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

A 47-year-old man was admitted to the hospital because of general convulsion, loss of consciousness and hyperthermia. A diagnosis of acute heat stroke was made clinically and neuroradiologically. As the consciousness level ameliorated, he developed severe abulia and mutism, then cerebellar ataxic syndrome (viz. truncal ataxia, hypermetria, ataxic speech and nystagmus). An MRI (diffusion weighted image; DWI) disclosed abnormal diffuse high signal intensity of the cerebellar cortex with reduced apparent diffusion coefficient (ADC). Two months later after the onset, truncal ataxia and dysarthria significantly improved, while dysmetria of the extremities rather worsened. At that time, the abnormal signal intensity of the cerebellar cortex disappeared, and the cerebellum became atrophic. The cerebellar blood flow was significantly decreased on brain SPECT (99mTc-ECD). The abnormal DWI signal intensity of the cerebellar cortex in the present patient may represent the cytotoxic edema of Purkinje cells resulting from heat stroke-related hyperthermia It is essential to repeat MRI examination for cerebellar pathology and to obtain better insight into sequelae in patients with acute heat stroke. Protirelin tartrate seemed to be valid for improvement of abulia in the present patient. Further study is indicated.
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PMID:[An acute severe heat stroke patient showing abnormal diffuse high intensity of the cerebellar cortex in diffusion weighted image: a case report]. 1999 44

We describe a case of bilateral caudate nucleus infarction caused by cardioembolic stroke associated with a variant circle of Willis. The patient was an 81-year-old man with atrial fibrillation who presented with a sudden disturbance of consciousness. When he became more alert a few days later, he was abulic with no spontaneous speech or activity. A magnetic resonance imaging scan of the brain revealed cerebral infarction of bilateral caudate nucleus heads and the left frontal lobe. The left A1 segment was absent on 3-dimensional computed tomography angiography. One year later, abulia had completely resolved. Bilateral caudate nucleus infarction with variant circle of Willis is rare.
J Stroke Cerebrovasc Dis 2012 Nov
PMID:Bilateral caudate nucleus infarction associated with a missing A1 segment. 2217 27

Anhedonia and abulia are syndromes often presented as components of various psychiatric and neurological disorders, including depression, schizophrenia, stroke, multiple sclerosis and brain injury. On the basis of the hypothesis that alterations in the dopaminergic motivational system might be involved in the etiopathogenesis of these clinical phenomena, the antidepressant agomelatine is a highly interesting candidate substance for their treatment because of its indirect dopaminergic effects resulting from its melatoninergic and partial anti-serotoninergic properties. Systematic clinical studies are urgently needed to test the hypothesis that agomelatine might be a clinically useful and versatile anti-anhedonic and/or anti-abulic substance.
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PMID:Agomelatine: an agent against anhedonia and abulia? 2431 Oct 62

A 55-year-old woman was admitted with a 3 days history of increasing lethargy with bradyphrenia and apathy. She progressively developed severe somnolence with marked abulia, right hemiparesis, right hemianopsia, and pseudobulbar palsy. Brain magnetic resonance imaging showed the rare image of bilateral acute anterior choroidal artery infarction. Pseudobulbar mutism and in rare cases abulia have been described in acute anterior choroidal artery infarction contralateral to an older lesion in mirror position. Although neurologic deterioration is not infrequent in anterior choroidal artery territory infarcts, the absence of focal neurologic signs on admission is rare and did not raise suspicion of acute stroke.
J Stroke Cerebrovasc Dis 2014 Sep
PMID:Bilateral anterior choroidal artery infarction presenting with progressive somnolence. 2510 36

Behavioral dysexecutive disorders are highly prevalent in patients with neurological diseases but cannot be explained by cognitive dysexecutive impairments. In fact, the underlying mechanisms are poorly understood. Given that socioemotional functioning underlies appropriate behavior, socioemotional impairments may contribute to the appearance of behavioral disorders. To investigate this issue, we performed a transnosological study. Seventy-five patients suffering from various neurological diseases (Alzheimer's disease (AD), Parkinson's disease (PD), frontotemporal lobar degeneration, and stroke) were included in the study. The patients were comprehensively assessed in terms of cognitive and behavioral dysexecutive disorders and socioemotional processes (facial emotion recognition and theory of mind). As was seen for cognitive and behavioral dysexecutive impairments, the prevalence of socioemotional impairments varied according to the diagnosis. Stepwise logistic regressions showed that (i) only cognitive executive indices predicted hypoactivity with apathy/abulia, (ii) theory of mind impairments predicted hyperactivity-distractibility-impulsivity and stereotyped/perseverative behaviors, and (iii) impaired facial emotion recognition predicted social behavior disorders. Several dysexecutive behavioral disorders are associated with an underlying impairment in socioemotional processes but not with cognitive indices of executive functioning (except for apathy). These results strongly suggest that some dysexecutive behavioral disorders are the outward signs of an underlying impairment in socioemotional processes.
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PMID:Does impaired socioemotional functioning account for behavioral dysexecutive disorders? Evidence from a transnosological study. 2705 57

A 75-year-old woman presented with consciousness disturbance accompanied by hematemesis. Brain imaging revealed ischemia in the bilateral caudate nuclei and right cerebral watershed area due to stenosis of the right anterior cerebral artery (ACA) and bilateral internal carotid arteries (ICA), and hypoperfusion in the right caudate nucleus. The patient's only symptom was abulia, which gradually resolved. Further brain scans showed that the ICA stenosis had improved, although the right ACA stenosis persisted. This was a rare case of bilateral caudate nucleus infarctions with a hemodynamic etiology.
J Stroke Cerebrovasc Dis 2018 Sep
PMID:Bilateral Caudate Nucleus Infarctions Following Upper Gastrointestinal Bleeding. 2980 81

A 62-year-old male presented to hospital with acute aphasia. His past medical history was significant for a previous left middle cerebral artery stroke, from which he fully recovered, hypertension, dyslipidemia, coronary artery disease, one episode of atrial fibrillation postoperatively, and thalidomide exposure in utero. Although initially he was thought to be aphasic, on further examination, he demonstrated significant abulia. His level of consciousness was normal, and neurological examination was otherwise unremarkable. A CT angiogram of the head and neck was performed. The patient was not a candidate for acute therapy, as he had established stroke on imaging, and the time of onset was unclear.
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PMID:Rare Bilateral Caudate Infarction in a Patient with a Common Circle of Willis Variant. 3123 Jun 3


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