: This 82 year-old right-handed male was driving
his car when he suddenly became aware of a spinning
sensation and feeling as though he were "drunk".
He pulled the car over to the side to the side of
the road, and after a few minutes, he again was asymptomatic.
A few hours later, he noted side by side double vision
which cleared when either eye was closed. He began
to experience a rotary or whirling sensation with
rapid position change. Two days later he consulted
This symptomatology suggests neurologic dysfunction
in which of the following areas?
A. Cerebral cortex
B. Visual pathways
C. Brain Stem
D. Cerebellar system.
The sudden onset of Neurologic Dysfunction at this
age is most suggestive of :
A. Vascular disease
B. Diabetes mellitus
C. Central nervous system neoplasm
D. A demyelinating disorder, such as late onset MS.
history revealed that six months prior to the onset
of these neurologic symptoms, he became aware of intermittent
claudication. He has had no known cardiac disease,
hypertension, or diabetes mellitus. About five years
ago, he had two episodes of spontaneous epistaxis
a few days apart, but otherwise, there has been no
evidence of blood dyscrasia. Eight years ago, he had
a subtotal gastrectomy for peptic ulcer disease, and
since then has been asymptomatic.
family history reveals that his mother died during
the influenza epidemic in 1917. She had diabetes late
in life. One sister also possibly is a diabetic. His
father died at age 42 trauma. Two siblings have a
history of heart disease.
examination reveals an alert, well-nourished gentleman,
who appeared considerably younger than his stated
age. Blood pressure 195/80, both arms, sitting. The
dorsalis pedis and posterior tibial pulses were absent
bilaterally. The carotid pulsations were strong bilaterally.
There was a Grade II systolic bruit in the left supraclavicular
area. No intracranial bruit was present. There was
no evidence of impairment of mentation. On gait testing
there was unsteadiness and swaying with rapid turns
and difficulty performing tandem walking. There was
slight slowing of left foot tapping. The pupils were
2mm bilaterally and reacted normally.
were minimal atherosclerotic changes in the retinal
vessels, and no appilledema was present. There was
diplopia on left lateral gaze and to a greater extent
on right lateral gaze. The images were horizontally
displayed. With extreme right lateral gaze, there
was unilateral nystagmus of the right eye with impairment
of full medial gaze in the left eye. There was a suggestive,
but not definite, left lateral rectus palsy. The rest
of the cranial nerves were normal.
examination was intact to superficial, deep and discriminative
modalities. Motor examination revealed no paresis
or cerebellar deficit, and the reflexes were equal
and active bilaterally with no abnormal reflexes present.
The Abnormalities of ocular motility can best be ascribed
A. A conversion reaction
B. Drug effect
C. Interruption of the median longitudinal fasciculus
D. Involvement of the dentate nucleus of the cerebellum
Which of the following statements are true?
A. A bruit over an extracranial vessel in the neck
always indicate stenosis of the artery being ausculated
B. Because of flow patterns, a bruit may be present
over the unobstructed side
C. Significant stenosis may be present without a bruit
D. All systolic bruits over the carotid arteries are
pathological and require further investigation.
: This patient was hospitalized, and was found
to have normal skull films, an unremarkable electroencephalogram
and brain scan and normal spinal fluid. He was mildly
diabetic, and was placed on a diabetic diet. A surgical
consultation was obtained. The vascular surgeon felt
that consideration of surgical repair was not indicated
because of the patient's age, and the fact that his
disease most likely was in the basilar-vertebral distribution.
Because of his history of peptic ulcer disease, epistaxis
and absence of clinical evidence that his stroke was
progressive or recurrent, it was elected not to give
his anticoagulation. Over the next four months, his
clinical signs gradually improved, although he continued
to experience mild diplopia on extreme right lateral
Which of the following situations calls for anticoagulation?
A. Transient insufficiency attacks
C. Completed stroke
D. Recurrent cerebral emboli
Which of the following may precipitate a transient
insufficiency attack in a patient with underlying
A. Orthostatic hypotension
B. Cardiac arrhythmia
C. Embolic plaque from atherosclerotic lesion
D. Hypercoagulable state
E. All of the above.
C The phenomenon of diplopia indicates a loss of normal
conjugate eye movements. This is usually due to a
lesion of the brain stem or one of the nerve innervating
the eye muscles. In myasthenia gravis, diplopia can
occur with the defect at the neuromuscular junction.
A Neurologic deficit that begins suddenly, if it is
not a seizure disorder, is usually either vascular
in origin or a manifestation of a demyelinating process
such as multiple sclerosis. In demyelinating disease,
the onset of neurologic deficit is rarely lightening-like,
but rather evolves over a period of several hours
at the least. Vascular disease, regardless of the
kind of circulatory disorders, characteristically
begins abruptly. This is true regardless of whether
the underlying mechanism is embolism, hemorrhage,
or ischemic thrombosis. Since demyelinating disease,
especially those that are rapid on onset, involve
primarily younger individuals, the sudden onset of
neurologic deficit in an adult almost always indicates
a disorder of blood supply of some variety.
C Nystagmus of the abducting eye on attempted lateral
gaze with limitation of movement of the adducting
eye is termed internuclear ophthalmoplegia and is
caused by a lesion of the median logitudinal fasciculus
in the brain stem.
C Physiologic bruits are fairly common, especially
in young males where they appear are rather localized
systolic bruits at the base of the right carotid.
This bruit increases with heart rate and can be altered
with position. Pathologic bruit usually does not change
significantly with alteration of heart rate or position.
If a vessel is completely occluded, a bruit will not
be present over that vessel, but may be heard over
the contralateral vessel as flow in this channel shows
a compensatory increase.
There is general agreement that 1) if the patient's
clinical syndrome is one of transient insufficiency
attacks, 2) if the diagnosis is reasonably certain,
3) if other correctable factors have been treated,
and 4) if no contraindication is present, that anticoagulation
will decrease the number of insufficiency attacks
is most patients, and in some will stop them completely.
It is not entirely clear, however, that anticoagulation
in the patient with TIA's results in a decreased incidence
of eventual cerebral infarction.
There is lesser agreement over the use of anticoagulation
in the stroke-in-evolution syndrome and in recurrent
cerebral emboli. Because of the not insignificant
incidence of anticoagulation induced intracerebral
hemorrhage, many have been reluctant to use anticoagulation
in these two situations. Other evidence, however,
indicates that on balance the patient will benefit
from immediate anticoagulation. The evidence and clinical
opinion is therefore divided in these two situations.
Most authorities, however, tend to favor immediate
anticoagulation in both situations. In the "completed
stroke" syndrome there is general agreement that
chronic anticoagulation does not prevent the recurrence
of further cerebral infarctions and is therefore not
E The major supply of the vertebral-basilar system
is the brain stem and the occipital lobes. Thus, with
either vertebral-basilar insufficiency or complete
occlusion, one finds variable symptoms and signs referable
to brain stem dysfunction: Cerebellar signs may also
occur. Nystagmus, hemiparesis and bilateral Babinski's
are very common. Horner's syndrome may occur if the
appropriate pathways in the brain stem are interrupted.
Hypothalamic dysfunction as manifested by wide fluctuations
in blood pressure and temperature may occur. "Crossed"
motor and sensory syndromes may be found.
There is general agreement that chronic use of vasodilators
is not of significant
benefit in the patient with the usual variety of atherosclerotic
cerebrovascular disease. In some patients, vasodilators
may induce orthostatic hypotension which can be deleterious.
In the initial phase of a vascular occlusion, however,
several authors favor the use of vasodilators, especially
papaverine hydrochloride. This has been debated in
literature, however, sincere there is evidence that
in certain situations vasodilation may shunt blood
from an ischemic area. Seizures as a manifestation
of cerebrovascular disease occur primarily with cerebral
embolus and intracerebral hemorrhage. Although they
do occur, they are very infrequent in the acute stage
of a cerebral thrombosis. They are extremely uncommon
in any form of basilar artery disease. The basilar-vertebral
distribution is also a very uncommon site for a cerebral
embolus regardless of its origin or etiology. In most
patients who have sustained a stroke, a lumbar puncture
is indicated. This is primarily to rule out subarachnoid
or intracerebral hemorrhage.
E The phenomenon of transient cerebral insufficiency
attacks has received considerable interest and study
over the past several years. At the present time,
it would appear that many mechanisms are involved
in precipitating such an event. In any one individual,
these factors may be multiple and careful evaluation
of each possibility is indicated. In some patients
the episodes are clearly associated with mechanisms
that cause orthostatic hypotension, such as urinating
after arising from sleep. Occasionally, Strokes-Adams
attacks and other cardiac dysrhythmias may present
primarily as a TIA. It has been clearly documented
that emboli may arise from an atherosclerotic lesion
in the more proximal vascular bed. These emboli may
consist of small thrombi or cholesterol crystals.
TIA's also occur in the setting of hyperlipidemia,
increased platelet adhesiveness, and other situations
that result in a hypercoagulable state. The mechanism
of vasospasm has been debated at great lengths and
it is still unclear whether this is a significant
factor in producing TIA's. Anemia and electrolyte
disturbances may also be contributory.