5th article Flashcards
1
Q
A 69-year-old man was admitted to this hospital because of
A
dizziness and vomiting.
2
Q
The patient had been well until 4:15 a.m. on the day of admission, when he became
A
dizzy, diaphoretic, and weak and had sensations of rocking and counterclockwise movement after he rolled onto his stomach in bed.
3
Q
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
A
tilting to the left but did not fall.
4
Q
The symptoms worsened throughout the
A
morning; they were most severe with head movements and were associated with increasing nausea and, after 10 a.m., vomiting.
5
Q
He called his doctor’s office because of concern that he was having
A
a stroke. He was advised to go the hospital and called emergency medical services
6
Q
On examination, his skin was
A
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.
7
Q
The patient reported
A
- facial tingling in the area surrounding the eyes, including
- the malar eminence, and
- a mild headache.
8
Q
He noted that his visual perception momentarily
A
lagged behind his eye movements, and the lag was more severe when looking to the right than to the left.
9
Q
He had
A
no diplopia, blurred vision, tinnitus, decreased hearing, difficulty swallowing, changes in sensation or strength, palpitations, chest pain, fever, or shortness of breath.
10
Q
He reported an episode of
A
self-limited positional vertigo that had occurred several years earlier.
11
Q
He had
A
- hypertension,
- hyperlipidemia,
- asthma,
- sleep apnea (for which he intermittently used continuous positive airway pressure at night),
- depression,
- meralgia paresthetica (a painful mononeuropathy of the lateral femoral cutaneous nerve),
- erectile dysfunction, and
- recurrent localized herpes simplex virus infection.
12
Q
His daily medications included
A
rosuvastatin, valsartan, hydrochlorothiazide, duloxetine, aspirin, and a multivitamin.
13
Q
He also received, as needed,
A
- a topical lidocaine patch for meralgia paresthetica;
- gabapentin for pain;
- vardenafil (though he had not taken it recently);
- fluticasone propionate nasal spray and inhaler,
- albuterol, and loratadine for wheezing and asthma; and 6. valacyclovir.
14
Q
He swam regularly, drank
A
wine daily, and did not smoke.
15
Q
His siblings had
A
- arthritis and
2. hypercholesterolemia, and his children and grandchildren were healthy.
16
Q
On examination, the patient was
A
alert and oriented.
17
Q
The skin was
A
pale and diaphoretic.
18
Q
The blood pressure was 123/89 mm Hg, and the pulse 58 beats per minute; the other vital signs and oxygen saturation were
A
normal.
19
Q
The sensation of light touch was slightly
A
- decreased over the malar eminence and the
2. jaw on the left side and was normal over the eyelids, frontalis muscle, and upper neck.
20
Q
There was
A
- nystagmus on left lateral gaze, and
- sustaining left lateral gaze required some effort;
- the eye movements were slower from midline to the left than from midline to the right.
21
Q
He was able to reproduce the
A
sensation of delayed visual return, which was more severe when moving his head to the right than to the left.
22
Q
When he was not supported, he tilted
A
to the left.
23
Q
He walked
A
cautiously and slowly, with a slightly broad-based gait, and was unable to perform tandem walking.
24
Q
Deep-tendon reflexes were slightly more
A
- brisk on the right side than on the left side.
2. The remainder of the neurologic and general examinations was normal.
25
The blood level of carbon dioxide was
low --> 21.9 mmol per liter (reference range, 23.0 to 31.9),
26
the level of glucose was
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]),
27
the level of phosphorus was
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
28
the anion gap was
high --> 16 mmol per liter (reference range, 3 to 15).
29
Blood levels of other electrolytes, calcium, and magnesium were
normal, as were results of the complete blood count and tests of coagulation, renal function, and liver function;
30
screening for troponin I was
negative.
31
An electrocardiogram (ECG) showed
1. sinus rhythm at a rate of 59 beats per minute and
| 2. no acute ischemic changes.
32
Lorazepam, ondansetron, and intravenous fluids were administered, and the patient’s condition partially
improved.
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
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;
34
there was
no intracranial hemorrhage, extraaxial collection, mass effect, or midline shift.
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
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.
36
Dr. Ning: Did you sit up?
| The Patient: I sat up
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.
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
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.
38
The day before the episode, I swam
three fourths of a mile, mostly doing a freestyle stroke, as part of my training for a triathlon.
39
First, I will try to identify the anatomical localization and cause of the present illness from the history provided. The patient is a
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.
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
central origin.
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
unilateral weakness and loss of sensation.
42
Patients with supratentorial lesions (i.e., lesions in the frontal, parietal, temporal, or occipital lobe) can present with
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.
43
Patients with infratentorial lesions (i.e., lesions in the brain stem or cerebellum) can present with
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.
44
In this case, what led to think that the lesion is localized to the brain stem and cerebellum?
1. the constellation of symptoms and
| 2. the lack of cortical signs indicate that the lesion is localized to the brain stem and cerebellum.
45
Occasionally, patients with a mass or demyelinating lesion adjacent to the cerebral ventricles or aqueduct can have
rapid-onset hydrocephalus, which is associated with symptoms similar to those seen in this case.
46
However, what clues suggested that the pt has focal neurovascular event?
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.
47
There are several crucial signs in this case. The first important sign is that the
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.
48
The maneuver can cause
paradoxical embolic stroke by forcefully opening a patent foramen ovale and allowing venous clots to travel to the brain.1
49
Change in body position can also move
otoliths in the semicircular canals of the inner ear2 or stretch vertebral blood vessels traveling inside the cervical spinous processes.
50
Cardiac ischemia triggers
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.
51
On rare occasions, during vertebrobasilar stenosis or clotting, low flow due to cardiac failure can trigger
brain-stem ischemia, which is manifested as central vertigo.
52
In addition, the brain can activate autonomic instability,3 and posterior-circulation infarcts can be associated with
hyperhidrosis.4-6
53
The spinning sensation, or true vertigo, is of
central origin (Table 1).2,7
54
Peripheral vertigo (a dysfunction of the peripheral vestibular system) is
more prevalent than central vertigo in the general population, but peripheral vertigo should be a diagnosis of exclusion in patients with vascular risk factors.
55
Central vertigo is associated with lesions in the
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.
56
Vertebrobasilar stroke should be considered because its consequences are
devastating; it is associated with up to 50% mortality.8
57
what is crucial for putting his acute symptoms in the context of other risk factors?
Assessment of the patient’s medical history is crucial for putting his acute symptoms in the context of other risk factors.
58
It is important to identify
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]).
59
This patient had
1. meralgia paresthetica and
| 2. erectile dysfunction, which may point to underlying diabetes or uncontrolled hypertension;
60
we often discover glucose intolerance or diabetes during a diagnostic workup for
stroke.
61
Chronic inflammatory conditions (e.g., recurrent localized herpes simplex virus infection and arthritis) may contribute to
clotting and vascular risk factors.
62
Furthermore, the patient, as an avid swimmer and triathlete, is at risk for
neck injury. In view of the risk factors, a vascular cause of his symptoms (i.e., acute stroke) is likely.
63
Clinical examination can help to distinguish
central vertigo from peripheral vertigo (Table 1).
64
The presence of asymmetric deep-tendon reflexes indicates a
central phenomenon, but diabetic neuropathy can obliterate these reflexes.
65
In central horizontal nystagmus, the fast phase is toward
the side of the lesion, indicating involvement of the left cerebellum in this case.
66
The loss of facial sensation in this patient may be related to focal injury in the
medulla near the fifth cranial nerve.
67
The examination is localized to a partial territory of the
posterior inferior cerebellar artery (Fig. 1);
68
a full-blown infarct of a posterior inferior cerebellar artery (Fig. 1B and 1C), or the lateral medullary syndrome, is relatively
rare, since the vascular pathological features have various thromboembolic distributions.9,10
69
In the United States, stroke is the leading cause of
serious long-term disability; one person dies from stroke every 4 minutes, and one in four patients with stroke have recurrent strokes.
70
The two major types of stroke are
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
71
Symptoms of the two types differ but can overlap as a result of
1. anatomical variance,
2. handedness, or
3. other genetic factors.11
72
Hemorrhagic strokes are roughly classified according to
location; the subtypes are
1. subarachnoid,
2. epidural,
3. subdural, and
4. intraparenchymal.
73
In this patient, the lack of
1. early severe headache and
| 2. lack of progression to global alterations in consciousness make subarachnoid hemorrhage an unlikely diagnosis.
74
Epidural hemorrhage, commonly due to
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.
75
In persons in this patient’s age group (i.e., >65 years of age), subdural hemorrhage can cause
progressive focal neurologic changes, especially after trauma, and an acute-on-chronic subdural hemorrhage can cause seizures in those who are taking anticoagulant drugs.
76
Recently recognized causes of intraparenchymal hemorrhage, such as
cerebral amyloid angiopathy, may result in an indolent disease course and cognitive changes.12
77
Intraparenchymal hemorrhage due
to hypertension is a possible diagnosis in this case; it commonly occurs in the cerebellum and basal ganglia.
78
It is very important to distinguish ischemic stroke from
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.
79
The incidental intraaxial lesion cannot explain the symptoms; such a lesion could cause
seizures but not fixed deficits.
80
Venous strokes due to cerebral venous thromboses are less common than
arterial ischemic strokes; they develop over days or weeks and frequently go undetected.
81
what are the clinical signs that prompt an urgent workup for cerebral venous thrombosis?
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.
82
Arterial strokes, which account for the majority of ischemic infarcts, comprise
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.
83
Age, cognitive status, sex, and race were traditionally used to identify stroke subtype; older age is associated with
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
84
This patient crosses these traditional stroke categories. He is at risk for
atherothrombotic disease because of
1. his age and
2. the presence of hyperlipidemia and
3. hypertension.
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
younger age, such as
1. traumatic dissection and
2. paradoxical embolism due to a patent foramen ovale.
86
If his previous episode of vertigo was associated with a transient ischemic attack, then a likely diagnosis is
thrombotic stroke because emboli seldom affect the same territory repeatedly.
87
The patient will need to undergo an individualized diagnostic workup (Table 3). He will undergo
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
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
heart and since large-vessel arterial disease and cardioembolic disease can coexist, in part because they have shared cardiovascular risk factors.1
89
The brain is the “upstairs neighbor” of the heart and on the receiving end of ischemic injury, and thus
monitoring circulatory brain–heart communication is crucial for stroke prevention.
90
For example, the right-to-left shunting through a patent foramen ovale not only allows clots to go
through but also
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).
91
In summary, in view of the
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.
92
A cardioembolic event is also in the differential diagnosis. Because the risk factors for and the causes of various stroke subtypes can
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.
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
the cerebellum.
94
We were concerned that he had a traumatic dissection that caused
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.
95
CT without the administration of contrast material was performed to rule out the presence of hemorrhage.
The patient then underwent MRI and magnetic resonance angiography (MRA).
96
Clinical Diagnosis
Cerebellar ischemic stroke, possibly due to vertebral-artery dissection.
97
DR. MingMing NING’s DIAGNOSIS
| Cerebellar ischemic stroke due to
vertebralartery dissection, with artery-to-artery emboli in a partial territory of the posterior inferior cerebellar artery.
98
Discussion of Imaging
| Dr. Rosenberg: Dr. Gonzalez, would you make the diagnosis for us?
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);
99
the abnormality is hypointense on the apparent-diffusion- coefficient images, a finding that confirms that this is an
acute infarction.
100
On T2-weighted images (not shown) and fluid-attenuated inversion recovery images (Fig. 2B),
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.
101
MRA revealed
1. normal,
2. widely patent,
3. bilateral carotid and right vertebral arteries (Fig. 2C);
102
however, the left vertebral artery is
poorly visualized (Fig. 2D).
103
Images from MRI scans suggest
acute left cerebellar infarction due to a dissection of the left vertebral artery.
104
CT angiography was performed to confirm the diagnosis of
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.
105
Discussion of Management
| Dr. Rosenberg: Dr. Ning, would you tell us how you would manage this case?
Dr. Ning: Appropriate management and secondary prevention of acute ischemic stroke must target the underlying cause.
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
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.
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
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.
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.
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;
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,
such as this one, with spinal arthritis.
110
Understanding the cause of the initial stroke is the
best way to prevent recurrence.
111
In this case, it is important to understand the
course of the vertebral artery as it travels within the cervical spinous processes (Fig. 1A).
112
The “elbow” of the artery (Fig. 1A, segment III) is likely to tear during
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).
113
Exercise has benefits that generally outweigh the risks, but the patient should be counseled about
bow-hunter’s syndrome and the risk of vertebral-artery dissection.
114
Dynamic transcranial Doppler ultrasonography to monitor intracranial flow during head turning can gauge limits in range of motion.
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.
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
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:
116
The patient was admitted to the neurology service.
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.
117
Results of a cardiac ultrasound examination and routine laboratory studies were
normal. There were no arrhythmias on 24-hour Holter monitoring.
118
Two months after discharge, a CT angiogram showed persistent
1. nonvisualization of the cervical portion of the left vertebral artery and
2. better visualization of the intradural portion;
119
anticoagulation therapy was continued, with the plan to perform
repeat imaging in 3 months.
120
Seven months after discharge, a repeat CT angiogram showed
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.
121
The intradural left vertebral artery and the dominant right vertebral artery were
patent.
122
His symptoms had completely resolved, and he was back to performing high level physical activities. The decision was made to discontinue
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
123
A Physician: Swimming the freestyle stroke involves a lot of head turning. Were you advised to stop swimming freestyle after your stroke?
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.
124
Anatomical Diagnosis??
Dissection of the left vertebral artery and cerebellar infarction.
