NEUROPSYCHIATRIC ASSESSMENT OF PATIENTS WITH HYPERKINETIC AND HYPOKINETIC MOVEMENT-DISORDERS

Citation
I. Litvan et al., NEUROPSYCHIATRIC ASSESSMENT OF PATIENTS WITH HYPERKINETIC AND HYPOKINETIC MOVEMENT-DISORDERS, Archives of neurology, 55(10), 1998, pp. 1313-1319
Citations number
57
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00039942
Volume
55
Issue
10
Year of publication
1998
Pages
1313 - 1319
Database
ISI
SICI code
0003-9942(1998)55:10<1313:NAOPWH>2.0.ZU;2-8
Abstract
Background: The role of the basal ganglia in neuropsychiatric behavior s is not well known. Anatomical, neurophysiological, and neurochemical evidence supports the notion of parallel direct and indirect basal ga nglia thalamocortical motor systems, the differential involvement of w hich accounts for the hypokinesia or hyperkinesia observed in basal ga nglia disorders. Objectives: To evaluate the neuropsychiatric manifest ations of patients with a hyperkinetic movement disorder, such as Hunt ington disease (HD), vs a hypokinetic disease, such as progressive sup ranuclear palsy (PSP). To verify if patients with HD show a greater fr equency of hyperactive behaviors leg, agitation, irritation, euphoria, or anxiety), while those with PSP exhibit hypoactive behaviors leg, a pathy). Patients and Methods: The Neuropsychiatric Inventory, a tool w ith established validity and reliability, was administered to 29 patie nts with HD (mean +/- SD age, 43.8 +/- 2 years) and 34 with PSP (mean +/- SD age, 66.6 +/- 1.2 years), matched for education, symptom durati on, and overall degree of dementia. Results: There was no difference b etween the groups in the total Neuropsychiatric inventory scores. Howe ver, there was a double dissociation in behaviors: patients with HD ex hibited significantly more agitation (45%), irritability (38%), and an xiety (34%), whereas patients with PSP exhibited more apathy (82%) (P< .01). Euphoria was present only in patients with HD. Conclusions: We f ound that patients with HD manifested predominantly hyperactive behavi ors, while those with PSP manifested hypoactive behaviors. Based on ou r findings and the anatomical lesions known to occur in these disorder s, we suggest that the hyperactive behaviors in HD are secondary to an excitatory subcortical output through the medial and orbitofrontal co rtical circuits, while in PSP the hypoactive behaviors are secondary t o hypostimulation.