PARKINSONISM

- a neurological syndrome.

EPIDEMILOGY In India there is a low prevalence of

Parkinson’s disease. We find it in Parsi community of Mumbai.

Even though we find early onset of PD and may even be seen due to mutations.

In ancient India Mucuna pruriens was in used in the treatment of PD.

But worldwide PD is found in 6 million people.

Neurological disorders reduce the quality of life.

ETIOLOGY:- They are of following types:1.primary75%

2.secondary.25%

1.Primary:

a) They may due to genetic causes. The mutation in alpha-synuclein, parkin, UCH1, DJ1, PINK1, LRKK cause PD cause oxidative stress on mitochondria. This in turn leads to nigrostriatal death.

b) Some environmental factors.

Secondary causes:-1.vascular diseases:-

2.Infectious and post infectious.Eg:- lyme disease is caused by 3 types of bacteria belonging to genus borrelia.

Neurosyphilis and AIDS. Some toxins such as Mn, cyanide,

methanol, carbon monoxide, pesticides. And some medications such as

methyldopa, CCB, lithium and dopamine depleting agents such as reserpine.

Rarely it is also due hyoparathyroidsm due to basal ganglia calcification, repeated trauma , etc.

PATHOPHYSIOLOGY:- Basal ganglia consists of:-

1.corpus sriatum(caudate nucleus and putamen).

2.Globus pallidus.

3.Substantia nigra.

*They mediate the extrapyramidal motor activity.

Basal ganglia

Extrapyramidal surface of brain:

The cerebral cortex and the substantia nigra both project towards corpus straitum.

The corpus striatum(caudate nucleus and putmen) projects into globus pallidus to thalamus and they regulates involuntary movement.

The nigro striatal neurons make motor connections to corpus striatum by 2 types of neurons which contain D1 (excitatory) and D2(inhibitory) receptors.

The D1 (excitatory) are glutaminergic and D2 (inhibitory) are GABAminergic.

D1=excitatory receptors= acetylcholine as transmitter=direct.

D2=inhibitory receptors=dopamine as transmitter=indirect.

WHAT HAPPENS IN PARKINSONISM? Inhibitory component dopamine is

deficient and its concentration on basal ganglia is low.

There is a pathological lesion in basal ganglia and corpus striatum.

This occurs due to dopaminergic neuron degeneration.

The dopamine is deficient so D2 receptors are less stimulated.

Dopamine deficiency

PICTURE SHOWING SUBSTANTIA NIGRA DEGENERATION.

As the dopaminergic neurons have their cell bodies in substantial nigra. And as the corpus striatum receives dopamine from substantia nigra degeneration of these neurons causes decrease in the functional amount of dopamine.

So eventually Parkinsonism is due to imbalance between acetylcholine and dopamine.

Normal levels of dopamine and acetylcholine balanced.

SIGNS AND SYMPTOMS:

Tremor when sitting and in rest and may be present only to one side.

Stiff muscles and aching muscles of leg, neck, face and other muscles of body.

Slow limited movement i;e bradykinesia.

Insomnia and nightmares are seen at very early stage before tremor.

Person showing Parkinson's disease symptoms.

Weakness of face and throat muscles making it harder to talk or to swallow.

Difficulty with walking called gait instability and postural instability.

COMPLICATIONS OF PARKINSON’S :

Depression and anxiety. Sexual dysfunction Sleep disorders. Urinary incontience.

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