Journal CMEs

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Leonard Lachover, MD, and John Dziuba, MD

Needs Assessment: Psychiatrists prescribe both typical and atypical antipsychotics on a daily basis. The awareness of the frequency and severity of potential side effects of neuroleptics is essential for good patient care. Oromandibular dystonias may be accompanied by a dislocated jaw; however, this diagnosis may not be recognized. Physicians should be aware of the signs and symptoms of jaw dislocation so as to obtain proper consultation with oral surgeons. Missing the diagnosis of jaw dislocation can cause prolonged, dangerous, and unnecessary suffering for the patient.

Learning Objectives:
• Recognize the potential to induce oral-buccal-lingual dystonic side effects when using neuroleptic medications.
• Identify signs and symptoms of jaw dislocation secondary to neuroleptic-induced oromandibular dystonias.
• Apply the emergency treatment for acute dystonia.
• Recognize the importance of thorough and complete diagnosis when dealing with a patient experiencing side effects from antipsychotics.

Target Audience: Primary care physicians and psychiatrists.

CME Accreditation Statement: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the Mount Sinai School of Medicine and MBL Communications, Inc. The Mount Sinai School of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Credit Designation: The Mount Sinai School of Medicine designates this educational activity for a maximum of 3 AMA PRA Category 1 Credit(s)TM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Faculty Disclosure Policy Statement: It is the policy of the Mount Sinai School of Medicine to ensure objectivity, balance, independence, transparency, and scientific rigor in all CME-sponsored educational activities. All faculty participating in the planning or implementation of a sponsored activity are expected to disclose to the audience any relevant financial relationships and to assist in resolving any conflict of interest that may arise from the relationship. Presenters must also make a meaningful disclosure to the audience of their discussions of unlabeled or unapproved drugs or devices. This information will be available as part of the course material.

This activity has been peer-reviewed and approved by Eric Hollander, MD, chair and professor of psychiatry at the Mount Sinai School of Medicine, and Norman Sussman, MD, editor of Primary Psychiatry and professor of psychiatry at New York University School of Medicine. Review Date: July 23, 2007.

Drs. Hollander and Sussman report no affiliation with or financial interest in any organization that may pose a conflict of interest.

To receive credit for this activity: Read this article and the two CME-designated accompanying articles, reflect on the information presented, and then complete the CME quiz. To obtain credits, you should score 70% or better. Early submission of this posttest is encouraged to measure outcomes for this CME activity. Please submit this posttest by August 1, 2009 to be eligible for credit. Release date: August 1, 2007. Termination date: August 31, 2009. The estimated time to complete all three articles and the quiz is 3 hours.

Primary Psychiatry. 2007;14(8):70-72

 

Dr. Lachover is clinical assistant professor in the Department of Psychiatry and Behavioral Neurosciences at Wayne State University School of Medicine in Detroit, Michigan. Dr. Dziuba is chief of psychiatry at Sinai-Grace Hospital and assistant professor in the Department of Psychiatry and Behavioral Neurosciences at Wayne State University School of Medicine.

Disclosure: The authors report no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Leonard Lachover, MD, Clinical Assistant Professor, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, The Ardmore Clinic, 14230 W. McNichols, Detroit, MI 48235; Tel: 313-966-2100; Fax: 313-966-4916; E-mail: keshet18@aol.com.

 

 


 

 

Abstract

A 26-year-old African-American male diagnosed with bipolar disorder with psychotic features was referred for outpatient treatment following inpatient hospitalization. The patient developed dysarthria after receiving oral and intramuscular haloperidol at the hospital. The patient’s oral symptoms were not affected by change of antipsychotic or addition of benztropine. A neurologic evaluation indicated a dystonia secondary to haloperidol. The consultant recommended an increase of benztropine that proved unsuccessful. A suggestion of botulinum injections into the jaw was not pursued. His oral symptoms worsened to include difficulty chewing and jaw tightness. The persistence of symptoms resulted in a referral to an oral surgeon. The patient’s evaluation revealed bilateral anterior temporal-mandibular joint dislocation. Manual reduction of the dislocations under general anesthesia relieved all oral symptomatology.

 

Introduction

The development of acute dystonic reactions due to antipsychotic use is well known and widely described. The clinical picture involves the rapid development of sustained muscular contractions involving the tongue, jaw, neck, eyes or entire body. The movements produced may be twisting or torsional and may be accompanied by pain and fear. The dystonia may manifest as trismus, blepharospasm oculogyric crisis, grimacing, forced jaw opening, protrusion of the tongue, or glossopharyngeal muscle contraction.1

Approximately 10% of patients exposed to typical antipsychotics will experience a dystonic reaction.1 This usually occurs within the first 4 days of treatment.2 The proposed mechanism of action has been postulated to be dopaminergic hyperactivity in the basal ganglia that occurs when central nervous system levels of an antipsychotic begin to fall. Risk factors include young adults, male gender, and history of cocaine use. Treatment involving a high-potency neuroleptic, especially when an intramuscular injection is used, also increases the risk.1 The occurrence of acute dystonias in patients treated with atypical antipsychotics, though reported, is felt to be rare.3-5

The following is a case of an African American male diagnosed with a dystonic reaction secondary to antipsychotic use. Traditional treatments of benztropine and a medication switch failed to alleviate the symptoms. Neurologic consultation did not provide relief. A consultation by an oral surgeon produced an unanticipated finding that led to complete symptom relief.

 

Case Report

A 26-year-old African American male was referred for outpatient care immediately following discharge from a psychiatric hospital. He related a 2-month history of increasing manic and psychotic symptoms prior to his inpatient stay. His symptoms included grandiose thoughts, decreased sleep, racing thoughts, rapid speech, auditory hallucinations, and paranoia. His interest in religion had also increased. He was forced to take a leave from his job as a community center director due to the severity of his illness.

The patient related that he was initially treated with oral haloperidol in the hospital and later given an intramuscular injection of haloperidol. The patient stated he had trouble speaking after the injection. He said he had difficulty being understood. He expressed embarrassment over his difficulty in enunciating words. He related that these symptoms arose quickly and had been unremitting. His inpatient psychiatrist changed his medication to quetiapine and he was discharged. He was told his speech difficulty “would go away.”

 At the initial meeting, the patient was intrusive, religiously preoccupied, and delusional. He had increased verbal productivity; however, he was dysarthric. He did not speak clearly and was difficult to understand. Efforts to obtain his hospital records and ascertain whether haloperidol decanoate was utilized in his treatment were unsuccessful. The patient told us of prior psychiatric treatment for mood symptoms and psychosis. He had been previously prescribed, at various times, antipsychotics, selective serotonin reuptake inhibitors, and benzodiazepines.

The patient’s psychiatric diagnosis was bipolar disorder with psychotic features. The patient was maintained on quetiapine and a mood stabilizer was recommended. Initial observation was that his speech difficulty was a dystonic reaction to the haloperidol. Benztropine 1 mg BID was begun. A consultation with a neurologist specializing in movement disorders was also arranged.

The patient was seen frequently over the next few weeks. Valproic acid was initiated and the benztropine titrated upwards to 2 mg BID. The patient’s psychiatric symptoms diminished and eventually went away, but his dysarthria remained.

The neurologist determined that the speech difficulty was an oromandibular dystonia related to the haloperidol given on the inpatient unit. He did not believe quitiapine was a contributing factor. Benztropine was increased to 2 mg TID. The neurologist stated that the oral symptoms would disappear in 2–9 months. He also recommended botulinum injections to the masseter muscles in order to hasten the patient’s recovery. The patient declined the injections.

The patient’s oral symptoms did not improve with the increase in benztropine. He began to complain of additional symptoms. He said he had difficulty chewing solid foods and was losing weight. He complained of headaches which he associated with “jaw tightness.” A consultation with an oral surgeon was scheduled.

The patient showed a remarkable change during his next visit to the clinic. He spoke clearly, effortlessly, and without difficulty. He was easily understood. He reported eating normally. He denied jaw pain or discomfort. He felt his speech had returned to normal and he was symptom free. The patient related he had been suffering from a dislocated jaw. He said the dentist’s examination and x-rays revealed bilateral anterior dislocations of both temporal-mandibular joints. His treatment consisted of being placed under general anesthesia and having the dislocated jaw manually reduced. The patient reported immediate relief of symptoms. He said he had mild jaw soreness related to the procedure for a few days that then went away.

Benztropine was discontinued but quetiapine and valproic acid were maintained. The patient did clinically well for 1 year and then left treatment. He did not experience any more jaw difficulties.

 

Discussion

This is a case of jaw dislocation occasioned by haloperidol-induced acute oromandibular dystonia. Although rare, this clinical scenario has been previously reported with dopamine-blocking agents used as antiemetics and antipsychotics.2 A review of the literature teaches that jaw dislocation should be considered in all cases of acute oromandibular dystonia.

The classic description of jaw dislocation associated with acute dystonia was provided by O’Hara6 in 1958. In this case, a 45-year-old woman underwent surgery and experienced persistent nausea and vomiting post operatively. She was treated with prochlorperazine injections (a derivative of phenothiazine). On her fifth day of treatment she experienced a tonic spasm of the trunk and face. The painful spasmodic contractions were most marked in the platysma and muscles of mastication. The most striking aspect throughout her episode was the facial contortions in which two teeth were chipped and the jaw was dislocated to the right. Kraak7 and Ryan and LaDow8 also reported cases of prochlorperazine-producing spasms of the masticatory muscles in patients treated for nausea. These dystonic reactions resulted in temperomandibular dislocations.

The occurrence of jaw dislocation resulting from antipsychotics has also been documented. O’Connor and colleagues9 wrote of a 21-year-old male who developed an oral-buccal-lingual dystonia after being given intramuscular haloperidol. In addition, the patient displayed facial asymmetry, difficulty swallowing, salivary drooling, and an inability to close his mouth. X-rays revealed an anterior dislocation of the right temperomandibular joint. Multani and Varma10 reported a case of a 33-year-old woman treated for hallucinations and delusions with haloperidol. In her 14th day of treatment, she developed orofacial dystonia with resultant jaw dislocation. Ibrahim and Brooks11 also reported a case of neuroleptic-induced temperomandibular joint dislocation. Undt and colleagues12 reported a case of recurrent temperomandibular dislocations in a psychiatric patient treated with haloperidol.

The emergence of acute dystonia in a patient requires immediate treatment. For example, laryngeal dystonia may be fatal if untreated.13 Kaplan and Sadock1 reported that intramuscular anticholinergics or intramuscular or intravenous diphenhydramine almost always alleviate the symptoms. They also stated that intravenous diazepam, amobarbital, caffeine sodium benzoate, and hypnosis have reported effectiveness. Corre and colleagues14 emphasized that patients treated for dystonic reactions should be closely monitored for at least 48–72 hours after initial therapy. They cited numerous cases of patients who were successfully treated in an emergency department only to experience recurrence of symptoms within the next few days. The continued use of oral anticholinergics, in these situations, should be considered.1 Their utilization should last a few weeks prior to attempts to gradually taper. The recurrence of dystonias is an indication for restarting anticholinergics.15 Prophylatic use of anticholinergics to prevent initial symptom emergence is a common treatment approach.16

The suspicion of oramandibular dislocation should result in a referral to an oral surgeon for further investigation and treatment. Clinical signs of jaw dislocation include pain, inability to completely close the mouth, deviation of the jaw to the side or forward protrusion of the mandible, difficulty swallowing, drooling from the mouth, difficulty chewing, and difficulty articulating.10

This case report illustrates the importance of continued clinical investigation when standard treatments do not produce expected results. It stresses the need for a physician to reassess his clinical conclusions when a patient’s progress stalls. The physician‘s ability to consider rare and unusual possibilities can improve a patient’s care and outcome. The physician is well served by seeking alternative opinions when clinical progress is unexpectedly delayed. When one hears the sounds of galloping hoofs approaching, the possibility of a zebra’s arrival should not be discounted.

 

Conclusion

Patients presenting with oromandibular movement disorders deserve a thorough evaluation to determine an accurate diagnosis. Oromandibular dystonia is a serious and painful antipsychotic side effect, and the possibility of jaw dislocation should be carefully excluded. Delay in diagnosis causes unnecessary suffering for the patient. The suspicion of jaw dislocation should result in consultation and referral for further evaluation and treatment. PP

 

References

1. Kaplan H, Sadock B. Dopamine receptor antagonists: antipsychotics. In: Kaplan H, Sadock B. Pocket Handbook of Psychiatric Drug Treatment. Lippincott Williams & Wilkins, Baltimore, MD: 1993:122-123.
2. Dressler D, Benecke R. Diagnosis and management of acute movement disorders. J Neurol. 2005;252(11):1299-1306.
3. Raja M, Azzoni A. Novel antipsychotics and acute dystonic reactions. Int J Neuropsychopharmacol. 2001;4(4):393-397.
4. Alevizos B, Papageorgiou C, Christodoulou GN. Acute dystonia caused by low dosage of olanzapine. J Neuropsychiatry Clin Neurosci. 2003;15(2):241.
5. Dew R, Hughes D. Acute dystonic reaction with moderate dose ziprasidone. J Clin Psychopharmacol. 2004;24(5):563-564.
6. O’Hara VS. Extrapyramidal reactions in patients receiving prochlorperizine. N Engl J Med. 1958;259(17):826-828.
7. Kraak JG. A drug initiated dislocation of the temporomandibular joint: report of case. J Am Dent Assoc. 1967;74(6):1247-1249.
8. Ryan M, LaDow C. Subluxation of the temporomandibular joint after administration of prochlorperazine. J Oral Surg. 1968;26(10):646-648.
9. O’Connor M, Rooney MD, Nienaber CP. Neuroleptic-induced dislocation of the jaw. Br J Psychiatry. 1992;161:281-282.
10. Multani HS, Varma GK. Dislocated jaw concealed by dystonia. Psychosomatics. 1982;23(6):671.
11. Ibrahim ZY, Brooks EF. Neuroleptic-induced bilateral temporomandibular joint dislocation. Am J Psychiatry. 1996;153(2):293-294.
12. Undt G, Weichselbraun A, Wagner A, Kermer C, Rasse M. Recurrent mandibular dislocation under neuroleptic drug therapy, treated by bilateral eminectomy. J Craniomaxillofac Surg. 1996;24(3):184-188.
13. Christodoulou C, Kalaitzi C. Antipsychotic drug-induced acute laryngeal dystonia: two case reports and a mini review. J Psychopharmacol. 2005;19(3):307-311.
14. Corre KA, Niemann JT, Bessen HA. Extended therapy for acute dystonic reactions. Ann Emerg Med. 1984;13(3):194-197.
15. Kaplan H, Sadock B. Biological therapies. In: Kaplan H, Sadock B. Synopsis of Psychiatry. 8th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1998:980.
16. Goff DC, Arana GW, Greenblatt DJ, et al. The effect of benztropine on haloperidol-induced dystonia, clinical efficacy and pharmacokinetics: a prospective, double-blind trial. J Clin Psychopharmacol. 1991;11(2):106-112.