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Spinal Shock
Published in Kelechi Eseonu, Nicolas Beresford-Cleary, Spine Surgery Vivas for the FRCS (Tr & Orth), 2022
Kelechi Eseonu, Nicolas Beresford-Cleary
The most likely diagnosis is spinal shock. This is a sudden and reversible loss of neurological function, including reflexes, rectal tone, and muscle tone below the level of an acute spinal cord injury (SCI). It is characterised by flaccid areflexic paralysis, bradycardia, hypotension (due to a loss of sympathetic tone) and an absent bulbocavernosus reflex (characterised by involuntary anal sphincter contraction in response to squeezing the glans penis/clitoris or tugging on an indwelling Foley catheter).
Spinal Injuries
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
For each mechanism of injury described earlier, there may be complete or incomplete (partial) cord injury. The distinction between complete and incomplete cord injury cannot, however, be made until the patient has recovered from spinal shock. Spinal shock is defined as the complete loss of all neurological function, including reflexes, anal tone and autonomic control, below the level of spinal cord injury. Spinal shock is unrelated to hypovolaemia or neurogenic shock and is effectively spinal concussion. It usually involves a period of 24–72 hours of complete loss of sensory, motor and segmental reflex activity with flaccid paralysis and areflexia below the level of the injury. Despite this profound paralysis, areas of the cord are still capable of a full recovery. Therefore, assessment of neurological status (ASIA Score) for outcome prediction reasons must be done after this period.
Pathophysiology of Spinal Shock
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Siobhán M. Hartigan, Elizabeth A. Rourke, Roger R. Dmochowski
Following initial injury to the spinal cord, a cascade of events occurs that results in complete/permanent injury. The initial clinical scenario in acute spinal shock, occurring within minutes of the primary injury, is due to compromise of motor, sensory, and autonomic systems resulting in flaccid paralysis, areflexia (absent somatic activity), and autonomic dysfunction driven by neurogenic shock.4 Spinal cord shock can last days to weeks (typically 4–12 weeks) following the primary injury with studies demonstrating spinal cord edema at its peak around 3 days after injury.5,6
Nurses and physiotherapists’ knowledge levels on autonomic dysreflexia in a rehabilitation hospital
Published in The Journal of Spinal Cord Medicine, 2023
Autonomic dysreflexia (AD) is a clinical condition that occurs mostly through uncontrollable sympathetic activity that is triggered by a sensory stimulus in patients with spinal cord injuries. AD, which can develop as a result of stimulation below the lesion level in cutaneous or visceral organs, is frequently observed with lesions above the T6 level, but can also occur in lesions up to T10. Several causes may trigger AD attacks; bladder distention and/or irritation are responsible for 80% of cases.3–6 Although AD characteristically occurs after the spinal shock period at the chronic phase of the injury, it can also occur in any time following the injury. The first attack is usually observed within approximately six months following the SCI, however, it can be observed in 5.2% of cases within the first month.8,9
Factors influencing thigh muscle volume change with cycling exercises in acute spinal cord injury – a secondary analysis of a randomized controlled trial
Published in The Journal of Spinal Cord Medicine, 2022
Maya G. Panisset, Doa El-Ansary, Sarah Alison Dunlop, Ruth Marshall, Jillian Clark, Leonid Churilov, Mary P. Galea
Spinal cord injury (SCI) results in substantial muscle atrophy below the neurological lesion, with significant repercussions for functional recovery and longer-term health.1 The acute physiological response to traumatic SCI involves a period of spinal shock, which may take some weeks to resolve.2 The combination of flaccid paralysis and decreased activity in the acute period causes rapid atrophy of skeletal muscle tissue. Loss of 33–45% of thigh muscle cross-sectional area (CSA) occurs as early as six weeks after SCI.3 Further atrophy (27–56%) has been reported from 6–24 weeks in patients with complete lesions.4 Atrophy occurring prior to neurological recovery may delay functional outcomes, as muscle strength must be regained.5 In animal studies, wheelchair immobilization in the first few weeks post-injury was associated with ongoing deficits in stepping behavior and coordination for months after re-mobilization.6 On the other hand, sensory feedback from rhythmic limb movement during locomotor training and cycling exercise in animal studies is thought to drive improvements in functional recovery after SCI via promotion of exercise-dependent neuroplasticity.7 Another study found that muscle to body weight ratios were maintained in both the plantaris and soleus muscles with four weeks of passive cycling (PC), initiated one week after injury in rats.8
Inspiratory muscle training is feasible and safe for patients with acute spinal cord injury
Published in The Journal of Spinal Cord Medicine, 2019
The annual incidence of traumatic spinal cord injury (SCI) is approximately 15 per million in Australia, 16 per million in western Europe and 39 per million in North America.1,2 Of the injuries recorded in Australia, 53% involved cervical segments and 32% thoracic segments, with incidences of 15% and 19% for complete tetraplegia and thoracic paraplegia respectively.3 Respiratory complications are a leading cause of morbidity and mortality in the SCI population as a result of denervation of the inspiratory and expiratory respiratory muscles.4–11 The risk of respiratory complications is further increased by the autonomic dysfunction associated with the initial period of spinal shock post-SCI, resulting in mucus hypersecretion, bronchoconstriction, bradycardia and hypotension.7,8 This predisposes patients with SCI to atelectasis, sputum retention, respiratory infection and ultimately respiratory failure.6,8,10–14