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

The medical records and autopsy data of patients over the age of 70 years at death with a diagnosis of cortical artery infarction (CAI) in the Yokufukai Geriatric Hospital were reviewed. Among 690 autopsied cases from 1981 to 1988, there were 45 cases (21 men and 24 women) with CAI available for this study. Fourteen cases (31.1%) suffered CAI while hospitalized for another disorder. Their ages at death ranged from 70 to 102 years with a mean of 82.4 years. From the results of this neurological and psychological analysis, the residuals of senile stroke were classified into six subtypes: 1) cerebrovascular dementia, 2) cerebrovascular Parkinsonism, 3) pseudobulbar palsy, 4) chronic stage of aphasia, 5) slowly-progressive decreased motivation or spontaneity without dementia, 6) the so-called bedridden state (prolonged vegetative or apallic state). Sixty-nine percent had anamnetic hypertension before the stroke. The ages at which they became bedridden ranged from 69 to 102 years with a mean of 81.8 years. Within one year after becoming bedridden, 83.3% of all patients died. The bedridden state in the elderly with residual CAI indicated a poor prognosis within one year after stroke. Causes of death included brain death in 22.3% of all patients, pneumonia in 20.0%, and digestive bleeding in 8.9%.
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PMID:[Cerebrovascular disease in the elderly--a clinicopathological study of 45 autopsied cases with cortical artery infarction]. 189 27

We studied 13 patients with supranuclear lower cranial nerve ("pseudobulbar" or "suprabulbar") palsy of acute onset. While seven patients had had a prior stroke, six patients had no history of stroke. Eight patients experienced a complete bilateral supranuclear lower cranial nerve palsy, which was isolated in five patients and associated with hemiplegia and with hemiparesis in three patients. Pseudobulbar palsy was partial in five patients. Only one patient had neuropsychologic impairment. The pseudobulbar features improved or recovered within a few weeks in all patients. The common characteristic of the lesions on computed tomography or magnetic resonance imaging was the interruption of the corticonuclear pathways contrasting with marked sparing of the corticospinal pathways in both hemispheres. These lesions were either an opercular infarct, or a deep infarct in the corona radiata or internal capsule, or a lenticular hemorrhage. Hypertension was the most prevalent concomitant. Our findings suggest that acute pseudobulbar or suprabulbar palsy has rather stereotyped anatomic-vascular correlates and time course.
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PMID:Acute pseudobulbar or suprabulbar palsy. 202 63

CT examination in 100 patients affected by chronic cerebrovascular insufficiency showed a normal picture in 16 cases, while 84 subjects showed different degrees of atrophy, generalised and focal, controlateral or sometime omolateral to the infarct, with differing patterns. The mean age of subjects with normal CT was significantly lower in comparison with patients with definite atrophy. Besides the neurological picture and the time course, the patients' psychiatric status was also assessed: no definite relationship seems to exist between psychiatric disturbances and brain atrophy. Pseudobulbar syndrome was found in 46 cases and many of them showed cortical and mainly ventricular atrophy. This picture was very seldom found in patients with vertebro-basilar insufficiency. Localised cortical atrophy, on the contrary, was often associated with ischaemic stroke. The incidence of predisposing risk factors (hypertension, diabetes mellitus or high lipid levels) was greater in subjects with brain atrophy and older age than in patients with normal CT scan.
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PMID:[CT findings in chronic cerebrovascular insufficiency (author's transl)]. 729 86

A survey was carried out on a large family presenting the symptoms of familial arteriopathy (CADASIL) recently mapped to chromosome 19. This is characterised clinically by recurrent subcortical infarcts developing into pseudobulbar palsy and subcortical dementia, and radiologically by early MRI abnormalities. To characterise this familial condition, 43 members older than 20 years and spreading over four generations were studied clinically (31 living, 12 deceased), genetically, and radiologically by MRI (n = 31). Twenty out of 43 were found to be clinically symptomatic and of these 13 out of 31 had MRI abnormalities. Genetic studies mapped this condition to the locus of CADASIL (lod score > 3). The natural history suggests a chronological clinicoradiological staging of this phenotype of CADASIL: stage I between 20 and 40 years with frequent migraine-like episodes and well delineated lesions of the white matter; stage II between 40 and 60 years with stroke-like episodes, bipolar or monopolar-like psychotic disorders, coalescent lesions of the white matter, and well delineated lesions of the basal ganglia; and stage III over 60 years with subcortical dementia, pseudobulbar palsy, diffuse leukoencephalopathy, and multiple well delineated lesions of the basal ganglia. This phenotype differs from the other two previously described by high frequency of migraine, frequency of psychotic disorders, and early neurological manifestations. The new acronym "cerebral autosomal dominant arteriopathy with subcortical infarcts, leukoencephalopathy, and migraine" (CADASILM) is proposed to better describe this particular subvariety of CADASIL.
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PMID:New phenotype of the cerebral autosomal dominant arteriopathy mapped to chromosome 19: migraine as the prominent clinical feature. 750 94

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited arterial disease of the brain recently mapped to chromosome 19. We studied 148 subjects belonging to seven families by magnetic resonance imaging and genetic linkage analysis. 45 family members (23 males and 22 females) were clinically affected. Frequent signs were recurrent subcortical ischaemic events (84%), progressive or stepwise subcortical dementia with pseudobulbar palsy (31%), migraine with aura (22%), and mood disorders with severe depressive episodes (20%). All symptomatic subjects had prominent signal abnormalities on MRI with hyperintense lesions on T2-weighted images in the subcortical white-matter and basal ganglia which were also present in 19 asymptomatic subjects. The age at onset of symptoms was mean 45 (SD [10-6]) years, with attacks of migraine with aura occurring earlier in life (38.1 [8.03] years) than ischaemic events (49.3 [10.7] years). The mean age at death was 64.5 (10.6) years. On the basis of MRI data, the penetrance of the disease appears complete between 30 and 40 years of age. Genetic analysis showed strong linkage to the CADASIL locus for all seven families, suggesting genetic homogeneity. CADASIL is a hereditary cause of stroke, migraine with aura, mood disorders and dementia. The diagnosis should be considered not only in patients with recurrent small subcortical infarcts leading to dementia, but also in patients with transient ischaemic attacks, migraine with aura or severe mood disturbances, whenever MRI reveals prominent signal abnormalities in the subcortical white-matter and basal ganglia. Clinical and MRI investigations of family members are then crucial for the diagnosis which can be confirmed by genetic linkage analysis. The disease is probably largely undiagnosed.
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PMID:Clinical spectrum of CADASIL: a study of 7 families. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. 756 22

Vascular dementia is usually sporadic and associated with definite risk factors. Several cases also occur in a familial fashion, and may affect middle-aged or even younger subjects. Recently, an autosomal dominant inheritance was demonstrated in two unrelated French families, the members of which were affected by stroke-like episodes culminating in progressive dementia. Genetic linkage analysis assigned the disease locus to chromosome 19q12. We report an additional kindred of Italian origin in which at least 16 subjects presented leukoencephalopathic alterations. Recurrent strokes, psychiatric disturbances, dementia, and in 2 members, tetraplegia and pseudobulbar palsy were the hallmarks of this syndrome. Notably, 5 asymptomatic individuals had neuroradiological signs of leukoencephalopathy. Pathological examination of 1 subject revealed a widespread vasculopathy of the perforating arterioles, characterized by deposition of eosinophilic-congophilic material that did not immunostain with antibodies against prion protein, beta-amyloid, cystatin C, transthyretin, or heat-shock protein 70 and was similar to that described in the French families. Based on the maximum lod score, the most likely location for the disease locus was also mapped to chromosome 19q12, and found to coincide with the CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) locus. The present results confirm the existence of a nosologically distinct, autosomal dominant cerebrovascular disease, presenting with recurrent subcortical ischemic strokes independent of vascular risk factors.
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PMID:An Italian kindred with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). 765 71

A 28-year-old, previously healthy, normotensive woman suddenly developed an acute pseudobulbar palsy with dysarthria, dysphagia, hypernasal voice and mild right arm paresis. Extensive laboratory investigations excluded all other possible causes of acute pseudobulbar palsy (neoplastic, inflammatory, demyelinative, myasthenic) and an MRI study demonstrated bilateral isolated thalamic infarcts. Oral contraceptives and smoking were the only possible stroke risk factors found and cerebral diaschisis the most tenuous explanation proposed. To our knowledge, this is the first report indicating that bilateral thalamic infarction on specific nuclei could be manifested as acute pseudobulbar palsy.
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PMID:Bilateral thalamic infarcts presenting as acute pseudobulbar palsy. 775 Aug 10

The potential causes of neurogenic oropharyngeal dysphagia in cases in which the underlying neurologic disorder is not readily apparent are discussed. The most common basis for unexplained neurogenic dysphagia may be cerebrovascular disease in the form of either confluent periventricular infarcts or small, discrete brainstem stroke, which may be invisible by magnetic resonance imaging. The diagnosis of occult stroke causing pharyngeal dysphagia should not be overlooked, because this diagnosis carries important treatment implications. Motor neuron disease producing bulbar palsy, pseudobulbar palsy, or a combination of the two can present as gradually progressive dysphagia and dysarthria with little if any limb involvement. Myopathies, especially polymyositis, and myasthenia gravis are potentially treatable disorders that must be considered. A variety of medications may cause or exacerbate neurogenic dysphagia. Psychiatric disorders can masquerade as swallowing apraxia. The basis for unexplained neurogenic dysphagia can best be elucidated by methodical evaluation including careful history, neurologic examination, videofluoroscopy of swallowing, blood studies (CBC, chemistry panel, creatine kinase, B12, thyroid screening, and anti-acetylcholine receptor antibodies), electromyography, and magnetic resonance imaging (MRI) of the brain, plus additional procedures such as lumbar puncture and muscle biopsy as indicated. Little is known about aging and neurogenic dysphagia, specifically the relative contributions of natural age-related changes in the oropharynx and of diseases of the elderly, including periventricular MRI abnormalities, in producing dysphagia symptoms and videofluoroscopic abnormalities in this population.
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PMID:Neurogenic dysphagia: what is the cause when the cause is not obvious? 780 24

Forced laughter generally occurs in bilateral or diffuse lesions of the brain and is generally associated with pathologic crying. We report the cases of 3 patients in whom temporary forced laughter occurred after unilateral supratentorial infarction demonstrated by CT scan or MRI. In all cases, the lesion was exclusively subcortical and involved the striatocapsular region. For all patients the laughter occurred during the recovery phase of motor deficit and was 'pure' without associated weeping or other clinical features of pseudobulbar palsy. In all cases, the laughter attacks had become much less frequent or had totally disappeared 1 or 2 months after the stroke. According to a 'motor' hypothesis, a unilateral striatocapsular lesion may lead to temporary deregulation of the expression mechanisms.
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PMID:Temporary forced laughter after unilateral strokes. 813 36

Foix-Chavany-Marie Syndrome or anterior opercular syndrome constitutes the cortical form of pseudobulbar palsy. Its most common etiology is stroke in the region of either operculum. Clinically it can be characterized by severe dysarthria and facio-pharyngo-glosso-masticatory dysplasia with automatic-voluntary dissociation. An inversion of this classical dissociation can be seen in patients with emotional paralysis in the face, in whom asymmetry of emotional expression but conservation of voluntary movement can be seen. The lesional topography of this inverse dissociation corresponds to the supplementary motor area. both processes support the existence of an anatomical base which is different for emotional movements and voluntary types. We describe the clinical case of a 65 year old woman with a history of breast cancer who presented a subacute and progressive clinical picture of dysphagia and severe dysarthria. Upon neurological examination slight velo-palato-pharyngea was noticed; most relevant was paralysis of the facial muscles for either emotional or automatic movements while voluntary innervation was maintained. Neuroradiological studies show the presence of brain metastasis located in both Roland opercula. Although the neuroanatomic bases for automatic-voluntary dissociation remain unclear, our case lends weight to the evidence that impulses for voluntary and emotional movements originate in different cortical areas or else take a different route through the brain. We have been unable to find any cases of biopercular lesion with inverse dissociation described in the literature we reviewed.
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PMID:[Biopercular lesion with inverse dissociation]. 855 92


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