Ergotamine dependency--a review.
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Biomedical subjects
Publications and source records attributed to J R Saper.
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Based on our clinical experience and the data reviewed and presented in this report, we propose that a state of physical dependency to ergotamine tartrate exists. This dependency state is characterized by the irresistible and dependable use of ergotamine tartrate and is contingent upon a self-sustaining, rhythmic headache/medication cycle that reflects the dependency. The headache and accompaniments (withdrawal headache?) represent the primary withdrawal symptoms. The presence of this state appears to render patients refractory to other forms of preventative therapy, which can be effective only when ergotamine is discontinued and the cycle broken. If the condition is left untreated, it is likely though by no means certain that the more traditional aspects of ergotism will evolve, although variable susceptibility and tolerance to ergotamine tartrate have been demonstrated. The mechanism of this disorder remains uncertain but might be related to the influence of ergotamine tartrate on the limbic-hypothalamic-pituitary-adrenal axis and other aminergic centers (locus ceruleus), areas considered by some as the central loci for the pathogenesis and associated symptoms of migraine.
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Secondary metabolic encephalopathy is a diffuse disorder of the brain caused by an extracerebral process. Underlying causes include oxygen deprivation, systemic metabolic disease, and drug intoxication. Symptoms and signs usually suggest a generalized disturbance of brain function: alterations in the level of consciousness; diffuse and, occasionally, focal motor abnormalities; and seizures. Electroencephalography in most instances gives evidence of generalized neuronal disturbance. Early diagnosis is important because encephalopathy secondary to an extracerebral process is potentially reversible. Treatment is directed toward reversal or control of the underlying process, supportive care, and prevention of complications such as infection, electrolyte imbalance, and cerebral edema.
A case is reported of a 28-year-old woman with central core disease who prior to muscle biopsy was diagnosed to have muscular dystrophy. Histologic evaluation confirmed a diagnosis of central core disease, a nonprogressive or slowly progressive disorder of voluntary muscle belonging to a group of muscle diseases called benign congenital myopathies. The clinical and pathologic features fo this benign disorder are reviewed. Two sons were examined and found to be normal.
The complications resulting from increased intracranial pressure are serious and include visual impairment, compromise of venous and arterial circulation, and brain herniation. Thus, early diagnosis of increased pressure is essential. The presence of papilledema is important in making the diagnosis; however, important exceptions exist. Diagnostic lumbar puncture is not usually a recommended procedure. The choice of therapeutic agents depends mainly on the urgency of the clinical situation and the clinician's experience. The hypertonic osmotic diuretics rapidly reduce elevated intracranial pressure but, with the exception of glycerol, must be restricted to urgent situations because of complications associated with their use.
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