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

Increasing doses of pilocarpine, 100-400 mg/kg, were given intraperitoneally to mice and the resulting behavioral, electroencephalographic and neuropathological alterations were studied. No behavioral phenomena were observed in mice treated with the lowest dose of pilocarpine. Occasional tremor and myoclonus of hindlimbs were found in animals which received pilocarpine in a dose of 200 mg/kg. At doses of 300, 325 and 350 mg/kg, pilocarpine produced a sequence of behavioral alterations including staring spells, limbic gustatory automatisms and motor limbic seizures that developed over 15-30 min and built up progressively into a limbic status epilepticus lasting for several hours. The highest dose of pilocarpine, 400 mg/kg, was generally lethal to mice. Pilocarpine produced both interictal and ictal epileptiform activity in the electroencephalogram (EEG). The earliest EEG alterations appeared in the hippocampus and then spread to cortical areas. EEG seizures started 10-15 min after injection of large doses of pilocarpine, 300-350 mg/kg. Ictal periods lasted for 1-2 min, recurred every 5-10 min and were followed by periods of depression of the EEG activity. By 30-45 min paroxysmal activity resulted in a status epilepticus. Examination of frontal forebrain sections with light microscopy revealed a widespread damage to several brain regions including the hippocampus, amygdala, thalamus, olfactory cortex, neocortex and substantia nigra. Scopolamine, 10 mg/kg, and diazepam, 10 mg/kg, prevented the development of convulsive activity and brain damage produced by pilocarpine. The results emphasize that excessive and sustained stimulation of cholinergic receptors can lead to seizures and seizure-related brain damage in mice. It is proposed that systemic pilocarpine in mice provides a useful animal model for studying mechanisms of and therapeutic approaches to temporal lobe epilepsy.
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PMID:Seizures produced by pilocarpine in mice: a behavioral, electroencephalographic and morphological analysis. 649 17

The antagonism of some benzodiazepine (Bz) actions by physostigmine was investigated in 4 Papio papio baboons. As a model of these actions, the myoclonus induced in this species by clonazepam i.m. administration was used. The baboon develops, 20-30 min after Bz i.m. injection, a non-epileptic myoclonus characterized by clinical symptomatology (jerks involving mainly the neck and the trunk bilaterally), by the absence of any correlative EEG discharge, and by its facilitation during movement. This Bz-induced myoclonus resembles the intention myoclonus of human patients, as seen for example after anoxia. In the present series, the effect of physostigmine i.v. injection on the frequency of clonazepam-induced myoclonus was tested. Physostigmine produces a rapid and total abolition of the myoclonus, and this effect lasts for a period which corresponds to the pharmacological activity of physostigmine. On the contrary, atropine i.v. injection considerably increases the amount of Bz-induced myoclonus. These results allow the existence of an anticholinergic action of benzodiazepines, reversed by physostigmine, and the theory that the myoclonus would be the consequence of a cholinergic system depression to be hypothesized.
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PMID:Physostigmine antagonizes benzodiazepine-induced myoclonus in the baboon, Papio papio. 652 40

Patients should be aware of alterations in sleep with age, and they should not have unrealistic expectations. Drinking or taking sleeping pills is not likely to be a long-term solution to a sleep problem. Chronic difficulty in sleeping raises the possibility of sleep apnea, nocturnal myoclonus or depression, all of which commonly appear after 40. In the absence of these and other, less common disorders, sleep can often be improved by exercise, regular habits and removal of any disturbing elements from the bedroom.
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PMID:Sleep after forty. 669 39

Drugs with improved potency and specificity are becoming available for the pharmacologic manipulation of serotonin neurons in brain. Both enhancement and impairment of serotoninergic function can now be achieved by drugs acting through different mechanisms. Drugs of this sort are not only valuable tools for exploring functional roles of serotonin neurons but they have real or potential value in the treatment of diseases like mental depression, obesity, myoclonus or other movement disorders, pain, hypertension, and endocrine dysfunction.
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PMID:Pharmacology of central serotonin neurons. 699 97

Polygraphic recordings of the sleep of patients complaining of insomnia has led to recognition of specific patterns of disturbed sleep corresponding to different etiologies of insomnia. This study presents results of polygraphic recordings of the sleep of 26 patients with chronic pain for which no physical cause can be found. All 26 also complained of insomnia. Sleep parameters of this group were compared with those to two other groups also complaining of insomnia: 12 patients whose disturbed sleep was judged secondary to psychiatric disorder, and 16 patients with the subjective complaint of insomnia in whom no objective evidence of sleep disturbance could be demonstrated. The three groups differed significantly in terms of their sleep parameters. The pain patients slept less than the subjective insomnia patients. The sleep disturbance of the psychiatric patients was more severe than that of the chronic patients. Several chronic pain patients showed evidence of nocturnal myoclonus; several also showed alpha rhythm intrusions into their sleeping electroencephalograms. The study verifies that chronic pain patients do experience significant sleep disturbance and raises several questions concerning relationships among chronic pain, sleep disturbance, and psychiatric illness, particularly depression.
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PMID:Disturbed sleep in patients complaining of chronic pain. 708 3

Intrahippocampal infusion of nanogram amounts of the neurotoxin kainic acid were used to investigate possible relationships between the convulsive and the local neurodegenerative properties of the amino acid. Bilateral hippocampal depth electrodes and cortical leads were employed to provide simultaneous and continuous electroencephalographic records following kainate injection in unanesthetized freely-behaving rats. In every animal, morphological analysis was performed 3-5 days after administration of kainic acid and attempts were made to correlate neuronal destruction with electroencephalographic patterns. Doses as low as 500 pg kainate led to behavioral sequelae consisting of grooming, scratching and enhanced locomotor activity. In a roughly dose-dependent fashion (range 500 gp-250 ng), these behaviors increased in frequency and at the highest doses the rats also displayed wet-dog shakes, stereotype mouth movements and occasional facial myoclonus. Apart from these automatisms, generalized motor seizures were never seen. Following kainic acid, a spectrum of electroencephalographic changes could occur consisting of one or more of the following: high voltage fast activity, slow and fast high voltage spiking, paroxysmal bursts, spindle bursts or postictal depression periods. The combination of any two of these changes were defined as an ictal episode if they occurred in all four leads simultaneously. Upon morphological examination, only the highest dose used (250 ng) resulted reliably in the degeneration of CA3, CA4 and, partly, CA1 pyramidal cells on the injected side. While the duration of electroencephalographic changes at this dose was significantly higher than at any of the lower doses, the number of seizures or the total time spent in seizures was not different at 250 ng from that at 50 ng. At the latter dose, however, only marginal cell damage could be found. Our data indicate that very low doses of kainic acid directly applied to hippocampal CA3 neurons, can elicit bilateral changes in the electroencephalogram indicative of repetitive limbic seizures which are not necessarily accompanied by neuronal degeneration. At higher doses (250 ng), kainic acid treatment results in both seizure activity and nerve cell death but the two effects appear mechanistically unrelated. While there is no clear-cut dose-response relationship between neuronal damage and seizures, extended electroencephalographic changes of a 15-30 Hz fast activity or simple spiking phenomena may be instrumental for the degenerative process. This dissociation between convulsive and neurodegenerative properties of kainic acid, however, does not argue against a role of an endogenous substance related to kainic acid in the etiology of temporal lobe seizure disorders.
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PMID:Intrahippocampal kainic acid, seizures and local neuronal degeneration: relationships assessed in unanesthetized rats. 717 85

Four patients with an acute overdose of carbamazepine were examined with serial blood level determinations. The clinical spectrum consisted of coma, respiratory depression, seizures, myoclonus, nystagmus, hyperreflexia, hyporeflexia, delayed gastric emptying with cyclic coma, ataxia, sinus tachycardia, and atrioventricular conduction delay. Carbamazepine elimination half-lives varied from 10 to 29 hours, and in one case carbamazepine-10,11-epoxide was measured and had a half-life of 24 hours.
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PMID:Acute carbamazepine toxicity resulting from overdose. 719 79

Of 842 consecutive patients with movement disorders seen over a 71 month period, 28 (3.3%) were diagnosed as having a documented or clinically established psychogenic movement disorder. Tremor was most common (50%) followed by dystonia, myoclonus, and parkinsonism. Clinical descriptions of various types are reviewed. Clinical characteristics common in these patients included distractability (86%), abrupt onset (54%), and selective disabilities (39%). Distractability seems to be most important in tremor and least important in dystonia. Other diagnostic clues included entrainment of tremor to the frequency of repetitive movements of another limb, fatigue of tremor, stimulus sensitivity, and previous history of psychogenic illness. On examination, 71% had other psychogenic features. Over 60% had a clear history of a precipitating event and secondary gain and 50% had a psychiatric diagnosis (usually depression). Twenty five per cent of patients presented with combined psychogenic movement disorder and organic movement disorder; 35% resolved and this subgroup had a shorter duration of disease than those who are unresolved. Psychogenic movement disorder represents an uncommon diagnosis among patients with movement disorders. The ability to make a diagnosis rests on the presence of a multitude of clinical clues and therapeutic action should be taken as early as possible.
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PMID:Psychogenic movement disorders: frequency, clinical profile, and characteristics. 756 21

Encephalitis lethargica (von Economo's encephalitis), pandemic from 1917 to 1926, opened a window on the study of behavioral consequences of infection-induced subcortical disorder. Widely varying acute manifestations included extrapyramidal disorders, myoclonus, eye movement disorders, paralyses, delirium, mood changes, inverted diurnal rhythms, and catatonia. Major pathological changes involved the substantia nigra, globus pallidus, and hypothalamus. A symptom-free recovery period was often followed by postencephalitic disturbances, typically parkinsonism in adults and conduct disorder in children. Occurrence of depression, mania, obsessive-compulsive disorder, and hyperactivity in post-encephalitic patients anticipated current concepts of the role of the basal ganglia in mood, personality, and obsessional syndromes. Observations of deferred onset and "tardy" hyperkinesias presaged current theories of the pathophysiology of tardive dyskinesia.
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PMID:Encephalitis lethargica: lessons for contemporary neuropsychiatry. 758 Feb 5

Sleep is disturbed in 90% of patients with major depression. Disordered sleep physiology may persist after clinical remission of depression, suggesting either that sleep disruption is a trait characteristic of recurrent depression or that depressed patients acquire new habits that perpetuate sleep-related problems. This article reviews the data suggesting a common pathophysiology between sleep and depression. It then focuses on a strategy for evaluating and treating sleep disruption in depressed patients. Treatment must have a conservative goal of restoring sleep quality to the pre-episode level. The treatment of sleep disruption relies primarily on optimal treatment of the depression itself. This includes evaluation and treatment of comorbid medical disorders, substance use (e.g., caffeine, alcohol), and sleep disorders (e.g., nocturnal myoclonus, sleep apnea). The effects of the different classes of antidepressant medications on sleep architecture are presented. Nonpharmacologic strategies for improving sleep, such as behavior modification, relaxation, and phototherapy, are discussed. Finally, the risks and benefits of hypnotic use in the depressed patient and a treatment algorithm for the acute and chronic use of hypnotics are considered.
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PMID:Treatment of sleep disturbances in depressed patients. 784 8


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