Movement Disorders


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Movement Disorders

  1. 1. A PRESENTATION ON ABNORMAL MOVEMENT DISORDERS<br /> Dr. Aarthy Joseph<br /> Prof. Dr. Mageshkumar’s Unit<br />
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  5. 5. PATIENT1 PATIENT2<br />15 year, female, no family history •60 year, female, known diabetic <br />1 week H/O abnormal movements•2 day H/O abnormal movements<br />Systemic examination •Systemic examination <br />Biochemical and hematological • RBS- 320, urine ketones- neg,<br />Routine investigations- normal other investigations- normal<br />• CXR and ECG- WNL •CT brain<br />• ASO titre- 200 •Neurology opinion <br />•CT brain and MRI brain<br />•Neurology opinion <br />•Cardiology opinion<br />•Ophthalmology opinion<br />•Serum ceruloplasmin<br />•Urinary copper<br />
  6. 6. DIAGNOSIS AND MANAGEMENT<br /> PATIENT1 PATIENT2<br />RHEUMATIC CHOREA HYPERGLYCEMIA INDUCED CHOREA<br />TREATMENT<br />Penicillin Glycemic control with insulin<br />Haloperidol Fluid correction<br />
  7. 7. CHOREA<br /><ul><li>Greek word meaning DANCE
  8. 8. Involuntary, rapid, irregular, jerky, purposeless, random, nonrhythmichyperkinesia
  9. 9. Present at rest, increased by activity, tension, emotional stress and self consciousness, and disappear in sleep
  10. 10. Most characteristic in the distal parts of upper extrimities</li></li></ul><li>CHARACTERISTIC FEATURES:<br />One extremity, hemichorea or generalised<br />Piano playing movements<br />Milkmaid grip<br />Parakinesia<br />Hypotonia and pendular DTR<br />Hyperpronation<br />Snake, darting, flycatcher tongue- Motor impersistence<br />
  11. 11. CAUSES<br />Hereditary – Huntington’s disease, benign hereditary chorea, neuroacanthocytosis, dentatorubro-pallidoluysian atrophy<br />Metabolic and endocrine disorders - Wilson disease, nonketotichyperglycemia, hypoglycemiahypobetalipoproteinemia, lipid storage diseases, Kernicterus, hyperthyroidism<br />Paroxysmal - Paroxysmal kinesogenicchoreoathetosis, paroxysmal dystonicchoreoathetosis<br />
  12. 12. <ul><li>Rheumatic choreaSyndenham’s chorea, Chorea gravidarum</li></ul>Drug induced - Neuroleptics, levodopa, oral contraceptives, cocaine, phenytoin<br />Toxins - Alcohol intoxication and withdrawal, carbon monoxide, manganese, mercury<br />Other choreas associated with systemic disease-<br />SLE, antiphospholipid antibodies, Polycythemiavera, AIDS<br />Rarely- Stroke, Vascular malformation, tumours<br />
  13. 13. RHEUMATIC CHOREA<br />After infection with group A ß-hemolytic streptococcus<br />25% of cases of acute rheumatic fever <br />Average age of onset is 5-15 years<br />Girls > boys<br />According to the 1992 modification of the Jones criteria, chorea alone is sufficient for diagnosis of RF<br />Imbalance among the dopaminergic system, intrastriatal cholinergic system, and inhibitory gamma-aminobutyric acid (GABA) system<br />
  14. 14. Cross-reactivity between group A ß-hemolytic streptococcus and the basal ganglia<br />Diagnosis of SC may be difficult. Chorea alone is sufficient for diagnosis providing other causes of the condition have been excluded<br />ASO titre may be elevated<br />Echocardiogram may show carditis<br />Volumetric MRI shows enlargement of the basal ganglia in affected patients without other abnormalities<br />Resolves spontaneously in 3-6 months<br />Recurrences<br />Treatment-<br />Chronic Penicillin prophylaxis for 10 years<br />Steroids<br />Haloperidol, Valproate<br />
  15. 15. CHOREA WITH NONKETOTIC HYPERGLYCEMIA <br />Focal neurological symptoms may provide the first clinical clue for the presence of non ketotichyperglycemia<br /> Seizures, chorea, Chorea – ballismus syndrome &focal neurological deficits<br />Pathogenesis- depletion of GABA, Cerebral hypoperfusion<br />T1 weighted MRI- hyperintense basal ganglia lesion<br />SPECT studies- Striatalhypoperfusion and striatalhypometaboli<br />Neurological symptoms improve with correction of hyperglycemia.<br />
  16. 16. REFERENCES<br />-DeJong’s The Nurological Examination<br /> -Harrison’s Principles of Internal Medicine<br />-Web references from medscape<br />
  17. 17. THANK YOU!!<br />