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R.W. Haley, R. Armitage, F.J. Bonte, W.W. Bryan, C.M.
Cullum, J.L. Fleckenstein, E.M. Frohman, R.F. Hoffman, J. Hom, A. Matt
Maddrey, W. Marshall, P.J. Orsulak, F. Petty, P.S. Roland, A.G. Shoup,
M.H. Trivedi, P.C. Van Ness, R.G.Victor, W. Vongpatanasin, G.I. Wolfe
Departments of Internal Medicine, Neurology, Nuclear Medicine,
Otolaryngology, Psychiatry, and Radiology, University of Texas Southwestern
Medical Center, Dallas, Texas
We studied a 48 year old white male 27-year veteran officer
of U.S. Army Special Forces, who developed a debilitating neurological
condition shortly after the Gulf War, and his identical, non-military
twin. Qualified in Airborne, Ranger, Special Forces, underwater combat
diving, and free fall parachuting, the officer served in 7 regions of
the world including Operation Just Cause, speaks three languages, received
service awards, and was fit on periodic Army HALO/SCUBA physical examinations
through1990. In the Gulf War he commanded a battalion and received the
Legion of Merit and Valorous Unit Citation. Within a year of the war,
he developed stuttering; slowed thinking; difficulty writing, pronouncing
polysyllabic words, and learning new information; problems with balance
descending stairs; apractic slowness in initiating actions such as stepping
on the brake in his car; middle and terminal insomnia; and moderate fatigue.
For several months at a time, he experienced paroxysms of coughing, severe
myalgias, hot flashes and night sweats, and worsening of fatigue, triggered
by exposure to fumes. Evaluation in the CCEP yielded diagnoses of mild
post-traumatic stress disorder (PTSD) and "adult-type ADD."
Our evaluation comparing the officer with his twin confirmed the negative
findings on routine medical tests including rheumatologic and pulmonary
evaluations, neurologic examination, nerve conduction testing, somatosensory
evoked potentials, brain MRI and blood testing. However, psychiatric evaluation
including SCID and CAPS found no evidence of present or lifetime PTSD.
Sleep studies revealed normal sleep latency and REM but multiple awakenings
in the last 2/3 of sleep, central sleep apnea (>30 per hour), and loss
of circadian rhythm of tympanic membrane temperature. Night sweats were
accompanied by temperature spikes to 40° C. High resolution 3-dimensional
full volume brain SPECT scans found reduced blood flow in the right putamen
and left temporal lobe. Auditory brainstem response found asymmetrical
delayed conduction in the upper brain stem and delay of the event-related
potential (P300). Platform posturography revealed vestibular ataxia. Infrared
oculography showed increased saccadic latency with decreased velocity
and acceleration. Quantitative EEG showed excess beta activity. Microneurography
found sympathetic nerve hyperactivity. 24-hour urine analysis found excess
norepinephrine excretion. Neuropsychological testing indicated cognitive
impairment not typical of commonly diagnosed neurologic conditions. Postwar
this officer developed chronic organic brain dysfunction, not found in
his twin, that was not detectable by standard medical testing.
Keywords: Persian Gulf Syndrome; Brain Stem; Putamen
Supported by the Perot Foundation and cooperative agreement
DAMD17-97-2-7025 |
