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Parkinson’S Disease

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  • 1. Parkinson’s disease Dr. Osman Sadig Bukhari
  • 2.
    • Parkinson’s disease is an idiopathic
    • progressive degenerative disease of the
    • dopaminergic neurones in za substantia
    • nigra resulting in:
    • 1- Bradykinesia or akinesia
    • 2- Resting tremors
    • 3- Muscle rigidity causing restricted
    • mobility
  • 3.
    • Prevalence
    • - world wide
    • - 1: 1000 general population increasing sharply
    • over the age of 60.
    • - M> F
    • Aetiology
    • - unknown
    • - no infective agent
    • - no enviromental factor ( dis world wide)
    • - ? Less in tobacco smokers (nicotine)
    • - ? MPTP, a pyridine cpd cause similar syndrome
    • ( enviromental MPTP like herbicide?) - ? Genetic factors, clusters of early onset Parkinson’s
    • in some families ? Mutation in parkin gene on
    • chromosome 6
  • 4.
    • Pathology
    • - progressive degeneration with eosinophilic
    • inclusion bodies ( Lewy bodies) in za neurones
    • of substantia nigra & other basal ganglia nuclei
    • - loss of melanin & dopamine that correlate with the degree of akinesia
    • - imbalance between dopaminergic & cholinergic
    • neurotransmitters.
  • 5.
    • Clinical features
    • - Symptoms develop over moths & several years
    • 1-Pill rolling tremors of za hands, often unilateral, is the most common initial feature. It is eventually becomes bilateral involving the UL, LL & jaw. It diminishes on voluntary movement an increases by emotion.
    • 2- Slowness of movement or bradykinesia is
    • usually by za family. There is difficulty in
    • initiating movements including fine finger move
    • 3- Rigidity causes stiffness . It is lead pipe and
    • cogwheel rigidity.
  • 6.
    • 4- Stooping posture, festinant & shuffling
    • gait wz reduced limb swinging
    • Propulsion & retropulsion are characteri
    • There is postural instability & falls.
    • 5- Masked expressionless face wz reduced
    • blinking.
    • 6- Monotonous speech progressing to
    • slurring & eventually lost.
    • 7- Micrographia
    • 8- Drooling of saliva, dysphagia, constipati
    • urinary troubles
    • 9- Excessive sweating & greasy skin.
  • 7.  
  • 8.
    • 10- Power remains normal, reflexes may
    • be increased, planters remain flexor
    • and sensations are normal.
    • 11- Cognitive fns preserved at least early,
    • dementia develops in late stages,
    • anxiety & depression are common
    • 12- No remission & za rate of progression
    • is variable wz death resulting from
    • chest infection, UTI & bed sores
  • 9.
    • Diagnosis
    • - characteristic clinical picture
    • - careful history & examination to exclude other
    • causes of Akinetic – rigid syndromes i.e.
    • secondary causes of parkinsonism
    • 1- Drug induced parkinsonism e.g neuroleptics,
    • reserpine, methyldopa, tricyclic antidepressants
    • mainly cause slowness & rigidity wz little tremor
    • 2- Post encephalitis lethargica
    • 3- Toxins e.g MPTP, CO, Mn
    • 4- CVAs, hypoparathyroidism, trauma & SOL
    • 5- Wilson’s disease & athetoid C. palsy in childr
  • 10.
    • 6- Progressive supranuclear palsy
    • 7- Multiple system atrophies:
    • - Olivo – ponto – cerebellar degeneration
    • - Pry autonomic failure ( Shy Drager syndr)
    • 8- Alzeheimer disease
    • 9- Huntington's chorea
  • 11.
    • Management of Parkinson’s disease
    • A- identify 2ry causes of parkinsonism & TR
    • e.g withdrawal of neuroleptics, penicillamine
    • for Wilson’s.
    • B- Drug therapy to restore dopaminergic/
    • cholinergic balance, but
    • - not curative
    • - greatly improve za quality of life
    • - should only be started when za functional
    • disability interferes wz life.
  • 12.
    • 1- Dopaminergic drugs act through
    • - replacement of neuronal dopamine e.g
    • L dopa which is za natural precursor of
    • dopamine & crosses BBB ( dopamine not)
    • - releasing dopamine from its stores and
    • inhibiting its re uptake e.g amantadine
    • - prolonging za action of dopamine by selectiv
    • inhibition of its metabolism e.g selegline
    • - dopamine receptor agonists e.g bromocriptine
    • 2- Anti muscarinic anti cholinergics reduce
    • cholinergic activity by inhibiting acetyl choline
    • esterase e.g benzhexol.
  • 13.
    • ** drug induced parkinsonism is best treated by anti muscarinic drugs & not by L dopa since
    • neuroleptic drugs block dopamine receptors.
    • Individual drugs
    • 1- Levodopa (L dopa )
    • - a a precursor of dopamine wz short ½ life 1,5h
    • - dopamine can not be used as it is rapidly
    • destroyed peripherally (gut, liver & blood) by
    • MAO inhibitor & catechol O –methyl transferase
    • and does not cross BBB.
    • - peripheral dopa decarboxylase inhibitors which
    • do not cross BBB are combined with L dopa in
  • 14.
    • therapeutic doses to avoid large doses of L dopa
    • e.g Sinemet ( cabidopa + L dopa 1 : 10) :
    • 110, 250mg. OR Madopar ( benserazide + L dop
    • 1:4: 65.5, 125, 250mg.
    • - With combination low doses of L dopa are used
    • and side effects are reduced:
    • (N, V, post hypotension, arrhythmias, dyskin
    • confusion, agitation, hallucination, depressio
    • long term problems of end of dose deterior
    • and on off swings)
    • - L dopa interaction wz non selective MAO-I
    • causes hypertensive crisis. In this situation L dopa dopamine Noradrenaline HT.
  • 15.
    • 2- Amantadine
    • - anti viral
    • - less effective than L dopa but may
    • enhance its effect
    • - mainly used in early mild cases
    • - dose: 100-300mg/d
    • - SE= post hypot, ankle edema & livedo
    • reticularis.
  • 16.
    • 3- Bromocriptine
    • - dopamine receptor agonist
    • - ½ life 5hrs, therefore smoother action than
    • L dopa & no fluctuation in action
    • - dose: 10-80mg starting wz 1.25mg e.g
    • Parlodel (2.5 &10mg)
    • - used in long term L dopa problems
    • - SE= similar to L dopa.
  • 17.
    • 4- Selegline
    • - selective B MAO-I
    • - It delays break down of dopamine & prolongs
    • its action
    • - main use in those wz long term L dopa
    • problems e.g end of dose deterioration
    • - anti depressant also
    • - e.g eldepryl 5mg X2. SE= similar to L dopa.
    • - no hypertensive cheese reaction (tyramine)
    • which occur wz non selective MAO-I which
    • prevent degradation of dietary amines by
    • MAO-I. Tyramine is degraded by type A MAO-I
  • 18.
    • 5- Entacapone
    • - COMT inhibitor
    • - Used to reduce end- of- dose fluctuation
    • in response to L dopa.
    • 6- Anti muscarinic anti cholinergics
    • - Act by blocking Ach in za CNS restoring the
    • imbalance created by decreased dopaminergi
    • activity.
    • - most effective in drug induced parkinsonism and in mild cases sp. tremor, rigidity and sialorrhMoea. Not used I n > 65, glucoma & BPH. SE= those of anti cholinergics.
  • 19.
    • - trihexyphenidyl (benzhexol 2mg), benz atropin
    • orphenadrine.
  • 20.
    • 3- General management of parkinsonism
    • - Positive attitude by encouraging physical
    • activity, physiotherapy & speech therapy
    • - Early mild cases: anti muscarinic & amantadine
    • -With progression of za disease dose of L dopa
    • needs to be increased wz more SEs which may
    • be overcome by reducing individual doses
    • and increasing za frequency of administration or
    • by using bromocriptine & selegline
    • - L dopa + carbidopa restore near normal
    • physical activity in 75%. Ultimately higher doses are required.
  • 21.
    • - long term therapy is associated with:
    • 1- end- of- dose fluctuation= swings from early morning akinesia to peak
    • dose dyskinesia.
    • 2- on- off swings= random fluctuation
    • from mobility to dyskinesia wz peak
    • plasma conc.
    • - Long term problems wz L dopa is treated
    • by: - gradual & partial substitution of
    • L dopa wz bromocriptine & selegline
    • effective in end- of- dose deterioration
    • - decreasing dose of L dopa & shortening za interval between doses.