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At least 163 records · Page 9Linked to original sources
PubMed1995

[Anarthria, progressive apraxia and extrapyramidal syndrome: an uncommon clinical form of corticobasal degeneration? A case studied by HMPAO Tc99m single-photon emission tomography].

A 48-year-old man presented with impaired joint movement and buccofacial apraxia. The disease progressed for six years associating an akineto-hypertonic syndrome, marked anarthria, saliva incontinence, bi-opercular syndrome, bucco-facial apraxia, severe global gestual apraxia and a frontal syndrom. Oculo-motricity and gait were normal. Magnetic resonance imaging of the brain demonstrated fronto-parietal atrophy and HMPAO Tc99 tomography revealed hypoperfusion of the cortex clearly predominating in the left parietal region. These particular findings with predominantly intense joint involvement is similar to the clinical picture in corticobasal degeneration--subcortical signs (progressively uncontrollable hypertonia) together with cortical signs (severe gestual apraxia). The neuroradiological imaging and functional results also suggest a degenerative process.

Apraxias↗
PubMed2002

The neurological bases of apraxia of speech.

Which site(s) of brain damage are associated with apraxia of speech (AOS)? There appears to be little agreement. The article first considers some reasons why not. Even allowing for factors that may have influenced findings, a definitive answer to the question of the neurological bases of AOS is not currently possible. The article goes on to look briefly at developments in the field of motor control, and limb and buccofacial apraxia in particular, that may hold clues to an answer or at least to asking the right questions. In particular, if AOS is to be understood as a motor disorder, then models compatible with motor control and its neurophysiological underpinnings must be sought. Current models of motor control and apraxia stress the sensorimotor, distributed, interactive nature of control across multiple brain areas.

Apraxia, Ideomotor↗
PubMed1988

Crossed buccofacial apraxia.

The cerebral hemisphere contralateral to the preferred hand is generally dominant for learned representational motor acts, including those involving buccofacial muscles. It is generally also language-dominant. This buccofacial apraxia has, with rare exceptions, been associated with left hemispheric lesions in right-handers. We describe two patients with severe buccofacial apraxia caused by large middle cerebral artery territory infarcts in the hemisphere ipsilateral to the preferred hand and nondominant for language. Neither patient had aphasia or major limb apraxia. Computed tomographic scans in the first patient and neuropathologic examination in the second failed to reveal an abnormality of the hemisphere contralateral to the preferred hand. Hence, in some individuals, the hemisphere controlling skilled representational buccofacial movements may not be the one that is dominant either for handedness or for language.

Aged↗
PubMed2003

Limb-kinetic apraxia in corticobasal degeneration: clinical and kinematic features.

Current concepts regarding the organisation of the motor system indicate the existence of a frontoparietal circuit involved in prehension and manipulation, whose damage may result in a motor behavioural disorder strongly resembling the one originally described as limb-kinetic apraxia. To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three-dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb-kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb-kinetic apraxia in patients with corticobasal degeneration.

Aged↗
PubMedDate not supplied

Screening for apraxia: a short assessment for stroke patients.

Apraxia is a disorder that involves impaired ability to execute previously learned movements that cannot be attributed to basic sensory or motor disturbances. A thorough assessment of apraxia typically entails both pantomiming and imitation of transitive (tool-related), intransitive (communication-related), and meaningless gestures, presented in an array of different, process-dependent sensory conditions. Precise and detailed assessment tools are often time-consuming and a shorter screening tool may be desirable for efficient surveillance of this disorder in stroke patients. In the present study, stroke patients (N = 37) were compared to healthy controls (N = 30) in their production of commonly used transitive and intransitive gestures. Five gestures (knife, flipper, tweezers, okay sign, cab hailing) were consistently performed with poorer accuracy in stroke patients when compared to healthy controls. The combination of gestures that best captured apraxic performance was statistically determined based on Z-score data. Results provide a shortened and sensitive method of detecting apraxia in stroke patients.

Apraxias↗
PubMed1987

Ideomotor apraxia in patients with dementia of Alzheimer type.

Ideomotor apraxia was checked in a carefully selected group of patients with Alzheimer's dementia, all in the mild stage of the disease. It was shown that ideomotor apraxia is not an early neuropsychological feature. When compared with other cognitive measures, the speed of deterioration of ideomotor apraxia appears to be particularly slow.

Aged↗
PubMed1993

Slowly progressive apraxia: two case studies.

Two patients with a slowly progressive and severe motor apraxia are presented. In one case, there was only apraxia; in the other there was moderate memory disturbance and a mild decline of global intellectual ability, suggesting a more widespread cognitive dysfunction. In this second case, recognition of the correct use of objects was also severely impaired, suggesting a disturbance of motor knowledge. In both cases, apraxia was asymmetrical, and associated with a contralateral atrophy of the upper parietal cortex, suggesting a differential involvement of separate action systems for each hand.

Aged↗
PubMed1986

The clinical examination for motor apraxia.

The signs and symptoms of motor apraxia are described both for ideomotor and ideational apraxia. Typical errors are described. For ideomotor apraxia a list of tasks is given. The many conceptual and psychometric problems that still await an answer are briefly discussed.

Apraxias↗
PubMed1985

Contrasting speech patterns in apraxia of speech and phonemic paraphasia.

This study was designed to determine if perceptual phonological analysis would reveal distinctions between patients with apraxia of speech and patients with phonemic paraphasic speech. Test findings from 10 Broca's aphasics with apraxia of speech were compared to findings from 10 paraphasic speakers (5 conduction and 5 Wernicke's aphasics). Several marked differences were revealed. Predominant locus of errors and relative difficulty of different classes of phonemic segments were significant discriminators. There was a nonsignificant trend for substituted phonemes to be further from target phonetically in the paraphasic patients. In addition, the two groups showed certain consistent differences in the types of errors they produced. Apraxic patients produced many errors of transitionalization, while sequencing errors were more typical of the patients with phonemic paraphasia. The findings are interpreted in relation to a neuropsychological model of speech. It is suggested that phonemic paraphasia represents a breakdown mainly in the retrieval of phonological word patterns, while apraxia of speech is characterized predominantly by a disturbance in encoding phonological patterns into appropriate speech movements.

Adult↗
PubMed1987

Persisting apraxia in two left-handed, aphasic patients with right-hemisphere lesions.

Apraxia usually follows a left hemisphere lesion in right-handers with left hemisphere speech representation. Apraxia following a right hemisphere lesion in left-handers is rare, however, and not well documented in the literature. Two left-handed patients are described in whom apraxia and aphasia followed a right hemisphere lesion. Both the apraxic and the aphasic deficits improved but were still demonstrable 6 weeks following the infarct. The data are consistent with those for right-handers with left hemisphere lesions in suggesting some overlap of anatomical structures for the control of speech and praxis.

Aged↗
PubMedDate not supplied

Oculomotor apraxia: the presenting sign of Gaucher disease.

Oculomotor apraxia may be idiopathic or a symptom of a variety of diseases. In Gaucher disease, oculomotor deficit is characterized by a failure of volitional horizontal gaze with preservation of vertical movements. We present 2 sisters, 6 1/2 and 5 1/2 years of age, in whom the presenting sign was oculomotor apraxia. Oculomotor apraxia has not been previously reported as the presenting manifestation of Gaucher disease.

Apraxias↗
PubMed2004

Crossed apraxia of speech: a case report.

The present study reports on the first case of crossed apraxia of speech (CAS) in a 69-year-old right-handed female (SE). The possibility of occurrence of apraxia of speech (AOS) following right hemisphere lesion is discussed in the context of known occurrences of ideomotor apraxias and acquired neurogenic stuttering in several cases with right hemisphere lesion. A current hypothesis on AOS-the dual route speech encoding (DRSE) hypothesis-and predictions based on DRSE were utilized to explore the nature of CAS in SE. One prediction based on the DRSE hypothesis is that there should be no difference in the frequency of occurrence of apraxic errors on words and non-words. This prediction was tested using a repetition task. The experimental stimuli included a list of minimal pairs that signaled voice-voiceless contrasts in words and non-words. Minimal-pair stimuli were presented orally, one at a time. SE's responses were recorded using audio and videotapes. Results indicate that SE's responses were characterized by numerous voicing errors. Most importantly, production of real word minimal pairs was superior to that of non-word minimal pairs. Implications of these results for the DRSE hypothesis are discussed with regard to currently developing perspectives on AOS.

Aged↗
PubMed2005

Early-onset ataxia with oculomotor apraxia with a novel APTX mutation.

Early-onset ataxia with oculomotor apraxia and hypoalbuminemia is an autosomal recessive cerebellar ataxia characterized by oculomotor apraxia, peripheral neuropathy, and hypoalbuminemia. Mutations in aprataxin gene located at chromosome 9q13 have been identified recently in Japanese and European patients. This study reports two cases of siblings with early-onset ataxia with oculomotor apraxia and hypoalbuminemia, which manifested early onset before 2 years of age with relatively rapid progression and severe dystonia. Both of the siblings were compound heterozygotes with aprataxin gene mutations, 689 insT and G692A, in exon 5 that encodes the histidine triad domain of the aprataxin protein. The novel missense mutation, G692A, was not present in 40 unrelated and unaffected individuals.

Adolescent↗
PubMed2000

Congenital ocular motor apraxia with autosomal dominant inheritance.

PURPOSE: To document congenital ocular motor apraxia in five first-degree relatives. METHODS: Case series. Five family members with a history of horizontal head thrusting had neuro-ophthalmologic evaluation. Magnetic resonance imaging of the brain was obtained in the proband. RESULTS: Four siblings (one boy and three girls) had congenital ocular motor apraxia. The father had head thrusting as a child and displayed residual signs of the disorder. Magnetic resonance imaging disclosed no central nervous system abnormalities in the father. CONCLUSION: Congenital ocular motor apraxia can be inherited as an autosomal dominant trait.

Adult↗
PubMed1997

On crossed apraxia. Description of a right-handed apraxic patient with right supplementary motor area damage.

GP, a right-handed woman, without evidence of familial left-handedness, showed clearcut bilateral ideo-motor apraxia and oro-facial apraxia after a vascular lesion of the right hemisphere, encroaching upon the fronto-mesial region. She scored normally in most other cognitive tests, including language, but showed signs of callosal disconnection, left anarchic hand and mild unilateral spatial neglect. This cognitive profile points to the possibility of praxis being localized to the right hemisphere in this right-handed patient. We argue in favour of individual variability of praxis dominance, and maintain that this dominance might be completely right-sided in some subjects. Moreover the anatomical locus of GP's lesion points to the possible role that the frontal lobes (and more specifically the Supplementary Motor Area) play in the genesis of apraxia.

Agnosia↗
PubMed1975

A tapping test in apraxia.

An enigma in understanding the mechanism of motor apraxia is why patients with disease restricted to the left hemisphere cannot imitate motions with the left hand despite intact visual motor apparatus. Liepmann suggested that motor memories are stored in the left hemisphere and that in apraxia these engrams are either destroyed or separated from the right hemisphere. If Liepmann's hypothesis is correct, then, in addition to poor performance on commands and imitation, there should be poor performance in a motor task. To ascertain if there is a motor defect of the non-paretic hand of apraxic patients, twenty apraxic patients were given a rapid finger tapping test and their performance was compared with the left hand performance of aphasic right hemiparetic non-apraxic controls. The aptaxic group performed this task significantly slower than the control group, thereby giving support to Liepmann's hypothesis of apraxia.

Aged↗
PubMed2000

Ideomotor apraxia, visuomotor control and the explicit representation of posture.

Ideomotor apraxia is normally viewed as a disorder of the representation or execution of action. However, the evidence from gesture imitation is that apraxic patients are unable to reproduce the final posture of a gesture but may not show abnormality in movement kinematics. This supports a hypothesis that impaired gesture imitation is due to a deficit in a conceptual representation of body posture rather than indicating a disorder specific to action control. The present study evaluated whether other aspects of apraxic behaviour might also be most consistent with a deficit in the representation of posture. Patients with left hemisphere damage and apraxia on gesture imitation had difficulty in reproducing a series of actions due to failure to adopt the required configuration of the hand whereas there was no consistent reduction in speed of response once the actions had been learned. They also tended to use an abnormal, clumsy grasp when using a spoon but this dissociated from accurate performance on other tests of manual dexterity where there was less scope for variation in configuration of the hand. These data suggest that the most common deficit in ideomotor apraxia is impaired ability to perform tasks where the goal is to reproduce or adopt complex hand configurations and that impaired execution of some types of action is secondary to this problem. This is consistent with a role for the human left parietal lobe in providing an explicit representation of posture which is used to guide some actions and to supplement a more primitive system of direct visuomotor control.

Adult↗
PubMed2006

[Autosomal recessive cerebellar ataxias with oculomotor apraxia].

INTRODUCTION: Autosomal recessive cerebellar ataxias (ARCA) comprise a phenotypically and genetically heterogeneous group of diseases. Recently, a subgroup of ARCA associated with oculomotor apraxia has been delineated. STATE OF THE ART: The ataxias with oculomotor apraxia (AOA) include four distinct genetic entities at least: ataxia-telangiectasia, ataxia telangiectasia-like disorder, ataxia with oculomotor apraxia type 1 (AOA1) and type 2 (AOA2). The responsible genes, ATM, MRE11, APTX and SETX respectively, are implicated in DNA-break repair mechanisms. CONCLUSION: We describe the phenotypic and genetic characteristics of these ataxias, based on a review of the literature and a personal study of AOA1 and AOA2 patients.

Apraxias↗