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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated 41 patients with unilateral right hemisphere strokes for hemiparesis, hemianopia, constructional apraxia, neglect, extinction, unilateral spatial neglect on drawing (USND), dressing apraxia, anosognosia, prosopagnosia, and motor impersistence. Low correlations were found among USND, neglect, and extinction. Constructional apraxia showed a higher correlation with USND than with hemianopia. Motor impersistence and anosognosia correlated with the severity of the hemiplegia. Left neglect, motor impersistence, and anosognosia tended to occur only with large strokes. Injury to the right parietal lobe appears to be an important determinant of USND and constructional apraxia. In most cases of motor impersistence, left neglect, and anosognosia, there was injury to the right parietal lobe and also to structures beyond the parietal lobe. In two cases, small deep lesions produced behavioral abnormalities comparable to those of larger superficial cortical lesions.
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PMID:Behavioral abnormalities after right hemisphere stroke. 668 79

A 72 year-old right handed woman had a right sided anterior choroidal artery infarction. She presented the triad of hemiplegia, hemianaesthesia, and homonymous hemianopsia, as well as complete non-determinant hemisphere syndrome that combined: disorientation for place and time, anosognosia, hemiasomatognosia, left spatial neglect, constructional apraxia and spatial fabulation concerning both the present time and the weeks that preceded the vascular event. Language and verbal memory were normal. Spatial memory could not be studied because of the severity of the neglect. The clinical course was poor: when tested one and a half year post-onset, the hemiplegia, the hemianaesthesia, and the hemianopsia as well as left spatial neglect remained severe. Vestibular caloric stimulation, carried out with left ear cold water irrigation, resulted in brief but clear-cut alleviation of the spatial neglect. An MRI with both axial and coronal slices showed a right-sided infarct affecting the whole posterior limb of the internal capsule including the genu, the posterior part of the globus pallidus, the anterior third of the cerebral peduncle and the amygdala but sparing the thalamus and the corona radiata. This crescent-shaped lesion transected entirely the thalamo-cortical connection fibers which resulted in a "thalamic exclusion". The measurement of brain glucose utilisation with (18F)-Fluoro-2-Deoxy-D-Glucose and positron emission tomography performed in the chronic phase (3 months post-onset) showed an exceptionally severe and widespread hypometabolism of the right hemisphere, relative to the left hemisphere, which correlated with both the unusual, severe and protracted non-dominant hemisphere syndrome. All the brain regions on the right side were hypometabolic relative to the left including the temporal region (mostly medial temporal), the left cerebellar lobe, the frontal lobe (mostly prefrontal region), the occipital region and the thalamus. The hypometabolism of the basal ganglia, the sensorimotor area and the parietal cortex was less severe. This most uncommon clinical-metabolic presentation presumably reflects a global thalamo-cortical disconnection inducing a diffuse dysfunction of the whole hemisphere.
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PMID:[Infarction in the area of the right anterior choroidal artery and minor hemisphere syndrome: clinical and metabolic study using positron-emission tomography]. 767 26

Following a massive infarction in the territory of the right sylvian artery, a right-handed patient with a left hemiplegia and anosognosia, developed a peculiar hypergraphia. It consisted of an inappropriate and permanent writing behaviour, disappearing only during sleep. Space-constructional components of writing were severely disturbed. Graphemes were poorly formed. The graphic disturbances were different from hypergraphia previously described in stroke patients who produced linguistically correct but semantically loose writing. They were also different from graphomania reported in a case of fronto-callosal glioma. Our case of anosognosic hypergraphia suggests a sudden loss of inhibition of writing activity of the left hemisphere. The term graphomimia is proposed to distinguish this writing behaviour from the cases of hypergraphia previously reported and from graphomania.
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PMID:[Anosognosic graphomimia: an uncommon variety of hypergraphia in right sylvian infarction]. 767 57

The stroke literature indicates that the explicit denial of hemiplegia, a form of anosognosia, is associated more commonly with right- than left-hemisphere lesions. Some investigators have suggested that this asymmetry may be an artifact and that the aphasia that often accompanies left-hemisphere dysfunction may mask some instances of anosognosia. Mechanisms suggested for anosognosia have been either "global" or "modular" in nature. Mechanisms posited in global explanations include psychological denial and general mental deterioration; modular explanations include feedback and feedforward theories. Videotapes of 54 patients with medically intractable seizures who had selective barbiturate anesthesia (Wada test) as part of their evaluation for seizure surgery were assessed for anosognosia of hemiplegia and aphasia after hemispheric anesthesia had worn off. The results suggest that, although aphasia may confound the reported rate of anosognosia for hemiplegia following left-hemisphere dysfunction, the frequency of anosognosia for hemiplegia is still higher with right- than left-side dysfunction. Anosognosia for hemiplegia and aphasia were dissociable, providing support for the postulate that awareness of dysfunction is mediated by a modular system.
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PMID:Dissociation of anosognosia for hemiplegia and aphasia during left-hemisphere anesthesia. 782 38

The traditional association between anosognosia for hemiplegia and the right hemisphere was investigated in 31 patients with unilateral temporal lobe pathology during intracarotid sodium amytal testing (ISA) before epilepsy surgery. Recall of arm weakness was examined by questioning at the end of the test, when memory for items presented during the hemiplegia was also examined. Significantly more patients were amnesic for left arm weakness than for right. Amnesia for right arm weakness (and speech arrest) was significantly associated with pathology in the temporal lobe on the non-injected side and with impaired recognition of the memory items. Amnesia for left arm weakness was independent of both. Examination of cases where injection was contralateral to a hemisphere without pathology, and which showed normal memory capacity under ISA conditions, revealed that 87% recalled right arm weakness, but only 22% recalled left arm weakness. Awareness of arm weakness during left hemiplegia was examined in nine patients. Five of them were not aware of the weakness. Three of the four others could not subsequently recall it. By inference from the generally unimpaired recall of right arm weakness, following left hemisphere inactivation by amytal, an intact right hemisphere is capable of both recognizing right arm weakness and mediating its subsequent recall. In contrast, the left hemisphere was aware of left arm weakness only in approximately 50% of cases and even when there had been awareness usually could not mediate its subsequent recall. The suggestion is made that the right hemisphere may have a specific mnestic function for arm weakness, and presumably for hemiplegia, additional to the gnostic function.
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PMID:Awareness of and memory for arm weakness during intracarotid sodium amytal testing. 789 7

The cause of anosognosia for hemiplegia (AHP) remains unclear. Weakness is detected when there is a mismatch between the expectancy of movement and the sensory perception of movement. The feed-forward hypothesis of AHP posits that there is a failure of detection because there is a loss of motor intention and expectancy of movement. We tested motor intention by measuring the activation of proximal muscles (pectoralis majoris) while subjects squeezed a dynamometer with each hand. We tested a group of normal controls, a group of patients with hemiparesis, a patient with neglect, a patient with resolved AHP, and a patient with persistent AHP. The patient with AHP did not contract either of his pectoralis muscles when asked to squeeze with his contralesional, paretic hand, yet he contracted both of them when squeezing the dynamometer with his ipsilesional hand. Normal controls, hemiparetic controls, and the patient with hemispatial neglect contracted both pectorales when asked to squeeze with each hand. The pattern of activation seen in the patients with persistent AHP and resolved AHP demonstrates a loss of motor intention and lends support to the feed-forward hypothesis of AHP.
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PMID:Anosognosia for hemiplegia: an electrophysiologic investigation of the feed-forward hypothesis. 793 25

We reported a rare case of cerebral infarction with somatoparaphrenia (SP) caused by involvement of the dominant cerebral hemisphere. The patient was 77-year-old right-handed woman who was noted to have atrial fibrillation, right hemiplegia, hemisensory disturbance and ipsilateral homonymous hemianopsia. Neuropsychologically, there were anosognosia (AG) for hemiplegia and SP arguing her hand as doctor's hand. In addition, there also were noted disorientation, right unilateral spatial neglect and mild amnestic aphasia. Brain CT and MRI demonstrated infarctions in the left lateral thalamus, internal capsule, lateral geniculate body, hippocampus, caudate nucleus and medial occipitotemporal gyrus. IMP-SPECT showed extensive hypoperfusion areas in the left cerebral hemisphere. These lesions were thought to have resulted from occlusion of the left anterior choroidal artery and partial occlusion of the left middle and posterior cerebral arteries caused by cardiogenic embolism. AG persisted and SP disappeared 80 days after the onset. While AG and SP are generally believed to be associated with non-dominant hemispherical lesion, the present case suggests the possibility that those symptoms were seen in the case of dominant hemispherical lesion without severe aphasia.
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PMID:[Somatoparaphrenia caused by the lesion in the dominant cerebral hemisphere--a case report]. 886 40

We report a 36-year-old woman with right hemiplegia, anosognosia, and rapidly deteriorating course. She was well until the end of January, 1995 when she had an onset of fever, sputum, and cough. A 5 x 5 tumor was found in her left lower lobe. She was admitted to the Pulmonary Medicine on May 24, 1995 when she was 36-year-old. General physical examination was unremarkable. Bone scintigraphy revealed increased uptake in the skull, sternum, right scapula, vertebrae, right femur, and in ribs. Cranial CT scan revealed a large mass lesion in the right frontal subcortical region with central low density and peripheral high density areas, and small low density lesions in the right thalamic area and in the right posterior frontal region; ring enhancement was observed in the latter two lesions. On the second day of admission, she noted left-sided weakness which improved by corticosteroid treatment. On June 17, there was a sudden onset of left hemiparesis and a neurologic consultation was asked. Upon neurologic examination, she appeared somnolent but could understand verbal commands. She showed constructional apraxia, neglect of the left hemisphere, and anosognosia. Cranial nerves were unremarkable. Motor-wise, she showed flaccid left hemiplegia. Deep tendon reflexes were exaggerated on the left and the plantar response was extensor bilaterally. Nuchal stiffness was noted. Her cranial CT scan on June 17 revealed enlargement of the right frontal mass lesion. The subsequent course was complicated by DIC and progressive worsening of her consciousness. On June 18, she was comatose and pupillary light reflex was lost. She developed Cheyne-Stokes respiration and expired on that evening. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had a primary adenocarcinoma in the lung with multiple metastases including the brain. The fulminant terminal course was ascribed to hemorrhage within the tumor and subsequent central type of transtentorial herniation. Opinions were divided regarding the cause of hemorrhage; some participants thought hemorrhage was caused by DIC. Post-mortem examination revealed an adenocarcinoma arising at the S6 segment of the left lung with multiple organ metastases. In the brain, a huge hemorrhagic metastasis was found in the right frontal lobe and a non-hemorrhagic metastasis in the right thalamic region. Probably, the size of the metastases influenced the occurrence of hemorrhage. The direct cause of the death was transtentorial herniation.
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PMID:[A 36-year-old woman with acute onset left hemiplegia and anosognosia]. 912 37

Feinberg et al. proposed that right-hemisphere-damaged stroke patients with anosognosia for hemiplegia (AHP) confabulate seeing stimuli on the left side but those without AHP admit to having inadequate visual information. This study examines the relationship between AHP and confabulation using selective anesthesia of the cerebral hemispheres. Seventeen patients with intractable epilepsy were tested during intracarotid methohexital infusion. For half of the trials, subjects were stimulated on their paretic hand with a material (sandpaper, metal, or cloth), and for the remaining trials they were not stimulated. The subjects were trained to use a pointing response to indicate if they been stimulated and the type of material they had felt. Admission of uncertainty was defined as pointing to a question mark. Confabulation was defined as any material response to a no-touch trial. During anesthesia of either hemisphere, subjects with and without AHP confabulated responses. The AHP and non-AHP groups did not differ in admission of uncertainty. Our results support the postulate that confabulation and AHP are independent disorders, and therefore confabulation cannot fully account for AHP.
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PMID:Anosognosia and confabulation during the Wada test. 937 15

Damage to the minor hemisphere or the right hemisphere of most right-handed subjects produces various neuropsychological disorders. Unilateral spatial neglect is the deficit to respond or orient to stimuli on the left side. The inferior parietal lobule is most frequently involved in the lesions of neglect patients, but lesions confined to the lobule may not cause chronic neglect. Severe and lasting neglect is frequently found in patients with an infarction in the territory of the middle cerebral artery or the anterior choroidal artery. Neglect is usually mild or moderate after frontal lesions. The most important mechanism of neglect seems to be disorders in spatial attention: rightward attentional bias, and impairment in disengagement and shift of attention from the right side. Directional hypokinesia is rarely observed in the chronic stage. Non-spatial factors, such as motivational deficit, insufficient compensation with verbal intelligence, or disuse of an appropriate spatial strategy may also contribute to the appearance of neglect. Anosognosia for hemiplegia is found in about half of patients with acute cerebrovascular accidents in the right hemisphere. Generalized attentional and intellectual deficits, diffuse brain atrophy or hypometabolism, and presence of multiple infarction may result in chronic anosognosia. Constructional disability is observed in about 30% patients with either hemisphere damage. Dressing apraxia is more frequent in right hemisphere damage. These two disorders, however, rarely appear as isolated neuropsychological deficits. Most patients show some of the accompanying disorders, such as unilateral spatial neglect, anosognosia, anosodiaphoria, and generalized attentional and intellectual impairment. By contrast, motor neglect may occur independently of the other disorders. Motor neglect follows damage to either hemisphere, although it occurs more frequently after right hemisphere damage. Neuropsychological deficits characteristic of right hemisphere damage may be unilateral spatial neglect in the acute and chronic stages and anosognosia for hemiplegia in the acute stage.
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PMID:[Neuropsychological disorders in minor hemisphere damage]. 957 65


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