Gait and dementia: moving beyond the notion of gait apraxia. Export

@article{citeulike:2163334, abstract = {Highest level gait disorders are produced by pathology in one or more structures in the cortical-basal ganglia-thalamocortical loop, which plays an important role in producing movements and postural synergies that meet personal desires and environmental constraints. Virtually all patients with dementia have pathology in one or more components of this loop, so highest level gait disorders are common in patients with dementia. The terminology surrounding these gait disorders is unnecessarily complex and too heavily influenced by the controversial concept of gait apraxia. Straightforward descriptive diagnostic criteria are needed. To this end, four core clinical features of highest level gait disorders are proposed: 1) inappropriate (counterproductive) or bizarre limb movement, postural synergies, and interaction with the environment, 2) qualitatively variable performance, influenced greatly by the environment and emotion, 3) hesitation and freezing, and 4) absent or inappropriate (counterproductive) rescue reactions. These core features follow logically from the physiology of the cortical-basal ganglia-thalamocortical loop and should be regarded as signs of pathology in this loop. A clinical rating scale based on these features should be developed to facilitate clinical diagnosis and clinicopathological correlation, while avoiding the ambiguities and controversies of gait apraxia.}, address = {Department of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.}, author = {Elble, R. J.}, citeulike-article-id = {2163334}, citeulike-linkout-0 = {http://dx.doi.org/10.1007/s00702-007-0743-3}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17510733}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17510733}, doi = {10.1007/s00702-007-0743-3}, issn = {0300-9564}, journal = {J Neural Transm}, keywords = {fog, gait, parkinsonism}, month = {October}, number = {10}, pages = {1253--1258}, posted-at = {2007-12-24 09:01:56}, priority = {2}, title = {Gait and dementia: moving beyond the notion of gait apraxia.}, url = {http://dx.doi.org/10.1007/s00702-007-0743-3}, volume = {114}, year = {2007} }

TY - JOUR ID - citeulike:2163334 L3 - citeulike-article-id:2163334 N2 - Highest level gait disorders are produced by pathology in one or more structures in the cortical-basal ganglia-thalamocortical loop, which plays an important role in producing movements and postural synergies that meet personal desires and environmental constraints. Virtually all patients with dementia have pathology in one or more components of this loop, so highest level gait disorders are common in patients with dementia. The terminology surrounding these gait disorders is unnecessarily complex and too heavily influenced by the controversial concept of gait apraxia. Straightforward descriptive diagnostic criteria are needed. To this end, four core clinical features of highest level gait disorders are proposed: 1) inappropriate (counterproductive) or bizarre limb movement, postural synergies, and interaction with the environment, 2) qualitatively variable performance, influenced greatly by the environment and emotion, 3) hesitation and freezing, and 4) absent or inappropriate (counterproductive) rescue reactions. These core features follow logically from the physiology of the cortical-basal ganglia-thalamocortical loop and should be regarded as signs of pathology in this loop. A clinical rating scale based on these features should be developed to facilitate clinical diagnosis and clinicopathological correlation, while avoiding the ambiguities and controversies of gait apraxia. IS - 10 JF - J Neural Transm SN - 0300-9564 AD - Department of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA. EP - 1258 TI - Gait and dementia: moving beyond the notion of gait apraxia. VL - 114 SP - 1253 KW - fog KW - gait KW - parkinsonism AU - Elble, RJ PY - 2007/10// UR - http://dx.doi.org/10.1007/s00702-007-0743-3 ER -