Grand rounds offer opportunity to discuss basics in medicine as applied on live cases. Neurological examination demands close observation of every action that child performs, even subconsciously. Over years, one learns to use various maneuvers to fish out subtle abnormalities if any. Following discussion is aimed at providing glimpses related to special issues that help in proper physical examination and interpretation of abnormal signs. It is not intended to discuss individual case scenario or conventional examination.
Observation and play techniques are essential means of monitoring intellectual, behavioral and motor functions in infants and young children. Beyond 4-5 years of age, neurological examination of more conventional. Gross motor functions can be screened by simple maneuvers such as hopping on each foot, tandem walking forwards and backwards and toe and heel walking. Standing with feet together, eyes closed and hands outstretched allows simultaneous assessment of abnormal movements and Romberg sign.
Finally finger-nose test adds further information.
Development assessment is important especially in infants and younger children. Developmental reflexes are pattern reflexes that help to evaluate general development of nervous system, though it does not localize the pathology. Abnormality is seen in either persistent of reflexes beyond the expected period, absence of expected reflex or asymmetrical reflex. Persistent ATNR may be the early sign of cerebral palsy. Simple screening of development is must at 3 months of age when moderate developmental delay should be made out. Holding head, recognizing mother, social smile, babble and hand to mouth coordination are achieve by this age. Absence of language development by 18 months demands proper evaluation for hearing, global development or abnormal behavior.
Observing the gait of a child gives clue to a probable lesion as in spastic hemiplegia, ataxia, extrapyramidal affection with shuffling gait, high stepping in peripheral lesion and waddling in muscular dystrophy. It is important to rule out contractures, scoliosis of spine or painful conditions. Abnormal movements are often accentuated while walking and can be easily observed.
Abnormal movements can be easily grouped as per their speed besides the site of affection. Slow movements are dystonia and athetosis, rapid jerky movements are ticks and chorea, rhythmic oscillatory movements are tremors and myoclonus.
Hypotonia may be non-neurological (non-paralytic) or neurological (paralytic or non-paralytic). Non-paralytic hypotonia is seen in malnutrition, chromosomal defects, congenital syndromes, benign congenial hypotonia, hypotonic cerebral palsy and myopathy of various etiologies. Paralytic hypotonia suggests lower motor neurone lesion.
Coma results from inadequate interaction between cerebral cortex and reticular activating system in diencephalons, midbrain and pons. Specific symptoms and signs that help in localization of lesion characterize each site of affection. Involvement of cerebrum and basal ganglia maintains normal breathing pattern, normal pupillary response and spontaneous movements of extremities with roving eye movements. Diencephalic affection results in periodic or Cheyne-Stokes breathing, positive doll's eye sign, small reacting pupils and decorticate posture. Midbrain involvement leads to hyperventilation, decerebrate posture, dilated pupils and dysconjugate gaze with loss of doll's eye reflex. Pons affection fixed dilated pupils with absence of eye movements and shallow irregular respiration. Rapid nostrocaudal deterioration suggests central tentorial herniation. Unilateral dilated pupil with midbrain dysfunction is characteristic of uncal herniation. Supratentorial mass lesion may present with either tentorial or uncal herniation.
Brain cell edema is categorized as cytotoxic – disruption of intracellular metabolism as in Reye's syndrome, SIADH, HIE or encephalitis, vasogenic – disrupted blood brain barrier as in trauma, abscess, tumor or infarct and interstitial as in case of acute hydrocephalus forcing CSF out of ependymal lining of ventricles. Dexamethasone is the drug of choice in vasogenic cerebral edema. Mannitol was considered useful for first 2-3 days in cytotoxic edema though present consensus suggests its use for just a dose or two, as it is not helpful beyond few doses.
Analyzing symptoms and physical signs to define anatomy of the lesion helps in clinical approach to neurological conditions.
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