The antiepileptic effect of allopurinol was assessed in a double-blind, randomized, placebo-controlled, cross-over trial in 84 patients with epileptic seizures refractory to standard antiepileptic ...drugs (AEDs). During a retrospective baseline period, patients experienced at least four seizures of any type per month. The effects of allopurinol and matching placebo were examined for 4-month periods. Allopurinol dosage was 150 mg daily for children weighing < 20 kg and 300 mg daily for other patients. Efficacy analysis based on the Wilcoxon rank-sum test was conducted for the 80 patients who completed the study. No significant period effect or treatment-period interaction was noted. Allopurinol significantly reduced total seizures (p = 0.005), and secondarily generalized seizures (p = 0.0015). Median seizure reduction for total seizures was 10.5 and 27.9% for secondarily generalized seizures. Subjective preferences by clinicians evaluated blindly significantly favored allopurinol. No significant change occurred in the plasma concentration of concomitant AEDs between treatment periods, but serum urate decreased by 32% during allopurinol treatment. No clinically relevant side effects or changes in routine laboratory clinical chemistry or hematology were ascribed to allopurinol.
Lack of dystrophin in
mdx mice leads to muscle fibre degeneration followed by the formation of new myofibres. This degeneration—regeneration event occurs in clusters. It is accompanied by ...inflammation and remodelling of the intramuscular terminal nerve fibres. Since the growth-associated protein B-50/GAP-43 has been shown to be involved in axonal outgrowth and synaptic remodelling following neuronal injury, we have investigated the presence of B-50 in gastrocnemius and quadriceps muscles of
mdx mice. Using immunocytochemistry we demonstrate increased presence of B-50 in terminal nerve branches at motor endplates of
mdx mice, particularly in the clusters of de- and regenerating myofibres. In comparison, the control mice displayed no B-50 immunoreactivity in nerve fibres contacting motor endplates. Our findings indicate that during axonal remodelling and collateral sprouting the B-50 level in the terminal axon arbours is increased although there is no direct injury to the motoneurons.
We suggest that the degenerating target and/or the inflammatory reaction induces the increased B-50 level in the motoaxons. The increased B-50 may be important for sprouting of the nerve fibres and re-establishment of synaptic contacts, and in addition, for maturation and survival of the newly formed myofibres.
The modifications in the CSF content of glutamate and GABA in patients afflicted with primary degenerative dementia (PDD) and olivo-ponto-cerebellar atrophy (OPCA) have been evaluated. Control ...subjects (with disk herniation) were also included in the study. The amino-acids assays were carried out utilizing enzymatic-bioluminescence technique. GABA levels in controls were 803 +/- 98 (n = 7) and in demented patients 702 +/- 98 (n = 7) pmol/ml. Glutamate levels were 2067 +/- 244 (n = 10) in controls, 1190 +/- 81 (n = 16) pmol/ml (vs controls p less than 0.01) in demented patients, and 1116 +/- 146 (vs controls p less than 0.01) in OPCA patients. These results suggest that CSF glutamate levels in severely demented patients might be a result of generalized neuronal loss in the brain with a reactive gliosis.
Twenty-two plasma amino acids were determined by means of ion-exchange chromatography in 16 previously untreated patients with generalized idiopathic epilepsy and in some of their first-degree ...relatives (26 subjects), and the results were compared with those obtained from a group of 50 healthy controls. The patients were subsequently treated with valproic acid for one month and then reexamined. In the epileptic subjects, statistical analysis showed significant alterations in the plasma levels of a group of amino acids, including the four associated with neuro-transmission (aspartate, glutamate, glycine, taurine); aspartate, glutamate and glycine levels were also altered in the first-degree relatives. Valproic acid therapy did not affect amino acid levels. If further confirmed, these alterations might be considered possible neurochemical markers of epilepsy.
The concentration of choline in the cerebrospinal fluid (CSF) of patients affected by primary dementia and in red blood cells (RBC) of depressed patients before and after treatment with lithium salts ...was determined using a chemiluminescent assay. The mean CSF concentration of choline was found to be 60 pmoles/ml (SD = 20 pmoles/ml) and this was lower than values obtained previously by spectrophotometric-colorimetric methods. Mean RBC choline concentrations before and after therapy with lithium salts were 20 nmoles/ml (SD = 16 nmoles/ml and 328 nmoles/ml (SD = 206 nmoles/l) respectively and these are similar to those reported previously (obtained by chemiluminescent and non-chemiluminescent methods).
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