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

Previous workers have clearly established that the central core limbic structures of the brain are primarily concerned in the production of amnesia of the axial or mesial type. The blood supply to these structures derives primarily from the posterior cerebral circulation. This was the rationale for Benson's work on 'amnesic stroke' in patients with posterior cerebral artery occlusion. We have extended this concept to show that a similar axial amnesia, as demonstrated by a classical response on Wechsler Memory Scale testing, exists in patients with vertebrobasilar insufficiency. Relative permanency of the amnesic syndrome was demonstrated by repeat testing at may be of assistance in the diagnosis of vertebrobasilar insufficiency.
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PMID:Memory disorder in vertebrobasilar disease. 11 97

Six patients with bilateral paramedian thalamic infarction were seen in a general hospital over a 4 year period. This distinct stroke syndrome was recognized by the features of disturbed vigilance, often episodic, with vertical gaze disorder. Other signs included an amnesic syndrome, convergence difficulty, third nerve palsies, eyelid retraction, dysarthria, ataxia and involuntary limb movements. Diagnosis was confirmed by CT brain scan or magnetic resonance imaging. A variety of risk factors for stroke were present. All patients improved but two had significant residual disabilities.
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PMID:Bilateral paramedian thalamic infarction: a distinct but poorly recognized stroke syndrome. 143 69

The clinical manifestations of thalamic hemorrhage frequently comprise hemiparesis, hemianesthesia, and oculomotor abnormalities. Since the advent of computed tomography, an amnestic syndrome following thalamic hemorrhage has been recognized, but the thalamic structures involved and the mechanism of amnesia have remained uncertain. We report a patient with sudden memory dysfunction following hemorrhage into the anterior nucleus of the left thalamus that was shown neuropathologically to disrupt the mamillothalamic fasciculus, one of the principal components of the limbic system. It is considered that the amnestic syndrome following thalamic (anterior nucleus) hemorrhage is due to interruption of the mamillothalamic fasciculus.
Stroke 1988 Jun
PMID:Amnesia following thalamic hemorrhage. Another stroke syndrome. 337 71

The paramedian diencephalic syndrome is characterized by a clinical triad: hypersomnolent apathy, amnesic syndrome, and impaired vertical gaze. We studied 4 cases with computed tomography evidence of bilateral diencephalic infarctions. Each case began abruptly with hypersomnolent apathy followed by fluctuations from appropriate affect, full orientation, and alertness to labile mood, confabulation, and apathy. Speech varied from hypophonia to normal; handwriting varied from legible script to gross scrawl. Psychological testing revealed poor learning and recall, with low performance scores. In 3 patients the predominant abnormality was in downward gaze.
Stroke
PMID:The paramedian diencephalic syndrome: a dynamic phenomenon. 356 93

Transient global amnesia is an unusual form of the amnestic syndrome in that it is completely reversible in most patients. The etiology of transient global amnesia is poorly understood, although involvement of the medial temporal lobe is most likely. The literature suggests that once an underlying structural lesion has been ruled out, cases can be divided into three groups: patients with a past history of migraine headaches, those who have no obvious underlying precipitating factors, and those with associated neurologic deficits during a spell and risk factors for cerebrovascular disease. Patients in the first group tend to have attacks at an earlier age and to have an increased recurrence rate but, like those in the second group, have a good prognosis. Patients in the third group often have onset later in life, and as many as 10% may have a stroke or dementia. Whether or not this is a higher incidence than should be expected in persons of this age group has not been determined. Although sophisticated testing may show persistence of the memory defect, most patients eventually recover completely.
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PMID:Transient global amnesia and the amnestic syndrome. 378 95

In this paper, we review the symptoms associated with damages to the frontal and/or temporal lobes. Similarities and differences between the symptoms observed after a stroke and in frontotemporal lobar degeneration are also discussed. Frontal lobe damages may lead to various apraxic disorders, including limb-kinetic, ideomotor, gait, buccofacial, and ocular motor apraxia. Language dysfunction can arise from perisylvian lesions as well as from extra-perisylvian regions. Broca's aphasia, Wernicke's aphasia, pure word deafness, and aphemia are typical examples of disorders caused by damages to the perisylvian region. Transcortical motor and anomic aphasias are mostly associated with damages to the extra-perisylvian region. Although it has been reported that executive dysfunction is associated with damages to the frontal lobe, it remains to be determined whether there is a cause-and-effect relationship between the 2. A combination of memory, attention, emotional, and mood disorders may underlie executive dysfunction. Patients with lesions in the inferior temporal lobe often present with various types of agnosia. Visual agnosia is common in semantic dementia, but is infrequent after a stroke in the temporal lobe. Prosopagnosia is a rare consequence of damages to the temporal lobe. Bilateral and right-sided lesions are likely to cause this disorder than left-sided lesions. Although, prosopagnosia is less frequently observed than visual agnosia in semantic dementia, it still is one of the common features of the disease. Bilateral injuries to the mesial temporal lobes have been known to induce a marked amnesic syndrome. It is devastating in that the patient can remember virtually nothing new. However, memories acquired before the injuries are mostly conserved and the patient can still learn motor skills.
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PMID:[The symptomatology of frontal and temporal lobe damages]. 1993 77

Strategic regions correspond to associative, limbic and paralimbic structures and related circuits, that underpin cognitive/behavioral functions. Strokes in these eloquent sites produce pictures of vascular dementia with syndromic features due to specific site lesion and/or interruption of their interconnections. This study aims at analysing subcortical strategic strokes that express similar cognitive/behavioral elements, by sharing common pathways. Patients (n=6) who attended in specialized ambulatory, were submitted to neuropsychological and neuroimaging assessments through MRI (GE Signa Horizon 1.5T) and brain SPECT (Millennium MG, ECD [TC-99m]). Stroke locations and respective main symptoms were: 1. anteromedian thalamus [L]: anterograde and retrograde amnesia (ARA), expression aphasia (EA), executive dysfunction (ED), apathy, and depression; 2. anterior thalamus [R]: ARA, inattention, apathy, and aggressiveness; 3. dorsomedian thalamus [L]: inattention, ED, anosognosia, and aggressiveness; 4. central paramedian thalamus [R]: EA, visual perception deficits (VPD), ED, infantility, and personality disorder; 5. caudate nucleus (ventral-head) [L]: VPD, ED, delirium, visual hallucinations, and personality disorder; and 6. anterior capsule [L]: VPD, ED, apathy, and depression. Vascular strategic syndromes connote the predominantly impaired cognitive/behavioral symptom of each site. Temporal and frontal disconnection symptoms were produced by disrupted MTT/hippocampal and IML/amygdala circuits expressing amnesic syndrome associated with heterogeneous dysexecutive syndrome, in all the cases, by disrupting frontal-basal ganglia-thalamus-cortical net, in three different levels of their pathway.
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PMID:Cognitive disconnective syndrome by single strategic strokes in vascular dementia. 2293 18

Unilateral cerebral ischemia of the hippocampus is very rare. This paper reviews the literature and presents the case of a 59-year-old woman with an amnestic syndrome due to a left hippocampal stroke. The patient suffered from retrograde amnesia which was most severe over the 2 days prior to presenting and a slight anterograde amnesia. In addition, a verbal memory disorder was confirmed 1 week after admission by neurological tests. As risk factors, arterial hypertension and a relative hyper-beta lipoproteinemia were found. This case shows that unilateral amnestic stroke, e.g. in the hippocampus region, may be the cause of an amnestic syndrome and should be included in the differential diagnostics.
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PMID:[Hippocampal stroke]. 2557 32