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)

We prospectively examined 11 patients with magnetic resonance imaging-documented infarction in the paramedian thalamopeduncular region, which is supplied by the superior mesencephalic and posterior thalamosubthalamic arteries. Variations in the size and rostral-caudal extent of infarction correlated with the following three clinical patterns: (1) With unilateral paramedian mesencephalic infarction, an ipsilateral third nerve paresis was accompanied by mild contralateral hemiparesis or hemiataxia. Contralateral ptosis and impaired upgaze were observed in two patients; one of them showed additional damage to the posterior commissure. (2) With bilateral infarction in the thalamopeduncular junction, involving the mesencephalic reticular formation, supranuclear vertical gaze defects were accompanied by impaired consciousness or memory, and mild aphasia in some patients. Persistent amnesia was observed only when the dominant anterior nucleus or mamillothalamic tract was damaged. (3) With larger thalamopeduncular infarcts, partial or complete third nerve paresis was combined with supranuclear gaze disturbance and delayed contralateral tremor. An unusual gaze disorder, a variant of the vertical "one-and-a-half syndrome," occurred with a small strategically placed lesion at the thalamopeduncular junction, best explained by selective damage to supranuclear pathways or partial nuclear involvement. The primary cause of these infarctions was embolism to the basilar apex or local atheroma at the origin of the posterior cerebral artery.
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PMID:Paramedian thalamopeduncular infarction: clinical syndromes and magnetic resonance imaging. 151 Mar 56

Effects of FKS-508 (AF102B; cis-2-methylspiro (1,3-oxathiolane-5,3')-quinuclidine), a novel M1-selective agonist, on central muscarinic responses in mice were examined in comparison with oxotremorine. FKS-508 was slightly less potent (6 times) in reversal of scopolamine-induced amnesia (passive avoidance failure), but far less potent (260 and 55 times) in producing hypothermia and tremor than oxotremorine. These results show that the selective M1 agonist FKS-508 differentiates highly between the central muscarinic effects.
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PMID:Central muscarinic activities of an M1-selective agonist: preferential effect on reversal of amnesia. 230 75

Flunarizine hydrochloride (FZ), a calcium entry blockade, has been used nationwide in Japan as a cerebral active vasodilator since October, 1984. The present paper reports 31 cases of FZ-induced Parkinsonism, depression and akathisia, referred to our hospital between October 1986 and September 1988. Out of the 31 patients, four including two with Parkinson's disease and one each with progressive supranuclear palsy and olivopontocerebellar atrophy showed worsening of their parkinsonian symptoms within a few months after FZ administration. The remaining 27 patients (7 males and 20 females) newly developed Parkinsonism after treatment with FZ. Symptoms appeared one week to two years (mean: 6.1 months) after starting FZ of a daily dose of 10 mg. FZ had been used in 6 patients for cerebrovascular episodes confirmed by clinical history or brain CT, and in the remainder, for dizziness, light-headedness, hypertension, amnesia or hypochondric neurotic complaints. Akinesia and bradykinesia progressed rather rapidly after onset, and patients became unambulatory within several months. Symptoms had worsened, and L-dopa, anticholinergic drugs, and bromocriptine had been ineffective until FZ was discontinued. Their Parkinsonism was characterized by marked akinesia, bradykinesia, and moderate rigidity. Masked face was seen in most of them. Tremor was absent at rest, and induced in 12 patients by posture and/or action. Sixteen patients were accompanied by depression, and five, by akathisia. Improvement began several weeks after withdrawal of FZ, and most patients recovered almost completely within a few months although mild rigidity and bradykinesia remained in some.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parkinsonism, depression and akathisia induced by flunarizine, a calcium entry blockade--report of 31 cases]. 258 81

We recently found that glucose injections attenuate amnesia and hyperactivity produced by scopolamine, a muscarinic antagonist. The present study examined whether glucose would augment behavioral effects produced by a muscarinic agonist, physostigmine. In experiment I, doses were first determined for which neither glucose (10 mg/kg) nor physostigmine (0.05 mg/kg) altered scopolamine-induced hyperactivity. However, combined glucose-physostigmine injections significantly reduced scopolamine hyperactivity. Experiment II evaluated the effects of glucose on physostigmine-induced tremors. Glucose (10, 100, and 250 mg/kg) or saline injections were given 20 min before physostigmine injections (0.4 or 0.05 mg/kg). Observations of glucose effects on the severity of physostigmine-induced tremors were then obtained at 5-min intervals for 25 min after physostigmine injections. Glucose (100 mg/kg) significantly facilitated the onset of tremors when injected before either dose of physostigmine, and augmented (at 100 and 250 mg/kg) tremor severity when injected before the lower dose of physostigmine. These findings indicate that glucose can facilitate the actions of a cholinergic agonist on two behaviors, locomotor activity and tremors, adding support to the view that circulating glucose levels can modulate central cholinergic function. More generally, the results provide additional evidence that circulating glucose levels can influence brain function.
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PMID:Blood glucose and brain function: interactions with CNS cholinergic systems. 320 15

The effects of a wide range of doses of systemically administered cysteamine were studied on locomotor behavior, passive avoidance memory, cortical and cerebrospinal fluid somatostatin-like immunoactivity and cortical levels of dopamine and norepinephrine. High doses of cysteamine (200 and 250 mg/kg s.c.) led to sustained locomotor activation. Doses of 150 mg/kg and above resulted in head and neck tremor and increased defecation. When cysteamine was administered immediately following the acquisition of a passive avoidance response, doses of 50 mg/kg and above resulted in significant attenuation of passive avoidance retention test performance. Cysteamine in doses of 50 mg/kg and above depleted cortical somatostatin-like immunoactivity by approximately 50%. The depletion of cortical somatostatin-like immunoactivity was accompanied by a rapid rise in somatostatin-like immunoactivity in cerebrospinal fluid. In addition to the depletion of somatostatin-like immunoactivity, high doses of cysteamine (150 mg/kg and above) produced changes in cortical levels of norepinephrine and dopamine, reminiscent of dopamine-beta-hydroxylase inhibition. The results of this series of experiments suggest that somatostatin, in addition to its effects on hormonal regulation, may play an important role in behavior and passive avoidance learning and memory. It is possible that the amnesia produced by cysteamine may have been due to the release of somatostatin into CSF from tissue stores, rather than somatostatin depletion per se. It is also possible that the catecholaminergic effects of high doses of cysteamine contribute to the behavioral deficits observed.
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PMID:Cysteamine-induced depletion of central somatostatin-like immunoactivity: effects on behavior, learning, memory and brain neurochemistry. 382 20

Effects of MCI-225, [4-(2-fluorophenyl)-6-methyl-2-(1-piperazinyl)thieno[2,3-d]pyrimidine monohydrate hydrochloride] on experimental amnesia were studied in rats and compared with those of THA [9-amino-1,2,3,4-tetrahydroacridine]. In the Morris-type water maze task, MCI-225 (1-10 mg/kg, PO) reduced the spatial learning impairment induced by scopolamine (0.5 mg/kg, IP). In a passive avoidance (PA) task, administration of MCI-225 prior to training (1-30 mg/kg, PO) lessened the carbon dioxide (CO2)-induced amnesia in a dose-dependent manner. MCI-225 (1-100 mg/kg) did not affect gross behavior. THA (0.1-3 mg/kg, PO) reduced scopolamine-induced learning deficits in the water maze task, but the effect was not significant. THA (0.3-3 mg/kg, PO) also ameliorated the CO2-induced amnesia, although slightly, in the PA task. THA (10 mg/kg, PO) increased locomotor activity and higher dose of THA (30 mg/kg, PO) induced tremor, hypersalivation, and muscle relaxation. These results suggest that MCI-225 lessens impairments in learning and memory without causing serious behavioral abnormalities.
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PMID:Effects of a novel compound MCI-225 on impaired learning and memory in rats. 809 Aug

The effects of physostigmine, tacrine and NIK-247 on scopolamine-induced impairment of a passive avoidance response were examined in rats. In addition, we investigated possible peripheral side-effects: miosis and salivation, and central side-effects: hypothermia and tremor which are mediated by cholinergic activation. Intraperitoneal injection of physostigmine reversed scopolamine-induced amnesia at a dose of 0.03 mg/kg. Antiamnesic effects of oral administration of tacrine and NIK-247 were observed at doses of 0.3 and 0.1-0.3 mg/kg, respectively. Intraperitoneal injection of physostigmine induced miosis, salivation, hypothermia and tremor at doses > or = 0.1, 0.3, 0.3 and 1 mg/kg, respectively. Oral administration of tacrine (at doses > or = 0.3 mg/kg) and NIK-247 (at doses > or = 3 mg/kg) produced miosis. Tacrine (at doses > or = 1 mg/kg) and NIK-247 (at doses > or = 3 mg/kg) produced hypersalivation. Hypothermia and tremor were observed after administration of tacrine (at doses > or = 10 mg/kg) and NIK-247 (30 mg/kg). The antiamnesic dose of physostigmine was 1/30-1/3 of doses with central or peripheral side-effects. The dose ratio of tacrine was 1/30-1; that of NIK-247 was 1/300-1/10. These results indicate that NIK-247 has higher safety and greater selectivity for cognitive functions than physostigmine or tacrine.
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PMID:Antiamnesic and cholinomimetic side-effects of the cholinesterase inhibitors, physostigmine, tacrine and NIK-247 in rats. 811 9

Diving deeper than 180 metres of seawater (msw) will impose neurological symptoms in most divers. Atactic signs and abnormal EEGs were found in five of 18 divers immediately after deep diving. Neuropsychological testing before and after deep diving in 64 divers revealed a reduction in autonomic reactivity (48%), increased hand tremor (27%) and impairment of spatial memory and reduced finger coordination (8%) after the dives. These results had not improved one year later. A follow-up study of 40 divers one to seven years after their last deep dive revealed that the divers experienced more problems of concentration and paresthesia in feet and hands than the controls. Two had had seizures, one had suffered episodes of transitory cerebral ischemia and one had experienced transitory global amnesia after the deep dives. In the future, oil installations at depths below 180 msw should be installed and maintained with remote control and robot technology.
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PMID:[Acute and chronic effects of deep diving on the nervous system]. 842 49

Dizziness in childhood is not an infrequent symptom, but epileptic vertigo is a rare condition in children. Here we report an 8-year-old Japanese boy with epileptic vertiginous seizures. At age 8 years, he visited Nippon Medical School Hospital because of a ten day history of dizziness. The dizziness occurred more than twenty times a day and he was hospitalized. On physical examination, the patient appeared normal and there were no abnormal neurological findings, including eye movement and cerebellar signs. Ophthalmoscopy, otoscopy, vestibular function test and hearing test were normal. Computerized tomography scanning and MR imaging of the head revealed no significant abnormality. The dizziness observed on admission comprised sudden brief attacks of rotatory sensation without amnesia regarding the event. Sometimes the attacks were accompanied by tremor like movement and numbness of the right hand, followed by postictal unsteadiness. Interictal EEG revealed spike-and-wave complexes in the central region dominantly in the light sleep stage. On ictal EEG, seizure discharges were observed to begin in the left central region and they increased in amplitude and subsequently propagated to the frontal and occipital regions. These findings were most suggestive of partial seizures. The patient was treated with carbamazepine and the seizures became well under control.
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PMID:[Epileptic vertiginous seizure in a Japanese boy: a case report]. 894 Aug 79

The bispectral (BIS) index and 95% spectral edge frequency (SEF) of the electroencephalograph (EEG) have been used to study the anesthetic and sedative effects of intravenously (i.v.) administered drugs. This prospective study was designed to evaluate the effectiveness of the BIS index and 95% SEF for assessing the level of propofol-induced sedation and amnesia during regional anesthesia. Ten consenting adult patients undergoing surgery with regional anesthesia were administered propofol in increments of 10-20 mg i.v., every 5-10 min until they became unresponsive to tactile stimulation (i.e., mild prodding or shaking). The BIS index and 95% SEF were continuously recorded from a bifrontal montage (Fp1-Cz and Fp2-Cz) using the Aspect B500 monitor. The depth of sedation was assessed clinically at 5- to 10-min intervals using the observer's assessment of alertness/sedation (OAA/S) scale, with 1 = no response to tactile stimulation to 5 = wide awake. Each patient was shown a picture of an animal (cat) prior to administration of an initial dose of propofol, 40 mg i.v.. Subsequently, patients were administered intermittent bolus doses of propofol, 10-20 mg i.v., and shown different pictures upon achieving OAA/S scores of 4, 3, and 2 during the onset of and recovery from propofol-induced sedation. Picture recall was tested upon arrival of the patient in the postanesthesia care unit (PACU). Of the two EEG variables studied, the BIS index exhibited a better correlation with the OAA/S scores during both the onset (Spearman's rho = 0.744) and recovery (Spearman's rho = 0.705) phases of propofol-induced sedation. With the increasing depth of sedation, there was a progressive decrease in the BIS index (OAA/S score of 5, BIS = 94.5 +/- 2.9; 4, 93.3 +/- 3.3; 3, 89 +/- 6.1; 2, 80.1 +/- 8.7; 1, 75.6 +/- 7.5; mean +/- SD). Conversely, there was a progressive increase in the BIS value during recovery from propofol sedation (OAA/S score of 1, BIS = 75.6 +/- 7.5; 2, 82.4 +/- 10.5; 3, 84.9 +/- 5.9; 4, 93.8 +/- 0.8). Although the changes in the 95% SEF values were less consistent during the onset phase, this EEG variable increased from 16.4 +/- 5.0 to 19.3 +/- 5.6 as the OAA/S score increased from 1 to 4 during the recovery phase. Patient recall of the intraoperative pictures decreased with increasing depth of sedation and decreasing BIS values (OAA/S:% BIS:% recall = 5:94.5 +/- 2.9:100%; 4:93.4 +/- 3:63%; 3:87.3 +/- 6.1:40%; 2:80.8 +/- 8.3:0%; 1:75.6 +/- 7.5:0%). The BIS index appears to be a useful variable for assessing the depth of propofol-induced sedation. Increasing depth of sedation was associated with a significant decrease in intraoperative picture recall.
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PMID:Electroencephalographic bispectral index correlates with intraoperative recall and depth of propofol-induced sedation. 898 22


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