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  • 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. Are the movements that you do not control; you make it so fast that your cerebrum doesn´t receive the information.
  • 3. Are the movements which we control. The Nervous System transmits the information of the action to the cerebrum.
  • 4. Reflex:When you blik, when somebody heats you, you shake. Voluntary movements: when you walk, you throw a ball, when you eat, …
  • 5. We blink 20.000 times a day. Yawns are contagious. The sneeze is an involuntary movement.
  • 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. Hyperkinetic hypokinetic Tremor(MC) PD(2nd MC) Chorea Apraxia Dystonia Hypothyroid slowness Ballism rigidity Myoclonus Tics Ataxia myokymia myorrhythmia
  • 8. Hypnogogic myoclonus Benign fasciculation without LMN disorder Physiological tremor Low amp, high freq
  • 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. 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.  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. “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.  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.  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.  Valproic acid is drug of choice  May respond to benzodiazepines e.g. clonazepam, piracetam, primidone, lamotrignine
  • 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.  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.  Chorea molles: Marked hypotonia with very minimal involun move Causes: rhumatic fever, encaphalitis huntington’s dis pergnency(chorea graviderum) congenital(rarely)
  • 19.  Anoxic brain damage ( post – CPR )  Systemic lupus erythematosis  Hepatic failure  Endocrine - Thyrotoxicosis - Addisons  Electrolyte - Low Ca, Mg, - High Na  Polycythemia rubra vera
  • 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.  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.  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.  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.  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. 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. 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.  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.  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.  Botulinum toxins  Medical: Dopa ant Dopa depleting agents Anticholinergics(trihexyphenidyl) Beclofen Clonazepam Anticonvulsant  Sx: Peripheral dennervation DBS U/l thalamotomy
  • 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.  Education  clonidine  Guanafacine  Atypical neuroleptics(resperidone, olanzapine)  Classical neuroleptics(haloperidol, fluphenazine)  Behavioural therapy
  • 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.  Harrison’s priciples of internal med  De jong’s neurology  Yellow oza & Dr S.S. desai  Dr Sheetal D vora