Neuropathophysiology of movement disorders in cerebral palsy.
Recent developments in understanding the pathophysiology of disordered motor control in cerebral palsy are reviewed. In spastic cerebral palsy, evidence for abnormal segmental as well as supraspinal control of motor neuron output exists. Impaired Ia inhibition of antagonist muscles has been suggested but recently contested. Evidence also supports the role of decreased presynaptic inhibition of Ia afferents and decreased nonreciprocal Ib inhibition. Furthermore, early cerebral injury results in reorganization of supraspinal (corticospinal) inputs to motor neuron pools. In extrapyramidal cerebral palsy, injury of basal ganglia or thalamus has been demonstrated. A scheme for understanding the neurochemical circuitry of the extrapyramidal system is discussed. Animal models and certain specific human diseases provide examples of how this circuitry may be disturbed, thereby resulting in an imbalance between the direct and indirect striatal output systems and in impaired motor control. Future studies employing postmortem neurochemical analysis, functional magnetic resonance imaging, and positron emission tomographic scanning may foster progress in this area.
Filloux
F M
FM
Department of Neurology, University of Utah School of Medicine, Salt Lake City, USA.
D000818:Animals; D000831:Animals, Newborn; D001479:Basal Ganglia / Q000033:anatomy & histology / Q000502:physiology; D002545:Brain Ischemia / Q000503:physiopathology; D002547:Cerebral Palsy / Q000503:physiopathology*; D005116:Extrapyramidal Tracts / Q000503:physiopathology; D006429:Hemiplegia / Q000151:congenital; D006801:Humans; D002534:Hypoxia, Brain / Q000503:physiopathology; D009069:Movement Disorders / Q000503:physiopathology*; D009128:Muscle Spasticity / Q000503:physiopathology; D051381:Rats