1. ACUTE DYSTONIC
REACTION AND TARDIVE
DYSKINESIA

2. OUTLINE
 Introduction
 Epidemiology
 Etiopathogenesis
 Clinical presentation
 Differential diagnosis
 Prognosis
 Management
 Conclusion

3. Introduction
Acute dystonic reactions or medication-induced dystonia, in general are movement disorders
characterized by
involuntary contractions of muscles, and typically develop within minutes to hours
following a trigger, such as medication. Usually presents as intermittent spasmodic or
sustained involuntary contraction of muscles in the face, neck, trunk, pelvis, extremities, and even
the larynx.
Aims of this study:
1. To know what it is
2. How it presents
3. How to prevent it from occurring

4. Epidemiology
 There is no racial attribution
 Incidence is greater in male than in female
 It is more common in children, teens, and young adults
 Risk decreases with age thus, Older individuals may carry less risk for the
development of dystonia because of limited number of D2 receptors with
aging

5. Ethiopathogenesis
 Although dystonic reactions are occasionally dose related extapyramidal side
effect, these reactions are more often idiosyncratic and unpredictable. They
reportedly arise from a drug-induced alteration of dopaminergic-cholinergic
balance in the nigrostriatum (i.e, basal ganglia).
 Recall that there are 4 dopaminergic pathways ( Nigrostriatal, Mesocortical,
Mesolimbic, Tubuloinfundibular).
Most drugs produce dystonic reactions by nigrostriatal dopamine D2 receptor
blockade which leads to an excess of the striatal cholinergic output.
 High potency D2 receptor antagonists are most likely to produce an acute
dystonic reaction.

6. Etiopathogenesis continues
 The primary cause of an acute dystonic reaction is the body’s reaction to
a medication. Acute dystonic reactions form one of the most commonly
experienced extrapyramidal side effects, which are medication-induced
movement disorders that range from dystonia to parkinsonism.
Most commonly, it occurs in response to antidopaminergic agents and
dopamine receptor antagonist, such as antiemetics (i.e., metoclopramide),
antipsychotics (i.e., haloperidol, Fluphenazine and chlorpromazine), and
antidepressants.
Acute dystonic reactions have been describe with every antipsychotics

7. Etiopathogenesis continues
Predisposing factors includes:
 A family history of dystonia and
 Viral infection
 Alcohol and cocaine use, increases risk.

8. Clinical presentation
 This often develop, dramatically and unpredictably, within minutes to days of initially
starting a medication,
Mental status is unaffected. Vital signs are usually normal. However the main features
are:
1. Torticollis – Contraction of head resulting in neck twisting to one side.
2. Tongue protrusion
3. Facial grimacing
4. Opisthotonos
Other symptoms that may be seen include:
1. Oculogyric crisis – fixed deviation of the eyes in one direction.
2. Buccolingual crisis
3. Trismus- lockjaw due to spasms of the muscles of mastigation.

9. Clinical presentation continues
5. Opisthotonic crisis- characteristic flexion posturing with arching of the back
6. Tortipelvic crisis – Typically involves, hip, pelvis, and abdominal wall muscles, causes
difficulty with ambulation
7. Forced jaw opening
8. Difficulty speaking

10. Differential diagnosis
 Anticholinergic toxicity
 Carbamazepine toxicity
 Conversion Disorder in emergency medicine
 Focal seizure
 Hypocalcemia
 Mandible dislocation
 Meningitis
 Neuroleptic malignant syndrome
 Pediatric status epilepticus
 Phenytoin toxicity
 Status Epilepticus

11. Differentials contin….
 Hemorrhagic Stroke
 Ischemic stroke
 Strychnine ingestion
 Tetanus
 Valproate toxicity

12. Management
 Non-pharmacological:
securing of the airway in laryngeal and pharyngeal dystonia to avoid
respiratory arrest.
 Pharmacologic treatment, typically with anticholinergic agents, resolves the reaction
within 10-30minutes. Continue medication for 48-72 hours to prevent relapse, as
follows:
• Benztropine 1-2mg PO bid
• Diphenhydramine 25-50mg PO qid
Arrange Psychiatric follow-up care if patient has a dystonic reaction while taking
neuroleptic medication. When continued neuroleptic therapy is necessary, maintain
patient on an anticholinergic agent or switch to a neuroleptic that is less likely to
produce an acute dystonic reaction.

13. Tardive dyskinesia
INTRODUCTION
 The Diagnostic and Statistical Manual of Mental Disorders, Fifth edition(DSM-V)
defines tardive dyskinesia as a medication-induced movement disorder that
persist despite discontinuation or change of the medication._x0000_
TD may be difficult to detect and recognize. It may coexist with non-TD movement
disorders such as
drug-induced tremor, akathisia, or acute dystonic reactions that obscure the
classic TD movements, and it is easily confused with movement abnormalities
including mannerisms and stereotypies that occur in psychiatrically ill patients.This
presentation introduces a clinical description of the classic features
of TD, summarizes the various types of tardive movement disorders,, discusses the

14. Etiology
Tardive dyskinesia (TD) is an iatrogenic hyperkinetic movement disorder
resulting from chronic administration of dopamine@A)-blocking agents,
including the typical antipsychotic agent_x0000_, especially the typical antipsychotics like;
(Chlorpromazine,Fluphenazine ,Haloperidol)
Current evidence suggests that the incidence of tardive dyskinesia is lower with
atypical antipsychotic agents such as clozapine, olanzapine, and risperidone than
with haloperidol
 certain antidepressants (e.g.,

 maprotiline), and some antinausea/ antiemetic compounds (e.g., prochlorperazine and

 metoclopramide). _x0000_

15. Epidemiology
 It occurs in approximately 25 percent of patients who receive

 neuroleptic agents for a 3-6months, and in 50 percent of these patients it

 becomes a chronic irreversible condition._x0000_
 Common in women
 Elderly
 Those with diffused brain dysfunction

16. Risk factors
 Prolong use of antipsychotic agents, especially the typical ones
 Mood disorders
 Patients with schizophrenia
 Other movement disorders
 Diabetes mellitus
 Greater than 50yrs of age
 Black race
 Post-menopause
 Learning disability
 Brain injury

17. Pathophysiology
 The cause of tardive dyskinesia is uncertain, but it could be due to hypersensitivity to dopamine as a result of
prolonged dopaminergic blockade. This explanation is consistent with the observations that tardive
dyskinesia may be aggravated by stopping antipsychotic drugs or by the administration of anticholinergic
antiparkinsonian drugs (presumably by upsetting further the balance between cholinergic and dopaminergic
systems in the basal ganglia).
 The most common Hypothesis concerning the neurochemical pathology of tardive dyskinesia are:
 Dopamine hypersensitivity
 Free radical-induced neurotoxicity
 GABA insufficiency
 Noradrenergic dysfunction

18. Clinical manifestation
Classic TD is characterized by
occurrence of abnormal movements in the lower face and distal limbs_x0000_
Typical facial movements include:
lip smacking,
chewing,
sucking,
puckering,
tongue writhing,
tongue protrusion,
jaw opening and closing, and
grimacing.
Usually described as choreiform movement (jerky movement) _x0000_

19. Differential diagnosis
 Huntington disease dementia
 Resting tremor
 Spontaneous dyskinesia
 Psychotic mannerisms
 Stereotypy

20. Treatment
 Minimize the use of anticholinergics. Although they probably do not contribute to
the etiology of the disorder, they often exacerbate its clinical manifestations
 Reduce neuroleptics to lowest acceptable doses. _x0000_This may, for the first few
weeks, worsen the TD but maximizes the likelihood of reversing the condition
over time. It may be possible to minimize or avoid the usual worsening during
neuroleptic reduction by employing a slowly tapering regimen.
 For clinically severe TD, divide daytime doses of neuroleptics to provide maximum
suppression. This strategy helps ameliorate the movements in up to 70 percent of
patients_x0000__x0000_ _x0000__x0000_

21.  DRUGS:
 valbenazine(Ingrezza) the first drug to treat tardive dyskinesia. Valbenazine is a
selective vesicular monoamine transporter 2 (VMAT2) inhibitor. These drugs modulate
the presynaptic packaging and release of dopamine into the synapse, and may offset
the movement-related effects of antipsychotics and other dopaminergic blockers.
 Dosage:Indicated for treatment of adults with tardive dyskinesia

 40 mg PO qDay x1 week, then increase to the recommended dose of 80 mg PO qDay

 40-60 mg qDay may be considered depending on response and tolerability

22.  2.Deutetrabenazine (Austedo) is a novel, highly selective vesicular
monoamine transporter type 2 (VMAT2) inhibitor. FDA has approved
deutetrabenazine tablets for the treatment of adults with tardive dyskinesia
(TD).deutetrabenazine, starting at 12 mg/day, with titration up to 48 mg/day over
a six-week period. This was followed by a six-week maintenance period at an
average dose of 38.3 mg/day.
 3.Clonazepam (1-4.5 mg/day) showed a decrease of TD symptoms

23. Conclusion
 Acute dystonic reactions and tardive dyskinesia are extapyramidal side effects of
medications , though idiosyncratic and iatrogenic respectively can be avoided
controlled as the case maybe.