Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 38-year-old man was admitted to Iwakuni National Hospital on July 6, 1978, with the complaints of difficulty seeing and walking. Two weeks before admission, he first experienced dizziness and it slowly progressed to uncontrollable tremor-like movements of the whole body. On admission, he was alert, oriented and afebrile. He had not experienced nausea, vomiting nor headache. He showed irregular horizontal oscillations of the eyes. Electronystagmographic study showed that this jerky eye movement appeared especially with changes of fixation of the eyes. It was also recorded during conjugate eye movement, and while he closed his eyes. He was ataxic, unable to walk, but no other abnormalities in cerebellar functions were observed. Spinal tap was performed and yielded watery clear cerebrospinal fluid containing 9/mm3 mononuclear cells. Clonazepam was given, 1.5 mg per day, for three days followed by doses of 3 mg per day. Improvement in walking was observed one week after starting the medication, when reserpine was started at a dose of 1 mg per day and increased to a dose of 1.5 mg per day in three days. One week after starting reserpine, opsoclonus improved markedly and he became able to read again. He was discharged home on September 3, 1978. Six months after admission, reserpine was decreased to 0.5 mg per day. Difficulty in reading developed within a month. Reserpine was given 1.0 mg per day and the doses was continuously given for next three months. One year after admission, he is back to his former occupation without medication. He complains of slight difficulty in reading for more than an hour, and in watching TV.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Opsoclonus-polymyoclonia syndrome suppressed with reserpine]. 371 80

A healthy young woman underwent arthroscopy of the right knee, for which she was given an enflurane anaesthetic. The anaesthetic was uneventful, but she started to show myoclonic jerky movements involving multiple muscle groups, except those innervated by the cranial nerves, while recovering from the anaesthetic. These jerky movements settled to the left side of her body. It was also associated with significant right frontal and retro-orbital headache. Serial neurological assessments were entirely negative. These symptoms took more than 48 hours to disappear. She recovered from this anaesthetic complication completely. An anaesthetic complication of this nature and duration has not been reported before in association with enflurane.
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PMID:Prolonged myoclonic contractions after enflurane anaesthesia - a case report. 744 13

A 38-year-old woman had an episode of headache, fever and convulsion in October, 1993. She became alert in two weeks, though weakness and atrophy remained in the upper limb muscles. She was diagnosed as Russian spring summer encephalitis (RSSE) based on several serological studies. Three kinds of involuntary movements were noted after recovery. These were spontaneous muscle jerks in the left arm, action tremor in the right arm and pathological associated-movement in the right leg. The movements were studied physiologically by electroencephalogram (EEG)-electromyogram (EMG) polygraphic recordings, jerk-locked averaging (JLA), magnetencephalography (MEG), and sensory evoked potentials (SEPs). The jerky movements in her left arm were observed at rest and aggravated by emotional stress. EEG-EMG polygraph showed that the jerks were sometimes associated with small spikes thus were considered to be due to epilepsia partialis continua (EPC). JLA analysis revealed a pre-myoclonus spike on the right hemisphere which preceded the onset of the jerk in the left first dorsal interosseous muscle by 25.2ms, which was equal to the magnetic cortical latency of that muscle. Jerk-locked magnetic field, obtained by averaging neuromagnetic activities with respect to the onset of myoclonus, showed that the spike preceding the jerk, originated from the right motor cortex. The spontaneous spikes were localized mainly on the right motor cortex. Sensory evoked potentials (SEPs) were normal in both size and latency. No hyperexcitability of the sensory cortex was demonstrated even by using paired stimulation SEPs. Based on these results, we conclude that the jerky movements in this patient were produced by abnormal spontaneous discharges in the motor cortex. The action tremor had a frequency of 4-5 Hz and its clinical features were compatible with cerebellar tremor. This is thought to result from a lesion in the left thalamus, affecting the cerebellothalamic pathways. Her right leg unintentionally moved whenever she began to move the hands. This was considered to be a pathological associated-movement due to dysfunction of the pyramidal tracts.
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PMID:[Involuntary movements observed in a patient with Russian spring summer encephalitis]. 881 Aug 52

Epileptic nystagmus is a quick, repetitive, jerky movement of the eyeball caused by seizure activity, which is unaccompanied by other ictal phenomena. We report a case of moyamoya disease with epileptic nystagmus. A 23-year-old woman presented with a headache and transient hemiparesis on her left side. Magnetic resonance imaging showed no ischemic or hemorrhagic stroke lesions. Digital subtraction angiography confirmed stenosis of the terminal portion of the right internal carotid artery and the formation of moyamoya vessels on the right side. 123I-N-isopropyl-iodoamphetamine (123I-IMP) single photon emission computed tomography (SPECT) showed decreased uptake in the right basal ganglia, frontal, and parietal regions. After electroencephalography (EEG) and a hyperventilation test were performed, nystagmus appeared and was accompanied with a declining level of consciousness. Ictal EEG during an attack showed no epileptiform discharge. Moreover, the patient sometimes experienced simultaneous upper limb-shaking and gelastic attacks. After superficial temporal artery to middle cerebral artery bypass surgery was performed on the right side, symptom frequency and duration gradually decreased. Decreased 123I-IMP SPECT blood flow in the right frontal region is considered a mechanism that causes the onset of epileptic nystagmus. It is presumed that the attack was caused by an ischemic abnormality in the saccade region of the frontal eye field. Moreover, revascularization can effectively treat the symptoms of moyamoya disease.
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PMID:Moyamoya disease with epileptic nystagmus: A case report. 3143 86