Disorders of Gait and Balance Classified
Abstracts & Commentary
Sources: Martin MP, O’Neill D. Vascular higher-level gait disorders—A step in the right direction? Commentary. Lancet. 2004;363:8; Liston R, et al. A new classification of higher-level gait disorders in patients with cerebral multi-infarct states. Age Ageing. 2003;32:252-258.
Martin and O’Neill called attention to and commented upon a revised classification of higher-level gait disorders (HLGD) proposed by Liston and associates.
In 1993, Nutt and associates classified gait disorders into lower, middle, and higher levels.1 The lower level comprises peripheral musculoskeletal and sensory disorders that can be compensated for by an intact central nervous system (CNS). Middle-level disorders include hemiplegic, paraplegic, and cerebellar ataxic, parkinsonian, choreic, and dystonic gaits in which the clinical neurological deficits are consistent with the gait disorder. In contrast, higher-level gait disorders are due to disturbances of CNS sensorimotor systems that cannot be accounted for by the neurological signs. Although HLGD can be due to frontal-lobe tumors and normalpressure hydrocephalus, the most common cause in the elderly is cerebrovascular disease.
Nutt et al subdivided HLGD into 5 categories: cautious gait, subcortical disequilibrium, frontal disequilibrium, isolated gait ignition failure, and frontal gait disorder. They based their categories on presumed anatomical location, on clinical phenomenology, or a mixture of both.
Liston et al have proposed a simplified classification of HLGD in the context of cerebrovascular disease. They subdivided HLGD into 3 categories: ignition apraxia, disequilibrium apraxia, and mixed picture (see Table). To validate their classification, they analyzed the clinical features of 13 patients with HLGD and radiologically proven cerebrovascular disease. Seven patients with infarcts in the basal ganglia (BG), thalamus, supplementary motor area (SMA) and/or periventricular white matter had ignition apraxia (gait ignition failure, shuffling, freezing). Six patients with infarcts in the parietal sensory cortex and frontal primary motor area (PMA) had equilibrium apraxia (poor balance and falls). Six elderly healthy relatives served as controls. The 3 groups were distinct with respect to step length, width of base and velocity of walking.
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Table Classification of HLGD in Patients With Cerebrovascular Disease |
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Commentary
The work of Liston et al builds upon the classification of Nutt et al and should prompt clinicians to read that excellent review of the neural control of gait and posture and its disorders. Neurologists, thus provided with an increased awareness and understanding of gait disorders, should be able to test the validity of the clinical subtypes of HLGD proposed by Liston et al in their own patients. At the present time, in the absence of effective medical or surgical treatment for HLGD due to cerebrovascular disease, even the best classification yields only a clinical distinction without a therapeutic difference. — John J. Caronna
Dr. Caronna, Vice-Chairman, Department of Neurology, Cornell University Medical Center; Professor of Clinical Neurology, New York Hospital, is Associate Editor of Neurology Alert.
Reference
1. Nutt JG, et al. Neurology. 1993;43:268-279.
Martin and ONeill called attention to and commented upon a revised classification of higher-level gait disorders (HLGD) proposed by Liston and associates.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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