Prolonged recurrent apnea (defined as a respiratory pause longer than 20 seconds) is often a life threatening clinical problem occurring in pre-term human neonates with the lowest birthweights and shortest gestational ages. Traumatic injury (hemorrhage/infarct) and/or delayed neural maturation of the brainstem respiratory pathways (myelineogenesis) and/or neuronal maturation are hypothesized as the cause of this derangement of pulmonary function. This may involve development of fiber tracts in the ponto-medullary area of the brainstem which are undergoing active myelination at 28-36 weeks of gestation. It is hypothesized that such physiological and anatomic abnormalities may be elucidated in the human neonate by noninvasive quantitative techniques of Brainstem Auditory and Somatosensory Evoked Potentials. Evoked Potentials are electrical signals generated by peripheral and central nervous system time-locked in response to auditory or somatosensory stimuli. Since auditory and somatosensory pathways converge in the region of the ponto-medullary junction (slightly rostral to the medullary regulatory pathways of respirations), these evoked potentials may reflect conduction in myelinated fiber tracts in this region. Such fiber tracts in the neonate with incomplete and/or delayed maturation may conduct impulses more slowly. Thus, they may show longer conduction times when compared to evoked potentials found in the """"""""normal"""""""" pre-term neonate. Using such measures of brainstem maturation, pre-term neonates with prolonged recurrent apnea will be longitudinally assessed (within 48 hours and at 2 weeks after birth) for physiological and anatomical evidence of pathologic disruption (hemorrhage/infarct) and/or delayed development of myelinated fiber tracts when compared with pre-term neonates without prolonged recurrent apnea. The present study is of clinical importance based on the fact that it may be possible to identify those infants predisposed to prolonged recurrent apnea and, thereby, prevent brain injury from recurrent hypoxia and sudden death - a lethal outcome from respiratory arrest.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08NS001005-05
Application #
3083641
Study Section
Neurological Disorders Program Project Review A Committee (NSPA)
Project Start
1985-07-01
Project End
1990-06-30
Budget Start
1989-07-01
Budget End
1990-06-30
Support Year
5
Fiscal Year
1989
Total Cost
Indirect Cost
Name
University of Kentucky
Department
Type
Schools of Medicine
DUNS #
832127323
City
Lexington
State
KY
Country
United States
Zip Code
40506
Gilmore, R L; Falace, P; Kanga, J et al. (1991) Sleep-disordered breathing in Mobius syndrome. J Child Neurol 6:73-7
Gilmore, R L (1990) Sensory evoked potentials in clinical practice. Semin Neurol 10:185-95
Gilmore, R L; Kasarskis, E J; Carr, W A et al. (1989) Comparative impact of paraclinical studies in establishing the diagnosis of multiple sclerosis. Electroencephalogr Clin Neurophysiol 73:433-42
Gilmore, R L; Nelson, K R (1989) SSEP and F-wave studies in acute inflammatory demyelinating polyradiculoneuropathy. Muscle Nerve 12:538-43
Gilmore, R (1989) The use of somatosensory evoked potentials in infants and children. J Child Neurol 4:3-19
Gilmore, R (1988) Use of somatosensory evoked potentials in infants and children. Neurol Clin 6:839-59
Reincke, H M; Gilmore, R L; Kuhn, R J (1988) High-dose lorazepam therapy for status epilepticus in a pediatric patient. Drug Intell Clin Pharm 22:889-90
Nelson, K R; Gilmore, R L; Massey, A (1988) Acoustic nerve conduction abnormalities in Guillain-Barre syndrome. Neurology 38:1263-6
Gilmore, R; Brock, J; Hermansen, M C et al. (1987) Development of lumbar spinal cord and cortical evoked potentials after tibial nerve stimulation in the pre-term newborns: effects of gestational age and other factors. Electroencephalogr Clin Neurophysiol 68:28-39