TL;DR: If the organism is severely damaged by acute non-specific nocuous agents such as exposure to cold, surgical injury, production of spinal shock, excessive muscular exercise, or intoxications with sublethal doses of diverse drugs, a typical syndrome appears, the symptoms of which are independent of the nature of the damaging agent or the pharmacological type of the drug employed.
Abstract: EXPERIMENTS on rats show that if the organism is severely damaged by acute non-specific nocuous agents such as exposure to cold, surgical injury, production of spinal shock (transcision of the cord), excessive muscular exercise, or intoxications with sublethal doses of diverse drugs (adrenaline, atropine, morphine, formaldehyde, etc.), a typical syndrome appears, the symptoms of which are independent of the nature of the damaging agent or the pharmacological type of the drug employed, and represent rather a response to damage as such.
TL;DR: There is a need for a better understanding of the syndrome of spasticity as well as the development of a valid and reliable assessment tool.
Abstract: Symptoms of spasticity are often experienced by individuals with spinal cord injury (SCI) following a period of spinal shock and, in many cases, these symptoms negatively affect quality of life. Despite its prevalence, spasticity as a syndrome in the SCI population is not always managed effectively. This is likely due to the fact that the syndrome can have various presentations, each with their own specific etiology. This overview summarizes the symptoms and pathophysiology of the various presentations of spasticity in the SCI population and discusses the currently accepted management techniques. There is a need for a better understanding of the syndrome of spasticity as well as the development of a valid and reliable assessment tool.
TL;DR: The historical background is provided followed by a description of a novel four-phase model for understanding and describing spinal shock, and clinical implications of the model are discussed.
Abstract: Spinal shock has been of interest to clinicians for over two centuries. Advances in our understanding of both the neurophysiology of the spinal cord and neuroplasticity following spinal cord injury have provided us with additional insight into the phenomena of spinal shock. In this review, we provide a historical background followed by a description of a novel four-phase model for understanding and describing spinal shock. Clinical implications of the model are discussed as well.
TL;DR: The late decrease in M-wave and flexor reflex amplitude in paraplegic patients suggests a secondary impairment/degeneration of premotoneuronal circuits and of motoneurons in patients with spinal cord injury.
Abstract: Objective: To investigate the adaptational changes in excitability of spinal neuronal circuits below the level of lesion from spinal shock to spasticity in patients with spinal cord injury (SCI). Methods: More than 6 months after an acute SCI, clinical follow-up examinations were paralleled by electrophysiologic recordings with tibial nerve stimulation (M-wave, F-wave, H-reflex, and flexor reflex). Results: During spinal shock, the loss of tendon tap reflexes and flaccid muscle tone were associated with low persistence of F-waves and loss of flexor reflexes, whereas H-reflexes were already elicitable. During the transition to spasticity , the reappearance of tendon tap reflexes and muscle tone and the occurrence of spasms was associated with the recovery of F-waves and flexor reflex excitability, whereas the H-to-M ratio remained about stable over months. At later stages (2 to 6 months after SCI) when clinical signs of spasticity became established, the electrophysiologic measures showed little change. In paraplegic patients, in contrast to tetraplegic patients, M-wave and flexor reflex amplitudes even decreased. Conclusions: The late decrease in M-wave and flexor reflex amplitude in paraplegic patients suggests a secondary impairment/degeneration of premotoneuronal circuits and of motoneurons. The divergent course of clinical signs of spasticity and their probable neuronal correlates indicates the occurrence of non-neuronal changes contributing to spasticity.
TL;DR: For patients with injury to bone and/or ligaments, the initial focus should be spinal immobilization and prevention of inducing injury to the spinal cord.