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[Slowly progressive dressing and constructional apraxia: symptomatological study, especially for dressing apraxia].

In 1982, Mesulam drew attention to a clinical picture characterized by slowly progressive aphasia without dementia, and since then, there have been many such reports. Recently, there have been 30 reports of slowly progressive apraxia. However, the nature of this apraxia is not uniform. We now report a patient with slowly progressive dressing and constructional apraxia. The patient is a 60-year-old right-handed woman with a 2-year history of a slowly progressive praxic disturbance. On admission, she was alert and aware of this difficulty. A neurological examination disclosed mild rigidity and myoclonus in her left hand. A neuropsychological assessment disclosed severe dressing apraxia, which was unlikely to be caused by dementia and moderate constructional apraxia. Her dressing apraxia was manifested in upper limbs, neck, trunk and lower limbs. However, she could express verbally the action of dressing. She also showed mild limb-kinetic apraxia, but neither ideational apraxia nor ideomotor apraxia was present. Aphasia and agnosia were also absent. On an MRI, the bilateral cerebral hemispheres were atrophic (right > left). A 99m-Tc ECD SPECT revealed decreased uptake in the right cerebral hemisphere and left frontal lobe, and an EEG showed slow waves over the right cerebral hemisphere. There have been 30 reports of slowly progressive apraxia. Most of these cases presented with slowly progressive clumsiness in one or both hands as an initial symptom, followed by constructional, ideomotor or dressing apraxia. Our patient differed from these cases in that dressing and constructional apraxia progressed slowly without any other apraxia except only mild limb-kinetic apraxia. There was a similarity between dressing apraxia of our patient and that of Marie's and Brain's original cases.

Activities of Daily Living↗
PubMed1994

Anosodiaphoria for dressing apraxia: contributory factor to dressing apraxia.

We report 2 patients with bilateral dressing apraxia. One patient had prominent bilateral dressing apraxia without severe constructional apraxia together with anosodiaphoria for dressing apraxia. The other patient had mild dressing apraxia with severe constructional apraxia and was aware of her disabilities. This dissociation implies that anosodiaphoria for dressing apraxia is an important factor in the severity of bilateral dressing apraxia. This also explains why automatic acts in dressing are more severely affected than when patients are asked to put clothing on in dressing examination.

Adult↗
PubMed1990

[A comparison of the influence of certain contextual factors on the symptoms of persons with acquired verbal apraxia and verbal developmental apraxia].

Data on the individual symptoms of patients with acquired apraxia of speech and developmental apraxia of speech is of theoretical significance in the study of this disorder. A comparison of individual symptoms may shed light on error patterns in apraxia of speech, the possibility of types of apraxia of speech and on 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; Van der Merwe, Uys, Loots, Grimbeek and Jansen, 1989) the symptoms of four patients with acquired apraxia of speech and one subject with developmental apraxia of speech were compared. The auditorily perceived symptoms and the deviations in voice onset time, vowel duration and utterance duration of all the subjects were compared. The results indicated that the frequency of occurrence of certain symptoms created individual error patterns but also that all subjects had the high occurrence of symptoms which reflect the nature of the disorder in common. The subject with developmental apraxia of speech had all symptoms in common with the other subjects but exhibited less deviancy in the temporal flow of speech and in the duration of the utterance. He presented with more sound substitutions than did the acquired group. The theoretical implications of the results are discussed.

Apraxias↗
PubMed1996

Modality specific naming and gesture disturbances: a case with optic aphasia, bilateral tactile aphasia, optic apraxia and tactile apraxia.

This study reports a patient who manifested optic aphasia, tactile aphasia, optic apraxia, and tactile apraxia following an operation for epidural left parietal haematoma. He could neither name nor pantomime the use of objects presented visually or tactually, but correctly performed semantic association tasks, thus demonstrating preserved recognition. He could name and pantomime the use of auditorily presented objects. Experimental results disproved that pantomime disorders were secondary to naming disorders, and suggested that modality specific aphasia and modality specific apraxia are independent clinical syndromes. CT scans showed injury to the posterior callosal radiations, the white matter of the angular gyrus, and the medial portion of the occipital lobe in the left hemisphere. We suggest that modality specific aphasia and modality specific apraxia can be explained by assuming a common semantic memory store.

Aphasia↗
PubMed2000

[Left unilateral melokinetic apraxia and left dynamic apraxia following partial callosal infarction].

A 69 year-old right-handed man suffered from an infarct in the left anterior cerebral territory's artery, involving the anterior and middle parts of the corpus callosum, and the cingulum. He had a right crural hemiparesis with a grasp reflex of the right hand, and ipsilaterally a melokinetic and a dynamic apraxia. Agility of the left fingers was lost: fast and nimble movements of theses fingers, and repetitive gestures of the left hand were defective. Execution of motor sequences with the left hand was disrupted by a lack of litheness in gesture series. By analogy with unilateral left ideomotor apraxia, we suggest melokinetic and dynamic apraxia could be symptomatic of an interhemispheric disconnection. Premotor cortex could have a dominance for both digital movements and programmation of gestual sequences. As a general rule, the left cortex could be preferentially activated by the nature of some tasks, particularly the execution of complex gestual series, which implie an internal speech. In theses conditions, an interhemispheric disconnection could lead some difficulties to make theses gestures with the left hand.

Aged↗
PubMed1993

Ideomotor apraxia without aphasia and aphasia without apraxia: the anatomical support for a double dissociation.

This study aimed to verify the existence of a double aphasia/apraxia dissociation. Apraxic patients without aphasia and aphasic patients without apraxia were included in a consecutive series of patients with cortical or subcortical CT documented vascular lesions in the left hemisphere. Of 699 patients, 10 were found to be apraxic but not aphasic and 149 aphasic but not apraxic. These findings indicate an aphasia/apraxia double dissociation. This suggests that praxis and language make use of two different, partly overlapping networks.

Aged↗
PubMed1992

[A case of apraxia and global aphasia without apraxia for axial body movement].

The case of a right handed 58 year old woman is presented who suffered an ischemic stroke after angiography following a vasospasm in the left internal carotid artery. The neuropsychological examination revealed global aphasia and severe apraxia for movements of the face and the extremities. However, the patient was able to carry out adequately axial movements to imitation and also to verbal command. These particular findings are discussed and explained within the context of the existing literature.

Aphasia↗
PubMed1996

The basal ganglia and apraxia.

Ever since Liepmann's original descriptions at the beginning of the century apraxia has usually been attributed to damage confined to the cerebral cortex and/or cortico-cortical connecting pathways. However, there have been suggestions that apraxia can be due to deep subcortical lesions, which raises the question as to whether damage to the basal ganglia or thalamus can cause apraxia. We therefore analysed 82 cases of such 'deep' apraxias reported in the literature. These reports consisted of a small number (n=9) of cases studied neuropathologically, and a much larger group (n=73) in which CT or MRI was used to identify the size and extent of the lesion. The reports were subdivided into (i) those with small isolated lesions which involved nuclei of the basal ganglia or thalamus only, and not extending to involve periventricular or peristriatal white matter; (ii) those with large lesions which involved two or more of the nuclei, or one or more of these deep structures plus damage to closely adjacent areas including the internal capsule, periventricular or peristriatal white matter; and (iii) lesions sparing basal ganglia and thalamus but involving adjacent white matter. The main conclusions to be drawn from this meta-analysis are that lesions confined to the basal ganglia (putamen, caudate nucleus and globus pallidus) rarely, if ever, cause apraxia. Lesions affecting the lenticular nucleus or putamen nearly always intruded into the adjacent lateral white matter to involve association fibres, in particular those of the superior longitudinal fasciculus and frontostriatal connections. Apraxia occurred with deep lesions of the basal ganglia apparently sparing white matter in only eight out of the 82 cases. Apraxia was most commonly seen when there were lesions in the lenticular nucleus or putamen (58 out of 72 cases) with additional involvement of capsular, and particularly of periventricular or peristriatal, white matter. Lesions of the globus pallidus (no cases) or caudate nucleus (three cases) rarely caused apraxia. The caudate lesions also had white matter involvement. Indeed, involvement of periventricular white matter alone caused apraxia. The vast majority of cases described with apraxia associated with deep lesions were in the left, dominant hemisphere. Ideomotor apraxia was described in most reports (72 out of 82 cases). Orofacial apraxia was less common (37 cases), usually with ideomotor apraxia. Ideational apraxia was rare (five cases), all with ideomotor apraxia. Apraxia was either bilateral or involved the left hand if there was a right hemiparesis, in those cases where descriptions were available. Lesions of the thalamus can sometimes cause apraxia (26 cases), even if there is no apparent involvement of white matter (12 cases). Small lesions confined to the thalamus can also sometimes cause apraxia (eight cases). The role of the thalamus in higher order motor control and apraxia remains to be determined. It is suggested that the term limb-kinetic apraxia should be retained to describe motor deficits in planning 'what to do', 'how to do it' and 'when to do it'; decisions which appear to involve activation of a complex distributed network of dorsolateral prefrontal cortex, supplementary motor areas, anterior cingulate regions and lateral premotor cortex. Such deficits need to be quantified. If they are present in patients with basal ganglia disease, over and above classical akinesia, bradykinesia and hypokinesia, then such patients could be said to exhibit limb-kinetic apraxia.

Apraxias↗
PubMed1994

The nature of apraxia in corticobasal degeneration.

Although apraxia is one of the most frequent signs in corticobasal degeneration, the phenomenology of this disorder has not been formally examined. Hence 10 patients with corticobasal degeneration were studied with a standardised evaluation for different types of apraxia. To minimise the confounding effects of the primary motor disorder, apraxia was assessed in the least affected limb. Whereas none of the patients showed buccofacial apraxia, seven showed deficits on tests of ideomotor apraxia and movement imitation, four on tests of sequential arm movements (all of whom had ideomotor apraxia), and three on tests of ideational apraxia (all of whom had ideomotor apraxia). Ideomotor apraxia significantly correlated with deficit in both the mini mental state examination and in a task sensitive to frontal lobe dysfunction (picture arrangement). Two of the three patients with ideomotor apraxia and ideational apraxia showed severe cognitive impairments. The alien limb behaviour was present only in patients with ideomotor apraxia. In conclusion, ideomotor apraxia is the most frequent type of apraxia in corticobasal degeneration, and may be due to dysfunction of the supplementary motor area. There is a subgroup of patients with corticobasal degeneration who have a severe apraxia (ideomotor and ideational apraxia), which correlates with global cognitive impairment, and may result from additional parietal or diffuse cortical damage.

Aged↗
PubMed2003

Upper and lower face and ideomotor apraxia in patients with Alzheimer's disease.

INTRODUCTION: Apraxia of face movement in Alzheimer's disease (AD) has been rarely investigated. This study aimed at investigating the frequency of lower (mouth, tongue and throat) and upper (eyes and eyebrows) face apraxia, in AD and its relationship with limb apraxia and severity of dementia. METHODS: Fifty seven patients with AD were tested with a new standardised test of face apraxia including upper and lower face movements, which uses an item-difficulty weighted scoring procedure, the IMA test, a test of ideomotor apraxia and the M.O.D.A., a means to assess dementia severity. RESULTS: Thirteen (23%) and 19 (33%) participants were below cut-off respectively on the upper and lower face apraxia test. Both sections of the Face Apraxia Test correlated significantly with the Ideomotor Apraxia Test. However, double dissociations between different types of apraxia were observed. Both the upper and lower face apraxia tests correlated significantly with the measure of dementia severity. CONCLUSIONS: The finding show that a proportion of AD patients fails face apraxia tests. Their face apraxia is interlinked with ideomotor limb apraxia, although dissociations are possible. Severity of dementia deterioration accounts for a good proportion of the variability of AD patients' performance on face apraxia tests.

Aged↗
PubMed1997

Apraxia in Parkinson's disease, progressive supranuclear palsy, multiple system atrophy and neuroleptic-induced parkinsonism.

We studied 45 non-demented patients with Parkinson's disease (PD), 12 with progressive supranuclear palsy (PSP), 10 with multiple system atrophy (MSA) and 12 with neuroleptic-induced parkinsonism (NIP) for the presence of apraxia. Our aim was to determine whether a standard comprehensive assessment of different praxic functions would demonstrate specific types of errors not attributable to bradykinesia, rigidity, tremor or any other abnormal elementary motor deficit. PD patients on chronic levodopa treatment were examined in the 'on' and 'off' (treatment) states. Based on apraxia assessment scores, bilateral ideomotor apraxia for transitive movements was found in eight (75%) and 12 (27%) of PSP and PD patients, respectively. Ideomotor apraxia was mainly characterized by spatial errors (i.e., external and internal configuration, body-part-as-object and trajectory). Four PSP but no PD patients exhibited ideomotor apraxia for intransitive movements. PSP as well as PD patients with ideomotor apraxia also had difficulties in imitating hand and finger postures, but none of them failed on pantomime comprehension and pantomime recognition/discrimination. Some PSP patients exhibited, in addition, a limbkinetic type of apraxia and a minority of them displayed deficits on tasks involving multiple steps. Neither MSA nor NIP patients showed any disturbance of praxic functions. There were no differences in age, disease duration, Mini Mental State Examination (MMSE), Unified Parkinson's disease Rating Scale and Hoehn-Yahr scores between apraxic and non-apraxic PD patients, and ideomotor apraxia scores were similar in the 'on' and 'off' states. A correlation was found between ideomotor apraxia scores in PD patients and deficits in frontal lobe-related neuropsychological tasks such as the Tower of Hanoi, verbal fluency and the Trail Making Test. Furthermore, PD patients with apraxia showed higher Hamilton depression scores than non-apraxic PD patients. In PSP patients, ideomotor apraxia scores correlated significantly with cognitive deficit as measured with MMSE. The presence or absence of cortical involvement, and its severity and distribution might determine the presence and type of apraxia in PD and PSP. Apraxia in these conditions would therefore reflect combined cortico-striatal dysfunction.

Adult↗