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

Controversy exists about whether depression following stroke represents a biologically mediated change or a psychological reaction to the deficits. We present a patient with an acute isolated personality change and depression following a lacunar infarct of the left internal capsule, who was unaware of his affective change. His anosognosia for the depression, which was abrupt and not accompanied by cognitive impairments, suggests that post stroke depression, at least in this case, is better explained by a biological than a psychological model.
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PMID:Depression with anosognosia following a left subcortical stroke. 1269

Persisting anosognosia after acute lesions is relatively rare, and no case studies to date have reported functional scanning investigation of this disorder. This is a case report of an 85-year-old right-handed Scottish woman, EN, who showed persistent anosognosia for hemiplegia following a haemorrhagic stroke. Extensive damage in the right hemisphere caused left upper and lower limb flaccid hemiplegia and severe left-sided neglect. Lack of awareness for her deficits was still present 2 years after the stroke, when neurological, neuropsychological, and SPECT examinations were performed. Testing revealed severe left unilateral neglect and poor performance on verbal fluency tasks. EN had age normal memory performance, and her object recognition and praxic abilities were preserved. She showed no global reasoning or language problems apart from her abnormal beliefs. EN believed that she was able to walk and carry out several activities, in a context of other disorders of belief. SPECT scan showed marked hypoperfusion in the right parietotemporal cortex and this extended to the associative cortex in the right frontal regions. The persistence of anosognosia in this patient cannot be explained by memory impairments or global cognitive decline. A possible account might be that alteration in awareness was maintained by contingent right frontal and/or parietal dysfunction causing a suspension or change in the ability to monitor and check the 'real' and especially to assess the veracity of mental contents.
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PMID:Belief and awareness: reflections on a case of persistent anosognosia. 1464 8

This study of anosognosia for hemiplegia investigated: whether it is homogeneous; specificity to plegia of unawareness; extension to different kinds of and objects of awareness regarding plegia; partiality of unawareness. Sixty-four hemiplegic stroke patients were assessed with control subjects on (a) motor and somatosensory function, immediately followed by participants' evaluations of performance; (b) conventional structured interview questions addressing awareness of various capacities: (c) Neglect, Mental Flexibility, General Mental State, Verbal Fluency, Short-Term Memory; (d) pre- and post-performance estimates of ability on the last two; (e) estimates of current ability on bilateral and unilateral tasks, addressed by questions in 1st- and 3rd-person forms, explanations of how overestimated tasks would be accomplished, attempts at 3 bimanual tasks and post-attempt estimates of ability on these. Anosognosia for plegia was mostly associated with right-brain damage. No single factor or combination accounted for all patients. Double dissociations indicated that anosognosia can be specific to plegia: and patients do not generally overestimate other abilities. Although unawareness of paralysis and of its consequences appear linked, the latter is more widespread and persistent. Double dissociation showed that concurrent unawareness of movement failures is a separate deficit from these. There was differential awareness of different aspects of plegia. Further, some patients who overestimated current bilateral task ability when asked in 1st-person form did not overestimate when asked how well the examiner, if he was in their current condition, could do each task. This suggests split awareness of a single aspect of plegia. Patients anosognosic on conventional questioning showed two distinctions. (1) Some were unaware of movement failures when they occurred; others were aware but quickly forgot such failures and seem unable to update long-term body knowledge. (2) Some patients' explanations of bimanual task performance reflect unawareness of hemiplegia; others' explanations were bizarre and imply some awareness. The latter group's deficit appears to be nonspecific and linked to right-hemisphere predominance of anosognosia, an account of which is offered. Anosognosia for hemiplegia is not a unitary phenomenon: several factors underlie deficits in bodily awareness.
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PMID:Anosognosia for plegia: specificity, extension, partiality and disunity of bodily unawareness. 1507 1

Normally, we are aware of the current functions of our arms and legs. However, this self-evident status may change dramatically after brain damage. Some patients with "anosognosia" typically are convinced that their limbs function normally, although they have obvious motor defects after stroke. Such patients may experience their own paretic limbs as strange or as not belonging to them and may even attribute ownership to another person and try to push their paralyzed limb out of bed. These odd beliefs have been attributed to disturbances somewhere in the right hemisphere. Here, we use lesion mapping in 27 stroke patients to show that the right posterior insula is commonly damaged in patients with anosognosia for hemiplegia/hemiparesis but is significantly less involved in hemiplegic/hemiparetic patients without anosognosia. The function of the posterior insular cortex has been controversially discussed. Recent neuroimaging results in healthy subjects revealed specific involvement of this area in the subject's feeling of being versus not being involved in a movement. Our finding corresponds with this observation and suggests that the insular cortex is integral to self-awareness and to one's beliefs about the functioning of body parts.
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PMID:Awareness of the functioning of one's own limbs mediated by the insular cortex? 1607 95

The psychopathology of stroke encompasses several psychiatric and behavioral disorders that have high prevalence in the geriatric population, reduce the patient autonomy and increase the caregiver's burden. These disorders are usually associated with other cognitive and neurological deficits, and are labelled as neuropsychiatric when the whole clinical picture is consistent with the specific dysfunction of a neural system or brain region. Thus the neuropsychiatry of stroke comprises disorders of the perception/identification of the self and the environment (anosognosia of hemiplegia, misidentification syndromes, confabulations, visual hallucinations, delirium and acute confusional state), amotivational syndromes (apathy and athymhormia), disorders of emotional reactivity (blunted affect, emotional incontinence, irritability, catastrophic reactions), poor impulse or ideation control (mania) and personality changes. The clinical profile of the subcortical vascular dementia also points to specific brain dysfunction (frontal-subcortical pathways) that manifests with behavioral (depression, emotionalism, irritability) and cognitive symptoms (psychomotor retardation, attention, executive and memory deficits). However, post-stroke depression and anxiety, which have a more variable clinical presentation and might be assimilated, for several aspects, to post-traumatic or adaptive disorders, are disorders less characterized in their neural correlates.
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PMID:[Psychopathology of stroke]. 1631 15

Anosognosia is one of the major problems in the treatment and care of Alzheimer's disease (AD) patients. The aim of the study was to determine the patient characteristics, psychiatric symptoms, and cognitive deficits associated with anosognosia, because these are currently poorly understood. Eighty-four patients who met the National Institute of Neurological and Communicative Disease and Stroke-Alzheimer's Disease and Related Disorders Association criteria for probable AD were examined for anosognosia based on the difference between questionnaire scores of the patient and their caregiver. The relationship of anosognosia with patient characteristics (age, age at onset, duration of illness, education, Mini-Mental State Examination (MMSE), Clinical Dementia Rating (CDR), Hyogo Activities of Daily Living Scale (HADLS)), psychiatric symptoms (Neuropsychiatric Inventory (NPI), Geriatric Depression Scale (GDS)), and cognitive function (Digit Span, Word Fluency Test, Trail Making Test, Stroop Test, Raven's Coloured Progressive Matrices Test) were studied. Anosognosia showed positive correlations with age, age at onset, duration of illness, CDR, HADLS, and NPI disinhibition, and negative correlations with MMSE and GDS. Regarding cognitive function, only Part III of the Stroop Test was a predictor of anosognosia. The severity of anosognosia increased with disease progression and with a later age at onset. Subjective complaints of depression requiring self-monitoring of mood tended to decrease and, in contrast, inhibition of socially unsuitable behavior became more difficult as anosognosia worsened. Regarding cognitive function, anosognosia appeared to be associated with response inhibition impairment. Both disinhibition, as a psychiatric symptom, and response inhibition impairment are known to be correlated with disturbance of orbitofrontal function, which therefore may be associated with anosognosia.
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PMID:Anosognosia in Alzheimer's disease: association with patient characteristics, psychiatric symptoms and cognitive deficits. 1640 Dec 46

Various competing hypotheses have been put forth to explain how it is possible for patients to be unaware of their own profound weakness. We investigated whether patients' retrospections after resolution of their anosognosia along with their clinical features are consonant with these hypotheses. Three well-educated and articulate men were interviewed about their stroke and their subsequent awareness of weakness. Psychological denial, general cognitive impairment, a faulty superordinate awareness system, lack of knowledge of stroke symptoms, and minimal curiosity as a personality trait were not satisfactory explanations for their anosognosia. Their self-observations and clinical presentations suggest that: (1) anosognosia for hemiplegia can be exquisitely domain-specific; (2) weakness, rather than being perceived automatically, must be discovered; (3) discovery of weakness is impeded by a feedforward intentional deficit which probably interacts with notions of ''body schema'' in complex ways; and (4) awareness of deficit emerges in a graded fashion.
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PMID:Anosognosia for hemiplegia: patient retrospections. 1657 88

This review examines the available literature on neuropsychological outcomes of stroke and the literature on the ability of specific areas of neuropsychological deficit to predict functional stroke outcome. The literature reviewed indicates that post-stroke deficits in executive function, memory, language, and speed of processing are common, with those identified as having progressive 'post-stroke dementia' presenting with a similar, though more impaired profile, with increased impairments particularly noted in the area of memory. It is clear that some aspects of neuropsychological functioning (e.g., presence of neglect, aphasia, anosognosia; and verbal memory and attention deficits) show promise as a means of predicting post-stroke functional outcomes. Examining the available literature, it becomes evident that there is a need for long-term, large scale (i.e., population based) follow-up studies, evaluating likely long-term neuropsychological outcomes of stroke and their prognostic utility.
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PMID:The impact of neuropsychological deficits on functional stroke outcomes. 1696 44

The aim of this study was to examine the association between anosognosia and unilateral neglect (UN), with special focus on age, stroke severity, lesion location and pre-stroke dementia. The basis of this investigation was a population-based stroke incidence study. Anosognosia was assessed using a questionnaire, and UN using a three-item version of the Behaviour Inattention Test, the Baking Tray Task and a test of personal neglect. Stroke severity was assessed using the NIH stroke scale. Patients with anosognosia were older, and they more often had pre-stroke dementia than patients having UN only. No particular lesion localization was associated with anosognosia, while UN was strongly associated with previously defined lesion sites, often in the parietal lobe. There was a borderline significance regarding stroke severity in patients having anosognosia compared with those with UN only. Patients with anosognosia had higher mortality than patients without, but when controlled for age and stroke severity, this effect was not independent. While UN is closely associated with 'classical' lesion sites, anosognosia is a condition that more often occurs in a previously impaired brain. For anosognosia, lesion location appears to be less important. Anosognosia also tends to occur with larger strokes.
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PMID:Anosognosia versus unilateral neglect. Coexistence and their relations to age, stroke severity, lesion site and cognition. 1722 14

Dejerine-Roussy Syndrome (thalamic pain syndrome) is characterised by the development of chronic, severe pain in the contralateral half of the body after a thalamic stroke. It is often largely refractory to treatment. In this paper we draw together a number of disparate pieces of knowledge to propose a novel therapy for this condition. There is already substantial evidence from neurological disease that the brain's left hemisphere serves to "smooth over" discrepancies in sensory input in order to impose order and maintain the existing view of the world around us. Conversely the right hemisphere acts on discrepant sensory input to cause a re-evaluation of one's world view. Based on this, it was proposed by Harris that pain is an organism's response to discrepancy. It is already known that cold water vestibular caloric irrigation of the ear leads to activation of a number of areas in the contralateral hemisphere - including the insular cortex. Indeed it is known that - presumably because it also activates the right parietal lobe - this technique can be used to treat anosognosia, somatoparaphrenia and neglect. In addition to being activated by vestibular stimulation, it has been shown that the posterior insula has a somatotopic map of the body for painful stimuli. We speculate that phylogenetically, close anatomical proximity between the pain and vestibular areas of the brain makes sense; as it would allow modulation of otherwise disabling chronic pain, when the organism makes a sudden movement to avoid a predator. Given Harris's theory we propose that post stroke thalamic pain may represent a pathological amplification of the thalamic posterior insular response to pain due to discrepant sensory input. Based on all the above we go on to hypothesise that cold vestibular caloric stimulation will be effective in treating Dejerine-Roussy Syndrome and we present provisional evidence from two patients which supports this conclusion. If our hypothesis is correct this will be the first time in clinical neurology that a chronic disorder, long considered refractory to treatment, is relieved by a simple non-invasive procedure.
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PMID:Can vestibular caloric stimulation be used to treat Dejerine-Roussy Syndrome? 1807 18


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