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Parkinson’s disease and parkinsonism

Parkinson disease (PD) is a progressive movement disorder marked by tremors, rigidity, slow movements (bradykinesia), and posture instability. It occurs when cells in one of the movement-control centers of the brain begin to die for unknown reasons. In Ayurveda Parkinson’s disease is called as Kampavata. It existed in ancient time and was called Kampavata. This was over 4500 years ago even though the disease acquired its present name from James Parkinson who redescribed the disease in 1817 A.D.

Usually beginning in a person's late fifties or early sixties, Parkinson disease causes a progressive decline in movement control, affecting the ability to control initiation, speed, and smoothness of motion. Symptoms of PD are seen in up to 15% of those ages 65-74, and almost 30% of those ages 75-84.
Most cases of PD are sporadic. This means that there is a spontaneous and permanent change in nucleotide sequences (the building blocks of genes). Sporadic mutations also involve unknown environmental factors in combination with genetic defects. The abnormal gene (mutated gene) will form an altered end-product or protein. This will cause abnormalities in specific areas in the body where the protein is used. Some evidence suggests that the disease is transmitted by autosomal dominant inheritance. This implies that an affected parent has a 50% chance of transmitting the disease to any child. This type of inheritance is not commonly observed. The most recent evidence is linking PD with a gene that codes for a protein called alpha-synuclein. Further research is attempting to fully understand the relationship with this protein and nerve cell degeneration.

Causes and symptoms
The immediate cause of PD is degeneration of brain cells in the area known as the substantia nigra, one of the movement control centers of the brain. Damage to this area leads to the cluster of symptoms known as "parkinsonism." In PD, degenerating brain cells contain Lewy bodies, which help identify the disease. The cell death leading to parkinsonism may be caused by a number of conditions, including infection, trauma, and poisoning. Some drugs given for psychosis, such as haloperidol (Haldol) or chlorpromazine (thorazine), may cause parkinsonism. When no cause for nigral cell degeneration can be found, the disorder is called idiopathic parkinsonism, or Parkinson disease. Parkinsonism may be seen in other degenerative conditions, known as the "parkinsonism plus" syndromes, such as progressive supranuclear palsy.
There are some known toxins that can cause parkinsonism, most notoriously a chemical called MPTP, found as an impurity in some illegal drugs. Parkinsonian symptoms appear within hours of ingestion, and are permanent. MPTP may exert its effects through generation of toxic molecular fragments called free radicals, and reducing free radicals has been a target of several experimental treatments for PD using antioxidants.
It is possible that early exposure to some as-yet-unidentified environmental toxin or virus leads to undetected nigral cell death, and PD then manifests as normal age-related decline brings the number of functioning nigral cells below the threshold needed for normal movement. It is also possible that, for genetic reasons, some people are simply born with fewer cells in their substantia nigra than others, and they develop PD as a consequence of normal decline.

The identifying symptoms of PD include:
• Tremors, usually beginning in the hands, often occuring on one side before the other. The classic tremor of PD is called a "pill-rolling tremor," because the movement resembles rolling a pill between the thumb and forefinger. This tremor occurs at a frequency of about three per second.
• Slow movements (bradykinesia) occur, which may involve slowing down or stopping in the middle of familiar tasks such as walking, eating, or shaving. This may include freezing in place during movements (akinesia).
• Muscle rigidity or stiffness, occuring with jerky movements replacing smooth motion.
• Postural instability or balance difficulty occurs. This may lead to a rapid, shuffling gait (festination) to prevent falling.
• In most cases, there is a "masked face," with little facial expression and decreased eye-blinking.
In addition, a wide range of other symptoms may often be seen, some beginning earlier than others:
• depression
• speech changes, including rapid speech without inflection changes
• problems with sleep, including restlessness and nightmares
• emotional changes, including fear, irritability, and insecurity
• incontinence
• constipation
• handwriting changes, with letters becoming smaller across the page (micrographia)
• progressive problems with intellectual function (dementia)

Ayurvedic Remedies:
In ayurveda the remedies include plants ontaining sources such as the seeds of Mucuna pruriens (Kauso). Vincia faba, the same chemical compound that has been used for Parkinson’s disease in the last 30 years. Seeds of Datura stramonium have an anticholinergic effect, similar to Artane and Cogentin. Banisterine from Banisteria caapi and Nicotiana tabacum has monoamine oxidase inhibitor that is similar to selegiline (deprenyl).
Mucuna is a twiner with trifoliate leaves, purple flowers, and turgid S-shaped pods covered with hairs that cause intense itching on contact with the skin. The plant belongs to the family Leguminosae, which is indigenous to India and has long been used in Ayurveda since ancient times. Overdose effects of Mucuna were also recognized in Ayurveda. These included headache, dystonia, fatigue, tremor, syncope, and thirst. Many of these could also occur from synthetic L-DOPA. In the modern times, two Indian scientists isolated L-DOPA from Mucuna in 1936 and published their results. However, at that time the role of L-DOPA in Parkinson’s was not known, hence not much attention was given to the discovery. Subsequently, when dopamine deficiency was linked to Parkinson’s disease in the 1960’s, scientists got interested in finding a source of L-DOPA for treatment of Parkinson’s disease. Because, the presence of L-DOPA was known to be present in the legume, initial attention was paid to extract levodopa from various Mucuna seeds and in fact, over a thousand plants were screened for the high content of L-DOPA. As L-DOPA was synthesized, further work on extraction of L-DOPA from beans was abandoned.

Other Ayurvedic Preparations:
Chaturbhuj Ras: 125 to 250 mg
Kaunch Churna:  2 to 5 gm

Yoga, Exercise and physical therapy
Regular, moderate exercise and Yoga has been shown to improve motor function without an increase in medication for a person with PD. Exercise helps maintain range of motion in stiff muscles, improve circulation, and stimulate appetite. An exercise program designed by a physical therapist has the best chance of meeting the specific needs of the person with PD. A physical therapist may also suggest strategies for balance compensation and techniques to stimulate movement during slowdowns or freezes

by Dr Raja Ram Dhungana

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