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The Nervous SystemParkinson's disease Synonyms : Parkinsonism; Shaking Palsy Clinical features, Diagnosis, Management, Prognosis, Nutrition, Herbs, Parkinson’s disease is a
progressive degenerative disease of the basal ganglia in the CNS causing
movements disorders that occur most commonly in the elderly (around age of 60)
but it may begin in childhood or adolescence (juvenile parkinsonism). It
affects about 1% of those older than 65 and 0.5% of those older than 40, both
sexes being affected equally. In
primary Parkinson’s
disease
(the most common type) there is marked degeneration
of the dopaminergic nigrostriatal tract with unknown cause (idiopathic). The
cell bodies of this tract are located in the substantia nigra in the midbrain
and axons extend to the corpus striatum (basal ganglia). It seems that overt
symptoms of Parkinsonism appear only when more than 80% of dopaminergic
neurons have been lost. The corpus striatum is also very rich in acetylcholine
which has excitatory function (dopamine acts as an inhibitor), so it appears
than symptoms result from an imbalance between these two (insufficient
dopaminergic inhibition). Secondary parkinsonism may develop as a result of some structural brain damage (tumour, stroke, encephalitis, head trauma, chronic poisoning) although the most common cause is treatment with antipsychotic (neuroleptic) drugs which produce parkinsonism by blocking dopamine receptors throughout the brain. In other words Parkinson-like syndrome is a side effect, though reversible, of neuroleptic drugs used in treatment of schizophrenia. Clinical features: < BACK TO TOP >
The
presenting feature is usually tremor
that starts in the hands and spreads to involve arms and legs; the tremor is
maximal at rest, diminishes during voluntary activity and is absent during
sleep; it gets worse on emotional tension or fatigue.
Muscle
rigidity
is detectable as an increased resistance to passive limb movement (plastic
‘lead pipe?type of rigidity); rigidity of the facial muscles gives the
face a mask-like appearance with mouth open and diminished blinking.
Voluntary
movements (e.g., cutting food, buttoning a shirt, writing) difficult to
initiate and consequently very infrequent and slow; the terms used to describe
this phenomena are bradykinesia and hypokinesia.
Patients
find it difficult to start walking; the gait becomes shuffling with short steps, and the arms are held flexed to the
waist and do not swing.
Once
walking is in progress patients cannot quickly stop or change direction and
they may even show tendency to run to prevent falling down (festination).
Signs
of autonomic nervous system dysfunction may be present (greasy skin,
constipation, urinary hesitancy, orthostatic hypotension).
Characteristically
there is normal sensory perception, muscle strength and reflexes are
preserved. Dementia affects about 50% of patients and depression is common. Diagnosis: < BACK TO TOP >
Diagnosis
is essentially clinical since no investigation is available to confirm
parkinsonism.
Brain
CT can be carried out in patients younger than 50 to exclude brain pathology.
In
patients in 2nd and 3rd decade clinical features similar to Parkinson’s disease may be caused
by Wilson’s disease (also known
as hepato-lenticular degeneration) which is an autosomal recessive deficiency
of copper carrying protein (ceruloplasmin) in blood that leads to deposition
of copper in the liver (chronic liver disease and cirrhosis) and brain.
In
Wilson’s disease there is low blood copper level, low blood ceruloplasmin,
raised urinary copper excretion, abnormal liver function tests and usually
copper deposits at corneo-scleral junction (greenish-brown Kayser-Fleischer
rings).
It is
important to avoid confusion of Parkinson’s disease with essential
tremor which is a benign hereditary condition (probably autosomal
dominant) that tends to increase with age (the reason why it is sometimes
incorrectly called senile tremor). Essential tremor characteristically increases with movements, and there are no movements disorders nor disorders of gait. Management < BACK TO TOP >
Drugs
used in treatment of parkinsonism act by counteracting deficiency of dopamine
in the basal ganglia or by blocking acetylcholine on muscarinic receptors. The most effective drug is levodopa, a dopamine precursor that easily passes the blood-brain barrier, where it is decarboxylated to dopamine. Levodopa is effective in most patients initially, bradykinesia/hypokinesia and rigidity are helped most, although tremor is often substantially reduced.
Efficacy of levodopa may be improved by combination with
peripheral decarboxylase inhibitors carbidopa [these combinations are
Sinemet, Kinson, Sinacarb] or benseraside [this combination is Madopar]. The main drugs in group of muscarinic antagonists are benzatropine [Cogentin], benzhexol [Artane], biperiden [Akineton] and procyclidine [Kemadrin] and they are usually given to supplement levodopa preparations. Other drugs are bromocriptine [Parlodel, Kripton, Bromohexal, Bromolactin], pergolide [Permax] and cabergoline [Cabaser] (drugs that directly activate dopamine receptors in the basal ganglia - dopamine agonists) and selegiline [Eldepryl, Selgene] (a monoamine oxidase type B inhibitor that reduces metabolism of dopamine in the brain and potentiates the actions of levodopa). Wilson’s disease is treated with penicillamine [D-Penamine] which binds copper, and the combined complex is soluble, passing out of the body via the kidneys. Prognosis < BACK TO TOP >
Nutrition < BACK TO TOP > Nutrition that alleviate or prevent Parkinson's disease :- Herbs < BACK TO TOP > Herbs that alleviate or prevent Parkinson's disease :- (source : -) |
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