![]() This will be apparent from the variable mechanisms of actions of anti-spasticity agents used in clinical practice. It seems highly likely that multiple mechanisms are operative in causation of human spasticity, many of which still remain to be fully elucidated. While simply speaking the increased muscle stretch reflex may be assumed to be due to an altered balance between the innervations of intra and extrafusal fibers in a muscle caused by loss of inhibitory supraspinal control, the delayed onset after lesion and the frequent reduction in reflex excitability over time, suggest plastic changes in the central nervous system following brain or spinal lesion. It is highly likely that in humans, reduction of spinal inhibitory mechanisms (in particular that of disynaptic reciprocal inhibition) is involved. The reflex hyperexcitability develops over variable period of time following the primary lesion (brain or spinal cord) and involves adaptation in spinal neuronal circuitries caudal to the lesion. The key to the increased excitability of the muscle stretch reflex (muscle tone) is the abnormal activity of muscle spindles which have an intricate relation with the innervations of the extrafusal muscle fibers at the spinal level (feed-back and feed-forward circuits) which are under influence of the supraspinal pathways (inhibitory and facilitatory). Clinically spasticity manifests as an increased resistance offered by muscles to passive stretching (lengthening) and is often associated with other commonly observed phenomenon like clasp-knife phenomenon, increased tendon reflexes, clonus, and flexor and extensor spasms. Spasticity, a classical clinical manifestation of an upper motor neuron lesion, has been traditionally and physiologically defined as a velocity dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex. Department of Neurology, Vivekananda Institute of Medical Sciences, Kolkata, India.Users should refer to the original published version of the material for the full abstract.Angshuman Mukherjee and Ambar Chakravarty* No warranty is given about the accuracy of the copy. However, users may print, download, or email articles for individual use. Copyright of Experimental Brain Research is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission.The data also indicate the need to use age-matched control subjects when comparing individuals with abnormalities resulting from disorders that occur at an old age. Activation of agonist and antagonist muscle pairs are most likely organized around a dual system of cortically and spinally mediated reciprocal inhibition that is altered by age. These data confirm the existence of cortical reciprocal inhibition reported previously in young humans and show that age reduces this inhibition similarly to the previously reported reduction of spinal reciprocal inhibition reported in old adults. The MEPs remained at control level in the FCR and were also unaffected in the first dorsal interosseus. The age by conditioning interval interaction ( P=0.001) showed that the MEPs in the ECR were significantly depressed at 14, 15, 16, 17, 18, and 19 ms (range 55.5-65.9% of control, all P<0.05) compared with control value of 100% and with old adults who showed no depression. The size of the control MEP in the ECR was also similar in young (0.98☐.10 mV) and old subjects (0.90☐.14 mV, P=0.686). The absolute TMS intensity, expressed as the percent of stimulator output, used to produce 1-mV control MEPs in the ECR was similar in young (mean 58.5, standard deviation ☑2.8%) and old adults (60.3☒0.3%, P=0.855). The test stimulus, delivered by transcranial magnetic stimulation (TMS) at 1-ms increments between 11 and 24 ms after the electrical conditioning stimulus, evoked motor potentials (MEP) in the extensor carpi radialis (ECR) and flexor carpi radialis (FCR). In young (age 27, n=6) and old (age 73, n=6) adults a mild conditioning electrical stimulus was delivered to the median nerve at the elbow. We examined the possibility that age also modifies cortical reciprocal inhibition. A widely observed age-related adaptation is the heightened activation of the antagonist muscles during voluntary movements. Abstract: Age alters the control of voluntary movement.
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