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Diagnostic dilemma: Drug withdrawal, borderline personality, and hyperthyroidism
CASE REPORT
BARUCH FISHMAN, Ph.D. ALAN BARASCH, M.D.
Diagnostic dilemma: Drug withdrawal, borderline personality, and hyperthyroidism Estimates of the incidence of medical illness in a psychiatric population range from 5% to 50%,' and in about 2% of all medical disorders the organic disturbance is the underlying cause of a psychiatric crisis. 2 Patients with hyperthyroidism, for example, can present a complex diagnostic dilemma because they manifest physical and psychological symptoms that may mimic anxiety disorders or manic depressive psychosis,"" and there are several reports'" of diagnostic and treatment difficulties. We describe a case of hyperthyroidism in a woman with borderline personality disorder, in which possible stimulant intoxication or sedative-hypnotic withdrawal further complicated diagnosis and treatment. Case report A 25-year-old single unemployed woman was admitted to the Payne Whitney Psychiatric Clinic from the emergency room after she requested hospitalization for drug detoxification, She reported heavy abuse of cocaine, methaqualone, and alcohol for several months, which had abruptly stopped a few days prior to admission because her supplier was hospitalized, She arrived for psychiatric examination looking adolescent in appearance and was also disheveled, wearing torn and dirty clothes, She undressed herself in public areas sayDr. Fishman is now a psychology fellow at Memorial Sloan-Kettering Cancer Center. and Dr. Barasch is clinical instructor of psychiatry at the Payne Whitney Psychiatric Clinic. New York. Reprint requests 10 Dr. Fishman at the Pain Service. Department of Neurology. Memorial Sloan-Kellering Cancer Center. 1275 York Ave., New York. NY 10021.
370
ing that she could not tolerate the heat, was hyperactive. restless, sexually disinhibited, and required active restraint. Her speech was loud and pressured, Her mood was euphoric and her affect was extremely labile, ranging from laughing and teasing to tearfulness and rage, Her thoughts were racing and tangential, but there were no abnormal perceptions, loosening of associations, or delusions, She reported sleep disturbances, weight loss but no decrease in appetite. and active suicidal ideation. She was hyperalert and highly distractible, but oriented to self, time, and place, Her higher cognitive functions were moderately impaired, but there was no evidence of delirium, Physical examination revealed SP of 130/50, temperature of 36°C, and pulse of 128. Routine admission laboratory tests, including complete blood cell count (CSC), electrolytes, and hepatic and renal functions, were within normal limits. Calcium and phosphorus values were minimally elevated with calcium at 10.6 mg/dL (normal 8,5 to 10.5 mg/dL) and phosphorus at 6.1 mg/dL (normal 2,2 to 4.2 mg/dL). A urine drug screen was positive only for diazepam, which the patient had received in the emergency room. The patient was the youngest of six siblings from a middleclass family, Since late adolescence she had experienced episodes of depression (but no mania), unstable family and social relationships, impulsive actions including sexual promiscuity, two abortions, multiple drug abuse, antisocial acts, temper outbursts, and two suicide attempts, This pattern was exacerbated after her father's death three years prior to admission. Never able to live away from her parents. she experienced intolerable anxiety and depression when alone. She had been treated for four years with psychotherapy, which she had abruptly terminated a few weeks prior to admission, The patient was diagnosed as: Axis I-mixed substance abuse, possible sedative-hypnotic withdrawal or PSYCHOSOMATICS
stimulant intoxication, and possible bipolar disorder, manic episode; and Axis II-borderline personality disorder. Initially, symptoms of insomnia, anxiety, irritability, and tachycardia were assessed as ongoing manifestations of sedative withdrawal, and the patient was begun on a detoxification regimen with diazepam, 10 mg every six hours. The symptoms of sexual disinhibition, affective lability, suicidal ideation, tantrums, and provocative behavior were seen as manifestations of a borderline personality disorder and were treated with firm limit setting. After 48 hours there was no improvement, and, assuming that we had underestimated the degree of sedative tolerance, we increased the diazepam dosage to 20 mg every six hours. However, during the following two days there was no sedation, and only minimal symptomatic improvement. On the fifth day of hospitalization a diagnosis of bipolar disorder, manic episode was definitively determined, and treatment with thiothixene and lithium carbonate was initiated. There was a rapid positive partial response, with improved sleep, reduced anxiety, and increased impulse control, but continued tachycardia, sweating, emotional lability, and disruptive behavior. On the eighth day of hospitalization the results of admission thyroid function tests arrived from the laboratory, and they revealed marked hyperthyroidism: triiodothyronine by radioimmunoassay (RIA) at 2.8 ng/mL (normal 0.8 to 2.0 ng/mL), thyroxine by RIA at 171 ng/mL (normal 45 to 120 ng/mL), free thyroxine index of 189 ng/mL (normal 45 to 120 ng/mL), and thyroid-stimulating hormone at 1.1 ng/mL (normal). A diagnosis of Grave's disease was made, and treatment with propranolol and propylthiouracil started. The thiothixene was tapered off, the lithium dosage was reduced, and the new level was maintained for six weeks. During this time the symptoms of insomnia, restlessness, sweating, tachycardia, and anxiety fully remitted, but the patient remained provocative, impulsive, and temperamental. Her thyroid functions returned to normal within four weeks. Two weeks later the lithium was discontinued, and she was discharged to a long-term residential drug rehabilitation program. Her discharge diagnosis was: Axis l-organic affective disorder secondary to hyperthyroidism; mixed substance abuse; and Axis II-borderline personality disorder. At a six-month follow-up she remained euthyroid and did not experience any of her initial symptoms except for disturbed and immature social behavior.
Discussion The presentation and hospital course of this patient exemplify the difficulties of diagnosis and treatment when complex interactions of biological, psychological, and social factors produce clinical phenomena that are consistent with several diagnostic formulations. Given the manifest history of drug abuse, our immediate intervention was to prevent a severe sedative withdrawal
MAY 1986· VOL 27· NO 5
syndrome through gradual detoxification, even though no drug traces were found in the urine. The somatic and anxiety symptoms were interpreted as withdrawal phenomena, and the behavioral disturbances were seen as characteristic of a borderline personality disorder. Ar. it turned out, the patient did not respond to the detoxification regimen (with diazepam up to 80 mg/d), and we had to change our diagnostic formulation. Now the physiologic symptoms, representing generalized somatic overactivation, and the behavioralpsychological disturbances were presumed to be the manifestations of an atypical manic episode, and we started treatment with lithium and thiothixene. Some of the symptoms responded immediately, and we expected that the other aspects of the patient's illness would respond over time. Thyroid function tests were ordered as part of a complete admission evaluation. In retrospect it seems that we did not consider seriously the possibility of thyroid dysfunction, and did not pursue aggressively the delay in receipt ofthe laboratory results, because there appeared to be at least two more common clinical explanations of the symptoms-sedative withdrawal or bipolar disorder. The discovery of hyperthyroidism forced a new diagnostic formulation, but while the somatic overactivation responded to antithyroid treatment, psychological and behavioral disturbances continued to be severe, and we were uncertain whether thyrotoxicosis could account for all the clinical phenomena. In this context we had to decide whether or not to continue maintenance treatment with lithium, which has documented antithyroid effects, >.8.'0 and therefore might have been r~ sponsible for the initial improvement reported in this case. In addition to the risk of falsely labeling the patient bipolar, combined treatment with lithium and propylthiouracil might result in hypothyroidism (myxedema) and depression. We decided to discontinue treatment with lithium, because the patient was transferred to a drug rehabilitation program that refused patients on psychotropic medication, and we considered drug rehabilitation to be the most important aspect of her long-term treatment. In retrospect, it is clear that the presenting affective syndrome was a manifestation of the overreaction of a fragile, borderline personality to the biological stress of acute hyperthyroidism, and even such hypomanic behavior as undressing in public was probably motivated in part by true heat intolerance, which is a common symptom of hyperthyroidism. 3.4 We report this case in order to alert psychiatrists to the complexities involved in the diagnosis and treatment of hyperthyroidism, and other medical conditions, in patients with already established psychiatric disorders. In our case, a borderline personality disorder and multiple drug abuse complicated the diagnostic and treatment dilemmas. In ad371
Case report
dition. clinical decisions made during treatment may complicate further treatment and confuse the final diagnosis. Treatment of presumed mania with lithium in cases of thyrotoxicosis'" may produce positive results because lithium acts as an antithyroid agent. If the successful treatment is interpreted as confirming the diagnosis of bipolar disorder. with continuation of lithium. the patient has to adjust to the psychosocial implications of having a major psychiatric disorder and tolerate possible drug side effects. while the un-
derlying thyrotoxicosis may remain untreated. Finally. we add to the previously described psychiatric manifestations of hyperthyroidism the observation that the acute condition can resemble. or be masked by. drul withdrawal or intoxication. In particular, patients mal abuse sedative-hypnotics in an attempt to medicate the anx iety and biological activation of hyperthyroidism, and thi: possibility needs to be considered in cases presenting witt similar drug-related syndromes. [
REFERENCES 1, Hall RCW: Medically induced psychiatric disease-An overview, in RCW Hall (ed): Psychiatflc Presentations of MedIcal Illness, New York. Spectrum, 1980. 2 Shepherd M: Mental health as an ingredient ot primary care, in Mentat Heatth Services in General Health Care Washington. DC. Institute of Medicine, National Academy of Sciences, 1979, p214. 3, Hall RCW: Psychiatric effects of thyroid hormone disturbance, Psychosomatics24:7-18,1983, 4, Lishman WA: Orgamc Psychiatry. Oxford. Blackwell Scientific. 1972 5, Wharlon RN: Accidental lithium carbonate treatment of thyrotoxicosis as mania, AmJ Psychiatry 137:747-748,1980
372
6 Katerndahl DA. Vande Creek L: Hyperlhyroidism and panic anacks, Ps~ chosomatics 24:491-496, 1983, 7. Folks DG: Organic affective disorder and underlying thyrotoxicosis, Ps~ chosomatics 25:243-249,1984, 8, Lazarus JH. Richards AR, Addison GM, et al: Treatment of thyrotoxicosi with lithium carbonate, Lancet2:1160-1163, 1974, 9, Shopsin B. Blum M. Gershon S: Lithium-induced thyroid disturbancE ComprPsychiatry 10:215-223, 1969, 10, McLarly DG. O'Boyle JH. Spencer CA, et al: Effect of lithium on hypotha lamic-pituitary-thyroid function in patients with affective disorders, B Med J 3:623-626, 1975,
PSYCHOSOMATICS
BARUCH FISHMAN, Ph.D. ALAN BARASCH, M.D.
Diagnostic dilemma: Drug withdrawal, borderline personality, and hyperthyroidism Estimates of the incidence of medical illness in a psychiatric population range from 5% to 50%,' and in about 2% of all medical disorders the organic disturbance is the underlying cause of a psychiatric crisis. 2 Patients with hyperthyroidism, for example, can present a complex diagnostic dilemma because they manifest physical and psychological symptoms that may mimic anxiety disorders or manic depressive psychosis,"" and there are several reports'" of diagnostic and treatment difficulties. We describe a case of hyperthyroidism in a woman with borderline personality disorder, in which possible stimulant intoxication or sedative-hypnotic withdrawal further complicated diagnosis and treatment. Case report A 25-year-old single unemployed woman was admitted to the Payne Whitney Psychiatric Clinic from the emergency room after she requested hospitalization for drug detoxification, She reported heavy abuse of cocaine, methaqualone, and alcohol for several months, which had abruptly stopped a few days prior to admission because her supplier was hospitalized, She arrived for psychiatric examination looking adolescent in appearance and was also disheveled, wearing torn and dirty clothes, She undressed herself in public areas sayDr. Fishman is now a psychology fellow at Memorial Sloan-Kettering Cancer Center. and Dr. Barasch is clinical instructor of psychiatry at the Payne Whitney Psychiatric Clinic. New York. Reprint requests 10 Dr. Fishman at the Pain Service. Department of Neurology. Memorial Sloan-Kellering Cancer Center. 1275 York Ave., New York. NY 10021.
370
ing that she could not tolerate the heat, was hyperactive. restless, sexually disinhibited, and required active restraint. Her speech was loud and pressured, Her mood was euphoric and her affect was extremely labile, ranging from laughing and teasing to tearfulness and rage, Her thoughts were racing and tangential, but there were no abnormal perceptions, loosening of associations, or delusions, She reported sleep disturbances, weight loss but no decrease in appetite. and active suicidal ideation. She was hyperalert and highly distractible, but oriented to self, time, and place, Her higher cognitive functions were moderately impaired, but there was no evidence of delirium, Physical examination revealed SP of 130/50, temperature of 36°C, and pulse of 128. Routine admission laboratory tests, including complete blood cell count (CSC), electrolytes, and hepatic and renal functions, were within normal limits. Calcium and phosphorus values were minimally elevated with calcium at 10.6 mg/dL (normal 8,5 to 10.5 mg/dL) and phosphorus at 6.1 mg/dL (normal 2,2 to 4.2 mg/dL). A urine drug screen was positive only for diazepam, which the patient had received in the emergency room. The patient was the youngest of six siblings from a middleclass family, Since late adolescence she had experienced episodes of depression (but no mania), unstable family and social relationships, impulsive actions including sexual promiscuity, two abortions, multiple drug abuse, antisocial acts, temper outbursts, and two suicide attempts, This pattern was exacerbated after her father's death three years prior to admission. Never able to live away from her parents. she experienced intolerable anxiety and depression when alone. She had been treated for four years with psychotherapy, which she had abruptly terminated a few weeks prior to admission, The patient was diagnosed as: Axis I-mixed substance abuse, possible sedative-hypnotic withdrawal or PSYCHOSOMATICS
stimulant intoxication, and possible bipolar disorder, manic episode; and Axis II-borderline personality disorder. Initially, symptoms of insomnia, anxiety, irritability, and tachycardia were assessed as ongoing manifestations of sedative withdrawal, and the patient was begun on a detoxification regimen with diazepam, 10 mg every six hours. The symptoms of sexual disinhibition, affective lability, suicidal ideation, tantrums, and provocative behavior were seen as manifestations of a borderline personality disorder and were treated with firm limit setting. After 48 hours there was no improvement, and, assuming that we had underestimated the degree of sedative tolerance, we increased the diazepam dosage to 20 mg every six hours. However, during the following two days there was no sedation, and only minimal symptomatic improvement. On the fifth day of hospitalization a diagnosis of bipolar disorder, manic episode was definitively determined, and treatment with thiothixene and lithium carbonate was initiated. There was a rapid positive partial response, with improved sleep, reduced anxiety, and increased impulse control, but continued tachycardia, sweating, emotional lability, and disruptive behavior. On the eighth day of hospitalization the results of admission thyroid function tests arrived from the laboratory, and they revealed marked hyperthyroidism: triiodothyronine by radioimmunoassay (RIA) at 2.8 ng/mL (normal 0.8 to 2.0 ng/mL), thyroxine by RIA at 171 ng/mL (normal 45 to 120 ng/mL), free thyroxine index of 189 ng/mL (normal 45 to 120 ng/mL), and thyroid-stimulating hormone at 1.1 ng/mL (normal). A diagnosis of Grave's disease was made, and treatment with propranolol and propylthiouracil started. The thiothixene was tapered off, the lithium dosage was reduced, and the new level was maintained for six weeks. During this time the symptoms of insomnia, restlessness, sweating, tachycardia, and anxiety fully remitted, but the patient remained provocative, impulsive, and temperamental. Her thyroid functions returned to normal within four weeks. Two weeks later the lithium was discontinued, and she was discharged to a long-term residential drug rehabilitation program. Her discharge diagnosis was: Axis l-organic affective disorder secondary to hyperthyroidism; mixed substance abuse; and Axis II-borderline personality disorder. At a six-month follow-up she remained euthyroid and did not experience any of her initial symptoms except for disturbed and immature social behavior.
Discussion The presentation and hospital course of this patient exemplify the difficulties of diagnosis and treatment when complex interactions of biological, psychological, and social factors produce clinical phenomena that are consistent with several diagnostic formulations. Given the manifest history of drug abuse, our immediate intervention was to prevent a severe sedative withdrawal
MAY 1986· VOL 27· NO 5
syndrome through gradual detoxification, even though no drug traces were found in the urine. The somatic and anxiety symptoms were interpreted as withdrawal phenomena, and the behavioral disturbances were seen as characteristic of a borderline personality disorder. Ar. it turned out, the patient did not respond to the detoxification regimen (with diazepam up to 80 mg/d), and we had to change our diagnostic formulation. Now the physiologic symptoms, representing generalized somatic overactivation, and the behavioralpsychological disturbances were presumed to be the manifestations of an atypical manic episode, and we started treatment with lithium and thiothixene. Some of the symptoms responded immediately, and we expected that the other aspects of the patient's illness would respond over time. Thyroid function tests were ordered as part of a complete admission evaluation. In retrospect it seems that we did not consider seriously the possibility of thyroid dysfunction, and did not pursue aggressively the delay in receipt ofthe laboratory results, because there appeared to be at least two more common clinical explanations of the symptoms-sedative withdrawal or bipolar disorder. The discovery of hyperthyroidism forced a new diagnostic formulation, but while the somatic overactivation responded to antithyroid treatment, psychological and behavioral disturbances continued to be severe, and we were uncertain whether thyrotoxicosis could account for all the clinical phenomena. In this context we had to decide whether or not to continue maintenance treatment with lithium, which has documented antithyroid effects, >.8.'0 and therefore might have been r~ sponsible for the initial improvement reported in this case. In addition to the risk of falsely labeling the patient bipolar, combined treatment with lithium and propylthiouracil might result in hypothyroidism (myxedema) and depression. We decided to discontinue treatment with lithium, because the patient was transferred to a drug rehabilitation program that refused patients on psychotropic medication, and we considered drug rehabilitation to be the most important aspect of her long-term treatment. In retrospect, it is clear that the presenting affective syndrome was a manifestation of the overreaction of a fragile, borderline personality to the biological stress of acute hyperthyroidism, and even such hypomanic behavior as undressing in public was probably motivated in part by true heat intolerance, which is a common symptom of hyperthyroidism. 3.4 We report this case in order to alert psychiatrists to the complexities involved in the diagnosis and treatment of hyperthyroidism, and other medical conditions, in patients with already established psychiatric disorders. In our case, a borderline personality disorder and multiple drug abuse complicated the diagnostic and treatment dilemmas. In ad371
Case report
dition. clinical decisions made during treatment may complicate further treatment and confuse the final diagnosis. Treatment of presumed mania with lithium in cases of thyrotoxicosis'" may produce positive results because lithium acts as an antithyroid agent. If the successful treatment is interpreted as confirming the diagnosis of bipolar disorder. with continuation of lithium. the patient has to adjust to the psychosocial implications of having a major psychiatric disorder and tolerate possible drug side effects. while the un-
derlying thyrotoxicosis may remain untreated. Finally. we add to the previously described psychiatric manifestations of hyperthyroidism the observation that the acute condition can resemble. or be masked by. drul withdrawal or intoxication. In particular, patients mal abuse sedative-hypnotics in an attempt to medicate the anx iety and biological activation of hyperthyroidism, and thi: possibility needs to be considered in cases presenting witt similar drug-related syndromes. [
REFERENCES 1, Hall RCW: Medically induced psychiatric disease-An overview, in RCW Hall (ed): Psychiatflc Presentations of MedIcal Illness, New York. Spectrum, 1980. 2 Shepherd M: Mental health as an ingredient ot primary care, in Mentat Heatth Services in General Health Care Washington. DC. Institute of Medicine, National Academy of Sciences, 1979, p214. 3, Hall RCW: Psychiatric effects of thyroid hormone disturbance, Psychosomatics24:7-18,1983, 4, Lishman WA: Orgamc Psychiatry. Oxford. Blackwell Scientific. 1972 5, Wharlon RN: Accidental lithium carbonate treatment of thyrotoxicosis as mania, AmJ Psychiatry 137:747-748,1980
372
6 Katerndahl DA. Vande Creek L: Hyperlhyroidism and panic anacks, Ps~ chosomatics 24:491-496, 1983, 7. Folks DG: Organic affective disorder and underlying thyrotoxicosis, Ps~ chosomatics 25:243-249,1984, 8, Lazarus JH. Richards AR, Addison GM, et al: Treatment of thyrotoxicosi with lithium carbonate, Lancet2:1160-1163, 1974, 9, Shopsin B. Blum M. Gershon S: Lithium-induced thyroid disturbancE ComprPsychiatry 10:215-223, 1969, 10, McLarly DG. O'Boyle JH. Spencer CA, et al: Effect of lithium on hypotha lamic-pituitary-thyroid function in patients with affective disorders, B Med J 3:623-626, 1975,
PSYCHOSOMATICS