Sunday, January 12, 2014
Living with parkinsons
This is a personal recount from a neurologist and how he found out that he had parkinsons disease.
Saturday, January 11, 2014
Parkinson's disease and dopamines role
Parkinson’s disease is a liberal neurological
disorder which affects the motor system and thus individual’s ability to move. It
is caused by the slow progressive degradation of neurons due to either genetic
or environmental effects and the lack of dopamine in the substantia nigra of
the brain. Dopamine is a neurotransmitter essential for the transfer of
neuronal signals from the brain to the spinal cord and eventually to the
appropriate muscles in the body. The shortage of dopamine in patients suffering
Parkinson’s disease thus leads to the impairment of their muscular function.
Dopamine is produced from the conversion of L-tyrosine through the intermediate product dihydroxyphenylalanaine (L-DOPA) in step-wise process catalyzed by specific enzymes. This process occurs in the dopaminergic neurons of substantia nigra.
The following shows the complete 2-step reactions
of dopamine production.
1) Catalysed by tyrosine 3-monooxgenase
L-tyrosine + THFA + O2 + Fe2+ → L-dopa
+ DHFA + H2O + Fe2+
2)
Catalysed by dopa decarboxylase
L-dopa
+ pyridoxal phosphate → dopamine +
pyridoxal phosphate + CO2
Signs of parkinson's
Excessive and unconscionable muscle
contractions are usually the initial symptoms of Parkinson’s disease. They
develop as the activity of dopaminergic neurons decreases. Also, the symptoms
and their severity differ from patient to patient.
Typical symptoms include:
o Tremor; Most apparent symptom and occurs in various parts of
the body, most commonly in the hand and fingers. May be diminished when rigidity
(another symptom) becomes severe.
o Rigidity; stiffness and constraint in the muscles leading to
pain in rigid areas as the continual contraction of the muscles proceeds.
o Hypokinesia; Difficulty to make movements especially small
movements (due to the reduced muscle movement in the limbs, one side or the
whole of the body) with the occurrence of pauses. Other stages include
Bradykinesia when muscles react slowly, hence slower movements and akinesia
when there is a loss of movement. Hyphophonia is another symptom whereby the
individual has soft voice due to the lack of coordination of the vocal muscles.
o Flexion of trunk; affecting and reducing the motility of
muscles around the oesophagus (spasms), small intestine, and stomach results in
constipation. In severe condition, posture of the body may be disturbed such as
the neck and shoulder are bent at a right angle respective to the trunk.
Festination occurs overtime.
o Urinary incontinence; loss control of urogenital muscles and
only develops in later stage of Parkinson’s disease. May lead to incompetence
o Lewy bodies; aggregation of protein inside neurons which
indicates cellular damage is occurring. Besides Parkinson’s disease, Lewy
bodies are also associated with dementia and other disorders.
Other
disorders such as depression, dementia, dystonia, and sleep disturbances may
also develop together with Parkinson’s disease.
Aldehyde dehydrogenase as neuronal protection
Although little is known about their role in
Parkinson’s disease however recent studies conducted show that there are
alterations of ALDH 1A1expression in the brain (substantia nigra) of
individuals with Parkinson’s disease. The level of activity of ALDH 2 was also
found to be abnormal in patients suffering the disease. Scientists are
currently doing more research on the basis of the unusual ALDH activity in
patients with Parkinson’s disease in hope that it could become the solution for
improved and more accurate diagnosis of the disease.
How can we treat parkinsons?
There are currently no cures for the loss of neurons in
individuals with Parkinson’s disease. Treatments are available only for the
symptoms of the disease.
Combination
of the drug Levodopa (L-dopa) with carbidopa is the most efficient treatment
that helps increase the conversion of L-dopa into dopamine in the brain while
minimising the side effects of Levodopa such as nausea. Such drug treatment could
last within 4 to 6 years as the effects of the drug will begin to subside (ie. Drug
dose becomes effective for shorter period of time that gradually wears off).
Symptoms of the disease such as tremor, muscle spasms of the neck, eyes and jaw
would then reappear again. Patients may choose to increase the dosage of the
drug however this comes with risky effects of dyskinesia.
Alternative drugs include:
·
Dopamine agonists – “imitates” the action of
dopamine in neurons of the brain. Although they are not as efficient as
levodopa, they do not wear off easily and last longer in the brain.
·
MAO B (Monoamine Oxidase B) inhibitors- Prevent
the breakdown of dopamine in brain caused by MAO B to slow down the loss of the
neurotransmitter. Side effect are in most cases are mild
·
Amantadine- Alleviate the effects of dyskinesia
and early mild symptoms of Parkinson’s disease. Usually prescribed together
with Levodopa-carbidopa.
Another
costly method is through a surgical procedure known as deep brain stimulation
(DBS). Electrodes are implanted within the body of the patient and are
connected with the generator in the chest. This allows electrical signals to
reach the brain and prevents the occurrence of the symptoms. DBS is usually
conducted to patients suffering from the later stages of Parkinson’s disease
(levodopa is no longer effective).
Fun Facts!
Find out if you have parkinsons with a phone call!
Famous people with parkinsons disease!
( P.S. if you are using an ad blocker, you will have to turn it off temporarily)
Subscribe to:
Posts (Atom)