PARKINSON’S DISEASE (PD)

Presented by – pankaj singh

History In western medical litreture it was discovered by the

physician Golen as shaking palsy in 175 A.D IN 1817 A detailed medical essay was published on the

subject by london doctor James parkinson Jean martin charcot was the first to truely recognise the

importance of docter james parkinson and renamed the disease which was formerly known paralysis agitans or shaking palsy after him

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DEFINITION

Involuntary tremulous motion, with

lessened muscular power, in parts not

in action and even when supported;

with a propensity to bend the trunk

forward, and to pass from a walking to

a running pace: the senses and intellect

being uninvolved (1817)

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Parkinsonism and parkinsons disease(idiopathic)

Parkinsonism is a clinical syndrome charecterised primarly by bradinesia with associated increased tone (rigidity)tremors and loss of postural reflexes .there are many causes but most common is parkinsons disease

When parkinsonism feature are present in a person without any established etiology it is called parkinsons disease

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Genetics

Mutation in parkin (a ubiquitin ligase that attaches ubiquitin to misfolded protein to promotes their transport to the proteasome for degradation and UCH-L1(which cleaves ubiquitin from misfolded protein to permit theri entry into the proteosome) are causative in other cause of familial PD

Mitochondrial dysfunction has also been implicated in familial PD.gene involed (parkin,PNKI,and DJ)

Having first degree are relative with PD Confers on a 2-3 times increased risk of developing parkinsonsim disease

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Genetics Genetic abnormalites resulting in protein misealding and

accumulation and mitochodrial dysfunction are found to be responsible for causing

Protein accumaltion can be due to increased formation or impaired clearance

Mutation in the park I gene encoding the protin alpha synuclein a main component of lewy body ,on the chromosome 4q are seen in early onset (mean age 46 year )parkinsons

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NATURAL HISTORY

Begin between 40-70 years of age Peak age of onset 6th decade Infrequent before30 years of age More common in men Trauma,emotinal upset overwork exposure to cold,rigid

personality etc are suggested to be predisposing factors to disease but none have evidence

Disease observed in all countries and all races

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TREMORS Often involves the hand Pin-rolling tremors(four per second)involing thumb and

fingersand charectestic Typically present when hand is at rest(hence the term resting

tremor) Voluntary movements dampens the tremors momentrly Complete relaxation (sleeping greatly reduces or abolishes

the tremor Also known as alternating tremors due to alternating burst of

activity in agonist and antagonist muscles in EMG

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Second common type is

A fine (seven to eight per sec ) tremors of the outstreched hands and fingers

Persists through out voluntary moments Not evident in resting position More easilly supressed by relaxation Lacks the alternating burst of action potential unlikeresting

tremors and resemble essential tremor Parkinsons disease patients may have either type of tremor

or both

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D Dx OF PARKINSONIAN SYNDROME

Idiopathic Parkinson’s disease

Drug induced – phenothiazines

Multiple cerebral infarct state.

Trauma – pugilistic encephalopathy

Toxin induced- MPTP, CO, Mn, Cu,

Parkinson’s plus syndromes

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ESSENTIAL TREMOR

Most common diagnostic error

10 times more common than PD

Postural or action tremor.

Titubation

Family history

B – Blockers help

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DRUG INDUCED PARKINSONISM Predictable

Neuroleptic Drugs (Both Typical And Atypical)

Hidden Neuroleptics – Metoclopromide

Prochlorperazine

Combination With Antidepressants (Fluphenazine )

Calcium Antagonist

Idiosyncratic› Lithium

› Sodium Valproate

› Amiodarone

› Mainly Tremor But Parkinsonism Reported. Adam and victor principle of neurology 10 ed

MULTIPLE INFARCT STATE

Related to Hypertension and other risk factors

Common mis-diagnosis.

Poor prognosis

Aspirin and Dipyridamole may be effective and safe

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VASCULAR PARKINSONISM

Binswanger’s encephalopathy

Insidious Onset

Gradual progression

Diffuse sub cortical white matter ischaemia.

2-3 % incidence of ‘pure’ vascular causes

No Acute or abrupt onset basal ganglia infarct

No lewy bodies or nigral degeneration

Confirmation: PM studies only

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DEMENTIA WITH LEWY BODIES Dementia

Fluctuating alertness

Hallucinations

Myoclonus more common

Tremor less common

More symmetrical

More rigid

Mild parkinsonism

Neuroleptic sensitivity

Less bradykinetic

Lewy bodies are abnormal dense core eosinophilic cytoplasmic inclusion aggregates of protein -alpha-synuclein of spherical masses surrounded by a halo of 10-nm-wide radiating fibrils that displace other cell components Adam victor principle of

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SURGERY

Deep Brain Stimulation

› Brain pacemaker, sends electrical impulses to brain to stimulate the subthalamic nucleus.

› Improves motor functions and reduce motor complications.

› Complications include: brain hemorrhage, seizures, death.

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TAKE HOME MESSAGES

Diagnosis of PD is clinical and can be difficult.

Every patient should be referred to secondary care

› to confirm the diagnosis and initiate treatment

Tt should only be started if there is functional impairment

Ldopa is the gold standard but DA cause much less dyskinesia

Follow up should be life long

Thank you

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