Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old woman hit her head during an automobile accident and was admitted to the hospital. One week later magnetic resonance imaging (MRI) showed a right frontal/parietal lesion. Among the behavioral sequelae were mild ataxia with trunkal instability and dysfluent speech accompanied by prominent shaking of the right leg, face and neck tension, and facial twitching. The speech-language pathologist thought the patient was not aphasic but rather was stuttering and treated her for about a month with pacing and "easy onset" techniques to which she showed fair response. The diagnostic question in this case is whether the stuttering was the result of the brain damage (neurogenic) or of the stressful events she had experienced (psychogenic). In this article we review her case and the process we used in arriving at an "expert" opinion.
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PMID:Sudden onset of "stuttering" in an adult: neurogenic or psychogenic? 951 89

If gallamine or d-tubocurarine gains access to the central nervous system it produces a myoclonus, a synchronized jerking of many skeletal muscles. Each jerk is accompanied by a slow wave in the inferior olive. The jerking continues for 24 h or more after the gallamine or d-tubocurarine can no longer be detected in the CSF. We report here that a novel substance appears in the CSF and persists for a long period of time, possibly as long as the twitching. This substance is not corticotrophin-releasing factor (CRF) nor does CRF or harmaline (a substance causing a tremor by an action on the inferior olive) lead to the appearance of the novel substance. At present the nature of this substance is not known.
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PMID:A novel substance associated with gallamine-induced myoclonus. 963 27

Theophylline toxicity has been recognized since its introduction into clinical medicine. Clarithromycin is a new oral macrolide antibiotic with excellent antibacterial activity and rare adverse effect. Patients with upper respiratory infection are often treated with theophylline and clarithromycin concurrently. We report a case of acute renal failure due to acute rhabdomyolysis caused by the interaction of theophylline and clarithromycin. A 72-year-old man visited our hospital because of coughing and a sore throat continuing for 1 week. He was diagnosed as having the common cold with a bronchial asthmatic symptom and was prescribed 200 mg/day of sustained-release theophylline for the treatment of asthma for 7 days. One week later, he visited our hospital again. Radiographic study of the chest revealed mild interstitial pneumonia and 200 mg/day of sustained-release theophylline and 400 mg/day of clarithromycin were administrated concomitantly. Five days after the second visit, the patient was admitted to our hospital because of generalized twitching, muscular weakness, high fever and serious general condition. He experienced generalized muscular twitching and tremor. Blood urea nitrogen was 106.1 mg/dl, serum creatinine was 7.4 mg/dl, serum creatinine kinase (CK) was 36,000 IU/l (normal 15-130 IU/l), CK isozyme revealed the following ratio: BB 0%, MB 1% and MM 99%. He was diagnosed as having acute renal failure with rhabdomyolysis caused by the interaction of theophylline and clarithromycin. Hemodialysis therapy was started. After 5 weeks, his serum creatinine was markedly decreased. It is well-known that clarithromycin enhances the serum concentration of theophylline by inhibition of the cytochrome P450-dependent pathway in hepatocytes. Theophylline toxicity may be enhanced when clarithromycin is administrated concomitantly, especially to elderly patients with dehydration.
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PMID:[A case of acute renal failure with rhabdomyolysis caused by the interaction of theophylline and clarithromycin]. 1044 97

The most venomous scorpion species are Buthotus tamulus of India, the Leiurus quinquestriatus and Androctonus crassicauda of North Africa and the Middle East, the Tityus serrulatus of Brazil, and the Centruroides suffussus of Mexico. The severity of scorpion envenomation varies with the scorpion's species, age, and size, and is much greater in children. Systemic intoxication reflects the overstimulation of the CNS, the sympathetic and parasympathetic nervous system. Severity ranges from local pain and paresthesia to fatal cardiotoxicity and encephalopathy. Symptoms include: agitation, tachycardia, vomiting, abdominal pain, salivation, diaphoresis, dehydration, muscle rigidity and twitching, tremor, seizures, coma, pupillary changes, hyperthermia, tachyarrythmias and occasionally bradyarrhythmias, hypertension, and less often hypotension, cardiac failure, and priapism in males. Laboratory abnormalities include: hyperglycemia, leucocytosis, transient elevation of cardiac and pancreatic enzymes, ischemic changes in the ECG, and evidence of cardiac dysfunction on echocardiography. The principles of management are: observation, cardiac monitoring, supportive treatment with intravenous fluids and electrolytes, and a meticulous use of cardiovascular agents: vasodilators, adrenergic antagonists, or calcium channel blockers in the hypertensive phase; and inotropic agents in the event of hypotension. Antiarrhythmics such as lidocaine, may be required. There is increasing evidence for the efficacy of specific antivenom. The advance in supportive care and antivenom efficacy has markedly improved the outcome of patients with scorpion envenomation.
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PMID:Clinical manifestations and management of scorpion envenomation. 1044 63

X-linked bulbospinal neuronopathy (XLBSN) or Kennedys disease is a rare inherited neuromuscular disease characterized by adult-onset muscle weakness, usually in a limb-girdle distribution. It is frequently misdiagnosed despite a distinctive clinical presentation, usually due to the absence of a clear family history, and perhaps also due to failure of recognition. Accurate diagnosis is crucial for genetic counseling purposes and because alternative diagnoses usually carry a poorer prognosis. We evaluated 4 patients with XLBSN and one symptomatic female heterozygote patient. Based on our clinical observations in these patients and a systematic review of previously reported cases, the following clinical and electrophysiologic features when present in the setting of adult-onset muscle weakness, are strongly suggestive of the disorder: 1) facial weakness, 2) facial twitching or fasciculations, 3) tongue weakness and atrophy, 4) postural hand tremor, 5) hypo- or areflexia, and 6) absent or low-amplitude sensory nerve action potentials despite clinically normal sensation. We also hypothesize regarding the possibility of partial expression of the abnormal XLBSN gene in a symptomatic heterozygote female patient.
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PMID:Distinguishing clinical and electrodiagnostic features of X-linked bulbospinal neuronopathy. 1056 82

It has been reported that mutations in the quorum-sensing genes lasI and rhlI in Pseudomonas aeruginosa result in, among many other things, loss of twitching motility (A. Glessner, R. S. Smith, B. H. Iglewski, and J. B. Robinson, J. Bacteriol. 181:1623-1629, 1999). We constructed knockouts of lasI and rhlI and the corresponding regulatory genes lasR and rhlR and found no effect on twitching motility. However, twitching-defective variants accumulated during culturing of lasI and rhlI mutants. Further analysis showed that the stable twitching-defective variants of lasI and rhlI mutants had arisen as a consequence of secondary mutations in vfr and algR, respectively, both of which encode key regulators affecting a variety of phenotypes, including twitching motility. In addition, when grown in shaking broth culture, lasI and rhlI mutants, but not the wild-type parent, also accumulated unstable variants that lacked both twitching motility and swimming motility and appeared to be identical in phenotype to the S1 and S2 variants that were recently reported to occur at high frequencies in P. aeruginosa strains grown as a biofilm or in static broth culture (E. Deziel, Y. Comeau, and R. Villemur, J. Bacteriol. 183:1195-1204, 2001). These results indicate that mutations in one regulatory system may create distortions that select during subsequent culturing for compensatory mutations in other regulatory genes within the cellular network. This problem may have compromised some past studies of regulatory hierarchies controlled by quorum sensing and of bacterial regulatory systems in general.
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PMID:Quorum sensing is not required for twitching motility in Pseudomonas aeruginosa. 1205 54

A distinct high-voltage rhythmic spike (HVRS) discharge characterized by a barrage of negative spikes oscillating at 5-12 Hz was observed in chronically implanted Long Evans rats. Spontaneous HVRS discharges were exhibited in 90% of 40 Long Evans rats and occurred during sudden arrest of ongoing behavior (immobility) with occasional facial/whisker twitching. However, the function of HVRS discharges in Long Evans rats remains inconclusive to date and has been associated with alpha tremor/mu rhythm, attentive mu wave, and absence seizure. To elucidate the function of HVRS discharges in Long Evans rats, several experiments were performed. In a 6-h recording session (12:00-18:00), HVRS activities primarily occurred in several specific vigilance states, being particularly abundant in a short-lasting period before vigilance changes. Several characteristics, such as durations, oscillatory frequencies, and interspike intervals (ISIs) of HVRS discharges, were altered during wake-sleep states. Oscillatory frequencies were negatively correlated with durations of HVRS segments. In addition, ISIs of a HVRS episode exhibited a crescendo-decrescendo pattern. These variable ISIs could explain why a negative correlation was found between oscillatory frequencies and durations of HVRS episodes. Moreover, HVRS discharges were demonstrated to have widespread and near-synchronous distribution to bilateral cortical areas. In addition, innocuous electrical stimuli were unable to stop ongoing HVRS discharges. By contrast, noxious stimuli elicited behavioral arousal and immediately terminated most HVRS discharges. Cortical-evoked potentials in response to mild electrical stimulation under HVRS discharges were different from those under waking state but resemble those under slow-wave sleep with a smaller magnitude. Moreover, the temporal and spectral characteristics of spontaneous HVRS activities were analogous to those of seizure activities induced by penicillin and pentylenetetrazol. The incidence of spontaneous HVRS discharges was significantly decreased by ethosuximide administration. Based on these results, HVRS discharge might not be associated with a voluntary mu-rhythm behavior, instead it behaves as an absence-like seizure activity. These results were also collaborated using other genetic absence-seizure rats, such as WAG/Rij and GAERS rats. Possible mechanisms for the generation and termination of paroxysmal HVRS discharges are also discussed.
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PMID:Is spontaneous high-voltage rhythmic spike discharge in Long Evans rats an absence-like seizure activity? 1282 56

This study examined the nociceptive effects of the intrathecal administration of various doses of the following endogenous excitatory sulphur-containing amino acids (SAAs): L-cysteic acid (L-CA), L-cysteine sulfinic acid (L-CSA), L-homocysteic acid (L-HCA) and L-homocysteic sulfinic acid (L-HCSA). For a period of 10min, rats were observed for spontaneous nociceptive behaviours (SNBs), including: tail elevation, twitching or licking; hindpaw elevation, licking or shaking; and caudally directed biting or scratching. The amount of time each rat spent eliciting these individual behaviours was recorded and a total time (in seconds) spent exhibiting SNBs was then calculated. To determine which glutamate receptors are primarily responsible for these nociceptive behaviours, we pretreated additional groups of rats with selective antagonists for N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid/kainate (AMPA/KA) and group I metabotropic glutamate receptors (mGluR1 and 5). Results indicate that SAAs dose-dependently produce SNBs that are attenuated by NMDA receptor and group I mGluR antagonists.
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PMID:Nociceptive effects of intrathecal administration of sulphur-containing amino acids. 1294

Paroxysmal 5- to 12-Hz high-voltage rhythmic spike (HVRS) activities, which are accompanied by whisker twitching (WT), are found in Long Evans rats, but the function of these HVRS activities is still debated. In four major functional hypotheses of HVRS discharges, i.e., alpha tremor, attention/mu rhythm, idling/mu rhythm, and absence seizure, the first two hypotheses emphasize WT behavior in HVRS bouts. Whisker movement is primarily determined by activation of intrinsic and extrinsic muscles. To clarify the role of WT in HVRS activities, simultaneous recording of the activities from the cortex and intrinsic/extrinsic and neck muscles were performed. Most HVRS bouts (68.8%) revealed no time-locked WT behavior in a 2-h recording session. In addition, WT primarily arose from active protraction due to activation of intrinsic muscles followed by passive retraction. A small portion of WT resulted from activation of both vibrissae muscles with dynamic frequency-dependent phase shifts. Onset of the rhythmic vibrissae EMG significantly lagged behind HVRS onset, and the mean duration of vibrissae muscle activity was one-third to a one-half of a HVRS bout. Moreover, a greater number of HVRS bouts were associated with a longer HVRS duration and higher oscillation frequency. Oscillation frequencies of HVRS activities without WT behavior were significantly lower than those with WT. Under peripheral sensory/motor blockade by xylocaine injection, oscillation frequencies of HVRS bouts significantly decreased, but no remarkable changes in the number or duration of HVRS bouts were observed. Compared with vibrissa muscle activity during WT and exploratory whisking, the duration of muscular activity in each cycle was apparently longer during whisking bouts. Based on these results, overemphasis of the role of WT on HVRS activities might not be appropriate. Instead, HVRS discharges may be associated with absence seizure or idling state. In addition, peripheral inputs, including WT, may elevate the oscillation frequency of HVRS bouts. Moreover, different muscular controls may exist between WT and whisking.
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PMID:Relation between activities of the cortex and vibrissae muscles during high-voltage rhythmic spike discharges in rats. 1562 92

A three year old Quarter Horse stallion was presented with a one year history of episodes of generalized muscle tremors and stiffness, and spasm of the muscles of facial expression, lasting 10-15 minutes. Between attacks, the horse was either normal or had a localized muscle tremor in the flank region. Episodes appeared unrelated to exercise. The major abnormal findings included 1) a rise in plasma potassium from a resting level of 4.4 to 7.9 mmol/L during an attack and 2) electromyographic findings of generalized increased insertion activity and myotonic discharges. The horse was treated with hydrochlorothiazide tablets for nine months, during which time no further attacks were noted. However, four months after the drug was stopped, sporadic focal muscle tremors reappeared; two months later, generalized attacks were seen. Despite reinstitution of the diuretic, a focal flank tremor persisted. Two related horses in the same stable also were reported by the owner to exhibit sporadic generalized muscle twitching. The abnormal findings of the present case differ from clinical syndromes previously reported in horses. Some similarities to hyperkalemic periodic paralysis in humans are noted.
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PMID:Episodic muscle tremors in a quarter horse: resemblance to hyperkalemic periodic paralysis. 1742 93


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