title: Brain imaging in patients with freezing of gait.
abstract: Freezing of gait (FOG) is a disabling gait disturbance with unknown cerebral pathophysiology. In this review, we discuss the functional brain imaging studies that address gait physiology and pathophysiology of FOG. Radiotracer metabolic studies show basal ganglia-cortical circuitry involvement in different aspects of gait control. FOG patients showed orbitofrontal and posterior parietal deficits and possibly predominant involvement of right-sided circuitry. We suggest that FOG results from neuronal circuitry dysfunction in right-sided parietal-lateral premotor circuits. These circuits incorporate sensory information into the control of gait. Furthermore, abnormal function of frontostriatal loops, which probably sheer cognitive and attentional activities is also a main factor in FOG. Gait-induced brain circuitry activation can not adequately be achieved when investigated subjects are in a supine rest position, as is the case in most present day imaging studies. Some radiotracer activation studies were performed after walking. Imagination of gait has been used in some radiotracer activation studies with positron emission tomography (PET) and in studies with functional magnetic resonance imaging (fMRI), showing cortical activation patterns involved in several aspects of gait control. For future investigation of FOG, it is suggested to design PET and fMRI studies which concentrate on activation of neuropsychological and sensory integration circuits.
authors.affiliation: Department of Neurology, University Medical Center Groningen (UMCG), University of Groningen, Groningen, The Netherlands. a.l.bartels@neuro.umcg.nl
authors.forename: Anna L
authors.initials: AL
authors.lastname: Bartels
authors.forename: Klaus L
authors.initials: KL
authors.lastname: Leenders
mesh_terms: D001921:Brain / Q000473:pathology*; D001931:Brain Mapping; D003952:Diagnostic Imaging / Q000379:methods*; D005684:Gait / Q000502:physiology*; D020233:Gait Disorders, Neurologic / Q000150:complications / Q000473:pathology*; D006801:Humans; D010300:Parkinson Disease / Q000150:complications / Q000473:pathology*