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Conclusion

Disorders of the basal ganglia share a distinctive pattern of cognitive deficits, predominantly in tests of frontal lobe function. A ‘frontostriatal’ pattern of cognitive impairment, consisting of a frontal lobe-like syndrome without primary amnesia or genuine cortical deficits such as apraxia, aphasia, or agnosia is the classical syndrome associated with basal ganglia diseases. Recent pathological investigations, however, have revealed widespread and moderate to severe cortical atrophy in PSP, CBD, and MSA. The greater cognitive decline of PSP patients in prefrontal-based cognitive functions is probably related to the prominent frontal deafferentiation associated with direct premotor and prefrontal involvement. Likewise, progressive and significant cortical involvement in prefrontal and posterior parietal areas explain the predominant dysexecutive and visuospatial deficits found in patients with MSA. Recent advances in immunohistochemistry and molecular genetics have helped to refine the nosological entity of FTDP-17. Mutations in the MAPT and PGRN genes determine the clinical and pathological heterogeneities previously described in patients with FTDP-17. Thus, the term FTD with parkinsonism seems more adequate than FTDP-17.

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