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The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
A central pain stimulus should be used for motor response; peripheral pain stimuli can invoke spinal reflexes and may result in an incorrect GCS assessment. A spinal reflex is a signal that travels via a sensory nerve to the spinal cord, producing a motor response from the spinal cord back to the periphery. The impulse does not travel via the brain and is not an indicator of motor function.
Spinal Cord Injury and Cerebral Trauma
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
The initial phase following acute SCI is that of spinal shock.7 This is related to the loss or the depression of most spinal reflex activity below the level of injury.8 Spinal shock is thought to result from the sudden withdrawal of facilitatory descending input from the supraspinal tracts, which disrupts transmission at synapses and stops interneuronal conduction in the distal cord.8 The loss of skeletal reflexes leads to flaccid paralysis and the loss of deep tendon reflexes. The duration of spinal shock varies widely, from several days to several months. It is not an “all or nothing” entity but depends on the extension and completeness of the spinal lesion. However, there is no generally accepted definition of spinal shock, since there are no high-level evidence studies on this issue. Nevertheless, Ditunno et al.9 have proposed a spinal shock model, which is very helpful in understanding this phenomenon. It includes an initial phase of loss of reflexes and three subsequent recovery phases.9 In addition to the effects on skeletal muscle, spinal shock may result in NLUTD. Indeed, it was generally assumed that patients with SCI have an acontractile detrusor during the spinal shock, but very recently detrusor overactivity was found in about 6 of 10 patients within the first 40 days after SCI.10 Overall, almost two-thirds of the patients showed unfavorable urodynamic parameters that jeopardized the lower and upper urinary tracts.10
Faecal Incontinence
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
P. Ronan O’Connell, Thomas Dudding
Local spinal reflexes are thought to contract the external sphincter in response to factors that threaten continence, such as raised intra-abdominal pressure, rectal distension and rectal contraction. These reflexes are probably modulated by higher cortical centres. In patients with spinal injuries, upper motor neurone lesions abolishes voluntary control of defaecation, but the anal reflexes are preserved. In these circumstances, most patients become constipated and reflex rectal evacuation can often be achieved by self-administered suppositories, digitation or enemas. Persons with complete spinal cord injuries below the level of the conus medullaris (lower motor neuron lesions) have disruption to the sacro-spinal reflex pathways. This leads to an areflexic bowel as well as lack of innervation of the EAS. Propulsion of stool still occurs by segmental colonic peristalsis mediated by the myenteric plexus, and this often leads to unplanned evacuation of stool which cannot be retained by the lax sphincter. Patients with incomplete lesions or cauda equina syndrome may have more variable symptoms. In those with a central prolapsed disc, often the entire sacral outflow is compressed and the external anal sphincter loses all innervation leading to a gaping anus and numbness in the perineum.
Transcutaneous spinal cord stimulation effects on spasticity in patients with spinal cord injury: A systematic review
Published in The Journal of Spinal Cord Medicine, 2023
Anas R. Alashram, Elvira Padua, Manikandan Raju, Cristian Romagnoli, Giuseppe Annino
Presynaptic inhibition from homonymous and heteronymous nerves is reduced after SCI,45 thus the post-activation depression of repetitively activated Ia afferents.9,10,46 Dysfunction in these presynaptic regulatory mechanisms after SCI results in an increased excitatory neurotransmitter release from Ia afferents. It contributes to the exaggerated stretch reflexes and hypertonia associated with spasticity.9,14 The continuous generation of Ia activity in multiple roots by tSCS, especially in those containing afferents from flexor nerves, would increase the level of presynaptic inhibition distributed to Ia terminals connected with ipsilateral limb muscles.26,47,48 Further, tSCS increases spinal reflex activity through evoked Hoffmann-like reflex activity resulting from activation of proprioceptive afferents.30–32
Augmented activity of the forearm extensor muscles induced by vibratory stimulation of the palm of the hand in individuals with subacute post-stroke hemiplegia
Published in Brain Injury, 2022
Nodoka Kimura, Mamiko Sato, Yasutaka Kobayashi, Eiichi Naito
A plausible explanation for our findings of a greater activity in the forearm extensors would be the induction of the AVR (15,16). Although the mechanism underlying the AVR is not fully understood, the neural mechanism that inhibits the agonistic flexors while facilitating the antagonistic extensors could be the presynaptic inhibition of the Ia afferent terminal or recurrent inhibition by Renshaw cells (41). These synaptic connections are controlled by descending pathways from the cortical level (15), and there is no spinal reflex circuit that generates the activity of the muscle antagonistic to a vibrated muscle at the spinal cord level (42). Furthermore, the AVR might be mediated by the long loop reflexes that comprise the motor response to somatosensory stimuli via the cerebral cortex (43,44). Therefore, the findings of the present study demonstrated that the activity of the forearm extensors could be generated by top-down modulation from the central nervous system.
Altered sexual function after central neurological system trauma is reflective of region of injury; brain vs spinal cord
Published in Brain Injury, 2020
Ian J. Baguley, Hannah L. Barden, Melissa T. Nott
While data confirm the importance of identifying and addressing sexual dysfunction following trauma (2), the region in which a CNS injury occurs would be expected to influence patterns of effect. For example, at a hypothetical level, the neurosexual impact of spinal cord injury (SCI) and traumatic brain injury (TBI) should differ. In SCI, spinal cord damage may directly impact on spinal reflex pathway function (e.g., for erection or orgasm) which are unlikely to be damaged following TBI. Conversely, TBI is more likely to produce neuroendocrine abnormalities, or to affect psychological and behavioral aspects of sex and sexuality (3). As a consequence of these patterns of change, people with combined TBI and SCI (termed Dual Diagnosis or DDx in this paper) could have elements of both patterns of altered sexual function following injury. The potential for people with DDx to experience greater neurosexual dysfunction than individuals with isolated spinal or brain injuries represents a testable hypothesis.