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)

On 6 properties in south-western Queensland an outbreak of nervous disease occurred horses due to ingestion of Swainsonia (Darling pea). Loss of condition, depression, hyperaesthesia and hyperexcitability were seen in affected horses. At autopsy of 2 horses generalised c ytoplasmic vacuolation was seen in the neurones of the central nervous system and in the liver, adrenal and thyroid. The clinical and pathological features were similar to those described in horses suffering from Swainsona poisoning in Australia and Astragalus and Oxytropis in North America.
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PMID:An outbreak of Swainsona poisoning in horses. 58 81

The clinical and psychological findings on 100 children with psychosomatic musculoskeletal pain seen at a major pediatric rheumatology referral center are reported. Most (76%) were female, median age was 13 years, and median duration of symptoms was 1 year. Multiple painful sites were common (66%). The pain was constant (63%) or intermittent (37%); 45% had hyperesthesia, and almost all maintained a cheerful affect when complaining of severe pain. Two predominant abnormal family milieu were seen. One was cohesive, stable, and organized, but intolerant of separation and individuation. The other was chaotic, emotionally unsupportive, with high levels of conflict. Members of the cohesive family type reported significantly less distress than members of chaotic families. Enmeshment between mother and child was common in both family types. Although frequently viewed as bright, most of these children had normal intelligence, and some had unrecognized academic difficulty. These children, compared with those with arthritis, had a significantly lower global well-being score. Clinical depression was unusual (11%). Most (97%) responded favorably to intensive physical and occupational therapy along with individual or family psychotherapy; 78% become symptom free or fully functional. Children with these signs and symptoms should have full psychological evaluations and respond well to treatment directed toward decreasing pain and restoring function.
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PMID:Psychosomatic musculoskeletal pain in childhood: clinical and psychological analyses of 100 children. 195 24

Intrathecal administration of glycine (strychnine) or GABA (bicuculline) but not opioid (naloxone), adrenergic (phentolamine) or serotonin (methysergide) receptor antagonists resulted in a dose-dependent organized agitation response to light tactile stimulation. This effect was maximally evoked by oscillating but not continuous stimulation applied to a dermatome corresponding to the levels of spinal cord acted upon by the intrathecal antagonist. Similar results were observed in chloralose-urethane anesthetized rats in which tactile stimulation evoked hypertensive responses following local tactile stimuli. The effects were only mildly depressed by even high doses of spinal morphine or DADL and not at all by ST-91 or baclofen. In contrast, intrathecal injections of glutamate receptor antagonists resulted in a dose-dependent depression of the strychnine evoked hyperesthesia with the ordering of activity being MK-801, AP-5, kynurenic acid, SKF10047 and ketamine. At doses below those which produced motor dysfunction, however, these agents had no effects on the hot-plate response latency. These data emphasize that low threshold afferent input is likely subject to an ongoing modulation, the loss of which results in a miscoding of the afferent stimulus yielding a pain relevant message. The lack of effect of agents having a powerful effect on somatic pain stimuli and the converse effects of glutamate receptor antagonists on the strychnine hyperesthesia at doses which do not affect the somatic pain response indicate discriminable processing systems, the characteristics of which resemble the clinical phenomenon observed in patients suffering from sensory dysesthesia following central and peripheral horn injury.
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PMID:Behavioral and autonomic correlates of the tactile evoked allodynia produced by spinal glycine inhibition: effects of modulatory receptor systems and excitatory amino acid antagonists. 254 67

The clinical and pathological features of 19 neonatal Holstein-Friesian calves affected with moderate to severe neurological disease are presented. Most calves were recumbent from birth, and many developed variable neurological signs including hyperaesthesia or depression, limb extension, head tremor, nystagmus, apparent blindness, and opisthotonos when stimulated. Consistent lesions of moderate to severe, diffuse, axonal swelling and loss, with Wallerian-type degeneration and myelin depletion in the spinal cord and brainstem, and occasionally in the midbrain and peripheral nerve roots, were observed. The lesions indicated a pre-natal insult affecting mainly motor areas of the foetal neuraxis, however the aetiology of the disorder remains undetermined. It is suggested that the calves may have been affected by a hitherto unrecognised disease entity for which we propose the term, degenerative axonopathy.
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PMID:Neurological disease associated with degenerative axonopathy of neonatal Holstein-Friesian calves. 273 93

We relate two cases of amineptine (Survector) overconsumption by patients cured for atypical depression with asthenia and activities deficit as the prevalent symptoms. Prescription of two tablets a day (0,200 g) was respected in one case during six months, and in the other case during two years, with therapeutic benefit on apragmatism. To no obvious reason, within few months both patients had gradually raised the doses to twenty tablets (2 g) and thirty tablets (3 g) respectively: we observed subexcitation, insomnia, sensorial hyperaesthesia, irritability, tachyphemia with dysarthria, anorexia with weight lost of more than 10 kg and amphetamine-like troubles without confusion or delusion, as a result of which both patients were treated for their addiction, in hospital. Treatment with clorazepate perfusions did not cause any physical dependence problems. However, psychological dependence was strong enough for one of the patients to go out, on the third day, against medical decision. As far as we know, in France, only one such case of addiction use at high doses and in single intakes is mentioned in the existing literature. However, our observations suggest that it might be necessary to re-assess the place of amineptine among new antidepressive molecules with psychostimulant abilities.
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PMID:[2 cases of amineptine dependence]. 614 28

Thallium poisoning is one of the most complex and serious toxicities known to man. The symptomatology of its toxicity is usually nonspecific due to the multi-organ involvement. The initial symptoms of thallium poisoning may include fever, gastrointestinal problems, delirium, convulsions and coma. Symptoms may appear rapidly, but more commonly the acute toxicity subsides to be replaced by a gradual development of mild gastrointestinal disturbances, polyneuritis, encephalopathy, tachycardia, skin eruptions, stomatitis, atrophic changes of the skin, nail changes (Mee's lines), and skin hyperesthesia (mainly in the soles of the feet and the tibia). Degenerative changes of the heart, liver and kidney, subarchanoid hemorrhage, bone marrow depression, and increased radiopacity of the liver may also occur. Development of psychotic behavior with hallucinations and dementia has also been reported. In humans the most characteristic sign of thallium toxicity is alopecia which usually appears in cases when death is delayed for 15-20 days. Other signs and symptoms may develop at any stage of toxicity. The current therapy for thallium poisoning is the use of prussian blue and potassium chloride. Potassium therapy is probably the single most effective agent in the treatment of thallium poisoning. Further research, however, is needed to find an optimal antidote for thallium.
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PMID:Thallium poisoning: a review. 633 55

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

Topically applied norepinephrine, dopamine, serotonin, GABA and glycine, and systemically administered clonidine, L-DOPA (plus carbidopa) and 5-hydroxytryptophan completely suppressed the cutaneous hyper-irritability produced in the trigeminal sensory distribution by picrotoxin overlying the caudal medulla. Cholinergic agents and apomorphine were ineffective. Of the positive compounds, norepinephrine, serotonin and GABA showed the shortest latencies and norepinephrine and serotonin required the lowest concentrations in order to inhibit the hyper-irritability. If L-DOPA (plus carbidopa) was injected after pre-treatment with FLA-63, the effects of L-DOPA did not appear. Similar depression of the hyper-irritability was caused by electrical stimulation of the central gray. The inhibitory effects of stimulation of the central gray was suppressed after administration of tetrabenazine, but again it produced markedly by injection of L-DOPA. From these observations it was concluded that the hyper-irritability could be suppressed by serotonergic as well as noradrenergic fibers terminating at the spinal trigeminal nucleus caudalis. The potential clinical use of L-DOPA in patients with hyperesthesia is discussed.
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PMID:Inhibitory mechanisms of the hyper-irritability caused by picrotoxin in the rat. 730

Bacterial meningoencephalitis most commonly affected lambs two to four weeks old (median three weeks, range three days to six months) with clinical signs of episcleral congestion, lack of suck reflex, weakness, altered gait and depression extending to stupor, but hyperaesthesia to auditory and tactile stimuli. Opisthotonos was observed during the agonal stages of the disease. Analysis of lumbosacral cerebrospinal fluid revealed a highly significant increase in protein concentration (P < 0.01) with a neutrophilic pleocytosis, but bacteriological culture yielded organisms in only a few cases. A response was achieved with high doses of dexamethasone and chloramphenicol in only one of 20 cases. Polyarthritis and liver abscesses in a number of lambs provided evidence of a previous bacteraemic or septicaemic episode but no definite source of the central nervous system infection was identified. In common with other infectious bacterial conditions which are prevalent during the early life of sheep, control measures should ensure an adequate transfer of passive antibody, repeated treatments of the navel, and hygienic conditions in the lambing and rearing environments.
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PMID:A field study of ovine bacterial meningoencephalitis. 798 44

Brain capillary function was assessed in 4- to 6-week-old calves given lead acetate (15 mg/kg of body weight) orally for 7 to 8 days. Neurologic signs of lead poisoning included CNS depression, blindness, and hyperesthesia. Brain capillaries were isolated from cerebral cortex of control and lead-treated calves and evaluated for metabolic indicators, ion transport, and prolyl hydroxylase activity. In lead-treated calves, the rate of glucose metabolism was less than half that in controls. Ion efflux of 45Ca or 36Cl from endothelial cell suspensions was not affected by lead treatment. Prolyl hydroxylase activity in endothelium and proline-to-hydroxyproline ratio in endothelial basement membranes were similar in control and lead-poisoned calves. Results indicate that lead may inhibit energy metabolism, but not ion transport or collagen biosynthesis in brain capillaries of calves and, compared with suckling rats, damage to the blood-brain barrier is less important. In calves, neuronal tissue may be the primary target for the CNS effects of lead.
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PMID:Effects of lead on glucose metabolism, ion flux, and collagen synthesis in cerebral capillaries of calves. 839 Dec 32


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