Max
06-19-2002, 08:43 AM
Assessment of spinal cord pathology following trauma using early changes in the spinal cord evoked potentials: A pharmacological and morphological study in the rat
Hari Shanker Sharma, PhD 1 *, Tomas Winkler, MD 2
1Laboratory of Neuroanatomy, Department of Medical Cell Biology, Box 571, Biomedical Centre, Uppsala University, SE-75123 Uppsala, Sweden
2Department of Clinical Neurophysiology, University Hospital, Uppsala, Sweden
email: Hari Shanker Sharma (sharma@medcellbiol.uu.se)
*Correspondence to Hari Shanker Sharma, Frödingsgatan 12, 28, SE-75421 Uppsala, Sweden
Funded by:
Swedish Medical Research Council 2710; Grant Number: JW/HSS
Göran Gustafsson Foundation (Sweden)
Astra-Zeneca (Mölndal, Sweden)
Alexander vin Humboldt Foundation (Bonn, Germany)
University Grants Commission (New Delhi, India)
Keywords
blood flow • blood-spinal cord barrier • drug influence • edema formation • spinal cord evoked potential • spinal cord • ultrastructure
Abstract
The possibility that spinal cord pathology following trauma can be assessed with early changes in the spinal cord evoked potentials (SCEPs) was examined in a rat model. Spinal cord injury (SCI) was produced in Equithesin-anesthetized (3 ml/kg, i.p.) rats through a longitudinal incision into the right dorsal horn at the T10-11 segments. The SCEPs were recorded with epidural electrodes placed over the T9 (rostral) segment of the cord. The SCEPs consisted of a small positive amplitude and a broad and high negative amplitude (NA). SCI resulted in an instant depression of the rostral NA that lasted for 1 h. However, the latency of NA continued to increase over time. At 5 h, spinal cord blood flow declined by 30% in the T9 segment, whereas the spinal cord water content and the permeability of the blood-spinal cord barrier (BSCB) were markedly increased. Damage to the nerve cells, glial cells, and myelin was quite common in the spinal cord, as seen by light and electron microscopy. Pretreatment with p-chlorophenylalanine, indomethacin, ibuprofen, and nimodipine attenuated the SCEP changes immediately after trauma and resulted in a marked reduction in edema formation, BSCB permeability, and blood flow changes at 5 h. However, pretreatment with cyproheptadine, dexamethasone, phentolamine, and propranolol failed to attenuate the SCEP changes after SCI and did not reduce the cord pathology. These observations suggest that early changes in SCEP reflect secondary injury-induced alterations in the cord microenvironment. Obviously, these changes are crucial in determining the ultimate magnitude and severity of cord pathology. © 2002 Wiley Periodicals, Inc. Muscle Nerve Supplement 11: S83-S91, 2002
[This message was edited by Wise Young on Aug 21, 2002 at 06:55 AM.]
Hari Shanker Sharma, PhD 1 *, Tomas Winkler, MD 2
1Laboratory of Neuroanatomy, Department of Medical Cell Biology, Box 571, Biomedical Centre, Uppsala University, SE-75123 Uppsala, Sweden
2Department of Clinical Neurophysiology, University Hospital, Uppsala, Sweden
email: Hari Shanker Sharma (sharma@medcellbiol.uu.se)
*Correspondence to Hari Shanker Sharma, Frödingsgatan 12, 28, SE-75421 Uppsala, Sweden
Funded by:
Swedish Medical Research Council 2710; Grant Number: JW/HSS
Göran Gustafsson Foundation (Sweden)
Astra-Zeneca (Mölndal, Sweden)
Alexander vin Humboldt Foundation (Bonn, Germany)
University Grants Commission (New Delhi, India)
Keywords
blood flow • blood-spinal cord barrier • drug influence • edema formation • spinal cord evoked potential • spinal cord • ultrastructure
Abstract
The possibility that spinal cord pathology following trauma can be assessed with early changes in the spinal cord evoked potentials (SCEPs) was examined in a rat model. Spinal cord injury (SCI) was produced in Equithesin-anesthetized (3 ml/kg, i.p.) rats through a longitudinal incision into the right dorsal horn at the T10-11 segments. The SCEPs were recorded with epidural electrodes placed over the T9 (rostral) segment of the cord. The SCEPs consisted of a small positive amplitude and a broad and high negative amplitude (NA). SCI resulted in an instant depression of the rostral NA that lasted for 1 h. However, the latency of NA continued to increase over time. At 5 h, spinal cord blood flow declined by 30% in the T9 segment, whereas the spinal cord water content and the permeability of the blood-spinal cord barrier (BSCB) were markedly increased. Damage to the nerve cells, glial cells, and myelin was quite common in the spinal cord, as seen by light and electron microscopy. Pretreatment with p-chlorophenylalanine, indomethacin, ibuprofen, and nimodipine attenuated the SCEP changes immediately after trauma and resulted in a marked reduction in edema formation, BSCB permeability, and blood flow changes at 5 h. However, pretreatment with cyproheptadine, dexamethasone, phentolamine, and propranolol failed to attenuate the SCEP changes after SCI and did not reduce the cord pathology. These observations suggest that early changes in SCEP reflect secondary injury-induced alterations in the cord microenvironment. Obviously, these changes are crucial in determining the ultimate magnitude and severity of cord pathology. © 2002 Wiley Periodicals, Inc. Muscle Nerve Supplement 11: S83-S91, 2002
[This message was edited by Wise Young on Aug 21, 2002 at 06:55 AM.]