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

Somatosensory evoked potential studies in nine patients with anosognosia for left hemiplegia and in one patient with anosognosia for right hemiplegia revealed an absence of response over either hemisphere on stimulation of the median nerve on the hemiplegic side. This apparent lack of cortical processing may underlie the impaired awareness of the hemiplegic side, manifested as anosognosia.
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PMID:Anosognosia for hemiplegia: somatosensory evoked potential studies. 103 81

Anosognosia, the verbally explicit denial of hemiplegia, is more often reported after right- than left-hemisphere lesions. However, this asymmetric incidence of anosognosia may be artifactual and related to the aphasia that often accompanies left-hemisphere lesions. Anosognosia has been attributed to psychological denial and the emotional changes associated with hemispheric dysfunction. Eight consecutive patients undergoing intracarotid barbiturate (methohexital) injections as part of their presurgical evaluations for intractable epilepsy were assessed for anosognosia after their hemiplegia and aphasia had cleared. After their left-hemisphere anesthesia, all subjects recalled both their motor and language deficits. However, after right-hemisphere anesthesia, none of the eight patients recalled their hemiplegia. These results suggest that anosognosia is more often associated with right- rather than left-hemisphere dysfunction and that it cannot be attributed to either psychological denial or the emotional changes associated with hemispheric dysfunction.
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PMID:Anosognosia during Wada testing. 156 54

An overall measure of the recovery of visual neglect in patients with an acute stroke is described: The "Visual Neglect Recovery Inde" (VNRI) expresses the amount of visual neglect on a battery of visual neglect tests as a percentage of complete recovery from the maximal visual neglect measurable. The principles underlying the development of the index are similar to those involved in the development of the Motricity Index for hemiplegia. A population of 68 survivors of stroke who presented with visual neglect at two to three days were followed for up to six months. The VNRI showed that neglect was greater in those with right hemisphere stroke than in those with left hemisphere stroke and that recovery was most rapid over the first 10 days and reached a plateau at three months. Most patients, including many with severe initial visual neglect, showed little visual neglect at three months. Stepwise regression analysis showed that the severity of visual neglect at three months and at six months post-stroke could be predicted by the severity of visual neglect and the presence of anosognosia at two to three days. A regression equation was produced which may enable clinicians to select patients for intensive treatment of visual neglect.
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PMID:Measuring visual neglect in acute stroke and predicting its recovery: the visual neglect recovery index. 161 6

We compared patients with unawareness of hemiplegia lasting more than 1 month after right hemisphere stroke with other patients with right hemisphere stroke who became aware of hemiplegia within a few days after onset. Patients with persistent unawareness invariably had severe left hemisensory loss and usually had severe left spatial neglect. They were almost always apathetic; their thought lacked direction, clarity, and flexibility, and they had at least moderate impairment of intellect and memory. Their right hemisphere strokes were large and always affected the central gyri or their thalamic connections and capsular pathways. In addition, there was evidence of at least mild left hemisphere damage, most commonly caused by age-associated atrophy. The pathogenesis of anosognosia for hemiplegia may involve failure to discover paralysis because proprioceptive mechanisms that ordinarily inform an individual about the position and movement of limbs are damaged, and the patient, because of additional cognitive defects, lacks the capacity to make the necessary observations and inferences to diagnose the paralysis. We discuss the implications of this "discovery" theory and contrast it with other explanations of anosognosia.
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PMID:The pathogenesis of anosognosia for hemiplegia. 194 7

We report investigations of the face processing abilities of SP, a right-handed woman who had suffered a subarachnoid haemorrhage from a right middle cerebral artery aneurysm. Although she could correctly assign visual stimuli to the 'face' category without difficulty, SP performed poorly on all other face processing, tasks, including 'closure' (Mooney faces), perception of facial expression, unfamiliar face matching, and identification of familiar faces. Identification of familiar people from nonfacial cues (names) remained relatively well-preserved, but severe impairments were evident on all face recognition tasks. Her errors mostly involved either failures to find a face familiar at all, or misidentification as another familiar person. In face-name learning tasks, there was evidence of 'covert' recognition of faces she failed to recognize overtly. SP's face processing impairment remained stable across a 20-month period of investigation, yet throughout this period she did not think that she had any problems in face recognition, and continued to show lack of insight into this impairment even when directly confronted with its consequences on formal testing. In contrast, SP showed adequate insight into other physical and cognitive impairments produced by her illness, including poor memory, hemiplegia, and hemianopia. We propose that her lack of insight into her face recognition problems involves a deficit-specific anosognosia, resulting from impairment of domain-specific monitoring abilities.
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PMID:Unawareness of impaired face recognition. 222 40

We encountered two patients with right middle cerebral artery infarction who showed a unique eye sign not described so far. Both had suddenly developed central facial weakness, hemiplegia and hemisensory deficit in the left side. Anosognosia for the left hemiplegia, motor impersistence and left unilateral spatial neglect were also present. Initially they showed difficulty in keeping their eyes closed to the same degree on both eyes. However, this symmetrical motor impersistence of eye closing developed into a differential pattern over the days. Thus, on verbal command to close the eyes, the right eye in the non-paretic side would be closed continuously and excessively and in the left eye in the paretic side would be closed slightly and impresistently. This dissociation of eye closure was not observed in spontaneous eye closure. This symptom is close to the contralateral motor impersistence of eye closure which has been attributed to the right hemispheric lesion. But the concurrence of the ipsilateral overcontraction of the orbicularis oculi has not been described to the authors' knowledge. We proposed a hypothesis on this unique right-left dissociation of eye closing behavior.
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PMID:[Right-left dissociation of voluntary eyelid closure following right middle cerebral artery infarction]. 236 31

A 65 year-old right-handed woman was admitted after the sudden onset of a right dense hemiplegia. C.T. showed a large left infarction in the middle cerebral artery territory. There was a slight anosognosia and neglect of the right space without confusion. She had aprosodia but no aphasia. On the other hand, there was a severe apraxia and all the components of Gerstmann's syndrome were present. This suggests an unusual sattering of hemispheric functional dominances.
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PMID:[Right hemiplegia and spatial neglect with apraxia and agraphia without aphasia in a right-handed patient]. 237 72

We reported a 72-year-old male with ischemic oculopathy due to ophthalmic artery stenosis followed by ipsilateral border zone infarction due to internal carotid artery stenosis. The patient had history of hypertension and diabetes mellitus. He had severe headache and visual disturbance of the right eye. He was diagnosed right neovascular glaucoma and left diabetic retinopathy (simple type), and received diuretics, beta-blockade and other anti-hypertensive drugs. One month later, he noticed left mild hemiparesis in a morning, and he experienced progression of left hemiparesis over a week. He was admitted to our hospital on the 11th day. He showed left complete hemiplegia, left sensory disturbance, anosognosia and left unilateral spatial neglect. His right eye was diagnosed neovascular glaucoma but left eye was normal. The 5th days CT showed low density area in the right terminal zone and bilateral periventricular lucency. At the same area, the 46th days MRI showed high intensity area in the T2-weighted image and low intensity area in the T1-weighted image. Cerebral angiography performed on the 33rd day, disclosed severe kinking at the cervical segment and 50% stenosis at the intracavernous segment in the right internal carotid artery, and 90% stenosis and post-stenotic dilatation of the right ophthalmic artery. Left internal carotid artery had each 60% stenosis at the cervical segment and the intracavernous segment. Left ophthalmic artery had severe stenosis from its beginning to distal part. This infarction was considered berder zone infarction by it's localization (terminal zone) and internal carotid artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of ischemic oculopathy followed by border zone infarction]. 258 88

Inverse ocular bobbing (IOB) is an uncommon abnormal eye movement. Its characteristics are slow downward eye movement with rapid upward return, a nadir at the extreme of downgaze position and horizontal roving eye movement. We present a case of IOB associated with cerebral embolism and diabetes insipidus. A 69 year-old right-handed woman was admitted because of a consciousness disturbance. She had been well until November 10, 1983, when she was found dysarthric and left hemiplegic. On admission, she was stuporous. There were conjugate deviation to the right, central left facial and hypoglossal palsy, left hemiplegia with spasticity, left hyperreflexia with positive pathologic reflex and anosognosia. A CT scan performed on November 11 showed extensive hypodense area in the region supplied by the right middle cerebral artery. A right carotid angiography revealed multiple occlusions in the top of the right internal carotid artery with poor collateral circulation. After admission, the level of consciousness gradually deteriorated and became comatose on November 18, when the following abnormal eye movements were observed. Following spontaneous horizontal roving eye movement, both eyes deviated downward slowly from midposition, taking 1 to 2 seconds to reach the nadir. The eyes then remained in the position for 1 to 15 seconds, followed by a rapid return to the midposition. These abnormal eye movements are compatible with inverse ocular bobbing (IOB) described by Knobler. Electronystagmography detected typical IOB and spontaneous upward nystagmus. There was no evidence of hypoxia when these abnormal eye movements were present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Inverse ocular bobbing associated with cerebral embolism and diabetes insipidus--a case report]. 274 84

A 74 year-old woman was admitted with a right hemiplegia resulting from a left infarct that had totally destroyed the territory supplied by the middle and anterior cerebral arteries. The patient presented with anosognosia and hemiasomatognosia and negligence of the right half-field. She was aprosodic, not aphasic, and there was a severe apraxia and total agraphia. These neuropsychological disorders are discussed in relation to the contradictory data relative to the manual lateralization of the patient. Findings in this case of a "crossed apraxia" show that management of language and of the propositional gestures are not necessarily ensured by the same hemisphere. It also appears that manual preference may be a poor clue for interpretation in terms of functional lateralization.
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PMID:[Right neglect with hemiasomatognosia, mental confusion, apraxia and agraphia without aphasia]. 383 99


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