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Pathophysiology

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Recent studies indicate that, besides changes in motoneuron activation (involuntary supraspinal descending inputs and inhibited spinal reflexes etc.), changes in muscle properties also contribute to the clinical appearance of limb spasticity and rigidity, which are frequently linked symptoms. In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are generally thought to be responsible for spastic movement disorders. Therefore, most antispastic treatments are directed at the reduction of reflex activity. In recent years, researchers have noticed a discrepancy between spasticity as measured in the clinic and functional spastic movement disorders, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behaviour of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fiber, collagen tissue, and tendon properties (e.g., loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organisation. Antispastic drugs can accentuate paresis and therefore should be applied with caution in mobile individuals (Dietz & Sinkjaer 2007).

Phadke et al. (2013) completed a review of articles published between 1989 and 2012 (n=24) using the EMBASE, CINAHL, and PEDro databases. The review examined the effect of triggers on spasticity. The authors found that the quality of the studies was moderate and included non-randomized trials, randomized trials with no effect and/or low study subject numbers or case reports. The authors found that factors increasing spasticity included pregnancy, posture, cold, circadian rhythm, and skin conditions as measured via objective clinical tests. Studies that relied on individual self-reports, revealed that bowel and bladder related issues, menstrual cycle, mental stress, and tight clothing were suspected to increase spasticity. There was no literature that reported on the increase in spasticity in response to heterotopic ossification, hemorrhoids, deep vein thrombosis, fever, sleep patterns and pain and conditions, even though these are thought to increase spasticity.