Inspite of extensive research the ideal drug therapy for idiopathic Parkinson's disease (PD) and its optimal timing remain uncertain. Levodopa still is the mainstay of therapy for PD. Little evidence exists to incriminate early institution of levodopa therapy in the development of motor fluctuations and dyskinesias in PD. These complications are probably a consequence of disease progression, and resultant inability to synthesize and store dopamine, and buffer the variability in dopamine availability. Therefore, withholding levodopa therapy until late stage of the disease is not warranted. Dopa agonists provide only a short-term benefit. The neuroprotective effect of selegiline remains to be established. There is not enough evidence to justify the current practice of initiating treatment for PD patients with expensive polypharmacy. Research into the development of inexpensive levodopa containing preparations needs to be encouraged.

Motor neuron disease, considered synonymous with amyotrophic lateral sclerosis (ALS), is seen frequently in India. Its aetiopathogenesis is one of the major enigmas in neuroscience. In India only a limited epidemiological data of this neurodegenerative disorder is available and the problem is further compounded by a lack of autopsy study on this devastating disease. We report the neuropathological findings of three autopsied cases diagnosed as amyotrophic lateral sclerosis on the clinical basis of weakness, wasting and fasciulations in all limbs. There was no involvement of the sensory, cerebellar and extra-pyramidal systems. Terminally all had profound respiratory muscle weakness as is the usual cause of death in patients with motor neuron disease. The major findings in the anterior horn cells of the spinal cord were significant and asymmetrical loss of motor neurons, increased central chromatolysis, presence of argyrophilic axonal spheroids, occurrence of Bunina bodies, hyaline bodies, and occasional neurofibrillary tangles. There was loss of axons in the anterior roots. Electron microscopic studies revealed accumulation of skeins of 10 nm neurofilaments, both in intraneuronal hyaline inclusions and the axonal spheroids. No definite temporal correlation in the evolution of the pathological lesions and the duration of the illness is evident in our study.

Motor evoked potentials were recorded in 25 patients with ischaemic stroke within 72 hours of onset by transcranial magnetic stimulation. Motor power was graded according to MRC grading and the disability by Ranking scale. The patients could be grouped into those with normal MEPs (Group I) - 5 (20 per cent), those with prolonged CMCT and/or abnormal MEP/CMAP ratios or prolonged interside difference in CMCT on the hemiparetic side (Group II) - 12 (48 per cent) and those with no elicitable cortical MEPs on the hemiparetic side (Group III) - 8 (32 per cent). Patients with greater weakness and disability tended to have more abnormal or absent MEPs. No definite correlation could be seen with the site of infarct and MEP abnormalities. Patients with no elicitable cortical MEPs (Group III) showed no significant improvement in motor deficit at six months follow up. Where as patients in whom normal or abnormal cortical MEPs could be elicited (Group I & II) showed significant improvement. Evaluation of MEPs by transcranial magnetic stimulation early in acute ischaemic stroke can be used to predict stroke outcome.

Eleven patients of ipsilateral seizures or ipsilateral neurological deficit were studied under the heading of ipsilateral cerebral events. Ipsilateral localisation was based on electroencephalogram (EEG) and computed tomography (CT) scan or both. Group A had 4 patients who had predominantly motor neurological deficit and ipsilateral pathology was evident on CT scan. Surgery re-confirmed the lesion in one case. Group B had 7 patients who had partial motor seizures with or without generalisation. EEG showed ipsilateral focus in all but only 3 patients revealed ipsilateral lesion on CT scan. All patients showed improvement on medical treatment except one case which underwent surgery. Various hypotheses are put forward for the ipsilateral phenomenon and the mechanism implicated are discussed.

Palmomentalis reflex (PMR) is a superficial polysynaptic, primitive reflex seen in normal population with higher incidence at the extreme of ages. It is exaggerated in upper motor neuron lesions involving corticobulbar tracts. We describe palmolevator labii superioris reflex - new variant palmomentalis reflex. The mechanism, pathway and diagnostic applications of PMR are discussed on recent studies.

A rare case of non Wegener's midline granuloma with bilateral thalamic involvement is presented. A 53 year old male presented with a nonhealing midline granuloma of nose for one year and right hemiparesis for five months with bilateral pyramidal signs. Biopsy from the nasal lesion picture of malignant midline reticulosis with angiocentric cellular infiltrate. Cranial CT scan reveled bilateral thalamic involvement.

Actinomycotic brain abscesses constituted 1 per cent of all brain abscesses treated in last eleven years. Computed tomographic finding of an irregular (nodular) thick unit or multilocular peripheral rim enhancing lesion were of some help in suspecting actinomycotic aetiology. The diagnosis was confirmed by bacteriological studies. A combined medical and surgical treatment produced excellent results.

A Case of a giant aneurysm of the internal carotid artery in an eleven years child is presented. The size of the aneurysm was 5 cm in its greatest diameter. The lesion presented with features of suprasellar mass, multiple lower cranial nerve paresis, ataxia, long tract signs and spontaneous, unprovoked bursts of laughter. Such a large size of aneurysm with features of mass effect involving the supratentorial as well as the infratentorial compartment is rarely encountered. Unprovoked bursts of laughter was a unique symptom in this child.