The nervous system
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella in Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
A reflex is initiated by the stimulation of a sensory receptor located at the peripheral end of an afferent or first-order sensory neuron. This afferent neuron transmits impulses to the gray matter of the spinal cord, which serves as an integrating center for the sensory input. It is within the gray matter that the afferent neuron will synapse with a neuron. When the afferent neuron synapses directly with an efferent or motor neuron, it forms a monosynaptic reflex. An example of this type of reflex is the stretch reflex. When the afferent neuron synapses with an interneuron, which then synapses with the motor neuron, it forms a polysynaptic reflex. An example of this type of reflex is the withdrawal reflex. Most reflexes are polysynaptic. The motor neuron then exits the spinal cord to innervate an effector tissue that carries out the reflex response.
Spinal Cord Injury and Cerebral Trauma
Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg in 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
Physiology of Micturition
Linda Cardozo, Staskin David in Textbook of Female Urology and Urogynecology - Two-Volume Set, 2017
Figure 23.5 Voiding reflexes. At the initiAtion of micturition, intense vesicAl Afferent Activity ActivAtes the brAinstem micturition center, which inhibits the spinAl guArding reflexes (sympAthetic And pudendAl outflow to the urethrA). The pontine micturition center (PMC) Also stimulAtes the pArAsympAthetic outflow to the blAdder And internAl sphincter smooth muscle. MAintenAnce of the voiding reflex is through Ascending Afferent input from the spinAl cord, which mAy pAss through the periAqueductAl grAy (PAG) mAtter before reAching the PMC. Afferent pAthwAy (colored dAshed line) from the detrusor ActivAtes spinAl reflex mechAnisms thAt induce firing in the somAtic cholinergic nerves to the externAl urethrAl sphincter (eus), sympAthetic Adrenergic nerves to the urethrAl smooth muscle, And cholinergic And nitrergic nerves to the urethrAl smooth muscle. bulbospinAl pAthwAys from the brAin cAn modulAte these spinAl reflex mechAnisms. urethrAl Afferents (blAck dAshed line) ActivAted by urine flowing through urethrA cAn further fAcilitAte pArAsympAthetic efferent outflow to the detrusor to complete voiding by meAns of A suprAspinAl pAthwAy pAssing through the PMC As well As A spinAl reflex pAthwAy. ACh, Acetylcholine; nePI, norepinephrine; no, nitric oxide; excitAtory (+) And inhibitory (-) mechAnisms.
Effect of inhibitory kinesiotaping on spasticity in patients with chronic stroke: a randomized controlled pilot trial
Published in Topics in Stroke Rehabilitation, 2022
Mahdad Mehraein, Zahra Rojhani- Shirazi, Ahmad Zeinali Ghotrom, Nasrin Salehi Dehno
In a recent study by Puce et al. (2021), the effect of KT on knee extensor spasticity was investigated in para-swimmers.54 In line with our study, they reported a significant decrease in the amplitude of stretch reflex 48 hours after KT, but MAS score did not change following KT.54 Despite the similarity between our results, they examined athletes and measured spasticity by stretch reflex. The H-reflex and stretch reflex have the same spinal circuitry.55 However, for H-reflex, Ia afferent axons are excited electrically and stretch reflex is elicited by the mechanical stimulation of group Ia and II afferent axons.55 Hence, our study is the first to highlight the specific effect of KT on the reflex component of muscle tone, which is spasticity in patients with stroke.
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
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.
Related Knowledge Centers
- Action Potential
- Alpha Motor Neuron
- Gamma Motor Neuron
- Muscle Contraction
- Muscle Spindle
- Reflex
- Spinal Nerve
- Spinal Cord
- Skeletal Muscle
- Golgi Tendon Reflex