Apraxia is widely used to describe one of the more disabling deficits following left strokes. The role of rehabilitation in treating apraxic stroke patients remains unclear. This systematic review was conducted to study the impacts of various rehabilitation interventions on the limb apraxia post-stroke. PubMed, SCOPUS, PEDro, CINAHL, MEDLINE, REHABDATA, and Web of Science were searched for the experimental studies that investigated the effects of the rehabilitation interventions on apraxia in patients with stroke. The methodological quality was rated using the Physiotherapy Evidence Database scale (PEDro). Six studies met our inclusion criteria in this systematic review. Four were randomized controlled trials, pilot ( = 1), and case study ( = 1). The scores on the PEDro scale ranged from two to eight, with a median of seven. The results showed some evidence for the effects of strategy training and gesture training interventions on the cognitive functions, motor activities, and activities of daily livings outcomes poststroke. The preliminary findings showed that the effects of the strategy training and the gesture training on apraxia in patients with stroke are promising. Further randomized controlled trials with long-term follow-ups are strongly needed.
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http://dx.doi.org/10.1080/23279095.2021.1900188 | DOI Listing |
J Neural Transm (Vienna)
January 2025
Section of Adult Neurology, Department of Internal Medicine, Chong Hua Hospital, Fuente, Cebu, Philippines.
Joubert Syndrome (JS) is a congenital cerebellar ataxia typically inherited in an autosomal recessive pattern, although rare X-linked inheritance can occur. It is characterized by hypotonia evolving into ataxia, global developmental delay, oculomotor apraxia, breathing dysregulation, and multiorgan involvement. To date, there are 40 causative genes implicated in JS, all of which encode proteins of the primary cilium.
View Article and Find Full Text PDFIntroduction: Apraxia of speech (AOS) is a motor speech disorder characterized by sound distortions, substitutions, deletions, and additions; slow speech rate; abnormal prosody; and/or segmentation between words and syllables. AOS can result from neurodegeneration, in which case it can be accompanied by the primary agrammatic aphasia (PAA), which when presenting together are called AOS+PAA. AOS can also be the sole manifestation of neurodegeneration, termed primary progressive AOS (PPAOS).
View Article and Find Full Text PDFCureus
December 2024
Department of Neurology, St. Joseph Medical Center, Stockton, USA.
Cerebellar mutism syndrome (also known as posterior fossa syndrome) has been mostly seen in pediatric patients after surgery for neoplastic disease and is characterized by mutism, with variable symptoms such as emotional lability, ataxia, apraxia, and hypotonia. While the mechanism is not precisely defined, it is thought to result from disconnections between the cortical and cerebellar brain networks. Presentation in adult patients is rare, with various etiologies including posterior fossa ischemia, hemorrhage, and tumors being most reported.
View Article and Find Full Text PDFNeurol Res Pract
January 2025
Department of Neurology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Str. 62, 50937, Cologne, Germany.
Background: Apraxia is a motor-cognitive disorder that primary sensorimotor deficits cannot solely explain. Previous research in stroke patients has focused on damage to the fronto-parietal praxis networks in the left hemisphere (LH) as the cause of apraxic deficits. In contrast, the potential role of the (left) primary motor cortex (M1) has largely been neglected.
View Article and Find Full Text PDFNeurobiol Dis
February 2025
Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany. Electronic address:
Corticobasal syndrome (CBS) is characterized not only by parkinsonism but also by higher-order cortical dysfunctions, such as apraxia. However, the electrophysiological mechanisms underlying these symptoms remain poorly understood. To explore the pathophysiology of CBS, we recorded magnetoencephalographic (MEG) data from 17 CBS patients and 20 age-matched controls during an observe-to-imitate task.
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