Hemiplegia

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37 Hemiplegia

Instruction

Carry out a neurological examination of this patient.

Salient features

History

• Obtain history of headache, seizures and loss of consciousness (more common in subarachnoid haemorrhage or intracerebral bleeds than in cerebral infarction)

• History of speech defects, sensory loss and weakness of face and limbs

• Risk factors: hypertension, smoking, diabetes mellitus

• History of functional status: swallowing, mobility, pressure sores, independence in activities of daily living, visual difficulties (for visual field defects).

Examination

• Unilateral upper motor neuron seventh nerve palsy.

• The arm is held to the side, the elbow is flexed and the fingers and wrist are flexed on to the chest.

• The leg is extended at both the hip and knee, while the foot is plantar flexed and inverted.

• Weakness of the upper and lower limbs on the same side with upper motor neuron signs: increased tone, hyper-reflexia and upgoing plantar response.

• Hemiplegic weakness of the upper limbs affects the shoulder abductor, elbow extensors, wrist and finger extensors, and small hand muscles.

• Hemiplegic weakness of the lower limbs affects hip flexors, knee flexors and dorsiflexors and evertors of the foot.

• Do not forget sensory signs, in particular joint sensation which is important in rehabilitation.

• Proceed by examining for:

• homonymous hemianopia and sensory inattention
• Horners syndrome (p. 176): contralateral to hemiplegia suggests carotid dissection
• carotid bruits
• speech defects
• atrial fibrillation with the pulse
• murmurs from the heart.

• Tell the examiner that you would like to check the patient’s BP and check the urine for sugar.

Diagnosis

This patient has had a stroke causing a right or left hemiplegia (lesion), which can be the result of either a vascular event, such as thrombosis, embolism or haemorrhage, or a neoplasm of the brain (aetiology). This patient is limited by hemiplegia and hemianopia (functional status).

Questions

What are the causes of hemiplegia?

About 80% of all strokes are caused by cerebral infarction resulting from thrombotic or embolic occlusion of a cerebral artery (J Neurol Neurosurg Psych 1990;53:16–22). The remainder 20% are caused by either intracerebral or subarachanoid haemorrhage.

Elderly:

• Vascular event (thrombosis, embolism or haemorrhage)

• Tumour

• Subdural haematoma

• Syphilis.

Youth:

• Multiple sclerosis

• Tumour

• Trauma

• Embolism: look for underlying valvular heart disease and atrial fibrillation

• Connective tissue disorder

• Neurosyphilis

• Intracranial infection: look for underlying acquired immunodeficiency syndrome (AIDS), otitis media, cyanotic heart disease.

How would you manage such a patient?

• Early hospital admission preferably to a dedicated stroke unit, which has been shown to produce long-term reductions in death, dependency and need for institutional care (BMJ 1997;314:1151–9)

• Aspirin given within 48 h of ischaemic stroke reduces the risk of death and recurrent stroke. The International Stroke Trial (Lancet 1997;349:1569–81) and the Chinese Stroke Trial (Lancet 1997;349:1641–9), each involved 20 000 patients and found that aspirin was associated with about 10 fewer deaths or recurrent strokes, but with slightly more haemorrhagic strokes. The International Stroke Trial reported no benefit from subcutaneous heparin given with or without aspirin

• FBC, ESR

• Urine sugar

• ECG

• Chest radiography

• Echocardiography (looking for source of emboli), CT and carotid digital subtraction angiography (DSA) in selected patients

• Carotid Doppler: prior to endartrectomy, presurgical evaluation of saccular aneurysm

• MRI: diffusion-weighted sequences allow early detection. MRI has a much higher sensitivity than CT for acute ischaemic changes, especially in the posterior fossa and in the first hours after an ischaemic stroke

• Physiotherapy, speech therapy and occupational therapy

• Control of risk factors: hypertension, hyperlipidaemia and diabetes; stop smoking and oral contraceptives.

Discuss the importance of blood pressure reduction in a patient with acute ischemic stroke

Randomized clinical trials suggest that patients with acute ischemic stroke treated with antihypertensive agents may have an adverse clinical outcome and increased mortality (BMJ 1988;296:737–41, Cerebrovasc Dis 1994;4:204–10).

Advanced-level questions

What are the measures used to determine the outcome after an acute stroke?

Some of the standard measures include:

• Barthel index: reliable and valid measure of the ability to perform activities of daily living such as eating, bathing, walking and using the toilet.

• Modified Rankin Scale: simplified overall assessment of function in which a score of 0 indicates the absence of symptoms and a score of 5 shows severe disability.

• Glasgow Outcome Scale: global assessment of function in which a score of 1 indicates good recovery, a score of 2 moderate disability, a score of 3 severe disability, a score of 4 survival but in a vegetative state, and a score of 5 death.

• NIH Stroke Scale: a serial measure of neurological deficit using a 42-point scale that quantifies neurological deficits in 11 categories. For example, a mild facial paralysis is given a score of 1 and complete right hemiplegia with aphasia, gaze deviation, visual field deficit, dysarthria and sensory loss is given a score of 25. Normal function without neurological deficit is scored as 0.

What is the role of thrombolysis in acute stroke?

Treatment with intravenous tissue plasminogen activator (tPA) when administered within 3 h after onset of the ischaemic event (and in the absence of any sign of brain injury on CT) improves clinical outcome at 3 months (N Engl J Med 1995;333:1581–7). The CT scan in these patients must be examined very carefully for evidence of hemispheric brain ischaemia, which may increase the risk of deterioration with or without cerebral haemorrhage, after thrombolytic treatment. An overview of previous trials found significant excesses of early and total deaths, and of symptomatic and fatal intracranial haemorrhages, after acute thrombolysis, but a significant reduction in death or dependency in patients randomized to treatment within 3 h of stroke onset (Lancet 1997;350:607–14). It remains unclear which patients are most likely to benefit or be harmed. Therapy with alteplase may be effective in patients who present 3–4.5 h after the onset of stroke symptoms

Note: If the examiner asks: ‘If a patient presents to you 60 min after the onset of a left hemispheric stroke; how long do you have to initiate thrombolytic therapy?’ The correct answer is 1 min, not 2 h! Time is neurons saved!

What is the role of anticoagulants in the immediate treatment of acute ischaemic stroke?

Anticoagulants (including unfractionated heparin, low-molecular-weight heparin or specific thrombin inhibitors) offer no short or long-term benefits in the immediate treatment of acute ischaemic stroke. Although the risks of deep venous thrombosis or pulmonary embolus are significantly reduced, these benefits are offset by a dose-dependent increased risk of intracranial or extracranial bleeding.

What are the important principles of rehabilitation after a stroke?

• Long-term use of aerobic training

• Exercises to enhance flexibility, balance and coordination

• Resistance exercises within daily activities.

What are the clinical features that would interest you for the rehabilitation of a stroke?

• Independence in activities of daily living: bathing, dressing, toileting, transferring, continence and feeding.

• Independence in more complex activities such as meal preparation, shopping, financial management, housekeeping, transportation, medication-taking and laundering.

What are key goals before and after discharge of a stroke patient?

• Before discharge the patient should be able to:

• provide reliable yes and no responses to questions
• express himself or herself in short phrases
• use the unaffected hand effectively for self-care
• walk 50 m slowly with hands-on supervision (with the aid of a cane and/or ankle–foot orthosis).

Note: The patient would be expected to require some physical help for self-care.

• After discharge:

• Physical, occupational and speech therapy with a focus on on training in skills needed to increase independence for activities of daily living both at home and in the community; successful learning of such personal skills may require 20 or more hours of practice
• Formal training of caregivers
• Depression should be identified and treated
• Improvement in movement and language skills is possible with further practice at any time after stroke (because of the plasticity of neural pathways that remain intact).

(See N Engl J Med 2005;352:1677.)

What is the prognosis in a patient with acute ischaemic stroke?

About 25% of stroke patients are dead within a month, about 30% by 6 months and 50% by 1 year. Prognosis is worse when it is caused by intracerebral and subarachnoid haemorrhage, where the 1-month mortality is close to 50%. Of those who survive the acute event, about half will experience some disability after 6 months (J Neurol Neurosurg Psych 1987;50:177–82).

What is the significance of carotid artery stenosis?

Carotid artery stenosis is an important predisposing factor for cerebrovascular ischaemic events, the risk increasing with the severity of the stenosis and the presence of symptoms.

For severe symptomatic stenosis (>70% narrowing), carotid endarterectomy is recommended.

For severe symptom-free stenosis, optimal management has yet to be defined: one meta-analysis of trials showed only a small absolute benefit from surgery in reducing the odds of ipsilateral stroke (BMJ 1998;317:1477–80). Also 45% of strokes in patients with asymptomatic stenosis with 60–99% narrrowing are attributable to lacunaes or cardioembolism (N Engl J Med 2000;342:1693–1700). Hence carotid endarterectomy cannot be routinely recommended.

For mild to moderate symptomatic stenosis (<70% narrowing), an antiplatelet agent such as aspirin is recommended. Persistent symptoms may necessitate use of other agents such as ticlopidine or clopidogrel, which reduce the relative risk for further ischaemic events slightly more than aspirin or anticoagulation with aspirin (CAPRIE trial, Lancet 1996;348:1329–39).

How would you manage a patient with a transient ischaemic attack?

• Advise to stop smoking

• Aspirin

• Duplex ultrasonography of the carotid vessels

• Carotid artery digital subtraction angiography

• MRI scan of the head. It has been argued that all patients with TIA should be scanned since permanent damage may be seen in the brain on MRI in about 25% of patients with TIAs. The best approach to such patients is using the ABCD scoring system:

• Age ≥60 years: 1 point
• BP elevation at first assessment (≥140/90 mmHg): 1 point
• Clinical feature of TIA: unilateral weakness: 2 points; speech impairment without weakness: 1 point
• Duration of TIA: 10–59 min: 1 point; ≥60 min: 2 points
• Diabetes: 1 point.

What do you understand by the term transient ischaemic attack?

An acute loss of focal cerebral or ocular function with symptoms lasting <24 h.

Why is it important to differentiate a carotid transient ischaemic attack from a vertebrobasilar attack?

Carotid TIAs may be amenable to surgery. Furthermore, a TIA in the anterior circulation is generally of more serious prognostic significance than a TIA in the posterior circulation.

What are the features of a carotid transient ischaemic attack?

Hemiparesis, aphasia or transient loss of vision in one eye only (amaurosis fugax).

What are the features of a vertebrobasilar transient ischaemic attack?

• Vertigo, dysphagia, ataxia and drop attacks (at least two of these should occur together)

• Bilateral or alternating weakness or sensory symptoms

• Sudden bilateral blindness in patients aged over 40 years.

What are the risk factors for stroke?

Hypertension, ischaemic heart disease, atrial fibrillation, peripheral vascular disease, diabetes, smoking, previous TIA, cervical bruit, hyperlipidaemia, raised haematocrit, oral contraceptive pill and cardiomyopathy.

Why is it important to treat transient ischaemic attacks?

Prospective studies have shown that within 5 years of a TIA:

• 1 in 6 patients will have suffered a stroke

• 1 in 4 patients will have died (from either stroke or heart disease).

What is the role of carotid endarterectomy in patients with a carotid transient ischaemic attack?

• For patients with severe stenosis (70–99%) the risks of surgery are significantly outweighed by the later benefits.

• For patients with mild stenosis (0–50% of cases) there is little 3-year risk of ipsilateral ischaemic stroke, even in the absence of surgery; consequently, any 3-year benefits of surgery are small and outweighed by its early risks (N Engl J Med 2000;342:1743–5).

• For patients with moderate stenosis (50–69% of cases) the balance of surgical risk and eventual benefit is still being evaluated.

What is the role of carotid angioplasties in patients with recent carotid artery transient ischaemic attacks who have severe stenosis of the ipsilateral carotid artery?

Carotid angioplasty has not been adequately assessed in patients with recent carotid artery TIAs or non-disabling ischaemic stroke and severe stenosis of the ipsilateral carotid artery, and hence it is not recommended. However, registry data suggest that carotid artery stenting may be useful in carefully selected patients. The results of the CREST (Revascularization Endarterectomy Versus Stenting Trial) trial (randomized trial funded by the NIH examining the role of carotid stenting) showed similar net outcomes with carotid artery stenting and carotid endarterectomy for the treatment of carotid stenosis. Whereas the International Carotid Stenting Study (ICSS) interim safety results at 120 days appeared to favour carotid artery stenting over carotid endarterectomy for patients with symptomatic carotid stenosis only.

What to you understand by ‘RIND’?

Reversible ischaemic neurological disease, in which symptoms and signs reverse within 1 week but not within 24 h.

What are lacunar infarcts?

Lacunar infarcts are seen in hypertensive patients and consist of small infarcts in the region of the internal capsule (causing partial hemiparesis or hemisensory impairment), pons (ataxia of cerebellar type, partial hemiparesis), basal ganglia or thalamus. They are often multiple. Lacunae are thought to be caused by occlusion of small branch arteries or by rupture of Charcot–Bouchard microaneurysms, producing a small haematoma that resolves leaving an area of infarction.

What are the deficits supplied by the anterior carotid artery?

The anterior carotid artery supplies the frontal lobes and the medial cerebral hemispheres with the exception of the visual cortex of the occipital lobes. Cortical areas supplied by this artery include the motor and sensory areas of the lower limbs, a ‘micturition centre’ and the supplementary motor cortex. Ischaemia in the territory of one anterior carotid artery produces weakness and mild sensory deficits in the opposite lower limb. Some patients with left anterior carotid artery ischaemia have a mild transient aphasia.

What do you understand by the term stroke?

Stroke is characterized by rapidly progressive clinical symptoms and signs of focal, and at times global, loss of cerebral function lasting >24 h or leading to death, with no apparent cause other than that of vascular origin (Bull Word Health Organ 1976;54:541–53).

How do you classify stroke?

The Bamford clinical classification of stroke has the following.

Total anterior circulation syndrome:

• Unilateral motor deficit of face, arm and leg

• Homonymous hemianopia

• Higher cerebral dysfunction (e.g. aphasia, neglect).

Parietal anterior circulation syndrome has any two of the following features:

• Unilateral motor and/or sensory deficit

• Ipsilateral hemianopia or higher cerebral dysfunction

• Higher cerebral dysfunction alone or isolated motor and/or sensory deficit restricted to one limb or the face.

Posterior circulation syndrome has one or more of the following features:

• Bilateral motor or sensory signs not secondary to brainstem compression by a large supratentorial lesion

• Cerebellar signs, unless accompanied by ipsilateral motor deficit (ataxic hemiparesis)

• Unequivocal diplopia with or without external ocular muscle palsy

• Crossed signs, for example left facial and right limb weakness

• Hemianopia alone or with any of the four items above.

Lacunar syndromes can be pure motor, pure sensory, ataxic hemiparesis or sensorimotor:

• Pure motor stroke:

• Unilateral, pure motor deficit
• Clearly involving two of three areas (face, arm and leg)
• With the whole of any limb being involved.

• Pure sensory stroke:

• Unilateral pure sensory symptoms (with or without signs)
• Involving at least two of three areas (face, arm and leg)
• With the whole of any limb being involved.

• Ataxic hemiparesis:

• Ipsilateral cerebellar and corticospinal tract signs
• With or without dysarthria
• In the absence of higher cerebral dysfunction or a visual field defect.

• Sensorimotor stroke;

• Pure motor and pure sensory stroke combined (i.e. unilateral motor or sensory signs and symptoms)
• In the absence of higher cerebral dysfunction or a visual field defect.

What advice would you give a stroke patient regarding driving?

The patient should be informed about driving regulations and the legal requirement to inform the Driver and Vehicle Licensing Authority need to be explained.

M. Fischer wrote one of the earliest descriptions on the effect of ‘occlusion of the internal carotid artery’ including transient cerebral ischaemia and ischaemic stroke (Arch Neurol Psychiatry 1951;65:346–77).

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