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.

9. Hyperkinetic hypokinetic
Tremor(MC) PD(2nd
MC)
Chorea Apraxia
Dystonia Hypothyroid slowness
Ballism rigidity
Myoclonus
Tics
Ataxia
myokymia
myorrhythmia

11. Hypnogogic myoclonus
Benign fasciculation without LMN
disorder
Physiological tremor
Low amp, high freq

12. 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

13. 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

14.  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

15. “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

16.  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

17.  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

18.  Valproic acid is drug of choice
 May respond to benzodiazepines e.g.
clonazepam, piracetam, primidone,
lamotrignine

19.  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

20.  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

21.  Chorea molles:
Marked hypotonia with very minimal involun move
Causes: rhumatic fever,
encaphalitis
huntington’s dis
pergnency(chorea graviderum)
congenital(rarely)

22.  Anoxic brain damage ( post – CPR )
 Systemic lupus erythematosis
 Hepatic failure
 Endocrine - Thyrotoxicosis
- Addisons
 Electrolyte - Low Ca, Mg,
- High Na
 Polycythemia rubra vera

23.  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

24.  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

25.  Dopamine receptor blockers
 Riluzole: corticostrial glutamate release
inhibitor
 Remacemide: glutamate/NMDA receptor
antagonist
 Co Q 10: UK mecha, possible behavioural
improvement
 Anti convulsant: valproate

26.  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

27.  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).

28. 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

29. 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

30.  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

31.  Secondary dystonias: neuroleptics, chronic
levodopa Rx, CO poisioning
 Dystonia plus syndromes: as a part of other
neurodegenrative disorder HD, PD, Wilson,
CBGD, PSP etc..

32.  Botulinum toxins
 Medical:
Dopa ant
Dopa depleting agents
Anticholinergics(trihexyphenidyl)
Beclofen
Clonazepam
Anticonvulsant
 Sx:
Peripheral dennervation
DBS
U/l thalamotomy

33.  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

34.  Education
 clonidine
 Guanafacine
 Atypical neuroleptics(resperidone,
olanzapine)
 Classical neuroleptics(haloperidol,
fluphenazine)
 Behavioural therapy

35.  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

36.  Harrison’s priciples of internal med
 De jong’s neurology
 Yellow oza & Dr S.S. desai
 Dr Sheetal D vora