Hostname: page-component-8448b6f56d-jr42d Total loading time: 0 Render date: 2024-04-19T11:36:09.541Z Has data issue: false hasContentIssue false
  • English
  • Français

Gait Apraxia in Multiple Sclerosis

Published online by Cambridge University Press:  02 December 2014

Nuhad E. Abou Zeid ,
Brian G. Weinshenker  and
B. Mark Keegan
Nuhad E. Abou Zeid
Affiliation:
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA
Brian G. Weinshenker
Affiliation:
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA
B. Mark Keegan*
Affiliation:
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA
*
Neurology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, Minnesota, 55905, USA
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Gait apraxia is a gait disorder not attributable to motor, cerebellar, or sensory dysfunction. Gait impairment is common in Multiple Sclerosis (MS), but is mostly attributed to spasticity and ataxia. Impairment ratings scales are designed accordingly and do not separately evaluate apraxia.

Objective:

To describe 15 patients with gait apraxia resulting from MS as their major functional impairment.

Methods:

The Mayo Clinic database (1994-2007) was searched for the terms MS and gait apraxia. Inclusion criteria: Definite MS, significant gait apraxia. Exclusion criteria: alternative disorder causing apraxia, predominantly spastic/ataxic gait disorder.

Results:

9 (60%) of the patients were women, and 12 (80%) had a progressive MS course. Gait apraxia was evident at a median of 8 years (range 0-34) following MS onset. Median EDSS at recognition of gait apraxia was 6.5 (range 5-8). Cognitive dysfunction was present in 11 (73%) and neurogenic bladder dysfunction in 14 (93%). The commonest MRI findings were confluent periventricular T2 lesions, T1 hypointensity and generalized cerebral atrophy with symmetrical ex vacuo ventricular enlargement.

Conclusion:

Gait apraxia can cause significant functional impairment in MS patients, and may be underrecognized. The natural course of the neurological deficit in such patients is unknown, and may differ from that of MS patients with other ambulatory disabilities.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 36 , Issue 5 , September 2009 , pp. 562 - 565
Copyright
Copyright © The Canadian Journal of Neurological 2009

References

1.Zadikoff, C, Lang, AE.Apraxia in movement disorders. Brain. 2005;128:1480–97.CrossRefGoogle ScholarPubMed
2.Nadeau, SE.Gait apraxia: further clues to localization. Eur Neurol. 2007;58:142–5.Google Scholar
3.Liston, R, Mickelborough, J, Bene, J, Tallis, R.A new classification of higher level gait disorders in patients with cerebral multi-infarct states. Age Ageing. 2003;32:252–8.CrossRefGoogle ScholarPubMed
4.Elble, RJ.Gait and dementia: moving beyond the notion of gait apraxia. J Neural Transm. 2007;114:1253–8.CrossRefGoogle ScholarPubMed
5.Kurtzke, JF.Rating neurologic impairment in multiple sclerosis: an expanded disability status scale (EDSS). Neurology. 1983;33:1444–52.Google Scholar
6.Polman, CH, Reingold, SC, Edan, G, Filippi, M, Hartung, HP, Kappos, L, et al.Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald Criteria”. Ann Neurol. 2005;58:840–6.Google Scholar
7.Kokmen, E, Naessens, JM, Offord, KP.A short test of mental status: description and preliminary results. Mayo Clin Proc. 1987;62:281–8.CrossRefGoogle Scholar
8.Kokmen, E, Smith, GE, Petersen, RC, Tangalos, E, Ivnik, RC.The short test of mental status. Correlations with standardized psychometric testing. Arch Neurol. 1991;48:725–8.CrossRefGoogle ScholarPubMed
9.Yakovlev, PI.Paraplegia of Hydrocephalus. (A clinical Note and Interpretation). Am J Mental Defic. 1947;51:571–6.Google Scholar
10.Franklin, GM, Nelson, LM, Filley, CM, Heaton, RK.Cognitive loss in multiple sclerosis. Case reports and review of the literature. Arch Neurol. 1989;46:162–7.CrossRefGoogle ScholarPubMed
11.Rascol, O, Fabre, N, Brefel-Courbon, C, Montastruc, JL.The pharmacologic treatment of gait ignition failure. Adv Neurol. 2001;87:255–64.Google Scholar
12.Bradley, WG Jr., Whittemore, AR, Kortman, KE, Watanabe, AS, Homyak, M, Teresi, LM, et al.Marked cerebrospinal fluid void: indicator of successful shunt in patients with suspected normal-pressure hydrocephalus. Radiology. 1991;178:459–66.Google Scholar
13.Liston, R, Mickelborough, J, Harris, B, Hann, AW, Tallis, RC.Conventional physiotherapy and treadmill re-training for higher-level gait disorders in cerebrovascular disease. Age Ageing. 2000;29:311–18.Google Scholar
14.Rubino, FA.Gait disorders. Neurologist. 2002;8:254–62.Google Scholar