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

Two more patients with triphasic waves (TW) on their EEGs in the absence of metabolic disturbances are described. One patient had coma associated with cerebellar hematoma, the other had mild dementia associated with idiopathic calcifications of the basal ganglia and normal auditory brainstem responses, subcortical and cortical somatosensory evoked potentials. Neurologic examination failed to show asterixis in both patients. The literature on nonmetabolic causes of TW was also reviewed, and the clinical and anatomic reports of 10 patients have been analyzed: 7 patients had focal brainstem-diencephalic lesions (craniopharyngioma: 2 patients; thalamic gliomas: 3 patients; pontine stroke: 2 patients), and 3 patients suffered from diffuse subcortical or multifocal encephalopathies (Binswanger's encephalopathy: 1 patient; cerebral carcinomatosis: 1 patient; multifocal cerebral lymphoma: 1 patient). From the clinical point of view, patients with nonmetabolic diseases causing TW presented either disturbance of higher cerebral functions with no asterixis or sudden onset of coma. It is concluded that TW may result from focal brainstem/diencephalic lesions or from diffuse subcortical or multifocal encephalopathies in the absence of concomitant metabolic abnormalities. Nonmetabolic causes of TW should be suspected in patients presenting with neurologic disturbances not associated with asterixis.
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PMID:Nonmetabolic causes of triphasic waves: a reappraisal. 236 53

Reports of 62 cases with a movement disorder associated with a focal lesion in the thalamus and/or subthalamic region were analyzed. Thirty-three cases had a lesion confined to the thalamus. Sixteen cases had a thalamic lesion extending into the subthalamic region and/or midbrain. Thirteen cases had a lesion in the subthalamic region or a subthalamic lesion extending into the midbrain. Nineteen cases with dystonia, 18 with asterixis, 17 with ballism-chorea, three with paroxysmal dystonia, and five with clonic or myorhythmic movements have been described. No case with isolated tremor has been described. In 53 cases with unilateral thalamic or subthalamic lesions, all but one with bilateral blepharospasm (associated with right posterior thalamic, pontomesencephalic, and bilateral cerebellar lesions) had dyskinesias in the limbs contralateral to the lesion. The other nine cases had bilateral paramedian thalamic lesions; seven developed bilateral dyskinesias, and the remaining two had unilateral dyskinesias. Regarding the 19 patients with dystonia, the two with bilateral blepharospasm had thalamic and upper brainstem lesions, and one with hemidystonia and torticollis had a subthalamic lesion. The other 16 patients all had a unilateral thalamic lesion with contralateral dystonia (10 hemidystonia, five focal dystonia affecting a hand and/or and one segmental dystonia involving face, arm, and hand). The exact location of the thalamic lesion was mentioned in 10 cases; the posterior or posterolateral thalamus was involved in six and the paramedian thalamus in four. These areas are more posterior or medial to the ventrolateral and ventroanterior thalamic nuclei, which receive pallido-thalamic and nigro-thalamic afferents. Two cases developed dystonia immediately after thalamotomy, and one case developed it 4 days after head trauma. The others initially had a hemiplegia and developed dystonia 1-9 months after the acute insult. Fifteen of the 17 patients with chorea had a unilateral lesion in the subthalamic nucleus or subthalamic region (eight due to infarcts, one to hemorrhage, five to mass lesions, and one to multiple sclerosis). All had contralateral hemichorea or hemiballism. One other case had bilateral chorea of the hands and tongue due to paramedian thalamic infarction. Another case with generalized chorea and thalamic atrophy was complicated by stereotaxic surgery. Thirteen of the 18 cases with asterixis had lesions confined to the thalamus. Eight were associated with thalamotomy, and five others had a stroke (four infarction and one hemorrhage) affecting the contralateral thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Movement disorders following lesions of the thalamus or subthalamic region. 799 Aug 45

Stroke-related nonepileptic transient dyskinesias are rare, and the site of ischemia remains often undetermined. Five cases out of 47 consecutive thalamic infarcts (10.6 per cent) are reported. Patients presented with monochorea (1 case), hemiballism-hemichorea (2 cases), choreoathetosis (1 case with subsequent arm painful dystonia and hand tremor), and asterixis (1 case). Magnetic resonance imaging demonstrated that the subthalamic nucleus was spared in all cases. Transient dyskinesias occurred at any time in the course of infarction (as a warning sign in 1 case, as an associated symptom in 3 cases, or during recovery in 1 case). Moreover, this study suggests that: 1) transient dyskinesias are mainly related to thalamic ischemic injury, and 2) small vessels disease is the main etiology.
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PMID:[Transient involuntary movement disorders and thalamic infarction]. 830 59

We prospectively studied motor symptoms in 32 patients with CT- or MRI-proven acute pure parietal stroke. A transient, mild, 'pseudoparesis' of the hand (90%), was noted, improved by visual attention and prompting, associated with non-awareness of muscle power (53%), transient soft pyramidal signs (50%), unilateral akinesia (100%) and motor hemineglect (37%) in non-dominant lesions. Lower motoneurone-type atrophy was not observed in this acute phase. We called 'poikilotonia' the striking unpredictable variations in muscle tone, ranging from extreme hypertonia to hypotonia, found in all patients. When maintaining postures, patients showed large oscillations (100%), laterodeviation or levitation of the arm (60%), especially in the case of large or posterior lesions, or, occasionally (3%), motor persistence or even hemicatalepsy (3%). Limb kinetic and manipulatory apraxia, with inadequate organization and anticipation of motor sequences and synergies, motor arrests, perplexity, unrecognizable gestures and loss of bimanual coordination, was a constant finding (100%). Other apraxias (62%) and difficulty in copying intransitive gestures of the hand (84%) were associated with posterior lesions involving the supramarginal gyrus. When reaching towards objects, all patients showed abnormal anticipatory hand shaping, but visuomotor ataxia (3%) was only seen with bilateral posterior stroke. Sensory (70%) or pseudocerebellar (4%) ataxia, was seen in both anterior and posterior lesions. Avoidance behaviors (34%) were not uncommon, but had no localizing value. Of the dyskinesias, hand dystonia (84%) was frequent, but athetosis (16%), asterixis (15%), postural tremor (15%), myoclonus (9%) and stereotypia (9%), were uncommon. The abnormal eye movements were unilateral hypo-akinesia of exploratory saccades (43%), abnormal ipsilateral pursuit and contralateral optokinetic nystagmus in the case of posterior lesions, and oculomotor apraxia with bilateral posterior lesions. In conclusion, parietal motor syndrome can be recognized during bedside examination, and probably reflects the loss of multiple sensory feedback to motor programs, especially those directed to the extrapersonal space.
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PMID:Parietal motor syndrome: a clinical description in 32 patients in the acute phase of pure parietal strokes studied prospectively. 987 53

The author describes 30 consecutive patients with unilateral stroke who had asterixis on presentation. The lesion location was as follows: thalamus in 19 (mostly, ventrolateral nucleus), frontal lobe in six, lenticulocapsular area in one, midbrain in two, and the cerebellum in two patients. Four patients had bilateral asterixis, and two patients with cerebellar lesions had ipsilateral asterixis. The asterixis may be caused by the abnormal control of arm posture maintenance due to functional dysregulation of the brainstem-spinal tracts from the cerebello-brainstem-thalamo-frontal lobe system.
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PMID:Asterixis after unilateral stroke: lesion location of 30 patients. 1122 2

Nuclear syndrome of the oculomotor nerve was first described in 1981, it is characterized by the association of an ipsilateral third nerve palsy with a paresis of elevation in the contralateral eye. This syndrome can be caused by vascular or tumoral lesions in the upper midbrain. It is rarely due to ischemic unilateral mesencephalic lesions, because ischemic lesions of the midbrain are usually integrated in a diffuse involvement of the brainstem and the thalamo-sub-thalamic region. In case of nuclear syndrome of the third nerve due to isolated upper midbrain infarct in the paramedian territory, dependent on branches of the basilar artery, oculomotor symptoms are frequently isolated. On the contrary, in fascicular syndromes of the third nerve, resulting from stroke in more lateral territories upon branches of the posterior cerebral artery, many neurological symptoms are associated with the oculomotor signs. We describe 3 patients presenting with a characteristic nuclear syndrome of the third nerve, resulting from a unilateral paramedian ischemic stroke in the upper midbrain, confirmed by cerebral CT scan or MRI examination. Clinical presentation differed in each case, and marked contralateral hemiparesia, cerebellar syndrome and focal asterixis were associated in various ways with the stereotyped oculomotor disorders. In the 3 cases, the nuclear syndrome of the third nerve was associated with fascicular involvement of the nerve, in an unusual clinical picture. The theoretical distinction between nuclear and fascicular syndromes is supported by the anatomical description of the arterial segmentation in the upper midbrain, which remains debated since the first description. According to the variability of clinical presentations, it seems that the arterial territories may be more variable than initially described. Therefore, ischemic lesions of the upper midbrain may involve some vascular borderzones with a high inter-individual variability. Upper midbrain strokes may thus lead to variable clinical pictures.
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PMID:[An ischemic syndrome of the oculumotor nucleus: associated clinical and anatomical variations on a theme]. 1367 21

Dyskinesias are infrequent presentations in acute stroke (1%). They can be found more frequently as delayed presentations after a stroke, but the prevalence is not available from the literature. The full spectrum of hyper- and hypo-akinetic syndromes has been described, but three main pictures are rather specific of an acute stroke: limb shaking, hemichorea-hemiballism and unilateral asterixis. Besides limb shaking, that seems to reflect a transient diffuse ischemia of the frontosubcortical motor pathway, lesions are described at all levels of the frontosubcortical motor circuit including the sensorimotor frontoparietal cortex, the striatum, the pallidum, the thalamic nuclei, the subthalamic nucleus, the substantia nigra, the cerebellum, the brainstem and their interconnecting pathways, as ischemic or hemorrhagic strokes. The preferentially late development of dyskinesia could reflect the return to a more ancestral motor control level, the most functional possible with the remaining configuration of structures, elaborated by brain plasticity after stroke.
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PMID:[Movement disorders in stroke]. 1876 Apr 32

Although rare, many different types of hyperkinetic and hypokinetic movement disorders have been described after both ischemic and hemorrhagic stroke in children and in adults. Current knowledge about these disorders comes from single case reports or small series of cases compiled from retrospective studies. Data from hospital-based studies suggest a prevalence of poststroke movement disorders ranging from 1.1 to 3.9%. However, despite the development of emergency care for stroke, these clinical syndromes remain insufficiently recognized. Poststroke movement disorders take place in the acute phase or following a variable delay after stroke onset, and could be transient or persistent. Dystonia is the most frequent movement disorder, occurring after a delay of several months, while chorea and hemiballism are most frequent in the acute stages. Amongst transient movement disorders, limb shaking is associated with high-grade stenosis or occlusion of the internal carotid artery, while myoclonus and asterixis are rare. From a pathophysiological point of view, most of these symptoms are induced by a lesion involving the basal ganglia, the thalamus, or the frontal subcortical pathways. In this article, we updated the clinical spectrum, neuropathophysiological mechanisms, and prognosis of stroke-induced movement disorders in adults and children.
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PMID:Clinical spectrum of movement disorders after stroke in childhood and adulthood. 2273 57

In 1949, asterixis was first described in patients with hepatic encephalopathy. It was quickly recognized that this phenomenon also occurs in other generalized encephalopathies and sometimes results from structural brain lesions. This paper is a study of asterixis in the general neurology clinic and on the inpatient neurology consultation service. The neurologists recorded the findings on inpatients and clinic patients for 12 consecutive months. Of the 1,109 inpatients with adequate examination, asterixis was documented in 97. Eighteen of the 97 cases were unilateral (18.6%) and 79 cases were bilateral (81.4%). Of the 614 outpatient visits with well documented examination, 6 (1%) individuals had asterixis. Since a small number of patients were examined more than once, the study yielded 103 individuals with adequate data for analysis. Asterixis resulted from varied causes: medications, renal disorder, hepatic dysfunction, pulmonary insufficiency, stroke and other brain lesions (including malignancy, subdural hematoma, and epidural abscess). Asterixis occurred in various patterns: in some cases it was easier to elicit in the upper extremities, in some it was easier to elicit in the lower limbs, and some it was solely or predominantly unilateral. The findings are discussed in light of the literature on asterixis with regard to its varied causes, patterns and presentations. Lastly, asterixis is examined from a historical perspective and the terminology is elucidated.
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PMID:Asterixis: a study of 103 patients. 2459 59

Asterixis as limb-shaking transient ischemic attack (TIA) is rare and poorly understood. Bilateral asymmetrical asterixis as limb-shaking TIA has not been reported in carotid stenosis. A 69-year-old gentleman presented with a TIA episode (dysarthria, right-arm weakness, and numbness). Bilateral asterixis was observed and was more severe on the right side. No prior infarcts were noted in the thalamus. Liver function was normal. A computerized tomography angiogram revealed 85%stenosis of the right internal carotid artery (ICA) and 65% stenosis of the left ICA. Three days after left ICA endarterectomy, the patient had complete disappearance of bilateral asterixis, with the right side showing initial improvement. The bilateral asterixis observed is proposed to be secondary to hemodynamic impairment and hypoperfusion of certain brain territory with resolution on revascularization.
J Stroke Cerebrovasc Dis 2015 Jan
PMID:Bilateral asymmetrical asterixis as limb-shaking transient ischemic attack in bilateral carotid stenosis. 2544 Mar 34


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