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

We report a 62-year-old man with ballism confined to the right leg, so-called monoballism. He was admitted to our hospital complaining of gait disturbance due to violent involuntary movements in the right lower extremity which had developed seven days before. He had a ten-years' history of hypertension and at age 57 had been diagnosed as having asymptomatic multiple cerebral infarcts. Until admission, he was taking antiplatelet drugs for the purpose of preventing thrombotic stroke. On neurological examination, he showed mild impairment of higher brain function, Horner's sign in the left eye, and typical ballism in the right lower extremity. Involuntary movements were never observed in the face and the other extremities. Surface electromyography also showed reciprocal burst discharges at about 1 Hz related to the ballistic movements in the right lower extremity. CT scan revealed a high density lesion surrounded by a low density in the left subthalamic area. MRI examination demonstrated a dumbbell shaped hemorrhage extending from the left subthalamic nucleus to the dorsomedial nucleus of the ipsilateral thalamus. Adding to the hemorrhage, many ischemic lesions were observed in the bilateral basal ganglia and thalamus including the left pallidum. The causal end of the hemorrhage apparently located in the anterior dorsomedial portion of the subthalamic nucleus. There were few reports concerning monoballism, especially monoballism limited to the lower extremity. Recent researches indicate that a subthalamic lesion reduces the excitatory control from the subthalamus to the internal segment of the globus pallidus, which leads to a disinhibition of the thalamus and gives rise to ballism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of thalamo-subthalamic hemorrhage presenting monoballism in the contralateral lower extremity]. 130 Feb 59

Over the past fifty years considerable clinical evidence has accrued to demonstrate involvement of the cerebral cortex in cardiac function. Hemispheric stroke is often associated with electrocardiographic (ECG) evidence of cardiac repolarisation abnormalities. In addition strokes of all types are associated with specific pathological changes in the ventricular myocardium (myocytolysis). These effects are not attributable to concomitant cardiac ischemic disease in the majority of cases. The insular cortex has recently been shown to contain a site of cardiac representation. Prolonged stimulation of this region in the rat produces ECG and cardiac pathological changes similar to those observed after human stroke. It is suggested that middle cerebral artery stroke in certain cases either directly or indirectly leads to insular disinhibition, and increased autonomic activity represented by cardiac changes which significantly influence prognosis.
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PMID:The insular cortex and the pathophysiology of stroke-induced cardiac changes. 162 48

The high affinity noncompetitive N-methyl-D-aspartate receptor antagonist CNS 1102 (aptiganel hydrochloride, Cambridge NeuroScience, Cambridge, MA.) is neuroprotective in preclinical models of stroke when administered as pretreatment or up to 60 minutes postischemia, and has potential for treatment of acute stroke or traumatic brain injury in man. A total of 55 healthy male subjects have participated in three separate studies to determine the clinical pharmacology of CNS 1102, 43 of whom have received CNS 1102 in doses of up to 100 micrograms/kg. Administration of CNS 1102 has been studied as a 15-minute intravenous infusion, as a 15-minute loading intravenous infusion followed by a 4-hour maintenance infusion, or as a fixed-dose intravenous bolus over 90 seconds. CNS 1102 in normal volunteers is well tolerated in total doses up to 32 micrograms/kg whether as a bolus injection, 15-minute infusion or 4-hour infusion. Central nervous system affects are evident within minutes of administration, implying rapid drug penetration. CNS 1102 has a large and variable volume of distribution (mean +/- standard deviation, 6.2 +/- 1.9 l/kg), variable clearance (115 +/- 77 l/h), and plasma half-life of approximately 4.5 hours. Adjustment of doses by subject weight does not improve variability of these parameters, and fixed doses may thus be administered. CNS 1102 causes dose-dependent elevation of blood pressure, accompanied by clinical evidence of vasoconstriction. Global cerebral blood flow is maintained, whilst middle cerebral artery flow velocity increases. Symptoms of light-headedness, disorientation and paresthesia progress through euphoria, disinhibition, and hallucinations to psychomotor retardation, paranoia and catatonia as total administered dose increases.
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PMID:Clinical pharmacology of CNS 1102 in volunteers. 748 14

Motor behaviors on the 'good side' of the body, i.e. ipsilateral to the hemispheric lesion, have not been studied systematically. We assessed motor behaviors in 20 consecutive patients during the acute phase (first 1-2 weeks) of a hemispheric stroke with hemiparesis. The behaviors were essentially rotations of the head, neck, eyes and trunk, orofaciopharyngeal or limb stereotypes, compulsive manipulation of the surroundings, or passive mobilization of the paralyzed arm or leg. These behaviors were found only with large infarcts in the territory of the internal carotid artery, middle cerebral artery and/or the anterior cerebral artery (ACA). All but two ACA infarcts involved the internal capsule and basal ganglia. The severity of the motor deficit and the presence of aphasia, neglect, or sensory loss were significantly correlated with the motor behaviors. Although the understanding of these behaviors remains unclear, we suggest that they may represent the clinical expression of early plastic changes of brain maps and circuits after an acute lesion; this is probably an active process induced by disinhibition, in order to establish new compensatory pathways.
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PMID:Hyperkinetic motor behaviors contralateral to hemiplegia in acute stroke. 881 36

Disinhibition syndromes, ranging from mildly inappropriate social behavior to full blown mania, may result from lesions to specific brain areas. Several studies in patients with closed head injuries, brain tumors, stroke lesions, and focal epilepsy have demonstrated a significant association between disinhibition syndromes and dysfunction of orbitofrontal and basotemporal cortices of the right hemisphere. Based on the phylogenetic origin of these cortical areas and their main connections with dorsal regions related to visuospatial functions, somatosensation, and spatial memory, the orbitofrontal and basotemporal cortices may selectively inhibit or release motor, instinctive, affective, and intellectual behaviors elaborated in the dorsal cortex. Thus, dysfunction of these heteromodal ventral brain areas may result in disinhibited behaviors.
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PMID:Mechanism of disinhibition after brain lesions. 904 3

During single word processing the negative cortical DC-potential reveals a left frontal preponderance in normal right-handers as well as in patients with a history of transient aphasia. Lateralization of DC-negativity therefore provides a reliable and robust method for the assessment of language dominance. In 11 stroke patients with permanent aphasia this physiological pattern changed to bilateral activation reflecting an additional right-hemispheric involvement in compensatory mechanisms in aphasia. Along with complete clinical recovery the classical aphasic syndromes revealed specific differences in changes of their lateralization patterns. In Broca's aphasia the initial right-hemispheric preponderance changed to a left frontal lateralization while in Wernicke's aphasia a presumably permanent shift towards the right hemisphere occurred. Differences in lateralization patterns might reflect different mechanisms of recovery such as the initial disinhibition of homologous areas contralaterally and subsequent collateral sprouting and synaptic modulation. The assessment of changes in lateralization of the cortical DC-potential during language tasks in a non-invasive, safe method with excellent time resolution that might provide further insights in the neural basis of recovery from aphasia.
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PMID:Language processing in aphasia: changes in lateralization patterns during recovery reflect cerebral plasticity in adults. 906 Aug 59

Symptoms consistent with dysfunction of the frontal lobes can occur following traumatic brain injury (TBI) or other types of acquired brain injury (stroke, aneurysm). These symptoms can include problems with short-term memory, attention, planning, problem solving, impulsivity, disinhibition, poor motivation, and other behavioral and cognitive deficits ("frontal lobe syndrome"). These symptoms may respond to certain drugs, such as dopaminergic agents. This case series describes results of using amantadine in 7 patients with this type of symptom profile (6 with TBI, 1 with meningitis following sinus surgery). Patients received neuropsychiatric examinations and serial neuropsychological testing. All patients showed some degree of positive response. One had side effects that resolved upon discontinuation of drug. The rationale for using dopaminergics is discussed, and pertinent literature is reviewed.
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PMID:Effect of amantadine hydrochloride on symptoms of frontal lobe dysfunction in brain injury: case studies and review. 914 1

Numerous studies in stroke patients suggest that the left frontal anterior region may be strategic for depression. However, these findings could not always be replicated. Some authors even deny any etiological contribution of lesion location to depression. The predominant role of the right hemisphere in secondary mania is well recognized. In disorders such as apathy, anxiety, catastrophe reactions and pathological laughing and crying, further studies are needed to determine the potential clinico-topographic correlations. Affective disorders are important to consider in stroke patients, since they may influence neurological recovery and may be responsive to treatment. Remarkable features of emotional behavior, such as disinhibition, denial, indifference, overt sadness and aggressiveness, are not rare during the acute phase of stroke and might be overlooked if not searched for systematically with appropriately designed scales. Some of these early behaviors, such as denial, may relate to the late development of depression, anxiety and other disorders. Systematic studies on large samples of patients may allow to establish which of these acute emotional behavioral changes are markers for the delayed development of mood disorders.
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PMID:Affective disorders following stroke. 928 28

Excessive activation of N-methyl D-aspartate (NMDA) receptors by endogenous glutamate (Glu) causes excitotoxic neuronal degeneration in acute central nervous system injury syndromes such as stroke and trauma. Early attempts to link NMDA receptor hyperactivity (NRHyper) to Alzheimer disease (AD) were stymied by evidence in 3 separate species (mice, rats, and monkeys) that, with advancing age, the NMDA receptor system becomes markedly hypoactive. While this would seem to argue against a role for NMDA receptors in AD, we have recently found in animal studies that, when the NMDA receptor system is rendered markedly hypoactive, a disinhibition syndrome is triggered in which low-grade chronic excitotoxic activity (fueled by acetylcholine and Glu) is unleashed that can cause a widespread pattern of neuronal degeneration resembling that seen in AD. Therefore, we postulate that NMDA receptor hypoactivity (NRHypo) associated with advancing age may have an important contributory role in AD and that the main difference between the aging AD brain and the aging "normal" brain is that a heavier burden of certain adjunctive risk factors may be present in the AD brain that promote the NRHypo state and increase the likelihood that widespread neurodegeneration will occur.
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PMID:Excitotoxic neurodegeneration in Alzheimer disease. New hypothesis and new therapeutic strategies. 934 69

In clinical stroke cardiovascular abnormalities are frequently neglected although they occur more often than it is generally assumed. However, cardiac arrhythmias, pathological ECG findings, and changes of circadian blood pressure patterns are significantly increased in patients with acute cerebrovascular lesions and are associated with an increased mortality. Several clinical studies have shown that cerebral infarctions may cause different cardiovascular abnormalities depending on the location and the size of the stroke. Hereby, the prolongation of the QT interval and the expansion of the QRS-complex as the most frequent ECG abnormalities are regarded as indicators of the electrical instability of the ventricular myocardium. Furthermore, cardiac enzyme increases are interpreted as an indicator of myocardial damage during the acute phase after cerebral ischaemia. Since the autonomic nervous system plays a major role in the regulation of blood pressure, alterations of sympatho-adrenergic activity can also affect the diurnal blood pressure profile. Some studies report frequent changes of the circadian blood pressure patterns with a decreased night-time blood pressure decline or a pathological night-time blood pressure elevation. Several studies proved the importance of infarct location. The insular cortex in particular has an important role in the genesis of the pathological activation of the sympathetic nervous system. Hence, a highly significant relationship between the extent of circadian blood pressure variation and percentage insular infarction could be found. Some findings implied that the mechanism of cardiovascular instability following stroke relates to the disinhibition of the insular cortex and a reacting augmentation of the sympathetic tone. A further important aspect is given by the strong evidence that sympathetic activation ] is lateralized following hemispheric brain infarction. Accordingly, patients with a right-sided hemispheric infarction showed a significantly diminished circadian blood pressure variation as compared with patients with left-sided hemispheric infarction. The results in patients with brain stem infarction were heterogeneous. On the one hand, patients with brain stem infarction had substantially higher mean plasma norepinephrine levels than did patients with hemispheric infarction; on the other hand, hemispheric lesions were associated with a significantly higher incidence of cardiac arrhythmias when compared to patients with brain stem infarction.
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PMID:Cardiovascular consequences of clinical stroke. 948 96


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