4th Year 2nd Semester 2nd Module Medicine III

L2: Cerebrovascular insufficiency & Hemiplegia

Cerebrovascular insufficiency
 State that results in obstruction in one or more arteries that supply the brain,
 May be localized(stroke) or generalized (coma)
 May be transient (TIA)or permanent (infarction)
Stroke
 A generalized reduction in cerebral blood flow due to systemic hypotension usually
produces syncope
 Global hypoxia-ischemia: widespread brain injury due to infarction in the border zones
between the major cerebral artery distributions if low cerebral blood flow persists for a
longer duration
 Hypoxic-ischemic encephalopathy: the constellation of cognitive sequelae that ensues
 Focal ischemia: usually caused by thrombosis of the cerebral vessels or by an emboli from a
proximal arterial source or the heart
 Intracranial hemorrhaqe: bleeding directly into or around the brain; produces symptoms
by:
a) mass effect of neural structures
b) toxic effect of blood itself
c) increasing intracranial pressure
Stroke Mimics (usually global rather than focal neurological symptoms)
• drug intoxication/withdrawal
• infections—herpes simplex encephalitis
• metabolic—hypoglycemia, renal failure, hepatic failure, hypoxia/hypercarbia, endocrine
disorders (thyrotoxicosis, myxedema, adrenal insufficiency)
• migraines • syncope
• seizures—Todd paralysis
• structural—trauma, tumors, subdural hemorrhage
Transient Ischemic Attack
 An ischemic episode causing transient focal neurologic symptoms without evidence of
infarct (on MRI) nor persistent symptoms following event.
 Symptoms: onset within 24 hours unilateral weakness or sensory symptoms, speech
disturbance, vision, ataxia, dysphagia, dysarthria, binocular diplopia
 Management
• Immediate assessment urgent CT/CTA or MRI/MRA,
• ECG, and laboratory investigations
• Control Bl P

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 4th Year 2nd Semester 2nd Module Medicine III
Hemiplegia
 Is total paralysis of the arm, leg, and trunk on the same side of the body. Severe or complete
loss of motor function on one side of the body.
 Hemiplegia is more severe than hemiparesis, where in one half of the body has less marked
weakness.
Causes:
• Cerebrovascular Accident (CVA) • Todd's Paralysis
• Thrombosis, Embolism or • Brain Tumor
hemorrhage Transient Ischemic • Infection (encephalitis, meningitis,
Attack (TIA) brain abscess)
• Migraine syndrome • Subdural empyema
• Head Trauma • Meningitis
• Brain Contusion • Nonketotic hyperosmolar coma
• Subdural Hematoma & Epidural • Vasculitis
Hematoma • Acute necrotizing myelitis
Thrombosis:
o Most common o Slowest Hours
o Wakes up in the morning with weakness
o History of TIA o Old age
Embolism:
o Fastest onset - Seconds o History of heart disease
o No progression {Max. deficit at o Younger age group
onset} o Major deficit ( heart to vessel )
Hemorrhage:
o H/o Prolonged hypertension o Vomiting
o Awake — stress o Altered consciousness
o Head ache o Convulsion
Pathogenesis:
• The exact cause of hemiplegia is not known in all cases.
• Brain is deprived of oxygen and this results in the death of neurons.
• When the corticospinal tract is damaged, the injury is usually manifested on the opposite
side of the body. This happens because the motor fibres of corticospinal tract, which take
origin from the motor cortex in brain, cross to the opposite side in the lower part of medulla
oblongata and then descend down in spinal cord to supply their respective muscles.

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 4th Year 2nd Semester 2nd Module Medicine III
Localization: Depending on the site of lesion in brain, the severity of hemiplegia varies.
 Internal capsule  Brainstem: Midbrain, Pons, Medulla
 Cortex  Spinal cord
 Subcortex - Corona radiata
Internal capsule
• Dense & uniform hemiplegia (UMN Facial )
• Hemisensory blunting
• Homonymous Hemianopia
Cortex
• Non dense nonuniform weakness • Apraxia
• Monoplegias • Cortical sensory loss
• Cortical signs • Convulsions
• Dysphasia
Subcortex
• Pattern of weakness similar to cortical
• Non dense non-uniform weakness
• No cortical signs
Brainstem
• Crossed hemiplegia
• Ipsilateral LMN CN palsy & contralateral hemiplegia
• Cerebellar signs
Spinal cord
• Rare
• No facial
• Brown sequard syndrome [hemiplegia on the side of involvement without face] lesion
above C5
• Effects below the level — UMN type motor loss and sensory loss
• At the level — LMN type
• Above the level — Hyperaesthesia
Midbrain
• Crossed cerebellar ataxia with ipsilateral third nerve palsy (Claude's syndrome):
• Weber's syndrome: third nerve palsy and contralateral hemiplegia:
• Bendict syndrome: Contralateral rhythmic, ataxic action tremor; rhythmic postural or
intention tremor with ipsilateral third nerve palsy

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 4th Year 2nd Semester 2nd Module Medicine III
Pons
• LMN Facial + contralateral hemiplegia
• +VI th Nerve + cotralateral hemiplegia
• + Lateral Gaze palsy + cotralateral hemiplegia
Medulla lateral Medullary syndrome
• Same side
• Homer's syndrome
• Loss of pain & touch on the face
• Cerebellar signs
• Palate weakness
• Opposite side
• Loss of pain and temperature sensation on the body and limbs
C/P: Onset and course:
• Acute onset and regressive course (vascular, infective, traumatic lesions).
• Gradual onset & progressive course (neoplastic lesions).
• Intermittent & relapsing course (multiple sclerosis)
Diagnosis: Hemiplegia is identified by clinical manifestations &examination
Signs & Symptoms: Vary from person to person.
• Difficulty with gait, Difficulty with balance while standing or arm and leg walking
• Having difficulty with motor activities, like holding, grasping or pinching
• Increasing stiffness of muscles
• Muscle spasms
• Difficulty with speech
• Difficulty swallowing food
• Significant delay during standing, smiling, crawling or speaking
• Behavior problems like anxiety, anger, irritability, lack of concentration or
• Emotions - depression
Clinical examination:
• General
° Pulse, BP, LN, Clubbing. neurocutaneous markers
° Other systems – DVS Valvular heart disease, CAD, Hypertensive heart disease
• Neurological examination
° Higher functions ° Reflexes
° Cranial nerves ° Sensory — +Cortical
° Tone ° Cerabellar
° Power Grade, symmetry ° Meningeal irritaion

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 4th Year 2nd Semester 2nd Module Medicine III

Features of UMN Lesions Features of LMN Lesions

• Weakness • Weakness
• Hypertonia • Hypotonia
• Deep reflex exaggerated • Loss of tendon reflex
• Loss of abdominal reflex • Fasciculation of muscle
• No muscle wasting • Contracture of muscle
• Distal muscle groups affected • Trophic changes
• Axial movements, extraocular, upper facial,
pharyngeal and jaw muscles are spared
• Extensor plantar

 Hemiplegia patients usually show a

characteristic gait. The leg on the
affected side is extended and internally
rotated and
 The upper limb on the same side is also
adducted at the shoulder, flexed at the
elbow, and pronated at the wrist with the
thumb tucked into the palm and the
fingers curled around it.

Investigations:
• Labs:
° CBC, lytes, urea, Cr, glucose, troponin,
° CK, PTT, INR, AST, ALT, ALP, bilirubin, total cholesterol, TGL, LDL, HDL,
homocysteine, ESR
• Imaging
° CT head without contrast
° MRI head (more sensitive than CT head in detecting acute ischemic stroke)
° angiogram (CT, MR, contrast)
° carotid Dopplers, echocardiogram (TEE > TTE)
• Special
° ECG—ST depression, QT prolongation, inverted T, prominent U waves
° holter monitor—evaluation for occult atrial fibrillation
° EEG—if seizures
° toxicology screen

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 4th Year 2nd Semester 2nd Module Medicine III
Ischemic stroke
Categories of treatment:
Designed to reverse or lessen the amount of tissue infarction and improve clinical outcome
1. Medical Support 4. Antithrombotic Treatment
2. IV Thrombolysis 5. Neuroprotection
3. Endovascular Techniques 6. Stroke Centers and Rehabilitation
1. Medical Support
• Immediate Goal: optimize cerebral perfusion in the surrounding ischemic penumbra
• Attention is also directed toward preventing the common complications of bedridden
patients:
° infections
° deep venous thrombosis (DVT)
• Blood pressure is lowered in:
° malignant hypertension
° concomitant myocardial ischemia
° BP >185/110 mmHg and thrombolytic therapy is anticipated
° B1-adrenergic blocker such as Esmolol can be a first step to decrease cardiac work and
maintain BP
2. IV Thrombolysis: rtPA:
Indications Contraindications
Clinical diagnosis of STROKE Sustained BP > 185/110 mmHg despite Rx
Onset of symptoms to time of drug Platelets LESS THAN 100,000;
administration is LESS THAN 3 HOURS Hematocrit LESS THAN 25%;
Glucose LESS THAN 50 or GREATER
THAN 400 mg/dl
CT scan show no hemorrhage or edema of Use of Heparin within 48 HOURS and
GREATER THAN 1/3 of the MCA territory prolonged PTT or elevated INR ; GI bleeding
preceding 21 DAYS
Age ≥ 18 years old Rapidly improving , minor stroke symptoms
Consent by patient or surrogate Prior stroke or head injury within 3
MONTHS; recent myocardial infarction
Major surgery in preceding 14 days
Coma or stupor

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 4th Year 2nd Semester 2nd Module Medicine III
3. Endovascular Techniques
• Vessels that involve a large clot volume and often fail to open with IV rtPA alone:
° middle cerebral artery (MCA)
° internal carotid artery
° basilar artery
• Endovascular mechanical thrombectomy:
° Adjunctive treatment of acute stroke in patients who are ineligible for, or have
contraindications to thrombolytics, or those who have failed to have vascular
recanalization with IV thrombolytics
4. Antithrombotic Treatment
Platelet inhibition:
• ASPIRIN: the ONLY antiplatelet agent that has been proven effective for the acute
treatment of ischemic stroke
• The use of aspirin within 48 hours of stroke onset reduced both stroke recurrence risk and
mortality minimally
Prognosis
• It is not a progressive disorder, except like in a growing brain tumor.
• Complications
° Neurologic — cerebral edema, seizures, hemorrhagic transformation of infarction with
or without hematoma, neurological deficits (dysphagia, falls, compressive neuropathies)
° Non-neurologic — myocardial infarction, arrhythmia, aspiration, pneumonia, UTI,
DVT, pulmonary embolism, malnutrition, pressure sores, orthopedic complications,
contractures, sleep disordered breathing, depression

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