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ACUTE DYSTONIC REACTION new.pptx
- 1. ACUTE DYSTONIC REACTION ANDTARDIVE DYSKINESIA
- 2. OUTLINE Introduction Epidemiology Etiopathogenesis Clinical presentation Differential diagnosis Prognosis Management Conclusion
- 3. Introduction Acute dystonic reactionsor 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 isno 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 dystonicreactions 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 Theprimary 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 factorsincludes: A family history of dystonia and Viral infection Alcohol and cocaine use, increases risk.
- 8. Clinical presentation Thisoften 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 Anticholinergictoxicity 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…. HemorrhagicStroke Ischemic stroke Strychnine ingestion Tetanus Valproate toxicity
- 12. Management Non-pharmacological: securing ofthe 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 TheDiagnostic 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 occursin 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 Prolonguse 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 causeof 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 TDis 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 Huntingtondisease dementia Resting tremor Spontaneous dyskinesia Psychotic mannerisms Stereotypy
- 20. Treatment Minimize theuse 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 dystonicreactions and tardive dyskinesia are extapyramidal side effects of medications , though idiosyncratic and iatrogenic respectively can be avoided controlled as the case maybe.