ABSTRACT
We have evaluated cortical excitability in nine patients affected by Wilson's disease (WD) using transcranial magnetic (TMS) and electric (TES) cortical stimulation and central silent period (CSP) data. A clinical score was derived from the sum of scores assigned to extrapyramidal, pyramidal and cerebellar signs. All patients underwent TMS. Motor evoked potentials (MEPs) from abductor pollicis brevis (APB) and tibialis anterior (TA) muscles were recorded. MEP threshold and amplitude, central motor conduction time (CMCT), CSP threshold, CSP and peripheral silent period (PSP) duration were measured. Three patients also underwent transcranial bifocal electric cortical stimulation (TES) and MEPs were recorded from the APB muscle, and CMCT, MEP threshold and amplitude were measured. TMS MEPs were absent from relaxed muscles in six patients and from contracted muscles in three. CMCT was prolonged in six patients. APB CMCT correlated with clinical score. In three patients in whom TMS revealed abnormal or no MEP, TES MEPs were of normal threshold and amplitude. The CSP threshold was increased in seven patients, and CSP was absent in one. These results suggest an intracortical presynaptic motor dysfunction in WD.
Subject(s)
Evoked Potentials, Motor/physiology , Hepatolenticular Degeneration/physiopathology , Magnetics , Motor Cortex/physiopathology , Movement/physiology , Muscle Contraction/physiology , Neural Inhibition/physiology , Adult , Electric Stimulation/methods , Female , Hepatolenticular Degeneration/diagnosis , Humans , Male , Middle Aged , Muscle, Skeletal/innervation , Muscle, Skeletal/physiopathology , Neural Conduction/physiology , Neural Pathways/physiopathology , Reaction Time/physiologyABSTRACT
Alcohol abstinence syndrome (AAS) occurs in alcohol dependent patients a few hours after ceasing to drink, first in the form of gastrointestinal and dysvegetative signs, then with the involvement of neurological functions. The results obtained in 15 patients selected according to DSM III criteria, treated with nimodipine (calcium entry blocker) in the acute phase and with reduced glutathione in the subacute phase are presented. All patients who, during treatment, did not take other drugs, showed a definite, fast improvement in symptoms, especially in neurovegetative symptoms. Administration of nimodipine, which seems capable of reducing the catecholaminergic drive, was very well tolerated. Treatment with reduced glutathione is justified by the fact that the inadequate intake of alcohol is responsible for liver changes and, particularly, for a significant reduction in liver levels of glutathione, a condition that makes the cell more exposed to attack on the part of substances that activate lipoperoxidation processes. The results obtained seem to confirm a protective action on the part of reduced glutathione.