The clinical underpinnings of two of the most common spasticity conditions, spastic cerebral palsy and multiple sclerosis, can be described as follows: in spastic diplegia, the upper motor neuron lesion arises often as a result of neonatal asphyxia, while in conditions like multiple sclerosis, spasticity is thought by some to be as a result of the autoimmune destruction of the myelin sheaths around nerve endings—which in turn can mimic the gamma amino butyric acid deficiencies present in the damaged nerves of spastic cerebral palsy children, leading to roughly the same presentation of spasticity, but which clinically is fundamentally different from the latter. Spasticity is assessed by feeling the resistance of the muscle to passive lengthening in its most relaxed state. A spastic muscle will have immediately noticeable, often quite forceful, increased resistance to passive stretch when moved with speed and/or while attempting to be stretched out, as compared to the non-spastic muscles in the same person's body (if any exist). As there are many features of the upper motor neuron syndrome, there are likely to be multiple other changes in affected musculature and surrounding bones, such as progressive malalignments of bone structure around the spastic muscles (leading for example to the scissor gait and tip-toeing gait due to ankle equinus or ankle planter flexion deformity in spastic cerebral palsy children. scissor gait is caused by spasticity of the hip adductor muscles while tip-toeing gait is caused by spasticity of the gastrocnemius-soleus muscle complex or calf musculature. Also, following an upper motor neuron lesion, there may be multiple muscles affected, to varying degrees, depending on the location and severity of the upper motor neuron damage. The result for the affected individual, is that they may have any degree of impairment, ranging from a mild to a severe movement disorder. A relatively mild movement disorder may contribute to a loss of dexterity in an arm, or difficulty with high level mobility such as running or walking on stairs. A severe movement disorder may result in marked loss of function with minimal or no volitional muscle activation. There are several scales used to measure spasticity, such as the King's hypertonicity scale, the Tardieu, and the modified Ashworth. Of these three, only the King's hypertonicity scale measures a range of muscle changes from the UMN lesion, including active muscle performance as well as passive response to stretch. Assessment of a movement disorder featuring spasticity may involve several health professionals depending on the affected individual's situation, and the severity of their condition. This may include physical therapists, physicians (including neurologists and rehabilitation physicians), orthotists and occupational therapists. Assessment is needed of the affected individual's goals, their function, and any symptoms that may be related to the movement disorder, such as pain. A thorough assessment will include analysis of posture, active movement, muscle strength, movement control and coordination, and endurance, as well as spasticity (response of the muscle to stretch). Spastic muscles typically demonstrate a loss of selective movement, including a loss of eccentric control (decreased ability to actively lengthen). While multiple muscles in a limb are usually affected in the upper motor neuron syndrome, there is usually an imbalance of activity, such that there is a stronger pull in one direction, such as into elbow flexion. Decreasing the degree of this imbalance is a common focus of muscle strengthening programs. Spastic movement disorders also typically feature a loss of stabilisation of an affected limb or the head from the trunk, so a thorough assessment requires this to be analysed as well. Secondary effects are likely to impact on assessment of spastic muscles. If a muscle has impaired function following an upper motor neuron lesion, other changes such as increased muscle stiffness are likely to affect the feeling of resistance to passive stretch. Other secondary changes such as loss of muscle fibres following acquired muscle weakness are likely to compound the weakness arising from the upper motor neuron lesion. In severely affected spastic muscles, there may be marked secondary changes, such as muscle contracture, particularly if management has been delayed or absent.
symptom of Amyotrophic lateral sclerosis
symptom of Multiple sclerosis
symptom of Myotonic dystrophy
symptom of Duchenne muscular dystrophy
symptom of Progressive supranuclear palsy
symptom of Japanese encephalitis
symptom of Myasthenia gravis
symptom of Romano–Ward syndrome