinion, the court should be cautious in approaching statistical evidence. Statistics relate to general trends, which may or may not relate to the specific circumstances of the case, see Benhaim at paras. 74-76, Andersen v. St. Jude Medical, Inc., 2012 ONSC 3660 at paras. 393-395 and Hacopian-Armen v. Mahmoud, 2020 ONSC 4946, at paras. 80-84. In the absence of “an evidentiary bridge” between general statistics and the plaintiff’s specific circumstances, statistical evidence may be entitled to limited weight. Ultimately, statistical probabilities are simply one piece of evidence that must be considered along with all of the evidence in determining whether the plaintiff has satisfied their burden on the issue of causation.

The Agreed Statement of Fact

[18] At the outset of the trial, counsel filed a comprehensive Agreed Statement of Fact that details the background medical evidence regarding stroke and stroke mechanisms, as well as the chronology of relevant events relating to Mr. Johnson. The Agreed Statement of Fact stipulates that the facts set out therein are agreed to without prejudice to the submissions of the parties may make about the relevance and weight to be given to any fact.[^3]

[19] In addition, the Agreed Statement of Fact stipulates that where a diagnosis or statement of opinion is referenced in a document contained in the Joint Book of Documents, the entries are admitted establishing the fact that the author of the entry reached those diagnoses or opinions at the time, and not for the truth or accuracy of those opinions.

The Parties

[20] The plaintiff, Mr. Johnson, is a former patient of the defendant physician, Dr. Rose-Anne Vieira, who discharged him from hospital on October 23, 2012, following an admission for acute stroke. The plaintiffs Jennifer Johnson and Roberta Johnson are Mr. Johnson’s wife and mother respectively.

[21] The defendant, Dr. Vieira, is a family physician licensed to practice medicine in Ontario and she was the physician most responsible for Mr. Johnson’s discharge from hospital on October 23, 2012.

Background on Stroke and Cervical Artery Dissection

[22] An ischemic stroke occurs when there is blockage of blood flow in part of the brain. When deprived of blood, which carries oxygen and glucose, brain cells die. This is known as an infarction.

[23] There are many different causes of stroke. Dissections of the cervical arteries (vertebral and carotid arteries) are a well-established cause of stroke, and a relatively common cause of strokes in young and middle-aged adults.

[24] A dissection refers to a tear that develops within an artery wall, leading to blood entering and splitting the inner layers of the vessel wall. This is known as an intramural hematoma. At the site of a dissection, the vessel diameter usually becomes narrowed from compression by the intramural hematoma. This can result in a mild, moderate, or severe narrowing of the vessel that can limit blood flow, or a complete vessel occlusion in which blood flow ceases. Blood clot formation inside the artery, known as thrombosis, can occur.

[25] The most common mechanism of stroke related to a dissection is thromboembolism, whereby clots that form at the site of a dissection can subsequently dislodge, travelling upstream and block blood flow within the brain. Strokes may also result from hemodynamic ischemia, (i.e., diminished blood flow), if the injured vessel becomes severely narrowed or occluded.

[26] There are four main arteries that carry blood to the brain: two carotid arteries travel up the front of the neck and into the head and two vertebral arteries travel up the back of the neck and into the head where they join to form the basilar artery. The vertebral and basilar arteries supply blood to the brainstem, cerebellum and back of the brain.

[27] Cervical artery dissections typically result from some form of head or neck injury, either major or minor trauma, or they may appear to occur spontaneously or associated with unrecognized or trivial trauma. The mechanism is usually a rapid or excessive neck movement (e.g., rotation or hyperextension) in a way that stretches and injures the artery wall. Dissections are usually painful (neck pain, headache, or facial pain) but may also be asymptomatic.

[28] The diagnosis of dissection is established by characteristic abnormalities on imaging studies of the blood vessels using CT, MRI, ultrasound, or catheter angiography.

[29] A stroke occurring as a complication of a dissection may occur immediately, but most often occurs in a delayed fashion (i.e., hours, days or weeks following the initial vessel injury). The typical temporal sequence is neck trauma, leading to artery dissection causing neck pain/headache and vessel narrowing/clotting, leading to a stroke.

Antithrombotic Medications for Stroke Prevention

[30] As most strokes arise from blood clots that originate from the blood vessels or the heart, medications are typically prescribed to lower the risk of clots that could lead to strokes. There are two main classes of anticlotting medications in clinical practice: antiplatelet drugs and anticoagulant drugs.

[31] Antiplatelet drugs include Aspirin and clopidogrel (Plavix). These drugs work by inhibiting blood platelets so they are less ‘sticky’ and less likely to form a clot.

[32] Anticoagulant drugs include Heparin and Warfarin. They work by inhibiting specific coagulation factors to interfere with the body’s ability to produce thrombin, thereby inhibiting the formation of fibrin clots.

[33] Heparin and Warfarin require monitoring with blood tests. The main advantage of antiplatelet drugs is that they have a lower risk of bleeding when compared to anticoagulants and are easier to use.

[34] As of 2012, the Canadian Stroke Best Practice Recommendations contained no specific recommendations pertaining to the treatment of cervical artery dissections.

Past Medical History

[35] In September of 2012, Mr. Johnson was 43 years old. He had a past medical history of diabetes, sleep apnea, anxiety, and depression. He was a non-smoker and did not suffer from hyperlipidemia, cardiac disease, or malignancy. He was taking insulin, Cipralex and Ativan.

[36] MRI scans of Mr. Johnson’s head performed on February 29, 2012, and September 18, 2012, were reported to be unremarkable.

[37] On September 22, 2012, Mr. Johnson attended the hospital complaining of dizziness, light-headedness, and nausea. A head CT scan performed on September 22, 2012, was reported to be unremarkable.

Chiropractor and Massage Therapy

[38] On October 15, 2012, Mr. Johnson attended an appointment at his chiropractor where a neck adjustment was performed. On October 16, 2012, he received massage therapy directed at his shoulders and neck. That night, he developed a significant headache.

October 17, 2012 - First Stroke

[39] On October 17, 2012, at approximately 2000 hours, Mr. Johnson went to the Emergency Room (ER) Department of the hospital complaining of a syncopal (fainting) episode. He reported that he had been vomiting since the morning, sweating and had a headache from the night before. He was also complaining of photophobia. He was given IV fluids, nausea and pain medication, and discharged.

October 18, 2012 – Family Doctor Visit

[40] On October 18, 2012, Mr. Johnson attended his family doctor, Dr. John Bolger, with ongoing complaints, including visual disturbances. Dr. Bolger sent him to an optometrist in the same building to rule out a retinal detachment. The optometrist, Dr. David Black, diagnosed a left sided homonymous hemianopia (loss of the left half of the field of vision in both eyes). Dr. Bolger recommended that Mr. Johnson go to the hospital to be assessed for a possible stroke.

October 18 to 23, 2012 – Admission to the Hospital for Acute Stroke

[41] On October 18, 2012, at approximately 1535 hours, Mr. Johnson arrived at the ER department of the hospital. A head CT scan documented a large hypodensity within the right occipital lobe indicative of an acute embolic ischemic stroke within the right posterior cerebral artery (PCA) territory, and small hypodensities in the inferior left cerebellar hemisphere compatible with infarcts (PICA territory).

[42] Mr. Johnson was admitted to the Stroke Unit at the hospital and assessed by a hospitalist. An ischemic stroke protocol was initiated, and Mr. Johnson was initially treated with a loading dose of Plavix 300 mgs at approximately 2050 hours, followed by subcutaneous Heparin 5,000 units to be administered twice, every 12 hours, and Aspirin 81 mgs daily starting on October 19, 2012, at approximately 0150 hours. Mr. Johnson had not been taking antiplatelet therapy prior to October 18, 2012.

[43] On October 21, 2012, Mr. Johnson was assessed by Dr. Crisp, a neurologist, who also initiated Crestor (cholesterol medication).

[44] On October 22, 2012, a brain MRI confirmed the diagnosis of an ischemic stroke within the right PCA territory affecting the occipital and posterior temporal regions. The suspected etiology was a vertebral artery dissection. The MR angiogram of the head and neck (the “MRA”) reported “hematoma within the left vertebral artery, concerning for dissection”.

Other Diagnostic Tests

[45] A carotid ultrasound study on October 19, 2012, reported normal carotids with no stenosis or plaque, and normal vertebral flows. A transthoracic echocardiogram performed the same day reported left ventricular lateral wall hypokinesis; left atrial diameter 3.9 cm (normal), normal left ventricular size, and no significant valve disease.

[46] On October 25, 2012, a transoesophageal echocardiogram, found no evidence of a cardiac source of embolism. The report indicated low normal left ventricular function, no atrial septal defect, no thrombus or mass. An ECG, telemetry and the echocardiogram performed during the October 18, 2012 admission, showed Mr. Johnson to be in regular sinus rhythm.

[47] Mr. Johnson had not been previously diagnosed with atrial fibrillation. In May 2012, he had seen neurologist Dr. Jiaravuthisan Somchai for intermittent “nonspecific dizziness”. A Holter monitor showed a normal sinus rhythm.

October 23, 2012 - Discharge

[48] On October 23, 2012, Mr. Johnson had improved and was in stable condition. He was discharged home by Dr. Vieira, at approximately 1029 hours on the following daily medications: Aspirin, Crestor, and Coversyl (blood pressure medication). He was discharged without the results of his MRA being fully appreciated.

[49] Dr. Vieira does not believe that she saw the MRA prior to discharge. Had Dr. Vieira seen the MRA, she would have called Mr. Johnson’s neurologist, Dr. David Crisp. Dr. Vieira would have asked for his opinion on how to proceed. Any further treatment decisions would have been made in consultation with Dr. Crisp. Dr. Vieira would have deferred to Dr. Crisp’s opinion in terms of treatment decisions.

October 23 to 29, 2012

[50] Mr. Johnson remained in stable condition from October 23, 2012, to October 30, 2012. He was mobile and able to communicate normally throughout that week. He did not report any concerning symptoms to his wife, Jennifer Johnson.

October 29, 2012 – Dr. Bolger

[51] On October 29, 2012, Mr. Johnson went to see Dr. Bolger to follow-up on his recent hospitalization. Dr. Bolger reviewed the MRA and contacted Dr. Crisp, and then instructed Mr. Johnson to return to the hospital immediately to start Heparin treatment.

October 29, 2012 – Readmission to Hospital

[52] At approximately 1250 hours on October 29, 2012, Mr. Johnson walked into the hospital and was readmitted. He was alert and oriented, and his gait was steady.

[53] An intravenous Heparin infusion was started at approximately 1630 hours. The dose of Heparin was guided by a standard Heparin dosing nomogram, starting with a single dose (bolus) and then continuous infusion to establish a target partial thromboplastin time (PTT) range of 50-70.[^4] Mr. Johnson was also given a starting dose of Coumadin (Warfarin) 10 mgs at approximately 1815 hours.

[54] Mr. Johnson remained in stable condition and did not exhibit or report any distress on October 29, 2012.

October 30, 2012 - Second Stroke

[55] In the afternoon of October 30, 2012, Mr. Johnson suffered a second stroke described as a new acute left cerebellar ischemic stroke. This presented initially in the late afternoon, and Mr. Johnson developed vertigo, headache, tinnitus, nausea and vomiting, and a tendency to fall to the left. A head CT scan completed at approximately 1510 hours was reported as unchanged in comparison with the study on October 18, 2012, with no new acute abnormalities. His Heparin infusion was stopped briefly at 1430 hours and then restarted at 1615 hours.

Clinical Deterioration

[56] On October 31, 2012, Mr. Johnson’s clinical condition worsened significantly. He had a fall that morning resulting in a left forehead laceration that was sutured. He was transferred to the Intensive Care Unit (ICU) for monitoring. A repeat head CT scan showed the development of a large left cerebellar infarct with mass effect, brainstem compression, obstructive hydrocephalus, and potentially tonsillar herniation. Within hours, Mr. Johnson deteriorated neurologically with reduced consciousness (Glasgow Coma Scale score 8 points). He required intubation and emergency ambulance transport to Toronto Western Hospital for neurosurgical treatment. He required an emergency posterior fossa decompressive craniectomy.

Rehabilitation

[57] Mr. Johnson subsequently required months of inpatient rehabilitation. The October 30, 2012 stroke resulted in neurological deficits and disability reflecting significant cerebellar dysfunction. He initially required a gastric feeding tube. He developed a pulmonary embolism in hospital. Following his hospital stay at Toronto Western Hospital, he was admitted to Toronto Rehabilitation Institute until August 6, 2013, and then transferred to Lakeridge Health Inpatient Rehabilitation Unit from August 6, 2013 to September 19, 2013.

[58] Mr. Johnson attended an outpatient stroke clinic appointment at Toronto Western Hospital on May 31 or June 1, 2013, at which time Dr. Casaubon documented that he was having ongoing symptoms of nausea, episodic headaches, vertigo, left upper limb tremor. His examination findings included left upper and lower limb ataxia (i.e., incoordination), dysarthria, diplopia, and nystagmus. He needed a walker to ambulate.

Cause of the Strokes

[59] The most likely underlying etiology of Mr. Johnson’s strokes was a dissection of his left vertebral artery. The mechanism of his October 17, 2012 stroke was embolic, most likely on the basis of an embolism (clot) that dislodged from the blockage in his left vertebral artery and occluded his right posterior cerebral artery.

[60] The vertebral artery dissection likely happened before October 17, 2012. The exact date of onset of the dissection is unknown; it may have correlated with his chiropractic treatment on October 15, 2012, or his massage therapy on October 16, 2012. Alternatively, the dissection may have predated his chiropractic treatment and massage therapy and may or may not have been exacerbated by one or both of them.

[61] The October 30, 2012 stroke is best explained by his left vertebral artery dissection, which either produced further emboli, blocking blood flow to smaller artery branches supplying the left cerebellum, and/or via hemodynamic ischemia due to reduction of blood flow within the left vertebral artery.

Duty and Standard

[62] Dr. Vieira had a duty to Mr. Johnson to exercise reasonable care in ordering his discharge from the hospital on October 23, 2012. Dr. Vieira breached the expected standards of care by failing to review the neck MRI (MRA) report prior to discharging Mr. Johnson.

Damages

[63] The parties have agreed upon the quantum of damages to be awarded.

The Expert Evidence

Dr. Louis Caplan

[64] Dr. Caplan is the plaintiffs’ expert. He was qualified to give expert opinion evidence as a stroke neurologist with respect to the diagnosis and treatment of ischemic stroke generally including the diagnosis, treatment and likely outcomes related to vertebral artery dissection, including the impact and consequences of any delay in treatment.

[65] Dr. Caplan is a world-renowned expert on stroke. He graduated from medical school in 1962, and following completion of his training has maintained a clinical practice for over 52 years, seeing somewhere between 15,000 and 20,000 stroke patients during that time. He is also a long-standing professor at Harvard University where he has supervised approximately 70 fellows from around the world. Dr. Caplan is the author of a leading textbook called Caplan’s Stroke: A Clinical Approach, which is now in its fifth edition. In addition, he has authored and co-authored other books and countless papers, articles and journals. He has also received a number of honours and distinctions reflecting his contribution to his chosen field of medicine.

[66] In terms of vertebral artery dissections, Dr. Caplan advised that he has personally treated somewhere around 200 individuals during the course of his lengthy career. He has also written extensively on vertebral artery dissections, including several articles published in leading medical journals.

[67] In terms of his “bottom-line” opinion, Dr. Caplan opined that if the plaintiff had been provided Heparin, an anticoagulant treatment, within the appropriate therapeutic timeframe, he would not have had the second stroke which led to his hospitalization and surgery. At a very high level, Dr. Caplan based this opinion on reviewing everything he knows and has read on vertebral artery dissection and stroke, and his experience over many years.

(i) Background Evidence on Stroke

[68] Dr. Caplan was asked to explain ischemic stroke, which is the type of stroke Mr. Johnson suffered. He explained that ischemia means a lack of blood flow. The brain is dependent on a constant supply of nutrition consisting of oxygen and sugar, which is supplied by blood vessels that supply the brain. When there is inadequate nutrition from a blood vessel, the part of the brain tissue supplied by that vessel dies or becomes infarcted. Initially, when blood supply is insufficient, the tissue stops functioning for a while but may not yet be irreversibly damaged. An infarct is when the damage to the tissue is irreversible. If an artery to the brain is blocked, it cannot supply blood adequately to that part of the brain which results in the death of brain tissue. This is an ischemic stroke.

[69] Dr. Caplan explained that the mechanism of ischemic stroke varies, though it is usually caused by embolism or thrombosis. An embolism is defined as a particle of material that originates in one place and then travels to a foreign place to block a blood vessel that supplies the brain. An embolism can arise from an artery, for example where a clot arises in the vertebral artery in the neck and then travels upstream to the brain. This is known as an inter-arterial embolism. If the embolism comes from the heart, it would be a cardiac embolism.

[70] A thrombotic stroke is something occurring locally within a vessel and can arise when a vessel becomes blocked because of a process within that vessel. As people get older, they often develop atherosclerosis, or plaque within an artery, that then blocks the artery and decreases the supply of blood to the brain. Damage to a vessel can be caused by several things, such as atherosclerotic plaque, inflammatory conditions, or dissection. This can also occur in vessels in the heart as a result of heart disease. As well, some people have blood that clots disproportionately easy, which can result in a clot in the heart or a vessel.

[71] Dr. Caplan was asked about vertebral artery dissection. He explained that “a dissection” simply means “a tear.” An arterial dissection or tear is likely to occur in parts of an artery that are moveable. The vertebral artery moves into the vertebral column, and it is loose between the origin and point where it “ducks” into the vertebral column. Dissection is most often caused by a sudden movement, for example a chiropractic adjustment or lunging movement.

[72] Dr. Caplan explained that an artery has three walls. It has an intima, which is an inner wall. It has a media, which is the middle wall which is partially connective tissue. Lastly, it has an outer wall called an adventitia. When the artery is torn, a clot develops and blood collects within the wall of the artery. When that occurs, the artery expands and the area that is expanding can tear through the intima, the inner lining of the artery, and inject that fresh blood into the lumen, which is a portion of the artery where blood flows.

[73] One type of dissection consists of blood within the wall of the artery in the intima medial and then within the lumen. It forms there because blood is injected from the blood bleeding from within the wall, or forms within the lumen as a result of compression and stasis. A second type of dissection in the outer wall of the artery can cause the outer part to bulge out forming an aneurysm which does not affect the lumen. Intima medial dissections are the type that often cause stroke.

[74] In terms of the symptoms of vertebral artery dissection, Dr. Caplan explained that there are three types of symptoms. The first type of symptoms relate to injuries to the vessels which have nerves along the outside. When vessels are damaged, pain is caused in the back of the head or in the neck on the same side as the dissection. The second type of symptoms relate to a lack of blood flow related to the area of the brain that is not getting enough blood. These symptoms can include dizziness, double vision, light-headed feeling, or altered vision. The third type of symptom relates to nerve pains caused when a dissection occurs on the outside of an artery.

[75] Ischemia, which is a lack of blood flow to the brain, is a medical emergency. When ischemia is present the goal is to prevent further ischemia by giving medicine to decrease the blood clot from forming, propagating and embolizing.

[76] Transient ischemic attacks occur when symptoms are temporary and go away on their own. A stroke occurs when there is a persistent injury resulting in death of tissue. The symptomology of stroke depends on the area of the brain affected and the functions controlled by that area.

[77] In terms of diagnosing a vertebral artery dissection, Dr. Caplan explained that if a patient, like Mr. Johnson, presents with a headache and stiff neck following a recent visit to a chiropractor, a likely vertebral artery dissection is “a pretty easy clinical diagnosis” based on the history of movement and the pain. As well, when a patient has ischemia and they present with dizziness, visual loss, double vision, or altered balance, which are symptoms related to an interruption of blood supply in the back of the brain, the issue is with the vertebral artery.

[78] In terms of the role of imaging with respect to the diagnosis of stroke, Dr. Caplan explained that the first step is to obtain an image of the brain, through either a CT scan or an MRI image. Abnormal areas shown in these images suggest the presence of dead tissue or stroke. Based on the area of the brain affected, doctors then focus on the arteries or vessels supplying blood to the area.

[79] Vessel imaging is done in three ways. A CT angiogram involves the use of IV dye and a CT scan. The dye travels through the blood vessels and can show if a vessel is narrowed, open or blocked. An MRI angiogram can be used to show areas of blood pooling. Lastly, vessels can also be catheterized for a digital subtraction angiogram.

[80] Sometimes the dissection itself can show on imaging and is commonly seen as a narrowing or blockage of the vessel. An intimal flap may also be seen when the intima or media is torn. In most cases, it is more difficult to actually see the lumen, but a doctor will be able to see if the lumen has been compromised.

(ii) Treatment of Stroke

[81] In terms of treatment, Dr. Caplan explained that there are two classes of antithrombotic treatment aimed at treating thrombus or blood clots within the circulatory system. These are anticoagulants and antiplatelets.

[82] Blood clots form through either the extrinsic or intrinsic clotting system. In terms of the extrinsic clotting system, where an artery has “rough spots” of plaque, platelets tend to stick or adhere to the wall of the artery and aggregate to form a clot that looks white. The platelet material is composed of platelets and fibrinogen, and it secretes a substance that promotes red blood cells to form along the clot and block the blood vessel. In order to prevent clots where there is irregular plaque within an artery, an agent such as Aspirin or Plavix is used. These agents, and others like them, are known to inhibit platelet activation and aggregation and prevent clots from forming.

[83] The second type of clot is often called a red clot, and it is composed mainly of red blood cells and thrombus resulting from the intrinsic system of circulating proteins within the blood which coagulate and form a clot. This occurs where there is stagnation or lack of blood flow. The blood sits and the system is activated, forming a clot. Anticoagulants such as Heparin or Warfarin are used to prevent red clots from forming. Anticoagulants work on the body’s vitamin K system. They prevent a clot from forming and also prevent a clot from spreading and adding new clot to its borders.

[84] When asked how a doctor might choose between therapies, Dr. Caplan explained that the first step would be to diagnose the patient to obtain all the necessary information in order to properly characterize what happened. Next, the doctor would try to find a randomized trial which included details matching the specific patient. Where the study proves that one treatment is better than another, the doctor would adhere to that treatment. However, in most circumstances, randomized trials do not provide an answer, in which case the doctor would consider what is known about the condition and treatment and the patient’s individual details, and then try to choose the treatment that seemed most appropriate.

[85] In cases of an arterial dissection, a red blood clot is formed, either from the lumen or from within the lumen. Platelets are not as active in such a scenario. The more logical treatment is an anticoagulant which will prevent the formation of a new clot or embolization from that clot. According to Dr. Caplan, the majority of neurologists, especially stroke neurologists, will treat with anticoagulants. Some use the newer anticoagulants and others continue to use Heparin and Warfarin.

[86] Dr. Caplan also explained that in cases of vertebral artery dissection resulting in a luminal clot, treatment with anticoagulants should start as soon as possible. Where vertebral artery dissection does not result in a luminal clot, the lumen is uncompromised and the usual treatment involves antiplatelet therapy.

[87] In terms of the efficacy of anticoagulant therapy, Dr. Caplan noted that in his experience, he could not recall a single case where a patient, having presented with a stroke or compromised lumen and then treated early with anticoagulant therapy, went on to suffer a further stroke.

(iii) The Cause of Mr. Johnson’s Stroke

[88] In relation specifically to Mr. Johnson’s chronology of presentation, Dr. Caplan noted that chiropractic treatment is a common cause of vertebral artery dissection. Dr. Caplan noted that Mr. Johnson’s MRA image showed the location of the dissection or blockage to be near the origin of the left vertebral artery, which originates from the subclavian artery and goes into the vertebral column. The blockage in this case occurred in the first part of the artery before the artery enters the vertebral column. Given its location, the dissection would be described as an extracranial dissection.

[89] In terms of the initial CT scan which revealed a hypodensity within the right occipital lobe indicative of an acute ischemic stroke, Dr. Caplan explained that Mr. Johnson had a clot in the lumen of the vertebral artery. When clots initially form, they are not adherent and can easily break off. With time, clots become more adherent and strokes do not occur.

[90] In Dr. Caplan’s view, the infarct in Mr. Johnson’s case was caused by an embolism. A red blood clot began in the neck where the dissection was. The clot went to vertebral artery inside the head, where it caused a lack of blood flow to the cerebellum resulting in an infarct in the cerebellum. A piece of that clot travelled up to the visceral artery to the posterior cerebral artery where it caused an infarct in the occipital lobe.

[91] According to Dr. Caplan, the only way for this to happen would be an embolus breaking off and temporarily blocking the vertebral artery intracranially inside the head, and then going upstream to the posterior cerebral artery. Dr. Caplan also explained that there may be some complementary function as a result of decreased blood flow. A normal vessel has high blood flow that helps wash out the embolus through the system. When a vessel is blocked, the embolus does not get pushed forward. The fact that the blood vessel was blocked at the neck would have impeded clearance of the embolism.

[92] Dr. Caplan explained that hemodynamic ischemia occurs where an arterial blockage in the neck region results in decreased blood flow, which causes other blood vessels to dilate in order to compensate. Where a local blood vessel is blocked, the blood supply is not restored and an infarct may nonetheless occur.

[93] Dr. Caplan explained that the size of infarct observed would only be caused by an embolism, though it would have been complemented by hemodynamic ischemia resulting from reduced blood flow. Mr. Johnson’s stroke was not purely hemodynamic.

(iv) Mr. Johnson’s Treatment

[94] Dr. Caplan observed that on admission to hospital on October 18, 2012, Mr. Johnson was assessed by a hospitalist and an ischemic stroke protocol was initiated. Mr. Johnson received a loading dose of Plavix, Heparin and Aspirin. Dr. Caplan explained that an ischemic stroke protocol involves various forms of imaging used to determine whether, and if so where a stroke has occurred, including the possible source or origin of the embolus.

[95] Dr. Caplan was asked about Mr. Johnson’s October 29, 2012 visit with his family physician, Dr. Bolger, which resulted in Dr. Bolger reviewing the MRA report and contacting Dr. Crisp. This visit concluded with Dr. Bolger instructing Mr. Johnson to return to hospital immediately to start Heparin. As set out in Dr. Bolger’s notes, “Dr. Crisp felt should never have been discharged and needs to return to LHO immediately for heparin x 1 week.”

[96] Based on this note, Dr. Caplan was asked to assume that Dr. Crisp’s view was that Mr. Johnson had been discharged prematurely and that he should have been administered Heparin prior to discharge.

[97] Following the meeting with Dr. Bolger on October 29, 2012, Mr. Johnson was readmitted to hospital where he was seen by Dr. Chong who stated the following in his treatment note:

This patient likely had a dissection with thrombous and then stroke. He’s actually about day 11 post acute event, and the benefit of intensifying his antithrombotic in this setting is actually controversial -- the few studies that do exist suggest that antiplatelet and anticoagulation are equivalent in the setting of cervical artery dissection, although most people do still anticoagulant for a variable length of time. I actually think a wide range of antithrombotic approaches at this stage would be within standard of care given the current evidence base, including just ongoing antiplatelet agents to full anticoagulation for 6 months. This was discussed with the patient and he has elected for the most aggressive approach which will be hospitalization for IV hpearin [sic] overlapped with warfarin.

[98] Dr. Caplan was asked about his understanding of the “controversy” referred to in Dr. Chong’s note. He stated that the controversy is about the best treatment as between antiplatelet and anticoagulant therapy. Dr. Caplan explained that the controversy has not been completely settled by randomized trials. Anticoagulants require more monitoring, more treatment including the use of Coumadin, and there is a higher risk of bleeding than with antiplatelet drugs.

[99] According to Dr. Caplan, the issue is “do you use an agent that is less likely to cause bleeding, but may be less effective, or an agent that is more effective, but may have a little bit more risk?” The answer is a matter of experience and is not universal. Not every doctor would use anticoagulant therapy. That said, Dr. Caplan noted that Mr. Johnson’s preference as expressed to Dr. Chong was to start the most aggressive therapy which was anticoagulation with Heparin and Warfarin.

(v) The CADISS Non-Randomized Study

[100] The CADISS Non-randomized study is a stroke study done in the United Kingdom and Australia on patients with carotid and vertebral artery dissections who were treated with either antiplatelets or anticoagulants. The trial results were not statistically significant. According to Dr. Caplan, there were too few cases involved in the study and it was not possible to ascertain whether there was any statistically significant difference between the treatments. There were very few strokes in the patient group entered in the study. Three patients on antiplatelet therapy had strokes and one patient on anticoagulant therapy had a stroke. However, given the limited number of people in the study, these results were not significant.

[101] Dr. Caplan wrote a letter to the editor of the Journal of Neurology expressing his view that the results of the CADISS study were not useful in considering acute treatment for patients with cervical artery dissection. Dr. Caplan explained that the CADISS study was not definitive, the entry criteria included patients who had dissections of the outer wall of the artery as opposed to the lumen, and the study involved patients who had had treatment started relatively late.

(vi) Dr. Caplan’s Opinion on Causation

[102] Dr. Caplan opined that if Mr. Johnson had not been discharged on October 23, 2012, and had been placed on anticoagulation therapy, he would not have had the second stroke and resulting disability. He explained,

Well, it certainly takes time sometimes for a clot to develop and the earlier you treat, the better. So if it takes a little bit of time to titrate, to get the treatment in the, in the appropriate level, targeted level, so that the earlier you treat, the better. So if, if the stroke did not occur for days after he was discharged from the hospital, had he been treated in the hospital, the anticoagulation, in my opinion, would have prevented a new clot from forming and embolizing and would have prevented the second stroke which was the one that led to the major disability, the surgery that was decompressive and his, his secondary problems.

[103] Contrary to Dr. Gladstone’s view, Dr. Caplan believed there would have been minimal risk to starting anticoagulation therapy during Mr. Johnson’s initial admission in hospital. Dr. Caplan noted that anticoagulation therapy has an increased risk of bleeding. That said, he opined that had Mr. Johnson been placed on anticoagulant therapy on October 22 or 23, 2012, he likely would not have experienced any bleeding complications. In his view, the risk of bleeding is very rare and if there is bleeding, it is usually not into the brain. Instead, the bleeding can be urinary or some other mild bleeding or bruising. Essentially, the risk of bleeding is theoretical.

(vii) Cross-Examination

[104] Dr. Caplan prepared two reports, a main report dated February 21, 2019, and a second report dated January 2, 2020, responding to Dr. Gladstone’s report. Dr. Caplan agreed that it was good practice in a report to set out the material reviewed in preparation of the report, though he agreed that he did not do so in this case. Nonetheless, he explained that he reviewed the hospital records and related imaging, though he could not specify which exact records he reviewed. He also acknowledged that when preparing his first report, he did not have any of the discovery transcripts which included evidence from Mr. Johnson, his family members and doctors.

[105] In terms of his first report, Dr. Caplan included a brief review of the essential facts which were set out in two paragraphs. Dr. Caplan agreed that he was initially asked to opine on the appropriateness of the overall treatment provided to Mr. Johnson, and not specifically the treatment provided by Dr. Vieira.

[106] When it was suggested to Dr. Caplan that his brief review of the essential facts contained some errors, he replied:

I don’t think there are errors. I think there are some omissions if that’s what you mean. There’s some things that you would want. Let me, let me be honest with you. I was asked at this time what my opinion was. I was under the impression that the courts are interested in truth, not just artificially every detail or every word that’s in a report. I would hope that that’s what the court is involved with, not just artificially looking just at a report, but looking at what the truth of the case is.

[107] Dr. Caplan ultimately acknowledged that his summary of the essential facts contained some errors and omissions, such as the date of the massage session the day following the chiropractic visit of October 15 and the fact that the imaging done on October 31 was a CT scan and not an MRI. Dr. Caplan agreed that Mr. Johnson did receive a subcutaneous dose of Heparin upon admission but explained that this form of Heparin treatment was geared towards preventing blood clots in the legs and not blood clots in the head.

[108] Dr. Caplan also agreed that Mr. Johnson was initially treated with 81 mgs of Aspirin starting on October 19, 2012, and carrying on to October 29, 2012. When asked whether Aspirin was an appropriate antiplatelet agent, Dr. Caplan stated, “That’s one that’s used, yes.” When asked if the dose of Aspirin was appropriate, Dr. Caplan noted that he was “very critical” of 81 mgs of Aspirin as an appropriate dose.

[109] Dr. Caplan explained that once a person has had a stroke, there would be concern over the initial stroke worsening and then a new stroke developing. In terms of a stroke worsening, Dr. Caplan noted that a lesion in the brain could develop edema resulting in the worsening of the stroke. Alternatively, a patient could get worse as a result of complications that are unrelated directly to the stroke. Dr. Caplan agreed that 25-35% of stroke patients would experience stroke worsening in the first few hours or days after the onset of the stroke. After the first few hours or days, the clot would tend to harden and the risk of worsening would decrease.

[110] In terms of a new stroke occurring, Dr. Caplan agreed that it would result from a different embolism, though it could occur near the location of the initial stroke. Dr. Caplan agreed that new stroke was different than a stroke worsening. Dr. Caplan agreed that the medication provided following an initial stroke, either antiplatelet or anticoagulation, is given in order prevent a new stroke from occurring.

[111] In terms of Mr. Johnson specifically, Dr. Caplan agreed that Mr. Johnson did not have a second stroke prior to being discharged, nor had he had a stroke upon returning to hospital on October 29, 2012.

[112] Dr. Caplan was asked specifically about his initial report, wherein he opined that if Mr. Johnson had been given Heparin followed by Warfarin during his October 19- 23, 2012 hospitalization, “the stroke worsening that he developed would not have developed.” Dr. Caplan agreed that he did not know whether Dr. Vieira was involved in Mr. Johnson’s treatment on October 19, 20, 21 and possibly 22.

[113] Dr. Caplan was asked about the entry in his report noting that when Mr. Johnson was discharged on October 23, 2012, he was prescribed 5 mgs of Crestor and 81 mgs of Aspirin daily. He agreed that these were not the only medications that Mr. Johnson was taking at the time. He also had medications for diabetes and for high blood pressure.

[114] Dr. Caplan agreed that Mr. Johnson suffered a second stroke on October 30, 2012, and further agreed that his initial report makes no mention of the second stroke. When asked whether this was something that he did not appreciate when writing his initial report, Dr. Caplan explained that the imaging actually showed a second stroke. He stated, “And I think I knew that he did have a new stroke on, on the 30^th. I don’t actually say that in words in the report, mea culpa. But the report is, is just, you’re being picayune.” Dr. Caplan then agreed that the fact that Mr. Johnson suffered a second stroke was a major fact in this case.

[115] Nonetheless, Dr. Caplan agreed that he failed to mention a second stroke in his initial report and instead described it as a “stroke worsening.” He further confirmed that there is distinction between a “stroke worsening” and a “second stroke.” He agreed that he had actually authored articles on “stroke worsening” and the concept was addressed in his textbook. When pressed on this issue, Dr. Caplan denied that he wrote his report flippantly or casually. He maintained that it would have been preferrable if he described the later occurrence as a second stroke and agreed that as written, the last sentence of his first report was incorrect. He agreed that in his second report he correctly noted that Mr. Johnson had suffered a second stroke, but denied that this change in his report was caused by his review of Dr. Gladstone’s report.

[116] Dr. Caplan was cross-examined about the CADISS study. He agreed that it was the only study he cited in his report and further agreed that it did not support his opinion. While he explained that he usually does not cite literature and studies in his reports, he knew that the CADISS study would come up in this case and therefore addressed it.

[117] When asked whether he could have done a literature review in preparation for his report, the following exchange occurred:

Q. So, so let me put it this way, just coming back to my point, a very simple one. You could have done a literature search in 2019 before you wrote this report, right?

A. I could have done a lot of things, sure, I could have come to Canada, I could have done anything before that. I didn’t think it was necessary.

Q. And you were too busy to do it?

A. I don’t know if I was too busy. I don’t remember what February was at that time. There are things in the report I could have done better that you’re very astute at pointing out. But what we’re at today is to try to get to the truth of what I think now. That’s the key for this case.

[118] Nonetheless, Dr. Caplan maintained that he had a familiarity with the literature on the issue and would have been current based on his involvement on the editorial boards of various medical journals.

[119] Dr. Caplan was asked whether he knew that the stroke guidelines in Canada, the United States and Europe, did not support his opinion on the use of anticoagulant therapy. He replied, “They don’t support any opinion” and explained that the guidelines do not conclusively clarify what the optimum treatment is. When pressed, Dr. Caplan agreed that the guidelines do not say that Heparin is better than Aspirin. However, he went on to explain that the guidelines are general in nature and there is insufficient data available to support a firm opinion on the issue.

[120] In his initial report, Dr. Caplan referenced the CADISS study and also referenced a letter he wrote to the Neurology Journal offering a critique. In cross-examination, he acknowledged that his letter did not relate to the later randomized CADISS study, but rather the CADISS-NR or non-randomized trial. His letter to the editor was published in 2013 and the final results of the CADISS randomized study were only released in 2019, though the results were available as of 2015. Dr. Caplan explained that his letter to the editor was based on the information he had available at the time he wrote the letter.

[121] Dr. Caplan’s letter to the editor regarding the CADISS-NR study received a reply from Dr. Markus, a noted colleague and friend of Dr. Caplan. Dr. Markus noted that Dr. Caplan’s comments regarding the timing of patient entry into the study was valid and went on to note that the ongoing randomized arm of the CADISS would be recruiting patients within seven days of symptom onset. Dr. Markus also noted that the non-randomized arm of the CADISS study included patients who would be ineligible for the randomized arm. Dr. Markus concluded his letter by noting “…whether anticoagulants or antiplatelets will be more effective during the acute phase can only be answered by randomized trials such as CADISS.” Dr. Caplan agreed that the purpose of his letter to the editor was to express his view that the treatment times for the non-randomized arm were not within the acute phase. In his view, the non-randomized arm of the study did not answer the question in relation to the preferred treatment of patients during the acute phase.

[122] In terms of the CADISS randomized study, Dr. Caplan agreed that the purpose of the study was to determine the recurrent stroke risk after carotid and vertebral artery dissection and whether antiplatelets or anticoagulants are more effective at reducing this risk. Dr. Caplan agreed that the CADISS study showed no difference between anticoagulant and anti-platelet therapy. The data on the study showed a low rate of stroke recurrence, approximately 2.5% in the per protocol (PPP) population, and approximately 2.4% in the intention to treat (ITT) population included in the study. Dr. Caplan noted, however, that the 2.5% recurrence rate did not include patients who had a recurrent stroke before treatment was started, and the patients in the study were not admitted to the study immediately after their first stroke.

[123] Nonetheless, Dr. Caplan agreed that Mr. Johnson met the inclusion criteria for the CADISS study and did not meet any of the exclusion criteria. As a result, to the extent that the CADISS study generated any data, that data would have applied directly to Mr. Johnson. Dr. Caplan agreed that the study suggested that the stroke recurrence rate was quite low. He agreed that the patients in the study were randomized into either antiplatelet or anticoagulant therapy groups, though he noted that the specific type of antiplatelet therapy was not defined or limited to treatment with 81 mgs of Aspirin. In fact, he noted that less than 22% of the antiplatelet group patients were treated with only Aspirin.

[124] When asked about the CADISS study’s conclusion that there was no evidence that antiplatelets or anticoagulants were more effective at reducing the risk of recurrent stroke, Dr. Caplan explained that this conclusion was reached because there was insufficient data. In other words, given the absence of sufficient data points, there was no definitive conclusion from the study.

[125] Dr. Caplan agreed that the results of the CADISS study were consistent with the findings of the CADISS-NR study. Dr. Caplan also agreed that there were “lots of other studies” comparing anticoagulant and antiplatelet therapy, including meta-analyses of world-wide literature, though he noted that these studies found that there were not enough end points in the statistics from which it was possible to make a definitive conclusion. He also noted that while anticoagulants were considered to present a higher risk of bleeding in the literature, that increased risk was not borne out statistically.

[126] The following exchange then occurred:

Q. And again to the extent that there is an extensive body of literature comparing these two treatments, you didn’t cite anything in support of what you are saying, do you agree?

A. No, I don’t agree. I think that’s a very global statement so if you look at the references that I’ve just told you about Schievink, there are other people that I have consulted and there are other surveys that have got, but I, I didn’t cite the world literature on this. I just cited my opinion, that’s what I was asked, what is my opinion. I didn’t go through the world literature about it.

And further on:

Q. So all of the literature worldwide which shows no difference between Heparin and Aspirin should be rejected in favour of your personal view, right?

A. No, I, what I said in the direct and let me just get back to it. I said what do you do if there aren’t trials that have a definitive answer? Actually, as the editor of the European Journal of Neurology, I ask people about that. So then you go on what you know about the condition, what you know about the results from you and from everybody else and then what the treatment is likely to do. You have to make a choice. You can’t say because ‘There’s no evidence-based trial, I’m not going to treat the patient.’ You have to make a decision and you make a decision based on a lot of factors. That individual patient, they’re druthers, what you’ve experienced, what other people experience, what you’ve read about. So you make a decision, you, there, most people that we see, there is not evidence-based trials that report a definitive answer.

[127] Dr. Caplan went on to express his views on the limitations of evidence-based medicine. He explained that in cases where he could recognize a patient in a trial, and where the trial had enough cases to provide a statistically relevant result, the advice of the trial should be followed. But, he noted, this was not possible in most cases. In his view, the CADISS trial failed to provide a definitive answer because “they didn’t get enough cases with end points.” Dr. Caplan maintained that his proposition was not that Heparin was better than Aspirin for all patients with vertebral artery dissections. Rather, he was saying that Heparin would have been better than Aspirin for Mr. Johnson when he was treated.

[128] The following conclusion from the CADISS randomized study was put to Dr. Caplan:

However, the low number of end points means that a very large sample size with many thousands would be required to detect the treatment difference between the two therapies, but the low rate of events suggest that any absolute effect on outcome even if, for example, there was a 25 percent reduction in risk would be very low.

[129] Dr. Caplan agreed with the conclusion and noted that a very large sample would be required in order to determine whether one therapy was better than the other. He noted that with rare illnesses, this was one of the limitations of evidence-based medicine. He also agreed that based on the low rate of events observed in CADISS, even if there were thousands of cases in a study the absolute effect on outcome would be very low. He agreed that it was possible that with thousands of cases, Heparin might be shown to be 5-10% better than Aspirin. However, he explained that even if that is what a study might show, it would still need to be “translated” to the individual patient. In other words, a doctor would still need to consider what the best treatment would be for a specific patient at a specific time. In fact, even if there was a clear difference between the treatments, it would not automatically mean that every individual patient would receive the leading treatment. It would depend on specific factors relating to the individual patient, including the patient’s own treatment choice.

[130] Dr. Caplan agreed that a second randomized study, TREAT-CAD, also examined treatments for vertebral artery dissections. When it was suggested to him that the TREAT-CAD study did not support his opinion, he replied, “It doesn’t come to any conclusion.” He explained that the study was inconclusive as there were not enough cases to get a statistically significant response.

[131] Dr. Caplan was shown the 2021 American Heart Association, American Stroke Association (AHA/ASA) guidelines for the Prevention of Stroke in Patients with Stroke and Transient Ischemic Attacks. He agreed that this guideline was authoritative and was used throughout the United States and in other parts of the world. Dr. Caplan explained that guidelines provide general rules that are mostly evidence based. He agreed that the guidelines set out various classes or strengths of recommendations as well as various levels signifying the quality of the evidence supporting the recommendations. In the section dealing with artery dissections, the AHA/ASA guidelines cite the CADISS study and note that the study “supports that there is equipoise between antiplatelets and anticoagulants in the first three months after a cervical artery dissection.” While Dr. Caplan agreed that this was the current guideline, he re-iterated that guidelines were simply general in nature. He agreed that the recommendation to treat with antithrombotic therapy was based on a consensus of expert opinion, which is the lowest evidentiary level used in the guidelines. In terms of the recommendation that in patients with ischemic stroke or transient ischemic attacks who are less than three months from arterial dissection it is reasonable to use either Aspirin or Warfarin to prevent recurrent stroke or transient ischemic attack, Dr. Caplan agreed that the evidentiary level was the second highest level of “Moderate quality of evidence from one or more randomize controlled trials.” He went on to state, “Reasonable, but not necessarily optimal, depending on the individual patient.” He explained that “reasonable” means that a doctor would use “reason” to consider which treatment was best. He also noted that the recommendation said nothing about the dose of Aspirin to be administered, nor did it give any details about the patient which the doctor would need to consider.

[132] Dr. Caplan agreed that his approach would be to determine the “optimal treatment” for the patient and that this is the approach he adopted in his second report on this matter. He agreed that if the evidence clearly suggested that one treatment was better than another, the preferred treatment would be the standard of care, subject to specific issues relating to the individual patient. Dr. Caplan reiterated that the guidelines were of limited relevance in determining which treatment would be optimal for a specific patient.

[133] Dr. Caplan was next asked about the AHA/ASA recommendations for the use of antithrombotic medications in secondary stroke prevention, which are not recommendations specific to dissection. The recommendations suggest the use of antiplatelet over anticoagulation therapy for minimizing the risk of bleeding and for secondary prevention of ischemic stroke in patients with non-cardioembolic ischemic stroke. These specific recommendations were supported by the highest level of evidence. Dr. Caplan agreed with these recommendations as general statements but explained that they would not assist in determining the specific treatment for Mr. Johnson. He described the recommendations as “irrelevant.”

[134] In terms of the Canadian Stroke guidelines published in the Canadian Journal of Neurological Sciences, Dr. Caplan agreed that they are authoritative and acknowledged the recommendation for antithrombotic therapy for individuals with a diagnosis of an acute or recent extracranial carotid or vertebral artery dissection. Dr. Caplan was then directed to the comment in the section dealing with Cervicocephalic Artery Dissection which states “there is an uncertainty about the comparative efficacy of antiplatelet therapy versus anticoagulation with Heparin or Warfarin.” Dr. Caplan agreed with this comment as a general statement. He also noted that unlike the AHA/ASA guidelines, the Canadian guideline did not specifically relate to the use of Aspirin but used the more general description “antiplatelet therapy.” Dr. Caplan also noted that the guideline directed doctors to make decisions “based on an individual risk/benefit analysis taking into consideration the imaging features of the dissection (presence and degree of stenosis, intraluminal thrombus, vessel occlusion, pseudoaneurysm), brain imaging, patient characteristics, and estimated bleeding risk.” In other words, the doctor would need to consider the individual details in the individual patient.

[135] Dr. Caplan was next shown the European Stroke Organization’s (ESO) guideline for the management of extracranial and intracranial artery dissection, published in the European Stroke Journal in 2021. Dr. Caplan agreed that these guidelines were based on a thorough analysis of literature including two randomized controlled trials (CADISS and TREAT-CAD), and 26 comparative observational studies. He agreed that these guidelines strongly recommend, based on evidence that has shown no difference between the benefits and risk of anticoagulants versus antiplatelets in the acute phase, that clinicians can provide either treatment option.

[136] Ultimately, Dr. Caplan agreed that all of the guidelines come to the conclusion that there exists no scientific evidence-based medicine that “would allow you on statistical evidence in trials to chose one over the other.” However, he also offered the following view:

I don’t think they’re relevant to a doctor choosing optimal treatment for this specific patient or any specific patient in general. They -- they -- we treat individual people. These are general rules which are – are reviewing what the evidence is. They’ve tried to be educational and educate people about treatment. If there is treatment that has been shown by the trials, it’s generally recommended, and then the doctor has to use his own judgment, knowing what he knows about the patient, about the patient’s background, about the patient’s disease, about the patient’s risk, about the patient’s druthers as what treatment to use.

[137] The following exchange then took place:

Q. You don’t think CADDIS is relevant to Mr. Johnson’s case?

A. I don’t think it gives you an answer that would be very helpful in -- in treatment.

Q. You don’t think there’s any study in the world, no paper in the world that’s helpful in analyzing Mr. Johnson’s case, right?

A. No, I didn’t say that. You said that. I just said the opposite. I said there are lots of data – Schievink’s article is one, I have an article in Nature National Review that goes over dissections and what the mechanism is, what the vessels look like, what the mechanism of stroke is, what the type of clots are, and then the doctor has to take that general information and what he knows about the patient and the patient’s (indiscernible), and decide on what’s the best treatment for that patient, and weighing benefits and risk. I don’t think they would get that from this -- these documents that you’re showing. About the general guidelines are educational, but they don’t tell the doctor what to give the patient. They’re not useful in that regard.

Q. So, we talked about this this morning, but you cited no literature from the worldwide literature supporting the notion that Heparin should be preferred to Aspirin here, right?

A. I didn’t say any literature, I knew that the -- the CADISS trial would come up, and so I mentioned the CADISS trial in it, so that it would be -- it could be discussed. That’s the only reason I mention it. In the reports I give, I very rarely – they’re – they’re not meant to be for publication in a -- in a medical journal. They’re meant to be reports about my opinion in the case. And that’s what I wrote in the reports, what my opinion was. You can take it or leave it, but that’s – that’s what I was asked to do.

Q. And you believe that your personal opinion should be preferred over the worldwide literature on the subject?

A. No, I didn’t give my -- my opinions about general treatment. All I gave my opinions about what I think would -- if -- if the patient had been given Heparin, my opinion was that he would not have developed a second stroke. That was my opinion. I didn’t say that everybody should get it. I’m just saying that if he had begotten it, that’s what the patient wanted, that’s what his neurologist wanted, if had gotten the treatment that his neurologist wanted and the patient wanted, I don’t think he would have had the second stroke. That was my opinion. I’m not offering suggestions for every patient or every doctor as to what to give to every patient. I’m just saying what the opinions were about Mr. Johnson. And that is not relevant in these guidelines.

[138] Dr. Caplan was asked about an article he co-authored in 1999 that was published in the Journal of Neurological Sciences. The article was called, “Heparin and oral anticoagulants in the treatment of brain ischemia.” In the first paragraph of the article, Dr. Caplan wrote, “The use of anticoagulants in the treatment of stroke is still a matter of debate. The benefit of Heparin in the acute phase of stroke and transient ischemic attacks remains unclear, despite its widespread use in both conditions.” The article also refers to an early survey of neurologists in the United States, which documented widespread use of Heparin in patients with acute stroke but also uncertainty regarding its efficacy and safety. Dr. Caplan noted he was also aware of a more recent survey wherein the majority of doctors prescribed anticoagulants. He did not cite the survey, nor could he recall specifics of the survey.

[139] In terms of Dr. Gladstone, Dr. Caplan agreed that he is a well-known and respected expert in the field of stroke medicine. He acknowledged that Dr. Gladstone is the Director of the Regional Stroke Centre at Sunnybrook Hospital, which is a leading stroke centre in Canada. He also acknowledged that Dr. Gladstone’s reports are well considered, thoughtful, well researched and well written. He offered that Dr. Gladstone’s reports “are very evidence based”, while also noting “mine are not so much dedicated to evidence-based medicine.” He agreed that Dr. Gladstone’s opinions are serious opinions to be taken with great consideration, and that Dr. Gladstone gave attention to detail with respect to the facts of this case. Lastly, Dr. Caplan agreed that he had not noted anything wrong in Dr. Gladstone’s reports.

[140] Turning to Mr. Johnson’s case specifically, Dr. Caplan was directed to Dr. Crisp’s note of October 19, 2012, dictated on October 21, 2012. In this note, Dr. Crisp states that “The big diagnosis to rule out here of course is a dissection in the vertebrobasilar system due to chiropractic adjustments.” Dr. Caplan agreed that he did not know when Dr. Crisp would have formed this opinion, but he believed it would have been when he first saw Mr. Johnson on October 19, 2012.

[141] Dr. Caplan reiterated his opinion that if Mr. Johnson had been given Heparin during his hospitalization between October 19 to 23, 2012, followed by Warfarin, he would not have had the new stroke. He clarified that as a matter of standard of care, some prudent doctors would have given Heparin and some prudent doctors would have given Aspirin or double antiplatelets. He explained, “I couldn’t argue with you that was against the standard of care. That’s really different than saying what was the best treatment or would that treatment have worked.”

[142] Dr. Caplan agreed that between October 19 and 23, Mr. Johnson was given Aspirin and this care did not fall below the required standard of care. He also agreed that Dr. Crisp’s note of October 21, 2012, makes no mention of anticoagulants. It only mentions antiplatelets. As such, it appeared to Dr. Caplan that Dr. Crisp was waiting on test results to suggest further treatment.

[143] Dr. Caplan was also taken to Dr. Chong’s note dated October 29, 2012, which was taken at the time of Mr. Johnson’s re-admission to hospital. In the note, Dr. Chong writes:

This patient likely had a dissection with thrombosis and then stroke. He’s actually about day 11 post acute event, and the benefit of intensifying his antithrombotic in this setting is actually quite controversial -- the few studies that do exist suggest that antiplatelet and anticoagulation are equivalent in the setting of cervical artery dissection, although most people do still anticoagulate for a variable length of time.

[144] Dr. Caplan agreed that what Dr. Chong wrote in his note was correct. That said, he also noted that Dr. Chong memorialized Mr. Johnson’s decision to elect for the most aggressive approach which was hospitalization for IV Heparin overlapped with Warfarin.

[145] In terms of the timing of Mr. Johnson’s stroke, Dr. Caplan indicated his belief that the arterial dissection occurred during the chiropractic adjustment on October 15, 2012. Mr. Johnson presented at hospital on October 17, 2012, showing symptoms of a stroke. In his view, the actual stroke occurred at some point in between October 15 and 17, 2012. The stroke was moderately large and very significant. Dr. Caplan agreed that the acute phase would last seven days, and he further agreed that Mr. Johnson had no new stroke prior to October 24 which would have been the end of the acute phase. The second stroke occurred 13 days later on October 30, 2012. Dr. Caplan did not agree that the Aspirin prevented a second stroke during the acute phase, though he agreed that Mr. Johnson was taking Aspirin during this time and did not suffer a second stroke until later.

[146] When asked about the appropriate timing of anticoagulation therapy, Dr. Caplan agreed that a doctor would need to be careful as to when to start anticoagulation therapy on a patient who had an ischemic stroke. He explained that the appropriate start time of such therapy would depend on the size of the infarct. Where the infarct was large, the risk of bleeding is higher so the doctor would have to weigh the benefits of the therapy versus the risk. Depending on the patient, a doctor might decide to not start anticoagulation right away. In order to make this assessment, the doctor would look at imaging of the patient to see if there was an infarct and also whether there was related hemorrhagic transformation. In Mr. Johnson’s case, there was no evidence of hemorrhage in relation to his first stroke.

[147] Dr. Caplan was asked whether he agreed with the following proposition, which was taken from the Canadian Stroke Best Practices guideline: “The optimal timing to start anticoagulation therapy after an ischemic stroke has not yet been well-defined by the clinical trial evidence.” Dr. Caplan explained that he could not really answer the question as it would be hard to devise a clinical trial that provided an answer. Dr. Caplan did agree with the guideline recommendation that the optimal timing of anticoagulation therapy should be based on an individual benefit/risk assessment, taking into account the clinical circumstances, stroke severity, infarct size, imaging appearances, risk of hemorrhagic transformation and estimated stroke recurrence risk.

[148] Dr. Caplan was also asked about the Canadian Stroke Best Practice guideline recommendations for the commencement of anticoagulation therapy, which provide as follows:

a. For patients with a brief transient ischemic attack and no visible infarct or hemorrhage on imaging, anticoagulation may be started with the first 24 hours;

b. For patients with a minor clinical stroke, small non-hemorrhagic infarct on imaging, anticoagulation may be started three days post-stroke;

c. For patients with moderate clinical stroke, moderate sized infarct on imaging, without hemorrhage on CT, anticoagulation may be started six to seven days post- stroke; and,

d. For patients with a severe clinical stroke, large size infarct on imaging, without hemorrhage on CT, anticoagulation may be started 12 to 14 days post-stroke.

[149] Dr. Caplan explained that these recommendations were very general statements that set out a general approach to timing. However, in his view, these recommendations were not very applicable. The timing of anticoagulation would depend on an assessment of a particular patient’s specific risk of re-embolization or re-developing a stroke. Dr. Caplan agreed that the larger the stroke, the greater the risk of hemorrhagic transformation. He further agreed that the risk of hemorrhagic transformation would be a factor causing a doctor to be careful in commencing anticoagulation therapy. This is because anticoagulation therapy carries a greater risk of bleeding when compared with antiplatelet therapy.

[150] In relation specifically to Mr. Johnson, Dr. Caplan described Mr. Johnson’s infarct as relatively small, and he would have placed him in the group of patients for whom anticoagulation therapy could commence immediately. Dr. Caplan agreed that the radiologist described Mr. Johnson’s stroke as “a large hypodensity.” Dr. Caplan was asked to assume that Mr. Johnson’s infarct was accurately described as large, and he was asked whether based on that assumption the commencement of anticoagulation therapy on October 29, 2012 conformed exactly with the Canadian Stroke Best Practices guidelines, which suggest a 12 day waiting period. He agreed, though he maintained that he would not describe Mr. Johnson’s infarct as large.

[151] When pressed on this issue, Dr. Caplan agreed that he did not specifically refer in his report to the CT scan done on October 18, 2012. He agreed that the radiologist describes a “large area of hypodensity” in this report, but he explains that the radiologist also states “there’s no space occupying lesion” which suggests that the infarction was not large. Dr. Caplan acknowledged that Dr. Gladstone included imaging and his interpretation of the imaging in his report. He did not disagree with Dr. Gladstone’s interpretation of the imaging.

[152] Dr. Caplan agreed that while there exists a difference of opinion as to which treatment should be given to which patients, his personal preference is anticoagulant therapy. His view is that anticoagulants are useful in certain settings of ischemic stroke, though Heparin should not be given indiscriminately to all acute brain ischemia patients. He agreed that the efficacy of Heparin has been inadequately tested in patients with defined stroke subtypes and occlusive vascular lesions.

[153] Dr. Caplan also agreed that based on his knowledge of thromboembolism pathophysiology and his clinical knowledge, he accepts the theory that Heparin will prevent red thrombus development propagation in embolism. His view is that Heparin is useful in treating patients who have stenosis or occlusion of large arteries. Dr. Caplan acknowledged that he uses this theory in practice and advocates this approach in his writing, including an article titled “Resolved: Heparin May Be Useful in Selected Patients with Brain Ischemia”, published in a 2003 Stroke Journal. He also agreed that he advocated the same approach in a book chapter, Acute Ischemic Stroke, he co-authored in an international text called Neurological Disorders: Course and Treatment, 2^nd Ed. When taken to the portion of the chapter relating to thrombotic treatment, Dr. Caplan agreed that he described his approach as a “strategy” to be used “until the results of randomized trials are available…” He agreed that he described his method as “hypothetical” and the results as “anecdotal and have not been tested scientifically.”

[154] Dr. Caplan’s cross-examination ended with the following exchange:

Q. And so if I take all of those words together, the words that you use in your writings and that we’ve just gone through to talk about your approach and your opinion in this case, I’m going to give you some words and, and you agree with me if you can, but these are the words that you had attached to this approach. The first one is “eclectic”, you used that word, right?

A. Yes, it depends on the individual patient.

Q. “Personal”, yes?

A. Yes.

Q. “Strictly hypothetical”, yes?

A. Well, I mean, I think there is some, I wouldn’t use the word “strictly”, I’d use the word, “hypothetical.”

Q. “Anecdotal”?

A. Yes, meaning there are no definitive trials.

Q. “Not tested scientifically”?

A. Yes.

Q. “Theoretical”?

A. Yes.

Dr. David Gladstone

[155] Dr. Gladstone is the defendant’s expert. He too was qualified to give expert opinion evidence as a stroke neurologist with respect to the diagnosis and treatment of ischemic stroke generally including the diagnosis, treatment and likely outcomes related to vertebral artery dissection, including the impact and consequences of any delay in treatment.

[156] Dr. Gladstone is a leading neurologist at Sunnybrook Health Sciences Centre and a scientist at the Sunnybrook Research Institute. In addition to his medical degree, he has also completed a Ph.D. in stroke neurology. He has been a practising neurologist for over 20 years with a focus on stroke neurology. During the course of his practice, he has directly encountered approximately 150 patients with vertebral artery dissections. He has also been indirectly involved in more than 100 other cases of dissection. As a scientist, Dr. Gladstone’s main area of focus has been clinical trials in secondary stroke prevention and the cardiac causes of stroke. He has been involved in conducting various randomized trials as a principal investigator. He was a site investigator working committee participant on the Navigate ESUS study, which was a randomized trial that compared anticoagulant therapy versus Aspirin for secondary stroke prevention in patients with embolic ischemic strokes.

[157] Dr. Gladstone has written and lectured extensively. He was the chair of the committee that produced the updated Canadian Stroke Best Practices Recommendations, Secondary Prevention of Stroke Module in 2020, on behalf of the Heart and Stroke Foundation of Canada. He also co-chaired the committee when it updated the recommendations in 2017.

(i) Overview of Opinion

[158] At the outset of his evidence, Dr. Gladstone was asked to opine on the efficacy as between antiplatelet and anticoagulant therapy in preventing stroke recurrence in the setting of arterial dissection. He explained that the “bottom line” is that both anticoagulant and antiplatelet therapy seem to have similar efficacy for secondary stroke prevention in patients with vertebral or carotid artery dissection. He noted that the published scientific evidence has not demonstrated the superiority of one over the other and that the practice guidelines have reflected this fact.

[159] In terms of his high-level opinion in relation to Mr. Johnson, Dr. Gladstone explained that he did a very detailed review of the medical records in order to understand the facts of the case specific to Mr. Johnson. He also considered clinical features, imaging features and the chronology of events. Based on his assessment, Dr. Gladstone opined that the stroke Mr. Johnson suffered on October 30, 2012, is unlikely to have been prevented with earlier treatment of Heparin and Warfarin had it been started a few days earlier, on or about October 22, after the MRI and MRA scans were available.

[160] Dr. Gladstone provided three main reasons for his opinion:

a. Mr. Johnson had an extensive occlusion in his left vertebral artery from the bottom to near the top so that it was both an extracranial and intracranial occlusion. This is considered a high-risk lesion;

b. There was really not a viable window of opportunity timewise for which anticoagulant therapy would likely have helped the plaintiff. This is based on a detailed review of the time sequence of events from the suspected onset of the plaintiff’s dissection and PCA stroke on October 17, the MRI and MRA on October 22, to when the second stroke occurred on October 30. Treating before the MRI on October 22 was not an option for various reasons and treating on that date or beyond was too late to make a difference; and,

c. His knowledge of antithrombotic medications, their benefits, risks and limitations, his personal clinical experience in seeing patients similar to the plaintiff, and in seeing other patients who have recurrent strokes in spite of being treated with anticoagulant medications.

(ii) Details of Opinion

[161] During his evidence, Dr. Gladstone reviewed images of Mr. Johnson’s brain and neck. These images were selected from the images he reviewed in preparation of his report and were taken at the hospital on October 18, 22 and 31, 2012. He explained that brain tissue typically shows up as a grey appearance on a CT scan and strokes are a darker colour, e.g., dark grey or black. Dark areas are called hypodensities and they represent tissue that has died. He pointed to dark areas involving the occipital lobe and explained this was a hypodensity indicative of acute ischemic stroke.

[162] Dr. Gladstone noted that the imaging confirmed the diagnosis of an acute ischemic stroke affecting predominantly the right occipital lobe, and this is in the territory of the specific blood vessel called the posterior cerebral artery of the brain. He explained that this is a condition that he has seen in “hundreds and hundreds” of patients with this type of stroke. The most common cause is a blood clot that blocks the posterior cerebral artery and cuts off flow to that part of the brain. He noted, “this fits with an embolic stroke mechanism.”

[163] With reference to the CT scan, Dr. Gladstone noted that the imaging showed that Mr. Johnson had suffered two strokes; a large stroke in the right occipital lobe described as a posterior cerebral artery territory infarct and a small one in the left cerebellar hemisphere. He described the posterior cerebral artery infarct as a “sizeable” and not small infarct and noted that its size had implications for treatment.

[164] In Dr. Gladstone’s view, a patient with an infarct of that size and location could not be safely started on an anticoagulant right away. He explained that such a patient would be typically started on Aspirin as a first-line treatment for secondary stroke prevention. He further explained that starting too soon with an anticoagulant agent would increase the risk of bleeding into the fresh infarct.

[165] In relation to the MRI images taken on October 22, 2012, Dr. Gladstone explained that the posterior cerebral artery infarct could be seen clearly and appears larger than it had on the CT scan taken on October 18, 2012. He noted that he could see “some hint” of bleeding from leaky blood vessels, with the observable dark areas within the core of the infarct. He then stated, “So when I see scans that look like this in the hospital, I would be scared to start any anticoagulation therapy…”

[166] Taking into account the large size of the infarct and the imaging appearance, Dr. Gladstone opined that Mr. Johnson had an infarct that would be at a higher than average risk for hemorrhagic transformation that could become symptomatic. Based on the literature and his observations of other patients, Dr. Gladstone was of the view that Heparin would be risky if given early after an infarct of this nature. He stated, “So the, the bottom line that I’m trying to convey is that in the situation like this, we have to be extremely cautious if we’re contemplating using an anticoagulant medication like Heparin.” He also indicated that he has seen many patients deteriorate neurologically and has seen fatal brain hemorrhages from overly aggressive initiation of anticoagulant therapy too soon after an acute ischemic stroke.

[167] When asked about the likely timing of anticoagulation for Mr. Johnson, Dr. Gladstone noted that the American Heart Association guidelines in Acute Stroke Management suggest a wait of 14 days in cases where a patient is expected to be at high risk for hemorrhagic transformation.

[168] Dr. Gladstone reviewed the images showing the location of the vertebral artery dissection. He explained that when imaging evidence suggests a vertebral artery dissection, blood clot formations are the likely cause of the strokes. When the blood clots dislodge, they travel upstream through the blood, up the vertebral artery all the way to the posterior cerebral artery where they get stuck and block blood flow. This is referred to as a thromboembolic stroke mechanism.

[169] While Dr. Gladstone agreed with Dr. Caplan that this mechanism was the likely cause of Mr. Johnson’s initial stroke, he noted that Mr. Johnson had an occlusion of almost the entire length of his vertebral artery, both extracranially and intracranially. As such, Mr. Johnson was not only at risk of thromboembolic stroke but also hemodynamic type ischemia. According to Dr. Gladstone, this could explain the second stroke suffered by Mr. Johnson on October 30, 2012. Further, in view of the occlusion to the artery, giving Heparin would have been “too little, too late.”

[170] In relation to the MRA imaging taken on October 22, 2012, Dr. Gladstone explained that it provided a better look at the upper part of the vertebral arteries. He traced the right vertebral artery from the bottom of the image, going up and joining to form the basilar artery at the centre. He said the corresponding left vertebral artery was supposed to be shown in the image, but it was absent because of the occlusion so blood flow through it could not be seen.

[171] Dr. Gladstone added that vertebral artery dissections are often localized to one segment of the artery and the rest of the artery above is widely open with blood flowing. Mr. Johnson’s image shows evidence of a vertebral artery dissection near the bottom left of the vertebral artery that resulted in an occlusion nearly the entire length of the vertebral artery. This was actually two pathologies in addition to the acute PCA territory infarct.

[172] Dr. Gladstone noted that Mr. Johnson had been prescribed Crestor, Coversyl and Aspirin on initial discharge. Crestor and Coversyl are drugs administered as part of the standard protocol for secondary stroke prevention. Aspirin, 81 mgs daily, is an antiplatelet therapy that is the most commonly prescribed medication for secondary stroke prevention. It is guideline recommended, with the “highest level of guideline recommendations.” Dr. Gladstone noted that Mr. Johnson had, on admission, also received a loading dose of Plavix, which is another antiplatelet medication that is used for secondary stroke prevention.

[173] Regarding the cause of the second stroke on October 30, 2012, Dr. Gladstone opined that based on the CT images from October 31, 2012, the stroke was likely caused by vertebral artery occlusion that resulted from the dissection. It was not caused by a lack of Heparin or Warfarin.

[174] After Heparin was administered to Mr. Johnson, his blood was tested on a PTT scale. PTT means Partial Thromboplastin Time, which is a measurement of the time it takes for blood to clot and is a way of measuring IV Heparin dosing. Dosing is individualized and based on body weight and PTT results. If the PTT is too high, bleeding risk increases. If it is too low for too long, it does not have the maximum effect.

[175] With reference to the PTT values set out in an appendix to the agreed statement of fact, Dr. Gladstone explained that the target range for Mr. Johnson was between 50 and 70 on the PTT scale. Dr. Gladstone explained the dosing was like adjusting a volume dial. Mr. Johnson started at 23 on the PTT scale, which is within normal limits for someone not on an anticoagulant. Mr. Johnson then received a starting bolus dose of Heparin followed by a continuous infusion. On the evening of October 29, 2012, Mr. Johnson’s PTT levels were at 44 and the target was around 60.

[176] Dr. Gladstone explained that Mr. Johnson’s PTT levels began to rise, nearly doubling. At the time of the stroke, Mr. Johnson was not fully anticoagulated though he was at approximately “two thirds of the way to reaching the target of 60”.

[177] However, despite being treated with various medications including Plavix, daily Aspirin, and Heparin and Warfarin beginning on October 29, 2012, Mr. Johnson had a left cerebellar acute ischemic stroke.

[178] Dr. Gladstone concluded:

And so, despite all of that the stroke still happened. And when I said a bit, you know, too little, too late, in terms of the Heparin starting, that’s because it was after his MR angiogram was done on October the 22nd which already showed occlusion of his vertebral artery. The real best candidates for Heparin are the ones who have a dissection, but the artery is still open. It hasn’t yet occluded and you’re aiming to try to prevent the new clot formation that could then occlude the artery. And so, in order to have done that, it would have meant that, you know, his Heparin would have been started way before the MRI, MRA studies were done on October the 22nd. But that even wasn’t in the cards because his diagnosis of a dissection wasn’t made until October the 22nd on the MR angiogram. So, there was no medical indication for Heparin or Warfarin to have been prescribed before that date.

[179] Dr. Gladstone went on to explain that the PTT table shows that Heparin, even if it had been administered on October 22, 2012, does not work immediately and takes time to increase to the therapeutic range, sometimes days or hours. He explained that his group had recently published data on this based on an audit of his clinical experience at Sunnybrook. The data showed that it takes more than 24 hours in a third of patients treated with Heparin to reach the therapeutic PTT range. According to Dr. Gladstone, this is one of the limitations of Heparin. Similarly, Warfarin is also slow to act, and it takes about a week to achieve its therapeutic effects.

[180] In addition, Dr. Gladstone clarified that Heparin does not dissolve blood clots. While other medications have this capability, Mr. Johnson was never a candidate eligible to receive them because there are specific criteria for their use and it would have been too dangerous due to a risk of bleeding in the brain. As a result, “… the only realistic hope with the use of Heparin and Warfarin is to help to minimize further clot propagation, but not to reverse the problem that had already developed.”

(iii) Dr. Gladstone’s View on Guidelines

[181] Dr. Gladstone commented that he was surprised to hear Dr. Caplan claim guidelines were irrelevant to Mr. Johnson’s case. He stated,

It’s frankly concerning that he doesn’t seem to value the importance of the guidelines. Guidelines have become international standards for medical practice nowadays. It used to be decades ago that a clinician would have an opinion or a preference about a treatment and recommend because he or she thought that, you know, that’s what should work. But now, we have a more scientifically sound, objective approach where we say well, lets see what actually does work or doesn’t work. And now we have a number of studies that have tested various treatments and we have a better sense of what is effective or not.

And so, we don’t want to get into a situation of over-estimating benefits of medications, or underestimating their risks. We look to the guidelines for credible, objective sources of information. The guidelines try to compile the best available evidence to date and the guidelines get updated on a continuous basis. And we want to follow the recommendations because the whole intent is to maximise the quality of patient care. We make sure that we, you know -- the guidelines are intended to help clinicians make very rational treatment decisions for their patients.

And so, I put a lot of weight in what the guidelines say. I accept the point that I think I heard Dr. Caplan make, and it’s correct, that the guidelines cannot cover every scenario or every medical condition or nuance, right? So, there can be some rare conditions that are not covered in the guidelines, but -- or some patients may not fit the, you know, the average patient that is intended to be covered by guidelines, but I think it’s very relevant in Mr. Johnson’s case because we have had guideline recommendations that are directly applicable to him when he was hospitalized in October 2012.

[182] On the issue of the applicable guideline in October 2012, Dr. Gladstone noted that in relation to secondary stroke prevention the main recommendation for most patients with an acute ischemic stroke was antiplatelet therapy with Aspirin, Plavix or other antiplatelet agent. This recommendation was consistent across guidelines from Canada, the United States, Australia, Europe and Asia. The guidelines did not recommend Heparin or Warfarin as first-line treatment for most patients with acute ischemic stroke.

[183] Dr. Gladstone explained that the 2017 and 2020 Canadian guidelines for a patient with a vertebral artery dissection or a carotid artery dissection, recommended antithrombotic therapy with either antiplatelet therapy or anticoagulant therapy. Both are considered acceptable, reasonable treatment options for secondary stroke prevention, and there is no preferential recommendation of one over the other.

[184] Similarly, the American guidelines also emphasize the uncertainty and recommend that either option is acceptable or reasonable. The same is true for the European guidelines, and the strength of that recommendation has been increased following the publication of the CADISS trial. As well, the European guidelines also recommend that if there is an arterial dissection that extends intracranially, then anticoagulation therapy is to be avoided because it creates a higher risk of subarachnoid hemorrhage, a type of brain bleed.

[185] When asked to comment on the absence of a preferential treatment in the guidelines, Dr. Gladstone explained that if there existed convincing evidence that one treatment was better than the other, it would be reflected in the guidelines. So, the fact that the guidelines do not make preferential recommendations of Heparin or Warfarin over antiplatelet therapy reflects the fact that the studies that have been conducted have not shown superiority, not only for dissection cases specifically but also for acute ischemic stroke patients in general. Dr. Gladstone then explained:

...it used to be decades ago that Heparin was used quite widely as a treatment right after an acute ischemic stroke until it was put to the test in randomized controlled trials. And there have been several of them now comparing Heparin based treatment strategies versus Aspirin in acute ischemic stroke…And the bottom line there is that there is no net benefit of Heparin when used after an acute ischemic stroke.

In fact, the most relevant studies as it pertains to this case, were studies that tested Heparin use for the first two weeks after an acute ischemic stroke, so exactly the timeframe that is under discussion for Mr. Johnson’s case. And those studies show no reduction in the rate of recurrent ischemic strokes with the use of Heparin based treatments, and there was a clear increased risk in causing bleeding complications with Heparin.

(iv) Dr. Gladstone’s View on Studies, Trials and Literature

[186] Dr. Gladstone discussed the Cochrane Collaboration Review, which was a meta-analysis of Heparin studies which involved more than 16,000 patients with stroke from four randomized controlled trials. This review found no reduction of recurrent ischemic strokes when the anticoagulation treatment was administered in the first two weeks. However, Heparin caused greater incidents of brain hemorrhage and internal bleeds. Heparin also actually increased the risk of death compared with Aspirin in a statistically significant fashion. In Dr. Gladstone’s view, this is the reason why the use of Heparin has fallen out of favour and the guidelines have not been recommending it.

[187] On the issue of the CADISS trial, Dr. Gladstone explained that CADISS was the first randomized controlled clinical trial comparing antiplatelet versus anticoagulant therapy for secondary stroke prevention in patients with dissection. Before the CADDIS trial, a number of observational studies were pooled into meta-analyses that did not show any statistically significant difference in favour of one treatment over the other.

[188] CADISS was conducted because there was still ongoing uncertainty in the medical community about the optimal treatment, there were different practice preferences, with some clinicians preferring one treatment over another. Both treatments were being used. The study was conducted in an attempt to resolve the issue and increase the strength of scientific evidence. It was undertaken with the premise that there did not seem to be a clear difference between treatments. In fact, had the existing evidence suggested otherwise, the trial would not have been approved.

[189] In Dr. Gladstone’s opinion, the fact that the CADISS trial was conducted is very strong evidence that at the time of the plaintiff’s stroke in 2012, there was no scientific evidence to support the use of Heparin as a treatment for him. It was a treatment option, as was antiplatelet therapy, but there was insufficient evidence to suggest that Heparin was going to be better or the right choice. The trial was ongoing at the time the plaintiff had a stroke. It started enrolling patients in 2008 and continued until 2013.

[190] According to Dr. Gladstone, the CADISS trial enrolled 250 patients who had experienced carotid or vertebral artery dissection. The average age was 49. About half of the patients had vertebral dissections and half had carotid dissections. Approximately 90% or more had also experienced an acute ischemic stroke or transient ischemic attack. Patients were enrolled and randomized early after the initial symptom onset, at an average of 3.65 days. Patients were then randomized into treatment groups of Aspirin or other antiplatelets, or Heparin and Warfarin.

[191] Dr. Gladstone noted that based on eligibility criteria alone, the patient profile in CADISS seemed to match Mr. Johnson’s situation: he was in his 40’s, had a vertebral artery dissection, and the treatment was applied within a time window that would have been relevant to Mr. Johnson’s treatment.

[192] The CADISS trial results showed that the overall rate of recurrent ischemic stroke was 2%, and there was no statistically significant difference between the treatment groups in terms of rate of recurrent strokes. The outcome of stroke or transient ischemic attack was 4% in each treatment group.

[193] The authors concluded that in this trial of 250 patients, they did not find any evidence of superiority of one treatment approach over the other. However, because of the sample size, if there was a true difference between the two treatment groups, many more patients would need to be enrolled in a larger trial. The authors estimated that 10,000 patients might be required in order to definitively conclude that there was no small difference in treatment effect. If there was a large difference favouring one treatment over the other, it probably would have been seen in the 250 patients used in the study, but it was not.

[194] While the CADISS trial did not demonstrate treatment superiority, it did document one major bleeding complication in the anticoagulant treated patients. There were no major bleeding complications in the antiplatelet group. A one year follow up was later published and it showed no long-term benefit as between the treatments.

[195] In response to Dr. Caplan’s view of the CADISS study, Dr. Gladstone noted that while the CADISS-NR study had patients with a relatively late entry date post onset of symptoms, the later CADISS randomized trial had patients on average enter the study within three to four days post onset. While he agreed with Dr. Caplan’s view that the late entry date “may have missed some potential benefit of Heparin”, he nonetheless was of the view that the CADISS study provided the best available randomized evidence. Moreover, he noted that the CADISS study results were consistent with the non-randomized observational studies and their meta-analyses.

[196] Dr. Gladstone also referenced the data from the Ontario Stroke Registry, which was a prospective registry involving about a dozen hospitals in Ontario. Over several years, every single consecutive patient who was hospitalized with an acute ischemic stroke was entered into the Registry and their data was tracked.

[197] Dr. Gladstone was one of the investigators with the Registry for many years, and he explained that it used a rigorous methodology and was considered to be a reputable registry. Based on the Registry data, a study was conducted to look at the outcome of 201 patients with dissection in Ontario between 2003 and 2008. One quarter of the patients had antiplatelet therapy and the rest were anticoagulation therapy. While the full manuscript was never published, the study was peer-reviewed, and the data was published in the abstract. The results of the study showed an overall rate of ischemic stroke or transient ischemic attack was 7% with no statistically significant difference between the two treatment groups.

[198] Dr. Gladstone also discussed the available meta-analyses. He explained that a meta-analysis combines the data from several individual studies into a single analysis, which increases the statistical power for the analysis. In terms of the hierarchy of levels of scientific evidence, the meta-analysis is “right near top” as it increases sample size and allows for more definitive conclusions.

[199] Dr. Gladstone referred to several meta-analyses. The first meta-analysis is the “Antithrombotic Drugs for Carotid Artery Dissections, Cochrane Database Systematic Review.” While this review examined cases of carotid artery dissections, the treatment approach is analogous to the treatment for vertebral artery dissections. The conclusion from this meta-analysis is that there was no significant difference between the two treatment approaches in terms of recurrent stroke rates.

[200] The second meta-analysis is the “Antiplatelets vs. Anticoagulants for Dissection” meta-analysis. This meta-analysis reviewed the result of the CADISS-NR study but also included a separate meta-analysis of the observational studies that had accrued to that point. This meta-analysis found no difference between the two treatment approaches.

[201] The third meta-analysis is the “Antiplatelets versus Anticoagulants for the Treatment of Cervical Artery Dissection: Bayesian Meta-Analysis.” This study examined composite outcomes including ischemic stroke, hemorrhagic stroke, and death. The conclusion of the authors of the study was that doctors should be favouring antiplatelet therapy as the first line of treatment rather than anticoagulant therapy. In view of the composite outcomes examined, the study “found a signal of additional benefit” to antiplatelet therapy. The study also observed that Aspirin is easy to use because it is a pill that can be taken orally, whereas Heparin requires IV infusion and hospitalization for monitoring. Anticoagulants are more costly than Aspirin, which is available over the counter.

[202] Dr. Gladstone also referenced a further meta-analysis from the Cochrane Library titled “Anticoagulants versus Antiplatelet Agents for Acute Ischemic Stroke”, by Dr. Sandercock. This meta-analysis, which included over 1,600 patients, compared Heparin versus Aspirin in the first two weeks after an acute ischemic stroke. The meta-analysis revealed that Heparin is potentially dangerous, doubling the risk of major bleeding complications and doubling the risk of hemorrhagic stroke without providing any additional benefit over Aspirin.

(v) Dr. Gladstone’s Final Opinion

[203] When asked whether recurrent strokes occur when a patient has been treated with Heparin, Dr. Gladstone explained that the reality of the currently available medications is that they are not fool proof. He noted that unfortunately recurrent strokes occur on a regular basis.

[204] When asked whether earlier initiation of Heparin would have made a difference in Mr. Johnson’s case, Dr. Gladstone replied:

My opinion is based on a careful review of the medical literature of what’s been published on this topic, and on a review of the particular medical facts in Mr. Johnson’s case, paying particular attention to his specific imaging features, and also the timing issues. And my opinion is that Mr. Johnson’s stroke that occurred on October 30th, 2012, would still likely have occurred even if Heparin and Warfarin had been administered earlier, starting right after his MRA and MRI scans were done on October the 22nd, and even if he had remained in hospital for longer and had not been discharged on October the 23rd. And my opinion in this matter is consistent with the published medical practice guidelines from all the major stroke societies around the world.

(vi) Cross-Examination

[205] Dr. Gladstone was asked about the significance of the results of the various studies. He acknowledged that studies such as the CADISS-NR revealed no statistically significant result. He agreed that as a matter of science, this meant that the results neither proved nor disproved the hypothesis.

[206] Dr. Gladstone agreed that at the time of Mr. Johnson’s stroke in 2012, there was no guideline that preferentially recommended anticoagulant therapy over antiplatelet therapy in the treatment vertebral artery dissection. The guidelines only definitively recommended antithrombotic therapy with either antiplatelets or anticoagulants.

[207] In terms of Mr. Johnson specifically, Dr. Gladstone agreed that anticoagulation with Heparin or Heparin bridged to Warfarin was one of several reasonable treatment options available between October 18 and October 30, 2012.

[208] Dr. Gladstone agreed that the overall rate of secondary stroke for both anticoagulation and antiplatelet treatments was roughly 2%. He also agreed that by way of mechanism of action or pathophysiologically, anticoagulants are more powerful anti-clotting agents, though he noted that they also had a higher risk of bleeding complications. He explained that the fact that anticoagulants are more powerful makes it tempting to think that they should be better for stroke prevention, but the clinical studies have not supported this conclusion in dissection cases.

[209] Dr. Gladstone acknowledged that Dr. Caplan’s theory is based on the pathophysiology of arterial dissection, which suggests that Heparin and Warfarin ought to be more effective than antiplatelet drugs for preventing red clots. He agreed that Dr. Caplan’s theory was very plausible and attractive, but went on to explain that it has not been borne out by the clinical studies. The following exchange then occurred:

Q. Again, Doctor, I think we’ve all established there’s no clinical studies.

A. I....

Q. But you still have to practice medicine, right?

A. I, I beg to differ. There have been numerous clinical studies that have informed us in this question of causation, in this case, and I’ve cited them in my reports. These are clinical studies in - observational studies, meta-analyses of the observational studies, and the CADISS randomized trial, and other studies that have been published subsequent to my reports, including a second...

Q. Like TREAT-CAD.

A. ...clinical trial. So, we actually have an enormous amount of clinical data that has addressed this topic.

Q. Okay. This is - Doctor, I agree there’s tons of data addressing this topic. Not one of those - not one of those studies you report comes up with a statistically significant result. Correct? Correct?

A. That is the conclusion, that one is not better than the other. Right.

Q. It’s not the conclusion. There was no statistical significance to any of those studies.

A. Well, there has been some variability in individual studies. Some observational studies have been conflicting, but when you combine them all together in a meta-analysis - because we like to see consistency of the results, and we put them all together, then the net result is that there is no observable clinically significant or statistically significant difference between the two different treatment approaches.

Q. So, there’s no statistically significant results. Correct?

A. That’s right, yes.

[210] In terms of the basis for his disagreement with Dr. Caplan, Dr. Gladstone relied on the fact that the available data from the clinical trials did not substantiate Dr. Caplan’s opinion. He also placed “a lot” of weight on the specific facts of Mr. Johnson’s case and, in particular, the fact that he had not only a vertebral artery dissection, but the dissection led to an extensive occlusion of the artery. He also had an acute ischemic stroke and a PCA territory infarct. Dr. Gladstone also placed a lot of weight on the imaging and the timeframe when the treatment could be administered.

[211] Dr. Gladstone was specifically challenged on his evidence regarding the possibility that Mr. Johnson had a hemodynamic occlusion to his artery which would not have been remedied by the use of Heparin. In particular, he was challenged on why this conclusion was not in his reports. Dr. Gladstone explained that in his report he stated that Mr. Johnson’s second stroke could have been caused from either hemodynamic occlusion or a blood clot. While he agreed that in his evidence in-chief, he described the possibility of hemodynamic occlusion as likely, he agreed that it was not possible to tell which was the cause. He stated, “It was likely either mechanism.”

[212] In terms of Dr. Crisp’s involvement, Dr. Gladstone agreed that Dr. Crisp expressed a preference for anticoagulation. He also agreed that this preference was accepted by Mr. Johnson, who wanted the most aggressive approach. Dr. Gladstone explained, however, that before prescribing Heparin, Dr. Crisp would have ideally had to review the imaging in order to determine the appropriate course of treatment. Dr. Gladstone was not prepared to simply assume that this had been done by Dr. Crisp.

[213] Regarding his experience, Dr. Gladstone was challenged on the basis that his specific subspecialty in terms of clinical and research work is hemorrhagic stroke. He agreed that hemorrhagic stroke is an area of interest but noted that his predominant research interest is secondary stroke prevention and the cardiac causes of stroke-like atrial fibrillation. He noted that he has published widely in the area of potentially preventable strokes. He also noted that dissection was “bread and butter” stroke neurology and something he had a lot of experience in within his clinical practice. He has seen patients who have had recurrent strokes despite anticoagulant therapies. He has a clinical and research interest in anticoagulant therapies and has published widely on recommendations for clinicians on how to prescribe and monitor anticoagulant therapy as safely as possible.

[214] Dr. Gladstone was also challenged on the basis that several of the studies he participated in and referred to in his reports did not specifically relate to arterial dissection. He agreed that none of these studies addressed cervical artery dissection, though he noted that he participated in drafting guidelines which addressed arterial dissections and were peer reviewed. Apart from the guidelines, Dr. Gladstone agreed that he had not written any peer reviewed articles specifically on dissection. While Dr. Gladstone wrote a book on stroke management that addressed acute ischemic stroke diagnosis and early treatment for prevention, it did not specifically address vertebral artery dissection. He agreed that he had not conducted any randomized clinical trials in respect of cervical artery dissection.

[215] In terms of CADISS, Dr. Gladstone agreed that CADISS was a feasibility study. In other words, it set out to determine how large a sample group would be needed in order to have a proper randomized clinical trial in relation to a relatively rare condition. However, he explained that it nonetheless provides the “best available evidence that we have to date.” Dr. Gladstone disagreed with the suggestion that the CADISS study provided “no evidence.” He explained that it simply failed to find a difference in favour of one treatment over the other.

[216] Dr. Gladstone was asked about treatment preferences, and he agreed that years ago anticoagulation was often the preferred initial treatment. This was reflected in a study done at Sunnybrook Hospital by the Canadian Stroke Consortium in 2003. Dr. Gladstone explained that in recent years, anticoagulant therapy has fallen out of favour as more and more studies have not supported it. He went on to note that “simple preference of medication” does not mean that the medication is better.

[217] In terms of Dr. Vieira’s treatment of Mr. Johnson, Dr. Gladstone agreed that it was substandard for Dr. Vieira to discharge Mr. Johnson without telling him that he had an arterial dissection. He also agreed that it would be substandard to discharge a patient without reviewing the imaging, particularly where there was a question about the source of the stroke. When challenged as to why he did not set out these views in his reports, Dr. Gladstone explained that he was tasked with focussing on causation and not standard of care. That said, he acknowledged that he had been asked to opine on standard of care as well, but explained that his focus was on the treatment Mr. Johnson was given and Dr. Vieira’s failure did not have implications in terms of treatment.

[218] In terms of the treatment of stroke generally, Dr. Gladstone explained that the standard approach is to give the patient Plavix and Aspirin and then to figure out what caused the stroke, and once that is done to treat accordingly. The doctor would then consult the specific guideline relating to the cause of the stroke and consider the appropriate treatment. The treatment would also need to be tailored to the specific patient.

[219] Dr. Gladstone was asked about the TREAT-CAD study. He explained that he had not referred to it in his report as it had not been published at the time. He agreed that it was an important study and explained that its conclusions support his opinion in this case. Dr. Gladstone further explained that the study did not prove the superiority or inferiority of either anticoagulant or antiplatelet therapy. He denied that this was simply another “failed study” that produced “no evidence.” In his view, the study failed to demonstrate any superiority or inferiority as between the two treatment choices.

[220] It was pointed out to Dr. Gladstone that in the TREAT-CAD study, patients in the Aspirin group received 300 mgs of Aspirin daily, while Mr. Johnson received 81 mgs of Aspirin daily which is the standard recommended in the Canadian and American guidelines. Dr. Gladstone then stated:

I think that there is a range of doses of Aspirin that’s used across the world. In Europe, they often favour a higher dose than in North America, but this has actually been studied, and there are trials, randomized trials that have compared low dose Aspirin to higher doses of Aspirin, and the bottom line is that there is no difference in the efficacy for stroke prevention between low dose and high dose, but the high dose is associated with a higher degree of side effects like stomach upset, stomach ulcers and bleeding side effects, and that’s why the -- I mean, we used to prescribe 1300 milligrams a day of Aspirin when I started my residency training. That was the standard.

[221] Dr. Gladstone further explained that various studies support the use of lower doses of Aspirin, though he agreed that none of those studies were specifically geared towards vertebral dissections. He also agreed that he did not have a study that compared 81 mgs of Aspirin to Heparin bridged with Warfarin in cases of vertebral dissection. That said, Dr. Gladstone noted that there was no reason to dismiss the many studies that have looked at different dosing of Aspirin.

[222] Dr. Gladstone agreed that the CADISS study did not specify the dosage of Aspirin as it was left to the clinician’s discretion, but many of the patients had dual antiplatelet therapy. In other words, they were taking more than one type of antiplatelet. CADISS revealed a 2% rate of secondary stroke and TREAT-CAD revealed an 8% rate of secondary stroke. The authors of an article published in UpToDate called “Cerebral and Cervical Artery Dissection: Treatment and Prognosis”, opined that one possible explanation for this discrepancy was that the patients in the TREAT-CAD study were using Aspirin monotherapy. Dr. Gladstone did not dispute this possible explanation but noted that it did not alter the conclusion of the trial.

[223] Dr. Gladstone also agreed that in the TREAT-CAD study all the recurrent strokes occurred in the antiplatelet group, but he explained that five of the seven strokes that occurred within that group occurred within the first day after initiation of the treatment, which is not the timing of when Mr. Johnson’s stroke occurred. While there were numerically more strokes in the antiplatelet group, when clinical patient outcomes were examined at three months, the outcomes were the same for both groups.

[224] Lastly, Dr. Gladstone agreed that dosages in various other studies he relied on were all well above 81 mgs of Aspirin daily. None of these trials and studies used 81 mgs of Aspirin.

Analysis and Findings

[225] I turn next to assessing the evidence and making factual and legal findings.

[226] I note at the outset that the sole issue in this case is causation. It is not a case about the standard of care, nor is it a case about informed patient consent. The issue of causation can be framed using the following two questions:

a. If Dr. Vieira had reviewed the imaging showing that the cause of Mr. Johnson’s initial stroke was related to a vertebral artery dissection, is it likely that Mr. Johnson would have been treated with Heparin?

b. If so, is it likely that Heparin would have prevented the second stroke on October 30, 2012?

[227] The plaintiffs argue that had Dr. Vieira reviewed the imaging, she would not have discharged Mr. Johnson. Instead, she would have consulted Dr. Crisp who would have diagnosed a vertebral artery dissection and would have kept Mr. Johnson in hospital. In doing so, Dr. Crisp would also have placed Mr. Johnson on Heparin bridged to Warfarin.

[228] The plaintiffs further argue that if Mr. Johnson had been placed on Heparin on or about October 23, 2012, he would have been fully “Heparinized” by October 31, 2012, which is the date when the stroke occurred. Lastly, they argue that the use of Heparin would likely have prevented the second stroke.

[229] The defendant argues that the plaintiffs have failed to establish both general and specific causation. In particular, the defendant argues that the plaintiffs have failed to prove the general proposition that Heparin is more likely than Aspirin to prevent a secondary stroke in cases of vertebral artery dissection. Further, the defendant argues that even if the general causation can be established, the plaintiffs have failed to prove that the administration of Heparin in this specific case would have likely prevented Mr. Johnson’s second stroke.

What Likely Happened to Mr. Johnson

[230] What happened to Mr. Johnson is mainly not in dispute. On October 15, 2012, Mr. Johnson had a chiropractic adjustment, followed by massage therapy on October 16, 2012. He developed a significant headache.

[231] On October 17, 2012, he went to the ER department of the hospital complaining of a fainting episode. He reported that he had been vomiting since the morning, sweating and had a headache from the night before. He was given IV fluids, pain and nausea medication and then discharged.

[232] On October 18, 2012, he went to see his family doctor, Dr. Bolger, and reported ongoing symptoms as well as visual disturbances. Fortuitously, Dr. Bolger saw fit to bring Mr. Johnson to an optometrist in the same building. The optometrist diagnosed homonymous hemianopia, which suggested a possible stroke.

[233] Mr. Johnson returned to hospital and was admitted. A CT scan of his head revealed a “large hypodensity” within the right occipital lobe, indicative of an acute embolic ischemic stroke. Some small hypodensities compatible with infracts were also observed in the inferior left cerebellar hemisphere.

[234] Mr. Johnson was admitted to the Stroke Unit where he was given antiplatelet therapy, including a loading dose of Plavix and 81 mgs of Aspirin daily. While he did receive Heparin, it was not related to the prevention of secondary stroke. The initial treatment of Mr. Johnson with antiplatelet therapy fell squarely within the standard of care. While there is an issue as to the appropriate dosage of Aspirin, the dosage Mr. Johnson received is the standard recommended dosage in Canada and elsewhere.

[235] According to Dr. Crisp’s note dictated on October 21, 2012, “the big diagnosis” to rule out is a dissection in the vertebrobasilar system stemming from the chiropractic adjustment. While Dr. Crisp was alive to the possibility of a vertebral artery dissection, this is not an instance where he viewed it as appropriate to commence anticoagulation therapy in advance of determining a cause.

[236] On October 22, 2012, the MRI and MRA imaging was performed and a report was prepared. The brain MRI confirmed the diagnosis of a sizeable acute ischemic stroke within the right PCA territory affecting the occipital and posterior temporal regions. The MRA of the head and neck reported a “lack of visualization” involving a portion of the left vertebral artery. The suspected etiology of Mr. Johnson’s stroke was a vertebral artery dissection.

[237] Mr. Johnson was discharged from hospital on October 23, 2012, before the vertebral artery dissection was diagnosed. Dr. Vieira had a duty to Mr. Johnson to exercise reasonable care in ordering his discharge from hospital on October 23, 2012. She breached the expected standard of care by failing to review the neck MRI (MRA) imaging report prepared on October 22, 2012, before discharging.

[238] Had Dr. Vieira seen the imaging report, she would have consulted Dr. Crisp, who was Mr. Johnson’s neurologist. She also would have deferred to any opinion he gave, and any further treatment decisions would have been in consultation with Dr. Crisp.

[239] Following discharge, Mr. Johnson remained on antiplatelet therapy of 81 mgs of Aspirin daily.

[240] On October 29, 2012, Mr. Johnson went to see his family physician, Dr. Bolger, who reviewed the imaging report that showed a vertebral artery dissection. Dr. Bolger contacted Dr. Crisp who had not yet seen the imaging report.

[241] According to Dr. Bolger’s note, Dr. Crisp felt that Mr. Johnson should never have been discharged and that he should return to hospital immediately to commence Heparin for one week.

[242] On Dr. Bolger’s advice, Mr. Johnson went immediately to hospital where he was admitted and given IV Heparin and Warfarin.

[243] In the afternoon of October 30, 2012, Mr. Johnson suffered his second stroke. This was an acute left cerebellar ischemic stroke. It was in a different location than the earlier stroke.

[244] The strokes were most likely caused by the dissection of Mr. Johnson’s left vertebral artery, which occurred at some point between October 15 and 16, 2012. The mechanism of the October 17, 2012 stroke was embolic, most likely caused by an embolism that dislodged from the blockage in his left vertebral artery and occluded his right posterior cerebral artery.

[245] The October 30, 2012 stroke also stems from the left vertebral artery dissection, which either produced further emboli, blocking blood flow to smaller artery branches supplying the left cerebellum, and/or via hemodynamic ischemia due to reduction of blood flow within the left cerebellar artery. Dr. Caplan’s view is that the second stroke was caused by an embolism to the left intracranial vertebral artery, though he allows for complementary hemodynamic ischemia. Dr. Gladstone’s view is that the second stroke was likely caused by a hemodynamic process, though he accepts that both processes are “likely causes.”

What Likely Would Have Happened

[246] I will address this issue in two parts. First, I will address whether it is likely that Mr. Johnson would have been hospitalized and placed on anticoagulant therapy had Dr. Vieira reviewed the MRI (MRA) imaging report. Second, I will address whether Mr. Johnson would likely not have had the second stroke if he had been on anticoagulant therapy as of October 23, 2012.

[247] In terms of the first issue, a problem arises in this case because Dr. Crisp, a former defendant, was not called as a witness, and as such there is no direct evidence from him as to what he would have done had he learned of the imaging report on October 23, 2012.

[248] The plaintiffs argue that what Dr. Crisp, a former defendant, would have done can be safely inferred from Dr. Bolger’s note of October 29, 2012, which they argue is admissible for the truth of its contents either as a business record under s. 35(2) of the Ontario Evidence Act, or in accordance with Ares v. Venner, 1970 CanLII 5 (SCC), 1970 S.C.R. 608. In the note, Dr. Bolger indicates that “Dr. Crisp felt should never have been discharged and needs to return to LHO immediately for heparin x 1 week.” The plaintiffs posit that the only reason why Mr. Johnson “should never have been discharged” was to administer Heparin, which is administered by IV and needs to be monitored in hospital. Indeed, the plaintiffs note that Dr. Gladstone agreed with this suggestion.

[249] In addition, the plaintiffs note that on October 29, 2012, when Dr. Chong gave Mr. Johnson his treatment options, Mr. Johnson elected for the “most aggressive approach” which was hospitalization with IV Heparin overlapped with Warfarin. The plaintiffs argue that while there is no direct evidence from Mr. Johnson as to what his treatment preference would have been on October 23, 2012, an inference arises that it would have been one and the same.

[250] Lastly, the plaintiffs note that treatment with anticoagulants would have been within the standard of care at any time between October 18, 2012 and October 30, 2012. In other words, it was essentially one of two treatments that reasonably could have been administered during that timeframe.

[251] The defendant argues that Dr. Bolger’s note is a hearsay statement of what Dr. Crisp said to Dr. Bolger, and neither Dr. Bolger nor Dr. Crisp were called as witnesses. While Dr. Bolger’s note was admitted as part of the Joint Book of Documents, counsel agreed upon the following stipulation:

Where the records contained in the Joint Book of Documents reference a diagnosis or statement of opinion those entries are admitted establishing the fact that the author(s) of the entry reached the diagnosis or opinions at the time, and not for the truth or accuracy of those opinions.

[252] Based on this stipulation, the defendant suggests that Dr. Bolger’s note is simply not evidence of the truth or accuracy of Dr. Crisp’s opinion regarding whether Mr. Johnson would have received Heparin on October 23, 2012. Moreover, the defendant notes that Dr. Bolger’s note, at best, relates only to October 29, 2012, and not to what Dr. Crisp would have done on October 23, 2012.

[253] The common law rule in Ares v. Venner, at p. 609, provides that records “made contemporaneously by someone having personal knowledge of the matters then being recorded and under a duty to make the…record should be received in evidence as prima facie proof of the facts stated therein.”

[254] In my view, Dr. Bolger’s note conveying Dr. Crisp’s opinion is admissible under the common law rule in Ares v. Venner.[^5] Both Dr. Bolger and Dr. Crisp would have been acting under a duty in terms of the creation of the record and comments contained therein. The note was contemporaneous with the examination by Dr. Bolger and the consultation with Dr. Crisp. Both Dr. Bolger and Dr. Crisp would have been acting under a duty.

[255] More importantly, there is no issue that Mr. Johnson left Dr. Bolger’s office and travelled to the hospital where he was re-admitted and placed on Heparin immediately. To the extent that the note suggests that Mr. Johnson needed to be re-admitted and placed on Heparin, that is exactly what happened and there is no challenge to the unfolding of these events. In other words, this is not a case where there can be any issue in terms of the reliability of the purported hearsay utterance.

[256] The more nuanced issue is what inferences can be drawn from Dr. Crisp’s stated opinion on October 29, 2012, as it relates to what would have happened on October 23, 2012 had Dr. Vieira consulted Dr. Crisp for his opinion at that time.

[257] On this issue, I note that the defendant argues that the record is insufficient to prove that Dr. Crisp would have been available to provide a consultation to Dr. Vieira on October 23, 2012. As well, the defendant submits that the evidence does not establish that Dr. Crisp would have administered Heparin on October 23, 2012, and further notes that on October 21, 2012 when Dr. Crisp suspected a vertebral artery dissection, his consultation note simply states that antiplatelet medication would be continued. As such, the defendant posits that had this been an urgent or clear case for the administration of Heparin, it would been ordered on October 21, 2012, once the vertebral artery dissection was suspected. In other words, Dr. Crisp would not have waited for confirmation of the vertebral artery dissection.

[258] The defendant notes that on the basis of the evidence before the court, Mr. Johnson suffered a significant infarct on or about October 17, 2012. Dr. Gladstone noted that the MRI scan from October 22, 2012 showed a large acute infarct, and he explained that infarcts very often have “leaky blood vessels” and are prone to bleeding. While Dr. Caplan referred to the stroke as “moderately large”, he did not quarrel with Dr. Gladstone’s interpretation of the imaging. According to Dr. Gladstone, Mr. Johnson was likely not a patient who could be safely started on an anticoagulant right away.

[259] Dr. Gladstone further opined that Mr. Johnson had an infarct that would have been at a higher than average risk for hemorrhagic transformation that could become symptomatic, which would have made the use of Heparin risky. Dr. Gladstone noted that in such a case, Heparin might be delayed in order to minimize risk to the patient. Dr. Gladstone further observed that in accordance with the Canadian Stroke Best Practice Recommendations published in 2020, a delay of 12-14 days would be appropriate for a patient who had a severe clinical stroke/large sized infarct.

[260] Lastly, the defendant further argues that there is insufficient evidence establishing that Mr. Johnson would have consented to Heparin treatment on October 23, 2012. The discussion about the associated risks of bleeding and the timing of the commencement of Heparin therapy would have been different on October 23, 2012, than the discussion memorialized in Dr. Chong’s note of October 29, 2012.

[261] Having considered this issue carefully, I am prepared to find that Dr. Crisp likely would have commenced anticoagulation on Mr. Johnson on or about October 23, 2012. I reach this conclusion for the following reasons. First, the note in Dr. Bolger’s file states that Dr. Crisp felt that Mr. Johnson should never have been discharged and that he needs to return to hospital immediately for Heparin. When this note is viewed in context, it clearly suggests that in view of the imaging that reveals the vertebral artery dissection, Dr. Crisp was of the view that Mr. Johnson should not have been discharged on October 23, 2012. Nothing had changed in Mr. Johnson’s presentation by October 29, 2012. The only change is that Dr. Bolger and Dr. Crisp came to appreciate the significance of the MRI and MRA reports. Dr. Crisp’s view that Mr. Johnson was to return to hospital immediately to start Heparin, in these circumstances strongly supports an inference that this is what his opinion would have been but for the premature discharge. Indeed, Dr. Gladstone himself acknowledged that the only reason to keep Mr. Johnson in hospital would be to administer Heparin, which is administered either by IV or subcutaneously.

[262] I am not prepared to find that the absence of evidence of Dr. Crisp’s availability on October 23, 2012, undermines the fact that this is likely what would have happened. The Agreed Statement of Facts specifically state that had Dr. Vieira noted the MRI and MRA imaging, she would have taken next steps in consultation with Dr. Crisp.

[263] I am also not prepared to find that there is no evidence that Mr. Johnson would have consented to Heparin treatment on October 23, 2012. When he presents at the hospital on October 29, 2012, he gives consent to “the most aggressive approach” as memorialized in the notes of Dr. Chong, which included a discussion of the fact that intensifying the antithrombotic treatment was “controversial.” Viewed in context, I am satisfied that had Dr. Crisp advised Mr. Johnson to take anticoagulation therapy on October 23, 2012, Mr. Johnson would have likely consented.

[264] Lastly, I accept Dr. Gladstone’s evidence that there may have been reasons why an anticoagulant would not have been the preferred treatment on October 23, 2012. In particular, I accept his evidence that Mr. Johnson had suffered a large infarct and that as a result there existed a higher than average risk of bleeding. His evidence on this point was logical, measured and in keeping with the current Canadian Stroke Best Practice Recommendations. That said, he acknowledged that in 2012, anticoagulation was the preferred treatment.

[265] I also do not accept Dr. Caplan’s attempt to describe the size of Mr. Johnson’s infarct as something other than large. In my view, Dr. Caplan’s evidence on this point appeared semantic and was contradicted by the evidence relating to the radiology findings as set out in the Agreed Statement of Facts. That said, I note that Dr. Caplan agreed that if an infarct was properly described as “large”, it would give a clinician “some pause” before initiating Heparin in view of the corresponding risk of hemorrhagic transformation.

[266] Ultimately, the issue is what Dr. Crisp would likely have done and not the correctness of Dr. Crisp’s decision or opinion. In my view, it is clear that Dr. Crisp would likely have placed Mr. Johnson on anticoagulation therapy had he been aware of the MRI and MRA imaging on October 23, 2012. While I accept that Dr. Gladstone would likely not have placed Mr. Johnson on anticoagulant therapy as early as October 23, 2012, that does not assist in determining what Dr. Crisp would likely have done. Indeed, it may well be that Dr. Gladstone would have disagreed with Dr. Crisp’s decision in this regard. However, Dr. Gladstone acknowledged that anticoagulation therapy with Heparin bridged to Warfarin would have been one of several reasonable treatment options for Mr. Johnson at this time. As such, Dr. Gladstone’s views are not greatly relevant on this issue.

[267] Based on the evidence before me, I am satisfied that had Dr. Vieira viewed Mr. Johnson’s MRI and MRA imaging on October 23, 2012, she would have consulted with Dr. Crisp who would likely have advised against discharge and would likely have placed Mr. Johnson on anticoagulation therapy. If anticoagulation therapy had started at that time, Mr. Johnson would have been fully “Heparinized” by October 30, 2012. In other words, Mr. Johnson’s PTT values would reached therapeutic levels of anticoagulation, though it is unclear when precisely this would have happened.

Would Anticoagulation Therapy Starting on October 23, 2012 Have Made a Difference?

[268] I turn lastly to the core issue in this case, which is whether it is likely that anticoagulation therapy starting on October 23, 2012 would have prevented the second stroke Mr. Johnson suffered on October 30, 2012.

[269] Having carefully considered the issue, I am not satisfied that Mr. Johnson’s second stroke would likely have been prevented. While it is possible that the switch to Heparin bridged to Warfarin may have prevented the second stroke, it is also possible that it may have either not prevented the stroke or may have resulted in Mr. Johnson suffering further complications such as bleeding.

[270] I start my analysis of this issue with some broad observations and findings on the expert evidence of Dr. Caplan and Dr. Gladstone, starting with their qualifications and then their methodologies, and finally ending with an assessment of their opinions.

[271] In short, for the reasons that follow, I prefer the evidence of Dr. Gladstone over the evidence of Dr. Caplan.

[272] Reduced to its core, Dr. Caplan’s evidence had an anecdotal, “just trust me” quality to it, especially on the key issue of the efficacy of Heparin versus Aspirin in the treatment of secondary strokes in cases of vertebral artery dissection. I find that his approach and methodology raised concerns about the objectivity and reliability of his evidence. Conversely, I find that Dr. Gladstone was an objective and balanced witness who, contrary to the suggestion of plaintiffs’ counsel, put no “spin” on his evidence. I find that he adopted a sound methodology, rooted in science and based on a detailed review and appreciation of the relevant studies, guidelines and medical literature. I also find that he approached the key issue in this case with an eye to the specific details of Mr. Johnson’s case, particularly the imaging.

(i) The Qualifications of the Experts

[273] There is no issue that both experts are eminently qualified to give expert medical opinion evidence on stroke and the cause of stroke. Dr. Caplan is one of the world’s leading experts. He is a professor at Harvard Medical School. He has literally “written the book” on stroke medicine, including a chapter on vertebral dissection. He has been extensively involved in the field for over 50 years and has treated between 15,000-20,000 stroke patients, including approximately 200 vertebral dissection cases.

[274] Dr. Gladstone is also a leading stroke neurologist practising at Sunnybrook Health Sciences Centre in Toronto. He is an assistant professor at the Department of Medicine, University of Toronto. He is also a scientist who has extensive clinical and research experience in this area of medicine, though his main area of research is generalized stroke prevention. He has treated approximately 150 cases of vertebral dissection and has been involved in an additional 100 cases of vertebral dissection in various consultative capacities. Dr. Gladstone has also been involved in drafting national stroke and cardiology guidelines. Dr. Gladstone described himself as a junior expert witness.

[275] In considering their expertise, I find that both experts are, more or less, on equal footing in terms of education, knowledge and experience. Dr. Caplan has more experience both as a doctor and as an expert witness. Dr. Gladstone is a scientist in addition to being a medical doctor. While Dr. Gladstone does not have as much experience or a research focus on vertebral dissection, he describes vertebral dissection as “bread and butter” neurology. Importantly, Dr. Caplan acknowledges Dr. Gladstone’s expertise and noted that his reports in this case were thorough, well researched and written and revealed no errors.

(ii) The Methodologies Used by the Experts

[276] In terms of their methodologies, Dr. Caplan explained that he approached this case from the perspective of determining the optimal treatment in view of Mr. Johnson’s specific presentation. He explained that evidence-based medicine has limitations in terms of deciding the optimal therapy for a specific patient. He also noted that the various available stroke guidelines were either “irrelevant” or of limited relevance in deciding what the optimal treatment would be for a specific patient. In addition, he noted that the available studies examining whether there was a difference between anticoagulant and antiplatelet therapy had “failed” and resulted in essentially “no evidence” on the issue. In his view, in the absence of any dispositive evidence suggesting a preferred treatment, the answer was to be arrived at clinically based on experience. On this issue, he explained that he considered the specific facts of Mr. Johnson’s case in order to arrive at his opinion that Mr. Johnson’s second stroke would likely have not occurred if he had been on anticoagulant therapy.

[277] Dr. Gladstone’s methodology was more focused on science-based evidence. He explained that in forming his opinion in this case, he conducted an up-to-date review of the available literature, studies, reviews and guidelines. He explained that he then considered the specific facts of this case in context with his knowledge base. His review of the facts of this case included a detailed assessment of the imaging that showed the size, nature and location of the strokes in Mr. Johnson’s brain. While Dr. Gladstone acknowledged that the available studies had not conclusively answered the question of which treatment was preferred, he did not share Dr. Caplan’s view that the studies had “failed” or had produced “no evidence.” His approach was more nuanced, and he explained that the studies suggested that if there was a difference in efficacy between the treatments it would likely be quite small.

[278] In assessing the methodologies used by both experts in arriving at their opinions, I find that Dr. Gladstone’s methodology and approach was most in keeping with the role of an objective expert whose aim was to provide the court with helpful evidence. I find that Dr. Caplan was quick to discount an entire body of scientific study and literature despite the obvious applicability to the issue raised in this case. Dr. Caplan’s approach was to essentially rely on his own personal anecdotes from his clinical practice to reach conclusions that were not supported by the body of literature and scientific studies on the issue. He agreed that his general preference is to treat patients like Mr. Johnson with Heparin. He conceded that his approach was hypothetical, anecdotal and not tested scientifically. While I do not entirely discount Dr. Caplan’s methodology and acknowledge that there is significant value in his years of clinical experience, I prefer the methodology employed by Dr. Gladstone.

(iii) The Comparative Merits of the Expert Opinions

[279] Before turning to the specific assessment of the expert opinions before the court, I note that there are some significant issues on which the experts are ad idem. These areas of agreement are important in considering what the likely result would have been had Mr. Johnson received Heparin on or about October 23, 2012.

[280] First, both experts agree that none of the available scientific studies and trials have demonstrated a preferential treatment as between anticoagulant and antiplatelet therapy. More specifically, neither of the two most relevant trials, the CADISS randomized trial and the TREAT-CAD trial, supported the view that Heparin was more effective than Aspirin for preventing secondary stroke in patients with vertebral artery dissection. To the extent that the TREAT-CAD study had more strokes in the antiplatelet group than in the anticoagulant group, I note and accept Dr. Gladstone’s explanation for the timing of those strokes, which mainly occurred in the first day following initiation of treatment and as such, did not undermine the fact that the trial showed no valid statistically significant difference.

[281] Second, the experts both agree that available guideline recommendations in Canada, America and Europe, uniformly suggest that treatment with either anticoagulant or antiplatelet therapy is an appropriate response in cases of vertebral artery dissection. Indeed, the most recent guideline, the 2020 Canadian Stroke Best Practice Recommendation, note that there is uncertainty about the comparative efficacy of antiplatelet therapy versus anticoagulation therapy and that either treatment is considered reasonable based on current evidence. Perhaps unsurprisingly, both experts agree that the choice to initially discharge Mr. Johnson on antiplatelet therapy and not anticoagulant therapy met the standard of care in the circumstances of this case.

[282] Third, the experts agree that the available literature, which includes meta-analyses and other studies, also show that there is no difference in efficacy as between anticoagulation and antiplatelet therapy. These studies include the CADISS non-randomized study which reviewed data from 1996 to 2011 and detected no statistical difference, though as Dr. Caplan pointed out, the entry point for patients in this study was later than he thought appropriate. The studies also included the 2002 Cochrane Database Systematic Review which was based on over 16,000 patients from four trials and showed no difference in treatment efficacy, though it observed the increased risk of bleeding associated with anti-coagulation. A subsequent Cochrane meta-analysis, published in 2015, involving over 23,000 patients, found no basis to change the conclusion that early anticoagulant therapy is not associated with either short or long-term benefits in ischemic stroke cases.

[283] Fourth, both experts agree that the treatment outcomes with either therapy reveal a low chance of secondary stroke, roughly 2%, and that to the extent that any studies show a difference in outcomes, it is not a statistically significant outcome.

[284] Fifth, both experts agree that in cases of vertebral artery dissection, blood clots are the cause of 90% or more of the related strokes. That said, both also agree that hemodynamic transformation or occlusion can account for a secondary stroke, though they disagree in terms of the presence of this mechanism in Mr. Johnson’s case.

[285] In view of these areas of agreement, the defendant argues that the plaintiffs have failed to establish general causation. In other words, they argue that the plaintiffs have failed to demonstrate the general proposition that Heparin may in some cases be more likely to prevent secondary stroke in vertebral artery dissection cases. There is merit to the defendant’s submission. However, I am not satisfied that this is the case. While the available medical evidence to date does not suggest that one treatment is better than the other, both experts seem to agree that the specific circumstances of an individual patient may warrant the choice of one treatment over another. Implicit in this is an acceptance that clinical judgment plays a role in deciding which treatment is best for a patient in a specific set of circumstances. This implies that in some cases, one treatment will be better than the other. In other words, as a general proposition, the treatment choice may impact the outcome. Indeed, both experts agreed that a doctor would need to make an informed clinical decision in deciding which treatment to give. It is not simply a coin toss. As well, both experts agreed that there are differences between the treatments that make them more or less amendable depending on the circumstances. Anticoagulant treatments are “stronger” than antiplatelet treatments. However, anticoagulant treatments also come with an increased risk of bleeding which in some cases militates against their early use.

[286] In my view, this is a case where the focus is properly on specific causation. In other words, would the use of Heparin starting on or about October 23, 2012, have likely prevented Mr. Johnson’s second stroke.

[287] On this issue, I now turn to my specific reasons for not accepting Dr. Caplan’s evidence. At the outset, I note that Dr. Caplan’s core opinion was that had Mr. Johnson received Heparin instead of Aspirin, his second stroke would likely have not occurred. Dr. Caplan appeared to primarily base this opinion on his personal anecdotal experience in treating approximately 200 patients with vertebral artery dissection using Heparin and Warfarin. He explained that he could not remember a single patient who had a second stroke.

[288] Dr. Caplan also explained that the cause of Mr. Johnson’s second stroke was thromboembolic, in other words caused by a blood clot, and he discounted the possibly of hemodynamic transformation as having anything more than a complimentary causative effect. In Dr. Caplan’s opinion, red blood clots are more logically treated by anticoagulants and not antiplatelets since they act to prevent a new clot from forming and prevent embolization from that clot. In his view, anticoagulant treatment should be started as soon as possible, particularly in those patients that have luminal compromise and clots.

[289] I find that while Dr. Caplan purported to place great weight on the specific facts of Mr. Johnson’s case, he got some of his facts wrong. The most glaring example stems from Dr. Caplan’s first report, wherein he opines in conclusion that the early administration of Heparin from October 19 to 23, 2012, would have prevented Mr. Johnson’s stroke from “worsening.” From a medical perspective, a “stroke worsening” is completely distinct from a “second stroke.” Dr. Caplan agreed that these were different issues and acknowledged that he had actually published on the subject of “stroke worsening.” Importantly, he also agreed that Mr. Johnson actually showed no signs of “stroke worsening.” Ultimately, he agreed that the conclusion to his first report was actually incorrect on this basis, though he maintained that it was simply poor word choice.

[290] In addition, Dr. Caplan could not recall what imaging had been done on Mr. Johnson during his October 18, 2012 admission. He offered no opinion in his reports concerning the imaging or the CT scan of October 18, 2012. Dr. Caplan was under the mistaken impression that Dr. Crisp assessed Mr. Johnson on October 19, rather than October 21, 2012. He noted the date of the chiropractic visit as October 16, 2012 and not October 15, 2012, which was important given the timing of the onset of the first stroke. As well, Dr. Caplan agreed that he did not review the discovery transcripts of all parties in advance of preparing his first report, despite agreeing that it would be important to review all the relevant information before providing an opinion. He agreed that he did not indicate in his report what materials he reviewed in preparing his opinion, nor did his report specifically cite the literature and studies he relied on. To the extent that Dr. Caplan’s report referred to the CADISS study, it did so because he knew “it would come up.”

[291] While some of these errors and omissions standing alone are not overly significant, when taken together they suggest a lack of care and diligence in assessing the specific facts of Mr. Johnson’s case. These errors and omissions also cast a shadow on Dr. Caplan’s opinion which purports to be specifically based on Mr. Johnson’s personal circumstances.

[292] More importantly, I find that his responses when challenged on these factual inaccuracies and omissions were overtly positional and argumentative, bordering on condescending. Indeed, while he offered a quick “mea culpa” when confronted with inaccuracies, he then went on to minimize the nature the errors, accused opposing counsel of being “picayune” and queried whether the exercise was about “getting at the truth.” When confronted with passages, he on more than one occasion noted that counsel “read the passage correctly” when it was obvious that he was being asked whether he agreed with the passage. He grew frustrated with counsel’s attempt to canvass the various studies and recommendations and suggested more than once that counsel was re-treading the same ground. The manner in which he responded to these objectively valid questions suggested a degree of unhelpful defensiveness, and a lack of objectivity that is fundamental to the expert’s task in helping the court. I was left with the sense that Dr. Caplan was going to defend his opinion no matter what, rather than objectively acknowledging the state of the science and how it impacted his opinion.

[293] The next problematic area of Dr. Caplan’s opinion is that he based his assessment on what the optimal treatment for Mr. Johnson would have been between October 19 and 23, 2012. His view was that Mr. Johnson should have been placed on Heparin “the earlier the better.” The admitted negligence by Dr. Vieira did not occur until October 23, 2012. The assessment of the causative impact of Dr. Vieira’s failure to review the imaging cannot be connected to treatment with Heparin prior to that date. Dr. Caplan does not specifically address the causal connection in relation to Dr. Vieira’s failure on October 23, 2012. As well, Dr. Caplan does not specifically address the fact that it takes time for Heparin to reach a therapeutic level. On the evidence before the court, the earliest that Mr. Johnson would have started Heparin would have been October 23, 2012. He would have been fully “Heparinized” at some point thereafter. Dr. Caplan’s evidence does not address this issue. In short, his evidence fails to directly address the causal issue that arises as a result of Dr. Vieira’s admitted negligence.

[294] I next consider Dr. Caplan’s specific treatment of the trials and guidelines. In short, as mentioned, I find that Dr. Caplan was too quick to discount the relevance of the trials and guidelines. I also do not accept his description of the studies as “failed” or as having provided “no evidence.”

[295] Dr. Caplan acknowledged that the available medical literature does not support the theory that the earlier initiation of Heparin would likely have prevented Mr. Johnson’s second stroke. However, he attempted to explain that the medical literature simply provided “no answer” as there were insufficient end points from which one could possibly get an answer. In other words, given the relative rarity of vertebral artery dissections resulting in recurring strokes, the available evidence cannot provide a conclusion on which treatment is preferential. In considering his evidence on this issue, I find that Dr. Caplan mischaracterized the available scientific evidence. The fact that years of study and writing, including randomized trials and extensive meta-analyses, have not demonstrated that one treatment is better than the other, is not demonstrative of a “failure” of the studies or “no evidence.” Rather, I accept, as Dr. Gladstone explains, that this body of study and literature demonstrates that either there is no statistically significant difference between the treatments, or the difference is of a small degree such that it would only be measurable with a very large sample size.

[296] In particular, I note that Dr. Caplan recognized the CADISS randomized trial as the leading study on the subject worldwide and agreed that it has been used in drafting stroke guidelines throughout the world since its publication. Dr. Caplan also agreed that the data from CADISS applied directly to Mr. Johnson, as he met the inclusion criteria for the study and none of the exclusion criteria applied to him. The authors of the CADISS study concluded, “we found no difference in efficacy of antiplatelet and anticoagulant drugs at preventing stroke and death in patients with symptomatic carotid and vertebral artery dissection.” This conclusion does not support Dr. Caplan’s opinion. It does not suggest that Heparin would likely have prevented Mr. Johnson’s second stroke.

[297] Dr. Caplan’s main criticism of CADISS is that its sample size prevented the determination of a preferential treatment. The authors of the CADISS study addressed this very issue when they noted that even with a sample size of “many thousands”, any absolute effect on outcome as between the two treatments would be “very low.” Dr. Caplan agreed that even if a larger test sample showed that Heparin was hypothetically, 5%, 10% or 25% better than Aspirin, the difference in outcomes would be very small given the percentage of persons who have second strokes. He suggested that if such a hypothetical differential was established, a doctor would still need to determine whether Heparin was the better treatment by considering the individual patients and their characteristics. Importantly, Dr. Caplan agreed that even if such a differential were established by the evidence, it would essentially mean that the patient would have a corresponding chance of a better outcome.

[298] In terms of Dr. Gladstone’s opinion, I find that his evidence overall was more cogent and objective. As indicated, I do not agree that he placed “spin” on his evidence. I reject the assertion that he did not testify in a forthright manner. To the contrary, he accepted that certain matters should have been more clearly stated in his report. He did not minimize or attempt to explain away the omissions. For instance, he agreed he did not specifically disclose in his report that he had treated 150 vertebral dissection cases and had other involvement in approximately 100 more. He readily agreed that this was an important omission. However, and unlike Dr. Caplan, he did not seek to base his opinion mainly on his clinical observations. While the plaintiffs invite the court to draw an adverse inference against him on the basis that he did not go further and explain how he treated his patients or what the results of his past treatments were, I decline to do so. The plaintiffs could readily have asked Dr. Gladstone this question. They chose not to. Moreover, this is not an instance where Dr. Gladstone was seeking to rely on his clinical experience in order to justify the core of his opinion.

[299] I turn next to Dr. Gladstone’s evidence on the cause of Mr. Johnson’s second stroke. On this issue, I note that the Agreed Statement of Facts states that the second stroke was caused by the vertebral dissection which either produced further emboli that blocked blood flow to smaller arteries supplying the left cerebellum, or via hemodynamic ischemia due to a reduction of blood flow. The plaintiffs fairly point out that, while Dr. Gladstone’s report mirrored the agreed facts, in his evidence in-chief, Dr. Gladstone went further and opined that hemodynamic ischemia was the likely cause of the second stroke. He appeared to base this on the presence of occlusion as seen in the imaging. The plaintiffs next note that in cross-examination, he backed off and agreed that both an embolism or hemodynamic ischemia were the “likely cause” of the second stroke.

[300] While I agree with the plaintiffs’ submission that the unfolding of Dr. Gladstone’s evidence on this issue was not perfect, I nonetheless accept his evidence and his explanation. In particular, I note that the evidence of occlusion was obviously visible on the imaging appended to Dr. Gladstone’s report and the imaging shown in court. In other words, there was a valid and objective basis for Dr. Gladstone’s belief that Mr. Johnson had an occlusion and that it played a role in causing the second stroke.

[301] I also accept the evidence that Heparin is not a “clot-buster”. Indeed, both experts agreed on this. Dr. Gladstone went further and noted that in view of the occlusion, even if the mechanism of the stroke was embolic, Heparin would have been too little too late, as it would not have been able to open the blockage. Ultimately, Dr. Gladstone opined that based on the occlusion of Mr. Johnson’s vertebral artery, Mr. Johnson was at high risk for secondary stroke, no matter what treatment he received. I accept this evidence. It makes sense in the context of the evidence as a whole, especially when considering the fact that Mr. Johnson had antiplatelet therapy and had also received some benefit from anticoagulation therapy when he had the second stroke.

[302] Dr. Caplan did not specifically refer to Mr. Johnson’s imaging in his report, nor did he do so in his evidence. This causes me some concern over his position that hemodynamic ischemia played, at best, a complementary role in Mr. Johnson’s second stroke. I prefer Dr. Gladstone’s evidence on this issue as it was supported by specific reference to the available imaging.

[303] I am also concerned over Dr. Caplan’s evidence that anticoagulant therapy would have been better than antiplatelet therapy in Mr. Johnson’s case because red clots respond better to anticoagulants. Dr. Gladstone agreed that the biological rationale underlying the proposition is “very plausible.” That said, Dr. Gladstone also explained the rationale was not supported by the available medical evidence. Moreover, he noted that a preference for one medication over another was not proof that one medication was better than another. As such, I find that Dr. Caplan’s evidence on this issue was likely overstated. It would have been more accurate for Dr. Caplan to state that antiplatelet therapy could have been better than antiplatelet therapy in Mr. Johnson’s case.

[304] On the whole, I prefer and accept Dr. Gladstone’s evidence on this issue. Importantly, I accept his evidence that the occlusion in Mr. Johnson’s artery is a factor that would have made Heparin less effective in the circumstances. Put another way, I find that the presence of occlusion undermines a finding that Heparin would likely have prevented the second stroke.

[305] Lastly, I will address the plaintiffs’ argument regarding the efficacy of the specific dosage of Aspirin taken by Mr. Johnson, which was 81 mgs daily, essential a “baby-Aspirin.” The plaintiffs argue that the validity of the CADISS study is undermined as the patients in the antiplatelet group in that study were not all on Aspirin alone. Some had Plavix, some Aspirin and Plavix, some Aspirin alone and a small number had Persantine. More importantly, the study does not reveal the specific dosage of Aspirin taken. In the TREAT-CAD study, the patients in the antiplatelet group were treated with 300 mgs of Aspirin daily. As well, Dr. Gladstone agreed in cross-examination that most of the available studies and analyses involved patients who were taking between 160 mgs and 300 mgs of Aspirin daily. The plaintiffs note that Dr. Caplan also expressed some disagreement with the 81 mgs dosage, though he did not get into this issue in any detail.

[306] The issue of dosage was specifically addressed by Dr. Gladstone. He explained that the studies he was aware of, albeit not in the context of vertebral artery dissection, showed no difference in efficacy between 81 mgs of Aspirin and the higher doses taken in some of the studies discussed. In fact, he noted that some of the evidence suggested a worse outcome. I accept his evidence on this point. Despite Dr. Caplan’s apparent misgivings, he did not specifically contradict it, nor did he point to any study suggesting the superiority of higher doses of Aspirin. In any event, the 81 mg dosage is the standard dosage used in Canada. The fact that the studies in the arterial dissection and/or ischemic stroke context had patients taking higher doses does not, on the evidence before me, undermine the results of those studies. In any event, there is no suggestion that the difference in outcome between 81mgs and 300 mgs of Aspirin would somehow prove that Heparin was more effective at preventing secondary stroke such as the one suffered by Mr. Johnson.

Conclusion

[307] For the reasons provided, I am satisfied that had Dr. Vieira viewed and appreciated the MRI and MRA imaging on October 23, 2012, she would have consulted with Dr. Crisp who would likely have advised against Mr. Johnson’s discharge. I find that Mr. Johnson would likely have been placed on anticoagulant therapy, specifically Heparin, as of that date.

[308] However, considering all the evidence, I am simply not satisfied that the switch to anticoagulant therapy would likely have prevented Mr. Johnson’s second stroke. At best, it may have possibly resulted in a different outcome, either better or perhaps even worse than the actual outcome. While I am cognizant that the plaintiffs need not prove causation with scientific precision, this is not a case where a common-sense inference can be used to bridge the evidentiary gap. The evidence taken as a whole simply does not support the conclusion either directly or by inference that Mr. Johnson’s second stroke would likely have been prevented had he been placed on Heparin instead of Aspirin at the time of his initial discharge from hospital. As such, the plaintiffs have failed to prove causation.

[309] I reach this conclusion with a significant amount of sympathy and understanding for Mr. Johnson and his family. He has suffered a life altering stroke with significant long-lasting consequences. I am certain that he and his family firmly believe that Dr. Vieira is responsible for this outcome and that he should be compensated as a result. While Dr. Vieira’s conduct falls below the standard of care required of doctors, the evidence does not establish that her conduct ultimately caused the second stroke.

[310] This is not an easy answer to accept. However, on this issue, I can do no better than to quote Dr. Gladstone who stated, “Unfortunately, recurrent strokes occur all the time, and every time someone has a stroke, it’s heartbreaking. And the reality is our currently available medications are just not foolproof. Unfortunately, our treatments do not prevent all strokes.”

[311] The action is dismissed.

[312] The parties are urged to agree on costs. If that is not possible, the parties are invited to file written costs submissions no longer than five pages in length, excluding appropriate appendices and caselaw. The defendant’s costs submissions will be due within 30 days of the release of these reasons. The plaintiffs’ submissions shall be due within 45 days. There shall be no right of reply.

[313] I wish to conclude by noting that this difficult case was efficiently and effectively presented by excellent counsel who demonstrated the highest level of skill, preparation and commitment throughout.

J. Di Luca J.

Released: May 1, 2023

ONTARIO

SUPERIOR COURT OF JUSTICE

BETWEEN:

WILLIAM JOHNSON, JENNIFER JOHNSON and ROBERTA JOHNSON

Plaintiffs

– and –

LAKERIDGE HEALTH CORPORATION, DR. MORRIS NEALE GINSBURG, DR. SHENIF LADAK, DR. DAVID CRISP, DR. ROSE-ANNE VIEIRA, DR. GEOFFREY DONSKY, JOHN DOE AND JANE DOE

Defendants

REASONS FOR decision

The Honourable Justice J. Di Luca

Released: May 1, 2023

[^1]: On consent, the action was dismissed as against Lakeridge Hospital Corporation and the other named doctors. The action was discontinued against John Doe and Jane Doe.

[^2]: In circumstances where multiple tortfeasors are all at fault, it may be appropriate for the court to apply a “material contribution to risk of injury test”, see Clements at para. 39. Counsel agree that this is not one of those cases.

[^3]: An Amended Agreed Statement of Fact was also filed at trial correcting a minor error in the original Agreed Statement of Fact.

[^4]: Mr. Johnson’s PTT values associated with his October 29, 2012 readmission are set out in Schedule “A” to the Agreed Statement of Fact.

[^5]: While the note may also be admissible as a business record under s. 35(2) of the Ontario Evidence Act, I need not decide this issue.