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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of intracerebroventricular (i.c.v.) or systemic injections of Met- or Leu-enkephalin, beta-endorphin, FK 33.824 (D-Ala2, MePhe4, Met(O5)-ol-enkephalin) and of morphine and naloxone have been studied in baboons, Papio papio, which spontaneously show photically induced epileptic responses. Animals were chronically implanted with epidural or deep recording electrodes and a cannula in one lateral ventricle, and tested whilst seated in a primate chair. In some animals the natural syndrome was enhanced by the prior administration of DL-allylglycine, 100--200 mg/kg, i.v. Met- or Leu-enkephalin, 1--10 mg, i.c.v., did not lead to any manifest focal or generalized seizure discharges. Nor did it lead to any consistent enhancement or reduction of photically induced myoclonic responses (as tested 5--10 min after injection). beta-Endorphin, 0.1--0.5 mg, i.c.v., did not enhance or impair photically induced myoclonic responses. FK 33.824, 0.1--0.5 mg, i.c.v., depressed respiration and slowed EEG background rhythms for 9--15 h. This was associated with a loss of myoclonic responses to photic stimulation. These effects were reversed for 20--40 min following the injection of naloxone, 1 mg/kg i.m. A depression of respiration and a slowing of EEG rhythms was seen beginning 5--20 min after FK 33.824, 2 or 4 mg/kg, i.v. The higher dose also abolished photically induced myoclonic responses. Naloxone, 1 mg/kg, definitively reversed these effects. Morphine, 5--10 mg i.c.v., tended to increase the latency to onset of generalized myoclonus during photic stimulation. Myoclonic responses were delayed or diminished after morphine, 5 mg/kg, i.m. Naloxone, 1--2 mg/kg i.m., reversed this effect. Naloxone, 0.2--5.0 mg/kg i.m., alone, did not significantly modify photically induced myoclonus, either in animals of low or high initial responsiveness, or in those pretreated with allylglycine.
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PMID:Effects of opiate-like peptides, morphine, and naloxone in the photosensitive baboon, Papio papio. 22 24

In six children, aged from 8 to 12 years, presenting with primary generalized epilepsy a significant rise in plasma ACTH and prolactin levels (as compared with levels measured 5 days later) was observed either during a generalized seizure demonstrated by EEG (3 cases) or within 1 hour of a generalized seizure (3 cases). The neurophysiological basis for these post-epileptic endocrine disturbances is a sudden depression of dopaminergic and GABA-ergic pathways. As a result, these endocrine changes, already well documented in adults, may be regarded as a good biological marker of the epileptic origin of a paroxysmal attack.
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PMID:[Post-crisis elevation of adrenocorticotropic hormone and prolactin in epileptic children]. 302 43

There are correlations between schizophrenia and the limbic seizure system on the one hand and the manic-depressive or bipolar syndromes and the generalized seizure system on the other hand, which are theoretically related to the different (although overlapping) neural substrates underlying the two major syndromes of psychosis. Evidence is reviewed that indicates that in ECT-responsive depression (with both bilateral and unilateral nondominant ECT) the modus operandi hinges on right-hemispheric neural events. At the same time the relevance of the complex interactions existing between limbic and generalized seizures, REM suppression, right limbic epilepsy and REM activation is discussed as well as the role of carbamazepine in these interactions.
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PMID:[Cerebral mechanisms of the efficacy of electroshock therapy]. 345 May 4

The neurophysiological systems subtending generalized seizures (activated by ECT) and temporal-limbic seizures are described as well as the interactions existing between the two seizure systems. There are correlations between schizophrenia and the limbic seizure system on the one hand and the manic-depressive or bipolar syndromes and the generalized seizure system on the other which are theoretically related to the different (although overlapping) neural substrates underlying the two major syndromes of psychosis. Evidence is reviewed that indicates that in ECT-responsive depression (with both bilateral and unilateral nondominant ECT) the modus operandi hinges on right-hemispheric neural events. Neurophysiological, neurological, and acoustic threshold evidence is discussed: all of which emphasizes the importance of the nondominant hemisphere in the genesis of endogenous depressions and in their treatment with convulsive therapies. In addition, studies showing that psychotropic agents with specific antidepressant effects produce asymmetric activation of the right hemisphere (EEG) are related to the above issues.
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PMID:Electroconvulsive therapy and lateralized affective systems. 351 73

We studied the effects of transauricular electroshock (ECS) on EEG and EMG patterns, and overt behaviors (wet-dog shaking and excessive grooming), caused by RX 336-M (7,8-dihydro-5',6'-dimethylcyclohex-5'-eno-1',2', 8',14 codeinone) in rats. Male, Sprague Dawley rats were prepared with cerebrocortical EEG and temporalis muscle EMG electrodes. In sham-shocked rats, RX 336-M (6 mg/kg, i.p.) induced behavioral activation, rapid forepaw movements, wet-dog shaking and excessive grooming; this syndrome was associated with EEG activation and EMG spiking. ECS alone produced a generalized seizure followed by postictal EEG slowing and behavioral depression. ECS suppressed the RX 336-M-induced behavioral syndrome and associated EEG and EMG responses. This attenuating action of ECS, presumed to involve the release of endogenous opioids, was antagonized when the rats were pretreated with naloxone (10 mg/kg, s.c.). Our results provide further evidence for the view that endogenous opioids are involved in the pathophysiology of certain postictal phenomena.
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PMID:EEG, EMG and behavioral evidence for the involvement of endorphin systems in postictal events after electroconvulsive shock in rats. 717 17

Effect of 3-sulfamoylmethyl-1,2-benzisoxazole (AD-810) on kindled seizures in the neocortex, hippocampus and amygdala was studied in comparison with that of clinically proved antiepileptics, and the differences in kindled seizure development in the three areas were also studied. The amygdala more rapidly developed a generalized seizure (kindled seizure) than the hippocampus and the neocortex. Although more days of stimulation were needed, the neocortex also developed a kindled seizure similar to limbic kindled seizures. Phenobarbital, carbamazepine, dipropylacetate and diazepam showed a depressant effect on the neocortical kindled seizures. Phenytoin showed a depressant effect only when it was administered intravenously. Phenobarbital and carbamazepine depressed the hippocampal kindled seizures, while phenytoin and diazepam had little effect. Phenobarbital and diazepam caused marked depression on the amygdaloid kindled seizures, but the effect of phenytoin, carbamazepine and dipropylacetate on them was weak or negligible. AD-810 showed a depressant effect on neocortical and hippocampal kindled seizures, but not on amygdaloid ones. The profile of AD-810 is similar to that seen with carbamazepine.
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PMID:Effects of 3-sulfamoylmethyl-1,2-benzisoxazole (AD-810) and some antiepileptics on the kindled seizures in the neocortex, hippocampus and amygdala in rats. 722 18

We retrospectively reviewed the charts of 12 subjects with brain injury who were treated with amantadine. Ten of the 12 subjects exhibited some improvement in cognitive and/or physical function while on amantadine. Areas most consistently showing improvement included focused and sustained attention and concentration, orientation, alertness, arousal, processing, time, and psychomotor speed, mobility, vocalization, agitation, anxiety and participation in therapy. Two of the three subjects with severe agitation showed dramatic resolution of the agitation. Eight of nine low-arousal subjects displayed an increased level of responsiveness. Areas with inconsistent response included memory, assaultiveness, and confusion. No response was seen in depression or sexual inappropriateness. Possible side-effects of amantadine were noted in five of the 12 subjects, and included pedal oedema, hypomania, generalized seizure, and visual hallucinations. This work suggests amantadine may play a role in neurobehavioural recovery of brain injury, and demonstrates the need for more in-depth study.
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PMID:Clinical use of amantadine in brain injury rehabilitation. 784 90

The aim of this investigation was to determine the incidence of seizure activity in the acute phase following traumatic brain injury. Compression contusion trauma was produced in the right parietal cortex in 19 artificially ventilated rats. Electroencephalographic recordings were carried out in 17 of the animals for 2 h following the impact. The extracellular levels of neuroactive amino acids were simultaneously monitored in 9 of the experiments using microdialysis. In 14 of the 17 animals a generalized seizure activity with an average duration of 59 s (range 30-101 s) was recorded. The mean time lag between trauma and seizure onset was 67 s (range 26-90 s). The seizure activity was consistently followed by post-ictal depression. The trauma was accompanied by a transient increase of aspartate, taurine, glutamate and glycine, in decreasing rank order. The seizure activity occurred when the levels of these neuroactive amino acids were elevated. It is concluded that the high incidence of seizure activity observed may be an important factor contributing to secondary ischemia after traumatic brain injury. Aspartate and glutamate, potentiated by glycine, may play a role in post-traumatic seizure activity.
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PMID:Epileptic seizure activity in the acute phase following cortical impact trauma in rat. 818 Aug

We report a case of spinal subdural haematoma with neurological deficit in a 36-yr-old woman following Caesarean section for severe preeclampsia and placental abruption. She had been taking chronic trifluoperazine treatment for depression. Her activated partial thromboplastin time (aPTT) was 49 sec (normal = 26-36) but all other tests of coagulation were normal. Epidural anaesthesia was attempted but, despite a negative test dose, injection of local anaesthetic resulted in a generalized seizure and general anaesthesia was induced. Seventy-two hours after delivery, she was found to have bilateral leg weakness, urinary incontinence, absent rectal sphincter tone and asymmetrical leg reflexes. The diagnosis of spinal haematoma was confirmed by magnetic resonance imaging. She underwent emergency laminectomy and made a full neurological recovery.
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PMID:Spinal subdural haematoma in a parturient after attempted epidural anaesthesia. 826 79

Electroconvulsive therapy, which works by creating a generalized seizure, is used most frequently to treat medication-resistant depression. Other indications for electroconvulsive therapy includes severe depression with suicidal ideation, acute mania and severe psychiatric illness with food and fluid refusal. Electroconvulsive therapy may be administered as an inpatient or outpatient procedure. Treatments are usually administered three times a week for six to 12 treatments. Before this therapy is used, a thorough medical and anesthetic history should be obtained, and a complete physical examination, an electrocardiogram and appropriate laboratory studies should be performed to rule out anemia, electrolyte imbalances, and cardiopulmonary and neurologic risk factors. Heart rate and rhythm, oxygenation, blood pressure and, often, the electroencephalogram are monitored continuously while the patient is anesthetized with a short-acting hypnotic agent and a muscle depolarizing agent. After electroconvulsive therapy, antidepressant or lithium therapy significantly reduces the symptom relapse rate.
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PMID:Electroconvulsive therapy: a guide for family physicians. 854 53


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