Thienylphencyclidine protection for the spinal cord of adult rats against extension of lesions secondary to a photochemical injury

1993 ◽  
Vol 78 (4) ◽  
pp. 603-609 ◽  
Author(s):  
Philippe Pencalet ◽  
Freddy Ohanna ◽  
Philippe Poulat ◽  
Jean-Marc Kamenka ◽  
Alain Privat
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neurological Impairment ◽  
Treated Group ◽  
Untreated Group ◽  
Spinal Cord Infarction ◽  
Adult Rats ◽  
Content Type ◽  
Arterial Blood ◽  
Cord Injury

✓ The purpose of this study was to evaluate treatment with the N-methyl-D-aspartate antagonist thienylphencyclidine (TCP) after spinal cord injury for its behavioral, electrophysiological, morphological, and immunohistochemical effects. Five minutes after a photochemical lesion was produced in rats at the T-8 level, the animals received TCP (1 mg/kg, intravenously) or TCP vehicle (saline). The animals were evaluated on Day 18 for neurological recovery by testing motor and sensory functions. The TCP-treated group showed less neurological impairment than the untreated group (p < 0.05 for inclined-plane stability and withdrawal reflex to extension). Somatosensory evoked potential testing was performed on Days 21 to 23 and the wave amplitude between the onset and P1 in the TCP-treated group was higher than in the untreated group (p < 0.05). Mean arterial blood pressure was not significantly modified after TCP injection. Morphometric studies of the lesion area in cross section revealed a significantly reduced spinal cord infarction in the TCP-treated group (p < 0.05). Immunohistochemical evaluation of the spinal cord in lumbar area showed an increased level of serotonin immunoreactivity in the dorsal horn of animals treated by TCP. These results demonstrate the efficacy of TCP in reducing secondary lesions after spinal cord injury in rats.

Neurological prognosis after traumatic quadriplegia

1979 ◽  
Vol 50 (5) ◽  
pp. 611-616 ◽  
Author(s):  
Frederick M. Maynard ◽  
Glenn G. Reynolds ◽  
Steven Fountain ◽  
Conal Wilmot ◽  
Richard Hamilton
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Injury ◽  
Head Injuries ◽  
Gunshot Wounds ◽  
Neurological Impairment ◽  
Treatment Protocols ◽  
Content Type ◽  
Cord Injury

✓ Between January, 1974, and December, 1976, 123 patients with traumatic quadriplegia were admitted to the California Regional Spinal Cord Injury Care System. The spinal cord injury resulted from gunshot wounds in five, from a stab wound in one, from neck injuries with no bone damage seen on x-ray studies in 10, and from fracture dislocations of the cervical spine in 107. One-year follow-up information was available on 114 patients. Neurological impairment using the Frankel classification system was compared at 72 hours postinjury to the 1-year follow-up examination. Fifty of 62 patients with complete injury at 72 hours were unchanged at 1 year. Five of these 62 patients had developed motor useful function in the legs or became ambulatory by 1 year, but all had sustained serious head injuries at the time of their trauma making initial neurological assessment unreliable. Ten percent of all cases had combined head injury impairing consciousness. Among 103 cognitively intact patients, none with complete injury at 72 hours were walking at 1 year. Of patients with sensory incomplete function at 72 hours postinjury, 47% were walking at 1 year; 87% of patients with motor incomplete function at 72 hours postinjury were walking at 1 year. Spinal surgery during the first 4 weeks postinjury did not improve neurological recovery. A method of analyzing neurological and functional outcomes of spinal cord injury is presented in order to more accurately evaluate the results of future treatment protocols for acute spinal injury.

Protein kinase inhibition by fasudil hydrochloride promotes neurological recovery after spinal cord injury in rats

2000 ◽  
Vol 93 (1) ◽  
pp. 94-101 ◽  
Author(s):  
Masahito Hara ◽  
Masakazu Takayasu ◽  
Kazuhiko Watanabe ◽  
Atsushi Noda ◽  
Teruhide Takagi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Protein Kinase ◽  
Treated Group ◽  
Neurological Recovery ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Protein Kinase Inhibition ◽  
Cord Injury ◽  
Fine Print

Object. In Japan fasudil hydrochloride (HA1077), a protein kinase inhibitor, is widely administered to prevent vasospasm in patients after subarachnoid hemorrhage. The effects of fasudil on experimental spinal cord injury (SCI) were investigated and compared with those obtained using methylprednisolone. Methods. Spinal cord contusion was induced in rats by applying an aneurysm clip extradurally to the spinal cord at T-3 for 1 minute. After injury three groups of rats were treated with intravenously administered saline (control), intraperitoneally administered fasudil (10 mg/kg), or intravenously administered methylprednisolone (four 30 mg/kg injections). Neurological recovery was evaluated periodically over 1 month by using a modified combined behavioral scale and histopathological examination. Leukocyte infiltration near the injury site was evaluated by measuring myeloperoxidase (MPO) activity at 24 hours. Spinal cord blood flow was measured at intervals up to 3 hours after injury by using laser Doppler flowmetry. In rats in the fasudil-treated group significant improvement in modified combined behavioral score was demonstrated at each time point, whereas in the methylprednisolone-treated rats no beneficial effects were shown. In the fasudil-treated group, reduction of traumatic spinal cord damage was evident histologically in the caudal portion of the injured areas, and tissue MPO activity in tissue samples was reduced. Spinal cord blood flow was not significantly different between fasudiltreated and control group rats. Conclusions. Fasudil hydrochloride showed promise of effectiveness in promoting neurological recovery after traumatic SCI. Possible mechanisms of this effect include protein kinase inhibition and decreased infiltration by neutrophils.

The effects of methylprednisolone and the ganglioside GM1 on acute spinal cord injury in rats

1994 ◽  
Vol 80 (1) ◽  
pp. 97-111 ◽  
Author(s):  
Shlomo Constantini ◽  
Wise Young
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Body Weight Loss ◽  
Ganglioside Gm1 ◽  
Rat Spinal Cord ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Fine Print

✓ Recent clinical trials have reported that methylprednisolone sodium succinate (MP) or the monosialic ganglioside GM1 improves neurological recovery in human spinal cord injury. Because GM1 may have additive or synergistic effects when used with MP, the authors compared MP, GM1, and MP+GM1 treatments in a graded rat spinal cord contusion model. Spinal cord injury was caused by dropping a rod weighing 10 gm from a height of 1.25, 2.5, or 5.0 cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. The lesion volumes were quantified from spinal cord Na and K shifts at 24 hours after injury and the results were verified histologically in separate experiments. A single dose of MP (30 mg/kg), given 5 minutes after injury, reduced 24-hour spinal cord lesion volumes by 56% (p = 0.0052), 28% (p = 0.0065), and 13% (p > 0.05) in the three injury-severity groups, respectively, compared to similarly injured control groups treated with vehicle only. Methylprednisolone also prevented injury-induced hyponatremia and increased body weight loss in the spine-injured rats. When used alone, GM1 (10 to 30 mg/kg) had little or no effect on any measured variable compared to vehicle controls; when given concomitantly with MP, GM1 blocked the neuroprotective effects of MP. At a dose of 3 mg/kg, GM1 partially prevented MP-induced reductions in lesion volumes, while 10 to 30 mg/kg of GM1 completely blocked these effects of MP. The effects of MP on injury-induced hyponatremia and body weight loss were also blocked by GM1. Thus, GM1 antagonized both central and peripheral effects of MP in spine-injured rats. Until this interaction is clarified, the authors recommend that MP and GM1 not be used concomitantly to treat acute human spinal cord injury. Because GM1 modulates protein kinase activity, protein kinases inhibit lipocortins, and lipocortins mediate anti-inflammatory effects of glucocorticoids, it is proposed that the neuroprotective effects of MP are partially due to anti-inflammatory effects and that GM1 antagonizes the effects of MP by inhibiting lipocortin. Possible beneficial effects of GM1 reported in central nervous system injury may be related to the effects on neural recovery rather than acute injury processes.

Transforaminal Lumbar and Thoracic Interventions and Ischemic Spinal Cord Injury

2016 ◽  
Author(s):  
Scott E. Glaser ◽  
Rinoo Shah
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Infarction ◽  
Supporting Evidence ◽  
Steroid Injections ◽  
Epidural Steroid Injections ◽  
Root Cause ◽  
Cord Injury ◽  
Epidural Steroid ◽  
Ischemic Spinal Cord Injury

Transforaminal epidural steroid injections have been shown to be associated with catastrophic neurologic complications secondary to spinal cord infarction. The reflexive, ad hoc response of practitioners to these injuries has been to recommend risk minimization strategies to prevent embolism of the injected particulate steroids and to use nonparticulate steroids. This focus on distal embolism as the sole or primary cause of catastrophic outcomes lacks conclusive supporting evidence and does not suffice to protect the patient from paraplegia as it fails to address the root cause of the complications. A root cause analysis of the procedure provides evidence that the injection technique itself—the “safe triangle”—creates a risk of arterial damage and sequelae leading to ischemia of the spinal cord. The evidence is strong that the only way to mitigate or eliminate the risk of paraplegia is to use a different technique to perform transforaminal injections: the Kambin triangle approach. This change in technique is the only definitive solution that addresses the root cause of these catastrophic sequelae associated with transforaminal epidural steroid injections. Key Words: Artery of Adamkiewicz, ischemic spinal cord injury, Kambin triangle, safe triangle, transforaminal epidural injection

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Therapeutic trial of hypercarbia and hypocarbia in acute experimental spinal cord injury

1984 ◽  
Vol 61 (5) ◽  
pp. 925-930 ◽  
Author(s):  
Ronald W. J. Ford ◽  
David N. Malm
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Mortality Rates ◽  
Therapeutic Trial ◽  
Tissue Preservation ◽  
Content Type ◽  
Experimental Spinal Cord Injury ◽  
Cord Injury ◽  
Fine Print

✓ Hypocarbia, normocarbia, or hypercarbia was maintained for an 8-hour period beginning 30 minutes after acute threshold spinal cord injuries in cats. No statistically significant differences in neurological recovery or histologically assessed tissue preservation were found among the three groups of animals 6 weeks after injury. No animal recovered the ability to walk. It is concluded that maintenance of hypercarbia or hypocarbia during the early postinjury period is no more therapeutic than maintenance of normocarbia. Mortality rates and tissue preservation data suggest, however, that postinjury hypocarbia may be less damaging than hypercarbia.

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