Cerebrovascular Disease Flashcards
- A 67-year-old woman with a history of type II diabetes mellitus and atrial fibrillation presents to the emergency room with right body weakness and slurred speech. The onset was sudden while she was brushing her teeth 1 h ago, and she was brought immediately to the emergency room. She has no complaints of word-finding difficulties, no dysesthesia, and no headache. She is taking warfarin. Physical exam findings include blood pressure of 205/90 and irregularly irregular heart beat. There is left side neglect with slurred speech. There is a corticospinal pattern of weakness of the right body, with the face and upper extremity worse than the lower extremity. Routine chemistries and cell counts are normal. Her INR is 1.8. 45. Which of the following should be done next?
A. Administer tissue plasminogen activator
B. Call a vascular surgery consult for possible endarterectomy
C. Order a brain CT
D. Order a cerebral angiogram
E. Start heparin
C
(Shuaib, p 58.) This is a good history for car- dioembolic stroke—sudden onset, cortical symptoms, atrial fibrillation, and subtherapeutic INR. The immediate goal should be to rule out an intracranial hemorrhage and confirm the diagnosis. Tissue plasminogen activator is the treatment for acute stroke in specific circumstances. How- ever, it is not yet certain that this is a stroke. It may be an intracranial hemorrhage, which would be a contraindication for tissue plasminogen activator. Additionally, an elevated INR in a patient on warfarin is a con- traindication for tissue plasminogen activator. Carotid endarterectomy is indicated for some cases when a transient ischemic attack or stroke is believed to be caused by carotid artery narrowing. It is not yet known what caused this patient’s event, and this procedure would rarely be done emergently. A cerebral angiogram would be indicated if you had strong suspicion of an aneurysm or vascular malformation. There is no reason to believe one of these is causing the patient’s symptoms. Heparin may be indicated if there is not an intracranial hemorrhage. This must first be established by CT or MRI.
- A 67-year-old woman with a history of type II diabetes mellitus and atrial fibrillation presents to the emergency room with right body weakness and slurred speech. The onset was sudden while she was brushing her teeth 1 h ago, and she was brought immediately to the emergency room. She has no complaints of word-finding difficulties, no dysesthesia, and no headache. She is taking warfarin. Physical exam findings include blood pressure of 205/90 and irregularly irregular heart beat. There is left side neglect with slurred speech. There is a corticospinal pattern of weakness of the right body, with the face and upper extremity worse than the lower extremity. Routine chemistries and cell counts are normal. Her INR is 1.8. The patient has an MRI that is consistent with an acute stroke. The most common cause of stroke is
A. Atherosclerosis
B. Fibromuscular dysplasia
C. Mitral valve prolapse
D. Arterial dissection
E. Meningovascular inflammation
A
(Victor,p825). Atherosclerosismayproducecerebral infarction by a variety of mechanisms, including emboli to the brain and local occlusion of atheromatous vessels. Platelet emboli may form on ulcer- ated atheromatous plaques in major vessel walls and ascend to the brain. The atherosclerotic plaque involves subintimal proliferation of smooth muscle, fatty deposits in the intima, inflammatory cells, and excessive elaboration of the connective tissue matrix in the vessel wall. Thrombi may form on the sur- face of the plaque and occlude the vessel, even if the plaque is not large enough to produce substantial narrowing of the vessel. Fibromuscular dys- plasia is a relatively uncommon cause of cranial vessel occlusion that devel- ops with segmental overgrowth of fibrous and muscular tissue in the media. Meningovascular inflammation is a rare process that occurs in some infectious or inflammatory disorders, such as syphilis, tuberculous meningitis, or sarcoid.
- A 67-year-old woman with a history of type II diabetes mellitus and atrial fibrillation presents to the emergency room with right body weakness and slurred speech. The onset was sudden while she was brushing her teeth 1 h ago, and she was brought immediately to the emergency room. She has no complaints of word-finding difficulties, no dysesthesia, and no headache. She is taking warfarin. Physical exam findings include blood pressure of 205/90 and irregularly irregular heart beat. There is left side neglect with slurred speech. There is a corticospinal pattern of weakness of the right body, with the face and upper extremity worse than the lower extremity. Routine chemistries and cell counts are normal. Her INR is 1.8.
A pure motor stroke is most likely with damage to the
A. Internal capsule
B. Cerebellum
C. Putamen
D. Caudate
E. Amygdala
A
(Victor, p 831.) Pure motor deficits are especially likely in hypertensive persons with small infarctions called lacunae. The
pure motor stroke is the most common type of lacunar stroke. The affected person usually has hemiplegia unassociated with cognitive, sensory, or visual deficits. The posterior limb of the internal capsule is the usual site of injury. The lacunae are assumed to develop because of an occlusive lesion in an arteriole that supplies the injured structure.
- A 67-year-old woman with a history of type II diabetes mellitus and atrial fibrillation presents to the emergency room with right body weakness and slurred speech. The onset was sudden while she was brushing her teeth 1 h ago, and she was brought immediately to the emergency room. She has no complaints of word-finding difficulties, no dysesthesia, and no headache. She is taking warfarin. Physical exam findings include blood pressure of 205/90 and irregularly irregular heart beat. There is left side neglect with slurred speech. There is a corticospinal pattern of weakness of the right body, with the face and upper extremity worse than the lower extremity. Routine chemistries and cell counts are normal. Her INR is 1.8.
A pure sensory stroke is most likely with damage to the
a. Internal capsule
b. Thalamus
c. Hippocampus
d. Globus pallidus
e. Pons
B
(Victor, p 839.) Pure sensory strokes are most likely in the same persons who are susceptible to pure motor strokes and other lacunae. With hypertensive injury to the posteroventral nucleus of the lateral thalamus, the affected person will report contralateral numbness and tingling. During recovery from this type of stroke, paradoxical pain may develop in the area of sensory impairment. This paradoxical pain associated with decreased pain sensitivity is referred to as the thalamic pain syndrome.
- A 61-year-old man with a history of hypertension has been in excellent health until he presents with vertigo and unsteadiness lasting for 2 days. He then develops nausea, vomiting, dysphagia, hoarseness, ataxia, left facial pain, and right-sided sensory loss. There is no weakness. On examination, he is alert, with a normal mental status. He vomits with head movement. There is skew deviation of the eyes, left ptosis, clumsiness of the left arm, and titu¬bation. He has loss of pin and temperature sensation on the right arm and leg and decreased joint position sensation in the left foot. He is unable to walk.
Magnetic resonance imaging (MRI) in this patient might be expected to show which of the following?
a. Basilar artery tip aneurysm
b. Right lateral medullary infarction
c. Left lateral medullary infarction
d. Left medial medullary infarction
e. Right medial medullary infarction
C
(Victor, pp 844–846.) Wallenberg, or lateral medullary, syndrome is due to infarction involving some or all of the structures located in the lateral medulla, including the nucleus and descending tract of the fifth nerve, the nucleus ambiguus, lateral spinothalamic tracts, inferior cerebellar peduncle, descending sympathetic fibers, vagus, and glossopharyngeal nerves. The patient with Wallenberg syndrome has ipsilateral ataxia and ipsilateral Horner syndrome. The trigeminal tract damage may produce ipsilateral loss of facial pain and temperature perception and ipsilateral impairment of the corneal reflex. The lateral spinothalamic damage produces pain and temperature disturbances contralateral to the injury in the limbs and trunk. Dysphagia and dysphonia often develop with damage to the ninth and tenth nerves.
- A 61-year-old man with a history of hypertension has been in excellent health until he presents with vertigo and unsteadiness lasting for 2 days. He then develops nausea, vomiting, dysphagia, hoarseness, ataxia, left facial pain, and right-sided sensory loss. There is no weakness. On examination, he is alert, with a normal mental status. He vomits with head movement. There is skew deviation of the eyes, left ptosis, clumsiness of the left arm, and titubation. He has loss of pin and temperature sensation on the right arm and leg and decreased joint position sensation in the left foot. He is unable to walk.
The dysphagia in this case is secondary to involvement of which of the following structures?
a. Nucleus solitarius
b. Nucleus and descending tract of CN V5
c. Nucleus ambiguus
d. Lateral spinothalamic tract
e. Inferior cerebellar peduncle
C
(Victor, pp 844–845.) The nucleus ambiguus, located in the ventrolateral medulla, contains the motor neurons that contribute to the ninth (glossopharyngeal) and tenth (vagus) cranial nerves. The motor neurons of the nucleus ambiguus innervate the striated muscles of the larynx and pharynx as well as provide the preganglionic parasympathetic supply to thoracic organs, including the esophagus, heart, and lungs. Injury to this nucleus and its pathways causes hoarseness and dysphagia.
- A 61-year-old man with a history of hypertension has been in excellent health until he presents with vertigo and unsteadiness lasting for 2 days. He then develops nausea, vomiting, dysphagia, hoarseness, ataxia, left facial pain, and right-sided sensory loss. There is no weakness. On examination, he is alert, with a normal mental status. He vomits with head movement. There is skew deviation of the eyes, left ptosis, clumsiness of the left arm, and titu¬bation. He has loss of pin and temperature sensation on the right arm and leg and decreased joint position sensation in the left foot. He is unable to walk.
Occlusion of which of the following arteries typically produces this syndrome?
a. Basilar artery
b. Vertebral artery
c. Superior cerebellar artery
d. Anterior inferior cerebellar artery (AICA)
e. Anterior spinal artery
B
(Victor, pp 842–846.) Most cases of lateral medullary infarction are due to occlusion of the vertebral artery. Several small branches of the distal vertebral artery supply the lateral medulla. In some cases, occlusion of the posterior inferior cerebellar artery (PICA) causes this syndrome. The PICA is the last large branch of the vertebral artery, and, when it is occluded, there may also be infarction of the inferior cerebellum accompanying that of the medulla.
- A 75-year-old man with a history of recent memory impairment is admitted with headache, confusion, and a left homonymous hemianopsia. He has recently had two episodes of brief unresponsiveness. There is no history of hypertension. Computed tomography (CT) scan shows a right occipital lobe hemorrhage with some subarachnoid extension of the blood. An MRI scan with gradient echo sequences reveals foci of hemosiderin in the right temporal and left frontal cortex. The likely cause of this patient’s symptoms and signs is
a. Gliomatosis cerebri
b. Multi-infarct dementia
c. Mycotic aneurysm
d. Amyloid angiopathy
e. Undiagnosed hypertension
D
(Osborn, pp 192–194.) Cerebral amyloid angiopathy (CAA), or congophilic angiopathy, is the most common cause of lobar hemorrhage in elderly patients without hypertension. The deposition of β-amyloid protein (the same as that found in Alzheimer’s disease) in brain blood vessels leads to disruption of the vessel walls, which predisposes them to hemorrhage. Patients are usually over age 70 and may present with multiple cortical hemorrhages with or without a history of dementia. At times, additional hemorrhages may be seen only on special imaging techniques, such as gradient echo MRI, which magnifies the effects of hemosiderin in regions of prior hemorrhage.
- A 22-year-old male abuser of intravenous heroin complains of severe headache while having sexual intercourse. Within a few minutes of that complaint, he develops right-sided weakness and becomes stuporous. His neurologic examination reveals neck stiffness as well as right arm and face weakness. An unenhanced emergency CT scan reveals a lesion of 3 to 4 cm in the cortex of the left parietal lobe. The addition of contrast enhancement reveals two other smaller lesions in the right frontal lobe but does not alter the appearance of the lesion in the left parietal lobe.
The diagnostic study most likely to establish the basis for this patient’s neurologic deficits is
a. HIV antibody testing
b. Cerebrospinal fluid (CSF) examination
c. Electroencephalography
d. Nerve conduction studies
e. Cardiac catheterization
B
(Victor, pp 902–903.) This young man almost certainly has numerous problems associated with his intravenous drug abuse, but the cause of his current complaints is most likely bleeding from a mycotic aneurysm. Aneurysms are specially likely to bleed during exertion, such as that associated with sexual intercourse or defecation. The fact that the lesion appeared largely the same on unenhanced and enhanced CT scans suggests that it is a hematoma. HIV antibody testing might reveal evidence of exposure to HIV, but, aside from establishing that the patient was at increased risk of opportunistic infections, that test would provide little insight into the cause of the acute neurologic syndrome. The CSF would be expected to be xanthochromic (yellow) with many (>20/µL) red blood cells (RBCs) or grossly bloody, thereby providing evidence of a recent subarachnoid hemorrhage. Electroencephalography would undoubtedly reveal an
asymmetric pattern associated with the left hemispheric lesion, but this too would provide little insight into the cause of the problem. Nerve conduc-tion studies would not clarify the basis for a lesion of the central nervous system, because they only examine structures of the peripheral nervous system. Cardiac catheterization might reveal valvular abnormalities, but these need not be associated with disease of the central nervous system.
- A 22-year-old male abuser of intravenous heroin complains of severe headache while having sexual intercourse. Within a few minutes of that complaint, he develops right-sided weakness and becomes stuporous. His neurologic examination reveals neck stiffness as well as right arm and face weakness. An unenhanced emergency CT scan reveals a lesion of 3 to 4 cm in the cortex of the left parietal lobe. The addition of contrast enhancement reveals two other smaller lesions in the right frontal lobe but does not alter the appearance of the lesion in the left parietal lobe.
The patient’s HIV antigen test is positive, but he has no depression of his CD4+ (helper) T lymphocyte count. Nerve conduction studies reveal general¬ized slowing in the legs, and EEG exhibits depressed voltage over the left parietal lobe. Cardiac catheterization suggests aortic valve disease, and his CSF is xanthochromic (yellow). The probable site of injury in the CNS is
a. An arterial wall
b. The ventricular endothelium
c. The pia arachnoid
d. The dura mater
e. The perivenular space
A
(Victor, pp 902–903.) The most likely explanation for this patient’s deficits is bleeding from a mycotic aneurysm. This type of aneurysm is usually relatively small and might not be evident on CT scanning or even on arteriography. An arteriogram would miss the lesion if it had destroyed itself when it bled or if the aneurysmal sac was completely thrombosed. The name mycotic is misleading. It suggests a fungal etiology, but it actually refers to the appearance of these aneurysms, which tend to be multiple. These aneurysms occur with either gram-positive or gram-negative infections, but the responsible organisms usually have relatively low virulence. Mycotic aneurysms form over the cerebral convexities with subacute bacterial endocarditis. The aneurysm develops from an infected embolus originating on the diseased heart valves and lodging in the arterial wall. Bleeding from these small aneurysms is largely directed into the subarach-
noid space. More virulent organisms that produce valvular heart disease are more likely to produce a meningitis or multifocal brain abscess with seeding of infected emboli to the brain. With acquired immune deficiency syndrome
(AIDS), a fungus could be the causative agent, but patients with endocarditis more typically have streptococcal or staphylococcal infections. Even if mycotic aneurysms form with endocarditis, they need not inevitably become
symptomatic.
- A 22-year-old male abuser of intravenous heroin complains of severe headache while having sexual intercourse. Within a few minutes of that complaint, he develops right-sided weakness and becomes stuporous. His neurologic examination reveals neck stiffness as well as right arm and face weakness. An unenhanced emergency CT scan reveals a lesion of 3 to 4 cm in the cortex of the left parietal lobe. The addition of contrast enhancement reveals two other smaller lesions in the right frontal lobe but does not alter the appearance of the lesion in the left parietal lobe.
Within 1 day of admission, the patient’s right-sided weakness began to abate, and within 1 week it completely resolved. On the fourth day of hospitalization, the patient abruptly lost consciousness and exhibited clonic movements starting in his right side and generalizing to his left side. The movements stopped within 3 min, but he had residual right-sided weakness for 24 h. CT scan was unchanged from that obtained on admission. The most appropriate treatment to institute involves
a. Heparin
b. Recombinant tissue plasminogen activator (r-TPA)
c. Lamotrigine
d. Phenytoin
e. Warfarin
D
(Victor, pp 356–360.) Anticoagulation with warfarin or heparin and thrombolysis with r-TPA or urokinase are contraindicated in anyone with an intracranial hemorrhage. Focal seizures that secondarily generalize after an intracerebral or subarachnoid hemorrhage occur frequently and are appropriately treated with an antiepileptic drug, such as phenytoin (Dilantin). Lamotrigine is an anticonvulsant, but would be a very poor choice in this case because this patient needs a drug that will be immediately therapeutic. Lamotrigine must be slowly titrated over many weeks when first started, because of the risk of severe rash.
- A 22-year-old male abuser of intravenous heroin complains of severe headache while having sexual intercourse. Within a few minutes of that complaint, he develops right-sided weakness and becomes stuporous. His neurologic examination reveals neck stiffness as well as right arm and face weakness. An unenhanced emergency CT scan reveals a lesion of 3 to 4 cm in the cortex of the left parietal lobe. The addition of contrast enhancement reveals two other smaller lesions in the right frontal lobe but does not alter the appearance of the lesion in the left parietal lobe.
The focal weakness lasting for 24 h was most likely attributable to
a. Intracerebral hemorrhage
b. Subarachnoid hemorrhage
c. Encephalitis
d. Todd’s paralysis
e. Hyponatremia
D
(Victor, pp 345–346.) That the patient had weakness after the seizure activity is evidence of a postictal paralysis, or Todd’s paralysis. Postictal weakness does not suggest extension of the bleeding or new areas of cerebrocortical damage, but imaging with CT scan is appropriate to exclude these possibilities. Postictal paralysis may last for many hours, or even days. The precise cause is unknown, but it appears to be due to some kind of neuronal exhaustion occurring after frequent repetitive discharges. It may reflect depletion of glucose in the neurons in the epileptic focus.
- A 16-year-old girl with complex partial seizures and mild mental retar¬dation has an area of deep red discoloration (port-wine nevus) extending over her forehead and left upper eyelid. A CT scan of her brain would be likely to reveal
a. A hemangioblastoma
b. A Charcot-Bouchard aneurysm
c. An arteriovenous malformation
d. A leptomeningeal angioma
e. A fusiform aneurysm
D
(Greenberg, 2/e, p 601. Victor, pp 1077–1078.) This patient has encephalofacial angiomatosis (Sturge-Weber syndrome), a congenital disturbance that produces facial cutaneous angiomas with a distinctive and easily recognized appearance, along with intracranial abnormalities such as leptomeningeal angiomas. Persons with the syndrome may be mentally retarded and often exhibit hemiparesis or hemiatrophy on the side of the body opposite the port-wine nevus. Both men and women may be affected, and seizures may develop in affected persons. The nevus associated with Sturge-Weber syndrome usually extends over the sensory distribution of CN#6, the first division of the trigeminal nerve. The lesion usually stays to one side of the face. Affected persons will usually also have an angioma of the choroid of the eye. Intracranial angioma is unlikely if the nevus does not involve the upper face. Deficits develop as the person matures and may be a consequence of focal ischemia in the cerebral cortex that underlies the leptomeningeal angioma. Hemangioblastomas are vascular tumors seen in association with polycystic disease of the kidney and telangiectasias of the retina (von Hippel-Lindau syndrome). Charcot-Bouchard aneurysms are very small and may be microscopic. They develop in patients with chronic hypertension and most commonly appear in perforating arteries of the brain. The lenticulostriate arteries are most commonly affected. Hemorrhage from these aneurysms is likely, and the putamen is the most common site for hematoma formation. Hemorrhage may extend into the ventricles and lead to subarachnoid blood. Other locations commonly affected include the caudate nucleus, thalamus, pons, and cerebellum. The dentate nucleus of the cerebellum is especially susceptible to the formation of Charcot-Bouchard aneurysms. Fusiform aneurysms are diffusely widened arteries with evaginations along the walls, but without stalks as occur with the typical berry-shaped structures of the saccular aneurysm. This type of aneurysm may be a late consequence of arteriosclerotic damage to the artery wall.
- A 72-year-old woman has the abrupt onset of right face and hand weakness, disturbed speech production, and a right homonymous hemi¬anopsia. This is most likely attributable to occlusion of the
a. Left middle cerebral artery
b. Left anterior cerebral artery
c. Left vertebrobasilar artery
d. Right anterior choroidal artery
e. Left posterior inferior cerebellar artery (PICA)
A
(Victor, pp 834–835.) The left middle cerebral artery supplies the cortex around the sylvian fissure, as well as some of the frontal lobe structures involved in speech. The optic radiation loops through the temporal lobe on its way to the occipital cortex and is usually damaged with occlusion of the middle cerebral artery. The speech disorder likely with an injury of the left frontal lobe is a Broca’s aphasia. Comprehension would be expected to be largely intact, but if the patient has damage to enough of the temporal lobe cortex, a Wernicke’s aphasia might develop. Choroidal artery occlusions might produce focal weakness, but speech problems would be less likely. Occlusion of the PICA can produce a variety of brainstem and cerebellar signs, but this combination of deficits would be unlikely with a lesion outside the cerebral cortex.
- A 39-year-old woman has diplopia several times a day for 6 weeks. She consults a physician when the double vision becomes unremitting, and also complains of dull pain behind her right eye. When a red glass is placed over her right eye and she is asked to look at a flashlight off to her left, she reports seeing a white light and a red light. The red light appears to her to be more to the left than the white light. Her right pupil is more dilated than her left pupil and responds less briskly to a bright light directed at it than does the left pupil.
Before any further investigations can be performed, the woman develops the worst headache of her life and becomes stuporous. Her physician discovers that she has marked neck stiffness and photophobia. The physician performs a transfemoral angiogram. This radiologic study is expected to reveal that the woman has
a. An arteriovenous malformation
b. An occipital astrocytoma
c. A sphenoidal meningioma
d. A pituitary adenoma
e. A saccular aneurysm
E
(Victor, pp 890–892.) The clinical picture suggests that a saccular aneurysm has become symptomatic by compressing structures about the base of the brain and subsequently leaking. Aneurysms enlarge with age and usually do not bleed until they are several millimeters across. Persons with intracerebral or subarachnoid hemorrhages before the age of 40 are more likely to have their hemorrhages because of arteriovenous malformations than because of aneurysms. Aneurysms occur with equal frequency in men and women below the age of 40; however, in their forties and fifties, women are more susceptible to symptomatic aneurysms. This is especially true of aneurysms that develop on the internal carotid on that segment of the artery that lies within the cavernous sinus. An angiogram is useful in establishing the site and character of the aneurysm. A CT scan would be more likely to reveal subarachnoid, intraventricular, or
intraparenchymal blood, but it would reveal the structure of an aneurysm only if it were several (>5) millimeters across. An MRI will reveal relatively large aneurysms if the system is calibrated and programmed to look at blood vessels. This patient had a transfemoral angiogram, a technique that involves the introduction of a catheter into the femoral artery; the catheter is threaded retrograde in the aorta and up into the carotid or other arteries of interest.
