This paper describes the evolution of the pathogenic concepts associated with the infection by the human immunodeficiency virus (HIV), with emphasis to the pathology of the nervous system. Although the first description of damage to the nervous system in the acquired immunodeficiency syndrome (AIDS) only appeared in 1982, the dramatic diffusion of the epidemic worldwide, as well as the invariably rapidly fatal outcome of the disease before the introduction of efficient treatment, generated from the beginning an enormous amount of research and re-thinking on a number of pathogenetic concepts. Less than 25 years after the first autopsy series on AIDS patients were published and the virus responsible for AIDS was identified, satisfactory definition and classification of a number of neuropathological complications of HIV infection have been established. This has led to the establishment of accurate clinical and biological diagnosis of the main neurological complications of the disease, which remain a major cause of disability and death in patients. Clinical and experimental studies have provided essential insight into the pathogenesis of CNS lesions and the natural history of the disorder. The relatively recent introduction of effective antiretroviral therapy in 1995-6 dramatically improved the course of prognosis of HIV disease. However, there remain a number of unsolved pathogenetic issues, the most puzzling of which remains the precise mechanism of neuronal damage underlying the specific HIV-related cognitive disorder (HIV-dementia). In addition, although antiretroviral therapy has changed the course of neurological complications, new issues have emerged, such as the lack of improvement or even paradoxical deterioration of the neurological status in treated patients. Interpretation of these complications remains largely speculative, partly because of the small number of neuropathological studies related to the beneficial consequence of this treatment.

Distal sensory polyneuropathy, which occur commonly in human immunodeficiency virus (HIV) patients can occur as a consequence of the disease itself or the antiretroviral treatment the patient is receiving. Among the antiretroviral agents, nucleoside analogues are commonly associated with neuropathy and the main underlying mechanism is thought to be the mitochondrial toxicity exhibited by these agents. Clinical presentation of antiretroviral induced neuropathy is similar to that associated with the HIV infection and in many patients they may overlap. Treatment is primarily symptomatic and certain pathogenesis-based approaches have shown promising results.

Until early 80's most patients presenting with lower motor neuron syndrome characterized by weakness, wasting, diminished reflexes, fasciculations, cramps and minimal sensory involvement would have been diagnosed as motor neuron disease- LMN variant. But similar clinical picture can be seen in various disorders right from degenerative illnesses like motor neuron disease to inflammatory ones like multifocal motor neuropathy (MMN). Some of them are potentially treatable conditions with immunomodulatory therapies and are associated with characteristic electrophysiological features and high serum antibody titers. Thus every patient presenting with pure motor LMN weakness and fasciculations should not be labeled as motor neuron disease and extensive electrophysiological search is warranted to diagnose these potentially treatable conditions, changing the grim prognosis to more favorable one.

The validity of Snodgrass and Vanderwart pictures and their norms derived on a western population on naming, familiarity, imageability and visual-complexity, is not established on a population with cultural background different from the west. We developed, therefore, a set of culturally appropriate pictures for and derived norms on Indians. Line-drawings of 103 concepts (67 from Snodgrass and Vanderwart, 36 new) from 10 semantic-categories were normed on 200 community-based older subjects. Only 31% of the Snodgrass and Vanderwart items showed a concept-agreement on the Indians comparable to western norms. Naming, familiarity and image-agreement mutually correlated but not with visual-complexity. Low-education and rural-residence tended to reduced concept-agreement. The output of this study will be of use in national and cross-national studies.

Intercommunications between musculocutaneous nerve and median nerve deserve important interest in view of their clinical significance. In the study of 50 upper limb specimens, the various communications between the musculocutaneous and median nerve in the arm were observed carefully. The communications between the two nerves were found in 13 arms. Variations in the present study involving the median nerve and musculocutaneous nerve are important in repairs for trauma to the shoulder and the understanding of the median nerve and the musculocutaneous nerve dysfunction.

Gelastic epilepsy is a rare but well recognized epileptic syndrome typically manifesting in early childhood. It is characterized by recurrent brief seizures with initial laughter or grimacing. Also known as "laughing" seizures, their association with hypothalamic hamartomas is well known in children and adults; however other structural causes have also been implicated. This study reports three cases of gelastic seizures, one each of Tuberous sclerosis, Left temporal gliosis and Hypothalamic Hamartoma with neuronal migration defect respectively. Though these seizures are usually pharmacoresistant and may end up as a severe epileptic encephalopathy and catastrophic epilepsy of childhood, all of our cases responded well to antiepileptic medication (carbamazepine and valproate). This study underscores the fact that certain brain abnormalities other than hypothalamic tumors are also associated with gelastic seizures. The clinical characteristic of seizures in these patients is different than those of isolated hypothalamic hamartomas and that these seizures can be well controlled with antiepileptic drugs.

A marked decrease in incidence has been observed for most central nervous system opportunistic infections after the use of highly active antiretroviral therapy. In developing countries, where highly active antiretroviral therapy is still unavailable, unusual patients are encountered. We are reporting an untreated patient who, in addition to progressive multifocal leukoencephalopathy, also had disseminated tuberculosis and oral candidiasis. Neuroimaging showed a very extensive white matter and gray matter involvement producing a picture of "JC virus encephalitis".

Central pontine myelinolysis (CPM), a neurologic disorder caused most frequently by rapid correction of hyponatremia, is characterized by demyelination that affects the central portion of the base of the pons. Central pontine myelinolysis occurs frequently in alcoholism and chronic liver disease. Clinical features usually reflect damage to the descending motor tracts and include spastic tetraparesis, pseudobulbar paralysis and the locked-in syndrome. Cerebellar ataxia with out weakness and pyramidal signs is extremely unusual. There are only very few reports of central pontine myelinolysis presenting as cerebellar ataxia.

Extramedullary haematopoiesis (EMH) as a cause of spinal cord compression in patients with thalassaemia major is very rare. Treatment of EMH includes the use of radiotherapy, hypertransfusion, laminectomy and chemotherapy in the form of hydroxyurea We report a presentation of progressive paraparesis due to a sacral mass in a 7 year old child undergoing repeated blood transfusions for thalassaemia major who had a dramatic improvement in symptoms after radiotherapy. A standard recommendation regarding the radiation dose required is not available but a dose of 20Gy delivered over 10 fractions seems to be effective and well tolerated.

With the advent of digital technology in the recording of the electroencephalogram (EEG) in the last decade, analogue paper-EEG machines have all but disappeared. While there are several advantages of digital EEG over its analog counterpart, like being paperless and therefore easy to store and the ability to change montages and filter settings during review, there is wide disparity in the standards of EEG recording, display and reporting in laboratories across the country. Colorful brain maps conveying little meaning are usually appended to reports. This article reviews the minimum standards that must be observed for recording digital EEG as recommended by the International Federation of Clinical Neurophysiology (IFCN) and illustrates the importance of use of appropriate derivations, montages, filters and gains during recording and review of digital EEG in the context of evaluation of patients with suspected epilepsy.