Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms of the anticonvulsant activity of cannabidiol (CBD) and the central excitation of delta 9-tetrahydrocannabinol (delta 9-THC) were investigated electrophysiologically with conscious, unrestrained cobalt epileptic rats. The well-known antiepileptics, trimethadione (TMO), ethosuximide (ESM), and phenytoin (PHT), were included as reference drugs. Direct measurements were made of spontaneously firing, epileptic potentials from a primary focus on the parietal cortex and convulsions were monitored visually. ESM and TMO decreased the frequency of focal potentials, but PHT and CBD exerted no such effect. Although CBD did not suppress the focal abnormality, it did abolish jaw and limb clonus; in contrast, delta 9-THC markedly increased the frequency of focal potentials, evoked generalized bursts of polyspikes, and produced frank convlusions. 11-OH-delta 9-THC, the major metabolite of delta 9-THC, displayed only one of the excitatory properties of the parent compound: production of bursts of polyspikes. In contrast to delta 9-THC and its 11-OH metabolite, CBD, even in very high doses, did not induce any excitatory effects or convulsions. The present study provides the first evidence that CBD exerts anticonvulsant activity against the motor manifestations of a focal epilepsy, and that the mechanism of the effect may involve a depression of seizure generation or spread in the CNS.
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PMID:The influence of cannabidiol and delta 9-tetrahydrocannabinol on cobalt epilepsy in rats. 11 6

In spastic patients the alpha-adrenergic blocking drug thymoxamine (Opilon Forte) was found capable of depressing most propioceptive reflex parameters within 1 min after intravenous administration. The action seems to be of CNS origin, probably exerted as a depression of spindle stretch sensitivity through descending alpha-adrenergic bulbospinal pathways, but an additional action on the mechanism of presynaptic inhibition is likely. With oral administration, the drug is also capable of depressing distressing clonus, and it is concluded that it deserves further testing as a spasmolytic.
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PMID:Depression of spasticity by alpha-adrenergic blockade. 14 2

Hoffman (H) reflexes were elicited from the soleus muscle during treadmill walking in 21 spastic paretic patients. The soleus and tibialis anterior muscles were reciprocally activated during walking in most patients, much like that observed in healthy individuals. The pattern of H-reflex modulation varied considerably between patients, from being relatively normal in some patients to a complete absence of modulation in others. The most common pattern observed was a lack of H-reflex modulation through the stance phase and slight depression of the reflex in the swing phase, considerably less modulation than that of normal subjects under comparable walking conditions. The high reflex amplitudes during periods of the step cycle such as early stance seems to be related to the stretch-induced large electromyogram bursts in the soleus in some subjects. The abnormally active reflexes appear to contribute to the clonus encountered during walking in these patients. In three patients who were able to walk for extended periods, the effect of stimulus intensity was examined. Two of these patients showed a greater degree of reflex modulation at lower stimulus intensities, suggesting that the lack of modulation observed at higher stimulus intensities is a result of saturation of the reflex loop. In six other patients, however, no reflex modulation could be demonstrated even at very low stimulus intensities.
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PMID:H-reflex modulation during walking in spastic paretic subjects. 178 8

Toxic reaction is the most common side-effect accompanying the local anesthetic administration. Toxic reaction symptoms may manifest as CNS symptoms or cardiovascular systems symptoms. Initially, the toxic reaction symptoms in CNS undergo the stage of stimulation, followed by the stage of depression. A case of toxic reaction to the usual dose of Cystocain DS for mandibular anesthesia in an 11-year-old girl is presented. The symptoms began with poor general condition, nausea, severe vertigo, pallor and excessive perspiration, followed by clonus-type muscular convulsions, with consciousness preserved. Upon hospitalization, convulsions were interrupted by i.v. administration of diazepam. Blood pressure returned to normal, circulation recovered and normal frequency and depth of breathing were resumed. To date, only one similar case of reaction to Cystocain DS was reported to the WHO. Mere possibility as well as seriousness and risk of the occurrence of such a situation require close therapist's observations of each patient receiving any type of local anesthetics.
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PMID:[Convulsions--reaction to intoxication with cystocain DS]. 213 12

Effects of intravenous administration of the serotonin precursor tryptophan (TRP) on serum prolactin, neuromotor function, subjective mood, and blood pressure and pulse were determined in nine depressed patients before and during placebo-controlled treatment with the monoamine oxidase inhibitor (MAOI) tranylcypromine. Tranylcypromine significantly increased the prolactin response to TRP. Four patients developed a distinctive neuromotor syndrome following TRP during tranylcypromine, but not placebo, treatment. Symptoms included hyperreflexia, ankle clonus, nystagmus, incoordination, tremor, myoclonic jerks, and nausea. There were no differences in peak prolactin, mood, or autonomic responses between patients with and without the syndrome, but those with the syndrome had received active tranylcypromine for a significantly shorter duration. Tranylcypromine had little effect on TRP-induced changes in mood or autonomic function, except for a modest enhancement of the TRP-induced rise in diastolic blood pressure. These results suggest that tranylcypromine treatment may enhance serotonin function in depression.
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PMID:Effects of tranylcypromine treatment on neuroendocrine, behavioral, and autonomic responses to tryptophan in depressed patients. 403 56

H-reflex amplitudes were recorded after stimulation of the tibial nerve and different electrical stimuli in 18 normal persons and 26 patients showing pyramidal spasticity (8 spastic spinal paralysis, 6 spastic hemiparesis, 12 spinal lesions). A just subthreshold stimulus of the tibial nerve facilitated the H-reflex in spastic patients slightly after about 300 ms (up to 113%), following an early strong facilitation (10 ms) and a longer lasting depression (20-200ms). Similar postinhibitory facilitation was obtained in spastic patients after ipsilateral stimulation of the plantar surface and after direct stimulation of the dorsal columns. Conditioning by contralateral stimuli of the posterior tibial nerve caused a slight late facilitation in both normal and spastic patients. This late facilitation did not correlate significantly with the severity of spasticity, but it was more pronounced in cerebral pyramidal lesions than in spinal ones. It is assumed that this postinhibitory facilitation is probably generated as a spinal rhythm, similar to the clonus, and that it is modulated from supraspinal structures.
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PMID:The late facilitation in H-reflex recovery cycles in different pyramidal lesions. 625 75

From the results obtained with the experimental series CORASIN (fast compression with He-N2-O2), a method of compression has been developed for the baboon (Papio papio) to dive deeper than 600 m. This method utilizes an exponential compression profile with stages of 40 min every 100 m and with the introduction of N2 before each stage from 200 m onward to maintain a concentration of 5.5%. Between 0 and 800 m, this procedure did not produce myoclonus or epileptic seizures; tremor appeared beyond 400 m (578 +/- 109 m) but remained slight. If N2 was not introduced, the tremor appeared earlier (266 +/- 52 m) and became severe; between 600 and 800 m, muscular hypertonus, myoclonus, and muscular cramps occurred. The modifications of the electroencephalogram were slight; the increase in slow activity did not exceed 300% with or without N2. Beyond 800 m, the compression procedure with N2 injections revealed new phenomena. There was a general depression of EEG activity starting at 800 m; from 1,000 m and deeper, there were periods of motor disturbances (hypertonus, spasms, and shaking), palpebral clonus, and eye movements associated with peak EEG activities localized in the posterior region of the skull that sometimes evolved toward an epileptic seizure localized in this region. These symptoms differed from the classical description of high-pressure nervous syndrome, which comprises an increase in tremor followed by convulsions. These differences may perhaps be linked to our compression procedure using N2 injection, to the effect of the pressure itself, or to a combination of the two.
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PMID:HPNS of baboons during helium-nitrogen-oxygen slow exponential compressions. 646 4

Sixteen patients with lathyrism, age ranging between 18 and 55 years and duration of illness between 2 and 25 years, underwent H reflex studies with the aim of studying motor neurone excitability. The patients had marked spasticity (Ashworth score ranging between 2 and 5) and mild to moderate leg weakness. Knee and ankle reflexes were exaggerated in all and the plantar response was extensor in 14 patients. The H reflex abnormalities included increased HM ratio indicating increased motoneurone excitability, significant lack of vibratory inhibition indicating altered transmission in the premotoneuronal portion of the H reflex pathway, and lack of reciprocal inhibition (P < 0.01). These H reflex abnormalities were not related to spasticity, weakness, clonus or plantar response. The H reflex recovery curve in 6 patients revealed increased excitability throughout the recovery curve. The secondary facilitation started and peaked slightly earlier than normal, and the late depression was not marked indicating change in excitability of motoneurones or of interneurones.
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PMID:H reflex studies in neurolathyrism. 752 Dec 88

Previous studies indicate that daily repetition of audiogenic seizures (AGS) leads to audiogenic 'kindling' with increased seizure duration and additional seizural behaviors. The present study examined the neuronal correlates of this phenomenon. Extracellular single neuron firing and concomitant convulsive behaviors associated with 14 repetitive AGS were evaluated in the genetically epilepsy-prone rat severe seizure strain (GEPR-9). An increase in the number of acoustically-evoked action potentials in neurons of the central nucleus of inferior colliculus (ICc) was observed by the second day of AGS repetition, and peaked at day four. The ICc responses remained at similar enhanced level through day 14. ICc neuronal responses were completely absent for approximately two min post-ictally after a single AGS in all animals, but 80% of the animals undergoing repetitive AGS consistently exhibited neuronal firing in this post-ictal period. Post-tonic clonus and an increased duration of post-ictal behavioral depression were also observed with repetitive AGS. The increased ICc neuronal firing was observed prior to the appearance of the post-tonic clonus component of repetitive AGS. This suggests that the ICc neuronal firing increase may subserve, at least, the initial increase in AGS severity. However, changes in neuronal firing in nuclei of the neuronal network for AGS efferent to the ICc may be responsible for the increased AGS severity that occurs after the fourth day of AGS repetition.
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PMID:Repetitive audiogenic seizures cause an increased acoustic response in inferior colliculus neurons and additional convulsive behaviors in the genetically-epilepsy prone rat. 896 82

Psychogenic tremor has become a rare movement disorder. Twenty-five patients from our movement disorder unit presented either with obviously nonorganic body shaking during stance or with extremity tremors. A sudden onset and a variable but rarely remitting course of the condition was common. The "coactivation sign of psychogenic tremor" and absent finger tremor were the most consistent criteria to separate them from organic tremors. Quantitative analysis of tremor shows decreasing amplitudes in most organic tremors when the extremity is loaded with additional weights. In contrast, we found an increase of tremor amplitude for most of the cases with psychogenic tremor. This might be caused by increased coactivation to maintain the oscillation. These clinical and electrophysiological features suggest a clonus mechanism induced by coactivation as the pathophysiological basis of psychogenic extremity tremor. Psychiatric evaluation did not show overt signs of hysteria for the majority of the patients. However, we found depression and functional somatic or psychosomatic conditions to be frequent among the patients. A reduced ability to cope with stressful situations may play a significant role. The clinical course of the condition is usually far from benign. We conclude that psychogenic tremor can be positively diagnosed by means of neurologic signs in the majority of patients and is not only a diagnosis of exclusion. The poor outcome makes early and serious neuropsychiatric attempts at therapy necessary.
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PMID:Diagnostic and pathophysiological aspects of psychogenic tremors. 953 44


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