The present paper deals with 21 types of neurological manifestations, some of them syndromes, observed by us in just under 600 cases of tuberculous meningitis over a period of more than a decade. Their incidence was high during this period because of prolongation of life and a greater number of recoveries with antituberculous treatment. The neurological syndromes seen at the onset or during the course of the disease are: (1) various types of paralyses such as hemiplegia and quadriplegia which are common, and monoplegia and cerebral paraplegia which are rare; (2) abnormal movements: hemiballismus is the most common, while Parkinsonian tremor, myoclonic jerks and disturbance of equilibrium due to midline cerebellar lesions caused by posterior fossa meningitis are rare; (3) the therapeutic paradox in which there is a neurological deterioration following chemotherapy; and (4) spinal leptomeningitis where the child presents with signs of spinal cord involvement; the meningitis may later extend intracranially in some of these cases. Infarction on the basis of large vessel involvement or ischaemia from jeopardisation of end-arterial circulation was responsible for the various paralyses. Border-zone necrosis of the subthalamic region, probably due to ischaemia from exudate in the Sylvian fissure, would seem to account for the hemiballismus. The clinical features and syndromes seen after the disease is well-established are: (1) cranial nerve palsies mainly involving the optic nerves, and the 3rd, 4th, 6th and 7th nerves; (2) various motor disturbances: decorticate and decerebrate spasms and rigidity and rarely flexor spasms; (3) a syndrome of acute increase in intracranial tension in a few cases which is often of grave prognosis: (4) neurological deficits caused by cerebellar hemispheric involvement seen rarely during recovery from meningitis; and (5) an interesting feature of the reappearance of neonatal reflexes in well-established cases of meningitis and often suggestive of an adverse prognosis. The pathogenesis of multiple cranial nerve involvement is obviously entrapment and rarely infiltration by the basal exudate of the cranial nerves in and around the interpeduncular fossa. Extensive damage to both cerebral hemispheres by infarction was responsible for the decorticate or decerebrate postures in about a third of the cases; in the majority this was a result of severe cerebral oedema or hydrocephalus; rarely there was oedema of the brain stem itself. Sudden rise in intracranial tension was brought about either by a rapid increase of internal hydrocephalus or, less frequently, by the acute development of cerebral oedema. Infarction of a cerebellar hemisphere was the most frequent cause of unilateral cerebellar syndromes. The various clinical pictures usually seen during or after recovery from the disease were: (1) hypothalamic-pituitary syndromes—(a) Cushing's syndrome, (b) obesity, (c) diabetes insipidus and (d) excessive sleepiness; (2) recurrent attacks of serous meningitis seen not infrequently in the past but less so today which often simulated atypical febrile fits or viral meningo-encephalitis; (3) postmeningitic encephalopathy, an infrequent complication presenting with various cerebral manifestations, usually seen after recovery from meningitis. The hypothalamic-pituitary syndrome seems to be the result of damage from excessive dilatation of the third ventricle and stretching of its floor, or from the direct effects of the basal exudate since it is most copious and adherent there; (4) post-lumbar puncture spinal epidermoid, a rare complication, was seen in 2 cases.