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)

Therapeutic efficacy of calcium channel blockers in stroke remains controversial, but previously used agents bind almost exclusively to L-type calcium channels. The newly-discovered N-type calcium channel is specific to neurons, and therapy involving blockade of this site has not been previously attempted. We assessed the neuroprotective effect of omega-conotoxin GVIA (CgTx), a blocker of N-type calcium channels, using both in vitro hypoxic injury to rat cortical neurons and an in vivo model of reversible spinal cord ischemia in the rabbit. In cell cultures, CgTx inhibited hypoxia-induced 45Ca accumulation and neuronal injury minimally, compared to the NMDA antagonist ketamine. In vivo, the duration of spinal cord ischemia which produced permanent paraplegia in 50% of control animals (ET50) was 24.0 +/- 2.6 min. Animals treated 2 h prior to ischemia with 0.5 nmol CgTx in the subarachnoid space had an ET50 of 26.9 +/- 1.8 min (P = 0.36). Animals treated 24 h prior to ischemia (all had persistent systemic tremor) had a ET50 of 28.9 +/- 1.8 min (P = 0.13). We conclude that pharmacologic modulation of the N-type calcium channel does not provide a significant protective effect against neuronal hypoxic-ischemic injury.
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PMID:Treatment with conotoxin, an 'N-type' calcium channel blocker, in neuronal hypoxic-ischemic injury. 208 77

Of 70 autopsied patients with the acquired immune deficiency syndrome (AIDS), 46 suffered progressive dementia that was frequently accompanied by motor and behavioral dysfunction. Impaired memory and concentration with psychomotor slowing represented the most common early presentation of this disorder, but in nearly one half of the patients either motor or behavioral changes predominated. Early motor deficits commonly included ataxia, leg weakness, tremor, and loss of fine-motor coordination, while behavioral disturbances were manifested most commonly as apathy or withdrawal, but occasionally as a frank organic psychosis. The course of the disease was steadily progressive in most patients, and at times was punctuated by an abrupt acceleration. However, in 20% of patients a more protracted indolent course was observed. In the most advanced stage of this disease, patients exhibited a stereotyped picture of severe dementia, mutism, incontinence, paraplegia, and in some cases, myoclonus. The high incidence and unique clinical presentation of this AIDS dementia complex is consistent with the emerging concept that this complication is due to direct brain infection by the retrovirus that causes AIDS.
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PMID:The AIDS dementia complex: I. Clinical features. 372 8

Serotonin mediated bulbospinal motor activities were examined in rats with experimental allergic encephalomyelitis (EAE)-induced-paraplegia. Treatment with monoamine oxidase inhibitors and L-tryptophan failed to elicit the components of the serotonin syndrome which involved levels of the neuraxis manifesting flaccid paralysis. Straub tail, hindlimb abduction and hindlimb rigidity did not occur. The motor responses represented at spinal segments just above the level of paraplegia, lateral head weaving and forepaw treading, were present but altered in the diseased rats. No impairment was evident in the production of head tremor or hyper-reactivity to accoustic and tactile stimuli. Similarly, in urethane-anesthetized EAE rats, serotonergically-evoked automatic swallowing activity was unchanged as judged by the effects of serotonin receptor agonists, and a serotonin precursor, a reuptake blocker and an antagonist. Our data support the conclusion that EAE-induced impairment of serotonergic neurotransmission is correlated with motor deficits manfested during the acute paralytic stage of the disease.
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PMID:Central serotonin receptor sensitivity in rats with experimental allergic encephalomyelitis. 696 16

Single-nerve fibre action potentials (APs) were recorded extracellularly from sacral nerve roots of people with spinal cord lesion (patients with paraplegia). Single-fibre APs of certain fibres were identified by the conduction velocity and the AP waveform, and simultaneous impulse patterns were extracted from the summed impulse traffic and analysed with respect to spacio-temporal relationships. The velocity values of components of compound APs, induced by electrical nerve root stimulation or electrical intravesical stimulation, were similar to the group conduction velocity values obtained from single-nerve fibre APs of natural impulse traffic. When changing the root temperature in one case from 32 degrees C to 35.5 degrees C, the group conduction velocities changed in the following way: secondary muscle spindle afferents (SP2): 40 m/s (32 degrees C) to 50 m/s (35.5 degrees C); bladder stretch afferents (S1): 31.3 to 40 m/s; bladder tension afferents (ST): 25 to 33.8 m/s; mucosal afferents (M): 12.5 to 13.8 m/s; alpha 1:-; alpha 2-motoneurons: 40 to 50 m/s; alpha 3: 33 to 40 m/s. The group conduction velocities showed different temperature dependence apart from SP2 fibres and alpha 2-motoneurons, which were therefore used for calibration. The distance between two Pacinian corpuscle (PC) receptors in a sacral dermatome of one paraplegic patient was calculated to be approximately 20 mm. A similar distance between PC receptors was found in a brain-dead individual. Receptor densities seem therefore to remain unchanged following spinal cord lesion. Motoneurons fired irregularly repeatedly with impulse trains. In paraplegics the oscillation periods and the interspike intervals of the impulse trains varied much more than observed for brain-dead and normal individuals. Motoneurons could therefore not always be identified by their pattern of oscillatory firing. Alternating long and short oscillation periods (T) could be measured in an oscillatory firing alpha 1 (T = 125 ms) and alpha 2-motoneuron (T = 150 ms). In both cases the average difference between the alternating oscillation periods was 5 ms. Tremor, alternating long and short oscillation periods, cellular oscillator properties, and recurrent excitation and inhibition are discussed with respect to the oscillator theory of the functioning of the human central nervous system. Mathematical predictions from populations of interacting biological oscillators are compared to measurements on neuronal network data.
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PMID:Classification, oscillatory and alternating oscillatory firing of alpha 1 (FF) and alpha 2-motoneurons (FR) in patients with spinal cord lesion. 893 96

Histochemical analysis of NADPH-diaphorase (NADPH-d) activity was performed on segments of the lumbar spinal cord in rabbit after 7 days pretreatment with the Ginkgo biloba extract Tanakan, and 30 min of ischemia followed by 24 h of reperfusion. In sections of the L5 segment of the spinal cord of untreated controls, NADPH-d-positive neurons were identified in the dorsal horns, in the pericentral region and occasionally in the ventral horns. The rabbits were completely paraplegic after 30 min of ischemia and 24 h of reperfusion. High NADPH-d activity was found in the wall of blood vessels in sections of the L5 segment and the numbers of NADPH-d-positive neurons in all sites was moderately elevated. After 7 days of Tanakan pretreatment, 30 min of ischemia and 24 h of reperfusion, the animals did not show paraplegia. Only a light tremor of the hind limbs was observed. NADPH-d activity in blood vessels and neurons was similar to that in controls. In the dorsal horns, NADPH-d positivity in neurons and fibres was increased. Our results indicate that Tanakan can scavenge free radicals produced during ischemia/reperfusion and may reduce reperfusion damage.
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PMID:NADPH-diaphorase activity in the spinal cord after ischemic injury and the effects of pretreatment with Ginkgo biloba extract (EGb 761). 1255 15

Spinocerebellar ataxia type 14 (SCA14) is an autosomal dominant neurodegenerative disorder, first described in a Japanese family, showing linkage to chromosome 19q13.4-qter. Recently, mutations have been identified in the PRKCG gene in families with SCA14. The PRKCG gene encodes the protein kinase Cgamma (PKCgamma), a member of a serine/threonine kinase family involved in signal transduction important for several cellular processes, including cell proliferation and synaptic transmission. To identify the disease-causing mutation in a large group of ataxia patients, we searched for mutations in the PRKCG gene. We ascertained 366 unrelated patients with spinocerebellar ataxia, either pure or with associated features such as epilepsy, mental retardation, seizures, paraplegia, and tremor. A C-to-G transversion in exon 4, resulting in a histidine-to-glutamine change at codon 101 of the PKCgamma protein, was identified in patients from a family with slowly progressive pure cerebellar ataxia. Functional studies performed in HEK293 cells transfected with normal or mutant construct showed that this mutation affects PKCgamma stability or solubility, verified by time-dependent decreased protein levels in cell culture. In conclusion, the H101Q mutation causes slowly progressive uncomplicated ataxia by interfering with PKCgamma stability or solubility, which consequently may cause in either case a decrease in the overall PKCgamma-dependent phosphorylation.
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PMID:A novel H101Q mutation causes PKCgamma loss in spinocerebellar ataxia type 14. 1618 24

Typical presentations of hyperthyroidism are palpitation, nervousness, tremor, malaise, and weight loss. Hyperthyroidism affects nearly every system in the body, and some patients may manifest neurologic or hematologic symptoms. Atypical presentations of hyperthyroidism often pose a great challenge in diagnosis and treatment. We report a case of Basedow's paraplegia and pancytopenia that was precipitated by hyperthyroidism. The unusual manifestations led to unnecessary examinations and delayed the treatment of hyperthyroidism. The classical symptoms of Basedow's paraplegia are subacute symmetric weakness of the lower extremities with areflexia and sparing sensation or sphincter involvement. Control of the hyperthyroidism mitigated the neurologic and hematologic complications and prevented unnecessary studies.
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PMID:Rare presentations of hyperthyroidism--Basedow's paraplegia and pancytopenia. 1937 62

Objectives. Our objective was to describe and analyze through a third party disinterested observer the results obtained by using motor cortex stimulation (MCS) for the treatment of central dysesthetic diffuse-distal type of paraplegic pain and intentional tremor secondary to the total removal of a cervical ependymoma. Design. Retrospective case report with discussion. Methods. A 69-year-old female, who after satisfactory removal of a cervical ependymoma, developed a central dysesthetic diffuse-distal type of paraplegic pain and intentional tremor associated with mild cerebellar deficit. Neurologic compromise became so intense that it prevented the patient from leading an independent lifestyle. Conservative treatments failed and a unilateral trial of MCS was performed. After a four-day satisfactory unilateral trial, a bilateral electrode, Resume II (Medtronic, Inc., Minneapolis, MN), was inserted through a small craniotomy and a dual-channel RF activated receiver was implanted. During the second month of follow-up an independent observer personally interviewed the patient and assessed results through a multimodal approach, encompassing several analog scales used to measure the different components of the painful experience; a daily life activities scale and drug intake. Results. Evoked painful phenomena were dramatically improved, but the steady component of pain was only moderately relieved. The patient's tremor improved to allow for the performance of simple movements such as independent eating. Conclusion. In this single case report MCS was extremely useful in eliminating almost all of the patient's pain-evoked phenomena. Both steady burning pain and tremor were also improved. This is only one case report and MCS warrants further investigation as to its utility in controlling central dysesthetic pain in paraplegia and postchordotomy dysesthesias.
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PMID:Bilateral motor cortex stimulation for the relief of central dysesthetic pain and intentional tremor secondary to spinal cord surgery: a case report. 2215 Aug 46

The First World War was a global war, beginning on 28 July 1914, until 11 November 1918. Soon after the beginning of the war, there was an "epidemic" of neurological conversion symptoms. Soldiers on both sides started to present in large numbers with neurological symptoms, such as dizziness, tremor, paraplegia, tinnitus, amnesia, weakness, headache and mutism of psychosomatic origin. This condition was known as shell shock, or "war neurosis". Because medically unexplained symptoms remain a major challenge, and considering the close relationship of symptoms described in shell shock with clinical neurology, we should study their history in order to improve future care.
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PMID:The relationship between the First World War and neurology: 100 years of "Shell Shock". 2859 93