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Tardive dyskinesia: An unrecognized cause of orofacial pain
oral medicine Editor: JAMES
W. LITTLE,
D.M.D.,
M.S.D.
School of Dentistry University of Minnesota 515 S.E. Delaware St. Minneapolis, Minn. 55455
Tardive dyskinesia: An unrecognized cause of orofacial pain Anne Bassett, M.D.,* Ronald A. Remick, M.D., F.R.C.P.(C),** and Bruce Blasberg, D.M.D., *** Vancouver, British Columbia, Canada UNIVERSITY
OF BRl’i-ISH
COLUMBIA
Tardive dyskinesia has not previously been discussed in the dental literature. It is a drug-induced movement disorder commonly involving the perioral and masticatory muscles. It can sometimes be a cause of orofacial pain. Two brief cases reports are provided as examples. Clinical features of tardive dyskinesia are presented to assist the dental practitioner in recognizing the syndrome. Suggestions for management are included. (ORAL SURC. ORAL MED. ORAL PATHOL. 61570-572, 1986)
I
n our Atypical Facial Pain Clinic’x2 we have diagnosed tardive dyskinesia, an involuntary movement disorder, as the medical disorder that was responsible for four patients’ (4/ 121, 3.3%) complaints of facial pain. Although tardive dyskinesia is not a common cause of orofacial pain, the presenting complaints and symptoms are quite characteristic of this disorder. It would not be unusual for a patient with tardive dyskinesia to first consult a dentist for treatment. However, tardive dyskinesia is a relatively new medical disorder that may be unfamiliar to many dentists. Accordingly, we offer a description of tardive dyskinesia to assist the dental clinician in recognizing this problem. CASE 1
A 63-year-old widow was referred for neuropsychiatric assessment on her “atypical facial pain.” She had seen severaldentistsbecauseof oral pain anddifficulty in eating with her dentures.She complainedof pain secondaryto
*Resident, Department of Psychiatry. **Clinical Associate Professor, Department of Psychiatry: Director, Atypical Facial Pain Clinic, Shaughnessy Hospital. ***Associate Professor, Oral Medicine, Faculty of Dentistry.
570
“playing with her mouth,” by which shemeantclenching her teeth. She saidthat shewasunableto stopthis habit. She attributed her dificulties to an ill-fitting set of completedenturesshe had received 4 years earlier, and three newersetsof completedentureshad not resolvedthe problem. Medical history revealedthat the patient wascurrently taking diazepam5 mgby mouththree timesa day, and the antipsychoticdrug methotrimeprazine,100mg at bedtime, for her “nerves.” She begantaking thesemedications6 years earlier, when her husbanddied, and she had been unableto decreaseor discontinuethem through the years without an exacerbationof her anxiety anddepression.On clinical examination, involuntary facial grimacing, mild lateral movementsof the jaw, lip-chewingmovements,and rhythmic involuntary movementsof the tongue were noted. The diagnosticimpressionwas that the orofacial pain wasdue to tardive dyskinesia,secondaryto the long-term use of the neuroleptic drug methotrimeprazine. At a follow-up assessment 2 years later orofacial movements were unchanged.The patient continuedto take methotrimeprazinein lower dosesfor her psychiatric disorder. CASE 2
A 60-year-oldwomanhad further assessment of orofacial pain, describedby her referring physicianasleft-sided jaw pain with headaches.The patient stated that her jaw
Volume Number
61 6
“gnawed away” on her left side, and she continually “chewed away” at her jaw. These oral movements occurred throughout the day when she was unaware of them, but they ceased when she consciously focused upon stopping them. The patient had seen two dentists, her family physician, a hypnotherapist, and an acupuncturist without relief. Through her life she had had extensive psychiatric treatment for depression. Her current medicines were amitriptyline, 150 mg daily, and the antipsychotic drug perphenazine, 4 mg daily. On examination, lateral jaw movements, lip-smacking movements, eye blinking, and an involuntary anteriposterior head rocking were noted. The diagnostic impression was that the facial pain syndrome was due to tardive dyskinesia resulting from long-term use of perphenazine. She was taking no neuroleptic medication at the 6-month follow-up. Her involuntary orofacial movements were unchanged. DlSCUSSlON
Tardive dyskinesia is a late-appearing movement disorder that occurs in patients who have taken neuroleptic (antipsychotic or “major” tranquilizer) drugs. Characteristically, the abnormal movements are involuntary or semivoluntary, and they include dyskinesias, chorea, and tics that involve the tongue, perioral, facial, and masticatory muscles. As these are often the initial and most prominently involved areas, the dentist may frequently be the first health professional to become aware of this distressing preventable condition. The patient might come to the dentist complaining of ill-fitting dentures or unwanted continual chewing motions attributed to a dental condition. Although tardive dyskinesia is a painless syndrome, secondary orofacial pain can result from chronic mild trauma between denture-bearing mucosa and dentures, which occurs with the abnormal movements. However, most patients would have no specific complaints, and in early or mild cases (the majority) the abnormal movements are not subjectively troublesome to the patient or particularly obvious to an untrained observer. During the examination of the patient, the dentist can recognize involuntary movements that commonly occur in tardive dyskinesia. Fine wormlike movements of the tongue can be seen in the early stages of the disorder. Later, there may be involuntary rhythmic movements of the tongue, both inside the mouth and protruding. Sucking, puckering, smacking, and grimacing movements of the mouth are typical. One may see chewing movement of the jaw and puffing of the cheeks. Although these movements are involuntary, they can be controlled briefly by voluntary effort (for example, when the patient is made consciously aware
Tardive dyskinesia
57 I
of the movement). This voluntary control is often accompanied by an unpleasant feeling of internal tension. The dyskinesia is worsened by anxiety or stress and intentional motor activity. Like all abnormal involuntary movements, they disappear during sleep. Thus, patients may notice that pain symptoms related to this disorder are less on awakening. The examiner may observe several associated signs. Involuntary choreiform movements sometimes occur in the limbs and trunk (for example, rocking movements of the trunk or legs, nodding of the head). If the patient is taking neuroleptic drugs at the time of examination, other side effects of these medications may be present. Dry mouth due to anticholinergic mechanisms that decrease salivation is particularly common. Pseudoparkinsonian side effects are frequently found: immobile facial expression, resting “pill-rolling” tremor, shuffling gait, and difficulty getting out of a chair. Notably, these parkinsonian neuroleptic side effects can mask the abnormal movements of tardive dyskinesia. Thus, a recent discontinuation or reduction in dosage of a drug may reveal previously masked symptoms. Essential to the diagnosis of tardive dyskinesia is a history of present or past use of any neuroleptic drug. Common examples of such medications are: chlorpromazine (Largactil), haloperidol (Haldol), thioridazine (Mellaril), trifluoperazine (Stelazine), methotrimeprazine (Nozinan, Levoprome, Veractil), perphenazine (Trilafon), and pimozide (Orap). These neuropharmacologic agents are indicated primarily for their antipsychotic property, most often for a schizophrenic illness and other psychoses. They are also used for other psychologic conditions (anxiety and behavior problems associated with mental retardation, dementia, personality disorders, depression) and some, such as the antinauseants prochlorperazine (Stemetil, Compazine) or metoclopramide (Maxeran, Reglan, Cerucal, Maxolon, Primperan), are used for nonpsychologic conditions. Every patient who is treated with neuroleptics is at some risk of developing tardive dyskinesia. However, the syndrome usually begins after several months or years of neuroleptic drug use. Paradoxically, stopping or reducing the dosage may unmask symptoms and usually aggravates the disorder. Tardive dyskinesia does not develop in every patient with long-term exposure to neuroleptic drugs. The most recent prevalence estimates indicate that the syndrome will be diagnosed in about 20% of those at risk of developing tardive dyskinesia.3 Risks appear to be increased for the elderly, women, and those patients with diffuse brain pathosis (the socalled organic brain syndromes).
572
Bassett, Remick,
and Blasberg
All involuntary movements of the mouth, even in a patient who is taking neuroleptic drugs, do not necessarily represent manifestations of tardive dyskinesia. There is a low rate of spontaneous abnormal movement disorders in the elderly, which increases with concurrent medical illnesses. There is about a 6% rate of spontaneous dyskinesia in schizophrenics.4 Other conditions that can be confused with tardive dyskinesia include habitual oral muscular activity secondary to ill-fitting dentures, Huntington’s disease, and reversible drug-induced chorea secondary to L-dopa (used in treatment of Parkinson’s disease), amphetamine, or methylphenidate (Ritalin). When a patient has clinical observable involuntary movements and a positive neuroleptic drug history, the dentist should suspect tardive dyskinesia. A patient with these signs should have a neuropsychiatric assessment by a specialist (psychiatrist or neurologist) familiar with movement disorders. Guidelines for dentists in obtaining such a referral have been suggested.5 The dentist should inform the patient of the abnormal movements noticed and recommend further evaluation by a specialist. The diagnosis remains a clinical one, however. There are no confirmatory tests for tardive dyskinesia. The disorder is reversible for more than one third of all patients who stop taking the neuroleptic drug.6 The likelihood of reversibility is greater in younger patients and increase with the time the patient has been off the medication (months to several years).’ A psychiatrist will be able to decide if the drug no longer seems necessary or if the psychiatric condition allows a gradual tapering and/or discontinuation of neuroleptic drugs. In nonpsychotic illnesses, other drugs or nonpharmacologic treatments are indicated as first-line therapies. For many patients with schizo-
Oral Surg. June, 1986
phrenic illness, however, stopping the drug exacerbates psychotic symptoms and the movement disorder must be tolerated as the lesser of the two evils. Unfortunately, there is no satisfactory treatment for tardive dyskinesia. A number of medications have been tried on experimental bases, but none has proved universally effective. Prevention is currently the only answer to the problem of tardive dyskinesia. A dentist’s recognition of possible tardive dyskinesia can be of invaluable assistance to the early detection and assessment for treatment of this distressing movement disorder. REFERENCES I. BIasberg B, Remick RA, Conklin R, Keller FD: Atypical facial pain in the elderly. Gerondontology 3: 77-81, 1984. 2. Remick RA, Blasberg B, Campos PE, Miles JE: Psychiatric disorders associated with atypical facial pain. Can J Psychiatry 28: 178-181, 1983. 3. Baldessarini RJ: Clinical and epidemiologic aspects of tardive dvskinesia. J Clin Psvchiatrv 46: 8-13, 1985. 4. Baldessarini RJ, Cole JO, Davis JM, Gardos G, Preskorn SH, Simpson GM, Tarsy D: American Psychiatric Association Task Force Report: Tardive Dyskinesia, Washington, D.C., 1980. American Psychiatric Association. 5. Blasberg B, Remick RA, Miles JE: The psychiatric referral in dentistry: indications and mechanics. ORAL SURG ORAL MED ORAL PATHOL 56: 368-371, 1983. 6. Jeste DV, Wyatt RJ: Therapeutic stategies against tardive dyskinesia: two decades of experience. Arch Gen Psychiatry 39: 803-816, 1982. 7. Jeste DV, Wyatt RJ: Prevention and management of tardive dyskinesia. J Clin Psychiatry 46: l4- 18, 1985. Reprint requests to: Dr. Ronald A. Remick Department of Psychiatry Health Sciences Centre Hospital Universitv of British Columbia Hospital 2255 Wesbrook Mall Vancouver, British Columbia V6T 2A I, Canada
W. LITTLE,
D.M.D.,
M.S.D.
School of Dentistry University of Minnesota 515 S.E. Delaware St. Minneapolis, Minn. 55455
Tardive dyskinesia: An unrecognized cause of orofacial pain Anne Bassett, M.D.,* Ronald A. Remick, M.D., F.R.C.P.(C),** and Bruce Blasberg, D.M.D., *** Vancouver, British Columbia, Canada UNIVERSITY
OF BRl’i-ISH
COLUMBIA
Tardive dyskinesia has not previously been discussed in the dental literature. It is a drug-induced movement disorder commonly involving the perioral and masticatory muscles. It can sometimes be a cause of orofacial pain. Two brief cases reports are provided as examples. Clinical features of tardive dyskinesia are presented to assist the dental practitioner in recognizing the syndrome. Suggestions for management are included. (ORAL SURC. ORAL MED. ORAL PATHOL. 61570-572, 1986)
I
n our Atypical Facial Pain Clinic’x2 we have diagnosed tardive dyskinesia, an involuntary movement disorder, as the medical disorder that was responsible for four patients’ (4/ 121, 3.3%) complaints of facial pain. Although tardive dyskinesia is not a common cause of orofacial pain, the presenting complaints and symptoms are quite characteristic of this disorder. It would not be unusual for a patient with tardive dyskinesia to first consult a dentist for treatment. However, tardive dyskinesia is a relatively new medical disorder that may be unfamiliar to many dentists. Accordingly, we offer a description of tardive dyskinesia to assist the dental clinician in recognizing this problem. CASE 1
A 63-year-old widow was referred for neuropsychiatric assessment on her “atypical facial pain.” She had seen severaldentistsbecauseof oral pain anddifficulty in eating with her dentures.She complainedof pain secondaryto
*Resident, Department of Psychiatry. **Clinical Associate Professor, Department of Psychiatry: Director, Atypical Facial Pain Clinic, Shaughnessy Hospital. ***Associate Professor, Oral Medicine, Faculty of Dentistry.
570
“playing with her mouth,” by which shemeantclenching her teeth. She saidthat shewasunableto stopthis habit. She attributed her dificulties to an ill-fitting set of completedenturesshe had received 4 years earlier, and three newersetsof completedentureshad not resolvedthe problem. Medical history revealedthat the patient wascurrently taking diazepam5 mgby mouththree timesa day, and the antipsychoticdrug methotrimeprazine,100mg at bedtime, for her “nerves.” She begantaking thesemedications6 years earlier, when her husbanddied, and she had been unableto decreaseor discontinuethem through the years without an exacerbationof her anxiety anddepression.On clinical examination, involuntary facial grimacing, mild lateral movementsof the jaw, lip-chewingmovements,and rhythmic involuntary movementsof the tongue were noted. The diagnosticimpressionwas that the orofacial pain wasdue to tardive dyskinesia,secondaryto the long-term use of the neuroleptic drug methotrimeprazine. At a follow-up assessment 2 years later orofacial movements were unchanged.The patient continuedto take methotrimeprazinein lower dosesfor her psychiatric disorder. CASE 2
A 60-year-oldwomanhad further assessment of orofacial pain, describedby her referring physicianasleft-sided jaw pain with headaches.The patient stated that her jaw
Volume Number
61 6
“gnawed away” on her left side, and she continually “chewed away” at her jaw. These oral movements occurred throughout the day when she was unaware of them, but they ceased when she consciously focused upon stopping them. The patient had seen two dentists, her family physician, a hypnotherapist, and an acupuncturist without relief. Through her life she had had extensive psychiatric treatment for depression. Her current medicines were amitriptyline, 150 mg daily, and the antipsychotic drug perphenazine, 4 mg daily. On examination, lateral jaw movements, lip-smacking movements, eye blinking, and an involuntary anteriposterior head rocking were noted. The diagnostic impression was that the facial pain syndrome was due to tardive dyskinesia resulting from long-term use of perphenazine. She was taking no neuroleptic medication at the 6-month follow-up. Her involuntary orofacial movements were unchanged. DlSCUSSlON
Tardive dyskinesia is a late-appearing movement disorder that occurs in patients who have taken neuroleptic (antipsychotic or “major” tranquilizer) drugs. Characteristically, the abnormal movements are involuntary or semivoluntary, and they include dyskinesias, chorea, and tics that involve the tongue, perioral, facial, and masticatory muscles. As these are often the initial and most prominently involved areas, the dentist may frequently be the first health professional to become aware of this distressing preventable condition. The patient might come to the dentist complaining of ill-fitting dentures or unwanted continual chewing motions attributed to a dental condition. Although tardive dyskinesia is a painless syndrome, secondary orofacial pain can result from chronic mild trauma between denture-bearing mucosa and dentures, which occurs with the abnormal movements. However, most patients would have no specific complaints, and in early or mild cases (the majority) the abnormal movements are not subjectively troublesome to the patient or particularly obvious to an untrained observer. During the examination of the patient, the dentist can recognize involuntary movements that commonly occur in tardive dyskinesia. Fine wormlike movements of the tongue can be seen in the early stages of the disorder. Later, there may be involuntary rhythmic movements of the tongue, both inside the mouth and protruding. Sucking, puckering, smacking, and grimacing movements of the mouth are typical. One may see chewing movement of the jaw and puffing of the cheeks. Although these movements are involuntary, they can be controlled briefly by voluntary effort (for example, when the patient is made consciously aware
Tardive dyskinesia
57 I
of the movement). This voluntary control is often accompanied by an unpleasant feeling of internal tension. The dyskinesia is worsened by anxiety or stress and intentional motor activity. Like all abnormal involuntary movements, they disappear during sleep. Thus, patients may notice that pain symptoms related to this disorder are less on awakening. The examiner may observe several associated signs. Involuntary choreiform movements sometimes occur in the limbs and trunk (for example, rocking movements of the trunk or legs, nodding of the head). If the patient is taking neuroleptic drugs at the time of examination, other side effects of these medications may be present. Dry mouth due to anticholinergic mechanisms that decrease salivation is particularly common. Pseudoparkinsonian side effects are frequently found: immobile facial expression, resting “pill-rolling” tremor, shuffling gait, and difficulty getting out of a chair. Notably, these parkinsonian neuroleptic side effects can mask the abnormal movements of tardive dyskinesia. Thus, a recent discontinuation or reduction in dosage of a drug may reveal previously masked symptoms. Essential to the diagnosis of tardive dyskinesia is a history of present or past use of any neuroleptic drug. Common examples of such medications are: chlorpromazine (Largactil), haloperidol (Haldol), thioridazine (Mellaril), trifluoperazine (Stelazine), methotrimeprazine (Nozinan, Levoprome, Veractil), perphenazine (Trilafon), and pimozide (Orap). These neuropharmacologic agents are indicated primarily for their antipsychotic property, most often for a schizophrenic illness and other psychoses. They are also used for other psychologic conditions (anxiety and behavior problems associated with mental retardation, dementia, personality disorders, depression) and some, such as the antinauseants prochlorperazine (Stemetil, Compazine) or metoclopramide (Maxeran, Reglan, Cerucal, Maxolon, Primperan), are used for nonpsychologic conditions. Every patient who is treated with neuroleptics is at some risk of developing tardive dyskinesia. However, the syndrome usually begins after several months or years of neuroleptic drug use. Paradoxically, stopping or reducing the dosage may unmask symptoms and usually aggravates the disorder. Tardive dyskinesia does not develop in every patient with long-term exposure to neuroleptic drugs. The most recent prevalence estimates indicate that the syndrome will be diagnosed in about 20% of those at risk of developing tardive dyskinesia.3 Risks appear to be increased for the elderly, women, and those patients with diffuse brain pathosis (the socalled organic brain syndromes).
572
Bassett, Remick,
and Blasberg
All involuntary movements of the mouth, even in a patient who is taking neuroleptic drugs, do not necessarily represent manifestations of tardive dyskinesia. There is a low rate of spontaneous abnormal movement disorders in the elderly, which increases with concurrent medical illnesses. There is about a 6% rate of spontaneous dyskinesia in schizophrenics.4 Other conditions that can be confused with tardive dyskinesia include habitual oral muscular activity secondary to ill-fitting dentures, Huntington’s disease, and reversible drug-induced chorea secondary to L-dopa (used in treatment of Parkinson’s disease), amphetamine, or methylphenidate (Ritalin). When a patient has clinical observable involuntary movements and a positive neuroleptic drug history, the dentist should suspect tardive dyskinesia. A patient with these signs should have a neuropsychiatric assessment by a specialist (psychiatrist or neurologist) familiar with movement disorders. Guidelines for dentists in obtaining such a referral have been suggested.5 The dentist should inform the patient of the abnormal movements noticed and recommend further evaluation by a specialist. The diagnosis remains a clinical one, however. There are no confirmatory tests for tardive dyskinesia. The disorder is reversible for more than one third of all patients who stop taking the neuroleptic drug.6 The likelihood of reversibility is greater in younger patients and increase with the time the patient has been off the medication (months to several years).’ A psychiatrist will be able to decide if the drug no longer seems necessary or if the psychiatric condition allows a gradual tapering and/or discontinuation of neuroleptic drugs. In nonpsychotic illnesses, other drugs or nonpharmacologic treatments are indicated as first-line therapies. For many patients with schizo-
Oral Surg. June, 1986
phrenic illness, however, stopping the drug exacerbates psychotic symptoms and the movement disorder must be tolerated as the lesser of the two evils. Unfortunately, there is no satisfactory treatment for tardive dyskinesia. A number of medications have been tried on experimental bases, but none has proved universally effective. Prevention is currently the only answer to the problem of tardive dyskinesia. A dentist’s recognition of possible tardive dyskinesia can be of invaluable assistance to the early detection and assessment for treatment of this distressing movement disorder. REFERENCES I. BIasberg B, Remick RA, Conklin R, Keller FD: Atypical facial pain in the elderly. Gerondontology 3: 77-81, 1984. 2. Remick RA, Blasberg B, Campos PE, Miles JE: Psychiatric disorders associated with atypical facial pain. Can J Psychiatry 28: 178-181, 1983. 3. Baldessarini RJ: Clinical and epidemiologic aspects of tardive dvskinesia. J Clin Psvchiatrv 46: 8-13, 1985. 4. Baldessarini RJ, Cole JO, Davis JM, Gardos G, Preskorn SH, Simpson GM, Tarsy D: American Psychiatric Association Task Force Report: Tardive Dyskinesia, Washington, D.C., 1980. American Psychiatric Association. 5. Blasberg B, Remick RA, Miles JE: The psychiatric referral in dentistry: indications and mechanics. ORAL SURG ORAL MED ORAL PATHOL 56: 368-371, 1983. 6. Jeste DV, Wyatt RJ: Therapeutic stategies against tardive dyskinesia: two decades of experience. Arch Gen Psychiatry 39: 803-816, 1982. 7. Jeste DV, Wyatt RJ: Prevention and management of tardive dyskinesia. J Clin Psychiatry 46: l4- 18, 1985. Reprint requests to: Dr. Ronald A. Remick Department of Psychiatry Health Sciences Centre Hospital Universitv of British Columbia Hospital 2255 Wesbrook Mall Vancouver, British Columbia V6T 2A I, Canada