Spasticity following spinal cord injury.

Spasticity is a hyper-excitable state of the reflex arcs in the spinal cord below the level of injury. Not only is the skeletal motor system affected, but bladder, bowel, blood pressure, and erection reflex mechanisms are also involved. Spasticity gradually emerges from the initial phase of spinal shock one to two months after the injury, and usually reaches a plateau of a mild to moderate degree in 3 to 4 months. Neurophysiological mechanisms indicate an increase in the alpha and gamma reflex systems and that central excitability through the interneurons is also involved in these systems. Excessive spasticity should be recognized as a substitute for pain in the spinal cord injured patient, as infections, calculi, pressure ulcers, and other normally painful conditions set off the hyper-sensitive reflexes causing more spasticity. Education and health maintenance is the best prevention of severe spasticity. Definitive treatment of incapacitating spasticity is to find and treat the underlying disease condition, as well as to introduce medication which will also suppress the spasm (Valium and/or Dantrolene). Muscle motor points and/or nerve blocks with neurolytic agents is perhaps the best technique for quietening excessive spasticity. Intrathecal neurolytic agents, anterior or posterior rhizotomies and cordectomies are not advocated even in severe incapacitating spasticity as they are too destructive. Selective longitudinal myelotomy is by far the best surgical technique for disrupting excessive spasticity, if any such procedure is to be done. Tendonotomies may be necessary in chronic contractures of joints after the muscle spasticity has been reduced. Excessive spasticity is not regarded as a normal state in the spinal cord injured patient. The cause should be sought and treated. Nerve destruction techniques should not be used unless medical and nursing techniques have failed. Prevention is so important and can be achieved by education, health maintenance, and especially motivation.     

Cerebrospinal fluid aluminum levels following deferoxamine

Deferoxamine is widely used in the diagnosis and treatment of aluminum toxicity and has a characteristic combination of side effects, including a poorly defined worsening of existing neurologic symptoms. However, to date, no measurement of cerebrospinal fluid (CSF) aluminum concentrations after deferoxamine exist. We report the case of a patient who developed acute neurological deterioration in conjunction with sepsis and elevated serum aluminum levels shortly after renal transplantation. Simultaneous values for blood and CSF aluminum were measured in response to deferoxamine and hemodialysis. The increase in CSF aluminum levels appears to parallel that seen in serum after deferoxamine. We hypothesize that this elevation in CSF aluminum may account for the observed neurologic deterioration after deferoxamine and postulate various pathophysiologic mechanisms that might be involved.     

Bowel dysfunction following spinal cord injury.

STUDY DESIGN: Review. OBJECTIVES: To outline the present knowledge of bowel dysfunction following spinal injury, and look at future directions of management and research. SETTING: Spinal Unit and Colorectal Unit, Christchurch, New Zealand. METHODOLOGY: Review. RESULTS: The underlying physiology of colorectal motility and defecation is reviewed, and consequences of spinal cord injury on defecation are reported. A discussion of present management techniques is undertaken and new directions in management and research are suggested. CONCLUSION: There is need for more intervention in regard to bowel function that could improve quality of life, but there is also a need for more research in this area.     

Cerebrospinal fluid lactate and lactate dehydrogenase levels as diagnostic aids in tuberculous meningitis

The value of cerebrospinal fluid (CSF) lactate and lactate dehydrogenase (LD) values as aids in differentiating tuberculous meningitis (TBM) from aseptic meningitis has been investigated. Using an upper limit of normal for CSF lactate levels of 2,75 mmol/l resulted in detection of 24 out of 26 cases of TBM (a sensitivity of 92%). If, however, a level of 3,85 mmol/l was taken as the upper limit of normal, then 18 out of 26 cases were detected (a sensitivity of 69%). Using 40 U/l as the upper limit of normal for LD levels detected 21 out of 38 cases of TBM (a sensitivity of 55%). Both tests may give normal values in the presence of TBM, but this should not cause specific antituberculosis therapy to be withheld. Neither test appears to hold marked advantages over conventional chemical analysis of CSF in differentiating TBM from aseptic meningitis.     

Pain and suffereing following spinal cord injury.

It is important to distinguish between the part played by possible pathological processes which can cause pain and those emotional problems which are often somatosized as pain. So much depends upon the patient's own ability to cope with his problem and communicate them effectively. The acceptance of his disability and of the strange feelings where once he felt his body has to take place. There is often a long period of time and experiences that the patient has to go through before he accepts the reality that he is paralyzed permanently and that he has to make a life that is worthwhile.     

Vocational outcome following spinal cord injury.

Study Design: Non-experimental (ex post facto) survey research design involving the use of a fixed alternative format questionnaire. Objectives: To investigate variables influencing vocational outcome, to identify barriers to gaining and sustaining employment and to identify the effects of variables on the type of work engaged in following spinal cord injury. The two sets of independent variables considered were, individual and injury-related factors (age at onset of injury, time since injury, extent/level of injury, highest educational qualification achieved pre-injury, and pre-injury occupation) and circumstantial factors (means of transport, access difficulties, perceived workplace discrimination, financial disincentives to work and perceived level of skill). Setting: The Princess Alexandra Hospital Spinal Injuries Unit, Queensland, Australia. Methods: Data on the variables and the vocational outcomes of having ever worked or studied post-injury, current employment status and post-injury occupation were obtained from survey responses. Demographical and medical data were gathered from medical records. Results: Forward stepwise logistic regression revealed that having ever worked or studied post-injury was associated with all individual and injury-related factors except pre-injury occupation, and two circumstantial factors, namely means of transport and access difficulties. Current employment was associated with all circumstantial factors as well as age at injury and pre-injury occupation. Standard multiple regression analyses revealed that post-injury occupation was correlated with all individual and injury-related factors as well as means of transport and perceived workplace discrimination. Conclusions: Tailored rehabilitation programs for individuals with characteristics associated with less successful vocational outcomes may facilitate their employment status after injury.     

Cerebrospinal fluid catecholamine levels and duration of spinal anaesthesia

The effects of catecholamines added to dibucaine on the duration of spinal anaesthesia and cerebrospinal fluid catecholamine levels were studied. Free norepinephrine levels increased from 0.107 ng.ml-1 before anaesthesia to 5.8 ng.ml-1 and 1,238 ng.ml-1 after 1.0 microgram or 100 micrograms norepinephrine had been added to the local anaesthetic. The effects of 2.5 micrograms of either norepinephrine or epinephrine added to dibucaine on the duration of motor blockade and sensory regression time were compared. The duration of both were significantly prolonged by added norepinephrine from 96 +/- 17 min to 193 +/- 20 min (sensory blockade) and from 116 +/- 14 min to 204 +/- 34 min (motor blockade), but were not changed by addition of epinephrine. These data suggest that a 2.5 micrograms dose of norepinephrine is sufficient to prolong the duration of spinal anaesthesia and more effective than the same dose of epinephrine.     

Cerebrospinal fluid lactate and lactate/pyruvate ratios in hydrocephalus.

Cerebral metabolism in 21 hydrocephalic patients was studied. Preoperative and postoperative specimens of cerebrospinal fluid (CSF) were obtained and the cerebral perfusion pressure (CPP) was calculated in each instance. The specimens of CSF were analyzed for lactate and pyruvate and the lactate/pyruvate (L/P) ratio was calculated for each sample. The L/P ratio, which reflects the redox state of the cell, was used to determine the extent of anaerobic metabolism. An inverse relationship was noted between CPP and lactate as well as the L/P ratio. In general, the level of anaerobic metabolism was decreased after insertion of a shunt.     

Xanthine oxidase in experimental spinal cord injury.

The excessive generation of free radicals is thought to be one of the major mechanisms leading to tissue injury in various pathological conditions, including ischemia, inflammation, and trauma. Conversion of xanthine dehydrogenase (XDH) to xanthine oxidase (XO) contributes to the formation of superoxide, an oxygen radical. We measured XDH and XO activity using a newly developed fluorometric assay in an experimental spinal cord injury model in rats. XO activity increased by more than 100% 4 h after spinal cord trauma. Total (XDH + XO) activity also increased by 96% during the same period. Allopurinol, an inhibitor of XO (100 mg/kg/day x 2 days, i.p.), completely inhibited plasma and spinal cord XO activity but did not affect posttraumatic edema determined by water content or polymorphonuclear (PMN) cell infiltration reflected by myeloperoxidase (MPO) activity in traumatized spinal cord. These results indicate that XDH conversion to XO may not be the major mechanism of oxygen radical formation in the pathogenesis of vasogenic edema or inflammatory response in this experimental spinal cord injury model in rats.     

Microvascular perfusion experimental spinal cord injury

Microperfusion of the spinal cords in cats was studied using a colloidal carbon perfusion technique following compression injury at 1/2 hour, 2 hours, 4 hours, 8 hours, 24 hours, and 51 days. Quantitative estimates of vascular filling were determined at these post-compression intervals. Microperfusion diminished in both the gray and white matter at 1/2 hour following injury and severe lack of perfusion was evident at 8 and 24 hours. Diminished filling of the vessels of gray and white matter seemed to parallel the degree of hemorrhagic necrosis of the gray matter. An increased number of vessels were evident in the spinal cords of long term survivals. The observation that microperfusion in the white matter of the spinal cord was diminished at 24 hours is at variance with some previous investigations. The hypoperfusion of the white matter found in this study suggests that ischemia plays a role in paraplegia resulting from experimental compression injury of the spinal cord.     

Leukotrienes in experimental spinal cord injury

Leukotrienes are a group of noncyclized fatty acid eicosanoids which are formed from the breakdown of arachidonic acid. They are potent mediators of inflammation and may contribute to secondary injury in the central nervous system. All mammalian tissue including cerebral cortex is capable of synthesizing these; however, clear documentation of leukotriene formation in the spinal cord is lacking. We subjected 55 rabbits to weight drops of 200, 300, and 400 gm/cm, respectively, on an exposed spinal cord. The traumatized spinal cord was removed after periods of 15, 30, and 45 minutes and 1, 2, 4, 8, and 24 hours. Radioimmunoassay for leukotriene B-4 was then performed on the specimens. Significant (p less than 0.05) elevation was noted in the 200 and 300 gm/cm groups with peak levels occurring in the first 4 hours. The 400 gm/cm group showed significant depression of values below control levels from 2 to 24 hours. We conclude that in sublethal central nervous system injury leukotrienes are produced in significant amounts and may contribute to secondary spinal cord injury.     

Anorectal physiology following spinal cord injury

PURPOSE: Spinal cord injured (SCI) patients have delayed colonic motility and anorectal dysfunction resulting in functional obstruction and constipation. This may be caused by changes in descending modulation from the central or sympathetic nervous systems. Anorectal dyssynergy may demonstrate similarities to that seen in the bladder following SCI. METHODOLOGY: Anorectal manometry was performed on 37 SCI volunteers. Patterns of rectal and sphincter function were identified. These patterns were then compared with questionnaire answers on bowel function and cystometrograms to identify a relationship between detrusor dyssynergy and anal sphincter tone. RESULTS: Rectal compliance and basal resting sphincter pressures were lower than normal values. Ramp rectal inflation demonstrated patterns of sphincter activity similar to that recorded in the patients' cystometrograms. There is no definite relationship of bowel function to the findings on manometry in SCI patients. CONCLUSIONS: SCI patients have abnormal anorectal function. Anorectal manometry results were able to be classified into four patterns on the basis of rectal pressure and sphincter tone in response to rectal distention. The patterns of anorectal manometry seen were similar to those in cystometrograms, however there is no definite relationship to bowel dysfunction. Spinal Cord (2000) 38, 573 - 580.     

Post-traumatic inflammation following spinal cord injury

Inflammatory reaction following a spinal cord injury (SCI) contributes substantially to secondary effects, with both beneficial and devastating effects. This review summarizes the current knowledge concerning the structural features (vascular, cellular, and biochemical events) of SCI and gives an overview of the regulation of post-traumatic inflammation.     

Post-traumatic growth following spinal cord injury

Context/objective

Examine the relationship of post-traumatic psychological growth (PTG), depression, and personal and injury characteristics in persons with spinal cord injury (SCI).

Design

Cross-sectional survey.

Setting

Community.

Participants

Eight hundred and twenty-four adults with SCI.

Interventions

None.

Outcome measures

Five items from the Post-traumatic Growth Inventory, reflecting positive change after injury in life priorities, closeness to others, new opportunities being available, stronger faith, and personal strength.

Results

Initial structural equation model testing of a conceptual model of personal and injury characteristics, violent etiology, depression, and PTG resulted in a poor fit. Model modifications resulted in an improved fit, but explained only 5% of the variance in PTG. Being female, younger, having less formal education, and less time since injury had significant relationships with PTG, whereas depression, violent etiology, and injury level/severity did not. In each PTG domain, between 54 and 79% of the sample reported at least some positive change after injury.

Conclusions

The results of this study, while promising, explained only a small portion of the variance in PTG. A majority of the sample experienced some positive change after injury, with the greatest change in discovering that they were stronger than they thought they were. Comparing means previously reported in a non-SCI sample of those who experienced trauma, positive change after injury was comparable for each PTG item except for new opportunities being available, which was significantly lower for those with SCI. Future directions of research include the development of theoretical models of PTG after SCI.     

Alteration of leukotriene C4 levels in experimental spinal cord injury]

Leukotriene C4 (LTC4) production in the guinea pig spinal cord following compression injury was determined by radioimmunoassay, in the same way thromboxane B2 (TXB2), a stable metabolite of thromboxane A2 (TXA2), was also measured. When the spinal cords were compressed under a 20 gram weight for 10 minutes, LTC4 levels reached peak values (2.2 +/- 0.4 pmol/g cord) 10 minutes after release, then gradually decreased until being undetectable 60 minutes later. TXB2 levels reached peak values (146.8 +/- 6.2 pmol/g cord) 5 minutes after the release from compression, the TXB2 level then gradually decreased, but remained at about 1/2 of the peak level even 60 minutes after the release. When the spinal cords were compressed with various weights, TXB2 production depended on the degree of compression, while LTC4 production was not affected by the compression injury. The LTC4 production confirmed in the injured spinal cords is suggestive of its relation to secondary disorders after spinal cord injury, spinal edema, in particular.