Transcript Session 2

NEUR 7510
Neurology Clerkship
Session 2:
Spells
Definitions
• Stroke: sudden loss of brain function due to
blockage or rupture of a blood vessel;
alternatively an acute brain related event
(focal/generalized)
• Embolic stroke: blockage of a vessel from a
proximal source
• Thrombotic stroke: in situ obstruction of blood
flow resulting in ischemia
• Lacunar infarction: small vessel related ischemic
stroke
• Hemorrhagic infarction: bleeding into the brain
and damaging brain tissue
Or
Carotid artery disease
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Atherosclerosis is common at the bifurcation of the common carotid artery
Stenosis of the internal carotid artery is a potentially treatable cause of:
– Ischaemic stroke
– Transient ischaemic attack
– Retinal infarction
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A patient with an asymptomatic 50% carotid stenosis has 1-2% per year risk
of a stroke
The risk of stroke increases with the degree of stenosis
Once a stenosis has become symptomatic the risk of a stroke is further
increased
Once an ischaemic stroke has occurred the risk of further stroke is ~10% in
the first year and ~5% in subsequent years
Assessment of stenosis
• Carotid bruits are an unreliable guide to severity of stenosis
• May be absent in patients with severe stenosis
Duplex ultrasound
Doppler recordings allow
assessment of flow at stenosis
Also allows imaging of arterial
anatomy
Intra-arterial angiography is the traditional
method of assessing degree of stenosis
4% risk of inducing further neurological
event
1% risk of permanent stroke
Lacunar infarct: This 52-year-old man with a history of poorly controlled hypertension
presented with right body numbness. Examination was significant for a blood
pressure of 182/96 mm Hg, retinal arterio-venous nicking and right-sided hemibody
hypesthesia to pinprick and temperature sensation. The T2-weighted axial image on
the left shows an area of high signal intensity within the left thalamus. The
corresponding diffusion-weighted MR image on the right shows an isolated area of
high signal intensity within the left thalamus.
What nonvascular processes mimic
stroke?
Brain MRIs Contrasting Bell's Palsy with a Central Pontine Infarct
Gilden, D. H. N Engl J Med 2004;351:1323-1331
100 patients with
cerebrovascular disease
• Subarachnoid
hemorrhage (5%)?
• Intraparenchymal
hemorrhage (20%)?
• Ischemia (75%)?
100 patients with cerebral ischemia
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25% Large vessel atherothromboembolism
25% Small vessel disease
25% Cardioembolism
5% Other conditions
20% Unknown
Types of brain hemorrhage
• Intraparenchymal
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Often hypertensive
Amyloid angiopathy
Into a tumor
Trauma related
Underlying vascular
abnormality
• Subarachnoid
– Trauma
– Related to an aneurysm
• Subdural
– Chronic versus acute; often
related to trauma or
bleeding propensity
• Epidural
– Acute often related to
trauma and injury to middle
meningeal artery
Coup and contre-coup
Injury
Epidural hematoma
Subdural hematoma
TRAUMA
AND
THE
BRAIN
Intraparenchymal hematoma
Diffuse axonal injury
In what four locations do spontaneous
(hypertensive) intracerebral
hemorrhages most commonly occur?
– Basal Ganglia
• Putamen - Contralateral hemiparesis, contralateral sensory loss,
contralateral conjugate gaze paresis, homonymous hemianopia, aphasia,
neglect, or apraxia
• Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze
paresis, or confusion
– Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze
paresis, homonymous hemianopia, miosis, aphasia, or confusion
– Brain stem (typically pons) - Quadriparesis, facial weakness,
decreased level of consciousness, gaze paresis, ocular bobbing, miosis,
or autonomic instability
– Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial
weakness, ipsilateral sensory loss, gaze paresis, skew deviation,
miosis, or decreased level of consciousness
– Lobar - Contralateral hemiparesis or sensory loss, contralateral
conjugate gaze paresis, homonymous hemianopia, abulia, aphasia,
neglect, or apraxia
Putamen (50%); thalamus (25%); pons/brainstem (10%); cerebellum (10%), and
cerebral hemispheres (5%)
64 yo RH Woman
• 5 min right arm weakness
• 2nd episode involved the leg
• What is the most likely anatomic
localization?
Exam:
AV nicking
Rt cervical bruit
Right facial weakness
Rt pronator drift w/ slow ffm & 4/5 wrist ext
Rt leg weakness
Rt toe: upgoing
Account for the
forehead symmetry
absence of sensory findings
good grip strength in the face of very slow finger tapping
symmetric reflexes
History reveals long-standing hypertension, MI 3 yrs prior, long
Tobacco use and rx for a diuretic
Pathological process
Mechanisms of injury
What is the patient was 30 yo?
Tests
Diagnostic studies: which are needed
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Coagulation studies
Drug/tox screen
Genetic studies/cholesterol/glucose/other
ECG/Rhythm monitoring
ECHO (TTE/TEE)
Arch study
Arteries: carotid ultrasound/CTA/MRA
4 vessel angiography
Brain CT/MRI/MRA/MRV/CTV
Management
• Preventive therapy?
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Blood pressure
Smoking
Blood sugar
Cholesterol
Exercise
Medications
Prevent complications?
Aid in recovery?
Risk factors?
Preventable?
Present management
– TPA
– Coumadin
– Antiplatelet
Medical management
• Stop smoking
• Pharmacological treatment of hypertension and diabetes
• Prophylactic aspirin
– Asprin prevents around 40 ‘vascular events’ per 1000 patients
treated for 3 years
– It should be started at 175-150 mg daily once ischaemic stroke
confirmed by CT
– It should also be given to those with asymptomatic stenoses
– The combination of aspirin and dipyridamole is no more effective
than aspirin alone.
Surgery for symptomatic stenosis
North American Symptomatic Carotid Endarterectomy Trial (NASCET)
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Compared endarterectomy plus medical treatment in those patients with
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Non-disabling stroke in 4-6 months prior to surgery
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Severe (70-99%) ipsilateral stenosis
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The risk of stroke or death over 2 years was reduced (9% vs. 26%) in surgery group
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5.8% randomised to surgery had stroke within 30 days
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Benefit also seen in those with more than 50% stenosis but not to same degree
European Carotid Surgery Trial (ECST)
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ECST risk of stroke or death over 3 years was reduced (12% vs. 22%) in surgery group
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7.5% randomised to surgery had stroke or died within 30 days of operation
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In those with mild (0-30%) and moderate (30-60%) symptomatic stenoses there was benefit from surgery
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Overall, In those with symptomatic stenoses
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Best results are seen in those with more severe stenosis
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Benefit only seen in institutions with low perioperative stroke and death rate
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Surgery indicated in those with severe stenosis (more than 70%) that have recently become symptomatic
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Operation should be performed by experienced surgeon
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Centres should audit their results and have a perioperative stroke rate of less than 7%
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Angina and hypertension should be well controlled pre-operatively
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If patient selection is poor or complication rate high then there will be no benefit from surgery.
Carotid angioplasty
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Angioplasty (± stent placement) is being used to dilate stenoses
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No published randomised trials
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In uncontrolled studies severe stenoses (more than 70%) have been dilated to less than 50%
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Re-stenosis often occurs and a significant risk of stroke during the procedure
Surgery for asymptomatic stenosis
Asymptomatic Carotid Atherosclerosis Study
• 1662 patients with more than 60% reduction in luminal diameter
• Randomised to either:
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Endarterectomy + medical treatment (aspirin 300 mg)
Medical treatment alone
Risk of ipsilateral stroke over 5 year period was reduced (5% vs. 11%) in surgery
group
2.3% in surgery group had stroke within 30 days of surgery
0.4% in medical group had stroke in same time period
Overall, benefit for those with asymptomatic stenosis but only the presence of a low
perioperative complication rate.
Asymptomatic Carotid Surgery Trial
• 3120 patients with more than 60% reduction in luminal diameter
• Randomised to either immediate or deferred carotid surgery
• Risk of stroke within 30 days of surgery was 3.1%
• Risk of stroke over 5 year period was reduced (3.8% vs. 11%) in surgery group
• Results were similar to ACAS study
58 yo LH Man
• 10 minute episode
– LUE tingling
– Within a minute spread to face & leg
– LUE & LLE would not work
• Anatomical localization?
• Exam
– Bruits: femoral, subclavian arteries
• Does the normal examination help or
hurt the presumed localization?
Questions
• Differential of transient focal neurologic
dysfunction and distinguishing features
• Long-term prognosis of a transient
ischemic attack (TIA)?
• Admission required?
81 yo M
• Acute onset of vertigo and nausea
• Rt leg unsteady & Rt facial numbness
• Anatomical localization?
Hoarse
Eyes move rapidly to Lt then slowly to Rt
Rt pupil 2 mm with ptosis; Lt pupil 4 mm
Rt face: reduced pp & temp
Palate pulls to Lt
RUE & RLE dysmetria
LUE & LLE decreased pp & temp
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Eye movements: Nystagmus
Defining central and peripheral vertigo
Differentiating central vs. peripheral vertigo
Diagnosis of this patient
Mechanism?
Treatment?
What are the cause & treatment of isolated
vertigo attacks?
• What if there was left hearing loss and facial
weakness?
• What it evolved slowly?
MRI Right Inferior Cerebellar Infarction in a Man with Acute Vertigo,
Vomiting, Nystagmus Elicited by Right, Left, or Upward Gaze, and
Severe Gait Instability.
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Axial T2-weighted image shows a highintensity signal (white) in the right inferior
cerebellum, with displacement of the
medulla. Neurosurgical intervention was
required because of brain-stem
compression with noncommunicating
hydrocephalus and progressive
deterioration in mental status. On the day
after surgery, the patient's mental status
rapidly improved. Over the next week, his
nystagmus resolved and he began walking.
The inset illustrates the vascular supply to
the inferior cerebellum. The inferior
cerebellum is perfused by the medial and
lateral branches of the posterior inferior
cerebellar artery (PICA) and the anterior
inferior cerebellar artery (AICA).7,8
Hotson, J. R. et al. N Engl J Med 1998;339:680-685
Dix-Halpike Test in BPV
Treatment of BPV
Schematic Drawing of Peripheral and Central Vestibular
Nystagmus with and without Visual Fixation.
Hotson, J. R. et al. N Engl J Med 1998;339:680-685
A 53-year-old man awoke in the morning with
acute dizziness. He staggered to the
bathroom, where he vomited repeatedly. When
he was seen at a local emergency room 12
hours later, he had left-beating nystagmus in
all positions of gaze but otherwise no focal
neurologic findings.
How should he be evaluated and treated?
The first task of the examining physician is to determine
whether the vertigo is of central or peripheral origin, since
some central causes of acute vertigo, such as cerebellar
hemorrhage or infarction, can be life-threatening and may
require immediate intervention.1
This differentiation can usually be made at the bedside on the
basis of the type of the spontaneous nystagmus, the results
of the head-thrust test (described below), the severity of the
imbalance, and the presence or absence of associated
neurologic signs.
Spontaneous nystagmus of peripheral origin is typically
horizontal with a torsional (rotational) component; it does not
change direction with a change in gaze.
By contrast, spontaneous nystagmus of central origin is
often purely horizontal, vertical, or torsional and usually
changes direction with changes in the position of the gaze.
The head-thrust test is a simple bedside test of the horizontal vestibuloocular reflex.2 It is performed by grasping the patient's head and applying
a brief, small-amplitude, high-acceleration head turn, first to one side and
then to the other. To start, the eyes should be about 10 degrees away
from the primary position in the orbit so that after a 10-degree head turn,
the eyes will be near the primary position. The patient fixates on the
examiner's nose and the examiner watches for corrective rapid eye
movements (saccades), which are a sign of decreased vestibular
response (i.e., the eyes move with the head rather than staying fixed on
the nose). If "catch-up" saccades occur after head thrusts in one direction
but not after those in the other direction, this indicates the presence of a
peripheral vestibular lesion on that side (in the labyrinth or the 8th nerve
including the root's entry zone in the brain stem).
Patients with an acute peripheral vestibular lesion typically can stand,
although they will veer toward the side of the lesion. By contrast, patients
with vertigo of central origin are often unable to stand without support.
Associated neurologic signs such as dysarthria, incoordination,
numbness, or weakness suggest a central origin.
The syndrome of acute, prolonged vertigo of peripheral origin is
commonly called vestibular neuritis, although other terms such as
"vestibular neuronitis," "labyrinthitis," "neurolabyrinthitis,"
and "unilateral vestibulopathy of unknown cause" have also
been used.3 The vertigo typically develops over a period of hours,
is severe for a few days, and then subsides over the course of a
few weeks. Some patients can have residual nonspecific
dizziness and imbalance that lasts for months. The condition is
thought to result from a selective inflammation of the
vestibular nerve, presumably of viral origin. The facts that the
disorder often has a viral prodrome, that it occurs in epidemics,
that it may affect several members of the same family, and that it
occurs more commonly in spring and early summer all support a
viral cause.3 Postmortem studies have found atrophy of the
vestibular nerve and the vestibular sensory epithelium that is
similar to the pathological findings with known viral disorders of
the inner ear, such as measles and mumps.4,5 Several viruses
selectively infect the labyrinth, the 8th nerve, or both in animal
A common feature of vestibular neuritis is selective
damage to the superior part of the vestibular labyrinth
(horizontal and anterior semicircular canals and utricle)
supplied by the superior division of the vestibular
nerve, with sparing of the inferior part (posterior
semicircular canal and saccule) supplied by the inferior
division.8
Benign paroxysmal positional vertigo (originating from
the posterior semicircular canal) often develops as a
sequela even if the patient has no remaining function in
the horizontal or anterior semicircular canal.3,9
Selective inflammation of the superior division of the
vestibular nerve10 or anatomical differences in the
bony canals of the two divisions11 might explain this
relative vulnerability.
A 27-year-old man
presented with a twoweek history of left
sensorineural hearing
loss and tinnitus.
T1-weighted gadolinium-enhanced axial
image through the posterior fossa at the
level of the cerebellopontine angle shows
the typical appearance of an acoustic
neuroma (vestibular schwannoma). The
larger, rounded portion (black arrow)
represents the cisternal component of the
mass, and the smaller, conical portion (white
arrow) represents the intracanalicular
component.
The tumor was resected through a left
suboccipital craniotomy. It involved both the
superior and inferior vestibular nerves. The
histologic diagnosis was acoustic neuroma.
The patient's postoperative course was
complicated by a pulmonary embolism,
which required placement of an inferior vena
caval filter. When the patient was last seen
four months postoperatively, he was deaf in
the left ear and had intermittent left-sided
tinnitus.
19 yo student
5 minutes of strange behavior:
– Abrupt blinking and picking at clothes
– Unresponsive to questioning
– Pushed roommated
– Walked aimlessly
– Cleared gradually
– Amnestic to event
Questions
• Type of event
• DDx: seizure, TIA, syncope
• Episodes
– Prodrome
– Spell
– Recovery
• Predisposing factors
• Define seizure and epilepsy
Questions II
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Prevalence
Lifetime risk of seizures
Is violence part of seizures
Tests?
– MRI vs. CT
• EEG
• Chances of a 2nd seizure after an unprovoked
single seizure
• Rx? Life long?
• Define status epilepticus
Thalamacortical Circuitry and EEG
Genetic Epilepsy
Hippocampal Sclerosis:
Mesial Temporal Lobe Epilepsy
Mesial Temporal Sclerosis
At the age of 23 years, he
reported seizures had begun
at 15 years old, after he had
been struck on the right side
of the head by his father and
had lost consciousness. The
seizures were preceded by
an aura of warmth on the
right side of the head;
occasionally, he had brief
myoclonic jerks before losing
awareness. His brother
added that the patient would
look to the right and then fall,
stiffen, and shake for several
minutes. Tongue biting and
incontinence accompanied
the seizures, which were
followed by confusion and
sometimes combativeness
for as long as 30 minutes.
• An 11-year-old right-handed boy was admitted to the
hospital because of a seizure.
• The child had been well until the day of admission, when
he stood up and fell, striking his head on a desk. He
became unconscious, with arms extended and pronated,
and had a right focal motor seizure that became
generalized and lasted 20 minutes. There was no
contusion, rash, or lymphadenopathy. Emergency
medical technicians found him confused, combative, and
unresponsive to verbal stimuli. He was brought to this
hospital.
• The boy's mother stated that he had developed normally
without any serious illnesses. An adult brother had died
of complications of the acquired immunodeficiency
syndrome (AIDS) several years earlier. The patient
resided with his mother, his stepfather, and two healthy
kittens. There was no history of fever, headache, rash,
visual problems, previous seizures, travel, exposure to ill
persons, or use of tobacco, alcohol, or illicit drugs.
Cat scratch encephalitis due to B. quinta
Questions III
• What are the systemic dangers of continued
convulsions?
• The dangers of ongoing seizures to the brain?
• The risks of intravenous phenytoin,
fosphenytoin, and valproic acid?
• Outline the treatment of convulsive status
epilepticus
• What are the Minnesota rules on driving and
epilepsy?
http://www.dps.state.mn.us/dvs/index.html
Anticonvulsants: need to check
Name
Half-life
Side effects
Serious S/Es
Phenytoin
12-24
ataxia
liver failure
Carbamazepine
8-12
above
Stevens-Johnson
Aplastic anemia
Valproate
8-12
Gapapentin
?
Neural tube defects
Liver
Confusion
?none
Questions
• Define therapeutic antiepileptic level
• Discuss teratogenecity of anticonvulsants
• Discuss dose adjustment during
pregnancy and postpartum
Vignette
• 24 yo man with atypical seizures
– Dropping objects at work
– Collapse w/o LOC during a joke
– Falling asleep at meetings
– Vivid dreams
• Diagnosis
• Test(s)
Treatments
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49 yo with obstructive sleep apnea
63 yo with restless legs syndrome
17 yo student bus ride @ 6:25 AM
47 yo with depression, anxiety & frequent AM
awakenings
• 67 yo woman whose spouse has requent
nocturnal myoclonus
• 41 yo man with multiple sclerosis and frequent
nocturnal extensor spasms
• 56 yo factory worker with frequent shift changes