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Parkinsonism And Motor Disorders

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Parkinsonism And Motor Disorders

  1. 1. Parkinsonism and motor disorders. Supervised by Dr- hajaj. Done by Ebrahim Al-Qunaibut.
  2. 2. OBJECTIVES. <ul><li>Define parkinsonism and describe its etiology. </li></ul><ul><li>Explain the pathological finding of pakinson`s disease. </li></ul><ul><li>List the symptoms and signs of parkinsonism. </li></ul><ul><li>Outline the management of parkinsonism. </li></ul>
  3. 3. INTODUCTION.
  4. 4. DEFINITION. <ul><li>It is a clinical syndrome characterized by diminished facial expression, stooped posture, slowness of voluntary movement, festinating gait, rigidity and tremor ( pill-rolling ). </li></ul><ul><li>This type of motor disturbance have in common damage to the nigro-striatal dopaminergic system. </li></ul>
  5. 5. ETIOLOGY. <ul><li>there is selective degeneration of pigmented dopaminergic neurons of the substantia nigra </li></ul><ul><li>There are few real clues as to the cause of parkinsonism. </li></ul><ul><li>1. Nicotine :- </li></ul><ul><li>PD is less prevalent in tobacco smokers than lifelong abstainers. </li></ul><ul><li>2. MPTP :- </li></ul><ul><li>Minute doses of the pyridine compound cause sever PD. </li></ul>
  6. 6. ETIOLOGY. <ul><li>3. Environmental agent :- </li></ul><ul><li>Environmental MPTP – like herbicide are implicated. </li></ul><ul><li>4. Encephalitis lethargica :- </li></ul><ul><li>Some survivors of viral encephalitis lethargica developed sever PD. </li></ul>
  7. 7. ETIOLOGY. <ul><li>5. Genetic factors :- </li></ul><ul><li>There are 3 mutated proteins which have been found in patients with PD. </li></ul><ul><li>a ) alpha – synuclein gene on chromosome 2 and account for autosomal dominant. </li></ul><ul><li>B ) ubiquitin carboxyl-terminal hydrolase L1 on chromosome 4 and also account for autosomal dominant </li></ul><ul><li>C ) parkin gene on chromosome 6 and found in families with autosomal recessive and some young. Account for most of cases below the age of 40. </li></ul>
  8. 8. ETIOLOGY. <ul><li>Mutant parkin proteins are unable to interact and ubquinate form of alpha – synuclein accumulate. </li></ul><ul><li>6. Drugs :- </li></ul><ul><li>Side effects of several antipsychotic drugs (i.e., phenothiazides, butyrophenones, reserpine) </li></ul>
  9. 10. PATHOLOGICAL EXAMINATION. <ul><li>Macroscopic examination :- </li></ul><ul><li>The typical finding are pallor of the substantia nigra and locus ceruleus. </li></ul><ul><li>Microscopic examination :- </li></ul><ul><li>there is loss of the pigmented catecholaminergic neurons in these regions associated with gliosis and Lewy bodies </li></ul>
  10. 11. LEWY BODY. <ul><li>Could be found in some of the remaining neurons. </li></ul><ul><li>Single or multiple. </li></ul><ul><li>Cytoplasmic, eosinoplic, round to elongated inclusion. </li></ul><ul><li>Have dense core surrounded by a pale hallo. </li></ul>
  11. 12. LEWY BODY. <ul><li>Composed of fine filaments. </li></ul><ul><li>These filaments are made of alpha – synuclein, parkin and ubiquitin. </li></ul><ul><li>May be found in other brainstem nuclei. </li></ul>
  12. 13. PATHOLOGICAL EXAMINATION. normal S. nigra depigmented S. nigra lewy body
  13. 14. SYMOPTOMS AND SIGNS. <ul><li>most symptoms do not appear until striata DA levels decline by at least 70-80%.  </li></ul><ul><li>There are 3 main clinical features in PD :- </li></ul><ul><li>tremor, rigidity and bradykinesia or akinesia. </li></ul>
  14. 15. TREMOR ( resting tremor ). <ul><li>It is asymptomatic at first. </li></ul><ul><li>Characteristic 4-7Hz pill-rolling. </li></ul><ul><li>PD present with resting tremor which is a rhythmical movement. </li></ul><ul><li>Resting tremors are present mostly during relaxation of the muscles and decrease with action. </li></ul><ul><li>Tremor consist of flextion and extension or pronation and supination Usually affect distal joints. </li></ul><ul><li>Nigrothalamic pathway is dopaminergic ( inhibtory ) and in PD it is affected. So ,, excessive impulses pass from thalamus to motor cortex ( halamocortical projection is excitatory ). This produce oscillation which cause tremor. </li></ul>
  15. 16. RIGIDITY. <ul><li>Define as an increase in resistance to passive movement. </li></ul><ul><li>Throughout the range of limb movement and is equal in opposing muscle groups. </li></ul><ul><li>Lead pipe or cogwheeling ??? </li></ul><ul><li>Rigidity is more easily felt when a joint is moved slowly and gently. </li></ul><ul><li>The flow of impulses in the basal nuclei is from cerebral cortex to neostriatum then to globus P. then again to cortex via thalamic nuclei. This feed back pathway is inhibited by dopaminergic nigrostriatal pathway which is already depleted. </li></ul>
  16. 17. G pallidus thalamus S nigra neostriatum GABA GABA Dopamine Dopamine tremor rigidity
  17. 18. BRADYKINESIA. <ul><li>Difficulty in initiating movement. Not rigidity. </li></ul><ul><li>Rapid fine finger movement ( piano – playing ) become indistinct. </li></ul><ul><li>Facial immobility give a mask-like semblance of depression. </li></ul><ul><li>Spontaneous blinking is reduced producing a serpentine stare. </li></ul>
  18. 19. OTHER SYMPTOMS AND SIGNS. <ul><li>Postural change :- </li></ul><ul><li>- stoop is characteristic. </li></ul><ul><li>- gait become hurrying (festinant) and shuffling with poor arm swinging. </li></ul><ul><li>- sometime called simian </li></ul><ul><li>- falls are common in later stage of PD. </li></ul>
  19. 20. OTHER SYMPTOMS AND SIGNS. <ul><li>Speech :- </li></ul><ul><li>- pronunciation initially monotone. </li></ul><ul><li>- progresses to tremulous slurring dysarthria. </li></ul><ul><li>- combination of akinesia, tremor and rigidity, speech may be lost completely (anarthria). </li></ul>
  20. 21. OTHER SYMPTOMS AND SIGNS. <ul><li>Heartburn. </li></ul><ul><li>Dementia. </li></ul><ul><li>Dribbling. </li></ul><ul><li>Dysphagia. </li></ul><ul><li>Constipation. </li></ul><ul><li>Weight loss. </li></ul><ul><li>Urinary difficulties (men). </li></ul>
  21. 22. DIAGNOSIS. <ul><li>A diagnosis of PD can be made with some confidence in patients who present with at least two of the three cardinal signs </li></ul><ul><li>rest tremor , rigidity, and bradykinesia </li></ul><ul><li>MR is normal </li></ul>
  22. 23. TREATMENT.

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