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

Anosognosia of hemiplegia is of interest for both pragmatic and theoretical reasons. We discuss several neuropsychological theories that have been proposed to explain this deficit. Although for psychological reasons people might deny deficits, the denial hypothesis cannot account for the hemispheric asymmetries associated with this disorder and cannot explain why some patients might deny one deficit and recognize another equally disabling deficit. There is some evidence that faulty feedback from sensory deficits, spatial neglect and asomatognosia might be responsible for anosognosia in some patients. However, these feedback hypotheses cannot account for anosognosia in all patients. Although the hemispheric disconnection hypothesis is appealing, disconnection is probably only a rare cause of this disorder. The feedforward intentional theory of anosognosia suggests that the discovery of weakness is dependent on attempted action and some patients might have anosognosia because they do not attempt to move. We present evidence that supports this theory. The presence of one mechanism of anosognosia, however, does not preclude the possibility that other mechanisms might also be working to produce this disorder. Although a large population study needs to be performed, we suspect that anosognosia might be caused by several of the mechanisms that we have discussed. On the basis of the studies of impaired corporeal self-awareness that we have reviewed, we can infer that normal self-awareness is dependent on several parallel processes. One must have sensory feedback and the ability to attend to both one's body and the space where parts of the body may be positioned or acting. One must develop a representation of the body, and this representation must be continuously modified by expectations (feedforward) and knowledge of results (feedback).
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PMID:Possible mechanisms of anosognosia: a defect in self-awareness. 985 62

Four patients had anosognosia for hemiplegia (AHP) as a manifestation of pontine infarction in the mediolateral region. Patients with AHP syndrome had no mental and neuropsychologic disturbances, and all had involvement of the medial or lateral part of the pons (medial or lateral pontine reticular nuclei). Brainstem lesions, which activate frontoparietosubcortical areas, may be a critical factor in the development of AHP syndrome.
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PMID:Pontine anosognosia for hemiplegia. 1044 40

Anosognosia for hemiplegia (AHP), i.e., unawareness of motor deficits and associated disorders, has been frequently reported, pre-dominantly following right hemispheric lesions. To a smaller extent, there are case reports of patients who give accounts of a feeling of strangeness concerning the contralesional limbs and sometimes attribute them to other persons. This "positive-variant" of AHP has been labeled "somatoparaphrenia" (SP). We report a case of SP in a 85-year-old woman with infarction of the right posterior cerebral artery and posterior parts of the right thalamus. She showed AHP and described her left side alternatively as her handicapped nephew and a clumsy cat. Misidentification of her daughter also occurred. With respect to the literature the predominant neuroanatomical features involved are lesions including right parietal cortex and/or posterior parts of the thalamus. Theories concerning the pathogenesis of this phenomenon comprise a denial of the illness, a lack of awareness caused by reduced sensory feedback and neglect, a misidentification or disturbance of the active discovery process considered necessary for realizing one's disorder.
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PMID:[Somatoparaphrenia. A positive variant of anosognosia for hemiplegia]. 1070 14

To clarify the relation between anosognosia for hemiplegia and confabulation, 11 patients with acute right cerebral infarctions and left upper limb hemiparesis were assessed for anosognosia for hemiplegia, illusory limb movements (ILMs), hemispatial neglect, asomatognosia, and cognitive impairment. Five of 11 patients had unequivocal confabulation as evidenced by ILMs. The presence of ILMs was associated with the degree of anosognosia (p = 0.002), with hemispatial neglect (p<0.05), and with asomatognosia (p<0.01). The results confirm that a strong relation exists between anosognosia for hemiplegia and confabulations concerning the movement of the plegic limb. There is also a strong relation between ILMs and asomatognosia.
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PMID:Illusory limb movements in anosognosia for hemiplegia. 1118 46

We report a patient with anosognosia for hemiplegia associated with a right pontine infarction. A 51-year-old woman with histories of hypertension and diabetes mellitus was admitted because of weakness of her left upper and lower extremities. On neurologic examination, she was alert and oriented without dementia. Visuospatial hemineglect was not present. Hemiparesis of her left upper and lower extremities was noted. Her brain MRIs showed a large infarction in the right pons. On admission, she could recognize her illness but was indifferent to her hemiplegia, so she said that there was not well-off for her life. Two weeks after the onset, her neurological symptoms gradually improved. Simultaneously, her interest in her hemiparesis increased. We proposed that, in the present patient, anosognosia for hemiplegia was caused by the pontine infarction. Since pontine anosognosia for hemiplegia has been rarely reported to date, it is expected that the findings of the present patient will be useful to the better understanding of mechanisms underlying anosognosia.
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PMID:[Anosognosia for hemiplegia in a patient with pontine infarction]. 1119 47

We evaluated consecutive stroke patients with an acute, unilateral lesion, in order to elucidate the anatomical correlates and the clinical course of sensory extinction phenomenon as well as its relation with unilateral spatial neglect (USN) and anosognosia for hemiplegia (AHP). Subjects consisted of 76 patients with right cerebral hemispheric lesions (RHL) and 43 with left cerebral hemispheric lesions (LHL). Twelve of 76 patients with RHL and 18 of 43 patients with LHL were excluded from this study, because of consciousness disturbance, aphasia, severe sensory disturbance, hemianopia, or severe dementia. All of the patients included in this study had an ischemic or hemorrhagic stroke, who admitted to our hospital within 24 hours after the onset of stroke. We repeatedly examined the patients to detect the presence of sensory extinction phenomenon, USN, and AHP from their acute to chronic stage. The incidence of extinction phenomenon in RHL was 33% (11/19 with cortical lesions and 10/45 with deep-seated lesions). When we excluded the patients with a lacunar stroke or TIA, 10 of 13 patients with subcortical lesions had sensory extinction phenomenon. Nineteen of 21 patients with RHL who showed sensory extinction phenomenon also accompanied USN, and twelve had associated AHP. The sensory extinction phenomenon disappeared within 20 days in 6 of 10 patients with subcortical lesions and 3 of 11 with cortical lesions. In contrast, three of 25 (12%) patients with LHL showed extinction phenomenon, the incidence being much rarer than the lesion in the right. Of these, two had USN and one had AHP together. All the deficits disappeared within 20 days after the onset of stroke in patients with LHL. Our studies may show that subcortical lesions present with extinction phenomenon more frequently than cortical lesions, although the phenomenon caused by the subcortical lesions of often disappear in a few weeks.
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PMID:[Sensory extinction phenomenon of double simultaneous stimulation: the analysis of consecutive stroke series with acute and unilateral lesions]. 1196 39

We report two patients presenting with a subacute right hemisphere stroke. These cases demonstrate a double dissociation between unilateral neglect and anosognosia for hemiplegia. The first patient suffered from a severe left hemiplegia associated with severe and persisting unilateral neglect. He appeared fully aware of his motor impairment. The second patient had a severe left hemiplegia, without any major sign of unilateral neglect on clinical tests nor on behavioural assessment. Nevertheless, he presented a severe and sustained anosognosia for hemiplegia. These case reports support the assumption that anosognosia and unilateral neglect, although they are frequently associated, may rely on independent mechanisms.
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PMID:[Double dissociation between unilateral neglect and anosognosia]. 1198 84

Unawareness of motor disorders (anosognosia) has often been reported after brain lesions, and it has been considered a temporary condition common in the acute and post-acute phases. The presence of anosognosia in a chronic phase (i.e. lasting more than few weeks) is a rare occurrence, thought to be the result of reasoning deficits which prevent patients from performing an adequate check of reality. Although this assumption is widely shared amongst researchers, only a few studies have actually addressed this issue. We report on the case of a patient (NS) who was still showing anosognosia for hemiplegia 1 year after a traumatic brain-head injury, while his reasoning abilities were well preserved. By means of a series of tests and experiments, we evaluated the main theoretical approaches. NS's long-lasting anosognosia is discussed in terms of a combination of clinical manifestations, whereby personal neglect and motor-sensory information play a key role in preventing awareness, whereas memory difficulties in updating pre-existing personal schema may be crucial in maintaining NS's anosognosic status.
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PMID:Chronic anosognosia: a case report and theoretical account. 1220

In recent years, research on unilateral spatial neglect has focused on dissociations between different aspects of the clinical syndrome, which is now considered by many students as a multi-componential disorder. Notwithstanding this leading view, there is at least one empirical argument which supports a unitary interpretation of the disorder. This is based on the observation, now replicated many times, that a variety of sensory stimulations (vestibular, optokinetic, transcutaneous mechanical vibration and nervous electrical, visual prism adaptation) involving a lateral change (left-right asymmetry) in the input pattern, affect in a very similar fashion virtually all manifestations of the syndrome, including: visuo-spatial neglect; hemianaesthesia (somatosensory hemi-inattention); extinction, hemiparesis, hemiplegia, and anosognosia for these motor disorders; somatoparaphrenia. These effects may be accounted for with reference to a spatial medium, articulated in a number of specific components, which is modulated by sensory input in a fundamentally similar fashion. Recent investigations concerning the neural bases of some of these stimulations support this view. In this chapter the case of the co-variation of the effects of vestibular stimulation on motor deficits and on anosognosia for hemiplegia is considered. The suggestion is made that one mechanism underlying anosognosia for hemiplegia is unawareness of a deficit of intention, or movement planning component, rather than, or in addition to, unawareness of a primary motor deficit. Temporary remission of anosognosia after vestibular stimulation may represent recovery from this neglect-related component, of which, as of other manifestations of the syndrome, patients are typically unaware. The recovered intention to move may allow the detection by the patient of the presence of a residual primary motor deficit, through a feedback mechanism.
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PMID:Anosognosia for left-sided motor and sensory deficits, motor neglect, and sensory hemiinattention: is there a relationship? 1269 68

The body scheme is a complex of memory patterns secured in the structures of the brain, where the parietal lobes play the most important role. Basic principles are given by the genetic programming of the structure and function along with the synthesis of information brought by means of sensory activity. The unitary perception of the body scheme is a dynamic image, enabling conscious and unconscious representation of our body, its parts, their functions, position, shape and/or movements. The recognition of the body scheme in humans is named somatognosia. Disorders of somatognosia include visceral and somatic phantom, phantom pain and other disorders related to the capability of communication by means of language: autotopoagnosia, hemiasomatognosia, pain asymboly, anosognosia of hemiplegia, anosognosia of blindness, deafness, neglect and other defects appearing at the neurologist's and psychiatrist's borderline of interest. Interest in the visceral phantom is usually much smaller than that in the phantom limb. The aim of this paper was to draw the to phantom phenomena in patients following rectum amputation and colostomy. A survey of contemporary knowledge about the body scheme and its disorders, cortical plasticity and the problem of cortical maladaptation are presented.
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PMID:[Somatognosis, body schema and the phenomena of somatic and visceral phantoms and phantom pain]. 1292 31


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