Stroke Case Histories and
Clinical Problem Solving
Cases prepared and presented by Dr. Robert Coni
Internal Medicine Residency Program
Grand Strand Medical Center
Objectives
1. Working through the case presentations and simulation questions in this
activity, the PGY-1 resident will be able to analyze the deficits and
scenarios to recognize stroke type and likely mechanism, identify
localization of the lesion in the nervous system, and will also develop a
strategy for further evaluation of the patient in the hospital and then use
the database collected to identify an effective strategy for secondary
stroke prevention. This will occur as the learner progresses through
clinical case presentation simulations and be assessed by answers
provided as the presentation deepens.
2. The PGY-1 physician will, by working through these case simulations,
review knowledge of and apply neuroanatomy to the neurological
examination function of lesion localization and will then adapt this
strategy for use in neurological assessment of other neurological
problems that are not stroke related and will be assessed on the
acquisition of this knowledge and ability while on the neurology rotation.
Objectives
1. The PGY-1 physician will review ischemic stroke types (large vessel,
branch vessel, and lacunar strokes) and understand the clinical
differences so as to recognize each readily from a clinical case scenario.
Transfer of this skill will be demonstrated during the neurology rotation.
2. The PGY-1 physician will review ischemic stroke mechanisms (embolic,
thrombotic, hemorrhagic, and low flow events) and understand the
presentation differences and recognize these when presented in a clinical
case scenario. Transfer of this skill will be demonstrated during the
neurology rotation.
3. The PGY-1 physician will order an appropriate stroke evaluation
determined by the presentation and clinical history, stroke type and
mechanism on hospitalized stroke patients and on simulation stroke
patients, and demonstrate, by using the data obtained as a result of this
workup, his/her knowledge of secondary stroke prophylaxis both on
rotation and within the case scenarios of this activity.
Case One
Case One
A 66 year old woman presents to the ED 40 mins after suddenly developing speech difficulty and weakness of
the right arm and leg. She was home, and well previously that morning when symptoms were observed by
family members. She became mute and slumped at the table. She has a past history of hypertension and takes
Atenolol and Amlodipine.
Her examination shows her to be afebrile, HR – 115; BP – 175/86 mmHg. Heart rhythm was irregularly irregular
and there were no Carotid bruits. Neurologic examination showed a lethargic woman who was arousable. She
followed some simple commands but had impairment of word fluency, anomia, and she could not repeat. Gaze
was deviated left and right lower facial droop was present. The right upper extremity was plegic and the lower
extremity on that side was weak. The left limbs had no drift when held out.
Where is her lesion; ie, what part of the brain is affected?
What is the most likely diagnosis?
Where is her lesion?
1. Right side of the brain in the brainstem.
2. Right side of the brain in the middle cerebral artery territory.
3. Left side of the brain in the brainstem.
4. Left side of the brain in the middle cerebral artery territory.
Answer is 4: This clinical description is that of a cortical lesion in the brain. The
lateralization to the left is evident based on a combination of right sided weakness
and left gaze preference. The language dysfunction is relevant as a “cortical sign”
which in this case is a sign of dominant hemisphere involvement. The description is
of an aphasia. The MCA distribution typically has weakness of the arm greater than
the leg and face. Gaze paresis is a frequent accompaniment with the patient
looking toward the lesion.
Knowing the patient’s handedness would be helpful but not necessary. Why?
- Most of the population is left brain dominant and right handed, but 80% of
left handed people are right brain dominant.
What would you expect her visual fields to show?
- Right hemianopsia; this is also a cortical sign.
What is the most likely diagnosis?
1. Acute embolic stroke.
2. Acute thrombotic stroke.
3. Transient ischemic attack.
4. Subdural hematoma.
Answer is 1. The history describes the clinical presentation of stroke.
The acute stroke syndrome is defined by sudden onset of neurological
deficits. A TIA has a similar onset but is limited with deficits appearing
suddenly and resolving over 15-30 mins, but by definitely by 24 hours.
Important to the definition of TIA is that imaging shows no infarct,
specifically a negative diffusion weighted image MRI.
What is the next diagnostic step?
1.
2.
3.
4.
A pre and post contrast CT scan of the brain.
A non-contrast CT scan of the brain.
A non-contrast MRI scan of the brain.
A pre and post CT scan of the brain with CTA of the head and neck.
Answer is number 2: The main concern is establishing the presence or
absence of intracerebral hemorrhage. Additional utility is to look for early
signs of cerebral ischemia. The CT scan is rather insensitive to acute
ischemia, thus, if there are signs of ischemia, the time of onset had to have
occurred on the order of hours before. An MRI is useful but in the acute
setting where decisions about management are critical, the CT is the most
useful. The CTA is useful and warranted after the non –contrast CT of the
brain in patients with a high NIHSS. Scores of 7 or higher often are associated
with large vessel occlusions which might be amenable to interventional
radiology procedures, but to assess, a CTA would be needed.
Of the following, which are part of the differential
diagnosis, mark all those that apply:
Seizure with postictal Todd’s paralysis
Subdural hematoma
Complicated migraine
Abscess
Brain tumor
Hypoglycemia
Multiple sclerosis
Herpes encephalitis
Intracerebral hemorrhage
Answer:
If you marked all of the answers you are correct. Each can mimic an
ischemic stroke. Usually there are differences in the onset with many
showing a subacute onset as opposed to sudden deficit. In the case of
seizure there are usually other tip offs including a history of some
preceding adventitious motor activity, tongue bite, incontinence or
sensory symptoms. Of course, hemorrhage is differentiated on the noncontrast CT scan of the brain.
Is this patient a candidate for thrombolytic therapy
provided there are no containdications?
1. No, even if the scan is negative, her BP at presentation would be a
contraindication.
2. No, even if her scan is negative, her NIHSS score can be estimated
to be around 20.
3. No, with a high NIHSS she might be better treated with a possible
interventional radiologic procedure for large vessel occlusion.
4. Yes, as long as there are no contraindications for giving IV tPA.
Answer: 4
The blood pressure restriction for IV tPA is >190 mmHg systolic and or
110 mmHg diastolic, which does not respond to intervention with IV
medications. When treated, if BP is reduced, the patient can be treated
with tPA. High NIHSS score is not an absolute contraindication for IV
tPA therapy. It is an indicator of possible large vessel occlusion (LVO),
with as much as 27% of patients having high NIHSS scores also
demonstrating LVO. This would be diagnosed by CTA of the head and
neck. This is performed in appropriate circumstances after the noncontrasted CT. Additionally, IV tPA can be given before an
interventional clot extraction.
Case One - Treatment
The non-contrast CT of the brain was negative. This patient was given
IV tPA. A CTA of the brain and neck was performed. The neck showed a
left carotid stenosis of approximately 65% and there was a partial
occlusion of the left MCA on brain CTA. After tPA, the patient began to
improve and interventional therapies were discussed with the family
however they refused.
Using stroke admission orders, the patient was routed to admission in
the ICU. Further evaluation revealed, an LDL of 106, HgbA1c of 5.8 and
an Echocardiogram showed an enlarged left atrium. Stroke admission
orders provide for all the needed tests and instituting appropriate
therapies at appropriate times, including DVT prophylaxis, therapy
evaluations and secondary prophylaxis.
Case One –Treatment Continued
What would appropriate secondary stroke prophylaxis be in this
patient?
1. Aspirin 81 mg daily
2. Aspirin 81 mg and Clopidogril 75 mg daily
3. 325 mg Aspirin
4. Anticoagulation (Warfarin or NOA)
Answer: 4 The etiology of this embolic stroke is atrial fibrillation.
Treatment of embolic stroke due to atrial fibrillation is anticoagulation
which reduces the incidence of stroke from about 7.5 % per year to 1.5
% per year.
Case One - Treatment
When should this treatment be instituted?
1. Immediately if the next CT is negative for bleeding.
2. In 5-7 days if the CT remains negative.
3. In two weeks at a minimum due to the size of the stroke.
4. At a six week follow-up visit.
Answer: 2
There is no reason to delay anticoagulation beyond this time frame.
Immediate anticoagulation is not warranted and places the patient at a
greater risk of hemorrhagic conversion of the stroke. A repeat non-contrast
CT scan should be done before starting anticoagulation to ensure there has
been no hemorrhagic change.
Case One - Treatment
The LDL was 106, thus the patient should be started on:
1. Any statin at low dose.
2. No statin is needed since LDL is less than 110.
3. Low dose atorvastatin (40 mg) or rosuvastatin (20 mg)
4. High dose atorvastatin (80 mg) or rosuvastatin (40 mg)
Answer: 4
High dose statin therapy is recommended in individuals ≤ 75 years of age
who have had a cerebrovascular event. Moderate doses are recommended
in those over 75 years of age. Generally, these two drugs are recommended
above others based on trials. A statin should be prescribed in any vascular,
stroke or TIA patient at discharge.
Case Two
Case Two
A 58 year old hypertensive, diabetic man presents to the ED with a chief complaint of experiencing
an odd sensation in the right hand for about four hours. This was first noted while he watched a
baseball game and he describes it as feeling numb. Later, after the game and as he prepared to eat
dinner, he noted difficulty grasping his utensils and bringing food to his mouth. He thought
symptoms would disappear but when his daughter called him he had difficulty getting to the phone
and mild trouble speaking due to slurring. His daughter encouraged him to go to the ED. He denied
swallowing or chewing difficulty, dizziness, leg involvement with weakness, or headache.
General physical examination was unremarkable except for moderate obesity. His BP was 156/88,
pules was 90 and regular. He was afebrile. Pulses were intact. Neurological exam showed normal
mental status and cranial nerve exam showed mild facial weakness on the right with nasolabial fold
flattening. He had mild pronation of the right arm with no drift. Rt arm strength was 4+/5 but there
was finger – nose – finger dysmetria. There was slowness to movement of the leg with no
dysmetria. Sensory examination was normal to cutaneous stimuli well as vibration. Toe response on
the right was mute. Last known normal was about 5 hours ago. His blood glucose was 274. He does
not use tobacco or drink alcohol. NIHSS was 6.
His initial head CT was normal with no evidence of ischemia or hemorrhage.
Where is his lesion? What structures could be affected?
What is the most likely diagnosis?
Case Two
Where is this patient’s lesion?
1. Anywhere in the left cortiospinal tract from the corona radiate to the
pons.
2. In the genu of the left internal capsule.
3. Anywhere in the right cortiospinal tract from the corona radiate to the
pons.
4. In the genu of the right internal capsule.
Answer: 1
The lesion is on the side opposite to the symptoms as the corticospinal tract
crossed at the decussation of the pyramids in the ventral medulla. It can be
located in any part of the tract above the pyramids.
Case Two
What is the diagnosis in this patient?
1. An acute ischemic embolic stroke.
2. An acute hemorrhagic stroke.
3. An acute embolic lacunar stroke syndrome.
4. An acute thrombotic lacunar stroke syndrome.
Answer: 4
Most all lacunar strokes are felt to arise from thrombotic occlusions of the terminal
arteriolar vessels, the parenchymal penetrating blood vessels. This patient’s
symptoms describe the clumsy hand – dysarthria syndrome. Can you name the
other recognized lacunar stroke syndromes? The syndrome most typically is
associated with pontine stroke but may also occur in the anterior limb of the
internal capsule or its genu, or corona radiate. In all the lacunar stroke syndromes,
there is a range of territories that may be infarcted to produce the syndrome.
Case Two
Please order the listed primary risk factors for lacunar small vessel disease?
 Hypertension
 Hypercholesterolemia
 Tobacco use
 Diabetes mellitus
Answer: 1, 4, 3, 2
What percentage of all ischemic stroke event present as small vessel disease?
1. 10%
2. 20%
3. 30%
4. 40%
Answer: 2 20 %
Case Two
The patient was not treated with tPA. What reason(s) should be documented
as to why he was not treated? Check all that apply.
 Treatment was contraindicated
 Blood glucose was too high
 His deficit was too mild
 His deficits were improving
 He was beyond the window of treatment
Answer: Only the last answer is correct. There were no contraindications for
tPA. Make sure you are familiar with contraindications for treatment with
tPA. His deficit was graded at 6. We generally treat all patients who qualify
for therapy based on presentation with an NIHSS of 4 or more. Hypoglycemia
is a reason to consider not treating with tPA but not hyperglycemia.
Case Two
Appropriate antithrombotic therapy for this patient is:
1. ASA, 81 mg daily
2. Clopidogrel 75 mg daily
3. Aggrenox (ASA and Dipyridamole) bid
4. Any of the above
Answer: 4
All agents are considered interchangeable. One needs to consider the
20 % incidence of non responders to Clopidogrel, the cost of the
agents, compliance with a regimen and tolerance. There is no evidence
that switching the agent after a treatment failure is indicated.
Case Two
His carotid ultrasound showed a 60% stenosis in the ipsilateral (left) carotid
artery. What would you recommend?
1. A follow-up study in 6 months.
2. CTA of the neck while in hospital to ascertain true stenosis.
3. MRA of the neck while in hospital to ascertain true stenosis.
4. Consider immediate carotid endarterectomy.
Answer: 2
A stenosis of ≥70% of the symptomatic artery should be evaluated for
surgery. A stenosis of less or closer to 60% might also be a candidate for CEA
but this is less rigid a recommendation and needs to be considered in the
context of the patient’s circumstance.
Case Two
His HgbA1c was 9.6%. Treatment of his elevated blood sugars should be approached in the
following manner:
1. Ultimate goal is HgbA1c ≤ 7.0, thus adjustments should address this.
2. Evidence suggests that blood sugar management is not critical during the acute phase.
3. Evidence suggests his blood sugar should be maintained at less than 180 mg/dl during
acute phase.
4. Tight glucose management is critical to his stroke recovery.
5. 1 and 3 are correct but not 2 and 4.
6. 1, 3 and 4 are correct but not 2.
Answer: 5
There is evidence that blood sugars > 180 should be avoided during the acute stroke phase
and that long term control of HgbA1c at or below 7.0 is probably optimal for secondary
stroke prevention.
Case Two
All of the following are true concerning blood pressure management in this
patient except:
1. Ultimate goal is BP ≤ 130/80 because of his diabetes.
2. He should be allowed permissive hypertension for the first 24 hours after
his stroke.
3. Treatment is best instituted with oral agents after 24-48 hours.
4. The best choices for intervention are a selective betablocker and thiazide
diuretic if needed.
Answer: 4 The optimal choices for BP control in a patient with
cerebrovascular disease are felt to be an ACE inhibitor and if needed a
diuretic, as long as renal function is acceptable. We allow permissive
hypertension for at least the first 24 hours then slowly seek to introduce
antihypertensives. Severely high systolic BP should be controlled as a
hypertensive urgency. In diabetes, the BP goal is is more stringent for
secondary prophylaxis and is less than or equal to 130/80.
Case Three
Case Three
A 78 year old African American woman awoke her family to use the bathroom as she
needed assistance. This was routine as she had undergone a left AKA for a non healing
infected diabetic foot ulcer after failed fem-pop bypass surgery about 8 weeks before. She
was conversant having awoken “normally for her” about 20 mins before she was found
unresponsive on the commode. She apparently yelled out but was unresponsive when the
family found her and she was slumped to the left. EMS was called and did not obtain a
medication list. The reported this as a stroke alert with left weakness. She was
hypertensive with a BP of 198/100 and a heart rate of 138. She experienced short runs of
NSVT.
When she arrived in the ED she was poorly responsive and required noxious stimuli to elicit
right sided movement which was non localizing and not posturing. She did respond
verbally. The left arm did not move to pain. The right body had increased tone. Her pupils
were 3 mm, sluggish but reactive. Corneal response was intact on the right but not the left.
She was reported to be blind in the left eye. There was a mute toe response on the right.
Her MSR on the right were brisk in the leg and could not be checked on the left. There was
left gaze preference. EOM slow to occulocephalic manuevers. Her initial CT of the brain
was negative.
Where is this patients lesion most likely to be?
Case Three
The patient went to CT scan while attempts were made to contact
family regarding her medications. Her BP increased despite attempts to
treat it and she remained tachycardic with an increasing but now
irregularly irregular HR. Her breathing became shallow and a decision
to intubate was made to protect her airway. After paralysis and
sedation were administered to accomplish this, her BP dropped and
she then developed unreactive small pupils.
A CTA of the head and neck were done at this point.
Case Three
What are you expecting from her CTA, where is the lesion?
1. Rt. Carotid artery occlusion. Rt MCA lesion.
2. Rt. Vertebral artery occlusion. Rt. Lateral medullary lesion.
3. A Basilar artery occlusion. Pontine lesion.
4. Rt posterior cerebral artery occlusion. Thalamus and occipital lesion.
5. Answer: This is a classic description of a basilar artery syndrome. Often
these patients present with weakness (> 50%) but have significant
changes of gaze, alertness, pupils and frequently they go on to develop
the “locked in syndrome” with no intervention. The autonomic instability
is an additional clue that she has brainstem involvement.
Case Three
What do you think precipitated the sudden change after intubation?
1) Increased intracranial pressure from early edema.
2) Hypotension precipitating decreased collateral circulation.
3) A direct effect of the neuromuscular used to ease intubation.
4) Hemorrhagic conversion.
Answer: 2
In all likelihood, hypotension provoked the worsening seen. There was no
evidence of increased ICP and if herniation were imminent, pupillary dilation
would be expected. There was no hemorrhage and although the medications
caused the hypotension, there was no direct effect of acetylcholine blockade
as the cause.
Case Three
This patient was administered IV tPA. What would be the next step in management?
1. Wait 30 to 45 minutes to see if there is a positive effect of tPA and admit to the ICU.
2. Force fluids and hyperventilate now that she is intubated.
3. Call a family conference to discuss DNR status and instituting palliative care measures.
4. Consider endovascular intervention by transfer to a tertiary care center.
Answer: 4
This patient is unstable and is in the time frame for possible posterior circulation
intervention. When an occlusion is present and these services are available, administer IV
tPA and then seek transfer as soon as possible. If the service is available at your institution,
then transfer to the angio/neurointerventional suite for immediate care. Remember, time
is brain. There is no need to wait for an effect as there is rarely any improvement
immediately evident in large vessel occlusions. Likewise, there is NO CONTRAindication to
doing an arterial endovascular procedure even after tPA is given IV. In fact the studies
which showed benefit from endovascular interventions published earlier this year included
patients given IV tPA first.
Case Three
Prior to transfer to the tertiary center your patient deteriorates and has
profound hypertension with lowering of her heartrate. Examination shows
small nonreactive pupils, no EOM by occulocephalics and posturing
bilaterally now. Why would this occur?
1. Cushing effect from propagation of the clot into the full basilar artery
along the pons.
2. Cushing effect from brain edema and swelling.
3. Cushing effect from clot breaking off the distal basilar and embolizing to
the rest of the brain.
4. A seizure has most likely occurred.
Answer: 1
This scenario can occur with posterior occlusions, and when it does, it
reinforces the need for urgent endovascular intervention, if available. The
patient has a poor prognosis but will likely die without endovascular clot
removal.
Case Four
Case Four
A 64 year old man with no history of hypertension or diabetes presented to the ED
with new onset of dizziness, swallowing problems and speech slurring. The
patient’s only risk factor was he was a smoker. Symptoms were noted when he
awoke in the morning. He also noted difficulty standing and described the
sensation as feeling as if he was being pushed. A CT scan of the brain was normal.
He was admitted for an acute onset of vertigo.
On examination, his BP was 162/90, pulse was 88 and regular. His general
examination was unremarkable. MS was normal. He was dysarthric and slightly
hoarse. He had a slight facial asymmetry. A neurologic consultation was obtained.
His EOM were intact but he had nystagmus at end gaze and his smooth pursuits
were lost leaving saccadic movement. You find his facial weakness is best
characterized as a Horner’s syndrome on the right. He had loss of facial pin and
cold temperature sensibility on the same side. There was right sided hemiataxia
and loss of pin and temperature on the left side. Reflexes and plantar responses
were normal. He could not stand to walk.
Where is the lesion?
Case Four
Where is the lesion?
1. Lt lateral medullary plate
2. Rt lateral medullary plate
3. Lt cerebellar peduncle
4. Rt cerebellar peduncle
Answer: 2 This patient exhibits the Wallenburg Syndrome or Lateral medullary plate syndrome.
What vessel is involved in the syndrome?
1. Rt posterior communicating artery
2. Rt Inferior cerebellar artery
3. Rt vertebral artery
4. Rt posterior cerebral artery
5. Answer: 3 The lesion might be in the vertebral artery ipsilateral to the lateral medullary plate
infarcted or it can involve only the posterior inferior cerebellar artery of PICA.
Case Four
What is the usual secondary prophylaxis in this syndrome? Check all that
apply:
 Smoking cessation
 Antiplatelet agent
 A statin
 A PEG tube insertion
 Anticoagulation
 Antihypertensive agents as indicated
Answers: 1,2,3,6 While a PEG might be needed in such a patient, it is not a
routine secondary prophylactic measure and does not help prevent another
stroke. The use of anticoagulation on a routine basis is not needed in lateral
medullary strokes. There may be some circumstances where It is warranted.
Case Four
What additional orders would not be needed in admitting this patient?
1. DVT prophylaxis
2. Thrombosis screen
3. Speech therapy, Occupational Therapy and Physical therapy assessments
4. Dysphagia screen
Answer: 2 These cases are treated as you would treat small vessel disease.
Thrombosis screening is often done in stroke in the young, but this
gentleman has risk factors, including tobacco abuse and hypertensive range
BP changes. Thrombosis screen may not give actionable information in
thrombosis and is more useful in embolic events.
Case Four
What is the prognosis for this man?
• Prognosis with rehabilitation is good. TRUE or FALSE
Answer: This syndrome is often incomplete and in these situations
prognosis is excellent. Dysphagia is a major complicating factor and can
lead to aspiration which changes the outlook. Consideration for a PEG
tube should be made early if dysphagia is stagnant and not improving.
In addition, patients often are slow to mobilize and are at risk for DVT.
Case Five
Case Five
A 32 year old woman presents with dizziness, neck pain, right sided
facial numbness and pain and a complaint of clumsiness developing
suddenly about 2-3 hours before. Further history and review of records
from the ED note that she was involved in a motor vehicle crash and
was seen in the ED 72 hours before for “whiplash”. At that time a CT
scan of the neck was normal and she was sent home. Now, a CT scan
of the head is obtained and this study is also normal. She was admitted
as she was having difficultly ambulating and she still had neck pain.
What test would you do?
Case Five
What test is most appropriate at this stage?
1. Echocardiogram
2. MRI of the brain
3. Brain stem auditory evoked potentials
4. Carotid duplex scan
Answer: 2. None of the other tests would assist with dx with her s/s
expect perhaps BAER, which is an OP test.
The MRI shows a lateral medullary infarct
Case Five
What would expect to find on examination? Hint: which side is the infarct
most likely on based on data so far?
1. Left sided ataxia
2. Left hemisensory loss to pin/temp
3. Left sided Horner’s syndrome
4. Right sided tongue deviation
Answer: 2
Sher has a history most consistent with the MRI scan abnormality, Rt lateral
medullary infarct. Horner’s and facial sensory change occur on the right as
does ataxia but contralateral hemisensory loss would be expected. The
hypoglossal nerve is not in the distribution of the lateral medullary plate, as
it is midline in the medulla. There is no hemiparesis in the syndrome.
Case Five
What do you think is the most likely mechanism for the syndrome in
this patient with this history?
1. Rt vertebral artery cardioembolic event
2. Rt PICA occlusion from small vessel disease
3. Rt vertebral artery occlusion due to dissection
4. Hypercoagulable state
Answer: 3
Given this history, a dissection is the most likely etiology.
Hypercoagulable states are a common cause for stroke in the young but
history suggests the dissection. In the same manner cardioembolism is
not suggested by history but can occur. Small vessel disease is unlikely
in this age group without risk factors.
Case Five
What treatment would you offer this patient?
1. Intravenous heparin and conversion to Coumadin for 3-6 months
2. Carotid endarterectomy
3. IV tPA
4. Intra-arterial tPA
5. Vertebral artery endovascular stenting
Answer: 1
Stenting is an option for severe origin stenosis and V-B insufficiency
symptoms but not dissection. Currently, data suggests that arterial
dissections, anticoagulation or antiplatelet agents might be used. A CEA
would not address the affected artery.
Case Six
Case Six
You are called to answer a neurological consultation request on a 72 year old man
admitted for bilateral fem-pop bypass for recurrent symptoms of claudication and a
history of PAD performed 3 days ago. There were intraoperative complications
associated with an abdominal aneurysm. Post-op he was encephalopathic and this
was felt to be due to effects of anesthesia and pain medications. He complained of
vague back pain, numbness and weakness of the legs and was noted to have
urinary retention. Today he was more alert and complained he could not move his
legs. The Physical Therapist examined him, and the patient was unable to lift his
legs. This finding led to your consultation.
A general physical examination reveals a BP of 134/86 and a pulse of 92. He was
afebrile. Neurological examination showed his MS had improved from prior notes
and he had a clear sensorium with normal speech and language. CN were normal.
UE strength was normal as was sensation and reflexes. His LE MSR were absent and
the legs were flaccid. There was a sensory level at around T8 to pin and
temperature. Vibration and proprioception were intact. In the ICU, he had a brief
episode of atrial fibrillation.
Where is the lesion? What is the problem?
Case Six
Where is the lesion?
1. Brainstem
2. Cauda equina
3. Conus medullaris
4. Thoracic spinal cord
Answer: Findings suggest a spinal cord lesion. It would be predicted to affect the thoracic
level at or slightly above the T8 segment. Conus medullaris syndrome may present with
sexual dysfunction and bowel and/or bladder dysfunction but would not be associated with
a T8 sensory level. The cauda equine syndrome can produce weakness of the legs with
numbness and decreased reflexes but also, not with a T spine sensory level.
On your review of the chart notes from surgery and anesthesia records, the patient had
significant hypotension for a good portion of the surgery from a combination of anesthesia
and blood loss when the surgeon had difficulty with the bypass on one side.
Case Six
What is the mechanism for this lesion?
1. Spinal cord compression
2. Embolic spinal artery stroke
3. Idiopathic transverse myelitis
4. Hypotension induced ischemia to the thoracic cord
Answer: 4 The symptoms suggest ischemia in the anterior spinal artery. This is very susceptible to
ischemia in the mid thoracic levels as the collateral circulation is poor at this level. Evolution has
endowed the cervical and lumbosacral cord segments with ample circulation via collateral flow. This
might be due to the abundance of neurons in the motor horns controlling limb muscles of the upper
and lower extremities. On the other hand, muscle output and thus neuronal load is minimal in the
thoracic segments and the blood flow is proportionally sparse. This leaves this region susceptible to
low flow states which we see in trauma, surgical aortic procedures, dissection of the aorta, blood
loss and iatrogenic low flow states.
These vessels are not prone to atheromatous states but compression can also lead to the ASA
syndrome defined by the patient here.
Case Six
What study would you perform to help confirm the diagnosis?
1. MRI of the thoracic spine
2. Lumbar puncture
3. CTA of the spinal arteries
4. Angiogram of spinal arteries
Answer: 1
This study should be able to identify the ischemic lesion. The etiology is
inferred by the history. Spinal angiography would be done in cases
where we are seeking malformations or hemorrhages but it is not
helpful in this historical situation.