The lecture has been given on May 7th, 2011 by Dr. Hassan Al-Jumaily.

2. Secondary:

3. Infectious: post-encephalitic parkinsonism

4. Toxins: manganese, carbon monoxide

5. Drugs: antipsychotics, reserpine

6. Hypoparathyroidism

7. Vascular

8. Parkinsonism-plus: associated with other neurologic diseases:

9. Striatonigral degeneration

10. Progressive supranuclear palsy

11. Shy-Drager syndrome

12. Normal pressure hydrocephalus

13. Alzheimer’s disease

14. Wilson’s disease

16. Rigidity: it is increase in tone (that’s increased resistance to passive movement), it is a characteristic feature of parkinsonism. The resistance is typically uniform throughout the range of movement which sometimes interrupted by tremor and called ‘cog-wheel rigidity’. In contrast to spasticity, where the increase in tone is of ten greatest at the beginning ‘clasp-knife’.

17. Hypokinesia (bradykinesia): it is the most disabling feature of the disease. It means slowness of voluntary movements and a reduction in automatic movements such as swinging the arms while walking. The patient’s face is relatively immobile called ‘masked face’, with widened palpebral fissures and infrequent blinking. The voice is slow and monotonous (poorly modulated), power is not diminished. The handwriting is small and tremulous ‘micrographia’.

18. Abnormal gait and posture: the patient generally finds it difficult to get up from bed or an easy chair and tends to adopt a flexed posture on standing. It is often difficult to start walking and the gait itself is characterized by small, shuffling steps with absence of the arm swing and there may be difficulty in stopping. In advanced cases, the patient tends to walk with increasing speed to prevent a fall, called ‘festinating gait’.

19. Other clinical features:

20. Blepharoclonus: fluttering of the closed eyelids

21. Blepharospasm: involuntary closure of the eyelids

23. Trihexyphenidyle (Artane)

24. Benztropine (Cogentin)

25. Procyclidine (Kemadrin)

27. Levodopa: it is unlike the anticholinergic drugs, it is often partically helpful against (hypokinesia), its side effects are nausea, vomiting, hypotension, abnormal movements and most common late complication is on-off phenomenon. Most of levodopa is broken down to its active metabolite (dopamine) outside the central nervous system by the enzyme (dopa decarboxylase) but does not cross the blood-brain barrier, so carbidopa is given with L-dopa in a combination known as (Sinemet) to limit the breakdown of L-dopa outside the central nervous system by inhibiting the effects of dopa decarboxylase enzyme. The carbidopa is generally combined with L-dopa in a fixed preparation (1:10 or 1:4) as Sinemet. Either Sinemet (10:100 mg) or (25:100 mg) orally three times daily.

28. Bromocriptine: it is an ergot derivative that directly stimulates dopamine receptors. The starting dose is 1.25 mg and the maintenance doses are usually between 2.5 to 10 mg orally, three times daily.

29. Pergolide: it is like bromocriptine an ergot derivative and dopamine receptor stimulator.

30. Selegiline: is mono amine oxidase inhibitor type B (MAOI-B), therefore; it inhibits the metabolic breakdown of dopamine, and enhances the antiparkinson effect. Some studies suggest that it can delay the progression of the disease.

31. Surgery: by thalamectomy and is rarely used

32. Physical therapy: physical therapy and speech therapy may benefit many patients.