Clinical Examination in Stroke Disease

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Learning objectives

  • Clinical signs of stroke
  • Examination of relevant systems

Useful Links

Clinical Examination

Assessment and examination commences with the arrival of the first responder or layperson to hopefully identify the suspected stroke. There are various quick and easy suggested screening formats and resources have been directed to educating the public in the typical signs of acute stroke. Recognising typical pattern combinations aids diagnosis and is key to a rapid and accurate diagnosis. Strokes are vascular syndromes and non-haemorrhagic strokes must match the syndrome of the 'culprit' artery occluded.

Clinical examination in stroke disease must define the deficit and resultant disabilities and also help focus investigations on the underlying aetiology. Must constantly ask "Where and why". In the acute situation when the time is short the NIH is a useful way to do a methodical neurological examination that covers patterns of deficits seen in a stroke. One must be doing this routinely. It is detailed in the appendix at the back. The general examination of a stroke patient is not confined to one system but should be from top to toe covering the neurological deficit and any suspected causative features or stroke complications.

Clinical Signs

  • Motor symptoms: weakness or clumsiness of one side of the body (hemiplegia or hemiparesis), or part of one side of the body. Think of weakness in terms of Face, arm, trunk (sitting up) and leg
  • Sensory loss: decreased sensation on one side of the body, or part of one side of the body. Screen by assessing face, arm and leg comparing side to side.
  • Dysphasia: impairment or loss of linguistic abilities, resulting in producing the content of speech (expressive dysphasia) as well as understanding speech (receptive dysphasia), reading (alexia) or writing (agraphia).
  • Visuospatial neglect: usually on the left side and associated with left hemiplegia and hemianopia seen with right cortical (non dominant) strokes
  • Visual disturbances: monocular blindness may be seen with strokes that involve the branches of the ophthalmic and posterior ciliary arteries
  • Hemianopia or quadrantanopia: with loss of vision to the weak side when the optic radiations are affected
  • Bilateral blindness with anosognosia : unaware and even denial that they have visual loss (Anton's syndrome)
  • Anosognosia: patient fails to appreciate that they have had a stroke. Rather blasé attitude. Will tell healthcare professions they are fine and try to walk when they plainly can't. A significant risk of falls.
  • Cerebellar Ataxia: seen with cerebellar strokes. Past pointing on same side as stroke, Nystagmus with fast phase to cerebellum affected, ataxia in limbs and gait, dysarthria
  • Dysarthria: due to damage to nerves controlling mouth/larynx/tongue. Can be cortical or brainstem.
  • Diplopia: typically a brainstem stroke
  • Dysphagia: Difficulty swallowing- seen with strokes affecting cortex, motor fibres or brainstem such as Lateral medullary syndrome
  • Horner's syndrome: miosis and slight ptosis suggests either a brainstem stroke e.g. Lateral medullary syndrome or carotid dissection. Shield the eyes and reduce lighting to allow the pupils to dilate and this will show and demonstrate any disparity in pupil sizeand the Horner's side the pupil will remain small.


  • Coma in stroke disease suggests a major bleed or infarct with raised intracranial pressure perhaps due to hydrocephalus or cerebral oedema. Most stroke patients are otherwise alert even with marked neurology.
  • Coma may suggest a malignant MCA infarct progressive coma may indicate need for urgent hemicraniectomy or shunting for developing hydrocephalus or with a large haemorrhage the need to consider surgical evacuation.
  • In a patient with a cerebellar bleed urgent clot evacuation is needed or ventricular drainage for obstructive hydrocephalus.
  • Somnolescence is different to coma - the patient appears to be sleeping rather than coma e.g. moves in bed, gets position of comfort but unrousable. Consider bilateral thalamic or other high brainstem infarction.

Causes of coma to be considered in a stroke patient

Always identify the cause and decide whether the action is needed or not.


  • Habitus: Marfan's disease, Ehlers-Danlos syndrome
  • Pregnancy is also a risk factor
  • Acromegalic or Cushingoid features may suggest endocrine hypertension
  • Nicotine staining (in heavy smokers always think is this carotid disease)


  • Splinter haemorrhages may suggest endocarditis or a manual worker (commoner in dominant hand),
  • Clubbing may suggest cyanotic congenital heart disease or endocarditis. Might suggest cerebral metastases from a lung tumour masquerading as a stroke. *Palmar erythema, spider naevi
  • Dupuytrens may suggest alcoholism with risks of ischaemic and haemorrhagic stroke
  • Arachnodactyly "spider fingers" seen in Marfan's and some connective tissue diseases with a higher risk of aortic incompetence, mitral valve prolapse and arterial dissection.


Facial Pulses

Look for temporal artery pulses and tenderness which may suggest a diagnosis of GCA in an older patient with a headache or visual symptoms. An absent or tender temporal artery is one of the criteria in the diagnosis of giant cell arteritis. Always document where there is a new headache or visual loss even transient resembling amaurosis fugax. Seen in those over 50 and can rarely cause a stroke. Check an ESR urgently and consider steroids and ophthalmic referral for confirming the diagnosis and temporal artery biopsy. Dynamic testing of facial pulses may help suggest if ipsilateral carotid occluded. This will cause external carotids to retrogradely supply the internal carotid artery territory. One place where the two systems meet is at the eye where the ophthalmic artery supplies.


  • Pallor from anaemia
  • Yellow discolouration from jaundice
  • Xanthelasma suggesting dyslipidaemia
  • Small miosed pupil and mild ptosis may suggest a Horner's syndrome due either to carotid artery dissection or an apical lung tumour or a lateral medullary infarct.
  • Complete or almost complete ptosis and dilated pupil pointing down and out suggests an oculomotor palsy in the midbrain or along its path. In some cases e.g. diabetes the pupil will remain intact.


Can be due to weakness of 3 muscles

  • Levator palpaebrae supplied by III e.g. midbrain infarction
  • Muller's muscle supplied by sympathetic e.g. Horner's syndrome e.g. Lateral medullary infarction
  • Frontalis supplied by VII and is least important and is not affected in UMN VII and so unaffected in stroke disease,

Causes of Ptosis

  • IIIrd nerve (Complete)
  • Horner's syndrome (Partial)
  • Myasthenia gravis
  • Botulism
  • Myopathies
  • Soft tissue problems


  • Dilated
  • Constricted

Cardiorespiratory Examination


  • Irregularly irregular pulse to look for AF. If suspected get an ECG to confirm.
  • Plateau pulse of Aortic stenosis
  • Collapsing pulse of AR
  • Jerky pulse of hypertrophic cardiomyopathy may also be useful.

Blood pressure

  • Ensure that an appropriately large cuff is used so as not to overestimate BP in obese patients
  • An uncontrolled BP > 185/110 mmHg is a contraindication to thrombolysis. Blood pressure is a major risk factor for both ischaemic and haemorrhagic stroke.
  • Blood pressure variability may also be important. Both systolic and diastolic values are important though

diastolic value tends to fall with age.

Jugular venous pressure

  • Elevated JVP can suggest congestive cardiac failure or volume overload.
  • SVC obstruction


  • Midline sternotomy - valve replacement or repair or coronary artery bypass grafting or cardiac transplant.
  • Pacemaker or AICD scar left or less commonly right infraclavicular fossa.

Palpation of the chest.

  • Palpable thrills
  • Left sternal heave representing RV hypertrophy and Pulmonary hypertension
  • Dyskinetic rocking motion - LV aneurysm

Apex beat

  • Any displacement which may suggest cardiac enlargement.
  • A palpable tapping S1 may be felt at the apex or medial to it suggesting mitral stenosis
  • A heaving apex might suggests aortic stenosis
  • Dynamic volume overloaded ventricle may suggest aortic incompetence

Auscultation of the heart

  • Systolic Murmur
  • Diastolic murmur
  • Pericardial sounds
  • Metallic valves

Carotid artery

Some stroke books say not to bother listening over the artery as stenosis may be silent and bruits may not mean stenosis and the decision to scan for disease should be based on symptomatology. Still, it's hard not to. If there is suspected occlusion of the internal carotid then external carotid flow may increase on the affected side and temporal and facial pulses may increase unilaterally as external carotid flow increases. A bruit over the carotid artery, eyeball, and the skull may suggest contralateral carotid occlusion due to increased flow on the side without the occlusion (Fisher's sign). To determine an internal from an external bruit, transiently compress the facial and temporal arteries this increases an internal carotid bruit and decreases an external one. Not part of the examination but as an aside avoid carotid sinus massage in any patient likely to have stroke disease. I would avoid it in any patient over 50. Concerns about dislodging plaques. A normal carotid doppler may make it a less risky procedure. There may even be a large scar running along the edge of the sternomastoid suggesting previous carotid endarterectomy.

Peripheral vascular disease

If the feet are cold and legs hairless then wise to assess peripheral pulses which may suggest peripheral vascular disease. Check ankle-brachial pressures. The blood pressure is reduced at the ankles if there is proximal significant narrowing.

Respiratory examination

  • Lung bases for signs of pulmonary oedema
  • Signs of long consolidation suggesting pneumonia
  • Pleural effusion
  • Consolidation
  • or stony dullness and reduced breath sounds suggesting pleural effusion with its many causes.

Abdominal and Genital examination

  • In the young patient angiokeratomas around the umbilicus might suggest Fabry disease.
  • Audible renal bruit may suggests renal artery stenosis and a cause of hypertension
  • Enlarged kidneys in adult polycystic kidney disease causing chronic hypertension and well-known association with Berry aneurysm and SAH
  • Young patient to look for radio-femoral delay due to Coarctation of the aorta.

Genital Exam

  • Sexually Transmitted disease: In the past syphilis was the scourge or neurologists and could cause basically any stroke symptom. Indeed Brocas's dysphasic patient had dysphasia due to a gumma and not a stroke. At this stage of neurological disease there is usually no genital evidence of primary or secondary syphilis. HIV should always be considered in all sexually active patients.
  • Ulcers on the genitals, however, may be due to Behcet's disease

Cortical dysfunction


Disinhibition, poor judgment, Emotional lability


  • C/L hemiparesis: damage to the primary motor cortex and associated
  • C/L Gaze Palsy: Unable to look to contralateral side
  • Cognitive : Apathy, indifference, Akinetic, Incontinence, Reduced verbal output
  • Gait apraxia: : Appearance of Basic reflexes: grasp reflex, pouting
  • Expressive dysphasia: Damage to Broca's area. (LF) May be fluent speech with nonsense content. May be aphasic
  • Ideational apraxia: Loss of ability to carry out learned complex tasks in the proper order</td></tr>


  • Contralateral Hemisensory loss: face, arm, leg and trunk. Reduced two point discrimination. Test each individually. Test both together then when looking for extinction.
  • Sensory agnosia: place a 50p piece or any coin or key or paperclip in someone's hand with their eyes closed and see can they determine what it is. Failure suggests astereognosis. Alternatively write a number on the palm 'What number is this'. Failure is agraphaesthesia
  • Contralateral homonymous hemianopia: Often an inferior quadrantopia

Non Dominant Parietal

  • Anosognosia: Patient does not comprehend that they have a neurological deficit usually on the left side. Vitally important as can lead to significant problems most notably a lack of insight. Despite a marked left hemiparesis patient will try to get out of chair to walk - leads to falls/injury. Patients will tell ED doctors and other healthcare staff that they are fine if it is taken at face value.
  • Dressing apraxia: Difficulty in dressing such as unable to put on their pyjama top and make it more difficult by pulling one sleeve inside out.
  • Geographical agnosia: Becoming disorientated and lost on the ward. Often find patient by the wrong bed.
  • Constructional apraxia: Unable to copy simple shapes and geometrical patterns.
  • Extinction: When stimuli presented bilaterally either visually or sensorily e.g. touch only one side is appreciated. Usually seen with non-dominant parietal lobe deficit. The way to separate this from sensory loss is that when stimulated individually touch is felt on the side which it is not felt when both sides are stimulated. This phenomenon also applies to the vision and should be looked for. *Asomatagnosia:Show patient their left hand and they failure to recognise it

Dominant Parietal

  • Receptive Dysphasia (Left): unable to follow basic commands e.g. close eyes or to touch ear. Try ever more complex instructions.
  • Acalculia: This is an inability to do simple calculations. Test arithmetic in keeping with educational background. May become important in managing money. *Alexia: Ask the patient to read from a newspaper or magazine
  • Agraphia: Unable to write.
  • Finger agnosia: Unable to identify individual fingers. Also unable to tell right from left. 'Show me your index finger'
  • Ideomotor apraxia: unable to voluntarily perform a learned task when given the necessary objects e.g. combing hair, 'show me how you would pour a cup of tea' - the patient uses his hand as the cup
  • Ideational apraxia: inability to initiate the action despite understanding the request


  • Contralateral homonymous hemianopia: Often a superior quadrantopia
  • Receptive dysphasia: Damage to Wernicke's area
  • Cortical deafness: May be seen with bilateral disease. Rarely seen with unilateral strokes,
  • Prosopagnosia: Can see a familiar face but fail to name them


  • Contralateral homonymous hemianopia: There may be sparing of central macular vision in infarcts of the posterior cerebral artery.
  • Cortical blindness: The pupillary responses to light are intact but light not perceived by the patient. May encompass Anton's syndrome where the patient is blind but denies visual loss where the patient is unable to direct voluntary gaze.
  • Visual hallucination: (positive phenomena) Flashing lights and fortification spectra can be seen with Migraine and some strokes.
  • Micropsia and macropsia: (positive phenomena) Seeing things bigger or smaller. Seen with Right occipital disease.

Assessing Motor Function

  • Inspection : Take care to look for wasting. Look at quadriceps and palpate muscle bulk. Specifically look at the thenar and hypothenar eminence, 1st dorsal interosseous, deltoids, extensor digitorum brevis. On the face, temporal wasting. Additionally look for scars, pressure, vascular and neuropathic ulcers. Always lift the legs and inspect the underside to see heels and between toes for lesions.
  • Tone: Assess upper limb tone in the wrist and elbow. Get the patient to relax and distract with irregular movements. Different types of altered tone are associated with disease. In the acute stroke the limbs are flaccid and hyporeflexic but this changes with time with increasing tone and extensor plantars and increased reflexes
  • Spasticity: increased tone seen with pyramidal weakness classically reduces as the joint is moved. High tone often gives way like a penknife and has been called "clasp knife". Best seen in forearm supination in upper limb and knee flexion in lower limb., Extrapyramidal: Lead pipe rigidity as the tone is constant through the range of movement. Becomes cogwheel when there is an overlying tremor. This is seen with Parkinson's disease. Gegenhalten: an erratic increase in tone in those with frontal lobe dysfunction also called "paratonia"
  • Power:Weakness in stroke disease follows a particular pattern. Weakness is predominantly in the upper limb extensors and the lower limb flexors. This pyramidal weakness disparity gives the particular flexed upper limb and extended lower limb appearance seen in stroke patients. Without strength in lower limb extensors to hold the knee straight walking would be much more difficult.

Grading power

can be again altered into + or -

  • 1. No contraction
  • 2. Flicker of contraction
  • 3. Active movement no gravity
  • 4. Active movement against gravity
  • 5. Active movement against gravity and resistance
  • 6. Normal power


Traditionally described as 0, +, ++, +++, ++++


  • Finger-nose test Ask the patient to touch nose and then your finger making sure the patient extends the full extension of elbow and back. Do this on both sides. There may be evidence of past pointing due to misjudgment of distance and speed. It may suggest cerebellar disease.
  • Heel-shin test: Patient runs heel down the opposite shin and lifts off back onto the patella. Notes speed and coordination.
  • Heel-toe walking: An old sobriety test as alcohol affected cerebellar function. Useful in subtle cases. It does assume the patient has a minimal pyramidal weakness and used really in mobile patients with subtle signs. Romberg's test Used to assess for a sensory ataxia. Usually seen in dorsal column disease where the patient has poor proprioception and closing the eyes leads to falling and loss of position sense.

Assessing Sensory Function

Much of this has been covered under parietal lobe function. A sensory loss tends to be complete along one side with large total anterior circulation strokes, thalamic strokes or those that take out the thalamocortical fibres. Look for Extinction when stimuli are presented bilaterally. See Parietal lobe higher functions for more information

Oxford Community Stroke Project classification

Abbreviations show S for syndrome when assessment is made before imaging. I for infarction After imaging when infarct without haemorrhage is demonstrated. H for haemorrhage After imaging when haemorrhage is demonstrated. The classification is useful clinically and prognostically and as an abbreviated way to communicate stroke type and severity.