HEMIPLEGIA
Hemiplegia, i.e. unilateral weakness, may be acute, chronic progressive or static.
• Acute hemiplegia of childhood is the major cause of concern in childhood, almost always suggestive of cerebrovascular accidents or strokes.
Severity of motor deficit is maximum at the onset of illness and recovery is usually faster than other causes.• Chronic progressive hemiplegia usually indicates: (a) focal CNS infections, e.g. brain abscess, tuberculoma,
(b) brain tumors, and (c) neurocutaneous disorders, e.g. Sturge-Weber syndrome, and (d) early stages of white matter degenerative disorders.
• Static hemiplegia usually denotes hemiplegic cerebral palsy due to: (a) perinatal hypoxic-ischemic insult, and (b) congenital malformations.
• Recurrent or alternating hemiplegia is seen in: (a) migraine, (b) hypercoagulable states, e.g. protein C or S deficiency, (c) vascular malformations, e.g. Moya- Moya disease, and (d) mitochondrial encephalopathies, e.g. MELAS (Myoclonic Epilepsy, Eactic Acidosis and recurrent Stroke-like syndromes.
• Todd paralysis is transient cause of unilateral weakness after seizures, which may be recurrent but does not last for more than 24 hours.
Diagnostic approach in hemiplegia aims to—(a) localize the site of lesion, and (b) identify probable cause on the basis of clinical and laboratory findings.
A. Clinical localization of lesion is possible up to certain extent, according to type of hemiparesis and presence of clinical signs (Table 18.22). Hemiplegia may be caused by any lesion from the cerebral cortex to upper few segments of spinal cord. Important localizing clues are:
• Side of hemiplegia: Hemiplegia is almost always contralateral to brain lesion, except in rare lower medullary lesions.
• Extent and severity of motor deficit: Internal capsule is the commonest site of lesion in dense hemiplegia,
| TABLE 18.22: Clinical localization of lesions | |
| Cortical | Non-dense contralateral hemiparesis Seizures Altered sensorium Motor aphasia (dominant side lesion) |
| C. radiata | As above, but without seizures |
| Int. capsule | Dense contralateral hemiplagia Contralateral sensory loss Supranuclear facial paresis |
| Midbrain | Contralateral hemiplagia + III/IV nerve palsy |
| Pons | Contralateral hemiplagia + Ipsilateral VII/VIII |
| Medulla | Contralateral hemiplagia + Ipsilateral bulbar palsy |
| Spinal cord | Ipsilateral hemiplagia, no cranial nerve palsies |
while cortical and sub-cortical lesions usually produce weakness limited in severity and scattered in extent.
• Side and type of facial palsy: Facial palsy is also contralateral and supranuclear in lesions at or above the level of upper pons. Ipsilateral infranuclear facial palsy, (i.e. contralateral to hemiplegia) indicates lesions at or below the lower pons.
B. Etiological identification of lesion is facilitated by:
• Onset and progress of lesion: Thromboembolic lesions generally present with sudden catastrophic onset over a few minutes and recovery starts within few days in most cases. On the other hand, hemorrhagic lesions develop more gradually and recovery is often unsatisfactory.
• History of head injury, diarrhea/vomiting, fever and systemic disorders, e.g. heart disease, bleeding disorders, sickle cell disease or hypercoagulable states.
• History of similar attacks in past (see causes of recurrent or alternating hemiplegia)
• Clinical examination suggestive of neurocutaneous markers, extracranial septic focus, signs of dehydration or systemic diseases.
C. Laboratory Investigations include:
• Neuroimaging with CT scan/MRI. Four-vessel angiography or MR angiography is necessary in suspected cases of cerbrovascular malformations.
• Relevant investigations to identify or exclude:
- Hematological causes: Sickling test, coagulation profile (prothrombin time, protein C and S levels, antithrombin), platelet count, etc.
- CNS infections: CSF examination (should be avoided in suspected bleeding disorders).
- Cardiac causes: ECG and echocardiography
- Connective tissue disorders: ESR, antinuclear antibodies, etc.
- Metabolic disorders — urine analysis, lactates, homocysteine levels, blood gas analysis for acidosis and enzyme studies.
Despite extensive investigations, underlying cause in acute hemiplegia of childhood remains unidentified in 60-70% cases.
Management of hemiplegia is largely supportive, including:
• General supportive measures, e.g. (i) nursing care (care of back, bowel and bladder), (ii) nutritional support, (iii) control of associated problems, e.g. seizures, raised ICP, etc.
• Physiotherapy, speech therapy and rehabilitation, should be started as early as possible.
• Specific therapy is of limited value in established case. However anti-thrombotic and anti-platelet therapy is required in cases of arterial ischemic strokes or cerebral sinovenous thrombosis, as discussed in Ch 18.7. Surgical evacuation of clot is indicated in cases of large hematoma.
• Preventive therapy depends on suspected cause. Salicylates, vasodilators and platelet inhibitors have been used to prevent recurrence of thromboembolic episodes.
18.9