Spasticity is a muscle control disorder that is characterized by tight or stiff muscles and an inability to control those muscles. In addition, reflexes may persist for too long and may be too strong (hyperactive reflexes).
Spasticity is caused by an imbalance of signals from the central nervous system (brain and spinal cord) to the muscles. This imbalance is often found in people with cerebral palsy, traumatic brain injury, stroke, multiple sclerosis, and spinal cord injury.
The cause of spasticity is not really known, but there are several theories. In general, spasticity develops when an imbalance occurs in the excitatory and inhibitory input to α motor neurons caused by damage to the spinal cord and/or central nervous system. The damage causes a change in the balance of signals between the nervous system and the muscles, leading to increased excitability in muscles.
One factor that is thought to be related to spasticity is the stretch reflex. This reflex is important in coordinating normal movements in which muscles are contracted and relaxed and in keeping the muscle from stretching too far. Although the end result of spasticity is problems with the muscles, spasticity is actually caused by an injury to a part of the central nervous system (the brain or spinal cord) that controls voluntary movements. The damage causes a change in the balance of signals between the nervous system and the muscles. This imbalance leads to increased activity (excitability) in the muscles. Receptors in the muscles receive messages from the nervous system, which sense the amount of stretch in the muscle and sends that signal to the brain. The brain responds by sending a message back to reverse the stretch by contracting or shortening.
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. Damage to the CNS as a result of stroke or spinal cord injury, alter the of peripheral nerves in the affected region. This change in input to bodily structures tends to favor excitation and therefore increase nerve excitability. CNS damage also causes nerve cell membranes to rest in a more state. The combination of decreased inhibition and an increased depolarized state of cell membranes decreases action potential threshold for nerve signal conduction, and thus increases the activity of structures innervated by the affected nerves (spasticity). 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.
- exaggerated deep tendon reflexes decreased endurance.
- decreased endurance.
Program for reducing spasticity
- Coral-Mine – 30 ml of water per 1 kg of weight (per day).
- H-500 – one capsule 2 times daily with a meal.
- Coral-Magnesium – one capsule 3 times daily with a meal.
- MindSet – one capsule 2 times daily with a meal.
- Folic Acid – one capsule 2 times daily with a meal.
- Griffonia – two capsules 2 times daily with a meal (in the first half of the day).
- Potassium – PentoKan, ApricoTabs (not in all regions available) 2 tablets 2 times daily. More potassium is found in Ultimate, 24/7 complex.
- B vitamins complex can be found in products such as TASTY B, Spirulina, Coral-Lecithin, Over 30, Daily Delicious Beauty Shake.
This program helps to reduce spasticity (I use the program myself).
Note: It is very important in parallel to do exercise – to train limited movements.
How to buy the products?
Acquisition of products is possible using a special discount card (free registration here).
After registration, you receive the number of the discount card, which will give you a 20% discount (for an unlimited period of time) for all products, purchasing in one of the Coral Club stores or on the Internet.