Physiology and pathophysiology of basalganglia: Impact on motor system function
Authors: Weicker Helmut , Kinscherf Ralf , Diserens Karin , Deigner Hans‐Peter , Strüder Heiko 
Published: December 2005

Non‐pyramidal muscular initiation by/of basalganglia differs from pyramidal, central, and spinal motor system regulation, but their synergistic cooperation increases the efficiency of central muscular motor functions. Corticostriatal pathways of neurons from motor areas in cortex excite by glutamate striatal GABA(gamma‐aminobutyric acid)ergic neurons via their receptors, causing the release of the inhibitory neurotransmitter GABA. Over direct and indirect projections GABAergic impulses reach several nuclei of basalganglia, while GABAergic impact is modulated by dopamine (DA) through inhibitory or excitatory DA receptor subtypes. Adequate DA release from nigrostriatal pathways of DAergic neurons of substantia nigra is essential for well adjusted propagation to motor exits of basalganglia. From basalganglia exit projections are forwarded to motor nuclei of thalamus whose basal activity can be attenuated by inhibition or increased by disinhibition. Impulses are projected from thalamus to motor areas in cortex, in which information on the conducted circuit through basalganglia is returned to basalganglia by corticostriatal loops, adapting the following projections from basalganglia according to the need. Simultaneously, thalamic output is projected via supplementary motor area to primary cortex and, thus, may also affect centrifugal pyramidal output. In addition to basalganglic motor pathways via thalamus to motor cortex, there also exist projections from substantia nigra reticularis to several areas of motor nuclei in the brain stem, which influence spinal motor system function, especially that of the γ‐motoneuron regulating extention of muscle spindle. Understanding of the physiological function of basalganglia has been immensely enriched by clarification of the pathophysiology of Parkinson's disease (PD) and its therapy. PD is characterized by resting tremor, rigidity, bradykinesia or slowness, gait disturbance, and postural instability. Hypokinetic, rigid syndrome of PD is caused by striatal disinhibition after degeneration of DAergic neurons in the substantia nigra pars compacta, which are essential for the control of motor performance. The cardinal symptomatology of the above mentioned motor system impairments in PD is also affected by the changes in motor behavior, particularly in the case of implicit learning and memory dysfunctions in striatum. In addition to the implicit deficit, cerebral dementia increases with duration of PD. Thus, explicit learning and memory function declines. Especially in the case of increasing bradyphrenia, anticipation of prefrontal association cortex as well as its propagation via frontal‐striatal pathways to associative sensomotor and motor areas with connection to motor cortex area 4, where centrifugal pyramidal projections originate, are disturbed. This process promotes the reduction of motor anticipative behavior in cortex and impairs the continuation of proper motor movements as well as their automatization. During execution of movements additional impairment of fluctuation in centripetal as well as centrifugal impulses cannot be corrected volitionally or by reflex in PD. They generally intensify the decline of non‐pyramidal and pyramidal synergistic cooperation. With increasing cardinal symptoms in PD, consequent specific medicamentous or invasive treatments are required. The systematic addressing of motor behavior in special reeducation programs can positively influence motor system functions. Particularly tremor and rigor, which are pronounced in the case of implicit motor system dysfunction, can partly be improved by increased explicit learning and memory function, supported by explicit mental movement initiation. Special training of prefrontal associations and a consecutive increase of central‐motor behavior associations can also reduce cerebral automatization deficits. By this, even in long existing PD, non‐pyramidal motor impairments can be affected and striatal dysfunctions symptomatically improved. Each motor input and output level and their central representation has to be evaluated individually and be corrected in this learning state, so that the summation of mistakes in the final phase is kept as small as possible. Thus, special didactical learning strategies should be applied with frequent controls.