Case 3

78 y.o. Caucasian male develops palpitations and chest pain. He has dyslipidemia and essential hypertension. Meds include Lipitor, Hydro-Diuril, ASA, Plavix, Atenolol. He had prior myocardial infarction one decade ago. He has no neurological dysfunction, however, he develops headache and dizziness when he takes his NTG for chest pain. He drinks a six-pack of beer daily.

Investigations

EKG
--atrial fibrillation
CT (brain)
--no abnormalities
MRI (brain)
--periventricular white matter disease

Evaluate stroke risk and potential stroke mechanisms in this patient

Cardiac
-- red clot formation (thrombin rich)
Cerebrovascular atherosclerotic carotid stenosis
-- white clot formation (platelet-fibrin rich)

Further diagnostic investigations

ECHO
--TTE
--TEE
Carotid ultrasound
MRA
CTA

ASA
Dipyridamole
Clopidogrel
Ticlopidine
Aggrenox
Coumadin

Treating MD believes patient is "too old" and "non-compliant" to take Coumadin. He is started on ASA 325 mgm daily. Three months later he awakens with left-sided headache and appears confused. Exam shows Wernicke aphasia and right homonymous hemianopsia. Pulse rate is 82 but irregular

Diagnostic Evaluation

- CBC and platelet count - normal
- EKG - atrial fibrillation
- CT - left temporal-parietal nonhemorrhagic infarct
- MRI - left temporal-parietal hyperintense lesion
- MRI with diffusion weighted imaging - multiple lesions in both hemispheres

- Recent lesion(s) within 10 to 14 days
- Most sensitive and earliest to detect ischemic lesion
- Based upon principle of Brownian motion
- With embolization would expect multiple lesions to be visualized with MRI

Hemorrhagic transformation
Re-embolization
Edema->mass effect->hydrocephalus->herniation
Seizure with prolonged postictal state
Complicating medical condition

Avoid

Hyperthermia
Hyperglycemia
Hypoxia
Hypercarbia
Hyperviscosity
Blood pressure extremes
--Hypertension
--Hypotension

Heparin
Coumadin

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Case 4

63 y.o. woman experiences an episode of sudden loss of vision in her left eye. She says this is similar to a shade being pulled down over the eye. Vision returns in 15 minutes.

She has no headache.

She has 3 similar episodes over 2 week period.

When she closes the involved eye, vision is normal in the opposite eye.

She goes to the eye doctor and he notes slightly elevated intraocular pressure and suggests she schedule "routine" appointment with PCP, and be followed as "glaucoma suspect".

She has high blood pressure, dyslipidemia, on no hormonal replacement.

What are potential mechanisms?

Vascular

Transient ischemia
--Hemorrhage
Electrical
--Focal seizure
--Migraine equivalent
....Spreading cortical depression
--Demyelination of MS type

Why not due to these mechanisms?

Metabolic
-- Hyper - or hypoglycemic electrolyte disorder does not cause focal impairments
-- Mass lesion does not cause sudden impairment of function
-- Medications - toxin, alcohol - do not cause focal impairments

Three days later she experiences an episode in which she loses the ability to speak and her right side becomes useless and paralyzed for 30 minutes. This resolves completely. The episode occurred after dinner at which she had 3 glasses of wine.

Primary eye disease

Optic nerve vascular disease
--Arteritis
----Giant cell
--Nonarteritic
----Carotid disease
Optic nerve demyelination
--Optic neuritis - multiple sclerosis
Ocular migraine
Medical condition
Coagulation disorder
--CRAO, CRV thrombosis
--APLA syndrome

Define these terms:

Transient ischemic attack
Reversible ischemic neurological deficit
Cerebral infarct with transient signs
Minor stroke
Major disabling stroke

What is goal of cerebrovascular disease management?

Vascular protection

Neuro protection

Goal of cerebrovascular management -
Prevent major disabling stroke
Do not consider prevention of reversible deficits as goal of therapeutic intervention.

Remember - Concept of ischemic tolerance

CT - nl
MRI - nl
Carotid duplex - occlusion of left internal extracranial) carotid artery
Severe 99% stenosis of left ICA with ulcerated plaque
Angiogram

Management - reperfusion strategies

Intravenous heparin
Thrombolytics
Antiplatelets
CEA
Angioplasty - stent

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Case 5

49 y.o. Afro-American hypertensive man develops occipital headache and dizziness. He is confused , disoriented and has brief episodes of transient blindness. Exam shows quiet inattentive state, left pronator drift, bilateral Babinski signs. Funduscopy shows hypertensive retinopathy. BP 250/145, P = 90 reg, R 18. Neck is supple.

PMH

Hypertension for 5 years. Meds include OH-diuril, atenolol, accupril and clonidine. Patient has several periods were he suddenly stopped his medication due to financial issues. This time he stopped meds 3 days ago. He has dyslipidemia for which he takes pravachol. Also has a diagnosis of "migraine" characterized by episodes of bilateral occipital headaches and dizziness; these are most intense upon awakening and disappear by noon.

Labs
CBC and platelet count - nl
BUN 38
Creatinine 2.8
Chest radiogram - cardiomegaly
EKG - left ventricular hypertrophy
ECHO - concentric hypertrophy with ejection fraction of 60%

Neuroimaging

CT - hypodense lesions in bilateral posterior parietal-occipital regions
MRI - hyperintense regions in both parietal-occipital regions

Ischemic stroke
Hemorrhagic stroke
--Intracerebral
--Subarachnoid
Venous sinus thrombosis
Intracranial mass
--Subdural hematoma
--Neoplasm

Definition of Stroke

Sudden
Onset
Focal
Neurological impairment
(negative symptoms)

Course

Stabilize
Deteriorate rapidly and die
Progress over 24 to 48 hours
Recurrence

Acute hypertensive vascular crisis

Rapid BP increase
Systolic > 240
Diastolic > 140
May occur: With encephalopathy
Without encephalopathy

End-organ signs of damage

Funduscopy - Hypertensive retinopathy

Cardiac - Congestive heart failure
Chest pain due to CAD
Dissecting aneurysm

Renal - Deteriorating renal function

Brain
- Ischemic stroke
----Large vessel
----Arteriole
-Hemorrhage

Hypertensive encephalopathy

Diffuse > focal signs
Altered mental state
Generalized seizures
Bilateral Babinski signs
Visual disturbances

Signs and symptoms
Effect posterior brain region: Due to cerebral autoregulation breakthrough at high level

Management
Rapid lowering of BP utilizing parenteral and controllable agent
Medical emergency that requires immediate therapy

Goal of therapy
Prevent or correct medical complications
Lower BP Diastolic by 1/3, but not below 95
Systolic by 1/3

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Case 7

Dr. R.J. is a 64 year-old surgeon. He awakens one morning and feels entirely well. While eating breakfast, he notes precipitous development of left-sided weakness. His speech becomes slurred, and he drops his fork. He feels dizzy and sees double. This persists for ten minutes and all symptoms rapidly and completely resolve. He does not seek medical care as he believes the symptoms are due to "low blood sugar" before breakfast as they resolve with food intake.

Past Medical History

He has hypertension for which he takes baby aspirin, hydrochlorothiazide and Metoprolol. He is relatively noncompliant with medication. He has had a prior myocardial infarction and still has occasional angina. He has intermittent claudication of legs and has been diagnosed with peripheral arterial vascular disease, but refuses vascular or cardiac surgery. ("All my friends are cardiac or vascular surgeons and all they want to do is operate, whether necessary or not.") He is obese, smokes one pack of cigarettes per day and has elevated blood cholesterol levels. He has no history of diabetes mellitus.

Subsequent course

He proceeds to his office to carry out his schedule for the day. He is fine until 30 minutes before his lunch break, when he suddenly develops a severe occipital headache and becomes dizzy with diplopia. He collapses and can not move his left side and can not speak.

Physical examination

BP 190/104 mm Hg (right arm, sitting)
P 80 regular
R 12, regular
Neck - supple, no neck vein distension
Heart & Lungs - normal
Pulse - symmetrical, no bruits

Mental state-Awake, eyes open but does not follow examiner commands, can not verbalize - phonate
Gait- Cannot stand due to severe weakness
Motor Quadriplegic with no motor response, motor tone reduced in all extremities
Reflexes Areflexic with extensor Babinski responses bilaterally
Sensory-No withdrawal response to pin prick
Cranial nerves-Pupils equal and respond to light; no horizontal eye movements with preserved vertical eye movements, bilateral facial weakness with preserved blink response; gag and palate movements preserved; aphonic

Laboratory studies

CBC - normal
Urinalysis - normal
Chest x-ray - enlarged heart
EKG - old anterior wall myocardial infarction

Imaging investigations
CT - Hypodense pons and cerebellum
MRI - Hyperintense pons, cerebellum, thalamus, and occipital cortex
MRA - High grade midbasilar stenosis

Treatment options

Thrombolytics
--Intravenous
--Intra-arterial
Anticoagulant
--Unfractionated heparin
--LMWH
Mechanical
-- Angioplasty
Stent

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Case 8

52 year-old hypertensive man awakens with left throbbing headache and vomits. When he gets out of bed, he is unsteady, dizzy and has horizontal double vision when he looks across the room. PMH indicates hypertension controlled with diuretic and ACE inhibitor.

Examination findings

MS - alert and attentive
Gait - broad-based ataxic with disequilibrium
Motor- no drift or hemiparesis
Reflex - symmetrical and plantar flexor response
Coordination - impaired heel-to-shin and normal finger-to-nose
CN - bilateral abucens paresis and left central facial weakness
PE - BP 220/120; P 52; R 10;
Neck - limitation of flexion

Hypertensive vascular complications

Hypertensive crisis with encephalopathy
Lipohyalinasis
Fibrinoid degeneration
Lacunes
Intracerebral hemorrhage
Accelerated atherosclerosis

Lacunar syndromes

Pure motor hemiparesis
Pure sensory stroke
Hemiparesis - hemianesthesia
Dysarthria - clumsy hand syndrome
Ataxic - hemiparesis

Putaminal
Caudate
Thalamic
Pontine
Mesencephalic
Cerebellar
Supratentorial
White matter

Management of cerebellar hemorrhages

HA
Vomiting
Elevated blood pressure
Treat and prevent seizures
Vasogenic edema - herniation
Hematoma evacuation
Hydrocephalus correction

Pitfalls of management

Avoid medications with these effects:
Increase bleeding
Reduce consciousness
Reduce respiratory drive
Impair neurological function
Cause GI bleeding
Impair renal function
Increase intracranial pressure

Watch cerebral perfusion pressure with neuro checks every 30 minutes

Discontinue or reverse any anticoagulant or antiplatelet medication

Hematoma Enlargement

Continued bleeding
--stretch-tear contiguous vessels
Edema formation
--vasogenic
Ischemia development
--cytotoxic
Rebleeding

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