2. Movement disorder
Emergencies
Any neurological disorder evolving acutely or
sub acutely
in which the clinical presentation is dominated
by a primary movement disorder and
in which failure to accurately diagnose and
manage the patient may result in significant
morbidity or mortality.
Balamurugan NamasivayamBalamurugan Namasivayam 22
3. Purpose
1) Identify the most important movement
disorder emergencies
2) Understand how are they managed
3) Recognize certain rare movement
disorders that should not be missed
(what I call, “don’t miss diagnoses”).
Balamurugan NamasivayamBalamurugan Namasivayam 33
6. Oculogyric crisis or
Acute dystonic reaction
A form of acute dystonia, it takes its name
from the tendency of the eyes to deviate
eye movements are only part of the
syndrome
opisthotonus and generalized rigidity,
anguish, multiple autonomic symptoms
Akathisia, forced gasping,gagging, loud
phonation, pallilalia
66
21. Paroxysmal autonomic
instability with dystonia. PAID
A complication of severe brain injury
Syndrome of
intermittent agitation,
diaphoresis,
hyperthermia,
hypertension,
tachycardia,
tachypnea, and extensor posturing.
22. Pathophysiology of PAID
Dysfunction of autonomic centers in the
diencephalon (thalamus or hypothalamus)
or their connections to cortical, subcortical,
and brainstem loci that mediate autonomic
function.
23. Criteria for PAID
Signs of PAID syndrome include
(1) severe brain injury,
(2) temperature > 38.5°C,
(3) Pulse > 130beats/min,
(4) respiratory rate > 40 breaths/ min,
(5) agitation,
(6) diaphoresis, and
(7) dystonia (ie, rigidity or decerebrate posturing).
The duration is at least 1 cycle per day for at least
3 days.
Finally, other conditions must be ruled out.
30. Sri Gokulam Hospital,SalemSri Gokulam Hospital,Salem Balamurugan NamasivayamBalamurugan Namasivayam 3030
Athetosis
Ballismus
Chorea
Topography is different and Clinical settings
are different.
39. Parkinsonism as movement
disorder emergencies
1. Fluctuations in response to levodopa
(new onset or sudden changes)
2. Involuntary movements (dyskinesia):
choreic or dystonic
3939
40. 4040
Late stage motor problems
Motor fluctuations
Related to duration and dosage of
levodopa therapy
Dyskinesias
Related to severity of the
disease
42. Situation leading to PHS
Stopping dopaminergic medications
Neuroleptic use
Motor fluctuations-
off periods, peri menstrural off
Metabolic disturbances
Dehydration
hypernatremia
4242
43. Management of PHS
Reintroduction of antiparkinsons
medications
Supportive care
Antipyretics
Rehydration
Bromocriptine 2.5mg tds
Dantrolene sodium10mg IV tds
4343
45. 4545
6 8 10 82
6412 10
Combination of motor fluctuation & Dyskinesias
YO-YO-ING
46. 4646
Combination of motor fluctuation &
Dyskinesias
YO-YO-ING
Repeated ups and downs of a yo yo
Dopamine receptors are intact but supersensitive
to allow dyskinesia (Pharmaco dynamic)
Short plasma off life leads to “OFF” state
(Pharmaco kinetic)
Plain levodopa Or Liquid preparation
(Not carbidopa/ COMT- prolonged unpredictable action)
Long acting DA may be tried (dopa sparing)
Levo dopa infusion via Intra duodenal pump
Surgery
51. 5151
Parkinsonism –Toxin induced
Bhatt MH, Elias MA, Mankodi AK. Acute and reversible parkinsonism due to organophosphate pesticide intoxication: five cases. Neurology
1999; 52(7):1467–1471.
Balamurugan N, Karthikeyan V, Bhaskar C. 1st Asian & oceanian parkinsons disease & movement disorders congress
2007 held at Singapore, Reversible Dystonic Parkinsonism after Organophosphate Poisoning,
Repititive or sustained or dynamic
Twisting or flexion/extention or abduction/adduction
Bullard: Suggested a release phenomenon in which loss of cortical and subcortical control of vegetative functions occurs, including regulation of blood pressure and temperature.
Thermoregulatory dysfunction may also be produced by hypothalamic dysfunction, as has been demonstrated experimentally6 and clinically.
The temperature elevations associated with PAID may also be explained, at least in part, by the hyper-metabolic state that accompanies sustained muscular contractions.
Boeve et. al : Expanded this concept by speculating that the mechanism likely involves activation (or disinhibition) of central sympathoexcitatory regions such as the para-ventricular hypothalamic nucleus, lateral periaqueductal gray substance, lateral parabrachial nucleus, or rostral ventricular medulla. Cortically provoked release of adrenomedullary catecholamines during PAID episodes may contribute to the rise in blood pressure as well as tachycardia and tachypnea.
Deepak Goel, Anil Singhal, Rajender K. Srivastav*, Amit Verma, Anurag Lamba. Magnetic resonance imaging changes in a case of extrapyramidal syndrome after acute organophosphate poisoning. Neurol India 2006 ; 54(2): 207-9.