5th article

Question 1

A 69-year-old man was admitted to this hospital because of

Answer 1

dizziness and vomiting.

Question 2

The patient had been well until 4:15 a.m. on the day of admission, when he became

Answer 2

dizzy, diaphoretic, and weak and had sensations of rocking and counterclockwise movement after he rolled onto his stomach in bed.

Question 3

The symptoms improved when he rolled into the supine position, and he slept until 7 a.m.; on awakening, the symptoms recurred. When walking, he sensed he was

Answer 3

tilting to the left but did not fall.

Question 4

The symptoms worsened throughout the

Answer 4

morning; they were most severe with head movements and were associated with increasing nausea and, after 10 a.m., vomiting.

Question 5

He called his doctor’s office because of concern that he was having

Answer 5

a stroke. He was advised to go the hospital and called emergency medical services

Question 6

On examination, his skin was

Answer 6

pale and dry and the blood pressure was 148/60 mm Hg; the other vital signs and the remainder of the examination were normal.

He was brought to the emergency department at this hospital, arriving approximately 9 hours after the onset of symptoms.

Question 7

The patient reported

Answer 7

1. facial tingling in the area surrounding the eyes, including
2. the malar eminence, and
3. a mild headache.

Question 8

He noted that his visual perception momentarily

Answer 8

lagged behind his eye movements, and the lag was more severe when looking to the right than to the left.

Question 9

He had

Answer 9

no diplopia, blurred vision, tinnitus, decreased hearing, difficulty swallowing, changes in sensation or strength, palpitations, chest pain, fever, or shortness of breath.

Question 10

He reported an episode of

Answer 10

self-limited positional vertigo that had occurred several years earlier.

Question 11

He had

Answer 11

1. hypertension,
2. hyperlipidemia,
3. asthma,
4. sleep apnea (for which he intermittently used continuous positive airway pressure at night),
5. depression,
6. meralgia paresthetica (a painful mononeuropathy of the lateral femoral cutaneous nerve),
7. erectile dysfunction, and
8. recurrent localized herpes simplex virus infection.

Question 12

His daily medications included

Answer 12

rosuvastatin, valsartan, hydrochlorothiazide, duloxetine, aspirin, and a multivitamin.

Question 13

He also received, as needed,

Answer 13

1. a topical lidocaine patch for meralgia paresthetica;
2. gabapentin for pain;
3. vardenafil (though he had not taken it recently);
4. fluticasone propionate nasal spray and inhaler,
5. albuterol, and loratadine for wheezing and asthma; and 6. valacyclovir.

Question 14

He swam regularly, drank

Answer 14

wine daily, and did not smoke.

Question 15

His siblings had

Answer 15

1. arthritis and

2. hypercholesterolemia, and his children and grandchildren were healthy.

Question 16

On examination, the patient was

Answer 16

alert and oriented.

Question 17

The skin was

Answer 17

pale and diaphoretic.

Question 18

The blood pressure was 123/89 mm Hg, and the pulse 58 beats per minute; the other vital signs and oxygen saturation were

Answer 18

normal.

Question 19

The sensation of light touch was slightly

Answer 19

1. decreased over the malar eminence and the

2. jaw on the left side and was normal over the eyelids, frontalis muscle, and upper neck.

Question 20

There was

Answer 20

1. nystagmus on left lateral gaze, and
2. sustaining left lateral gaze required some effort;
3. the eye movements were slower from midline to the left than from midline to the right.

Question 21

He was able to reproduce the

Answer 21

sensation of delayed visual return, which was more severe when moving his head to the right than to the left.

Question 22

When he was not supported, he tilted

Answer 22

to the left.

Question 23

He walked

Answer 23

cautiously and slowly, with a slightly broad-based gait, and was unable to perform tandem walking.

Question 24

Deep-tendon reflexes were slightly more

Answer 24

1. brisk on the right side than on the left side.

2. The remainder of the neurologic and general examinations was normal.

Question 25

The blood level of carbon dioxide was

Answer 25

low –> 21.9 mmol per liter (reference range, 23.0 to 31.9),

Question 26

the level of glucose was

Answer 26

high –> 164 mg per deciliter (9.1 mmol per liter; reference range, 70 to 110 mg per deciliter [3.9 to 6.1 mmol per liter]),

Question 27

the level of phosphorus was

Answer 27

low –> 1.2 mg per deciliter (0.4 mmol per liter; reference range, 2.6 to 4.5 mg per deciliter [0.8 to 1.5 mmol per liter]), and

Question 28

the anion gap was

Answer 28

high –> 16 mmol per liter (reference range, 3 to 15).

Question 29

Blood levels of other electrolytes, calcium, and magnesium were

Answer 29

normal, as were results of the complete blood count and tests of coagulation, renal function, and liver function;

Question 30

screening for troponin I was

Answer 30

negative.

Question 31

An electrocardiogram (ECG) showed

Answer 31

1. sinus rhythm at a rate of 59 beats per minute and

2. no acute ischemic changes.

Question 32

Lorazepam, ondansetron, and intravenous fluids were administered, and the patient’s condition partially

Answer 32

improved.

Question 33

Dr. R. Gilberto Gonzalez: Approximately 2 hours after the patient’s arrival, computed tomography (CT) of the brain, performed without the administration of contrast material, revealed

Answer 33

normal brain parenchyma and an extraaxial calcified lesion, 9 mm by 16 mm by 6 mm, in the left
parafalcine area over the high parietal convexity;

Question 34

there was

Answer 34

no intracranial hemorrhage, extraaxial collection, mass effect, or midline shift.

Question 35

When this event started, according to the history, you had rolled over in bed.
Can you describe to me exactly what happened?
The Patient: I woke up

Answer 35

1. lying on my stomach, and
2. the room was spinning.
3. I was sweating so profusely that I had to wring out my T-shirt and take it off.

Question 36

Dr. Ning: Did you sit up?

The Patient: I sat up

Answer 36

1. briefly. I went back to sleep on my back for a few hours and then woke up.
2. The spinning was less severe, but it was still there.

Question 37

Dr. Ning: I understand that you do a lot of vigorous exercise, including swimming. Had you
done anything unusual before this episode? The Patient: I generally

Answer 37

1. swim 5 days a week. I do

2. a freestyle stroke for 1 or 2 miles, or I occasionally do a 3. modified butterfly stroke or a breaststroke.

Question 38

The day before the episode, I swam

Answer 38

three fourths of a mile, mostly doing a freestyle stroke, as part of my training for a triathlon.

Question 39

First, I will try to identify the anatomical localization and cause of the present illness from the history provided. The patient is a

Answer 39

1. 69-year-old,
2. left-handed avid swimmer who,
3. after rolling onto his stomach in bed, noted
4. vertigo,
5. diaphoresis, and the development of progressive and fixed symptoms, including tilting to the left, nausea, vomiting, headache, oscillopsia (the visual perception of objects moving when they are actually stationary), and
6. changes in facial sensation.

Question 40

Neurologic symptoms can be localized to the central nervous system or the peripheral nervous system; most of the signs and symptoms in this case are of

Answer 40

central origin.

Question 41

The central nervous system is roughly divided into the supratentorial and infratentorial regions.

Abnormalities in the two regions have some common manifestations, such as

Answer 41

unilateral weakness and loss of sensation.

Question 42

Patients with supratentorial lesions (i.e., lesions in the frontal, parietal, temporal, or occipital lobe) can present with

Answer 42

cortical signs, such as

1. aphasia,
2. neglect,
3. difficulty with higher cognitive functions (e.g., calculation or praxis),
4. confusion, and
5. visual-field deficits.

Question 43

Patients with infratentorial lesions (i.e., lesions in the brain stem or cerebellum) can present with

Answer 43

cranial-nerve abnormalities and cerebellar signs, such as 1. dysarthria,

2. double vision,
3. difficulty swallowing,
4. nystagmus,
5. oscillopsia,
6. dysmetria,
7. ataxia,
8. gait imbalance,
9. nausea, and
10. vertigo.

Question 44

In this case, what led to think that the lesion is localized to the brain stem and cerebellum?

Answer 44

1. the constellation of symptoms and

2. the lack of cortical signs indicate that the lesion is localized to the brain stem and cerebellum.

Question 45

Occasionally, patients with a mass or demyelinating lesion adjacent to the cerebral ventricles or aqueduct can have

Answer 45

rapid-onset hydrocephalus, which is associated with symptoms similar to those seen in this case.

Question 46

However, what clues suggested that the pt has focal neurovascular event?

Answer 46

1. the sudden onset of illness and
2. the rapid progression within a few hours, in the absence of other subacute signs, are suggestive of a focal neurovascular event.

Question 47

There are several crucial signs in this case. The first important sign is that the

Answer 47

1. patient rolled over onto the abdomen in bed — that is, he performed a passive Valsalva maneuver.
2. The Valsalva maneuver is associated with
   - active coughing,
   - heavy lifting,
   - constipation, or
   - passive pressure on the abdomen that alters atrial pressure.

Question 48

The maneuver can cause

Answer 48

paradoxical embolic stroke by forcefully opening a patent foramen ovale and allowing venous clots to travel to the brain.1

Question 49

Change in body position can also move

Answer 49

otoliths in the semicircular canals of the inner ear2 or stretch vertebral blood vessels traveling inside the cervical spinous processes.

Question 50

Cardiac ischemia triggers

Answer 50

1. hyperactivity of the autonomic nervous system and is commonly associated with diaphoresis,
2. but it is rarely associated with true vertigo, a normal ECG, or negative screening results for troponin I.

Question 51

On rare occasions, during vertebrobasilar stenosis or clotting, low flow due to cardiac failure can trigger

Answer 51

brain-stem ischemia, which is manifested as central vertigo.

Question 52

In addition, the brain can activate autonomic instability,3 and posterior-circulation infarcts can be associated with

Answer 52

hyperhidrosis.4-6

Question 53

The spinning sensation, or true vertigo, is of

Answer 53

central origin (Table 1).2,7

Question 54

Peripheral vertigo (a dysfunction of the peripheral vestibular system) is

Answer 54

more prevalent than central vertigo in the general population, but peripheral vertigo should be a diagnosis of exclusion in patients with vascular risk factors.

Question 55

Central vertigo is associated with lesions in the

Answer 55

posterior fossa (i.e., the brain stem and cerebellum), and its symptoms — including

1. nausea,
2. vomiting (due to increased intracranial pressure),
3. inability to walk (due to ataxia or weakness), and
4. headache — can often be mistakenly attributed to gastroenteritis.

Question 56

Vertebrobasilar stroke should be considered because its consequences are

Answer 56

devastating; it is associated with up to 50% mortality.8

Question 57

what is crucial for putting his acute symptoms in the context of other risk factors?

Answer 57

Assessment of the patient’s medical history is crucial for putting his acute symptoms in the context of other risk factors.

Question 58

It is important to identify

Answer 58

1. traditional risk factors (e.g., hypertension and hyperlipidemia, both present in this patient), as well as
2. emerging risk factors (e.g., sleep apnea, migraine with aura, and
3. genetic variants such as CADASIL [cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy]).

Question 59

This patient had

Answer 59

1. meralgia paresthetica and

2. erectile dysfunction, which may point to underlying diabetes or uncontrolled hypertension;

Question 60

we often discover glucose intolerance or diabetes during a diagnostic workup for

Answer 60

stroke.

Question 61

Chronic inflammatory conditions (e.g., recurrent localized herpes simplex virus infection and arthritis) may contribute to

Answer 61

clotting and vascular risk factors.

Question 62

Furthermore, the patient, as an avid swimmer and triathlete, is at risk for

Answer 62

neck injury. In view of the risk factors, a vascular cause of his symptoms (i.e., acute stroke) is likely.

Question 63

Clinical examination can help to distinguish

Answer 63

central vertigo from peripheral vertigo (Table 1).

Question 64

The presence of asymmetric deep-tendon reflexes indicates a

Answer 64

central phenomenon, but diabetic neuropathy can obliterate these reflexes.

Question 65

In central horizontal nystagmus, the fast phase is toward

Answer 65

the side of the lesion, indicating involvement of the left cerebellum in this case.

Question 66

The loss of facial sensation in this patient may be related to focal injury in the

Answer 66

medulla near the fifth cranial nerve.

Question 67

The examination is localized to a partial territory of the

Answer 67

posterior inferior cerebellar artery (Fig. 1);

Question 68

a full-blown infarct of a posterior inferior cerebellar artery (Fig. 1B and 1C), or the lateral medullary syndrome, is relatively

Answer 68

rare, since the vascular pathological features have various thromboembolic distributions.9,10

Question 69

In the United States, stroke is the leading cause of

Answer 69

serious long-term disability; one person dies from stroke every 4 minutes, and one in four patients with stroke have recurrent strokes.

Question 70

The two major types of stroke are

Answer 70

1. ischemic (caused by a lack of blood flow and accounting for 87% of strokes) and
2. hemorrhagic (caused by a blood-vessel rupture and accounting for 13% of strokes).11

Question 71

Symptoms of the two types differ but can overlap as a result of

Answer 71

1. anatomical variance,
2. handedness, or
3. other genetic factors.11

Question 72

Hemorrhagic strokes are roughly classified according to

Answer 72

location; the subtypes are

1. subarachnoid,
2. epidural,
3. subdural, and
4. intraparenchymal.

Question 73

In this patient, the lack of

Answer 73

1. early severe headache and

2. lack of progression to global alterations in consciousness make subarachnoid hemorrhage an unlikely diagnosis.

Question 74

Epidural hemorrhage, commonly due to

Answer 74

traumatic injury of the middle meningeal artery, occurs in persons who are in a younger age group (i.e., <45 years of age) and whose skull and dura are more easily separated.

Question 75

In persons in this patient’s age group (i.e., >65 years of age), subdural hemorrhage can cause

Answer 75

progressive focal neurologic changes, especially after trauma, and an acute-on-chronic subdural hemorrhage can cause seizures in those who are taking anticoagulant drugs.

Question 76

Recently recognized causes of intraparenchymal hemorrhage, such as

Answer 76

cerebral amyloid angiopathy, may result in an indolent disease course and cognitive changes.12

Question 77

Intraparenchymal hemorrhage due

Answer 77

to hypertension is a possible diagnosis in this case; it commonly occurs in the cerebellum and basal ganglia.

Question 78

It is very important to distinguish ischemic stroke from

Answer 78

hemorrhagic stroke, because the treatments are completely different. Dr. Gonzalez has reviewed the crucial cranial CT scan, which rules out the diagnosis of clinically significant hemorrhage.

Question 79

The incidental intraaxial lesion cannot explain the symptoms; such a lesion could cause

Answer 79

seizures but not fixed deficits.

Question 80

Venous strokes due to cerebral venous thromboses are less common than

Answer 80

arterial ischemic strokes; they develop over days or weeks and frequently go undetected.

Question 81

what are the clinical signs that prompt an urgent workup for cerebral venous thrombosis?

Answer 81

1. Venous hypercoagulability,
2. worsening headache,
3. changes in visual acuity,
4. papilledema, or
5. the late development of a hemorrhagic lesion (due to venous congestion) should prompt an urgent workup for cerebral venous thrombosis.

Question 82

Arterial strokes, which account for the majority of ischemic infarcts, comprise

Answer 82

1. thrombotic (largevessel or small-vessel) strokes,
2. embolic (cardioembolic or paradoxical embolic) strokes, and
3. other vasospastic variants (Table 2).13,14 A large proportion (>30%) of arterial strokes are cardioembolic, regardless of the age group of the patients.

Question 83

Age, cognitive status, sex, and race were traditionally used to identify stroke subtype; older age is associated with

Answer 83

1. large-vessel atherosclerotic disease,
2. cognitive impairment with small-vessel disease, and younger age with traumatic dissection and congenital abnormalities.14-18 As the population lives longer, age may not be reliable in the identification of stroke subtypes, and an individual patient may have multiple causes of stroke.

New causes of strokes in the cryptogenic category (i.e., strokes of unclear cause after a standard workup) have been discovered, including genetic variants (e.g., CADASIL), subclinical paroxysmal atrial fibrillation undetected by short-term cardiac monitoring, and cardiac abnormalities (e.g., patent foramen ovale).18-20 Patent foramen ovale is associated with more than 40% of cryptogenic strokes.1

Question 84

This patient crosses these traditional stroke categories. He is at risk for

Answer 84

atherothrombotic disease because of

1. his age and
2. the presence of hyperlipidemia and
3. hypertension.

Question 85

However, he appears younger than his stated age and is a swimmer, and thus he is also at risk for stroke
subtypes associated with

Answer 85

younger age, such as

1. traumatic dissection and
2. paradoxical embolism due to a patent foramen ovale.

Question 86

If his previous episode of vertigo was associated with a transient ischemic attack, then a likely diagnosis is

Answer 86

thrombotic stroke because emboli seldom affect the same territory repeatedly.

Question 87

The patient will need to undergo an individualized diagnostic workup (Table 3). He will undergo

Answer 87

1. magnetic resonance imaging (MRI) of the brain and its vasculature, as well as
2. cardiac evaluation, because of the high prevalence of embolic stroke.19

Question 88

We have formed a cardioneurology clinic at this hospital to evaluate the health of the heart in terms of stroke risk and treatment, since up to 50% of ischemic strokes involve the

Answer 88

heart and since large-vessel arterial disease and cardioembolic disease can coexist, in part because they have shared cardiovascular risk factors.1

Question 89

The brain is the “upstairs neighbor” of the heart and on the receiving end of ischemic injury, and thus

Answer 89

monitoring circulatory brain–heart communication is crucial for stroke prevention.

Question 90

For example, the right-to-left shunting through a patent foramen ovale not only allows clots to go
through but also

Answer 90

increases oxidative stress in the blood, elevating the risk of future events.20 Blood lipid levels and inflammatory and individualized clotting profiles should be obtained to stratify stroke risk for future management (Table 3).

Question 91

In summary, in view of the

Answer 91

1. sudden-onset,
2. progressive,
3. fixed neurologic deficits,
4. the history of potential neck injury, and
5. the risk factors for thromboembolic disease, my leading diagnosis is ischemic stroke due to vertebral-artery dissection, resulting in artery-to-artery emboli in the territory of the posterior inferior cerebellar artery.

Question 92

A cardioembolic event is also in the differential diagnosis. Because the risk factors for and the causes of various stroke subtypes can

Answer 92

overlap, the next step is a comprehensive workup for stroke that includes vascular imaging, as well as cardiac and hematologic testing tailored to the patient’s risk factors.

Question 93

Dr. Rosenberg: Dr. Kim, would you tell us the thinking of your team during evaluation of the patient?

Dr. Kim: We were concerned that a vascular event, either hemorrhagic or ischemic stroke, had occurred between the time the patient went to bed and the time he first woke up, at 4:15 a.m. We believed that the event was most likely localized to

Answer 93

the cerebellum.

Question 94

We were concerned that he had a traumatic dissection that caused

Answer 94

a posterior-circulation infarct. Nine or 10 hours had already passed since symptom onset, so the window of time during which he could undergo thrombolysis with intravenous tissue plasminogen activator (t-PA) had closed.

Question 95

CT without the administration of contrast material was performed to rule out the presence of hemorrhage.

Answer 95

The patient then underwent MRI and magnetic resonance angiography (MRA).

Question 96

Clinical Diagnosis

Answer 96

Cerebellar ischemic stroke, possibly due to vertebral-artery dissection.

Question 97

DR. MingMing NING’s DIAGNOSIS

Cerebellar ischemic stroke due to

Answer 97

vertebralartery dissection, with artery-to-artery emboli in a partial territory of the posterior inferior cerebellar artery.

Question 98

Discussion of Imaging

Dr. Rosenberg: Dr. Gonzalez, would you make the diagnosis for us?

Answer 98

Dr. Gonzalez: MRI and MRA were performed. The diffusion-weighted images show a single
hyperintense abnormality involving the
1. medial left cerebellum and
2. vermis (Fig. 2A);

Question 99

the abnormality is hypointense on the apparent-diffusion- coefficient images, a finding that confirms that this is an

Answer 99

acute infarction.

Question 100

On T2-weighted images (not shown) and fluid-attenuated inversion recovery images (Fig. 2B),

Answer 100

a hyperintense abnormality is identified at precisely the same location as on the diffusion weighted images, findings that suggest that the acute infarction occurred more than 6 hours earlier.

Question 101

MRA revealed

Answer 101

1. normal,
2. widely patent,
3. bilateral carotid and right vertebral arteries (Fig. 2C);

Question 102

however, the left vertebral artery is

Answer 102

poorly visualized (Fig. 2D).

Question 103

Images from MRI scans suggest

Answer 103

acute left cerebellar infarction due to a dissection of the left vertebral artery.

Question 104

CT angiography was performed to confirm the diagnosis of

Answer 104

dissection; the images show a normal right vertebral artery, but the left vertebral artery is enhanced intermittently, confirming that the presence of a dissection is likely.

Question 105

Discussion of Management

Dr. Rosenberg: Dr. Ning, would you tell us how you would manage this case?

Answer 105

Dr. Ning: Appropriate management and secondary prevention of acute ischemic stroke must target the underlying cause.

Question 106

Management of acute Ischemic Stroke Thrombolysis with intravenous t-PA is first-line treatment for acute ischemic stroke. Major clinical trials of thrombolysis in patients with ischemic stroke did not exclude patients with dissection, and a meta-analysis suggested

Answer 106

no difference in the risk of hemorrhage in patients with dissection and in those without dissection.21,22 Intravenous t-PA can be efficacious if it is administered within 4.5 hours (or perhaps even longer) after symptom onset in selected patients,23-27 but the Food and Drug Administration has not yet approved its use beyond a 3-hour window.

At this hospital, patients give informed consent for the administration of intravenous t-PA within 4.5 hours after symptom onset, on a case-by-case basis.

Question 107

However, patients are ineligible if they do not know the time of symptom onset or if their presentation is delayed because of neurologic symptoms (e.g., in this case, the patient fell

Answer 107

back to sleep, possibly because of brain-stem ischemia that decreased consciousness). In patients with basilar-artery thrombosis with severe disability, such as those with the locked-in syndrome, intraarterial thrombolysis or clot retrieval can be performed up to 24 hours after symptom onset.

Ongoing clinical trials and innovative technology may help to widen the therapeutic window, and educating primary care providers to recognize early stroke symptoms can also be very useful.28-31 In the acute care setting, patients with largeterritory cerebellar or cerebral infarcts should be monitored in the neurologic intensive care unit for edema and herniation. Treatment can involve intravenous hyperosmolar therapy, placement of an external ventricular drain for hydrocephalus, or decompressive craniectomy.32

Treatment for dissection in patients who are not receiving acute care should be individualized.

It may seem risky and counterintuitive to administer anticoagulation therapy for a torn blood vessel, but cerebrovascular dissections are rarely actual ruptures of the vessel; more often, they are separations of the intima from the rest of the vascular wall, and the prothrombotic intimal flap can act as a source of distal emboli.

Patients with dissection within the intradural portion of the vertebral artery (Fig. 1A) who receive anticoagulation therapy are at increased risk for bleeding; unless a clot is advancing toward the basilar artery, anticoagulation therapy is not recommended.

On rare occasions, dissection occurs within the tunica media or adventitia, resulting in a pseudoaneurysm or vessel-wall rupture and subarachnoid hemorrhage33,34; this is more common in posterior-circulation intracranial dissections and spontaneous dissections associated with collagen vascular disease (e.g., Marfan’s syndrome and fibromuscular dysplasia). This patient does not have marfanoid features.

Our overall clinical experience indicates that the risk of hemorrhage is relatively low among patients with arterial dissection.35 Unless there is evidence of subarachnoid hemorrhage or extensive intracranial vertebral-artery dissection with the formation of a pseudoaneurysm, careful anticoagulation therapy for 3 to 6 months, to give injured vessels a chance to recanalize, can maximize the risk–benefit ratio for this patient, because the chance of emboli is highest within the first few months.

Question 108

Workup for Stroke and Secondary Prevention Table 3 lists indications for studies that should be tailored to the individual patient. Patients with multiple cardiovascular risk factors can have multiple simultaneous causes of stroke.

Answer 108

As the population lives longer and ages better, causes of stroke normally associated with younger age groups (e.g., traumatic dissection and patent foramen ovale) are affecting older patients;

Question 109

for example, paradoxical embolism can be caused by deep-vein thrombosis after hip replacement, or vertebralartery dissection can be caused by traumatic neck injury in patients,

Answer 109

such as this one, with spinal arthritis.

Question 110

Understanding the cause of the initial stroke is the

Answer 110

best way to prevent recurrence.

Question 111

In this case, it is important to understand the

Answer 111

course of the vertebral artery as it travels within the cervical spinous processes (Fig. 1A).

Question 112

The “elbow” of the artery (Fig. 1A, segment III) is likely to tear during

Answer 112

rotation of the joint at the level of C1 and C2.

In addition to dissection, older patients with cervical arthritic lesions can undergo the development of bow-hunter’s syndrome, which occurs when extreme rotation of the neck (such as the rotation that occurs during archery) occludes a vertebral artery in the neck and the other vertebral artery is already atretic or occluded (Fig. 1D).

Question 113

Exercise has benefits that generally outweigh the risks, but the patient should be counseled about

Answer 113

bow-hunter’s syndrome and the risk of vertebral-artery dissection.

Question 114

Dynamic transcranial Doppler ultrasonography to monitor intracranial flow during head turning can gauge limits in range of motion.

Answer 114

If the transcranial Doppler study shows poor flow and the patient becomes symptomatic during movement, then an intervention, such as a neck brace to limit range of motion or possibly stenting, may be indicated.

Question 115

Modification of Risk Factors
Since an individual patient can have overlapping causes of stroke, lifestyle modifications and the management of all risk factors (e.g., hypertension, diabetes, physical inactivity, and obesity) are keys to secondary stroke prevention.15,16

Answer 115

After epithelial injury due to dissection, the risk of atherosclerosis at the site of the injury becomes higher. Monitoring blood markers is helpful in individualized medical management.

For example, low-density lipoprotein (LDL) cholesterol levels below 70 mg per deciliter (1.8 mmol per liter) are associated with a significant decrease in the risk of stroke; however, substantially lower LDL cholesterol levels (i.e., ≤30 mg per deciliter [0.8 mmol per liter]) are associated with an increased risk of intracranial hemorrhage.36 Lifestyle modifications (e.g., healthful changes in diet, exercise, and alcohol consumption, as well as smoking cessation) and the treatment of obesity and sleep apnea are also important. Supervised neurorehabilitation is crucial for recovery,37 and treatment of depression and anxiety can improve motor outcomes after stroke.38

In summary, stroke often has multiple mechanisms, and thus a thorough, individualized workup ensures a comprehensive strategy for treatment and prevention.

Dr. Rosenberg: Dr. Kim, would you tell us what happened with this patient?

Dr. Kim:

Question 116

The patient was admitted to the neurology service.

Answer 116

1. Anticoagulation therapy with heparin was begun and was later transitioned to warfarin.
2. His symptoms gradually improved, and he was discharged on the fourth hospital day.

Question 117

Results of a cardiac ultrasound examination and routine laboratory studies were

Answer 117

normal. There were no arrhythmias on 24-hour Holter monitoring.

Question 118

Two months after discharge, a CT angiogram showed persistent

Answer 118

1. nonvisualization of the cervical portion of the left vertebral artery and
2. better visualization of the intradural portion;

Question 119

anticoagulation therapy was continued, with the plan to perform

Answer 119

repeat imaging in 3 months.

Question 120

Seven months after discharge, a repeat CT angiogram showed

Answer 120

1. persistent nonvisualization of the cervical portion of the left vertebral artery on early-phase images
2. but full opacification of the cervical portion on delayed images, with focal areas of luminal thrombus that were most prominent at the level of C4 and C5.

Question 121

The intradural left vertebral artery and the dominant right vertebral artery were

Answer 121

patent.

Question 122

His symptoms had completely resolved, and he was back to performing high level physical activities. The decision was made to discontinue

Answer 122

warfarin, and he resumed taking aspirin for secondary stroke prevention.

Careful control of his blood-pressure and lipid levels has been maintained.

Dr. Rosenberg: Are there questions for any of the discussants or the patient?

A Physician: Dr. Ning, would you have initiated treatment with intravenous t-PA if the patient had arrived within the 3-hour window?

Dr. Ning: I would have administered intravenous t-PA within 3 hours (or even 4.5 hours) after arrival if a CT scan showed no evidence of hemorrhage. Patients who receive intravenous t-PA are 30% more likely to have better outcomes at 3 months39; however, t-PA can trigger reperfusion injury37-40 and result in symptomatic intracerebral hemorrhage in 3.3 to 15.7% of patients.41-44

Continuing clinical and translational research regarding the timing of stroke and the widening of therapeutic windows for the administration of thrombolysis is important.23,29,30,37,40,45,46

Question 123

A Physician: Swimming the freestyle stroke involves a lot of head turning. Were you advised to stop swimming freestyle after your stroke?

Answer 123

The Patient: After my stroke, I was advised not to swim at all. I turned to other types of activity, including walking and running. After about 1 year, I resumed swimming and have had no further problems.

Question 124

Anatomical Diagnosis??

Answer 124

Dissection of the left vertebral artery and cerebellar infarction.