This article reviews the evidence for cortical involvement in shaping postural responses evoked by external postural perturbations. Although responses to postural perturbations occur more quickly than the fastest voluntary movements, they have longer latencies than spinal stretch reflexes, suggesting greater potential for modification by the cortex. Postural responses include short, medium and long latency components of muscle activation with increasing involvement of the cerebral cortex as latencies increase. Evidence suggests that the cortex is also involved in changing postural responses with alterations in cognitive state, initial sensory-motor conditions, prior experience, and prior warning of a perturbation, all representing changes in "central set." Studies suggest that the cerebellar-cortical loop is responsible for adapting postural responses based on prior experience and the basal ganglia-cortical loop is responsible for pre-selecting and optimizing postural responses based on current context. Thus, the cerebral cortex likely influences longer latency postural responses both directly via corticospinal loops and shorter latency postural responses indirectly via communication with the brainstem centers that harbor the synergies for postural responses, thereby providing both speed and flexibility for pre-selecting and modifying environmentally appropriate responses to a loss of balance.

The present study explored differences in dendritic/spine extent across several human cortical regions. Specifically, the basilar dendrites/spines of supragranular pyramidal cells were examined in eight Brodmann's areas (BA) arranged according to Benson's (1993, Behav Neurol 6:75-81) functional hierarchy: primary cortex (somatosensory, BA3-1-2; motor, BA4), unimodal cortex (Wernicke's area, BA22; Broca's area, BA44), heteromodal cortex (supple- mentary motor area, BA6beta; angular gyrus, BA39) and supramodal cortex (superior frontopolar zone, BA10; inferior frontopolar zone, BA11). To capture more general aspects of regional variability, primary and unimodal areas were designated as low integrative regions; heteromodal and supramodal areas were designated as high integrative regions. Tissue was obtained from the left hemisphere of 10 neurologically normal individuals (M(age) = 30 +/- 17 years; five males, five females) and stained with a modified rapid Golgi technique. Ten neurons were sampled from each cortical region (n = 800) and evaluated according to total dendritic length, mean segment length, dendritic segment count, dendritic spine number and dendritic spine density. Despite considerable inter-individual variation, there were significant differences across the eight Brodmann's areas and between the high and low integrative regions for all dendritic and spine measures. Dendritic systems in primary and unimodal regions were consistently less complex than in heteromodal and supramodal areas. The range within these rankings was substantial, with total dendritic length in BA10 being 31% greater than that in BA3-1-2, and dendritic spine number being 69% greater. These findings demonstrate that cortical regions involved in the early stages of processing (e.g. primary sensory areas) generally exhibit less complex dendritic/spine systems than those regions involved in the later stages of information processing (e.g. prefrontal cortex). This dendritic progression appears to reflect significant differences in the nature of cortical processing, with spine-dense neurons at hierarchically higher association levels integrating a broader range of synaptic input than those at lower cortical levels.

Freezing of gait (FoG) is an episodic, brief inability to step that delays gait initiation or interrupts ongoing gait. FoG is often associated with an alternating shaking of the knees, clinically referred to as knee trembling or trembling in place. The pathophysiology of FoG and of the concomitant trembling knees is unknown; impaired postural adjustment in preparation for stepping is one hypothesis. We examined anticipatory postural adjustments (APAs) prior to protective steps induced by a forward loss of balance in 10 Parkinson’s disease (PD) subjects with marked FoG and in 10 control subjects. The amplitude and timing of the APAs were determined from changes in the vertical ground-reaction forces recorded by a force plate under each foot and were confirmed by electromyographic recordings of bilateral medial gastrocnemius, tibialis anterior and tensor fascia latae muscles. Protective steps were accomplished with a single APA followed by a step for control subjects, whereas PD subjects frequently exhibited multiple, alternating APAs coexistent with the knee trembling commonly observed during FoG as well as delayed, inadequate or no stepping. These multiple APAs were not delayed in onset and were of similar or larger amplitude than the single APAs exhibited by the control subjects. These observations suggest that multiple APAs produce the knee trembling commonly associated with FoG and that FoG associated with a forward loss of balance is caused by an inability to couple a normal APA to the stepping motor pattern.

The supplementary motor area is thought to contribute to the generation of anticipatory postural adjustments (which act to stabilize supporting body segments prior to movement), but its precise role remains unclear. In addition, participants with Parkinson’s disease (PD) exhibit impaired function of the supplementary motor area as well as decreased amplitudes and altered timing of the anticipatory postural adjustment during step initiation, but the contribution of the supplementary motor area to these impairments also remains unclear. To determine how the supplementary motor area contributes to generating the anticipatory postural adjustment and to the impaired anticipatory postural adjustments of participants with PD, we examined the voluntary steps of 8 participants with PD and 8 participants without PD, before and after disrupting the supplementary motor area and dorsolateral premotor cortex, in separate sessions, with 1-Hz repetitive transcranial magnetic stimulation. Both groups exhibited decreased durations of their anticipatory postural adjustments after repetitive transcranial magnetic stimulation over the supplementary motor area but not over the dorsolateral premotor cortex. Peak amplitudes of the anticipatory postural adjustments were unaffected by repetitive transcranial magnetic stimulation to either site. The symptom severity of the participants with PD positively correlated with the extent that repetitive transcranial magnetic stimulation over the supplementary motor area affected the durations of their anticipatory postural adjustments. The results suggest that the supplementary motor area contributes to the timing of the anticipatory postural adjustment and that participants with PD exhibit impaired timing of their anticipatory postural adjustments, in part, due to progressive dysfunction of circuits associated with the supplementary motor area.

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