Distal symmetrical peripheral neuropathy is a common adverse experience in persons with HIV infection. This condition, which presents as a pain, numbness. burning and/or dysaethesia initially in the feet, is often multi-factorial in its origin. Nucleoside analogue reverse transcriptase inhibitors represent an important contributor to peripheral neuropathy. Specifically, around 10% of patients receiving stavudine or zalcitabine and 1 to 2% of didanosine recipients may have to discontinue therapy with these agents due to neuropathy. Prompt withdrawal of these therapies enables gradual resolution of signs and symptoms in most patients, although a period of symptom intensification may occur shortly after withdrawal. Risk factors for developing peripheral neuropathy during nucleoside analogue therapy include low CD4+ cell count (<100 cells/mm3), a prior history of an AIDS defining illness or neoplasm, a history of peripheral neuropathy, use of other neurotoxic agents including high alcohol (ethanol) consumption and nutritional deficiencies such as low serum hydroxocobalamin levels. Thus, patients at increased risk of peripheral neuropathy should potentially avoid the use of the neurotoxic nucleoside analogues or be more carefully monitored during therapy. Management of this problem includes patient education. prompt withdrawal of the likely causative agent (giving consideration not to leave the patient on a sub-optimal therapy regimen) and simple analgesia. with augmentation with tricyclic antidepressants or anticonvulsant agents when pain is severe. New agents that may assist in managing this condition include levacecarnine (acetyl-L-carnitine) and nerve growth factors such as recombinant human nerve growth factor.

The development of the host/graft interface of cerebellar and cerebral transplants was studied 1-60 days after operation. Grafts from fetal Wistar rats were transplanted to a cavity over the superior colliculus of adult rats by removing parts of the overlying cortex and hippocampus according to the Björklund/Stenevi technique. In sham-operated control rats, in which a cavity was made in the brain but no graft was implanted, the parenchyma bordering the entire cavity developed a complete glial-meningeal scar within 2 weeks after operation consisting of multilayered glial processes, a basal lamina, and fibroblasts (meningeal cells). A similar interface also developed between graft and host in the most superficial parts of the transplantation cavity. In the basal parts of the transplantation cavity, the host/graft interface consisted either of an incomplete sheet of astrocyte processes aligned in parallel to each other but without a covering basal lamina or of completely fused neuropil without any morphological signs of separation between host and transplant. It is concluded that these three zones of host/graft interface are established by differential interaction between the growing transplant and the host cicatrix. At the basal host/graft parenchymatous interface the fetal transplant interferes with the normal adult cicatrization process of the host, possibly by either releasing inhibitory factors or by preventing contact between the astroglia of the host and fibroblasts (meningeal cells). In white matter regions of the transplantation cavity, voluminous cysts developed, both in sham-operated controls and in graft recipients, which were invaded by transplanted neurons.

No abstract

PER seems safe in PWE with ID. It is better tolerated by PWE with Moderate to profound ID than PWE with higher functioning. Caution is advised when history of mental health problems is present. The standardised approach of the Ep-ID register UK used confirms that responses to AEDs by different ID groups vary between themselves and General population.