We performed a double-blind, placebo-controlled, crossover study to assess the effect of amantadine versus placebo on levodopa-induced dyskinesias in Parkinson's disease. We found a 24% reduction in the total dyskinesia score after amantadine administration (p = 0.004). This improvement was achieved without any influence on the severity of "on" period parkinsonism. The results confirm that amantadine reduces levodopa dyskinesias and support the hypothesis that dyskinesias can be reduced by blockade of excitatory pathways in the basal ganglia.
Hypoglycemia produced hemiplegia with right-sided predilection in 16 patients initially suspected of having suffered a stroke. Fifteen patients had no demonstrable brain disease, and the hemiplegia cleared rapidly once the hypoglycemia was corrected. Invasive investigations such as carotid arteriography are not required in most patients. The features of hypoglycemia hemiplegia suggest that a selective neuronal vulnerability and not underlying focal brain disease is responsible in most cases.
In a 16-year-old woman with systemic lupus erythematosus (SLE) and receiving a stable dose of sodium valproate (VPA) for the treatment of idiopathic generalized epilepsy, two episodes of severe aseptic meningitis developed after treatment with lamotrigine (LTG). Both episodes of aseptic meningitis resolved after discontinuation of LTG. Extensive investigations failed to disclose any other cause than a hypersensitivity reaction to LTG.Aseptic meningitis can occur as a rare reaction to several medications, most commonly nonsteroidal antiinflammatory drugs, trimethoprim-sulfamethoxazole, and intravenous immunoglobulin. We present a case of recurrent aseptic meningitis after exposure to LTG.A 16-year-old woman with idiopathic generalized epilepsy with tonic-clonic seizures was first seen with fever and headache after starting LTG, 25 mg, on alternate days in addition to her regular 1 g daily of VPA. She was not taking a nonsteroidal antiinflammatory drug or any other medication. Eighteen months earlier, SLE was suspected on the basis of hemolytic anemia, thrombocytopenia, antinuclear antibody titer >1:2,560 with a speckled staining pattern, and positive anti-double-stranded DNA, anti-Ro, and anti-La antibodies. Anti-Sm and anticardiolipin antibody testing was negative. She met three of the 11 American Rheumatism Association criteria for SLE (1). Her first generalized tonic-clonic seizure occurred at age 8 years. Electroencephalography showed several brief bursts of generalized spike and polyspike-and-wave complexes during hyperventilation and drowsiness consistent with primary generalized epilepsy. She remained seizure free until age 15 years, after which she had frequent generalized tonic-clonic seizures. VPA, 2 g/day was required
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