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Gait apraxia after bilateral supplementary motor area lesion
  1. S Della Sala1,
  2. A Francescani2,
  3. H Spinnler2
  1. 1Neuropsychology Research Group, Department of Psychology, University of Aberdeen, UK
  2. 2Third Neurology Ward, Department of Medicine, Surgery, and Dentistry, University of Milan, S Paolo Hospital, Milan, Italy
  1. Correspondence to:
 Professor S Della Sala, Department of Psychology, University of Aberdeen, AB24 2 UB Aberdeen, UK;


Objectives: The study aimed at addressing the issue of the precise nature of gait apraxia and the cerebral dysfunction responsible for it.

Methods: The case of a patient, affected by a bilateral infarction limited to a portion of the anterior cerebral artery territory is reported. The patient's ability to walk was formally assessed by means of a new standardised test.

Results: Due to an anomaly within the anterior cerebral artery system, the patient's lesion was centred on the supplementary motor regions of both hemispheres. He presented with clear signs of gait apraxia that could not be accounted for by paresis or other neurological deficits. No signs of any other form of apraxia were detected.

Conclusions: The clinical profile of the patient and the analysis of 49 cases from previous literature suggest that gait apraxia should be considered a clinical entity in its own right and lesions to the supplementary motor areas are responsible for it.

  • anterior cerebral artery
  • frontal lobes
  • trunk
  • gait apraxia
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  • * The syndrome of GA has been named differently by different authors—for example, “Torso apraxie” (trunk apraxia1) or “déséquilibration frontale” (frontal imbalance2). Some of the other labels conformed to the core deficit found—for example, “trepidante abasie”,3,4 “eingentümliche Ungeschicklichkeit” (remarkable clumsiness5), “bewegungstechnische Schwierigkeit” (loss of the technical requirements of the movements6), “Tapsigkeit” (gawky movements7), “Unbeholfenheit” (awkwardness8), slipping clutch syndrome,9 lower half parkinsonism,10,11 gait ignition failure.12 Some other labels referred to the authors' interpretation of GA—for example, melokinetic apraxia,13 “frontale ataxie” (frontal ataxia14), “gliedkinetische apraxie” (limb-kinetic apraxia, quoted by Westphal,15 “motorische Apraxie”,16 “corticale apraxie”,17 “innervatorische Apraxie” (innervatory apraxia6), “bilaterale motorische Apraxie”,18,19 frontal gait disorder,20 higher level gait disorder.21 However, these different terms, often derived from different conceptualisations of gait disorders, define syndromes that overlap more than is usually admitted.

  • Bruns14 quoted the work of earlier authors who noted the presence of stance and gait disorders in patients with frontal tumours. Among them, he (p 138) cited Wernicke35 who reckoned that a “hesitant gait has been often seen in patients with frontal tumours, it is well possible that in the future this sign will be considered as resulting from a direct insult to the frontal lobes” (p 323). Oppenheim36 described gait disturbances in nine of 11 patients with frontal tumours compared with only four of 10 patients with tumours elsewhere in the brain. Bernhardt (quoted by Bruns14 p 138) reported gait disturbances in 18 of 44 patients (40%) with frontal tumours but only in five of 41 (5%) patients with extrafrontal tumours. This testifies that the link between gait disturbances and frontal lesions predates the later discussion between its apraxic or ataxic nature.

  • The six patients with gait ignition failure reported by Atchison et al12 are not listed in table 3 because the authors explicitly maintain that the symptom they describe should be differentiated from GA. However, the authors acknowledged that gait ignition failure is due to frontal damage. We see no reasons to keep it separate from other manifestations of GA.

  • ** ”Sicherlich spielt auch fuer sie das Stirnhirn eine wesentliche Rolle, ob das linke vorwiegend und in welchen besonderen Anteilen, läβt sich noch nicht näher feststellen”.27

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