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Comparison of apraxia in corticobasal degeneration and progressive supranuclear palsy

*The contribution of the first two authors was equal and their names appear in the order determined by a coin toss.
From the Cognitive Neuropharmacology Unit (V. Pharr and Dr. Litvan), Defense & Veteran Head Injury Program, Henry M. Jackson Foundation, Rockville, MD; Psychology Department (Dr. Uttl), Oregon State University, Corvallis, OR; Department of Neurology (Dr. Stark), Hospital of the University of Pennsylvania, Philadelphia; Department of Psychology (Dr. Fantie), American University, Washington, DC; and the Cognitive Neuroscience Section (Dr. Grafman), National Institute of Neurological Disorders and Stroke, Bethesda, MD.

Address correspondence and reprint requests to Dr. Jordan Grafman, Cognitive Neuroscience Section, National Institute of Neurological Disorders and Stroke, NIH, Building 10, Room 5C205, MSC 1440, Bethesda, MD 20892-1440.

OBJECTIVE: To describe ideomotor apraxia in patients with corticobasal degeneration and those with progressive supranuclear palsy, two parkinsonian disorders that are often misdiagnosed due to the overlap in their clinical features, and to determine whether systematic apraxia testing is useful for differential diagnosis.

METHODS: Fourteen patients fulfilling National Institute of Neurological Disorders and Stroke–Society for Progressive Supranuclear Palsy clinical criteria for progressive supranuclear palsy, 13 patients fulfilling modified Lang criteria for corticobasal degeneration, and 12 normal healthy control subjects were given the Test of Oral and Limb Apraxia, which was scored according to the Florida Apraxia Battery for occurrence of various types of apraxic errors.

RESULTS: Both patients with progressive supranuclear palsy and corticobasal degeneration committed a greater number of apraxic errors than normal healthy control subjects on both transitive and intransitive tasks (p < 0.001 in both cases), but apraxia was much more severe in patients with corticobasal degeneration than progressive supranuclear palsy (p < 0.001). The index of apraxia severity, in combination with the assessment of the two key features of progressive supranuclear palsy (falls and vertical gaze palsy), correctly classified all patients.

CONCLUSIONS: Patients with corticobasal degeneration show more severe ideomotor apraxia than patients with progressive supranuclear palsy, and systematic assessment of ideomotor apraxia facilitates the differential diagnosis between patients with progressive supranuclear palsy and those with corticobasal degeneration.

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