The purpose of the study is to examine the relationship between the location of the initial onset of back pain as revealed by the subject's pain drawing and the site of maximum muscle tension at rest, while jaw-clenching and during a cold stressor, in men and women. Subjects were 30 males and 30 females divided into three groups of 10 males and 10 females each and designated according to back pain history as no back pain (NBP), upper back pain onset (UBP) and lower back pain onset (LBP). Six bipolar, bilateral electromyographic (EMG) recording sites were instrumented on each subject. EMG levels were recorded from the forehead, forearm, upper back, lower back, thighs and ankles under conditions of rest, jaw-clenching and a cold stressor. Seven hypotheses predicted that EMG levels would distinguish groups and gender of the subjects and that interactions would exist between site of pain onset and EMG elevations.

Neuropsychological tests have been used in differentially diagnosing schizophrenic and brain damaged populations. Research indicated some subgroups of schizophrenia exhibit certain symptoms of brain damage; and that schizophrenia involves difficulty in sensory integration. The Haptic Visual Discrimination Test (HVDT) designed to test tactilevisual integration, Bender Gestalt, and Information and Digit Symbol subtests of the WAIS were used to test performance abilities of forty schizophrenic subjects, forty subjects medically diagnosed as brain damaged (10 right hemisphere, 10 left hemisphere, and 20 diffuse), and normals as defined by the standardized age norm scores.

The present study investigates the effect of brain damage on verbal-spatial-cognitive (VSC) and sensorimotor (SM) measures included in the McCarron-Dial System (MDS). The subjects include 141 brain damaged adults and 42 psychiatric controls. The following research questions are addressed: (a) Does the brain damaged group differ significantly from controls? (b) Are there significant differences among left, right, anterior, posterior, and diffuse brain damaged groups? (c) Do early onset, late onset, acute, and chronic damaged groups differ significantly? and (d) Does a cerebral palsy group differ significantly from a non-CP brain damaged group?