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PubMed1987

Kepiński's functional structures, Kohonen's topological structures, aphasia and apraxia.

The concept of functional structures was introduced by Kepiński. At the Second Scandinavian Congress on Image Analysis in 1981 Kohonen provided evidence that the map of signals has the same topological order as the map of reactions. These topological concepts can be applied also to logical structures. The same is true also of functional structures described by Kepiński in schizophrenia, which may be created or destroyed, but their topological order remains unaltered. Functional structures change in obscuration and in hallucinogen-induced psychodelic states. Fixed pathological structures characterized by an altered topological order occur in paranoia. In the case of amnestic aphasia single elements of the topological functional structures fall out-these elements represent terms which patient is unable to recall. In motor aphasia, on the other hand, damage concerns the topological functional structures of speech related movements. In sensory aphasia damage concerns topological functional structures in the sensory area. In Goldstein's amnestic apraxia there is a loss of some elements of the topological functional structures governing the movements. In ideational apraxia the damage concerns topological functional structures representing entire sets of motor function and especially their creation. In ideomotor apraxia the respective topological functional structures are retained, albeit inaccessible, due to a disturbance in the motor association. In motor apraxia the damage seems to concern the topological functional structures governing precise movements and located at a lower level, i.e., closer to the effector. Constructive apraxia seems to result from the disturbed creation of the respective functional structures. Similarly the hypermotility of a maniacal type has a smooth and purposeful character, as far as the relation to a particular situation is concerned, which suggests that the respective topological functional structures are preserved. On the other hand, in the hyperkinetic phase of catatonic schizophrenia, in which the patient performs sequences of incoherent aimless movements without any relation to the current situation and environment, these structures are supposedly altered.

Aphasia↗

PubMed1999

Ideomotor apraxia in Alzheimer disease and left hemisphere stroke: limb transitive and intransitive movements.

OBJECTIVE: Ideomotor apraxia was studied in patients with Alzheimer disease (AD) and unilateral left hemispheric damaged (LHD) stroke to determine whether these groups differed. BACKGROUND: Given that the neuropathology of AD is bilateral and more diffuse than the localized involvement in patients after an LHD stroke, and given that the cognitive deficits in AD are more widespread than in LHD stroke, the authors predicted that patients with these disorders would differ in response to an auditory command task administered to evaluate ideomotor apraxia, and that the two patient groups would be significantly more impaired than healthy matched control subjects. METHODS: Twenty-one persons were studied, including equal numbers of patients with AD, patients with unilateral LHD stroke, and control subjects. An auditory command test of limb apraxia was administered and videotaped to score performance and to code spatial-temporal or content errors. RESULTS: The patients with AD and LHD stroke were significantly more impaired than healthy control subjects. Whereas the patients with AD and LHD stroke were equally apraxic and did not differ in their performance of transitive limb movements, the patients with AD were significantly more impaired than the patients with stroke when performing intransitive limb movements. A positive correlation was found between severity of dementia and severity of apraxia in the patients with AD. The patients with LHD stroke were as likely to make spatial-temporal as content errors when performing intransitive limb movements, whereas the patients with AD made content errors only. Error types produced with transitive limb movements did not differ between groups; spatial-temporal errors were the most common errors made both by patients with AD and patients with LHD stroke. CONCLUSIONS: As predicted, patients with AD and with LHD stroke were impaired when producing limb movements after auditory command, and both patient groups were significantly more impaired than the healthy adults. Patients with AD were significantly more impaired than patients with stroke when performing intransitive limb movements, and error types differed by group. Patients with AD and patients with stroke were equally impaired when performing transitive movements, and error types did not differ by group. Patients with ideomotor apraxia are often degraded in their production of transitive and intransitive movements, and the observation that performance may differ depending on the type of limb movement suggests that movement representations for transitive and intransitive movements may be at least partially independent.

Aged↗

PubMed2000

[Progressive anarthria: one case without lingual apraxia].

Progressive anarthria is a focal cortical degenerative disorder characterized by a profound, progressive alteration in speech without impairment in other cognitive domains. The first symptoms consist of an alteration in the articulation of speech producing telegraphic speech. The disorder invariably progress towards anarthria by deprogramming of the phonation and orolingual movements (bucophonetic apraxia). This type of apraxia is usually associated with orolinguofacial apraxia and it has been anatomofunctionally correlated with frontal opercular involvement of left predominance. The patient presented as progressive anarthria in the absence of manifest orolingual apraxia associated with a predominance of cortical atrophy in the right frontal operculum. This semiological dissociation emphasizes the importance of bucophonatory apraxia in the pathophysiology of progressive anarthria.

Apraxias↗

PubMed2000

[Progressive limb-kinetic apraxia with myoclonus focal atrophy in the postcentral gyrus and the supplementary motor area].

We report a 70-year-old right handed man with a 5-year history of slowly progressive clumsiness of his left hand. A neurological examination disclosed mild rigidity and myoclonus in his left hand. He showed limb-kinetic apraxia, but neither ideational apraxia nor ideomotor apraxia was present. Aphasia and agnosia were also absent. He was thought to have the primary progressive limb-kinetic apraxia clinically. Brain CT and MRI revealed focal atrophy in the right postcentral gyrus and the supplementary motor area. A positron emission tomography (PET) study showed diffuse decrement of cerebral blood flow, predominantly in the right hemisphere. The decrease in the uptake of [18F]-Fluoro-deoxyglucose also revealed glucose hypo-metabolism, especially in the right frontal and parietal lobe. Striatal [11C]NMSP and [18F]FDOPA uptake were also reduced in an asymmetric pattern. These findings suggest that our patient is likely to have corticobasal degeneration. Transcranial magnetic stimulation using double pulse paradigm revealed a decrease in the level of cortico-cortical inhibition in the motor cortex on the affected side. Our results indicate increase in the excitability of motor cortical neurons in primary progressive limb-kinetic apraxia, likely due to a decreased excitability of cortico-cortical inhibitory mechanism as a result of focal degeneration of cortical neurons.

Aged↗

PubMed1989

[The influence of certain contextual factors on voice onset time, vowel duration and utterance duration in verbal apraxia].

The concept of context sensitivity as borrowed from the coalition model has important implications for the interpretation of the symptoms of apraxia of speech and for a better understanding of the nature of the disorder. In this study which was part of the wider investigation into the effect of variation in contextual factors on apraxia of speech (van der Merwe, Uys, Loots and Grimbeek, 1987; 1988), the effect of two contextual factors namely sound structure and articulatory features on voice onset time, vowel duration and utterance duration was acoustically analysed. Four subjects with acquired apraxia of speech and one with developmental apraxia of speech were tested. Findings indicated that voice onset time is not context sensitive. Errors in voice onset time were not true substitutions with voiceless sounds but were inconsistent distortions due to an inability to keep interarticulator synchronization within the critical temporal boundaries of motor equivalence. Vowel and utterance duration were found to be context sensitive. The deviation in duration increased with increased complexity of the utterance. As was the case with the auditorily perceived symptoms, the temporal characteristics of apraxia of speech can also be classified into core symptoms and associated symptoms based on their context sensitivity.

Apraxias↗

PubMed1995

[Progressive severity of left unilateral apraxia in 2 cases of Alzheimer disease].

Two patients presented with progressive left unilateral motor apraxia and progressive visuo-spatial difficulties, including constructional apraxia, dressing apraxia, spatial dysgraphia and dyslexia, spatial acalculia and neglect of the left side, without significant changes in the other cognitive functions. In both patients, radiological tests demonstrated cortical atrophy, more marked in the retrorolandic areas. A diagnosis of Alzheimer's disease was made in the first patient by cortical biopsy and in the second patient by post-mortem examination. The second patient died from an intercurrent neoplastic condition early in the course. Post-mortem examination of her brain showed the atrophy to be predominantly in the superior parietal gyri. In these areas, in addition to neuritic plaques and neurofibrillary tangles, these was also severe gliosis and superficial spongiosis. These two cases were clinically different from cortico-basal degeneration, where the motor difficulties are associated with occulo-motor problems, extrapyramidal signs and involuntary movements of the "alien hand" type. These data confirm the presence of focal forms of Alzheimer's disease. The motor apraxia seen in our patients resembles the kinesthesic apraxia described by Luria.

Alzheimer Disease↗

PubMed1997

[Neuropsychological analysis in 2 cases of infarction in the left precentral gyrus--with special reference to apraxia of speech and agraphia].

It remains controversial whether agraphia can coexist in a case with apraxia of speech, and whether an apraxia of speech can be classified into a category of aphasia. We examined the presence of agraphia in 2 right-handed patients of apraxia of speech. Case 1 of mild agraphia showed an infarcted lesion in the left precentral gyrus extending to the neighboring white matter, which involving the arcuate fasciculus on MRI. Positron emission tomography (PET) indicated decrease of cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) in the infarcted lesion, but no decrease of CBF and CMRO2 in the Broca's area. In this case, agraphia was more conspicuous in "kanji" than in "kana" and severity of the agraphia was not correlated to that of speech disturbance on naming test. Case 2 without agraphia showed a small infarcted lesion in the left precentral gyrus, which did not extend to the deep white matter on MRI. Agraphia can coexist with apraxia of speech in a case with the lesion in the left precentral gyrus, in which the cortical lesion is relatively widespread or extends to the deep white matter. However, lack of etiological connection between the agraphia and the apraxia of speech was suggested. We could not confirm the location in the left precentral gyrus which is responsible for the agraphia.

Aged↗

PubMed1998

Speech, cognition, and imaging studies in congenital ocular motor apraxia.

Detailed neurological, speech and language, psychological, and neuroimaging studies were carried out in eight children with the diagnosis of congenital ocular motor apraxia. The neurological examination showed clinical evidence of cerebellar vermis abnormality (hypotonia and truncal ataxia) in all cases. Neuroimaging studies suggested that the site of neuropathological disturbance of congenital ocular motor apraxia was the inferior vermis. Half of the subjects had associated speech apraxia. The most likely location of brain disturbance, which was responsible for the speech apraxia, was also an as yet undefined area of the vermis. Psychological testing consistently revealed visual-spatial difficulties. These may have been secondary to cerebellar pathology or to developmentally inappropriate sensory input caused by the abnormal saccades. Children with speech apraxia appear to be slightly more affected neurologically than those with normal speech.

Apraxias↗

PubMed2002

Gait apraxia after bilateral supplementary motor area lesion.

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.

Apraxias↗

PubMed2001

Recessive ataxia with ocular apraxia: review of 22 Portuguese patients.

BACKGROUND: The recessive ataxias are a heterogeneous group of neurodegenerative disorders characterized by cerebellar ataxia associated with a number of different neurologic, ophthalmologic, or general signs. They are often difficult to classify in clinical terms, except for Friedreich ataxia, ataxia-telangiectasia, and a relatively small group of rare conditions for which the molecular basis has already been defined. OBJECTIVES: To study the clinical presentation and to define diagnostic criteria in a group of Portuguese patients with ataxia and ocular apraxia, an autosomal recessive form without the essential clinical and laboratory features of ataxia-telangiectasia. PATIENTS AND METHODS: We reviewed 22 patients in 11 kindreds, identified through a systematic survey of hereditary ataxias being conducted in Portugal. RESULTS: Age at onset ranged from 1 to 15 years, with a mean of 4.7 years. The duration of symptoms at the time of last examination varied from 5 to 58 years. All patients presented with progressive cerebellar ataxia, the characteristic ocular apraxia, and a peripheral neuropathy. Associated neurologic signs included dystonia, scoliosis, and pes cavus. Magnetic resonance imaging was performed in 16 patients, all of whom showed cerebellar atrophy. CONCLUSIONS: Ataxia with ocular apraxia may be more frequent than postulated before, and may be identified clinically using the following criteria: (1) autosomal recessive transmission; (2) early onset (for most patients in early childhood); (3) combination of cerebellar ataxia, ocular apraxia, and early areflexia, with later appearance of the full picture of peripheral neuropathy; (4) absence of mental retardation, telangiectasia, and immunodeficiency; and (5) the possibility of a long survival, although with severe motor handicap.

Adolescent↗

PubMed2003

Spasmus nutans and congenital ocular motor apraxia with cerebellar vermian hypoplasia.

BACKGROUND: Spasmus nutans and congenital ocular motor apraxia share clinical characteristics. However, their development in a patient with cerebellar vermian hypoplasia has not been previously described. OBJECTIVE: To report spasmus nutans and congenital ocular motor apraxia in a child with cerebellar vermian hypoplasia. DESIGN: Case report. SETTING: Tertiary-care hospital. Patient A 7-year-old boy with a history of spasmus nutans during infancy and developmental delay was referred for the evaluation of abnormal head and eye movements. RESULTS: The patient had impaired voluntary saccades and smooth pursuit in the horizontal plane and showed thrusting movements of the head during attempted gaze shift. Magnetic resonance imaging of the brain demonstrated cerebellar vermian hypoplasia, especially in the inferior portion. CONCLUSIONS: Spasmus nutans and congenital ocular motor apraxia may develop in patients with cerebellar vermian hypoplasia. In patients with congenital ocular motor apraxia, a history of spasmus nutans should be sought, and careful evaluation of the cerebellar vermis is needed during brain imaging.

Apraxias↗

PubMed2003

Right orbitofrontal tumor with pedophilia symptom and constructional apraxia sign.

BACKGROUND: Orbitofrontal abnormalities are associated with poor impulse control, altered sexual behavior, and sociopathy. OBJECTIVE: To describe a patient with acquired pedophilia and a right orbitofrontal tumor who was unable to inhibit sexual urges despite preserved moral knowledge. DESIGN: Case report. RESULTS: The patient displayed impulsive sexual behavior with pedophilia, marked constructional apraxia, and agraphia. The behavioral symptoms and constructional deficits, including agraphia, resolved following tumor resection. CONCLUSIONS: For patients with acquired sociopathy and paraphilia, an orbitofrontal localization requires consideration. This case further illustrates that constructional apraxia can arise from right prefrontal lobe dysfunction. Agraphia may represent a manifestation of constructional apraxia in the absence of aphasia and ideomotor apraxia.

Adult↗

PubMed2005

Interventions for apraxia of speech following stroke.

BACKGROUND: Apraxia of speech is a communication disorder that can affect stroke patients. Several different intervention strategies are undertaken by speech and language therapists working with this patient group. OBJECTIVES: To assess whether therapeutic interventions improve functional speech in stroke patients with apraxia of speech and which individual therapeutic interventions are effective. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (searched May 2004). In addition, we searched the following databases: the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 4, 2003); MEDLINE (1966 to April 2004); EMBASE (1980 to April 2004); CINAHL (1982 to April 2004); PsycINFO (1974 to April 2004); the National Research Register (searched April 2004); and Current Controlled Trials Register (searched May 2004). We reviewed reference lists of relevant articles and contacted authors and researchers in an effort to identify published and unpublished trials. SELECTION CRITERIA: We sought to include randomised controlled trials of non-drug interventions for adults with apraxia of speech following a stroke where the primary outcome was functional speech at six months follow up. DATA COLLECTION AND ANALYSIS: One author searched the titles, abstracts and keywords. Two authors examined the abstracts that might meet the inclusion criteria. Four authors were available to assess trial quality and to extract data from eligible studies. MAIN RESULTS: No trials were identified. AUTHORS' CONCLUSIONS: There is no evidence from randomised trials to support or refute the effectiveness of therapeutic interventions for apraxia of speech. There is a need for high quality randomised trials to be undertaken in this area.

Apraxias↗

PubMed1999

A kinematic study of progressive apraxia with and without dementia.

BACKGROUND: Prehension is an ideationally simple, cued movement requiring proximal (transport) and distal (manipulation) limb control. Patients with this syndrome of progressive apraxia are unable to perform many activities of daily living that require prehension. There is little known about how this syndrome kinematically disrupts such movements or whether concurrent dementia might play a critical role. OBJECTIVES: Using prehension as a paradigm for an ideationally simple, cued functional movement, we sought to (1) characterize the kinematic features of progressive apraxia in general, and (2) contrast the kinematic differences between apraxic patients with and without dementia. METHODS: Eight patients with the syndrome of progressive apraxia (including five without dementia, one of whom had autopsy-confirmed corticobasal ganglionic degeneration, and three with dementia, one of whom had autopsy-confirmed Alzheimer's disease) were compared with eight age-matched normal control subjects on a prehension task using an Optotrak camera system. RESULTS: Compared with control subjects, apraxic subjects had slowed reaction time, slowed transport and manipulation kinematics, greater lateral deviation from the linear prehension trajectory, greater intermanual asymmetry, motor programming disturbances, and mild transport-manipulation uncoupling. There were minor differences between the apraxia subgroups such as greater intermanual differences and impaired grip aperture velocity in the nondemented group, and overall slower movement in the demented group. CONCLUSIONS: There are major kinematic differences between apraxic and control subjects on a prehension task. The differences between clinical-pathologic subgroups are more subtle, and the movement disorder itself rather than concurrent dementia is the greatest determinant of motor disability.

Aged↗

PubMed1995

Progressive ideomotor apraxia: evidence for a selective impairment of the action production system.

We report a patient with slowly progressive bilateral limb apraxia associated with an asymmetrical focal degenerative process of the parietal lobes. Clinical assessment of praxis production suggested a striking deficit in controlling the spatiotemporal attributes of purposeful skilled limb movements, consistent with ideomotor apraxia. The precise nature of the action production impairment was further defined by objective three-dimensional computergraphic analysis of transitive movements which demonstrated significant kinematic deficits in spatial accuracy, timing, spatiotemporal coupling, and joint coordination. Gesture comprehension and discrimination were spared. Furthermore, detailed evaluation of the conceptual praxis system revealed that despite an almost complete inability to perform transitive movements accurately, abstract knowledge of tool function and action was remarkably well preserved. The critical dissociation between intact conceptual knowledge of action and impaired movement execution documented in this case points to a fundamental competence/performance dichotomy in apraxia and provides empirical support for cognitive models of praxis that divide the action system into distinct conceptual and production subcomponents. Within this theoretical framework, our patient's severe ideomotor apraxia is interpreted to represent a selective disruption of the action production system.

Apraxias↗

PubMed2000

The role of the dynamic body schema in praxis: evidence from primary progressive apraxia.

On an influential model of limb praxis, ideomotor apraxia results from damage to stored gesture representations or disconnection of representations from sensory input or motor output (Heilman & Gonzalez Rothi, 1993; Gonzalez Rothi et al., 1991). We report data from a patient with progressive ideomotor limb apraxia which cannot be readily accommodated by this model. The patient, BG, is profoundly impaired in gesturing to command, to sight of object, and to imitation, but gestures nearly normally with tool in hand and recognizes gestures relatively well. In addition, performance is profoundly impaired on imitation of meaningless gestures and on tasks requiring spatiomotor transformations of body-position information. We provide evidence that BG's apraxia is largely attributable to impairments external to the stored gesture system in procedures coding the dynamic positions of the body parts of self and others; that is, the body schema. We propose a model of a dynamic, interactive praxis system subserved by posterior parietal cortex in which stored representational elements, when present, provide "top-down" support to spatiomotor procedures computed on-line. In addition to accounting for BG's performance, this model accommodates a common pattern of ideomotor apraxia more readily than competing accounts.

Aged↗

PubMed2005

[Apraxias].

Apraxias are deficits in higher motor behaviour that are not primarily caused by elementary deficits of the sensorimotor system, communication problems, or dementia. These patients present with deficits such as imitating meaningful or meaningless gestures and in dexterity or purposeful use of objects. The different forms of apraxia originate from lesions of different levels/structures of the motor system, reflecting its complexity. Apraxias are caused by deficits in motor programmes generated in the frontal motor areas, in modality-specific higher sensorimotor control, or at the highest level of motor planning and motor conception. The types of apraxia differentially affect activities of daily living and hence show marked differences in the prognosis of recovery and the physiotherapeutic treatment required. Therefore, appropriate diagnosis and treatment of the different forms are of foremost clinical importance.

Apraxias↗

PubMed2005

[Apraxia--neuroscience and clinical aspects. A literature synthesis].

Apraxic phenomena occur in various neurological conditions. Selective motion control is viewed as the basic capacity to make fine and precise, isolated or independent face or limb movements. Its deficit can indicate limb-kinetic apraxia if it is not explained by paresis, somatosensory deafferentation, or ataxia. The core deficit in ideomotor apraxia could be deficient movement representations, i.e. the combination of invariant features of intrinsic and extrinsic coding for a given movement, which are most important when movements have to be performed outside their typical context. Ideational apraxia would be defined by a semantic deficit related to action. Frontal apraxia is characterised by an action-sequencing deficit. A detailed model is proposed regarding processes relevant to praxis.

Apraxias↗