So today I went to visit Dr. McKee at the Cleveland Clinic. Dr. McKee is the spasiticity doctor.
Spasticity is a feature of altered skeletal muscle performance in muscle tone involving hypertonia; it is also referred to as an unusual "tightness", stiffness, and/or "pull" of muscles.
Clinically spasticity is defined as velocity dependent resistance to stretch, where a lack of inhibition results in excessive contraction of the muscles, ultimately leading to hyperflexia (overly flexed joints). It mostly occurs in disorders of the central nervous system (CNS) impacting the upper motor neuron in the form of a lesion, such as spastic diplegia, but it can also present in various types of multiple sclerosis, where it occurs as a symptom of the progressively-worsening attacks on myelin sheaths and is thus unrelated to the types of spasticity present in neuromuscular cerebral palsy rooted spasticity disorders.
Precise cause aside, whenever there is a loss of muscle tone inhibition from the brain to the spinal cord such that muscles become overactive, this loss of inhibitory control can cause an ongoing level of contraction, with decreased ability for the affected individual to volitionally control the muscle contraction, and increased resistance felt on passive stretch.
The clinical underpinnings of two of the most common spasticity conditions, spastic diplegia 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 diplegics, leading to roughly the same presentation of spasticity, but which clinically is fundamentally different from the latter.
Overall, a defining feature of spasticity is that the increased resistance to passive stretch is velocity-dependent. Lance (1980) describes it this way: “...a motor disorder, characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex as one component of the upper motor neurone (UMN) syndrome”.[citation needed] Strangely, however, rather than being in the motor nerves as might be assumed to be the case, spasticity actually stems from the sensory nerves.[citation needed]
Spasticity is found in conditions where the brain and/or spinal cord are damaged or fail to develop normally; these include cerebral palsy, multiple sclerosis, spinal cord injury and acquired brain injury including stroke. Muscles affected in this way have many other potential features of altered performance in addition to spasticity, including muscle weakness; decreased movement control; clonus (a series of involuntary rapid muscle contractions often symptomatic of muscle over-exertion and/or muscle fatigue); exaggerated deep tendon reflexes; and decreased endurance.

Looking back on his past observations, I am showing improvement.  Improving in strength and tone. The walking time is still a meer 20 seconds in a 10 foot stretch. So my career as an Olympic sprinter is still far from reality.

I can even feel the improvement by longer times standing in the kitchen for one. So I guess its safe to say I wont be cutting my thumb off using my clever. Now if only the double vision can be decreased or even fixed!

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