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Perhaps the most intriguing disorders of body representation are those that are not due to primary disease of brain tissue. Strange and sometimes painful phantom limb sensations can result from loss of afference to the brain; and Complex Regional Pain Syndrome (CRPS)—the subject of the current report—can follow limb trauma without pathology of either the central or peripheral nervous system. This enigmatic and vexing condition follows relatively minor trauma, and can result in enduring misery and a useless limb. It manifests as severe pain, autonomic dysfunction, motor disability and ‘neglect-like’ symptoms with distorted body representation. For this special issue on body representation we describe the case of a patient suffering from CRPS, including symptoms suggesting a distorted representation of the affected limb. We report contrasting effects of mirror box therapy, as well as a new treatment—prism adaptation therapy—that provided sustained pain relief and reduced disability. The benefits were contingent upon adapting with the affected limb. Other novel observations suggest that: (1) pain may be a consequence, not the cause, of a disturbance of body representation that gives rise to the syndrome; (2) immobilisation, not pain, may precipitate this reorganisation of somatomotor circuits in susceptible individuals; and (3) limitation of voluntary movement is neither due to pain nor to weakness but, rather, to derangement of body representation which renders certain postures from the repertoire of hand movements inaccessible. [ABSTRACT FROM AUTHOR]

The reduction in saccade latency when the fixation point is removed (fixation offset effect–FOE) reflects the degree to which fixation neurons are under influence by a stimulus at fixation. Strategic manipulations of oculomotor readiness that bring these neurons under endogenous control reduce the magnitude of the FOE. Using an aging foreperiod paradigm, and the FOE as a marker for cortical control of reflexive fixation, we showed that, for both prosaccades and antisaccades, increasing preparation across the foreperiod reduced both saccade latency and the FOE. Consistent with Los’s trace conditioning account, these effects reflected greater preparation for trials when the current short foreperiod was preceded by a trial with a short foreperiod. The FOE was also smaller for antisaccades than for prosaccades demonstrating strategic modulation. However, the effects of trace conditioning were comparable in the two tasks, demonstrating that strategic and unconscious priming effects both independently modulate the control of ocular fixation. [ABSTRACT FROM AUTHOR]

Fourteen patients with a chronic, unilateral lesion restricted to the frontal lobe (twelve involving the frontal eye field (FEF)), nine patients with a chronic, unilateral lesion restricted to posterior association cortex (eight involving the intraparietal sulcus (IPS)), and twelve neurologically normal control subjects were studied in an anti-saccade task. A combination of manipulating cuing and fixation offset enabled us to examine the effects of chronic oculomotor lesions on both saccade preparation and voluntary control over ocular fixation. Patients with lesions of the FEF made more errors (reflexive glances) toward contralesional targets, whereas patients with IPS lesions made fewer errors toward contralesional targets. Patients with IPS lesions had increased latencies to initiate saccades away from contralesional targets. For FEF patients, the presence of a fixation point inhibited the initiation of contralesionally directed saccades less than those directed ipsilesionally. Saccade preparation in response to a cue did not reduce the inhibitory effect of a fixation point on initiating anti-saccades directed either ipsilesionally or contralesionally for either patient group. We conclude that chronic IPS lesions result in a reduced contralesional visual grasp reflex (VGR) and delayed utilization of visual signals in the contralesional field for planning voluntary eye movements. In contrast, patients with chronic FEF lesions are impaired in inhibiting the VGR toward contralesional signals, and manifest an asymmetry in the balance between fixation and saccade activity. Moreover, voluntary control of fixation is compromised after chronic damage to either frontal or parietal oculomotor cortex. [ABSTRACT FROM AUTHOR]