- Email: [email protected]
Mental Status Changes of Addison's Disease
Case Reports
15. Nelson JC. Jatlow PF: Neuroleptic effect on desipramine steady state plasma concentrations. Am J Psychiatry 137:1232-1234.1980 16. Chou T: Electrocardiography in Clinical Practice. Second Ed. New York, Grone & Strallon. 1986, pp 20-21
17. Bigger IT, Kantor SJ. Glassman AH, et a1: Cardiovascular effects of tricyclic antidepressant drugs. in Lipton MA. DiMascio A. Killam KF: Psychopharmacology: AGeneration of Progress. New York. Raven, 1978, pp 10331046
Mental Status Changes of Addison's Disease PETER A. S. JOHNSTONE, M.D., M.A., LT, MC, USN JAMES R. RUNDELL, M.D., MAJ, USAF, MC MARIA ESPOSITO, M.D., COL, USA, MC
ince Klippel' first discussed the concept [' encephalopathie addisonienne in 1899, it has been recognized that psychiatric signs and symptoms are common in primary adrenocortical insufficiency. From 64% to 84% of patients with Addison's disease present with or experience accompanying psychiatric symptoms. The complex clinical difficulties of treating Addison's disease have been the subject of several retrospective reviews 2- s and numerous case reports.~8 Engel and Margolin. 2 in 1941, described neuropsychiatric symptoms in 16 of 25 Addisonian patients. Episodic mood or behavioral changes, especially depression, apathy, or confusion, were common findings. Two patients were acutely psychotic. Sorkin,3 in 1949, found similar symptoms in 70% of 50 patients, including three instances of psychosis. In 1951, Cleghom 4 reported that apathy and negativism were present in 21 of 25 Addison's disease cases. One patient was paranoid. Stoll, as reported by Cleghom,s found psychiatric disturbances in 19 of the 29 patients in his series. Single case reports have described extreme psychiatric presentations and difficulties with actual diagnosis. Paranoia,6 schizophrenia,? and self-mutilation8 have been described. Addison's disease may go unrecognized, especially in the summer, when a suntan can mask hyperpigmentation and characteristic fatigue may be
S
VOLUME 31· NUMBER I • WINTER 1990
explained by summer-related overactivity. The following case history is an example of how the insidious onset of Addison's disease can make psychiatric symptoms appear more prominent than the underlying physical symptomatology.
Case History
Our patient, a 28-year-old white female. presented to her family physician on May I, 1986, with neck pain and diarrhea that had lasted for three months and decreasing menstrual flow lasting for one year that had progressed to amenorrhea. She had a history of urinary tract infections and numerous somatic complaints. She visited her physician about every three weeks. Her previous blood pressure had been 90/60 mmHg; previous beta-human chorionic gonadotropin (j}-HCG) and monospot were negative. She was married and had two children. She admitted to being very worried about the family's finances and under increased stress since her husband began medical school and she had begun providing day care for Received July 18. 1988; revised April 14. 1989; accepted May 5. 1989. From the Department of Psychiatry, Uniformed Services University of the Health Sciences. Bethesda. Maryland. Address reprint requests to Dr. Johnstone, Department of Professional Affairs, National Naval Medical Center. Bethesda. MD 20814. Copyright © 1990 The Academy of Psychosomatic Medicine. 103
Case Reports
three children to earn extra money.
The following laboratory results were obtained at this visit: thyroid stimulating hormone (TSH), 63.3 IU/ml; serum triiodothyronine (T3), 193 ng/dl (normal range, 90 to 190 ng/dl); serum thyroxine (T4)' 9.8 mg/dl (normal range, 4.5 to 12.2 mg/d1), triiodothyronine resin uptake (T3RU), 0.56 (normal range, 0.86 to 1.16); free thyroid index (T,), 5.5 mg/dl (normal range, 4 to 14 mg/dl); negative monospot; and a microsomal antibodies ratio of 1:1600 (normal ratio, I: 100). Results offollow-up thyroid function tests three weeks later were 123 IU/ml for TSH, 185 ng/dl for T3' 5.1 mg/dl for T4, 0.53 for T 3RU, and 2.7 mg/dl for T,. A diagnosis of Hashimoto's thyroiditis was made and levothyroxine 0.1 mg/day was begun. The TSH gradually returned to normal, falling to 11.5 IU/ml on June 12, about one month after therapy was begun, and to 1.5 IU/ml on July 10. However, because fatigue and diffuse muscle cramping continued, the levothyroxine dosage was increased to 0.15 mg/day on June 20. Because adequate thyroxine replacement had not relieved most of her symptoms, the patient returned to the clinic on July 29. Her complaints at that time included fatigue, muscle cramping, depression, forgetfulness, wide mood swings, and recurrence of suicidal ideation. She had difficulty anending to conversations, and she was less patient with her children. The physician agreed, at her insistence, to consult an endocrinologist. On August 4, an endocrinologist noted "her skin is orange." This hyperpigmentation was evident on her knees and elbows, and recent scars were more pigmented than older ones. The patient admined craving salt. Her blood pressure was 80/54 mmHG when supine and 70/50 mmHg when standing. A provisional diagnosis of Schmidt's syndrome (Hashimoto's thyroiditis and Addison's disease) was made, and an adrenocorticotropic hormone (ACfH) stimulation test was ordered. Results showed no detectable cortisol immediately, 30 minutes, or 60 minutes after AcrH infusion. Serum estradiol and follicle-stimulating hormone values were normal. Treatment with hydrocortisone in divided daily doses and fludrocortisone acetate supplementation resulted in a return to premorbid mental status.
Discussion The mechanisms of psychiatric illness in patients with Addison's disease are unknown. It is clear 104
that many of the changes are due to central nervous system effects of the hypoadrenal state. The wide spectrum of psychiatric presentations suggests a diffuse etiology; however, the universal findings of fatigue, apathy, and depression, together or alone, can frequently be explained by metabolic factors. Woodbury and associates9 found hyponatremia to be the predominant factor in brain excitability. Timiras and associates 10 felt that the effect was due to altered ratios of intracellular to extracellular sodium (increased) and potassium (decreased). Concurrent hyponatremia and hyperkalemia suggest a potential milieu for mental status changes. It is doubtful, however, that electrolyte changes alone could produce all the pictures seen or the wide range of symptoms. Another proposed mechanism for Addisonian mental findings is hypoxia associated with hypotension. 3 However, without a more critical hypoxic cause, the cerebral autoregulation of blood flow between 60 and 160 mmHg makes this unlikely. Hypoglycemia is another mechanism theorized for the mental changes of Addison's disease and Addisonian crisis. As early as 1941, Engel and Margolin II found a relationship between hypoglycemia, electroencephalographic (EEG) changes, and "severe personality changes." Of note, personality changes occur at significantly higher blood glucose levels in patients with adrenoconical insufficiency than in normals,I2 although this study has not been validated using today's more sensitive assays. Low serum glucocorticoid levels may contribute to Addisonian organic mental syndromes. One mechanism proposed by Henkin and associates is that decreased serum glucocorticoids increase axonal conduction velocityl3 and lower axonal membrane threshhold. '4 This alteration in excitability potential has been implicated in lower taste threshholds,lS increased auditory acuity;4 "improved ability to 'integrate' speech stimuli into meaningful pattems,,,14 increased latency of visual evoked potentials,I6 and more acute olfactory sensitivity.I' Treatment with prednisolone returned sensory levels to normal. Given the relationship between ACTH, endorphins, and the precursor for both, proPSYCHOSOMATICS
Case Reports
FIGURE 1. MaaestrudUre of proopiomelanoc:ortin (POMC) COOH
t--.o,· ···_··~iJ-·--···"'·_·-·_"' '-'" ._ _._ _-" -----1l.._, , _..~_-fC . . _." 41
81
~...
61
77
A,LPHA-END It
71
Numbe" re'er to emlno eclds within eech peptide Abbre.letlons: MSH: melanocyte-stimulating hormone ACTH: adrenocorllcotrophlc hormone BETA-LPH: Beta-lipotropin END: endorphin MET -ENK: methionine-enkephelln
opiomelanocortin (POMC), hyper-ACTH states may also be hyperendorphin states. Figure 1 illustrates the relationship of POMC to ACTH and endorphins. The association between endogenous opioids and psychosis is strengthened by the studies of Lindstrom and associates,18 in which six of nine schizophrenic patients, four of four bipolar patients, and four of four puerperal psychotic patients had elevated CSF endorphin levels that returned to normal after drug therapy. Further, phencyclidine (PCP) and meperidine's metabolite, normeperidine, may cause psychotic symptoms in predisposed individuals by stimulating opiate receptors, particularly delta, sigma, and "PCP" sUbtypes.19 Several studies have shown that naloxone can ameliorate auditory hallucinations in schizophrenics; Lehmann and associates2o found the greatest response in the patient with the greatest diurnal ACfH levels. These studies do not prove that psychoses are due to increased endorphins. In fact, it could be inferred that increased endorphins are a response to psychiatric illness. Further research may elucidate the role of endorphins in the etiology or amelioration of Addisonian mental changes. In summary, the exact mechanism of the VOLUME31·NUMBER I·WlNTER 1990
psychiatric component of Addison's disease remains unclear. It is possible that all the factors discussed here contribute to some degree, and their effects may be additive (see Figure 2). Other mechanisms may be involved. Fortunately, regardless of the etiology of Addison's disease, the treatment is always the same: remediate the adrenal insufficiency. In the vast majority of cases, treatment ameliorates both psychiatric and medical symptoms.
Conclusions Organic mental disorders due to Addison's disease may resemble other psychiatric illnesses. The unusual and labile nature of symptoms may misdirect an unsuspecting physician toward a personality disorder diagnosis. Conversely, psychiatric symptoms may be undertreated and underrecognized in endocrine patients. Several factors obscured the diagnosis ofour patient's condition. First, the fact that she was responsible for five children four years old or younger every day may have led to a belief that this was the cause of her fatigue. Second, the primary care physician believed that worsening psychiatric symptoms in the face of normal thylOS
Case Reports
FIGURE 2. Interrelations of possible metabolic facton In Addison's disease •
•
ZONA FASCICULAr A FUNCTION
Al TERED SENSORIUM
ZONA GlOMERUlOSA FUNCTION
r
I
roid function test values was an indication of levothyroxine underreplacement. Nevertheless, the endocrinologist did not presume that she was merely tanned. or that thyroiditis was the only endocrinologic abnormality. It is incumbent on the physician to consider organic etiologies first in patients who present with fatigue. neurasthenia, or mental status changes. Checking a complete blood count, elec-
trolyte panel, and liver and thyroid function tests as well as performing a thorough physical examination can yield fruitful results in such patients.
The opinions or assertions contained herein are the private ones ofthe authors and are not to be construed as the official views of the U.S. Department of Defense or the Uniformed Services University ofthe Health Sciences.
References I. Klippel M: Encephalopathie addisonienne. Rev Neural 7:898-899,1899 2. Engel GL. Margolin SG: Neuropsychiatric disturbances in internal disease. Arch Intern Med70:236-259. 1942 3. Sorkin SZ: Addison's disease. Medicine 28:371-425. 1949 4. Cleghorn RA: Adrenal conical insufficiency: psychological and neurological observations. Can Med Assoc J 65:449-454.1951 5. Cleghorn RA: Psychologic changes in Addison's disease. JClinEndocrinoI13:1291-1293.1953 6. Gonnan WF. Wonis SB: Psychosis in Addison's disease. Diseases ofthe Nervous System 8:267-271.1947 7. Sarai K: Case ofAddison's disease erroneously diagnosed as schizophrenia (Engl. transl.). Clin Endocrino/15:8488. 1967 8. Rajathurai A, Chazan BI. Jeans JE: Self-mutilation as a feature of Addison's disease. Br Med J 287:1027,1983
106
9. Woodbury OM. Cheng Cop, Sayers G. et a1: Antagonism of adrenoconicotrophic honnone and adrenal conical extract to deoxycorticosterone: electrolytes and electroshock threshold. Am J Physio/l60:217-227. 1950 10. Timiras PS. Woodbury OM. Goodman LS: Effect of adrenalectomy. hydroconisone acetate. and deoxyconicosterone acetate on brain excitability and electrolyte distribution in mice. J Pharmacol Exp Ther 112:80-93. 1954 II. Engel CL. Margolin SG: Clinical correlation of the electroencephalogram with carbohydrate metabolism. Arch Neurol Psychiatry 45:890-892. 1941 12. Thorn OW, Koepf OF. Lewis RA. et a1: Carbohydrate metabolism in Addison's disease. J Clin Invest 19:813832. 1940 13. Henkin RI. Gill JR. Warmolts JR. et al: Steroid-dependent increase of nerve conduction velocity in adrenal insufficiency.JClinlnvest42:94I.I963
PSYCHOSOMATICS
Case Reports
14. Henkin RI. Daly RL: Auditory detection and perception
in nonnal man and in patients with adrenal conical insufficiency: effect of adrenal conical steroids. J Clin Invest 47:1269-1280.1968 IS. Henkin RI. Gill JR. Banter FC: Studies on taste threshholds in nonnal man and in patients with adrenal conical insufficiency: the role of adrenal conical steroids and ofserum sodium concentration.J Clin Invest 42:727735. 1963 16. Ojemann CA. Henkin RI: Steroid dependent changes in visual evoked potentials. Life Sci 6:327-334. 1967 17. Henkin RI. Banter FC: Studies on olfactory thresholds in
nonnal man and in patients with adrenal cortical insufficiency: the role of adrenal conical steroids and of serum sodium concentration.J Clin Invest 45:1631-1639.1966 18. Lindstrom LH. Widerlov E. Gunne L-M. et al: Cerebrospinal fluid: clinical correlations to some psychotic states. Acta Psychiatr Scand 57: 153-164. 1978 19. Wise MG. Rundell JR: Concise Guide to Consultation Psychiatry. Washington. DC. American Psychiatric Press. 1988 20. Lehmann H. Nair NPV. Kline NS: Beta-endorphin and naloxone in psychiatric patients: clinical and biological effects. AmJ Psychiatry 136:762-766. 1979
Severe Claustrophobia in a Patient Requiring Hyperbaric Oxygen Treatment JAMES RANDOLPH
HILLARD.
M.D.
Case Report
tion treatment (7500 rads) to her mandible. The patient's sarcoma was cured. but her jaw was hypoplastic. Some teeth had been extracted and her mandible debrided when she was 24. At that time. she also underwent stomatorraphy and a split-thickness skin graft to cover bone exposed secondary to radionecrosis. At this time. the patient received a total of 20 hyperbaric oxygen treatments. each lasting 60 minutes. She tolerated the treatments and recovered well. despite claustrophobic symptoms. At the age of 34. the patient developed more dental problems. and funher extractions were recommended. Hyperbaric oxygen treatments (10 treatments of 90 minutes each) to prevent radionecrosis were also recommended. The patient was told that extraction and radiation accompanied by hyperbaric oxygen treatment carried a 7% risk of radionecrosis. but the same treatment without hyperbaric oxygen carried a 40% risk of developing necrosis. The patient reponed always having been nervous in enclosed spaces. such as the back seats of
The patient was a 34-year-old. white. female registered nurse who had been referred for hyperbaric oxygen treatment for prophylaxis of osteoradionecrosis secondary to dental extraction. At age 17. she had been diagnosed with a reticulum cell sarcoma that required excision of two tumors in her jaw plus radia-
Received March 23. 1989; revised April 19. 1989; accepted May 26. 1989. Address reprint requests to Dr. Hillard. Depanment of Psychiatry. University of Cincinnati College of Medicine. 231 Bethesda Avenue. ML559. Cincinnati. OH 45267-0559. Copyright © 1990 The Academy of Psychosomatic Medicine.
yperbaric oxygen therapy is the treatment of choice for an ever-increasing range of medical conditions. I Because claustrophobia is relatively common in the general population/·3 a substantial number of severely claustrophobic individuals are likely to require treatment with hyperbaric oxygen. This article describes the successful treatment of one such individual. The hyperbaric oxygen chamber is uniquely stressful for claustrophobic individuals because it is quite small, usually measuring seven feet by two feet by two feet. A long exposure time (60 to 90 minutes) is required, and because 15 to 30 minutes are required to depressurize following treatment. the patient cannot make a rapid escape should it seem necessary.
H
VOLUME 31 • NUMBER 1 • WINTER 1990
107
15. Nelson JC. Jatlow PF: Neuroleptic effect on desipramine steady state plasma concentrations. Am J Psychiatry 137:1232-1234.1980 16. Chou T: Electrocardiography in Clinical Practice. Second Ed. New York, Grone & Strallon. 1986, pp 20-21
17. Bigger IT, Kantor SJ. Glassman AH, et a1: Cardiovascular effects of tricyclic antidepressant drugs. in Lipton MA. DiMascio A. Killam KF: Psychopharmacology: AGeneration of Progress. New York. Raven, 1978, pp 10331046
Mental Status Changes of Addison's Disease PETER A. S. JOHNSTONE, M.D., M.A., LT, MC, USN JAMES R. RUNDELL, M.D., MAJ, USAF, MC MARIA ESPOSITO, M.D., COL, USA, MC
ince Klippel' first discussed the concept [' encephalopathie addisonienne in 1899, it has been recognized that psychiatric signs and symptoms are common in primary adrenocortical insufficiency. From 64% to 84% of patients with Addison's disease present with or experience accompanying psychiatric symptoms. The complex clinical difficulties of treating Addison's disease have been the subject of several retrospective reviews 2- s and numerous case reports.~8 Engel and Margolin. 2 in 1941, described neuropsychiatric symptoms in 16 of 25 Addisonian patients. Episodic mood or behavioral changes, especially depression, apathy, or confusion, were common findings. Two patients were acutely psychotic. Sorkin,3 in 1949, found similar symptoms in 70% of 50 patients, including three instances of psychosis. In 1951, Cleghom 4 reported that apathy and negativism were present in 21 of 25 Addison's disease cases. One patient was paranoid. Stoll, as reported by Cleghom,s found psychiatric disturbances in 19 of the 29 patients in his series. Single case reports have described extreme psychiatric presentations and difficulties with actual diagnosis. Paranoia,6 schizophrenia,? and self-mutilation8 have been described. Addison's disease may go unrecognized, especially in the summer, when a suntan can mask hyperpigmentation and characteristic fatigue may be
S
VOLUME 31· NUMBER I • WINTER 1990
explained by summer-related overactivity. The following case history is an example of how the insidious onset of Addison's disease can make psychiatric symptoms appear more prominent than the underlying physical symptomatology.
Case History
Our patient, a 28-year-old white female. presented to her family physician on May I, 1986, with neck pain and diarrhea that had lasted for three months and decreasing menstrual flow lasting for one year that had progressed to amenorrhea. She had a history of urinary tract infections and numerous somatic complaints. She visited her physician about every three weeks. Her previous blood pressure had been 90/60 mmHg; previous beta-human chorionic gonadotropin (j}-HCG) and monospot were negative. She was married and had two children. She admitted to being very worried about the family's finances and under increased stress since her husband began medical school and she had begun providing day care for Received July 18. 1988; revised April 14. 1989; accepted May 5. 1989. From the Department of Psychiatry, Uniformed Services University of the Health Sciences. Bethesda. Maryland. Address reprint requests to Dr. Johnstone, Department of Professional Affairs, National Naval Medical Center. Bethesda. MD 20814. Copyright © 1990 The Academy of Psychosomatic Medicine. 103
Case Reports
three children to earn extra money.
The following laboratory results were obtained at this visit: thyroid stimulating hormone (TSH), 63.3 IU/ml; serum triiodothyronine (T3), 193 ng/dl (normal range, 90 to 190 ng/dl); serum thyroxine (T4)' 9.8 mg/dl (normal range, 4.5 to 12.2 mg/d1), triiodothyronine resin uptake (T3RU), 0.56 (normal range, 0.86 to 1.16); free thyroid index (T,), 5.5 mg/dl (normal range, 4 to 14 mg/dl); negative monospot; and a microsomal antibodies ratio of 1:1600 (normal ratio, I: 100). Results offollow-up thyroid function tests three weeks later were 123 IU/ml for TSH, 185 ng/dl for T3' 5.1 mg/dl for T4, 0.53 for T 3RU, and 2.7 mg/dl for T,. A diagnosis of Hashimoto's thyroiditis was made and levothyroxine 0.1 mg/day was begun. The TSH gradually returned to normal, falling to 11.5 IU/ml on June 12, about one month after therapy was begun, and to 1.5 IU/ml on July 10. However, because fatigue and diffuse muscle cramping continued, the levothyroxine dosage was increased to 0.15 mg/day on June 20. Because adequate thyroxine replacement had not relieved most of her symptoms, the patient returned to the clinic on July 29. Her complaints at that time included fatigue, muscle cramping, depression, forgetfulness, wide mood swings, and recurrence of suicidal ideation. She had difficulty anending to conversations, and she was less patient with her children. The physician agreed, at her insistence, to consult an endocrinologist. On August 4, an endocrinologist noted "her skin is orange." This hyperpigmentation was evident on her knees and elbows, and recent scars were more pigmented than older ones. The patient admined craving salt. Her blood pressure was 80/54 mmHG when supine and 70/50 mmHg when standing. A provisional diagnosis of Schmidt's syndrome (Hashimoto's thyroiditis and Addison's disease) was made, and an adrenocorticotropic hormone (ACfH) stimulation test was ordered. Results showed no detectable cortisol immediately, 30 minutes, or 60 minutes after AcrH infusion. Serum estradiol and follicle-stimulating hormone values were normal. Treatment with hydrocortisone in divided daily doses and fludrocortisone acetate supplementation resulted in a return to premorbid mental status.
Discussion The mechanisms of psychiatric illness in patients with Addison's disease are unknown. It is clear 104
that many of the changes are due to central nervous system effects of the hypoadrenal state. The wide spectrum of psychiatric presentations suggests a diffuse etiology; however, the universal findings of fatigue, apathy, and depression, together or alone, can frequently be explained by metabolic factors. Woodbury and associates9 found hyponatremia to be the predominant factor in brain excitability. Timiras and associates 10 felt that the effect was due to altered ratios of intracellular to extracellular sodium (increased) and potassium (decreased). Concurrent hyponatremia and hyperkalemia suggest a potential milieu for mental status changes. It is doubtful, however, that electrolyte changes alone could produce all the pictures seen or the wide range of symptoms. Another proposed mechanism for Addisonian mental findings is hypoxia associated with hypotension. 3 However, without a more critical hypoxic cause, the cerebral autoregulation of blood flow between 60 and 160 mmHg makes this unlikely. Hypoglycemia is another mechanism theorized for the mental changes of Addison's disease and Addisonian crisis. As early as 1941, Engel and Margolin II found a relationship between hypoglycemia, electroencephalographic (EEG) changes, and "severe personality changes." Of note, personality changes occur at significantly higher blood glucose levels in patients with adrenoconical insufficiency than in normals,I2 although this study has not been validated using today's more sensitive assays. Low serum glucocorticoid levels may contribute to Addisonian organic mental syndromes. One mechanism proposed by Henkin and associates is that decreased serum glucocorticoids increase axonal conduction velocityl3 and lower axonal membrane threshhold. '4 This alteration in excitability potential has been implicated in lower taste threshholds,lS increased auditory acuity;4 "improved ability to 'integrate' speech stimuli into meaningful pattems,,,14 increased latency of visual evoked potentials,I6 and more acute olfactory sensitivity.I' Treatment with prednisolone returned sensory levels to normal. Given the relationship between ACTH, endorphins, and the precursor for both, proPSYCHOSOMATICS
Case Reports
FIGURE 1. MaaestrudUre of proopiomelanoc:ortin (POMC) COOH
t--.o,· ···_··~iJ-·--···"'·_·-·_"' '-'" ._ _._ _-" -----1l.._, , _..~_-fC . . _." 41
81
~...
61
77
A,LPHA-END It
71
Numbe" re'er to emlno eclds within eech peptide Abbre.letlons: MSH: melanocyte-stimulating hormone ACTH: adrenocorllcotrophlc hormone BETA-LPH: Beta-lipotropin END: endorphin MET -ENK: methionine-enkephelln
opiomelanocortin (POMC), hyper-ACTH states may also be hyperendorphin states. Figure 1 illustrates the relationship of POMC to ACTH and endorphins. The association between endogenous opioids and psychosis is strengthened by the studies of Lindstrom and associates,18 in which six of nine schizophrenic patients, four of four bipolar patients, and four of four puerperal psychotic patients had elevated CSF endorphin levels that returned to normal after drug therapy. Further, phencyclidine (PCP) and meperidine's metabolite, normeperidine, may cause psychotic symptoms in predisposed individuals by stimulating opiate receptors, particularly delta, sigma, and "PCP" sUbtypes.19 Several studies have shown that naloxone can ameliorate auditory hallucinations in schizophrenics; Lehmann and associates2o found the greatest response in the patient with the greatest diurnal ACfH levels. These studies do not prove that psychoses are due to increased endorphins. In fact, it could be inferred that increased endorphins are a response to psychiatric illness. Further research may elucidate the role of endorphins in the etiology or amelioration of Addisonian mental changes. In summary, the exact mechanism of the VOLUME31·NUMBER I·WlNTER 1990
psychiatric component of Addison's disease remains unclear. It is possible that all the factors discussed here contribute to some degree, and their effects may be additive (see Figure 2). Other mechanisms may be involved. Fortunately, regardless of the etiology of Addison's disease, the treatment is always the same: remediate the adrenal insufficiency. In the vast majority of cases, treatment ameliorates both psychiatric and medical symptoms.
Conclusions Organic mental disorders due to Addison's disease may resemble other psychiatric illnesses. The unusual and labile nature of symptoms may misdirect an unsuspecting physician toward a personality disorder diagnosis. Conversely, psychiatric symptoms may be undertreated and underrecognized in endocrine patients. Several factors obscured the diagnosis ofour patient's condition. First, the fact that she was responsible for five children four years old or younger every day may have led to a belief that this was the cause of her fatigue. Second, the primary care physician believed that worsening psychiatric symptoms in the face of normal thylOS
Case Reports
FIGURE 2. Interrelations of possible metabolic facton In Addison's disease •
•
ZONA FASCICULAr A FUNCTION
Al TERED SENSORIUM
ZONA GlOMERUlOSA FUNCTION
r
I
roid function test values was an indication of levothyroxine underreplacement. Nevertheless, the endocrinologist did not presume that she was merely tanned. or that thyroiditis was the only endocrinologic abnormality. It is incumbent on the physician to consider organic etiologies first in patients who present with fatigue. neurasthenia, or mental status changes. Checking a complete blood count, elec-
trolyte panel, and liver and thyroid function tests as well as performing a thorough physical examination can yield fruitful results in such patients.
The opinions or assertions contained herein are the private ones ofthe authors and are not to be construed as the official views of the U.S. Department of Defense or the Uniformed Services University ofthe Health Sciences.
References I. Klippel M: Encephalopathie addisonienne. Rev Neural 7:898-899,1899 2. Engel GL. Margolin SG: Neuropsychiatric disturbances in internal disease. Arch Intern Med70:236-259. 1942 3. Sorkin SZ: Addison's disease. Medicine 28:371-425. 1949 4. Cleghorn RA: Adrenal conical insufficiency: psychological and neurological observations. Can Med Assoc J 65:449-454.1951 5. Cleghorn RA: Psychologic changes in Addison's disease. JClinEndocrinoI13:1291-1293.1953 6. Gonnan WF. Wonis SB: Psychosis in Addison's disease. Diseases ofthe Nervous System 8:267-271.1947 7. Sarai K: Case ofAddison's disease erroneously diagnosed as schizophrenia (Engl. transl.). Clin Endocrino/15:8488. 1967 8. Rajathurai A, Chazan BI. Jeans JE: Self-mutilation as a feature of Addison's disease. Br Med J 287:1027,1983
106
9. Woodbury OM. Cheng Cop, Sayers G. et a1: Antagonism of adrenoconicotrophic honnone and adrenal conical extract to deoxycorticosterone: electrolytes and electroshock threshold. Am J Physio/l60:217-227. 1950 10. Timiras PS. Woodbury OM. Goodman LS: Effect of adrenalectomy. hydroconisone acetate. and deoxyconicosterone acetate on brain excitability and electrolyte distribution in mice. J Pharmacol Exp Ther 112:80-93. 1954 II. Engel CL. Margolin SG: Clinical correlation of the electroencephalogram with carbohydrate metabolism. Arch Neurol Psychiatry 45:890-892. 1941 12. Thorn OW, Koepf OF. Lewis RA. et a1: Carbohydrate metabolism in Addison's disease. J Clin Invest 19:813832. 1940 13. Henkin RI. Gill JR. Warmolts JR. et al: Steroid-dependent increase of nerve conduction velocity in adrenal insufficiency.JClinlnvest42:94I.I963
PSYCHOSOMATICS
Case Reports
14. Henkin RI. Daly RL: Auditory detection and perception
in nonnal man and in patients with adrenal conical insufficiency: effect of adrenal conical steroids. J Clin Invest 47:1269-1280.1968 IS. Henkin RI. Gill JR. Banter FC: Studies on taste threshholds in nonnal man and in patients with adrenal conical insufficiency: the role of adrenal conical steroids and ofserum sodium concentration.J Clin Invest 42:727735. 1963 16. Ojemann CA. Henkin RI: Steroid dependent changes in visual evoked potentials. Life Sci 6:327-334. 1967 17. Henkin RI. Banter FC: Studies on olfactory thresholds in
nonnal man and in patients with adrenal cortical insufficiency: the role of adrenal conical steroids and of serum sodium concentration.J Clin Invest 45:1631-1639.1966 18. Lindstrom LH. Widerlov E. Gunne L-M. et al: Cerebrospinal fluid: clinical correlations to some psychotic states. Acta Psychiatr Scand 57: 153-164. 1978 19. Wise MG. Rundell JR: Concise Guide to Consultation Psychiatry. Washington. DC. American Psychiatric Press. 1988 20. Lehmann H. Nair NPV. Kline NS: Beta-endorphin and naloxone in psychiatric patients: clinical and biological effects. AmJ Psychiatry 136:762-766. 1979
Severe Claustrophobia in a Patient Requiring Hyperbaric Oxygen Treatment JAMES RANDOLPH
HILLARD.
M.D.
Case Report
tion treatment (7500 rads) to her mandible. The patient's sarcoma was cured. but her jaw was hypoplastic. Some teeth had been extracted and her mandible debrided when she was 24. At that time. she also underwent stomatorraphy and a split-thickness skin graft to cover bone exposed secondary to radionecrosis. At this time. the patient received a total of 20 hyperbaric oxygen treatments. each lasting 60 minutes. She tolerated the treatments and recovered well. despite claustrophobic symptoms. At the age of 34. the patient developed more dental problems. and funher extractions were recommended. Hyperbaric oxygen treatments (10 treatments of 90 minutes each) to prevent radionecrosis were also recommended. The patient was told that extraction and radiation accompanied by hyperbaric oxygen treatment carried a 7% risk of radionecrosis. but the same treatment without hyperbaric oxygen carried a 40% risk of developing necrosis. The patient reponed always having been nervous in enclosed spaces. such as the back seats of
The patient was a 34-year-old. white. female registered nurse who had been referred for hyperbaric oxygen treatment for prophylaxis of osteoradionecrosis secondary to dental extraction. At age 17. she had been diagnosed with a reticulum cell sarcoma that required excision of two tumors in her jaw plus radia-
Received March 23. 1989; revised April 19. 1989; accepted May 26. 1989. Address reprint requests to Dr. Hillard. Depanment of Psychiatry. University of Cincinnati College of Medicine. 231 Bethesda Avenue. ML559. Cincinnati. OH 45267-0559. Copyright © 1990 The Academy of Psychosomatic Medicine.
yperbaric oxygen therapy is the treatment of choice for an ever-increasing range of medical conditions. I Because claustrophobia is relatively common in the general population/·3 a substantial number of severely claustrophobic individuals are likely to require treatment with hyperbaric oxygen. This article describes the successful treatment of one such individual. The hyperbaric oxygen chamber is uniquely stressful for claustrophobic individuals because it is quite small, usually measuring seven feet by two feet by two feet. A long exposure time (60 to 90 minutes) is required, and because 15 to 30 minutes are required to depressurize following treatment. the patient cannot make a rapid escape should it seem necessary.
H
VOLUME 31 • NUMBER 1 • WINTER 1990
107