Transcript Slide

Neurology Board Review
Stroke and Spinal Cord Disorders
Diagnosis of acute stroke
• Head CT without contrast = initial test of choice to identify
hemorrhagic stroke.
• MRI can identify acute ischemia or a nonvascular cause.
• Hemorrhagic stroke cannot be reliably distinguished from
ischemic stroke on clinical grounds alone. Coma,
meningismus, seizures at onset, vomiting, headache, and a
diastolic blood pressure greater than 110 mm Hg makes
hemorrhagic stroke more likely.
• CT angiography is commonly used to identify patients who
may benefit from endovascular treatment or to identify
potential sources of hemorrhage.
Transient Ischemic Attack
• Any focal neurologic deficit caused by impaired cerebral
blood flow that lasted <24 hours
• The ABCD2 score (based on Age >60, Blood pressure
>140/90, Clinical presentation, Duration of symptoms, and
the presence of Diabetes) to stratify risk of subsequent
stroke.
• The risk of subsequent stroke at 90 days approaches 10% in
patients who have a TIA, with the highest risk in the first 48
hours
• Hospital admission is recommended for all patients seen
within 72 hours of initial symptoms whose ABCD2 score is at
least 3.
Ischemic Stroke
• Defined by presence of cerebral infarction on imaging,
but may not be seen if the infarct is small or located in
the brainstem.
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20% of ischemic strokes are cardioembolic
20% from large artery atherosclerosis
25% are small subcortical infarcts
30% are cryptogenic strokes, for which no cause is
identified
• 5% have rare causes, such as cerebral artery dissection
or vasculitis.
Treatment of acute ischemic stroke
• Recombinant tissue plasminogen activator (rtPA) is effective within 3
hours of acute ischemic stroke.
• National guidelines recommend that treatment be initiated within 1
hour of arrival at the emergency department.
• Risk factors for hemorrhage after tPA include large infarct size, poor BP
control, hyperglycemia, and treatment after the appropriate time
window.
• tPA requires ICU x 24 hrs. Avoid surgical procedures and antithrombotic
treatment for 24 hours.
• Prior to tPA, BP should be <185/110 mm Hg, which can be achieved by
labetalol or nicardipine infusions.
• After tPA infusion, BP target is <180/105 mm Hg.
• In patients ineligible for tPA, blood pressures up to 220/120 mm Hg are
permitted with the intention of improving cerebral perfusion
tPA Exclusion Criteria
• Minor or rapidly
improving symptoms
• Seizure at stroke onset
• Other stroke or trauma
within 3 months
• Major surgery within 14
days
• History of intracerebral
hemorrhage
• Sustained BP ≥185/110
• Suspicion of SAH
• Arterial puncture at
noncompressible site
within 7 days
• Received heparin within
48 hours and PTT
elevated
• INR >1.7
• Plt <100,000
• Glc <50 or >400
Hemorrhagic Stroke
• Intracerebral hemorrhage
– Use labetalol or nicardipine infusion for aggressive BP control if
SBP>200 mm Hg
– If SBP >180 mm Hg, target SBP <160 if no elevated ICP or <140 if
elevated ICP
– Reverse anticoagulation as quickly as possible. The efficacy and
safety of platelet transfusions in the setting of antiplateletassociated ICH have not been established.
– If elevated ICP, need medical stabilization followed by surgical
evacuation of the hematoma. Intubation and short-term
hyperventilation followed by osmotherapy with either mannitol
or hypertonic saline.
– Cerebral hemorrhage may obscure an underlying tumor, so
need repeat imaging 4 to 6 weeks after the initial event.
Hemorrhagic Stroke
• Subarachnoid hemorrhage
– Typically caused by a ruptured cerebral aneurysm
– If CT head is negative for SAH but the clinical suspicion
remains high, do lumbar puncture to look for erythrocytes and
xanthochromia.
– Angiography to delineate the anatomy of a ruptured cerebral
aneurysm and to rule out other causes of subarachnoid
hemorrhage, such as intracranial arterial dissection or mycotic
aneurysms.
– Causes of decline in neurologic status after SAH are rebleeding
and elevated ICP (cerebral edema, hydrocephalus) in the acute
setting, and arterial vasospasm 5 days or more after the
hemorrhage.
– Nimodipine to prevent vasospasm.
Dural Venous Sinus Thrombosis
• Venous thrombosis should be considered if there are focal
neurologic symptoms; often accompanied by severe headache, a
depressed level of consciousness, and seizures. 50% have
papilledema.
• Most common location is the superior sagittal sinus.
• Cavernous sinus thrombosis results in a characteristic neurologic
syndrome that includes lesions of cranial nerves III, IV, V (V1 and
V2), and occasionally VI.
• Risk factors: hypercoagulable disorders, malignancy, trauma,
systemic inflammatory disorders, severe dehydration or infection,
or pregnancy.
• Definitive treatment for venous thrombosis has not been
established, but most experts recommend anticoagulation for 6
months, even in the setting of ICH.
Carotid and Vertebral Artery Dissection
• Rare cause of stroke but should be considered in persons
younger than 50 years.
• The presence of a partial Horner syndrome (ptosis and
miosis without anhidrosis) with head or neck pain should
prompt investigation for ICA dissection.
• Obtain MRI of the soft tissues in the neck
• Anticoagulation for 3 to 6 months is commonly used in
treating arterial dissection.
Secondary Stroke Prevention
• HTN is the greatest risk factor. To prevent recurrent stroke, aim
for BP<140/80
• Goal LDL<100
• Symptomatic extracranial ICA stenosis > 70% is a risk factor for
recurrent stroke. Carotid endarterectomy (gold standard) has a
higher risk of perioperative myocardial infarction, but angioplasty
and stenting has a higher risk of perioperative stroke, especially if
>70 years old.
• No benefit of percutaneous closure of patent foramen ovale for
stroke prevention.
Secondary Stroke Prevention
• Antiplatelet agents are recommended over anticoagulation in
patients with stroke who have intracranial atherosclerosis
because warfarin was associated with an increase in mortality.
• For stroke prevention in patients without atrial fibrillation, the
most commonly used aspirin dosage is 81 mg/d.
• Clopidogrel is better for stroke prevention in patients with
peripheral arterial disease
• Clopidogrel or aggrenox for patients with recurrent ischemic
stroke despite optimal risk factor management while treated
with aspirin.
• The combination of aspirin and clopidogrel is not commonly
used in patients without cardioembolic stroke unless they have
vascular stents or a previous myocardial infarction
Compressive Myelopathies
• Spinal cord compression is neurologic emergency, can occur in cases of
metastatic neoplasm, vertebral fracture (pathologic or traumatic), epidural
abscess, or epidural hematoma.
• Neck or back pain is often the initial symptom, followed rapidly by weakness,
sensory changes, and bowel or bladder dysfunction
• Chronic spinal degenerative changes also can cause a compressive myelopathy,
with progressive weakness, numbness, spasticity, and bladder impairment
• MRI of the spinal cord to diagnose
• High-dose corticosteroids, most often dexamethasone, is indicated for
traumatic spinal cord injury or epidural metastases.
• Decompressive surgery followed by radiotherapy for metastatic tumors.
Decompressive surgery provides the best chance for future ambulation.
Leukemia, lymphoma, myeloma, and germ-cell tumors are very sensitive to
radiation and may not require surgery.
Noncompressive Myelopathies
• Idiopathic transverse myelitis: postinfectious syndrome
(usually after viral gastroenteritis or URI) with a subacute
weakness, sensory changes, and bowel or bladder
dysfunction and is sometimes preceded by back pain or a
thoracic banding sensation.
– Dx: clinical features of the syndrome, evidence of
inflammation (such as contrast enhancement of the lesion on
MRI or leukocytosis in the cerebrospinal fluid), and exclusion
of other potential causes.
– Tx: Intravenous methylprednisolone (1 g) x 3-5 days.
Transverse myelitis that is refractory to steroids may require
plasmapheresis or cyclophosphamide. Recurrence of
symptoms beyond 30 days of initial onset suggests the
presence of other diseases, such as multiple sclerosis.
Noncompressive Myelopathies
• Infectious causes: HSV, VZV, West Nile virus, Lyme,
neurosyphilis, HIV, tuberculosis
• Vascular causes: Spinal cord infarction (eg. anterior spinal
artery). Acute bilateral weakness, loss of pain and
temperature sensation, but vibration and position sense are
often spared because of the redundant vascular supply to the
posterior aspect of the cord. Diagnose by angiography.
• Metabolic causes:
– Severe vitamin B12 deficiency may result in a subacute combined
degeneration of corticospinal tracts and the dorsal columns.
Replacement therapy will usually halt progression of but may not
improve symptoms.
– Copper deficiency can be clinically indistinguishable from vitamin
B12 deficiency.
A 37-year-old woman presents with 1-week history of headache.
The headache is constant, worse when she first awakens, and characterized
by a feeling of increased pressure. She reports no other focal neurologic
symptoms. The patient has a 10-pack-year history of smoking. Her only
medication is a low-dose estrogen oral contraceptive.
On physical examination, temperature is normal, BP 112/78 mm Hg,
pulse 62/min and regular, RR 16/min; BMI is 37. Bilateral papilledema is
noted. The Valsalva maneuver increases the headache pain. All other
general and neurologic examination findings are unremarkable.
Laboratory studies show a normal leukocyte count, a platelet count
of 322,000/µL (322 × 109/L), an INR of 1.1, and an activated partial
thromboplastin time of 36 s.
An MRI of the brain without contrast is normal.
Which of the following is the most appropriate next diagnostic test?
A. Cerebral angiography
B. Lumbar puncture
C. Magnetic resonance venography
D. Measurement of serum lupus anticoagulant level
• This patient should next undergo magnetic resonance venography. Her
headache, (worse in AM and with Valsalva) is consistent with elevated ICP.
Combined with her history of tobacco and oral contraceptive use, and the
presence of papilledema, she most likely has dural sinus venous thrombosis.
Dural sinus venous thrombosis may also present with focal neurologic
findings, seizures, and mental status changes.
• Risk factors include conditions that predispose to spontaneous thromboses
(inherited or acquired thrombophilia, pregnancy, OCP use, malignancy,
sepsis, head trauma).
• Magnetic resonance venography is the most sensitive imaging modality for
detecting the thrombus and the occluded dural sinus or vein.
• The recommended treatment is smoking cessation, discontinuation of oral
contraceptives, and systemic anticoagulation to prevent sequelae related to
elevated intracranial pressure for 6 months if no hypercoagulable disorder is
found.
A 71-year-old woman is evaluated in the emergency department 90
minutes after onset of left-sided weakness and slurred speech. She has a history of
type 2 diabetes mellitus. Medications are glyburide and metformin.
On physical examination, blood pressure is 178/80 mm Hg, pulse rate is
60/min and regular, and respiration rate is 16/min. No carotid bruits are heard. On
neurologic examination, left facial weakness and left arm and leg weakness are
noted; weakness is more pronounced in the left arm than left leg.
Labs:
aPTT 36s
Platelet count 410,000
INR 0.9
Creatinine 1.1
CT scan of the head without contrast is normal.
Six hours after tPA infusion, her blood pressure is 190/90 mm Hg and pulse
rate is 68/min; the neurologic examination findings are unchanged except for
increasing anxiousness.
Which of the following is the most appropriate next step in treatment?
A. Aspirin
B. Cryoprecipitate
C. Diazepam
D. Nicardipine
E. Nitroprusside
• Treatment guidelines indicate that after tPA infusion, BP should be <180/105 mm
Hg. Nicardipine and labetalol are options to reduce the blood pressure to avoid
intracerebral hemorrhage.
• Aspirin should be avoided. Treatment antithrombotic and antiplatelet
medications must be withheld for at least 24 hours after tPA administration
• Intracerebral hemorrhage due to thrombolytic therapy presents with headache,
nausea, vomiting, and a worsening of the neurologic exam. If clinically suspected,
tPA infusion should be stopped and a repeat CT of the head obtained. If ICH
present, consider cryoprecipitate and platelet infusion. However, in the absence
of documented intracerebral bleeding, the administration of these agents is not
indicated.
• Diazepam also should not be administered. Although the patient's hypertension
may be anxiety induced, treatment of the hypertension to prevent intracerebral
hemorrhage is the priority. Additionally, benzodiazepines in the setting of acute
stroke may impair recovery from neuronal injury and thus should be avoided.
• Nitroprusside is relatively contraindicated in patients with acute ischemic stroke
or hemorrhage because of the possibility of increasing intracranial pressure.
A 57-year-old man has a follow-up evaluation 3 months after discharge from
the hospital, where he was treated for an ischemic stroke. He has a history of
hypertension, dyslipidemia, and peripheral arterial disease for which he has required
no revascularization procedures. Medications are enalapril, hydrochlorothiazide,
rosuvastatin, and aspirin.
On physical examination, blood pressure is 138/68 mm Hg, pulse rate is
68/min and regular, and respiration rate is 16/min. Cardiac examination reveals no
carotid bruits. Neurologic examination shows only a right pronator drift.
Results of laboratory studies show a platelet count of 340,000/µL (340 ×
109/L), a serum creatinine level of 1.1 mg/dL (97.2 µmol/L), and an LDL cholesterol
level of 68 mg/dL (1.76 mmol/L).
A head CT scan and a brain MRI show a left pontine infarct. An
electrocardiogram shows normal sinus rhythm with no ischemic changes. A
transthoracic echocardiogram and a magnetic resonance angiogram of the head and
neck are normal.
Which of the following is the most appropriate treatment?
A. Add clopidogrel
B. Add ticlopidine
C. Add warfarin
D. Substitute clopidogrel for aspirin
E. Substitute warfarin for aspirin
• This patient should receive clopidogrel instead of aspirin. He has a small
subcortical infarction and a history of peripheral arterial disease. The Clopidogrel
versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) study showed that
clopidogrel was superior to aspirin in preventing ischemic stroke, MI, and death,
with the benefit being greatest among participants with peripheral arterial
disease. The combination of aspirin and dipyridamole could be another
appropriate option for secondary stroke prevention.
• The combination of aspirin and clopidogrel for ischemic stroke prevention was
associated with a slight reduction in risk of ischemic stroke, but this was offset by
hemorrhagic complications.
• Although ticlopidine has been shown to be superior to aspirin in preventing
recurrent stroke, it can cause agranulocytosis and thrombotic thrombocytopenic
purpura.
• For noncardioembolic ischemic strokes, aspirin and warfarin were shown to be
equivalent in the Warfarin-Aspirin Recurrent Stroke Study (WARSS). This patient
has no evidence of atrial fibrillation or other high-risk cardioembolic symptoms
that necessitate treatment with warfarin or direct thrombin inhibitors.
• The combination of aspirin and warfarin does not provide any additional
protection against recurrent ischemic stroke and is associated with greater rates
of hemorrhagic complications.
A 34-year-old woman is evaluated in the emergency department for acute
onset of a severe headache. She has hypertension treated with lisinopril.
On physical examination, blood pressure is 160/100 mm Hg, pulse rate is
78/min, and respiration rate is 12/min. General medical examination findings are
normal. Neurologic examination shows that she is somnolent but readily arousable,
with symmetric and briskly reactive pupils and a left arm drift.
Results of routine laboratory studies are normal. A CT scan of the head
shows a subarachnoid hemorrhage, with a thick clot in the right sylvian fissure, but
no hydrocephalus or cerebral edema. Angiography shows a 10-mm right middle
cerebral artery aneurysm.
The patient undergoes urgent aneurysmal clipping with no complications
and is started on nimodipine. She is transferred to the intensive care unit and has
no further symptoms until 6 days after initial evaluation, when she is less
responsive and has new left arm paralysis on neurologic examination.
Which of the following is the most appropriate next diagnostic step?
A. CT angiography of the head
B. Electroencephalography
C. Lumbar puncture
D. MRI of the brain
• The patient with subarachnoid hemorrhage should undergo CT angiography of
the head. The complications after SAH are classified as early vs late. In the first
48 hours after hemorrhage, aneurysm rerupture and hydrocephalus are the
principal causes of neurologic deterioration. Starting at day 5, the risk of cerebral
arterial vasospasm emerges.
• CT angiography can diagnose cerebral vasospasm. Treatment includes induced
hypertension. Intra-arterial therapy with calcium channel blockers or angioplasty
of the artery in spasm may be performed.
• Convulsive and nonconvulsive status epilepticus, which is associated with poor
neurologic outcome, is common and underdiagnosed after hemorrhagic stroke. If
neuroimaging does not find a cause of neurologic decline, EEG may be an
appropriate next step.
• Lumbar puncture may be useful to measure intracranial pressure and diagnose
postoperative meningitis. Repeat imaging, however, is first required to ensure
that no mass effect is present that could precipitate cerebral herniation.
• MRI may provide information on cerebral infarction but is less accurate than
other means for determining vasospasm.
A 78-year-old woman is evaluated in the emergency department 12 hours
after onset of left-sided weakness and slurred speech. She reports being unable to
swallow water at home. She has a history of hypertension and type 2 diabetes
mellitus, both of which she tries to control with lifestyle modifications.
On physical examination, blood pressure is 190/90 mm Hg, pulse rate is
68/min and regular, and respiration rate is 16/min. Cardiac examination reveals no
carotid bruits. Neurologic examination reveals facial weakness on the left side,
severe dysarthria, left-sided hemiplegia, left-sided sensory loss, and normal mental
status.
Results of laboratory studies show a serum creatinine level of 1.1 mg/dL
(97.2 µmol/L) and no serum troponins; urinalysis findings are normal.
A CT scan of the head shows a faint hypodensity in the right posterior limb
of the internal capsule. An electrocardiogram shows normal sinus rhythm with no
ischemic changes. A chest radiograph is normal.
Which of the following is the most appropriate treatment of this patient's elevated
blood pressure?
A.
B.
C.
D.
E.
Intravenous hydralazine
Oral candesartan
Oral labetalol
Oral nitroglycerin
No treatment is required
• This patient does not require treatment of her elevated blood
pressure (190/90 mm Hg) at this time. Because her initial evaluation
occurred 12 hours after her acute ischemic stroke, she is not a
candidate for tPA. The American Heart Association guidelines allow
blood pressures of up to 220/120 mm Hg in patients with ischemic
stroke who are ineligible for tPA, unless evidence of end-organ
damage (active ischemic coronary disease, heart failure, aortic
dissection, hypertensive encephalopathy, acute kidney failure, or
preeclampsia/eclampsia) exists. Treatment with antihypertensive
agents in the acute setting may lead to neurologic worsening due to
a decline in cerebral perfusion in the area of the tissue at risk.
• The blood pressure target of less than 220/120 mm Hg is maintained
until hospital discharge to home or a rehabilitation facility, at which
time patients can begin or resume taking antihypertensive
medication.
A 76-year-old man is evaluated for an episode of left-handed weakness
involving all five digits that occurred yesterday and gradually subsided over 3 hours.
He has had two similar episodes in the past 2 weeks. He reports no other problems
and has no pertinent personal or family medical history. An exercise stress test
performed 1 year ago had normal results. His only medication is aspirin, 81 mg/d.
On physical examination, blood pressure is 156/78 mm Hg and pulse rate is
76/min and regular. Cardiac examination reveals a right carotid bruit. Other physical
examination findings are normal.
Results of laboratory studies show a serum LDL cholesterol level of 156
mg/dL (4.04 mmol/L).
An electrocardiogram shows normal sinus rhythm with no evidence of
ischemia. A carotid duplex ultrasound shows 80% to 99% stenosis of the right
internal carotid artery, which is confirmed by CT angiography. An MRI of the brain
shows a 5-mm infarct in the right middle cerebral artery distribution.
Which of the following will have the greatest impact in reducing the risk of
recurrent stroke in this patient?
A. Carotid endarterectomy
B. Carotid stenting
C. Clopidogrel
D. Simvastatin
• This patient should be referred for immediate R ICA carotid endarterectomy.
He has had an acute ischemic stroke caused by symptomatic high-grade
carotid stenosis. Carotid endarterectomy has been shown to be highly
effective in reducing the risk of recurrent stroke (number needed to treat,
17) in the immediate poststroke period. With symptomatic carotid stenosis,
the risk of recurrent stroke is 1% per day for the first 2 weeks after a stroke
or transient ischemic attack, which indicates that the greatest benefit is
gained when the procedure is performed early.
• Endarterectomy was superior to stenting because stenting poses a greater
risk of perioperative stroke than does endarterectomy.
• No evidence supports the use of clopidogrel in the acute poststroke period
in patients with symptomatic high-grade carotid stenosis. Antiplatelet agents
generally provide only a marginal benefit in reducing the risk of stroke
compared with surgery.
• Statins have yet to be established as safe or efficacious in the immediate
poststroke setting.
A 62-year-old woman is evaluated in the stroke unit for a 2-day
history of difficulty speaking and right arm weakness. She has a history of
hypertension and dyslipidemia and a 35-pack-year smoking history.
Medications are lisinopril, atenolol, simvastatin, and aspirin.
On physical examination, blood pressure is 148/78 mm Hg, pulse
rate is 84/min and regular, and respiration rate is 12/min. Other general
medical examination findings are normal. Neurologic examination shows
mild sensory aphasia and right arm drift.
An MRI of the brain shows an acute infarct in the left middle
cerebral artery distribution that appears embolic. A magnetic resonance
angiogram of the head and neck is normal. An electrocardiogram shows
sinus rhythm and is normal. Telemetry performed over the next 3 days
shows occasional premature ventricular complexes. A transesophageal
echocardiogram shows no intracardiac thrombus, normal left atrial
appendage velocities, and a patent foramen ovale with an atrial septal
aneurysm. No evidence of deep venous thrombosis is found.
Which of the following is the most appropriate next step in management?
A. Percutaneous PFO closure
B. Prolonged cardiac rhythm monitoring
C. Surgical closure of the PFO
D. Warfarin
• This patient's condition should be managed with prolonged cardiac rhythm
monitoring. She has infarcts that appear embolic on an MRI and no evidence
of proximal arterial disease. As such, her stroke is classified as a cryptogenic
ischemic stroke. According to data from recent studies, up to 25% of
patients with cryptogenic ischemic stroke have paroxysmal atrial
fibrillation on prolonged cardiac monitoring.
• A diagnosis of atrial fibrillation would be the only reason for this patient to
start warfarin for stroke prevention, and this patient has not yet been
demonstrated to have atrial fibrillation. No clinical trials have shown the
superiority of warfarin compared with aspirin in the prevention of recurrent
cryptogenic stroke, even in the presence of a PFO.
• The risk of recurrent stroke in patients with a PFO is low. Percutaneous or
surgical closure of a patent foramen ovale has not been shown to reduce the
risk of ischemic stroke in patients with an otherwise cryptogenic stroke.
A 56-year-old man is evaluated in the emergency department 7
hours after onset of right-sided weakness. He has a history of hypertension
and osteoarthritis. Medications are hydrochlorothiazide and daily aspirin.
On physical examination, the patient is fully awake and interactive.
Blood pressure is 220/110 mm Hg, pulse rate is 86/min and regular, and
respiration rate is 16/min. No papilledema is detected. Neurologic
examination findings include slurred speech, a lack of movement in the right
arm, trace antigravity movement in the right leg, and profound sensory loss
to all modalities on the right side.
Results of laboratory studies show an INR of 1.2, a platelet count of
375,000/µL (375 × 109/L), and a serum creatinine level of 1.4 mg/dL (124
µmol/L). Urine toxicology results are positive for cocaine.
A CT scan of the head without contrast shows a right thalamic
intracerebral hemorrhage with intraventricular extension and mild
enlargement of the ventricles
Which of the following is the most appropriate treatment?
A. External ventricular drain placement
B. Labetalol infusion
C. Metoprolol intravenously
D. Platelet transfusion
•
The patient should receive an infusion of labetalol. He has an intracerebral hemorrhage
likely due to HTN, cocaine, and (possibly) aspirin. Hematoma expansion is an important
predictor of a poor outcome in intracerebral hemorrhage, and HTN is one of the principal
risk factors for expansion. In this patient, SBP should be lowered by an intravenous
infusion of antihypertensive medication, with monitoring of vital signs every 5 minutes,
particularly because the systolic blood pressure is greater than 200 mm Hg. Because
labetalol is unlikely to interact with cocaine and cause an increase in blood pressure, it is
the appropriate option.
•
In patients whose systolic blood pressure is greater than 180 mm Hg, a target blood
pressure of 160/90 mm Hg is reasonable as long as there are no signs of elevated
intracranial pressure; if intracranial pressure is elevated, a target systolic blood pressure
of 140 mm Hg appears to be safe, according to recently published guidelines.
•
External ventricular drain placement is inappropriate in this awake and interactive
patient, despite the hydrocephalus seen on imaging. If the patient were to develop
impaired consciousness, then CSF shunting may be necessary to reduce elevated
intracranial pressure.
•
Metoprolol is contraindicated in patients with cocaine intoxication because of unopposed
α-activity potentially leading to coronary, and potentially cerebrovascular,
vasoconstriction.
•
Whether platelet transfusions improve outcomes in patients with intracerebral
hemorrhage or prevent hematoma expansion in patients taking antiplatelet agents
remains unknown.
A 76-year-old woman is evaluated in the emergency department for a 2week history of difficulty walking and four episodes of falling backward. The patient
was previously mobile and independent with the use of a walker. She has an 8-year
history of Parkinson disease characterized by bilateral tremors at rest, generalized
bradykinesia and rigidity, start hesitation and freezing, postural instability, and a
tendency to retropulse. She also has osteoarthritis of the knees and spine but no
dementia. Medications are levodopa-carbidopa and acetaminophen.
Physical examination reveals a thin, alert patient with a kyphotic posture.
Vital signs are normal. Bilateral mild hand tremors at rest, neck flexion, and a
markedly increased neck tone are noted. The legs are stiff, with three beats of
clonus elicited by ankle dorsiflexion, and the toes are upgoing. The arms and hands
have normal strength. Sensory examination shows decreased vibration perception
to the mid-shins. Her deep tendon reflexes are brisk, with spread, and the plantar
responses are extensor. She has difficulty lifting her legs off the gurney and is
unable to stand because of leg weakness. Gait and balance cannot be tested
because of her inability to stand.
Which of the following is the most appropriate next step in management?
A. CT myelography
B. Head CT
C. Increased dosage of levodopa-carbidopa
D. Lumbar puncture
E. MRI of the cervical spine
•
An MRI of the cervical spine should be obtained. Acute onset of leg weakness and an
inability to walk suggest a cause other than Parkinson disease, and could be caused by
compressive cervical myelopathy. Her physical exam is notable for increased tone with
ankle clonus, hyperreflexia, extensor plantar responses, and profound leg weakness.
Her arm strength and reflexes are normal, which suggests the possibility of spinal cord
compression from a combination of cervical arthritis, stenosis, and trauma.
•
Although CT myelography can also establish the diagnosis of cervical myelopathy and
may be needed in patients in whom MRI is precluded, this technique is difficult to
perform on an emergent basis and does not produce images of the spinal cord
parenchyma.
•
A CT of the head will not show compression of the cervical spine.
•
This patient's symptoms are not consistent with a worsening of her Parkinson disease,
and thus increasing her dosage of levodopa-carbidopa is unlikely to be helpful.
•
A lumbar puncture with CSF examination would help diagnose Guillain-Barré syndrome,
which can cause a rapidly progressive subacute paraplegia. However, the clinical
scenario and examination findings make this diagnosis unlikely
A 59-year-old woman is evaluated in the emergency department for a
4-day history of low back pain, leg weakness, and urinary incontinence. She was
discharged from the hospital 1 week ago after undergoing a lumbar diskectomy
as treatment for lumbosacral radiculopathy. Additional history includes
nonvalvular atrial fibrillation with good systolic function and hypertension.
Medications are warfarin, metoprolol, and acetaminophen as needed.
On physical examination, temperature is 36.6 °C (97.9 °F), blood
pressure is 145/65 mm Hg, and pulse rate is 68/min. Strength testing reveals
3/5 weakness in the right leg and 4/5 weakness in the left leg. Reflexes are 2+ in
the arms, 1+ in the left patellar region, and 0 in the right patellar region and
bilateral Achilles tendons. Laxity of the anal sphincter is noted.
Laboratory studies show an erythrocyte sedimentation rate of 3 mm/h,
a leukocyte count of 5800/µL (5.8 × 109/L), and an INR of 3.0. MRIs of the
lumbosacral spine show a compressive epidural lesion at L2 through L5.
Which of the following is the most appropriate management?
A.Add high dose methylprednisolone
B.Add vancomycin and ceftazidime
C.Discontinue warfarin and reverse the anticoagulation
D.Perform a lumbar puncture
• The most appropriate management for this patient is discontinuation of
warfarin and reversal of the anticoagulation. She most likely has cauda
equina syndrome secondary to external compression of the spinal cord by a
spinal epidural hematoma. Her recent surgery is a risk factor, which was
likely exacerbated by early reinitiation of warfarin after the procedure.
Stopping the warfarin and reversing the anticoagulation should be
performed in preparation for subsequent surgical decompression.
• Adding high-dose methylprednisolone to her treatment regimen is
inappropriate because none of the clinical, laboratory, or imaging findings
suggests the presence of an inflammatory disorder.
• Although an epidural abscess is part of the differential diagnosis in this
patient, the lack of fever, elevated leukocyte count, or elevated erythrocyte
sedimentation rate makes the diagnosis highly unlikely and intravenous
administration of antibiotics inappropriate
• Lumbar puncture in this patient in her current state of anticoagulation is
likely to exacerbate the underlying epidural hematoma.
A 63-year-old man is evaluated in the emergency department for a
2-day history of mid-back pain, leg weakness, and urinary incontinence. He
was treated with surgical resection for prostate cancer 1 year ago. He has no
other medical history of note.
On physical examination, temperature is 36.8 °C (98.2 °F), blood
pressure is 138/60 mm Hg, and pulse rate is 94/min. Bilateral leg weakness,
decreased sensation to pinprick below the T9 level, and mild laxity of the
anal sphincter are noted.
Laboratory studies show a PSA of 34 ng/mL (34 µg/L) and a normal
CBC. An MRI of the thoracic spine shows a contrast-enhancing epidural
lesion causing spinal cord compression.
In addition to starting intravenous corticosteroids, which of the following
interventions is likely to provide the best chance for future ambulation in
this patient?
A. Androgen-deprivation therapy
B. Chemotherapy
C. Decompressive surgery
D. Radiation therapy
• This patient should next undergo decompressive surgery which provides the best
chance for future ambulation. The most common cause of spinal cord
compression is tumor metastasis to a vertebral body, which results in direct
extension into the epidural space or a pathologic fracture. Pain is the most
common initial presenting symptom, with neurologic symptoms typically evolving
later. Corticosteroids should be administered immediately in patients with
suspected spinal cord compression for improved pain management and
prevention of further neurologic impairment. When feasible, decompressive
surgery should be performed next, followed by radiation therapy.
• Although radiation therapy does provide benefit for most tumor types, evidence
from clinical trials shows that the addition of surgical decompression before
radiation therapy is superior to radiation therapy alone, and direct head-to-head
comparisons show more long-term benefit from surgery than radiation therapy.
• Androgen-deprivation therapy (with a GnRH agonist or surgical castration) is used
as adjuvant therapy in patients with high-risk disease and as first-line treatment
in patients with an increasing PSA after initial definitive therapy for prostate
cancer or in those with metastatic disease. It is not an effective treatment for
spinal cord compression.
• Chemotherapy is not an effective treatment for metastatic cancer causing spinal
cord compression unless the tumor is highly sensitive to chemotherapy, such as
lymphoma.
A 54-year-old man is evaluated for a 9-month history of progressively
worsening paresthesia in the legs that has recently spread to the hands and a 6month history of an ataxic gait. 3 years ago he had gastric bypass surgery. He takes
a daily multivitamin, iron, ascorbic acid, calcium, and vitamins D, B6, and B12.
On physical examination, temperature is 37.2 °C (99.0 °F), blood pressure
is 110/60 mm Hg, and pulse rate is 70/min; BMI is 31. Neurologic examination
shows decreased vibratory sensation in the hands and feet and decreased position
sense in the feet. Hip flexion strength is 4/5 bilaterally, and reflexes are 3+
throughout with upgoing toes.
Labs:
Hgb 12.9
MCV 102
Vit B12 590
RPR nonreactive
T2-weighted MRIs of the cervical and thoracic spines show slight hyperintensity in
the posterior columns from approximately C4 through T9 with no contrast
enhancement.
Which of the following serum levels should be measured next?
A. Copper
B. Folate
C. 25-OH vitamin D
D. Thiamine
E. Vitamin A
• This patient's serum copper level should be measured next to detect
copper deficiency. The Roux-en-Y gastric bypass is a dual-mechanism
bariatric surgery combining a small gastric reservoir, which restricts oral
intake, with a small-bowel bypass, which induces mild malabsorption.
Nutritional deficiencies of vitamin B12, iron, calcium, folate, and 25hydroxyvitamin D are common in patients after gastric bypass. Less
frequently, deficiencies of magnesium, copper, zinc, vitamin A, other Bcomplex vitamins, and vitamin C may occur.
• This patient has a myelopathy (as evidenced by the hyperreflexia and
upgoing toes) localizing to the posterior columns and bilateral
corticospinal tracts. Common entities that cause dysfunction in this
pattern are vitamin B12 deficiency, neurosyphilis, and copper deficiency.
• Folate, vitamin D, thiamine, and vitamin A deficiencies are not associated
with myelopathy.