Physiology of neglect syndrome

Hat tip to Kim Meador, AAN notes from 2000 course on physiology of cognition

Contralesional visual P3 event related potential is consistently abnormal among patients with visual neglect (increased latency and decreased amplitude). (L'Hermitte et al. Arch Neurol 1985 42:567-573). Monkeys with lesion induced neglect have normal early but abnormal late components on the SEP (N2 and P3) (Watson RT et al. Neurology 1986; 36:636-640 and Watson RT et al. Arch Neurol 1977; 34: 224-227).

In humans, SEP reliably differentiates those with extinction/tactile neglect/tactile joint sense. (Maugiere et al. Paris Rev Neurol 1987; 143:643-656). VEP's are normal is visual neglect patients who have no conscious knowledge of visual stimulation (Vallar et al. Neurology 1991; 41: 1918-1921). A delay does occur in steady state visual VEP's in contralesional field of neglect patients, especially at high but not low frequencies (Spinelli et al. Neuroreport, 1996) and consistent with loss of contrast sensitivity in neglected field (Angellini et al. 1998 COrtex) and worse in left lower field implying vertical as well as horizontal neglect. VEP and blood flow both improve with direction of head/gaze to right (Nadeau et al. JNNP 1997).

PET scan studies of tactile extinction were performed (Remy et al Neurology 1999). Left hand stimuli activated SII regions, but not right SM1 region. Bilateral stimuli showed suppression of right SM! but also both SII regions. Compensation is inhibited by overstimulation of both sides.

In healthy humans, PET shows selective activation of right prefrontal and parietal cortex irrespective of side stimulated on somatosensory and visual vigilance tasks.

Amphetamines decrease habituation in the midbrain, to already detected stimuli thereby increasing vigilance (Cite).