Gait apraxia after bilateral supplementary motor area lesion. (1/14)

OBJECTIVES: The study aimed at addressing the issue of the precise nature of gait apraxia and the cerebral dysfunction responsible for it. METHODS: The case of a patient, affected by a bilateral infarction limited to a portion of the anterior cerebral artery territory is reported. The patient's ability to walk was formally assessed by means of a new standardised test. RESULTS: Due to an anomaly within the anterior cerebral artery system, the patient's lesion was centred on the supplementary motor regions of both hemispheres. He presented with clear signs of gait apraxia that could not be accounted for by paresis or other neurological deficits. No signs of any other form of apraxia were detected. CONCLUSIONS: The clinical profile of the patient and the analysis of 49 cases from previous literature suggest that gait apraxia should be considered a clinical entity in its own right and lesions to the supplementary motor areas are responsible for it.  (+info)

Paraneoplastic chorea: case study with autopsy confirmation. (2/14)

A 67-year-old man presented with a 7-month history of insidiously progressive chorea, ataxia, and vertigo. Neurologic examination revealed deficits referable to the basal nuclei, cerebellar vermis, and vestibular nuclei. Small-cell lung cancer was diagnosed by fine-needle biopsy of a parahilar mass. After chemotherapy, the patient's chorea worsened. Anti-Hu antibodies were present in serum and cerebrospinal fluid. Microscopic examination of the brain at autopsy revealed diffuse perivascular lymphocytic infiltrates, microglial activation, and neuronophagia throughout the neuraxis, including the brainstem, cerebellum, lenticular nuclei, striatum, and cerebral cortex. Prominent loss of Purkinje cells was seen in the cerebellar vermis and hemispheres to a lesser degree. Chorea is extremely rare as a paraneoplastic manifestation of cancer. The florid presentation and the positive findings contrasted with an unremarkable MRI of the brain. This case illustrates the preeminence of symptoms and signs over negative MRI findings in paraneoplastic encephalitis.  (+info)

A new classification of higher level gait disorders in patients with cerebral multi-infarct states. (3/14)

BACKGROUND: cerebral multi-infarct states may lead to gait disorders in the absence of cognitive impairment. Where these gait disorders occur in the absence of neurological signs they have been termed gait apraxia or more recently higher-level gait disorders. In this paper we hypothesise three main types based on presumptive sites of anatomical damage: (a) Ignition Apraxia, where damage is predominantly in the supplementary motor area and its connections, with good responses to external clues; (b) Equilibrium Apraxia, where damage is predominantly in the pre-motor area in its connections, with poor responses to external cues and (c) Mixed Gait Apraxia. SUBJECTS: the clinical features and measured gait parameters of 13 patients with cerebral multi-infarct states and higher-level gait disorder are described (7 with Ignition Apraxia and 6 with Equilibrium Apraxia) along with those of 6 healthy elderly control subjects. METHODS: baseline gait characteristics were assessed on a walkway, which measured the following: step lengths, width of base and velocity. RESULTS: measured baseline gait parameters support the above hypothesis. CONCLUSIONS: it is suggested, though not proven, that patients with Ignition Apraxia could have problems with internal cueing due to lesions in the supplementary motor area or its connections whereas those with Equilibrium Apraxia could have dysfunction predominantly in the pre-motor area and its connections.  (+info)

Walking difficulties in patients with Alzheimer's disease might originate from gait apraxia. (4/14)

OBJECTIVES: To investigate whether gait apraxia is a possible cause for some of the walking abnormalities shown by patients with Alzheimer's disease. METHODS: 60 patients with Alzheimer's disease, selected as being free from overt extrapyramidal impairment or other potential causes of walking deficits, were assessed with a new test evaluating aspects of walking and related movements. Norms for this test were collected from a sample of 182 healthy volunteers. RESULTS: 40% of the Alzheimer group performed below the cut off score on this test, and half performed poorly. Performance of the Alzheimer group in the walking skills test correlated highly with scores in a test assessing limb apraxia and with dementia severity. CONCLUSIONS: Gait apraxia may be the cause of walking disorders found in a subgroup of patients with Alzheimer's disease. Its detection is made easier by the use of a standardised test, but still relies heavily on the exclusion of other causes of walking deficits. It is a recognisable and independent form of apraxia.  (+info)

Apraxia in movement disorders. (5/14)

The definition of apraxia specifies that the disturbance of performed skilled movements cannot be explained by the more elemental motor disorders typical of patients with movement disorders. Generally this does not present a significant diagnostic problem when dealing with 'higher-level' praxic disturbances (e.g. ideational apraxia), but it can be a major confound in establishing the presence of limb-kinetic apraxia. Most motor disturbances characteristic of extrapyramidal disorders, particularly bradykinesia and dystonia, will compromise the ability to establish the presence of loss of dexterity and deftness that constitutes this subtype. The term 'apraxia' has also been applied to other motor disturbances, such as 'gait apraxia' and 'apraxia of eyelid opening', that perhaps are misnomers, demonstrating the lack of a coherent nomenclature in this field. Apraxia is a hallmark of corticobasal degeneration (CBD) and historically this has received the most attention among the movement disorders. Corticobasal degeneration is characterized by various forms of apraxia affecting limb function, particularly ideomotor apraxia and limb-kinetic apraxia, although buccofacial and oculomotor apraxia can be present as well. The syndrome of parkinsonism and prominent apraxia, designated the 'corticobasal syndrome' (CBS), may be caused by a variety of other central nervous system pathologies including progressive supranuclear palsy (PSP), Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementias. Distinct from the CBS, PSP and Parkinson's disease can demonstrate varying degrees of apraxia on selected tests, especially in those patients with more severe cognitive dysfunction. Diseases that cause the combination of apraxia and a primary movement disorder most often involve a variety of cerebral cortical sites as well as basal ganglia structures. Clinical-pathological correlates and functional imaging studies are compromised by both this diffuse involvement and the confusion experienced in the clinical evaluation of apraxia in the face of the additional elemental movement disorders. Finally, although apraxia results in clear disability in patients with the CBS, it is not clear how milder ideomotor apraxia found on specific testing contributes to patients' overall day-to-day motor disability.  (+info)

Lengthening and transfer of hamstrings for a flexion deformity of the knee in children with bilateral cerebral palsy: technique and preliminary results. (6/14)

Between July 2000 and April 2004, 19 patients with bilateral spastic cerebral palsy who required an assistive device to walk had combined lengthening-transfer of the medial hamstrings as part of multilevel surgery. A standardised physical examination, measurement of the Functional Mobility Scale score and video or instrumented gait analysis were performed pre- and post-operatively. Static parameters (popliteal angle, flexion deformity of the knee) and sagittal knee kinematic parameters (knee flexion at initial contact, minimum knee flexion during stance, mean knee flexion during stance) were recorded. The mean length of follow-up was 25 months (14 to 45). Statistically significant improvements in static and dynamic outcome parameters were found, corresponding to improvements in gait and functional mobility as determined by the Functional Mobility Scale. Mild hyperextension of the knee during gait developed in two patients and was controlled by adjustment of their ankle-foot orthosis. Residual flexion deformity > 10 degrees occurred in both knees of one patient and was treated by anterior distal femoral physeal stapling. Two children also showed an improvement of one level in the Gross Motor Function Classification System.  (+info)

Association between the metabolic syndrome and its components and gait speed among U.S. adults aged 50 years and older: a cross-sectional analysis. (7/14)

BACKGROUND: To examine the relationship between the metabolic syndrome and its components and gait speed among older U.S. men and women. Whether these associations are independent of physical activity was also explored. METHODS: Eight hundred and thirty-five men and 850 women aged > or =50 years from the continuous National Health and Nutrition Examination Survey 1999-2002 were examined. We used the definition of the metabolic syndrome developed by the U.S. National Cholesterol Education Program Adult Treatment Panel III. Gait speed was measured with a 6.10-meter timed walk examination. RESULTS: The prevalence of the metabolic syndrome was 40.2% in men and 45.6% in women (P = .127). The prevalence of gait speed impairment was 29.3% in men and 12.5% in women (P < .001). No association was found between the metabolic syndrome and gait speed impairment. After including the individual components of the metabolic syndrome in a logistic model adjusted for age and leisure-time physical activity, abdominal obesity, low HDL cholesterol, and high fasting glucose were significantly associated with gait speed impairment among women (adjusted odds ratio [AOR] = 0.48, 95% confidence interval [CI] = 0.26 to 0.89; AOR = 2.26, 95% CI = 1.08 to 4.75; and AOR = 2.05, 95% CI = 1.12 to 3.74, respectively). Further adjustment for race/ethnicity, education, smoking status, alcohol consumption, arthritis status, and use of an assistive device attenuated these associations; among women, abdominal obesity and low HDL cholesterol remained significantly associated with gait speed impairment (AOR = 0.37, 95% CI = 0.18 to 0.76 and AOR = 2.45, 95% CI = 1.07 to 5.63, respectively) while the association between hyperglycemia and impaired gait speed attenuated to nonsignificance. CONCLUSION: Among women, gait speed impairment is associated with low HDL cholesterol and inversely with abdominal obesity. These associations may be sex-dependent and warrant further research.  (+info)

Backward walking in Parkinson's disease. (8/14)

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