Movement disorder

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Movement disorder

  1. 1. Dr Hardik K ParmarDr Hardik K Parmar Student of Dr S.S.DesaiStudent of Dr S.S.Desai But expression of a well made manBut expression of a well made man appears not only in his face,it is in his limbs and joints also.appears not only in his face,it is in his limbs and joints also. - walt whitman- walt whitman
  2. 2. Are the movements that you do not control; you make it so fast that your cerebrum doesn´t receive the information.
  3. 3. Are the movements which we control. The Nervous System transmits the information of the action to the cerebrum.
  4. 4. Reflex:When you blik, when somebody heats you, you shake. Voluntary movements: when you walk, you throw a ball, when you eat, …
  5. 5. We blink 20.000 times a day. Yawns are contagious. The sneeze is an involuntary movement.
  6. 6. Basal ganglia are group of the neuclei located subcorticallywhich take part in motor movements of body. Abnormal increment or decrement in its parts causes various movements disorders.
  7. 7. Hyperkinetic hypokinetic Tremor(MC) PD(2nd MC) Chorea Apraxia Dystonia Hypothyroid slowness Ballism rigidity Myoclonus Tics Ataxia myokymia myorrhythmia
  8. 8. Hypnogogic myoclonus Benign fasciculation without LMN disorder Physiological tremor Low amp, high freq
  9. 9. DISORDER LESION Chorea Striatum, STN(red neucleus) Athetosis Diff hypermyelination of corpus striatum & hypothalamus Dystonia U.K.(Basal motor neuclei) Hamiballismus H’age in C/l STN Rest & postural tremors Mid brain, sup cerebeller pudencle
  10. 10. Rhythmic Involuntary movements Of fingers, hand, arms, legs,tongue, or head Due to alternatecontaction and relaxation of oppo mus groups Sometimes they can be so fine that they cant be easily recognised Put a paper on dorsum of an out streched hand MC cause is anxiety OTHERS: Psychogenic,Post traumatic(2- 8 Hz), Rx: Propranolol, Primidone, gabapentine, BZD
  11. 11.  Athotosis, Ballismus, Chorea & Dystonia Should not be thought as a separate entity but as a different manifestation of same spectrum as they often coexist Tics:cant be suppresed by voluncontrol
  12. 12. “rapid, brief, shock-like, jerky, involuntary movements”  May be caused by active muscle contraction - positive myoclonus  May be caused by inhibition of ongoing muscle activity - negative myoclonus ( eg. Asterixis )  Generalised - widespread throughout body  Focal / segmental – restricted to particular part of body Hypnogogic: occurs during sleep
  13. 13.  Action myoclonous: asso with voluntary movements  Reflex/startle: In response to external stimulus  Reversible: Renal failure, hypocalcemia  D/D from tics: interfere with normal movements & not suppressible
  14. 14.  Symptomatic i.e secondary to disease process - Neurodegenerative eg. Wilson’s disease - Infectious e.g CJD, Viral encephalitis - Toxic e.g. penicillin, antidepressants - Metabolic - anoxic brain damage - hypoglycemia - hepatic failure ( “ asterixis” ) - renal failure - hyponatremia….. And others
  15. 15.  Valproic acid is drug of choice  May respond to benzodiazepines e.g. clonazepam, piracetam, primidone, lamotrignine
  16. 16.  Rapid, flinging, rotatory, Violent movement of larger amplitude of axial or prox parts of limb, irreguler, U/l, disapp during sleep   Almost always unilateral and therefore known as HEMIBALLISMUS  Patient may hurt himself  Can lead to exhaustion
  17. 17.  Semi purposive, darting, jerky, short-lasting, centrifugal, affecting limbs (face & tongue sos)  Hypotonia + but reflexes are also +nt  May be hyperextended joints  In the limbs chorea refers more to distal movements ( as proximal movements usually called ballismus)  Patients often attempt to conceal involuntary movements by superimposing voluntary movements onto them e.g. an involuntary movement of arm towards face may be adapted to look-like an attempt to look at watch
  18. 18.  Chorea molles: Marked hypotonia with very minimal involun move Causes: rhumatic fever, encaphalitis huntington’s dis pergnency(chorea graviderum) congenital(rarely)
  19. 19.  Anoxic brain damage ( post – CPR )  Systemic lupus erythematosis  Hepatic failure  Endocrine - Thyrotoxicosis - Addisons  Electrolyte - Low Ca, Mg, - High Na  Polycythemia rubra vera
  20. 20.  Mainly children / adolescents  Complication of previous group A streptococcal infection  Usually no recent history of infection  Acute / subacute onset  May have behavioural problems  Usually remits spontaneously
  21. 21.  Chorea of any cause that begins in pregnancy  May represent recurrence of Sydenham’s chorea.  Most commonly associated with anti- phospholipid syndrome +/- SLE  Usually resolves spontaneously
  22. 22.  Dopamine receptor blockers  Riluzole: corticostrial glutamate release inhibitor  Remacemide: glutamate/NMDA receptor antagonist  Co Q 10: UK mecha, possible behavioural improvement  Anti convulsant: valproate
  23. 23.  Slow, snake-like, writhing, worm-like movements of dynamic in nature starting at fingers and then spreades proximally which causes abduction & int rotation of UL  Increased on voluntary movements  Disapp during sleep  Can also affect face and tongue  Often use term “ choreoathetosis ” due to overlap between syndromes ( chorea referring to less smooth , more jerky movements)  Causes: CP, hepatic failure
  24. 24.  Sustained or repetative involuntary mus contraction freq asso with twisting and assumption of abnormal postures.  Due to co-contraction of agonist and antagonist muscles in part of body  Can be thought of as an athetoid movement that “gets stuck” for a period of time; thus, a patient with choreoathetosis may perform an involuntary movement in which his hand and fingers are twisted behind his head. He may hold this position for a few moments before his hand moves back in front of his body.  The part of the movement when the limb was held, unmoving, in an abnormal position would be considered a dystonia ( may occur alone).
  25. 25. Idiopathic torsion dystonia (oppenheim’s dystonia)  Hereditary and sporadic forms  Variable inheritence(AD)  DYT 1 gene mutation on Chr-9-protein torsin A  High incidence in Ashkenazi Jews  Onset may be in childhood / adulthood(<26yr)  Affects limbs then progress prox  Trial of L-dopa usually initiated  Level of disability variable
  26. 26. DRD or segawa variant (DYT 5)  Affects production of tyrosine hydroxylase and thereby formation of dopamine  1-12yrs, foot dystonias that interefers with walking which worsens as day progresses and disapp during sleep  Excellent response to L-dopa
  27. 27.  Blepharospasm: involuntary forceful closure of eyes  OMD: mus of lower face, lips, tongues (MEIG’S syn is combo of bleph &OMD)  Torticollis :Tendency of neck to twist to one side.  spasmodic dystonia: involves vocal cords(choking due to adductor mus involv)  Limb dystonias: writer’s cramps, musician’s cramp
  28. 28.  Secondary dystonias: neuroleptics, chronic levodopa Rx, CO poisioning  Dystonia plus syndromes: as a part of other neurodegenrative disorder HD, PD, Wilson, CBGD, PSP etc..
  29. 29.  Botulinum toxins  Medical: Dopa ant Dopa depleting agents Anticholinergics(trihexyphenidyl) Beclofen Clonazepam Anticonvulsant  Sx: Peripheral dennervation DBS U/l thalamotomy
  30. 30.  Recurrent, sterotyped, seemingly purposeless abnormal movements  May be suppressed voluntarily or with distraction  Voluntary suppression leads to anxiety and a build-up of internal unrest.  Worsen under stress
  31. 31.  Education  clonidine  Guanafacine  Atypical neuroleptics(resperidone, olanzapine)  Classical neuroleptics(haloperidol, fluphenazine)  Behavioural therapy
  32. 32.  Movement disorders are often difficult to define precisely, but have similar differential diagnoses.  They are often a manifestation of a more widespread neurological or internal medical problem.  Other than the specific treatments mentioned, most details of therapy are beyond the scope of this lecture  In some cases treatment includes treatment of underlying cause e.g. Wilson’s disease
  33. 33.  Harrison’s priciples of internal med  De jong’s neurology  Yellow oza & Dr S.S. desai  Dr Sheetal D vora

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