Double dissociation between unilateral neglect and anosognosia

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.     

General intellectual impairment in chronic right hemisphere damaged patients with anosognosia: a group study

The study evaluates the possible relations between cognitive impairment, persisting anosognosia for hemiplegia and peripersonal neglect. Thirty eight chronic right hemisphere stroke patients were divided in three age- and education-matched groups: A (n = 13) patients with left hemiparesis, peripersonal neglect, and anosognosia for hemiplegia; B (n = 12) patients with left hemiparesis and peripersonal neglect, and C (n = 13) patients with left hemiparesis only. We used MMSE and WAIS Verbal IQ and verbal subtests to assess cognitive impairment in patients, in order to avoid a bias due to visuospatial deficit, which is common in patients with neglect. VIQ, Information, Digit Span and Vocabulary WAIS subtests as well as MMSE were found to be significantly lower in group A versus group B. No difference was found in any test between groups B and C, indicating a general worse cognition in patients compared to those without anosognosia for hemiplegia. Patients with anosognosia for hemiplegia also showed larger brain lesions and, more frequently, frontal, parietal, temporal and basal ganglia involvement, particularly if they had low verbal IQ, indicating a relationship between cognitive impairment, persisting anosognosia for hemiplegia and large right hemisphere lesions.     

General intellectual impairment in chronic right hemisphere damaged patients with anosognosia: A group study

The study evaluates the possible relations between cognitive impairment, persisting anosognosia for hemiplegia and peripersonal neglect. Thirty eight chronic right hemisphere stroke patients were divided in three age- and education-matched groups: A (n?=?13) patients with left hemiparesis, peripersonal neglect, and anosognosia for hemiplegia; B (n = 12) patients with left hemiparesis and peripersonal neglect, and C (n?=?13) patients with left hemiparesis only. We used MMSE and WAIS Verbal IQ and verbal subtests to assess cognitive impairment in patients, in order to avoid a bias due to visuospatial deficit, which is common in patients with neglect. VIQ, Information, Digit Span and Vocabulary WAIS subtests as well as MMSE were found to be significantly lower in group A versus group B. No difference was found in any test between groups B and C, indicating a general worse cognition in patients compared to those without anosognosia for hemiplegia. Patients with anosognosia for hemiplegia also showed larger brain lesions and, more frequently, frontal, parietal, temporal and basal ganglia involvement, particularly if they had low verbal IQ, indicating a relationship between cognitive impairment, persisting anosognosia for hemiplegia and large right hemisphere lesions.     

The pathogenesis of anosognosia for hemiplegia

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.     

Anosognosia for hemiplegia in a patient with pontine infarction]

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.     

An anatomical account of somatoparaphrenia

Somatoparaphrenia is a delusional belief whereby a patient feels that a paralyzed limb does not belong to his body; the symptom is typically associated with unilateral neglect and most frequently with anosognosia for hemiplegia. This association of symptoms makes anatomical inference based on single case studies not sufficiently specific. On the other hand, the only three anatomical group studies on somatoparaphrenia are contradictory: the right posterior insula, the supramarginal gyrus and the posterior corona radiata, or the right medial or orbito-frontal regions were all proposed as specific lesional correlates. We compared 11 patients with and 11 without somatoparaphrenia matched for the presence and severity of other associated symptoms (neglect, motor deficits and anosognosia). To take into account the frequent association of SP and neglect and hemiplegia, patients with and without somatoparaphrenia were also compared with a group of fifteen right brain damage patients without neglect and hemiplegia. We found a lesion pattern involving a fronto-temporo-parietal network typically associated with spatial neglect, hemiplegia and anosognosia. Somatoparaphrenic patients showed an additional lesion pattern primarily involving white matter and subcortical grey structures (thalamus, basal ganglia and amygdala). Further cortical damage was present in the middle and inferior frontal gyrus, postcentral gyrus and hippocampus. We propose that somatoparaphrenia occurs providing that a distributed cortical lesion pattern is present together with a subcortical lesion load that prevents most sensory input from being processed in neocortical structures; involvement of deep cortical and subcortical grey structures of the temporal lobe may contribute to reduce the sense of familiarity experienced by somatoparaphrenic patients for their paralyzed limb.     

Anosognosia for hemiplegia with preserved awareness of complete cortical blindness following intracranial hemorrhage

A 51-year-old woman presented with anosognosia for hemiplegia (AHP), neglect, and a complete loss of vision, for which she was almost immediately aware. Neuroimaging studies revealed intracranial hemorrhages in the medial temporal lobes bilaterally, extending back to the occipital cortex, but sparing the calcarine cortex. A large right frontal-parietal hemorrhage which extended to the posterior body of the corpus callosum was also observed. The patient's vision slowly improved, and by 11 months post onset, formal visual fields revealed improvement primarily in the left upper quadrants only. In contrast, resolution of her AHP occurred between the 26th and 31st day post onset. Awareness of motor impairment was correlated with her ability to initiate finger tapping in her left hemiplegic/paretic hand. During the time she was unaware of her motor deficits but aware of her visual impairments, her dreams did not reflect concerns over visual or motor limitations. The findings support a "modular" theory of anosognosia.     

Illusory limb movements in anosognosia for hemiplegia

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.     

Somatoparaphrenie Eine “Plusvariante” der Anosognosie für Hemiplegie

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.