anticonvulsant/atrofia

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[Evaluation of bone atrophy by microdensitometry and effect of active vitamin D3 (1 alpha-OH-D3) administration in patients receiving anticonvulsants].

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Attention has been paid to bone atrophy caused by oral anticonvulsants. Bone atrophy has been judged on X-ray picture in combination with measuring bio-chemical parameters such as serum calcium (Ca), phosphorus (P) and alkaline phosphatase (Alp), and assessing X-ray findings such as bone density and

Multilevel transneuronal degeneration after brain damage. Behavioral events and effects of anticonvulsant gamma-aminobutyric acid-related drugs.

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Recent morphologic and behavioral studies of the effects of gamma-aminobutyric acid agents on transsynaptic degeneration after cortical and striatal damage are reviewed and discussed. Following unilateral lesions of the anteromedial cortex, mild atrophy appears in the ipsilateral striatum and

Folic acid concentrations in cerebrospinal fluid in relation to anticonvulsant drugs and cerebral atrophy.

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[Folic-acid deficiency due to long-term anticonvulsant therapy as a causal factor of cerebellar degeneration (author's transl)].

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Paradoxical deterioration in seizure control due to anticonvulsant-induced hypocalcaemia.

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Hepatic cytochrome P450 enzyme induction is associated with certain antiepileptic drugs (AEDs) and may result in hypocalcaemia secondary to vitamin D deficiency. We report a case of a 44-year-old man with a history of epilepsy, who presented with breakthrough seizures after having previously been

Long term anticonvulsant therapy and cerebellar atrophy.

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Anticonvulsant action of diphenylhydantoin in mice with genetic cerebellar degeneration.

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The Anticonvulsant and Neuroprotective Effects of Oxysophocarpine on Pilocarpine-Induced Convulsions in Adult Male Mice.

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Epilepsy is one of the prevalent and major neurological disorders, and approximately one-third of the individuals with epilepsy experience seizures that do not respond well to available medications. We investigated whether oxysophocarpine (OSC) had anticonvulsant and neuroprotective property in the

Berberine exerts an anticonvulsant effect and ameliorates memory impairment and oxidative stress in a pilocarpine-induced epilepsy model in the rat.

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Though new antiepileptic drugs are emerging, approximately a third of epileptic patients still suffer from recurrent convulsions and cognitive dysfunction. Therefore, we tested whether berberine (Ber), a vegetable drug, has an anticonvulsant property and attenuates memory impairment in a pilocarpine

[Endogenous anticonvulsant and neuroprotective agents].

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Elucidation of the biochemical basis of neuronal degeneration following seizures, ischemia or hypoglycemia appears to be one of the most urgent problems of contemporary science. Close attention has been devoted to endogenous anticonvulsant and/or neuroprotective agents which help to maintain a

Preclinical toxicology of the anticonvulsant calcium valproate.

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The oral toxicity of the anticonvulsant calcium valproate with selected comparisons to valproic acid and sodium valproate was evaluated in mice, rats and Beagle dogs. Median lethal doses of the three forms of valproate in rodents ranged from 1100 to 3900 mg/kg. Clinical signs in acute studies and

Mental deterioration in epilepsy due to folate deficiency.

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Folate deficiency in 50 epileptic children aged 5 to 18 years was treated with a combination of folic acid and vitamin B(12). Improvement in mental condition occurred from five to eight weeks after beginning treatment in some of the younger children; no change was noticed, however, in 31. Similarly,

Valproate and spinal muscular atrophy (Review).

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Childhood spinal muscular atrophy (SMA) is an autosomal recessive disorder caused by mutations in the survival motor neuron (SMN) gene. The severity of the disease is dictated by the copy number of a second copy of the gene, known as SMN2, with higher copy numbers associated with milder forms of

Different effects of valproic acid on photoreceptor loss in Rd1 and Rd10 retinal degeneration mice.

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OBJECTIVE The histone-deacetylase inhibitor activity of valproic acid (VPA) was discovered after VPA's adoption as an anticonvulsant. This generated speculation for VPA's potential to increase the expression of neuroprotective genes. Clinical trials for retinitis pigmentosa (RP) are currently

Anticonvulsant and neuroprotective effects of oligosaccharides from Lingzhi or Reishi medicinal mushroom, Ganoderma lucidum (Higher Basidiomycetes).

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An oligosaccharide fraction isolated from the mycelium of the Lingzhi or Reishi medicinal mushroom Ganoderma lucidum (GLOS) was separated by size-exclusion chromatography. The chemical structure of GLOS consists of a disaccharide repeating unit [-4-β-1-Galf(1-6)-O-(β-Glcp)-1-]n (n=3,4). In addition,

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