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PubMed2001

Changes in synaptic inputs to sympathetic preganglionic neurons after spinal cord injury.

Spinal cord injury (SCI) leads to plastic changes in organization that impact significantly on central nervous control of arterial pressure. SCI causes hypotension and autonomic dysreflexia, an episodic hypertension induced by spinal reflexes. Sympathetic preganglionic neurons (SPNs) respond to SCI by retracting and then regrowing their dendrites within 2 weeks of injury. We examined changes in synaptic input to SPNs during this time by comparing the density and amino acid content of synaptic input to choline acetyltransferase (ChAT)-immunoreactive SPNs in the eighth thoracic spinal cord segment (T8) in unoperated rats and in rats at 3 days or at 14 days after spinal cord transection at T4. Postembedding immunogold labeling demonstrated immunoreactivity for glutamate or gamma-aminobutyric acid (GABA) within presynaptic profiles. We counted the number of presynaptic inputs to measured lengths of SPN somatic and dendritic membrane and identified the amino acid in each input. We also assessed gross changes in the morphology of SPNs using retrograde labeling with cholera toxin B and light microscopy to determine the structural changes that were present at the time of evaluation of synaptic density and amino acid content. At 3 days after SCI, we found that retrogradely labeled SPNs had shrunken somata and greatly shortened dendrites. Synaptic density (inputs per 10-microm membrane) decreased on ChAT-immunoreactive somata by 34% but increased on dendrites by 66%. Almost half of the inputs to SPNs lacked amino acids. By 14 days, the density of synaptic inputs to dendrites and somata decreased by 50% and 70%, respectively, concurrent with dendrite regrowth. The proportion of glutamatergic inputs to SPNs in spinal cord-transected rats ( approximately 40%) was less than that in unoperated rats, whereas the GABAergic proportion (60-68%) increased. In summary, SPNs participate in vasomotor control after SCI despite profound denervation. An altered balance of excitatory and inhibitory inputs may explain injury-induced hypotension.

Amino Acids↗
PubMed2005

Upregulation of EphA3 receptor after spinal cord injury.

Spinal cord injury (SCI) releases a cascade of events that leads to the onset of an inhibitory milieu for axonal regeneration. Some of these changes result from the presence of repulsive factors that may restrict axonal outgrowth after trauma. The Eph receptor tyrosine kinase (RTK) family has emerged as a key repellent cue known to be involved in neurite outgrowth, synapse formation, and axonal pathfinding during development. Given the nonpermissive environment for axonal regeneration after SCI, we questioned whether re-expression of one of these molecules occurs during regenerative failure. We examined the expression profile of EphA3 at the mRNA and protein levels after SCI, using the NYU contusion model. There is a differential distribution of this molecule in the adult spinal cord and EphA3 showed an increase in expression after several injury models like optic nerve and brain injury. Standardized semi-quantitative RT-PCR analysis demonstrated a time-dependent change in EphA3 mRNA levels, without alterations in beta-actin levels. The basal level of EphA3 mRNA in the adult spinal cord is low and its expression was induced 2 days after trauma (the earliest time point analyzed) and this upregulation persisted for 28 days post-injury (the latest time point examined). These results were corroborated at the protein level by immunohistochemical analysis and the cell phenotype identified by double labeling studies. In control animals, EphA3 immunoreactivity was observed in motor neurons of the ventral horn but not in lesioned animals. In addition, GFAP-positive cells were visualized in the ventral region of injured white matter. These results suggest that upregulation of EphA3 in reactive astrocytes may contribute to the repulsive environment for neurite outgrowth and may be involved in the pathophysiology generated after SCI.

Animals↗
PubMed2004

Assistive technology and computer adaptations for individuals with spinal cord injury.

Spinal cord injury (SCI) commonly occurs in individuals during important years for formation of vocational goals, resulting in low post-injury employment rates and higher costs to society. Individuals with SCI who are employed have improved quality of life. Assistive technology, often available at modest cost, can help individuals with SCI to compensate for functional limitations, overcome barriers to employability, enhance technical capacities and computer utilization, and improve ability to compete for gainful employment.

Adult↗
PubMed2004

Degenerative and regenerative mechanisms governing spinal cord injury.

Spinal cord injury (SCI) is a major cause of disability, and at present, there is no universally accepted treatment. The functional decline following SCI is contributed to both direct mechanical injury and secondary pathophysiological mechanisms that are induced by the initial trauma. These mechanisms initially involve widespread haemorrhage at the site of injury and necrosis of central nervous system (CNS) cellular components. At later stages of injury, the cord is observed to display reactive gliosis. The actions of astrocytes as well as numerous other cells in this response create an environment that is highly nonpermissive to axonal regrowth. Also manifesting important effects is the immune system. The early recruitment of neutrophils and at later stages, macrophages to the site of insult cause exacerbation of injury. However, at more chronic stages, macrophages and recruited T helper cells may potentially be helpful by providing trophic support for neuronal and non-neuronal components of the injured CNS. Within this sea of injurious mechanisms, the oligodendrocytes appear to be highly vulnerable. At chronic stages of SCI, a large number of oligodendrocytes undergo apoptosis at sites that are distant to the vicinity of primary injury. This leads to denudement of axons and deterioration of their conductive abilities, which adds significantly to functional decline. By indulging into the molecular mechanisms that cause oligodendrocyte apoptosis and identifying potential targets for therapeutic intervention, the prevention of this apoptotic wave will be of tremendous value to individuals living with SCI.

Animals↗
PubMed2002

Sympathetic sudomotor skin activity in human after complete spinal cord injury.

Spinal cord injury (SCI) causes serious disturbances in autonomic innervation and malfunction of the sympathetic nervous system that controls the pelvic organs, blood pressure, skin temperature and sweating. We studied sympathetic sudomotor pathways in 6 healthy subjects and 14 patients with sensory and motor complete SCI on cervical, thoracic and lumbar level. Sympathetic skin responses (SSRs) were provoked by auditory bursts and electrical stimulation of median, pudendal and tibial nerve and recorded from the palmar and plantar skin. The SSRs in healthy subjects occurred generally with the same pattern and with similar latencies suggesting a common sudomotor pathway mediating the SSR. Appearance or absence of the SSRs in SCI following stimulation above the lesion depend on the spinal level of lesion and on the location of stimulation. Lesions below T3 show palmar and lesions below T12 palmar and plantar SSR. Pudendal nerve stimulation evoked plantar SSRs in patients with complete cervical and thoracic SCI. No SSRs were obtained in patients with lesions at L1 and more caudal. SSRs following pudendal nerve stimulation in complete SCI above the level L1 are mediated by sacral somatic afferents and a sympathetic pathway originating at the upper lumbar level. The underlying sacro-lumbar reflex circuit is organized on spinal level and requires intact lumbar segments. Tibial nerve stimulation was not found to elicit SSRs below a SCI lesion and we suppose that this type of electrical stimulation cannot activate the spinal sudomotor reflex circuit.

Adrenergic Fibers↗
PubMed1995

Urodynamic evaluation in spinal cord injuries.

Spinal cord injury, regardless of its level, causes flaccid paralysis during the shock phase affecting the detrusor and rectal musculature. Then, depending on the level and severity of the lesion, the bladder gains spasticity or remains flaccid. Monitoring the reflex behaviour of detrusor and sphincter activities helps to select the treatment modalities. Thirty patients with cord injuries of various levels have been urodynamically tested at 3-month intervals. The shock phase of the acutely tested patients lasted about 8-9 weeks. Eventually, 23 of the cases were hyperreflexic, while 7 cases remained areflexic: 2 had detrusor-sphincter dyssynergia. The response to treatment has been investigated by cystometrographical and electromyographical methods.

Adolescent↗
PubMed1993

Urologic complications of spinal cord injury.

Spinal cord injuries in the past were associated with a very high mortality, predominantly from urologic complications and sepsis. Improvements in the urologic and medical management of these patients have significantly decreased the morbidity and mortality. Many complications may still develop during the urologic management, however. Periodic follow-up is thus essential to recognize and treat urologic complications in order to preserve renal function.

Adult↗
PubMed2000

[Electric stimulation in muscle training of the lower extremities in persons with spinal cord injuries].

Spinal cord injured persons have limited possibilities to perform physical training. By use of computerized, feed-back controlled electrical stimulation of the gluteal, the hamstrings and the quadriceps muscles cycle ergometry can be performed by the spinal cord injured individual. The cardiovascular demands of this training is higher than with voluntary upper body training using the intact innervated muscles. The inactivity related conditions caused by the spinal cord injury are reversed in part by regular electrically stimulated training. An increase is seen in maximal oxygen consumption, in the insulin stimulated glucose uptake and in the muscular mass and bone mineral content of the lower extremities. Electrically induced cycle ergometry is thoroughly investigated, relatively safe, but time consuming. As this training in addition results in the same well being as seen by training in able bodied individuals it can be recommended for motivated patients.

Electric Stimulation Therapy↗
PubMed2004

[Physiopathologic aspects and nursing care in the rehabilitation of subjects with spinal cord injury].

Spinal cord injury can cause neurological damage such as alterations in the motor, sensitive and autonomic function. In this paper, details of clinical complications such as PVT, infection, respiratory insufficiency, pressure ulcers, autossomic disreflection, orthostatic hypotension, sphincteral-vesical and intestinal disfunctions, are related. And will also present prophylactic and therapeutic nursing care interventions designed for the well-being and improvement in life quality for patients.

Humans↗
PubMed1995

Thyroid hormone changes in chronic spinal cord injury.

Spinal cord injury (SCI) impacts metabolic function and deranges various hormonal axes. Previous studies characterizing thyroid hormones in SCI reported depressed triiodothyronine (T3) and thyroxin (T4), primarily in acute tetraplegics. These studies cited an 11-13 percent incidence of low T3 syndrome (LT3S) in SCI patients, with an increased incidence in tetraplegics (20-36 percent). The purpose of this study was to evaluate thyroid function and determine the incidence and clinical relevance of LT3S in the chronic SCI population. Thyroid function tests were performed on 30 chronic SCI patients (14 tetraplegics and 16 paraplegics) and 30 age- and gender-matched controls. Mean T3 and T4 levels were significantly depressed in SCI patients relative to controls, while T3 resin uptake (T3RU) values were significantly elevated. LT3S only occurred in the SCI population with an incidence of 23.3 percent. SCI patients with LT3S did not differ significantly from those without in the level or completeness of injury, age or the interval since injury. They did, however, have co-existent pathology: decubiti, urinary tract infections, etc. When SCI patients with normal T3 were compared with controls, they still had depressed mean T3 levels. We conclude that LT3S occurs frequently in the chronic SCI population and suggest that depressed serum T3 levels may predispose SCI patients to sick euthyroidism in the face of minor pathologic insult.

Activities of Daily Living↗
PubMed1986

Psychosocial responses to spinal cord injury.

Spinal cord injury (SCI) is devastating both physiologically and psychologically. The psychosocial responses to SCI are the focus of this article. The following nursing diagnoses as they relate to the acute SCI population are examined in detail: disturbance in self-concept (body image, self-esteem, and role performance); powerlessness; functional grieving; and alteration in family process. Each nursing diagnosis will be explored in depth.

Adaptation, Psychological↗
PubMed1992

The rehabilitation of children with spinal cord injury.

Spinal cord injured children have special needs because of their potential for physical, intellectual, psychological and social growth. The overriding goal for comprehensive medical rehabilitation is to provide services required by the child for maximal recovery and to compensate for lost or impaired function while permitting the fullest development of potential in all areas. Because spinal cord injuries in childhood are not common, it is imperative that rehabilitation should be comprehensively coordinated and directed by a single specialist taking overall responsibility for the chronic phase of management. Rehabilitation involves the child and his family, a hospital-based and rehabilitation centre-based team and a school. Every effort must be made to prevent medical and/or physical complications that could interfere with rehabilitation or lead to greater disability.

Adolescent↗
PubMed1995

Prevalence and impact of wrist and shoulder pain in patients with spinal cord injury.

Spinal cord injury (SCI) patients experience varying degrees of wrist and shoulder pain. Previous studies indicated that 30 to 64 percent of SCI patients reported chronic shoulder pain. The purpose of this study was to identify the prevalence of chronic wrist and shoulder pain, to determine which activities caused or exacerbated the pain, and assess functional and emotional responses to chronic pain and identify ways in which the pain might be reduced. Eight hundred SCI patients were surveyed by questionnaire with 451 (66 percent) responding. In addition, 30 patients were available for clinical observation and evaluation. Data was evaluated using the Statistical Analysis System and the Cornell Personal Adjustment Scale. Results indicated that wrist and shoulder pain were more prevalent than previously indicated (72.7 percent of respondents reported some degree of chronic pain in one or both of these areas), wheelchair propulsion and transfers caused most pain and also increased the degree of pain. Patient's age, neurologic level and time since injury were not statistically significant in the study and emotional responses did not significantly vary between groups with and without pain. Further, it was noted that among the pain group, various routine therapies were not effective. We conclude that alternative methods for wheelchair propulsion and transfers, which lessen stress and cumulative trauma, need to be developed for SCI patients in order to diminish the incidence of chronic upper limb pain.

Activities of Daily Living↗
PubMed1999

Psychosocial implications of spinal cord injury.

Spinal cord injury (SCI) is a devastating event that has not only physical but also social and psychological ramifications for both the injured person and the family. Within one brief moment, a person's world will be changed forever. Like a ripple on the water, one injured family member affects the entire family system. This article will identify the social and psychological forces that impact the injured person's quality of life along with that of his or her family and the interventions that can be instituted by acute care personnel.

Adaptation, Psychological↗