Parkinson’s disease презентация

Syed Baseeruddin Alvi (09)

resting tremor, rigidity, flexed posture, “freezing,” and loss of postural reflexes.
Studied and discovered by James Parkinson (1817) which he called the shaking palsy and by the Latin term paralysis agitans.
Pathology shows loss of neuromelanin-containing monoamine neurons, particularly dopamine (DA) neurons in the substantia nigra pars compacta.

monoamine neurons.
The loss of DA content in the nigrostriatal neurons accounts for many of the motor symptoms which is due to neuronal degradation
Six cardinal clinical features of parkinsonism:

or no functional impairment

Stage 2:
Bilateral or midline involvement, without balance impairment

Stage 3:
Impairment of righting reflex

Stage 4:
Fully developed and severely disabling

Stage 5:
Confinement to bed or wheel chair.

of dopamine, is the single most effective agent in the treatment of PD .
It is inert both therapeutic & adverse effects are due to decarboxylation , central and peripheral respectively .
In practice it is always administered in combination with peripherally acting inhibitor of aromatic L-amino acid decarboxylase ( carbidopa , benserazide)

muscles
muscular spasms most often affecting the tongue, jaw, eyes, and neck
mental changes, such as depression, psychotic episodes, paranoia, and suicidal tendencies.
less serious adverse reactions include anorexia, nausea, vomiting, abdominal pain, dry mouth, difficulty in swallowing, increased hand tremor, headache, and dizziness.

excess in Parkinson’s disease) in the CNS. Drugs with anticholinergic activity are generally less effective than levodopa.

Other adverse reactions may include skin rash, urticaria urinary retention, tachycardia, muscle weakness, disorientation, and confusion.

COMT inhibitors:

These drugs prolong the effect of levodopa by blocking (COMT). When given with levodopa, the COMT inhibitors increase the plasma concentrations and duration of action of levodopa.

fever
Other adverse reactions are orthostatic hypotension, sleep disorders, excessive dreaming, and muscle cramps

Dopamine receptor agonists (non ergot):

It is thought that these drugs act directly on postsynaptic dopamine receptors of nerve cells in the brain, mimicking the effects of dopamine in the brain.

disturbances, abnormal involuntary movements, and headache.

Selective MAO-B Inhibitors:

By interfering with one of the enzymes that break down dopamine (monoamine oxidase, or MAO-B), they can enhance and prolong the effect of each dopamine molecule.