Presentation about Parkinson Disease for UG Medical students Parkinsonism Epidemiology Management Prognosis Complications

1. PARKINSON’S DISEASE
SANDRA SAJU
VII th Semester
TMA

2. PARKINSONISM
• Parkinsonism: A group of disorders producing abnormalities of BG
function. cardinal features:
o Rest tremor
o Rigidity
o Bradykinesia, and
o Gait impairment
• PD / Idiopathic Parkinsonism : most common.
• Secondary Parkinsonism : Viruses, tumors, toxins and drug induced.
• Parkinsonism plus syndromes : Conditions mimicking PD but are
caused by other Neuro-degenerative diseases.

3. Progressive loss of dopamine containing
neurons is a feature of normal aging;
however, most people do not lose the
70% to 80% of dopaminergic neurons
required to cause symptomatic PD.

4. EPIDEMIOLOGY
• Onset between 40 and 70 years of age.
• Affects men and women of all races, all occupations, and all countries
equally.
• Men are (1.5 times) more prone .
• Mostly idiopathic.
• Mutations in PINK1,PARKIN ,ALPHA SYNUCLEIN genes
• Risk factors: exposure to pesticides, rural living, stress...
• Reduced risk with cigarette smoking and caffeine.

5. pathophysiology
BASAL GANGLIA : Regulates the flow of information from the cerebral
cortex to the motor neurons of the spinal cord.
 loss of the dopaminergic neurons of the pars compacta.
 Without dopamine, inhibitory influences are lost and excitatory
mechanisms are unopposed.
 Neurons of basal ganglia are over stimulated.
 Excess muscle tone, tremors & rigidity

7. CLINICAL FEATURES
Assymetric onset of symptoms.

8. Bradykinesia:
Slowed ability to start and continue movements.
Akinesia - Expressionless face(poker/maskedface)
Postural instability :
Impaired balance.
The patients suffers frequent falls. This symptom is
not seen in early stages.

9. Other symptoms

10. ON NEUROLOGIC EXAMINATION
 Muscle strength / reflexes remain normal, plantar responses are flexor.
 There is a paucity of facial expression (hypomimia).
 The blink reflex may be exaggerated & fail to habituate (glabellar tap sign).
 Eye movements are normal to standard clinical testing.
 Sensation is normal & intellectual abilities are not affected initially.
As the disease progresses, 1/3 develop cognitive impairment.

11. ATYPICAL PARKINSONISM
More widespread neurodegeneration. (w/o Lewy bodies)
Early speech and gait impairment, absence of rest tremor, no asymmetry,poor or no response
to levodopa, and an aggressive clinical course.
 Multiple-system atrophy
Manifests as a combination of parkinsonian, cerebellar, and autonomic features
MSA-p and MSA-c
 Progressive supranuclear palsy
slow ocular saccades, eyelid apraxia, and restricted eye movements ,impairment of downward
gaze.
Atrophy of the midbrain with relative preservation of the pons- hummingbird sign.
 Corticobasal ganglionic degeneration
asymmetric dystonic contractions and clumsiness of one hand coupled with cortical sensory
disturbances manifest as apraxia, agnosia, focal myoclonus, or alien limb phenomenon.

12. SECONDARY PARKINSONISM
• Associated with drugs, stroke, tumor, infection, or exposure to toxins.
• Dopamine-blocking agents such as the neuroleptics are the commonest cause.
Finally, parkinsonism can be seen as a feature of other degenerative disorders such
as Wilson’s disease, Huntington’s disease dopa-responsive dystonia, and
neurodegenerative disorders with brain iron accumulation
( PANK–associatedneurodegeneration)

13. DIAGNOSIS
The diagnosis is made clinically, as there is no diagnostic test for Parkinson's
disease.
 Parkinsonism associated with rest tremor, asymmetry, and a good response
to levodopa is
more likely to predict a correct diagnosis of PD.

14. Alternative Diagnosis

15. Investigations
• Imaging techniques are useful only for research purposes.
• Imaging of the brain dopamine system with (PET) or (SPECT) shows reduced uptake
of striatal dopaminergic markers, particularly in the posterior putamen.

16. TREATMENT
Medications , surgery and exercise are available for Symptomatic treatment.
Levodopa: Converted into Dopamine within nigrostriatal neurons.
Administered with a DDC inhibitor-Carbidopa ,to prevent peripheral metabolism of
L-Dopa.

17. Dopamine agonists: pramipexole , ropinirole
It mimics Dopamine.
Used in early stages of PD.
Longer duration than L Dopa.
Not effective as Levodopa in reducing symptoms .

18. MAO-B inhibitors: selegiline, rasagiline
increase the level of dopamine by decreasing it’s degradation.
Used to treat very mild symptoms.
This treatment is less effective than Levodopa but can be used to increase the
time of effect of Levodopa.
COMT INHIBITORS: tolcapone and entacapone
Increase the elimination half-life of levodopa and enhance its brain availability.

19. Other drugs
Amantadine: An antiviral drug which aids in increased Dopamine production.
Central-acting anticholinergic drugs such as trihexyphenidyl and benztropine.
Decrease level of acetylcholine to achieve a balanced level with Dopamine.

20. FURTHER MANAGEMENT

21. Physiotherapy& rehabilitation:
Patients at all stages of Parkinson's disease benefit from
physiotherapy, which helps reduce rigidity& corrects abnormal
posture.
Speech therapy may help in cases where dysarthria & dysphonia
interfere with communication.

22. PROGNOSIS
 Variable& depends partly on the age of onset.
 If symptoms start in middle life, the disease is usually slowly progressive &
likely to shorten lifespan because of the complications of immobility &
tendency to fall.
 Onset after 70 is unlikely to shorten life or become severe.

23. MOTOR COMPLICATIONS SEEN IN PD

24. COMPLICATIONS

25. References
 https://www.youtube.com/watch?v=VIEUEV9wlyI
 file:///C://parkinsonsdiseaseppt-121007130452-phpapp01.pdf
 https://www.slideshare.net/drcramanan/parkinsons-disease-37094427
 http://www.psychiatrictimes.com/special-reports/management-psychosis-parkinson-disease
 HARRISON’S neurology in clinical medicine, 33rd edition.
 https://dodoodad.com/parkinsons-disease-symptoms-and-treatments