Innovative approach to headaches.
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Biomedical subjects
Publications and source records attributed to G A Mellick.
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Two patients presented with life-threatening motor paresis after ingestion of leaves from the tree tobacco plant (Nicotiana glauca ). In addition to severe muscle weakness, bulbar palsies, flexor muscle spasm, hypertension, nausea, vomiting, and respiratory compromise were reported or observed. These are the fourth and fifth reported cases of a toxicologic emergency apparently caused by the alkaloid, anabasine, an isomer of nicotine found in the tobacco tree plant. The effects of this plant ingestion can mimic other better-known causes of paresis or paralysis. In areas of the country where the plant is indigenous, this toxicologic condition should be considered in the differential diagnosis of patients presenting with paresis or paralysis.
The authors report rapid cluster headache relief in a 43-year-old man with a 5-year history of refractory cluster headache. The patient described complete headache relief within 10 minutes of taking 10 mg of methylphenidate (Ritalin) when used to abort the onset of his headaches. Subsequently, a scheduled Ritalin dose taken each morning was sufficient to prevent his nightly headaches. In addition, 1 week of prophylactic methylphenidate therapy halted the series of cluster headaches. This is the first reported case of relief of cluster headaches with methylphenidate.
The use of the recently released anticonvulsant, gabapentin (Neurontin), in the treatment of severe and refractory reflex sympathetic dystrophy (RSD) pain in six patients ranging in age from 42 to 68 years is reported. Satisfactory pain relief obtained in all six patients suggests that this medication is an effective treatment for RSD pain. In addition to pain control, early evidence of disease reversal in these patients is suggested. Patient 6 is the first documented case of successful treatment and cure of the RSD pain syndrome using gabapentin alone. Specifically, reduced hyperpathia, allodynia, hyperalgesia, and early reversal of skin and soft tissue manifestations were noted. Gabapentin was chosen because it has properties similar to other anticonvulsant drugs and because previous studies have shown that it is well tolerated and appears to have a benign efficacy-to-toxicity ratio. It was considered an acceptable and compassionate therapeutic choice because previous medical and surgical approaches had been ineffective for these patients, who represent the first case series documenting the use of gabapentin for pain management. Presently, the mechanism of pain relief in these patients is unknown. In this article, the pathophysiology of RSD is discussed, and a mechanism by which gabapentin provides pain relief is proposed. In view of encouraging results in these and other RSD patients, further scientific investigation is needed to delineate the role of gabapentin in the treatment of reflex sympathetic dystrophy.
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Medical treatment of hemifacial spasm has generally been ineffectual. This report describes a 36-year-old man with a 7-year history of right hemifacial spasm who responded to felbamate (Felbatol) at doses of 1800-2800 mg per day. During treatment, he was able to achieve complete control of all spontaneous facial muscle spasms at rest. Activated hemifacial spasms, initiated by chewing, speaking, smiling, or grimacing were reduced in frequency and intensity of contraction by 40%-50%. Spontaneous worsening of the hemifacial spasms occurred at a dose of 3600 mg/day. Control of the hemifacial spasm was regained at a lower dose. This is the first reported use of felbamate for the control of hemifacial spasm. Microvascular decompression of the facial nerve has been the only known effective treatment for this condition. Successful felbamate therapy would provide an alternative to those patients for whom surgery is not a treatment option.
A 15-year-old boy ingested 19.6 g (15 g verifiable) phenytoin sodium approximately four hours before emergency department presentation. The patient survived the suicide attempt with only supportive care, despite the ingestion of 392 mg/kg and a peak serum level of 100.8 micrograms/mL. A wide spectrum of physical findings consistent with acute massive ingestion of phenytoin was noted. This case report and a review of cases reported in the English literature of acute single anticonvulsant ingestion further delineate the clinical presentation of acute phenytoin overdose.
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