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In Parkinson's disease, one of the most troublesome dilemmas is the treatment of levodopa-induced dyskinesia. After a few years, chronic treatment with levodopa is associated with the development of dyskinesias. Strategies to delay or to reduce dyskinesias are based on the change of levodopa dosing or the early use of dopamine agonists. Dopamine agonists with different pharmacological profile are available. Our paper was aimed to analyse the clinical impact and the management of dyskinesias with dopamine agonists.

The modulation of trigeminal reflex excitability in migraine patients was evaluated during the asymptomatic phase by studying the effects of attention, habituation and preconditioning stimulus on the R2 and R3 components of the blink reflex (BR). Fifty patients suffering from migraine without aura, 20 affected by migraine with aura and 35 sex- and age-matched controls were selected. In subgroups of migraine with-aura and without-aura patients, and normal controls, the blink reflex was elicited during different cognitive situations: (a) spontaneous mental activity; (b) stimulus anticipation; (c) recognition of target numbers. In the remaining subjects, R2 and R3 habituation was evaluated by repetitive stimulation at 1, 5, 10, 15, 20, 25 and 30 s intervals. The R2 and R3 recovery curves were also computed. A reduced R3 threshold with a normal pain threshold was found in migraine with-aura and without-aura patients; the R3 component was not significantly correlated with the pain thresholds in patients and controls. The R2 and R3 components were less influenced by the warning of the stimulus in migraine without-aura and migraine with-aura patients, in comparison with the control group. A slight increase of both R2 and R3 recovery after preconditioning stimulus was also observed in migraine patients, probably caused by a phenomenon of trigeminal hyperexcitability persisting after the last attack. The abnormal BR modulation by alerting expresses in migraine a dysfunction of adaptation capacity to environmental conditions, probably predisposing to migraine.

Epidemiological studies performed to identify the possible cause of Multiple Sclerosis (MS) suggest that an environmental agent could be involved in its etiopathogenesis. For a long time it has been hypothesized that this agent was a virus, but until now no virus specific to MS has been consistently identified. Animal models indicate that the demyelination of the central nervous system can be induced by certain families of viruses, but the implication of this in the etiopathogenesis of MS has not been clearly demonstrated. Morbilliviruses were the most studied. Research on this subject arose from the observation of the similarity between the brain lesions occurring in MS and encephalitis caused by the measles virus (Subacute Sclerosing Panencephalitis). Antimeasles, antirubella, antiherpes zoster antibodies have been found in the blood and the cerebrospinal fluid of MS patients, but the relationship between this finding and the disease is not clear. It has recently been proposed that the pathogenetic immune response in the brain of MS patients might be directed predominantly towards antigens of a DNA virus, such as JCV. This preferentially infects glial cells and causes a demyelinating syndrome in immunodeficient subjects, called Progressive Multifocal Leucoencephalopathy. The target JC viral antigens in MS could be synthesized during transient viral reactivation. A recent hypothesis is that retroviruses may intervene in the etiopathogenesis of MS. Strong interest has been taken in HTLV-I after its identification in Tropical Spastic Paraparesis, a disease with certain similarities to MS. Serologic and polymerase chain reaction findings from various authors have suggested an association between this human retrovirus and MS. However more recent data are not consistent with this. Current experiments aimed at detecting retroviral particles in long-term cultured peripheral blood monocytes and cerebrospinal fluid mononuclear cells in MS could clarify whether these cells provide a reservoir for such viruses, with a latency of many years without expression at brain level.