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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cocaine causes serious neurologic and neuropsychiatric complications. Cocaine-induced seizures are common and appear to be due to the local anaesthetic actions of this compound. Cocaine induced stroke has varied mechanisms. With ischemic stroke there is severe vasospasm induced by rises in brain catecholamines. These changes can persist for many weeks and can be demonstrated using single-photon emission computerized tomography (SPECT). In many patients with psychiatric symptoms such as psychosis or mania, SPECT demonstrates similar changes in cerebral blood flow. In fact, some of the psychiatric symptoms induced by cocaine may be due to decreases in cerebral blood flow. In cocaine abuse, treatment strategies based on decreasing cerebral vasospasm need to be developed.
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PMID:Neuropsychiatric effects of cocaine: SPECT measurements. 148 93

Neuropsychiatric disorders following stroke are common, and pathologic involvement of specific regions or functional systems results in behavioral syndromes similar to idiopathic psychiatric syndromes. Depression occurs in up to half of all stroke patients and is most frequently associated with left anterior cortical and subcortical infarctions. Mood changes interfere with cognitive, functional and social recovery. Treatment with heterocyclic antidepressants, stimulants, and electroconvulsive therapy is efficacious in most patients. Mania, delusions, hallucinations, personality alterations, obsessive-compulsive disorder, and changes in sexual behavior are less common but have also been described in post-stroke patients. Each behavioral syndrome is associated with a specific pattern of brain involvement. Investigation of these phenomena contributes to understanding the cerebral basis of psychiatric disorders.
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PMID:Neuropsychiatric aspects of stroke. 206 51

The prevalence, diagnosis, clinical presentation, evolution, and treatment of depression and mania following stroke are discussed. Among the many studies presented in the review is one that indicates major depression following right hemisphere lesions is associated with a positive family history of psychiatric disorder and lesions involving the parietal cortex. The co-occurrence of major depression and generalized anxiety disorder is associated with cortical lesions, while depression alone is associated with subcortical lesions. A recent study has also shown a strong association between mania and direct or indirect dysfunction of the basotemporal cortex in the right hemisphere. Possible mechanisms for both mania and depression following stroke are presented, and ideas for future directions in research are suggested.
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PMID:Current research in affective disorders following stroke. 213 55

The use of calcium channel blockers is usual in cardiology today, but seem to spread to others specialties, particularly in the field of neuropsychiatry. The authors report the major clinical studies in neurology (treatment of migraines, epilepsia, dizziness and ischemic stroke) where flunarizine and nimodipine seem to have an important role. In psychiatry, their introduction is more recent. However, some encouraging results have been noted in the treatment of panic disorder, Gilles de la Tourette disease and mania.
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PMID:[Use of calcium inhibitors in neuropsychiatric pathology]. 219 69

A retrospective review of the records of 755 patients seen by a psychiatric consultation-liaison service in a general hospital was performed. The authors found that 87% of manic patients and 38% of depressed patients had a diagnosis of organic mood disorder. The most frequent precipitants of mania were corticosteroids, human immunodeficiency virus (HIV) infection, and temporolimbic epilepsy. The most frequent precipitants of depression were stroke, Parkinson's disease, and HIV infection.
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PMID:Causes of organic mood disorder. 252 Oct 90

Previous investigations by our group and others have demonstrated that poststroke depressions are not fully explained by the severity of associated impairment. We have consistently found, however, a strong association between development of major depression and left anterior brain injury. Recent studies have demonstrated that either left anterior cortical or subcortical lesions may lead to the development of major depression and that preexisting subcortical atrophy may play an important permissive role in the development of major depression. Patients with a mild degree of ventricular enlargement perhaps related to perinatal damage may be more likely to develop poststroke major depression following a lesion of the left frontal cortex or left basal ganglia than a patient without preexisting atrophy. Poststroke mania, on the other hand, is strongly associated with right hemisphere lesions as well as a preexisting subcortical atrophy and sometimes a family history of affective disorder. Thus, mania following brain injury may require the convergence of two factors: a right hemisphere brain injury and either a preexisting subcortical atrophy or a genetic vulnerability. PET scan findings have suggested that the biochemical response of the two hemispheres to stroke may be different. Right hemisphere stroke produces an increase in serotonin receptor binding, which is not found following comparable left hemisphere strokes. Within the left hemisphere, the lower the serotonin binding, the more severe the depression. This suggests that the right but not the left hemisphere may have an ability to increase serotonin binding in noninjured regions, producing a biochemical "compensation" for damage. This differential biochemical response to injury between the right and left hemisphere may partially explain why left hemisphere injury leads to depression and right hemisphere injury (in special circumstances) lead to mania. There remain, however, numerous unanswered questions and many important areas for future research. Although this area of neuropsychiatry is just beginning to develop, it is hoped that insights gained from studying mood disorders in brain-injured patients may also help to illuminate mechanisms involved in affective disorder in patients without brain injury.
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PMID:Mood disorders following stroke: new findings and future directions. 260 85

Empirical studies have recently demonstrated that major and minor depressive disorders occur in 30-50% of stroke patients, and last more than one year without treatment, although they do respond to tricyclic antidepressants. These mood disorders are not strongly associated with severity of impairment, demographic characteristics, social supports or prior personal history, but major depression is often strongly associated with left frontal or left basal ganglia lesions and pre-existing subcortical atrophy. While the aetiology of these mood disorders remains unknown, serotonergic or noradrenergic dysfunction may play a role. Mania is a rare complication of stroke: the clinical presentation and response to treatment are usually the same as mania without brain injury. Post-stroke mania is strongly associated with both a right hemisphere lesion in a limbic-connected area and a second predisposing factor, such as genetic loading for affective disorder, pre-existing subcortical atrophy or seizure disorder. This disorder may be mediated through frontal lobe dysfunction. The lesion method represents a potentially fruitful technique for investigating the mechanisms of affective disorder.
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PMID:Affective disorders and cerebral vascular disease. 267 74

Twelve patients who developed mania after a brain lesion are reported. Ages ranged from 20 to 83 years. Five patients had brain tumors (three frontal meningiomas, one temporal meningioma, and one temporal astrocytoma), four patients had stroke lesions (one frontal, one temporal, and two thalamocapsular), two patients had a traumatic frontal closed head injury, and one patient had a pituitary adenoma resection. Although seven patients had lesions restricted to the right hemisphere, four had bilateral or midline damage and one had a left hemisphere lesion. Damage to structures functionally connected to the obitofrontal cortex, mainly in the right hemisphere, seems to be associated with secondary mania. The possible roles of monoaminergic, genetic, and perinatal factors in the pathogenesis of secondary mania are discussed.
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PMID:Mechanisms of mania after brain injury. 12 case reports and review of the literature. 327 15

Six hundred and sixty-one patients with stroke, confirmed by CT scan or at autopsy, were reviewed in order to evaluate the frequency of presentation with altered mental state. Nineteen patients (3%) had presented with delirium, an organic delusional state, the acute onset of dementia, or mania, mimicking psychiatric illness. All had focal cerebrovascular lesions which were usually, but not invariably, right sided. None had a previous history of cognitive impairment, psychiatric disease, drug abuse, or alcohol excess. Neurological signs were absent or mild and transient, and therefore easily missed. Post-mortem examinations in four patients showed localised cerebral infarctions with no evidence of multiple lesions, Alzheimer's disease, or metabolic encephalopathies. The possible causative factors are discussed and the evidence of asymmetrical cerebral representation of emotion, and for a relationship with epilepsy, is reviewed.
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PMID:Inobvious stroke: a cause of delirium and dementia. 347 Nov 94

This study investigated emotional change following stroke at acute (2-week), 2-month, and 6-month time intervals. Five dimensions of emotional functioning were examined in a sample of 19 stroke subjects: indifference, inappropriateness, depression, mania, and pragnosia (a defect in the pragmatics of social communicative style). Results showed that, at the 2-month point, differential recovery rates become apparent depending on hemispheric side of the stroke lesion. Increased indifference, inappropriateness, and depression appear to account for these results and suggest a slower rate of recovery on these variables in the left hemisphere group (LH n = 9) compared to the right (RH n = 10). Results further indicate that, at the 6-month point, emotional functioning in RH subjects appears to worsen. In contrast, emotional recovery in LH subjects seems to stabilize at this time. Clinical implications of these findings in terms of type and timing of intervention are discussed.
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PMID:Emotional sequelae of stroke: a longitudinal perspective. 783 3


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