Neuropsychiatric Assessment of Patients With Hyperkinetic and Hypokinetic Movement Disorders

Abstract

We found that patients with HD manifested predominantly hyperactive behaviors, while those with PSP manifested hypoactive behaviors. Based on our findings and the anatomical lesions known to occur in these disorders, we suggest that the hyperactive behaviors in HD are secondary to an excitatory subcortical output through the medial and orbitofrontal cortical circuits, while in PSP the hypoactive behaviors are secondary to hypostimulation.

Involvement of Sensorimotor, Limbic, and Associative Basal Ganglia Domains in L-3,4-Dihydroxyphenylalanine-Induced Dyskinesia

“…Nonetheless, a fundamental consequence of the present study is that we cannot continue analyzing LID by investigating only motor areas, thus rendering unreliable all studies that do not pay attention to the anatomofunctional organization of cortico-basal ganglia loops. Seeing LID as either "caused" by unwanted involvement of associative and limbic areas or simply as having the cognitive and limbic abnormal counterparts of LID ("consequence"), as is often reported in hyperkinetic disorders (Klawans, 1988;Litvan et al, 1998), might have different clinical consequences. For instance, if electrophysiological investigations support the causative hypothesis, modulating the activity of nonmotor regions would reduce severity of LID, thereby offering new drug targets for treatment of this debilitating condition.…”

Clinical Motor and Cognitive Neurobehavioral Relationships in the Basal Ganglia

“…Hypokinesia is a disinhibition or increase in spontaneous movement (tics, tremors). It is thought that hypokinesia and hyperkinesia may relate to hypoactive behavior and hyperactive behavior associated with subcortical hypo-stimulation or hyper-stimulation of medial and orbitofrontal cortical circuits [10]. It is important to review these connections further to understand the role of basal ganglia in control of cognitive function.…”

“…Five fronto-subcortical circuits unite regions of the frontal lobe (the supplementary motor area; frontal eye fields; dorsolateral, prefrontal, orbito-frontal and anterior cingulate cortices) with the striatum, globus pallidus and thalamus in functional systems that mediate volitional motor activity, saccadic eye movements, executive functions, social behavior and motivation [10,11].…”

“…The basal ganglia then sends inhibitory outflow by GABA fibers from the globus pallidus and putamen to specific thalamic nuclei. The thalamus has excitatory fibers that return to the cortex [10]. Abnormalities of direct and indirect pathways result in different pathological functions.…”

Huntington disease as a dual diagnosis disorder: Data from the national research roster for Huntington disease patients and families

“…Psychiatric manifestations occur more frequently in HD than other dementias and basal ganglia disorders, and often resemble schizophrenia, bipolar, and unipolar syndromes, obsessive-compulsive disorder, or their variants (Anderson et al, 2001;Folstein and Folstein, 1983;Mendez, 1994). HD causes progressive atrophy and neuronal loss in cortical-striatal circuits corresponding to a progressive triad of motor, cognitive, and psychiatric symptoms (Cummings, 1993;Halliday et al, 1998;Joel, 2001;Litvan et al, 1998;Paulsen et al, 2001;Thieben et al, 2002;Vonsattel et al, 1985)]. …”