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

Persistent depression of mood following stroke and acute psychiatric disturbances in conjunction with infarcts in the right hemisphere has been well reported. Sometimes its psychiatric features were most salient although neurological signs could not be elicited. We treated two patients with infarcts in the right hemisphere. The first developed depression with melancholia, the second a bipolar disorder. We question whether aprosodia or mood neglect may give a melancholic profile of depression following right hemisphere damage.
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PMID:[Mood disorders and right hemisphere infarction]. 269 75

Increasing evidence indicates that subtypes of bipolar disorder differ not only in symptomatology and associated clinical features, but by differences in age at onset, illness course, and response to treatment. Secondary manic states differ from typical bipolar states and are often especially difficult to treat. Although the correction of the underlying organic factors (toxic, metabolic, or infectious) may effectively reverse the manic presentation, many organic factors are not reversible (trauma, stroke, and aging), and the presence of these etiologic factors can complicate traditional antimanic treatments. Lithium may be effective for treating patients with secondary mania, but data from published studies show that in this population the associated adverse effects often limit its usefulness. Anticonvulsants appear to offer an effective alternative. Divalproex sodium, in particular, has been shown to be an effective and well-tolerated treatment in open trials in the elderly and other patient groups with secondary mania. Controlled clinical trials are necessary to confirm the efficacy and tolerability of mood-stabilizing anticonvulsants in the treatment of secondary mania.
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PMID:Secondary mania: diagnosis and treatment. 1124 98

New onset rapid cycling bipolar disorder is rare in late life. The authors report the case of an 87 year old woman who first developed this disorder at age 82 and was successfully treated with valproate and L-thyroxine. The contribution of aging, hypothyroidism and stroke to the etiology of this woman's disorder is discussed. The pharmacological management of rapid cycling bipolar disorder in the elderly is also reviewed.
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PMID:New onset rapid cycling bipolar disorder in an 87 year old woman. 834 71

Numerous emotional and behavioral disorders occur following cerebrovascular lesions. Depression is the most common of these, affecting up to 40% of patients. Clinical correlates of post-stroke depression include severity of physical and cognitive impairment as well as location of brain injury. Perhaps the most compelling reason to identify post-stroke depression, however, is its substantial impact on recovery in activities of daily living, cognitive function, and survival. Antidepressant medication has been shown to effectively treat depression, although its administration may require careful clinical monitoring. Other post-stroke emotional/behavioral disorders include mania, bipolar disorder, anxiety disorder, apathy, and pathological crying. Controlled studies have not documented the effect of these disorders on long-term recovery, but the potential impact of syndromes such as mania and apathy on rehabilitation efforts or pathological crying on social functioning are evident. With the exception of pathological crying, which has been shown to respond to antidepressant drug therapy, the other post-stroke emotional/behavioral disorders need to be evaluated in controlled treatment trials for response to therapy.
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PMID:Neuropsychiatric consequences of stroke. 904 57

The authors describe 9 patients with bipolar affective disorder associated with cerebrovascular lesions. Eight had negative family histories of affective disorders and late age at onset (after age 40) of manic-depressive symptoms. Only one, with positive family history of affective disorders, developed mood swings before age 40. Clinical subtypes of bipolar disorder and patterns of affective cycling in these stroke patients resembled those previously reported in functional bipolar disorder. Five patients had concurrent hyperkinetic movement disorders, and one depressed patient presented with unilateral left-sided parkinsonism that disappeared during a manic switch. In most patients, bipolar affective disorder was associated with right hemisphere lesions that involved subcortical and midline structures. Findings suggest that damage to frontal-basal ganglia-thalamocortical circuits by subcortical vascular lesions may simultaneously provoke disorders of movement and mood regulation.
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PMID:Poststroke bipolar affective disorder: clinical subtypes, concurrent movement disorders, and anatomical correlates. 908 51

The appearance of bipolar affective disorder after stroke depends on the presence of two factors: a predisposing factor of either genetic loading or subcortical atrophy, and a lesion of specific corticolimbic pathways involving the right hemisphere. Whether cyclothymia and seasonal affective disorder further predispose to poststroke affective disorder is not clear. A case is described which highlights these issues. The aetiological factors, pathophysiology, and diagnosis are discussed.
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PMID:Seasonal cyclothymia to seasonal bipolar affective disorder: a double switch after stroke. 941 20

Social insight, specifically the ability to represent thoughts and feelings ('theory of mind'), may have a circumscribed and dedicated neurological substrate. Evidence of deficits in 'theory of mind' following acquired lesions would support this idea. Previous studies of lesions resulting from stroke or head injury have been hampered by lack of detailed lesion information and pre-lesion documentation. We report the case of a 76-year-old man who, following a standard surgical procedure to treat bipolar affective disorder, showed evidence of impaired 'theory of mind'. This case, which is the first of its type, may contribute to the search for the brain basis of social insight.
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PMID:Acquired mind-blindness following frontal lobe surgery? A single case study of impaired 'theory of mind' in a patient treated with stereotactic anterior capsulotomy. 1111 57

Lithium, the major drug used to treat manic depressive illness, robustly protects cultured rat brain neurons from glutamate excitotoxicity mediated by N-methyl-D-aspartate (NMDA) receptors. The lithium neuroprotection against glutamate excitotoxiciy is long-lasting, requires long-term pretreatment and occurs at therapeutic concentrations of this drug. The neuroprotective mcchanisms involve inactivation of NMDA receptors, decreased expression of pro-apoptotic proteins, p53 and Bax, enhanced expression of the cytoprotective protein, Bcl-2, and activation of the cell survival kinase, Akt. In addition, lithium pretreatment suppresses glutamate-induced loss of the activities of Akt, cyclic AMP-response element binding protein (CREB), c-Jun - N-terminal kinase (JNK) and p38 kinase. Lithium also reduces brain damage in animal models of neurodegenerative diseases in which excitotoxicity has been implicated. In the rat model of stroke using middle cerebral artery occlusion, lithium markedly reduces neurologic deficits and decreases brain infarct volume even when administered after the onset of ischemia. In a rat Huntington's disease model, lithium significantly reduces brain lesions resulting from intrastriatal infusion of quinolinic acid, an excitotoxin. Our results suggest that lithium might have utility in the treatment of neurodegenerative disorders in addition to its common use for the treatment of bipolar depressive patients.
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PMID:Neuroprotective effects of lithium in cultured cells and animal models of diseases. 1207 10

A number of biological risk factors have been tentatively identified for unipolar and bipolar disorder in the elderly. The list includes genetic factors as well as medical illness in general and vascular disease in particular. Most of these risk factors have been identified on the basis of cross sectional studies rather than longitudinal studies. There is a need for long term epidemiologic and prevention studies (in the case of modifiable risk factors). The modifiable risk factors include medical illness in general and vascular disease in particular. An example is the use of antidepressants following stroke to prevent the onset of depression. Of particular interest is the role of vascular risk factors and MRI changes suggesting subtle cerebrovascular disease in the development of depression and bipolar disorder in late life. The changes have been established using both clinical samples and in the case of depression in cross sectional epidemiologic samples. The location of these cerebrovascular changes has contributed to our understanding of the regions of the brain implicated in the pathophysiology of depression. Further longitudinal and preventive studies are needed to conclusively demonstrate these as biological risk factors.
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PMID:Biological risk factors in late life depression. 1218 25

N-methyl-D-aspartate (NMDA) glutamate receptor antagonists are used in clinical anesthesia and are being developed as therapeutic agents for preventing neurodegeneration in stroke, epilepsy, and brain trauma. However, the ability of these agents to produce neurotoxicity in adult rats and psychosis in adult humans compromises their clinical usefulness. In addition, an NMDA receptor hypofunction (NRHypo) state might play a role in neurodegenerative and psychotic disorders, like Alzheimer's disease, bipolar disorder and schizophrenia. Thus, developing pharmacological means of preventing these NRHypo-induced effects could have significant clinically relevant benefits. NRHypo neurotoxicity appears to be mediated by a complex disinhibition mechanism that results in the excessive stimulation of certain vulnerable neurons. Here we report our findings that five agents (phenytoin, carbamazepine, valproic acid, lamotrigine, and riluzole), thought to possess anticonvulsant activity because they inhibit voltage-gated sodium channels, prevent NRHypo neurotoxicity. The ability of tetrodotoxin, a highly selective inhibitor of voltage-gated sodium channels, to prevent the same neurotoxicity suggests that inhibition of this ion channel is the likely mechanism of action of these five agents. We also found that three other anticonvulsants (felbamate, gabapentin and ethosuximide), whose mechanism is less clear, also prevent NRHypo neurotoxicity, suggesting that inhibition of voltage-gated sodium channels is not the only mechanism via which anticonvulsants can act to prevent NRHypo neurotoxicity. Several of these agents have been found to be of clinical use in bipolar disorder. It would be of interest to determine whether these agents might have therapeutic benefits for conditions in which a NRHypo state may exist.
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PMID:Antiepileptic drugs and agents that inhibit voltage-gated sodium channels prevent NMDA antagonist neurotoxicity. 1219 17


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