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PubMed2005

Familial cognitive impairment with ataxia with oculomotor apraxia.

Ataxia with oculomotor apraxia is an autosomal recessive inherited disease characterized by childhood onset of progressive cerebellar ataxia, oculomotor apraxia, and progressive motor peripheral neuropathy. The mean age at onset is approximately 4.7 years, with oculomotor apraxia appearing a few years later. Diagnosis is based on molecular genetic analysis for mutations of the aprataxin (APTX) gene (chromosome 9p13.1; ataxia with oculomotor apraxia 1). Ataxia with oculomotor apraxia 2 is caused by an unknown gene mutation at locus 9q34. We describe two siblings, born to consanguineous parents, who had clinical features of cerebellar ataxia, tremor, dysarthria, oculomotor apraxia, and motor peripheral neuropathy. Brain magnetic resonance imaging showed cerebellar atrophy and mild brainstem atrophy. Electromyography showed signs of axonal neuropathy. The molecular genetic analysis demonstrated the APTX mutation W279X at locus 9p13.3 (ataxia with oculomotor apraxia 1 disease), and psychologic studies showed mild cognitive impairment. We suggest that mentation can be compromised in ataxia with oculomotor apraxia 1.

Adolescent↗

PubMed2001

Comparison of apraxia in corticobasal degeneration and progressive supranuclear palsy.

OBJECTIVE: To describe ideomotor apraxia in patients with corticobasal degeneration and those with progressive supranuclear palsy, two parkinsonian disorders that are often misdiagnosed due to the overlap in their clinical features, and to determine whether systematic apraxia testing is useful for differential diagnosis. METHODS: Fourteen patients fulfilling National Institute of Neurological Disorders and Stroke-Society for Progressive Supranuclear Palsy clinical criteria for progressive supranuclear palsy, 13 patients fulfilling modified Lang criteria for corticobasal degeneration, and 12 normal healthy control subjects were given the Test of Oral and Limb Apraxia, which was scored according to the Florida Apraxia Battery for occurrence of various types of apraxic errors. RESULTS: Both patients with progressive supranuclear palsy and corticobasal degeneration committed a greater number of apraxic errors than normal healthy control subjects on both transitive and intransitive tasks (p < 0.001 in both cases), but apraxia was much more severe in patients with corticobasal degeneration than progressive supranuclear palsy (p < 0.001). The index of apraxia severity, in combination with the assessment of the two key features of progressive supranuclear palsy (falls and vertical gaze palsy), correctly classified all patients. CONCLUSIONS: Patients with corticobasal degeneration show more severe ideomotor apraxia than patients with progressive supranuclear palsy, and systematic assessment of ideomotor apraxia facilitates the differential diagnosis between patients with progressive supranuclear palsy and those with corticobasal degeneration.

Aged↗

PubMedDate not supplied

[Crossed apraxia secondary to a right parietal infarct].

INTRODUCTION: Crossed apraxia is an unusual alteration in praxic function due to a cerebral lesion which is contralateral to that which would be expected. We report a case of crossed apraxia due to a right parietal lesion in a left handed patient who had been obliged to be right handed. We discuss the peculiar neuropsychological profile and possible relation of this to left handedness. CLINICAL CASE: A 75 year old man, left handed but obliged to use the right hand, suffered an acute episode of alteration in the management of utensils (lids, taps, medicine containers), although he maintained his usual social behaviour and orientation. On neurosomatic examination no focal deficits were observed. On MMST he scored 29/30, on the Edinburgh questionnaire he scored 35 (left handed dominance). On a Barcelona PIENC battery his scores were in the pathological range for subtests on understanding orders, carrying out symbolic gestures and imitating gestures, in perceiving super imposed images and visual memory. MRI showed a right parietal laminar infarct. CONCLUSIONS: The patient showed clear bilateral ideo motor apraxia, which could not be justified/explained by visuo spatial agnosia secondary to a right parietal ischaemic lesion. It is usually considered that ideatory and ideomotor apraxias are due to left hemisphere lesions, whilst contsructive apraxia and apraxia related to dress are due to right hemisphere lesions. In this case, there was ideomotor apraxia secondary to a right parietal lesion, that is to say a crossed ideomotor apraxia, without crossing of other neuropsychological functions. This supports the theory of independence of hemisphere dominance for different cognitive functions. The frustrated left handedness of the patient might be related to the greater probability of unusual hemisphere dominance for ideomotor praxis function in this particular case.

Aged↗

PubMedDate not supplied

Congenital ocular motor apraxia: imaging findings.

PURPOSE: To determine the frequency of cerebellar and cerebral abnormalities on brain imaging studies in children with congenital ocular motor apraxia. METHODS: Brain imaging studies were performed in 19 children with typical congenital ocular motor apraxia who were in the care of a visual impairment program at a children's hospital. Independent clinical review categorized the subjects as having partial (n = 10) or expanded (n = 9) congenital ocular motor apraxia on the basis of extent of associated speech or neurodevelopmental problems. Fifteen CT studies and 13 MR examinations of the brain performed in these children were reviewed independently by two pediatric neuroradiologists. Radiologic findings were agreed on by consensus. RESULTS: Cerebellar abnormalities were found in 12 of 19 cases. The cerebellar vermis was small in 10 children. A small cerebellar vermis was the only abnormality in five of 10 children with partial congenital ocular motor apraxia and in two of nine children with expanded congenital ocular motor apraxia. Among seven children with a small vermis examined with high-resolution MR imaging, the inferior portion of the vermis was preferentially involved in each case. Of these seven subjects, none of four with partial congenital ocular motor apraxia but two of three with expanded congenital ocular motor apraxia had an abnormality of the superior portion of the vermis. Miscellaneous supratentorial lesions affecting both gray and white matter were found in six subjects. Five of the 19 children had normal imaging findings. CONCLUSION: Inferior vermian hypoplasia is the most common abnormality in children with congenital ocular motor apraxia.

Apraxias↗

PubMed1998

Pathologic correlates of apraxia in Alzheimer disease.

OBJECTIVE: To examine the neuroanatomical correlates of apraxia in Alzheimer disease. PATIENTS: Twenty-three patients with clinically overt Alzheimer disease. DESIGN: Anterograde study and neuropathologic case series. Clinical severity was assessed using the Global Deterioration Scale. Ideomotor praxis was examined on transitive and intransitive movements and meaningless gestures, and dressing ability was evaluated clinically. Constructive praxis was tested using a 3-dimensional figure copying task. Correlations between neurofibrillary tangle and senile plaque densities and praxis test performance were studied using stepwise logistic regression models. SETTING: Studies were conducted at the Psychiatric and Geriatric Hospitals of the University of Geneva School of Medicine, Geneva, Switzerland. MAIN OUTCOME MEASURES: Odds ratios to estimate the associations between neurofibrillary tangle and senile plaque densities in each neocortical area and the presence of ideomotor, dressing, and constructional apraxia. RESULTS: Statistically significant relationships were found between neurofibrillary tangle densities in the anterior cingulate cortex and ideomotor and dressing apraxia and between neurofibrillary tangle densities in the superior parietal, posterior cingulate, and occipital cortex and constructional apraxia. Senile plaque counts did not correlate with praxic performance. CONCLUSIONS: These results suggest that ideomotor and dressing apraxia are associated with mild damage of the anterior cingulate cortex, whereas constructional apraxia is related to the disruption of cortical pathways mediating visuospatial cognition in Alzheimer disease. Senile plaque densities do not represent a valuable pathologic correlate of apraxia in this disorder.

Aged↗

PubMed2004

Apraxia.

In this review, we present a summary of some of the most pertinent new research on aspects of apraxia. Rather than attempt a review of all neurologic syndromes that have been identified as forms of apraxia, such as buccofacial, truncal, apraxia of eye opening, and apraxia of speech, we focus on current literature and trends in the study of limb apraxia. Although the classic empirical approach to the study of apraxia has been through systematic neuropsychologic assessment of various aspects of the syndrome, questions remain regarding the exact neural substrate that forms the foundation of the praxis system. More recent work using sophisticated neuroimaging methods has yielded a wealth of new data that contributes significantly to our understanding of the neuroanatomic correlates of this complex disorder. In addition, the results of recent sophisticated neuropsychologic studies have suggested modifications to classic cognitive models of apraxia. A discussion of current work and directions for future research are also provided.

Apraxias↗

PubMed2006

Evaluation of ideomotor apraxia in patients with stroke: a study of reliability and validity.

OBJECTIVE: This aim of this study was to determine the reliability and validity of an established ideomotor apraxia test when applied to a Turkish stroke patient population and to healthy controls. SUBJECTS: The study group comprised 50 patients with right hemiplegia and 36 with left hemiplegia, who had developed the condition as a result of a cerebrovascular accident, and 33 age-matched healthy subjects. METHODS: The subjects were evaluated for apraxia using an established ideomotor apraxia test. The cut-off value of the test and the reliability coefficient between observers were determined. RESULTS: Apraxia was found in 54% patients with right hemiplegia (most being severe) and in 25% of left hemiplegic patients (most being mild). The apraxia scores for patients with right hemiplegia were found to be significantly lower than for those with left hemiplegia and for healthy subjects. There was no statistically significant difference between patients with left hemiplegia and healthy subjects. CONCLUSION: It was shown that the ideomotor apraxia test could distinguish apraxic from non-apraxic subjects. The reliability coefficient among observers in the study was high and a reliability study of the ideomotor apraxia test was therefore performed.

Adult↗

PubMed2002

Sensitivity of different ADL measures to apraxia and motor impairments.

OBJECTIVE: To determine whether specifically designed activities of daily living (ADL) observations can measure disability due to apraxia with more sensitivity than the Barthel ADL Index, a conventional functional scale. DESIGN: Cross-sectional study. SETTING: Rehabilitation centres and nursing homes. SUBJECTS: One hundred and six left hemisphere stroke patients with apraxia, hospitalized in rehabilitation centres and nursing homes. MEASURES: ADL observations, Barthel ADL Index, an apraxia test, Motricity Index, Functional Motor Test. RESULTS: Multivariate analyses showed that the specific ADL observations were associated with severity of apraxia (and not with motor impairments). The Barthel ADL Index was associated with motor impairments (and not with severity of apraxia). CONCLUSION: The assessment of disability in stroke patients with apraxia cannot rely only on the Barthel ADL Index. In addition, the specific ADL observation procedure is needed to measure disability due to apraxia.

Activities of Daily Living↗

PubMed1998

Outcome of strategy training in stroke patients with apraxia: a phase II study.

OBJECTIVE: Evaluation of a therapy programme for stroke patients with apraxia. The programme is based on teaching patients strategies to compensate for the presence of apraxia. This programme was designed for assessment and treatment by occupational therapists. DESIGN: The outcome was studied in a pre-post test design. Measurements were conducted at baseline and 12 weeks later. SUBJECTS: Thirty-three stroke patients with apraxia were treated at occupational therapy departments n general hospitals, rehabilitation centres and nursing homes. MAIN OUTCOME MEASURES: The following measurements were conducted: an apraxia test, a motor functioning test, observation of activities of daily living (ADL), Barthel Index, and an ADL questionnaire for the therapist and the patient. RESULTS: The patients showed large improvements in ADL functioning on all measures and small improvements on the apraxia test and the motor functioning test. The effect sizes for the disabilities, ranging from 0.92 to 1.06, were large compared to the effect sizes for apraxia (0.34) and motor functioning (0.19). The significant effect of treatment is also seen when individual improvement and subjective improvement are considered. Measured with the Barthel Index for instance, 71% of the patients improved. CONCLUSIONS: These results suggest that the programme seems to be successful in teaching patients compensatory strategies that enable them to function more independently, despite the lasting presence of apraxia.

Activities of Daily Living↗

PubMed2001

Neural and cognitive bases of upper limb apraxia in corticobasal degeneration.

OBJECTIVE: To investigate the neural and cognitive bases of upper limb apraxia in corticobasal degeneration (CBD). METHODS: Eighteen patients with CBD underwent a cognitive neuropsychological assessment of apraxia and resting [(18)F]-fluorodeoxyglucose PET scanning. Two complementary measures of apraxia were computed for each modality of gesture production. First, a performance score measured error frequency during gesture execution. Second, as a more stringent test of the integrity of the praxis system, the correction score measured the patient's ability to correct his or her errors on a second attempt. For each measure type, a cut-off score for the presence of apraxia was defined with regard to healthy controls. Using each cut-off score, the regional cerebral glucose metabolism of patients with CBD with apraxia (i.e., performing below cut-off score) was compared with that of patients with CBD without apraxia. RESULTS: Mean performance scores were below normal values in all modalities. Anterior cingulate hypometabolism predominated in patients with CBD who performed below the cut-off performance score. At variance, mean correction scores were below normal values for gesture imitation only. Hypometabolism in superior parietal lobule and supplementary motor area characterized patients with CBD who were unable to correct their errors at the same rate as control subjects did. CONCLUSIONS: Distinct neural networks underlie distinct aspects of the upper limb apraxic deficits in CBD. Extending previous findings of gesture production deficits in CBD, the use of complementary measures of apraxic behavior discloses a visuoimitative upper limb apraxia in CBD, underlain by a metabolic decrease in a parietofrontal neural network.

Aged↗

PubMed1991

Ideomotor apraxia in Huntington's disease.

The pattern of movement errors in ideomotor apraxia suggests an abnormality in selection and sequencing of component movements. Individuals with Huntington's disease were evaluated prospectively for the presence of apraxia, and aspects of motor and cognitive function were correlated with apraxic errors. Based on a conservative apraxia rating, ideomotor apraxia occurred in three (33%) of nine patients with a mean duration of disease of 10.4 years. Only two (22%) individuals made no apraxic errors, however, and the group as a whole made apraxic errors in 26% of movements. Apraxia was associated with errors in imitation of nonsymbolic movements but not with errors in recognition of gestures. It correlated significantly with duration of disease and with progressive abnormalities of posture but not with other individual aspects of elementary motor or cognitive function. These associations indicate that apraxia in Huntington's disease may be due primarily to involvement of subcortical motor structures rather than cerebral cortex.

Adult↗

PubMed1998

The apraxias are higher-order defects of sensorimotor integration.

The classical features of motor disorders due to neurological disease affecting the pyramidal pathways, cerebellum and basal ganglia in humans are well known. What is less understood is the clinical world of apraxia--'inability to perform purposeful skilled movements in the absence of any elementary motor (weakness, akinesia, abnormal posture or tone) or sensory deficits, or impaired comprehension or memory'. Much of what clinicians call apraxia is a failure of gesture production to command, due to problems of transcoding language into motor action, without motor deficit in ordinary life. However, damage to premotor regions and superior parietal lobules provokes devastating spontaneous higher-order motor deficits, including limb-kinetic apraxia, diagnostic apraxia, visuomotor apraxia and ideational apraxia.

Apraxias↗

PubMed1998

Limb-kinetic apraxia.

Five cases of limb-kinetic apraxia following primary degenerative cerebral pathology are reported. Apraxia appeared as the main symptom and was not concomitant to aphasia or to widespread cognitive impairments. Apraxia was not a consequence of elementary motor or sensory deficits, lack of coordination, or the result of the presence of rigid-akinetic symptoms. The apraxia was usually unilateral, being present in both routine activities and testing sessions and consisting of the coarse, unilateral, awkward execution of correctly planned movements. Conceptual knowledge of the movements and their ideational plan was spared. The characteristics of apraxia fit the definition of limb-kinetic apraxia originally proposed by Liepmann. The pertinent literature is reviewed.

Aged↗

PubMed2000

Cognition in action: testing a model of limb apraxia.

Assessment of limb apraxia is still suffering from Liepmann's legacy and performance in gesture-processing tests is generally rendered by classifying patients' profile according to the classic clinical labels of ideomotor and ideational apraxia. At odds with other cognitive functions, interpretation of apraxia has suffered from a lack of a reliable model which does justice to its complexity. Recently such a model has been proposed (Rothi et al., 1991, 1997). In this article a modified version of this model is presented and predictions are made according to its functional architecture. Five different patterns of impairment of gesture processing are postulated. To validate the predicted performance profiles, 19 left-hemisphere-damaged patients were assessed by means of an ad hoc battery of four praxis tests. Four of the five predicted apraxia patterns were observed, the fifth being more equivocal. These results support the need to overcome the simplistic dichotomous view of apraxia and confirm the fruitfulness of a model of normal gesture processing in order to understand dissociations in apraxia.

Aged↗

PubMed1976

Constructional apraxia in patients with discrete missile wounds of the brain.

Sixty patients with missile wounds confined to one of the four quadrants of the brain were investigated. All patients had neurosurgical verification of the limits of their lesions. The incidence and severity of constructional apraxia was studied using the WAIS Block Design and Object Assembly subtests, and the Bender Gestalt Test. A uniformly significant caudality effect was obtained with more posteriorly localized lesions resulting in more severe constructional apraxia. A significant laterality effect was obtained on two of three criterion measures with uniformly inferior performance by patients with right hemisphere lesions. The magnitude of the laterality effect, however, was less than that of the caudality effect for all criterion variables. The degree of severity of constructional apraxia in patients with right posterior lesions was uniformly greater than that of patients with other quadrant loci. The incidence of constructional apraxia in the four quadrants varied as expected with the left anterior lesion sample showing very little evidence of constructional apraxia, while the right posterior sample showed a high incidence of such deficits. The absolute incidence of significant constructional apraxia in all samples was suprisingly low. This finding might be partially accounted for by the age and general good health of the subjects studied, the relative absence of general cognitive impairment in the majority of subjects, and the discrete nature of the lesions.

Adolescent↗

PubMed2003

Patterns of limb apraxia in primary progressive aphasia.

Primary progressive aphasia (PPA) is a syndrome characterized by a progressive language deficit without other dementia features for at least two years (). Other deficits that are likely to co-exist with aphasia, such as apraxia, have only been investigated in a few case studies and only at a rudimentary level for the most part. In this study we investigate the frequency and severity of apraxic deficits in PPA patients. Ten PPA patients and twelve aged-matched healthy adults performed eight transitive gestures to pantomime and to imitation. Gesture performance was measured along five movement dimensions and a composite score based on the arithmetic mean of the five dimensions was calculated. Overall, PPA patients performed worse than controls with both pantomime and imitation. Furthermore, individual comparisons revealed that out of the three apraxia patterns described by (pantomime alone, imitation alone, or apraxia in both conditions), the most frequent pattern in PPA patients was apraxia in both conditions. This result corresponds with previous findings in populations of stroke and Alzheimer's patients. Considering the occurrence of apraxia in this population, this study supports the idea that a comprehensive apraxia assessment should be administered in cases of PPA.

Aphasia↗

PubMed1999

A diagnostic test for apraxia in stroke patients: internal consistency and diagnostic value.

The internal consistency and the diagnostic value of a test for apraxia in patients having had a stroke are presented. Results indicate that the items of the test form a strong and consistent scale: Cronbach's alpha as well as the results of a Mokken scale analysis present good reliability and good scalability. The diagnostic value of the test was determined by comparison of test results in three groups of patients: 44 stroke patients with apraxia (patients), 35 stroke patients without apraxia (patient controls), and 50 healthy nursing home residents with no history of stroke (normal controls). The diagnostic value is expressed by means of the sensitivity and specificity and the predictive value of the test. In addition, Receiver Operator Characteristics (ROC) curves are presented. The sensitivity and specificity of the apraxia test appear to be good: all values are higher than 80%. The test also has high predictive value. The ROC curves illustrate that the test is sufficiently discriminative to allow a differentiation between persons with apraxia and persons without apraxia.

Adult↗

PubMed1984

Lesion size and location in ideomotor apraxia.

Lesion size correlated positively with the severity of apraxia in the acute (one month) and chronic (one year) stage in 177 stroke patients, but accounted for only 25 per cent of the variance of the apraxia scores. Apraxia was measured on a standardized battery and defined in relation to normal controls. Lesions visualized by CT were traced objectively and measured on standard templates. Small lesions (less than one-tenth of the hemispheric volume) producing moderate or severe apraxia were mostly frontal and close to the body of the lateral ventricle. The lesions of the deep parieto- and occipitofrontal and anterior callosal fibres seem to be crucial in apraxia, rather than the parietal cortex as traditionally claimed. Large lesions (more than three-tenths of the hemisphere) without apraxia were associated with atypical asymmetries in half of the cases, as measured by the torque and the width of the frontal and occipital lobes on CT scan, suggesting a right hemisphere role in sparing and recovery of praxis.

Adult↗