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Handbook of Clinical Neurology 2008
Topics: Apraxias; Brain; Functional Laterality; Gestures; History, 19th Century; History, 20th Century; Humans
PubMed: 18631699
DOI: 10.1016/S0072-9752(07)88016-X -
Revue Neurologique Feb 2003
Review
Topics: Apraxia, Ideomotor; Apraxias; Diagnosis, Differential; Humans; Neurologic Examination
PubMed: 12660580
DOI: No ID Found -
Cortex; a Journal Devoted To the Study... Aug 2017
Topics: Apraxias; Humans; Psychomotor Performance
PubMed: 28410626
DOI: 10.1016/j.cortex.2017.03.010 -
Topics in Stroke Rehabilitation 2008Apraxia of speech (AOS) is an acquired adult neurogenic communication disorder that often occurs following stroke. The purpose of this article is to review current... (Review)
Review
Apraxia of speech (AOS) is an acquired adult neurogenic communication disorder that often occurs following stroke. The purpose of this article is to review current research studies addressing the diagnostic and therapeutic management of AOS. Traditional definitions and characteristics are compared with current features that assist in the differential diagnosis of AOS. Prognostic indicators are reviewed in addition to how neuroplasticity may impact treatment in chronic AOS. Treatment techniques discussed include the articulatory kinematic approach (AKA), use of augmentative/alternative communication devices, intersystemic facilitation/reorganization, and constraint-induced therapy. Finally, the need to address functional communication through support groups, outside the therapeutic environment, is discussed.
Topics: Apraxias; Communication Disorders; Diagnosis, Differential; Humans; Neuronal Plasticity; Stroke; Stroke Rehabilitation
PubMed: 19008207
DOI: 10.1310/tsr1505-484 -
Seminars in Speech and Language Feb 2018Apraxia of speech (AOS) is a motor speech disorder that disrupts the planning and programming of speech motor movements. In the acute stage of stroke recovery, AOS... (Review)
Review
Apraxia of speech (AOS) is a motor speech disorder that disrupts the planning and programming of speech motor movements. In the acute stage of stroke recovery, AOS following unilateral (typically) left hemisphere stroke can occur alongside dysarthria, an impairment in speech execution and control, and/or aphasia, a higher-level impairment in language function. At this time, perceptual evaluation (the systematic, although subjective, description of speech and voice characteristics) is perhaps the only "gold standard" for differential diagnosis when it comes to motor speech disorders. This poses a challenge for speech-language pathologists charged with the evaluation of poststroke communication abilities, as distinguishing production impairments associated with AOS from those that can occur in aphasia and/or dysarthria can be difficult, especially when more than one deficit is present. Given the need for more objective, reliable methods to identify and diagnose AOS, several studies have turned to acoustic evaluation and neuroimaging to supplement clinical assessment. This article focuses on these recent advances. Studies investigating acoustic evaluation of AOS will be reviewed, as well as those that have considered the extent that neuroimaging can guide clinical decision making. Developments in the treatment of AOS will also be discussed. Although more research is needed regarding the use of these methods in everyday clinical practice, the studies reviewed here show promise as emerging tools for the management of AOS.
Topics: Apraxias; Diagnosis, Differential; Humans; Neuroimaging; Speech; Speech Acoustics; Speech Disorders; Speech Production Measurement; Stroke
PubMed: 29359303
DOI: 10.1055/s-0037-1608853 -
Neuropsychological Rehabilitation 2012Apraxia is a higher level motor deficit that occurs when processing a goal-directed action. The apraxic deficit can manifest itself in absence of sensory input deficits... (Review)
Review
Apraxia is a higher level motor deficit that occurs when processing a goal-directed action. The apraxic deficit can manifest itself in absence of sensory input deficits or motor output deficits, neglect, frontal inertia or dementia. According to a clinical classification still largely in use, there are two main forms of limb apraxia: ideomotor (IMA) and ideational (IA), observed when a patient is required to imitate a gesture or use an object, respectively. In the present review, we examined only the cognitive treatments of both types of limb apraxia of a vascular aetiology. Despite the high prevalence of limb apraxia caused by left brain damage, and the fact that apraxia has been known for over a century, the literature regarding its rehabilitation is still very limited. This is partly due to the nature of the recovery from the deficit, and in part to the automatic-voluntary dissociation. Here we review those treatments that have proved most successful in helping patients to recover from limb apraxia.
Topics: Apraxias; Cognitive Behavioral Therapy; Humans; Stroke; Stroke Rehabilitation; Treatment Outcome
PubMed: 22324430
DOI: 10.1080/09602011.2012.658317 -
Brain : a Journal of Neurology Feb 1996Ever 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... (Review)
Review
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.
Topics: Apraxias; Basal Ganglia; Humans; Magnetic Resonance Imaging; Neurology; Tomography, X-Ray Computed
PubMed: 8624692
DOI: 10.1093/brain/119.1.319 -
Brain Research. Cognitive Brain Research Mar 1996Ideomotor apraxia is a symptom of left hemisphere damage. Patients with ideomotor apraxia commit errors when imitating movements with their left, non-paralyzed hand.... (Review)
Review
Ideomotor apraxia is a symptom of left hemisphere damage. Patients with ideomotor apraxia commit errors when imitating movements with their left, non-paralyzed hand. This has been taken as evidence for a motor dominance of the left hemisphere. It has been hypothesized that the left hemisphere is dominant for internal preprogramming of skilled movements of either hand. We investigated the kinematics of movement trajectories of imitation of meaningless gestures. Group analysis confirmed that hesitant, feedback-controlled movement prevail in patients with apraxia, but analysis of single cases revealed the existence of kinematically normal movements leading to apractic errors. Enhanced reliance on feedback-control appears to be a compensatory strategy rather than the source of apractic errors. In a second study we explored the alternative hypothesis that patients with apraxia lack a general concept of the human body which is necessary to mediate the translation of a target position seen on the model into a target position on the patient's body. Imitation of movements was examined on oneself and on a mannikin. Patients with apraxia who made errors when imitating on themselves committed errors also when imitating on the mannikin. Taken together, both studies support the view that the source of errors in the imitation of gestures is to be sought at a conceptual level. This casts doubts on the alleged dominance of the left hemisphere for motor control.
Topics: Apraxias; Dominance, Cerebral; Humans; Manikins; Movement
PubMed: 8713550
DOI: 10.1016/0926-6410(95)00034-8 -
Brain : a Journal of Neurology Jun 1983A 43-year-old woman suffered a spontaneous corpus callosum disconnection, resulting in apraxia and apraxic agraphia confined to the left hand. She initially had a...
A 43-year-old woman suffered a spontaneous corpus callosum disconnection, resulting in apraxia and apraxic agraphia confined to the left hand. She initially had a functionally total callosal disconnection. With time, the splenium of the corpus callosum became functional, and a computerized tomographic scan performed five months after the onset showed infarction of only the body of the corpus callosum. Concomitant with this improvement in callosal function, the apraxia changed from ideational (loss of the concept of skilled movements) to classic ideomotor apraxia. A temporal analysis of this case provided support for Liepmann's (Liepmann, 1900; Liepmann and Maas, 1970) hypothesis that there is a centre for visuokinaesthetic (space-time) engrams in the left hemisphere of right-handed patients that controls skilled motor acts in either hand. This patient's recovery also allowed us a better understanding of the mechanisms underlying various types of apraxia.
Topics: Adult; Agraphia; Apraxias; Cerebral Infarction; Corpus Callosum; Female; Humans; Radiography
PubMed: 6850274
DOI: 10.1093/brain/106.2.391 -
Journal of Neurology Jul 2012Upper limb apraxia, a disorder of higher motor cognition, is a common consequence of left-hemispheric stroke. Contrary to common assumption, apraxic deficits not only... (Review)
Review
Upper limb apraxia, a disorder of higher motor cognition, is a common consequence of left-hemispheric stroke. Contrary to common assumption, apraxic deficits not only manifest themselves during clinical testing but also have delirious effects on the patients' everyday life and rehabilitation. Thus, a reliable diagnosis and efficient treatment of upper limb apraxia is important to improve the patients' prognosis after stroke. Nevertheless, to date, upper limb apraxia is still an underdiagnosed and ill-treated entity. Based on a systematic literature search, this review summarizes the current tools of diagnosis and treatment strategies for upper limb apraxia. It furthermore provides clinicians with graded recommendations. In particular, a short screening test for apraxia, and a more comprehensive diagnostic apraxia test for clinical use are recommended. Although currently only a few randomized controlled studies investigate the efficacy of different apraxia treatments, the gesture training suggested by Smania and colleagues can be recommended for the therapy of apraxia, the effects of which were shown to extend to activities of daily living and to persist for at least 2 months after completion of the training. This review aims at directing the reader's attention to the ecological relevance of apraxia. Moreover, it provides clinicians with appropriate tools for the reliable diagnosis and effective treatment of apraxia. Nevertheless, this review also highlights the need for further research into how to improve diagnosis of apraxia based on neuropsychological models and to develop new therapeutic strategies.
Topics: Apraxias; Cognition Disorders; Disability Evaluation; Gestures; Humans; Neuropsychological Tests; Upper Extremity
PubMed: 22215235
DOI: 10.1007/s00415-011-6336-y