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At least 739 records · Page 41Linked to original sources
PubMed1985

Therapeutic blood levels of phenytoin in treatment of paroxysmal choreoathetosis.

Eight patients with paroxysmal choreoathetosis received phenytoin therapy, starting from 50 mg of oral phenytoin with a gradual increment of the dose. After successful control of the paroxysmal attacks, blood levels of phenytoin in these patients were measured by enzyme immunoassay. The mean phenytoin blood level was 5.2 +/- 3.2 micrograms/ml, with a range of 1.1-10.9 micrograms/ml. It is proposed that phenytoin can be maintained at a lower level in the treatment of paroxysmal choreoathetosis than in seizure control.

Adolescent↗
PubMed1988

Choreoathetosis induced by ordinary phenytoin levels, explained by high free fraction?--A case report.

Choreoathetosis was induced by phenytoin therapy in an 81-year-old epileptic woman. The plasma concentration of phenytoin was 59 to 80 mumol/L when side effects appeared. Choreoathetosis at ordinary plasma levels has previously been attributed to a preexisting brain damage. In this case, however, it may be explained by a high free fraction (19%) of the phenytoin plasma concentration.

Aged↗
PubMed2000

Paroxysmal dyskinesias as a paradigm of paroxysmal movement disorders.

Paroxysmal dyskinesias are genetically and clinically heterogeneous. Paroxysmal kinesigenic choreoathetosis is frequently familial, with autosomal-dominant transmission. Benign infantile convulsions can be observed in these families and both diseases as linked to the pericentromeric region of chromosome 16. Two different forms of paroxysmal dystonic choreoathetosis are distinguished on clinical grounds, by the presence or absence of spasticity, and genetically, as they are linked with loci on different chromosomes. Among the paroxysmal disorders, these diseases may belong to the group of channelopathies.

Athetosis↗
PubMed2005

Surgical treatment of cervical myeloradiculopathy associated with movement disorders: indications, technique, and clinical outcome.

OBJECTIVE: Movement disorders may be associated with advanced cervical myeloradiculopathy, which represents a major management challenge. We report on eight patients with movement disorders causing progressive cervical myeloradiculopathy who were treated successfully by cervical decompression and reconstruction. RESULTS: The mean age of our patients was 44 years with a male/female ratio of 3:1. The average duration of symptoms prior to presentation was 10 months. The most common levels decompressed and reconstructed were C3-C4 and C4-C5. Six cases showed improvement, and two cases showed stabilization of neurologic status at a mean follow-up of 21 months. Our management strategy and results are interpreted in the context of a systematic review of the literature in which 78 cases are reported. CONCLUSIONS: Movement disorders cause premature cervical spondylosis most commonly involving the C3-C4 and C4-C5 levels. Ventral pathology with kyphotic angulation requires corpectomy or discectomy with or without posterior decompression and reconstruction. Decompression should always be combined with segmental internal fixation. Perioperative use of botulinum toxin and halo vest immobilization can increase the rate of clinical success but requires vigilance to minimize complications. Laminectomy with lateral mass fixation may be used successfully in the absence of kyphotic deformity.

Adult↗
PubMed1982

Dyskinesias: nursing care and surgical intervention.

The dyskinesia syndromes are a group of physically, socially and psychologically debilitating diseases. Many patients may be helped through medical management consisting of drugs, physical and speech therapy, and vocational rehabilitation. However, when medical management fails to palliate symptoms, surgical intervention may be the patient's alternative. The ultimate goal of therapy is to lead an improved quality of life. As a neurosurgical nurse, you have an important role in achieving that goal.

Activities of Daily Living↗
PubMed1977

Choreoathetosis during phenytoin treatment.

A patient with symptomatic epilepsy receiving only phenytoin developed choreoathetosis and orofacial dyskinesias. These movement disorders disappeared when the drug was stopped and reappeared when the patient was challenged. Throughout the period of treatment, concentrations of phenytoin in serum were consistently low within the therapeutic range. Interfering symptoms from the cardiovascular system and the absence of some classic symptoms of phenytoin intoxication (nystagmus and dysarthria) contributed to delay the diagnosis. The patient died in hospital and autopsy of the brain showed rather localized encephalomalacies of corpus striatum. The pathogenic action of phenytoin and the role of preexisting brain lesions are discussed. Phenytoin must be suspected as the cause, when patients on this drug present with uncontrolllable epilepsy or neurological or mental deterioration.

Aged↗
PubMed1989

Electroencephalographic findings of hereditary dentatorubral-pallidoluysian atrophy (DRPLA).

The electroencephalograms (EEGs) of 22 patients suffering from hereditary DRPLA were studied. Epileptoform patterns were observed in 14 patients (63.6%) with epileptic seizures. The epileptoform patterns most frequently observed were those atypical spike-wave complexes. Slow wave bursts were seen in 18 patients (81.8%). Photosensitivity was revealed in six (27.3%) patients, all of whom presented progressive myoclonus epilepsy (PME) syndrome. Abnormal background activity was evident in 17 (77.3%) patients. These abnormalities in EEG were more severe in patients in the PME type than those of the A (ataxia) and AE (ataxia and epilepsy) types.

Adolescent↗
PubMed1995

Paroxysmal kinesigenic choreoathetosis associated with prenatal brain damage.

We describe a 15 year old patient with paroxysmal kinesigenic choreoathetosis. Neurological examinations revealed a paresis of the right arm and hand that was similar to ulnar nerve palsy, a right homonymous hemianopsia and an ocular movement disturbance of smooth pursuit to left. Attacks of dystonic spasms began abruptly, usually following running, and lasted less than 5 min. Magnetic resonance imaging displayed a linear area of increased signal in the T2-weighted images along the lateral margin to the left putamen, atrophies of the frontal and temporal opercula and a large porencephalic cyst in the left parieto-temporo-occipital region. A cerebral blood flow study with single photon emission computed tomography showed hypoperfusion of the lenticular nucleus and the regions corresponding to the atrophies and the porencephalic cyst. Electroencephalograms during the attacks could not demonstrate epileptic abnormality. Only the neuronal plasticity of an immature brain could explain the discrepancy between the observed huge lesions of the brain and the minor neurological symptoms present. Attacks of paroxysmal kinesigenic choreoathetosis might occur when the basal ganglia maturate to some extent, even if the lesions in the brain were caused before birth.

Adolescent↗