390 Emergency Medicine
The head CT may initially appear normal and starts to show the extent
of injury within 6 to 12 hours after the onset of symptoms.
(a)Current guidelines recommend that thrombolytics be administered
within 3 hours (180 minutes) of the patient’s symptom onset. Any patient
whose symptoms are present upon waking up from sleep is excluded
because it cannot be certain when the symptoms began. (b)The general
consensus in the neurology literature is to nottreat hypertension in patients
with acute ischemic stroke unless they are candidates for thrombolysis and
their BP is >185 mm Hg systolic or 100 mm Hg diastolic. Labetalol is often
recommended over nitroprusside. Labetalol preserves normal cerebral autoreg-
ulationwhereas nitroprusside, a vasodilator, may divert blood from the
injured tissue and cause increased ischemia. Heparin therapy (c)has not
been shown to reduce stroke-related mortality or disability in the setting of
acute stroke. If the patient is not a candidate for thrombolytics, aspirin (e)
should be given in the setting of acute ischemic stroke. Maintenance therapy
with daily aspirin or another antiplatelet agent has been shown to help reduce
stroke recurrence after a TIA.
355.The answer is e.(Rosen, pp 1522-1524.)Myasthenia gravisis an
autoimmune disease of the neuromuscular junctionthat is more common
in women in their twenties and thirties and men in their seventies and
eighties. Myasthenia gravis results from autoantibodies directed against the
nicotinic acetylcholine receptor at the neuromuscular junction. This leads
to destruction of acetylcholine receptors and competition with acetylcholine
for the remaining receptors. Muscular weaknessandfatigabilityare the
hallmarks of myasthenia gravis. Ocular symptoms manifest early and include
ptosis, diplopia, and muscle weakness. Symptoms usually worsen as the day
progresses. Diagnosis is usually made by the edrophoniumorTensilon test.
(a)Botulism is a toxin-mediated disease that causes acute weakness by
the irreversible binding of botulinum toxin to the presynaptic membrane
of nerves subsequently inhibiting the release of acetylcholine. The classic
presentation of botulism is a descending, symmetric paralysis. Unlike myas-
thenia gravis, botulinum toxin decreases cholinergic output, which may lead
to anticholinergic signs, such as dilated pupils, dry skin, urinary retention,
constipation, and increased temperature. (b)Lambert-Eaton myasthenic
syndrome is often associated with small-cell carcinoma of the lung. Autoan-
tibodies cause a decreased release of acetylcholine from presynaptic nerves.
However, with repeated stimulation, the amount of acetylcholine in the
synaptic cleft increases leading to an improvement of symptoms throughout