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Stroke: Clinical Features &

Complications
Dr A Sinha
ST2 Clinical Pharmacology
St George’s Hospital
[email protected]
Learning Objectives
Definition of stroke and classification
Prevalence and Importance
Natural History and Clinical Presentation of Stroke
Differential Diagnosis
Management
Complications
Definitions
Stroke or cerebrovascular accident (CVA): A clinical
syndrome, characterised by disruption of cerebral
vascularity, typified by rapidly developing signs of
focal or global cerebral dysfunction lasting more than
24 hours or leading to death.

Transient Ischaemic Attack (TIA): A clinical


syndrome, of presumed vascular origin, typified by
rapidly developing signs of focal or global cerebral
dysfunction resolving within 24 hours
Stroke Classification
(1) Ischaemic- thrombotic or embolic event causing
blockage of the blood supply to the cerebrum (80%)
(2) Haemorrhagic- rupture of a cerebral blood vessel
leading to extravasation of blood into the cerebrum
and its surrounding tissue compromising neural
perfusion (20%)
Relevance
Stroke is the neurological disease of modern times
In one year 3 people in every 2000 will have a stroke
For those over the age of 75 this rises to 20 people in
every 2000 every year
After heart disease and cancer it remains the third most
common cause of death after heart disease and cancer
Natural History and Risk Factors
Ischaemic Strokes: Underlying pathology is (usually)
atherothromboemolism
Haemorrhagic Strokes: Underlying pathology is
vascular rupture
Ischaemic Stroke
Risk Factors for Thrombosis and
Embolism
High blood pressure
Smoking
Diabetes
Elevated Cholesterol
Atrial Fibrillation
Structural heart lesions (e.g.. post-MI mural thrombus,
endocarditis, patent foramen ovale with DVT)
Thrombophillic States and Vasculitic States
Haemorrhagic Stroke
Risk Factors for Vascular Rupture
Hypertension
Arterio-Venous Malformations
Trauma
Clinical Presentation
Variable!
Presentation often depends on the area of the brain that
has been damaged
Anatomy of the brain
Brain consists of two cerebral hemispheres (dominant
and non-dominant), the cerebellum and the brain stem.
The brain stem contains autonomic centres and houses
the nuclei of the cranial nerves
The cerebellum is involved with balance and planning
of movements
The cerebrum is involved with higher functions
(speech, spatial awareness etc)
Anatomy of the Brain
Neuroanatomy
Frontal Lobe

Parietal Lobe

Temporal Lobe

Occipital Lobe
Neuroanatomy
Frontal Lobe

Parietal Lobe

Temporal Lobe

Occipital Lobe
Vascular Anatomy
Three main cerebral arterial territories:
Anterior Cerebral Artery
Middle Cerebral Artery
Posterior Cerebral Artery
Penetrating Arteries extend into the brain tissue itself
Verterobasilar Circulation supplies the brain stem
Vascular Anatomy
Linking Function to Structure
Frontal Lobe- Higher intellectual function (mood,
personality, frontal eye fields, language)
Parietal Lobe- Language (reading, writing) calculation,
Visuo-spatial function, Higher sensory function, visual
pathways
Temporal Lobe- Memory, language, visual pathways
Occipital Lobe- Visual cortex and association areas
Specialist Areas
Specialist Areas
Specialist Areas
Clinical Presentation
Global Dysfunction
Stupor or Coma
Confusion or agitation/memory loss
Seizures
Delirium
Clinical Presentation
Focal Dysfunction
Aphasia (incoherent speech or difficulty understanding
speech)
Facial weakness or asymmetry
Incoordination, weakness, paralysis, or sensory loss of
one or more limbs
Ataxia (poor balance, clumsiness, or difficulty
walking)
Visual loss (Monocular or binocular; May be partial
loss of the field)  
Differential Diagnosis
Trauma: Extradural haematoma, Subdural
haematoma
Infection: Meningitis/encephalitis
Intracranial mass: Tumour, Abscess
Inflammation: SLE
Migraine with persistent neurological signs
Metabolic causes : Hyperglycaemia, Hypoglycaemia,
Narcotic abuse, Alcohol abuse, Hypothyroidism
Patterns of deficit
Total Anterior Circulation Infarct (TACI). Significant
Damage of both Anterior and Middle Cerebral
Arteries:
Hemiplegia
Hemianopia
Cortical Deficit (dysphasia, visuo-spatial loss)
Partial Anterior Circulation Infarct (PACI). Partial
Damage of both Anterior and Middle Cerebral
Arteries: Two of the above
Patterns of Deficit
Posterior Circulation Infarct. Damage to the posterior
cerebral artery and Vertebrobasilar circulation:
Limb or gait ataxia
Dysarthria
Dysconjugate gaze
Nystagmus
Amnesia
Bilateral visual field defects  
Patterns of Deficit
Lacunar Infarct: Damage to small penetrating vessels:
Decreased sensation of face and limbs on one side of
the body without abnormalities of higher brain
function, motor function, or vision
Investigations and Diagnosis
Aim is to establish the cause and prevent recurrence
Full blood count, ESR, U and Es, glucose, lipids,
clotting
Chest radiograph and ECG
CT scan
Management
Ischaemic Strokes- Aspirin 300mg and Simvastatin
40mg and compression stockings if not contra-
indicated
Admission to acute stroke ward, assessment of
swallow reflex, intensive nursing, early physiotherapy,
occupational therapy and social services need to be
instigated
Complications
Wide ranging!
Complications
Complications
Complications
Complications
Complications
Complications
Complications
Complications
At 1900 At 2000
Complications
Malnutrition and aspiration
DVT and PE
Falls and fracture
Epilepsy
Spasticity
Pneumonia
Bedsores
Prognosis
TACS: 60% dead at one year. 20% living
independently
PACS: 15% dead at one year. 50% living
independently
Lacunar: 10% dead at one year. 70% living
independently
POCS: 20% dead at one year. 60% living
independently

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