Psychiatric effects of thyroid hormone disturbance

RICHARD C. W. HALL, M.D.

Psychiatric effects of thyroid hormone disturbance Psychosomatic illness review: No.5 in a series Neuroendocrine disorders often present and/or are associated with psychiatric signs and symptoms.. The author reviews the literature on psychiatric findings in hypothyroidism and hyperthyroidism and provides recommendations for diagnostic and treatment procedures.

ABSTRACT:

Disturbances of endocrine function are among the most common physical causes for the production of what appears to be primary psychiatric disease. I·) This paper reviews psychiatric, physical, and laboratory findings associated with hypothyroidism and hyperthyroidism, and presents recommendations for diagnosis and treatment. HYPOTHYROIDISM History and symptoms In 1874, Gu1l4 reported on a "cretinoid state occurring in an adult female" who had psychiatric symptoms. Four years later, Ord5 coined the term "myxedema" and commented that mental changes were

frequently associated with this condition. Ten years later, the Clinical Society of London6 published a detailed report that defined the symptoms of 109 patients with myxedema. The majority of their findings remain valid. The Society concluded that "delusions and hallucinations occurred in nearly half of the cases," and that "insanity" was seen in an equal number of patients. The report defined the characteristic "insanity" of myxedema as "acute or chronic mania or dementia melancholia with a marked preponderance of suspicion and self-accusation." The frequency of an initial psychiatric presentation for myxede-

Dr. Hall is chief of staff of the VA Medical Center, Memphis, associate dean for veterans affairs, and professor ofpsychiatry and ofinternal medicine at the University of Tennessee College of Medicine. Reprint requests to him at VA Medical Center, 1030 Jefferson A ve., Memphis. TN 38104. JANUARY 1983' VOL 24 • NO 1

ma seems to be decreasing, perhaps because of better and more available medical care, which interrupts the disease at an earlier stage. Early reviews of the literature suggested that psychosis did indeed occur in the 50% range reported by the Clinical Society.6.8 More recent studies, however, suggest that the current incidence of psychosis in myxedematous patients is between 5% and 15%. As described in the literature (there are several hundred case reports on the psychiatric course and symptoms),9.21 the characteristic course of slowly progressive myxedema seems to be one of progressive mental slowing, with a decline in memory function, speech, and learning ability. Perceptual changes progress, with distortion of hearing, taste, vision, and smell. Delusions and frank hallucinations or psychosis occur as the disease becomes more advanced. The typical manifestations of myxedema madness were described in 1949 by Ascher,20 who emphasized the prominence of psychiatric symptoms in his classic review of 14 cases in which the 7

Thyroid hormone disturbance

diagnosis of myxedema had not been previously established. All of these patients presented with psychotic changes, and ten had been admitted to a mental ward for observation under the Lunacy Act. In nine of the 14, "there was a dramatic and complete recovery of sanity with thyroid treatment." Two patients partially improved when treated, one remained unchanged, and two died. In discussing the cases, Ascher called attention to the very important fact that myxedema causes psychosis: If one observer can encounter this number in four years. it must mean that there are many others. Possibly there are many cases in mental hospitals which have not been diagnosed. If the diagnosis is borne in mind by psychiatrists a number of otherwise hopeless psychoses may be cured. and the awareness of an organic cause for one psychosis may lead to the discovery of physical causes for others which are at present dismissed as of psychological or idiopathic origin.

Ascher suggested that the patient's history was of little help in initially establishing the diagnosis, although it was of great utility in confirming the diagnosis once it had been suspected. That was because symptoms are "admitted rather than complained of.... The mental slowness of the illness itself smothers self-criticism. In fact, you get no history of myxedema if you are not thinking of myxedema when you take that history." Ascher defined the following symptoms as most common in his patients: general tiredness, weight gain, vague aching pains in the legs, memory impairment, constipation, deafness, loss of hair, dry skin, and 8

cold intolerance. He noted that changes in facial appearance, alterations of voice, and snoring were often complained of by the patient's relatives. Most of his cases were women. Although no characteristic psychosis occurred, in all cases he noted that the most frequent presentation was depression or an agitated paranoid state. Other presentations for the condition described in the literature are: chronic insidious personality change with lability of mood, anxiety, and emotional withdrawal; gradually progressive depressive disorder simulating psychogenic depression; a paranoid schizophrenia-like syndrome; rapidly developing psy-

Psychiatric symptoms may be the earliest or most prominent signs or symptoms reported by the hypothyroid patient. chotic depression; and a mania-like presentation with paranoid ideation and agitation.8.11.14.21.24 The most characteristic picture of rapidly developing myxedema is one of generalized agitation, with progressive disorientation, persecutory delusions, hallucinations, and intermittent bouts of lethargy and extreme restlessness. Patients are often extremely irritable, delusional, paranoid, and complain of auditory and/or visual hallucinations. Hypersexuality during these states has also been reported. 19 St01l2 1 describes the classic personality changes as follows: "One is impressed by the marked personality changes present in advanced cases: irritability, untruthfulness, suspicion, delusions, retarded cerebration, inability to concentrate,

introversion and failing memory are conspicuous." Ruhberg22 believed that "every case of uncomplicated myxedema presents with a mental state, the essential features of which are fatigability and psychomotor retardation." Etiology of mental symptoms A variety of theories have been developed to explain the occurrence of mental changes in hypothyroid patients. Early theories2S suggested that myxedematous psychosis was a direct result ofcerebral hypometabolism or of the production of central nervous system toxins. Other theories26.2 7 surmised that the psychosis was due to cerebral edema, enzymatic changes in the brain, or diminished cerebral blood flow. Easson 28 proposed that mental symptoms were related to "a rapid change in internal stimuli and external perception which may not allow the physiological and emotional readjustment necessary to maintain an integrated concept of body stability." This theory had the added advantage of explaining the fact that some patients became worse when treatment was initiated: "Further internal adjustment, albeit towards normality, often caused a worsening of the myxedematous patient's emotional state." Other authors29 have noted that the severity of mental symptoms is greater in elderly patients an~ in persons with rapidly changing levels of thyroid hormone. The cerebral effects of the hypothyroid state were well depicted by Scheinberg and associates26 in their study of eight myxedematous patients with sensory impairment. He documented a 38% decrease in cerebral blood flow, a 27% decrease in cerebral oxygen and glucose consumption, and a 91% increase in PSYCHOSOMATICS

cerebrovascular resistance in these patients. He suggested that there was a specific correlation between disturbed metabolism and altered mental state. Of note to the practicing clinician are the findings of Blume and Grabow30 and Crevasse and Logue,31 who established that unusual neurologic symptoms may precede other signs of myxedema. These authors reported on the early occurrence of cerebellar ataxia and peripheral neuropathy as presenting symptoms of hypothyroidism. The EEG effects of myxedema have been studied by a variety of authors, with mixed findings. Browning and associates 32 were unable to correlate the EEG pattern and the clinical symptoms of hypothyroid patients. Libow and Durelp3 demonstrated slowing and flattening of the EEG in delirious myxedematous patients. Logothetis34 also reported EEG slowing and flattening, and suggested that these changes were associated with hyperthyroid psychosis. He noted the resolution of these abnormalities when the patient was returned to the euthyroid state. Using a carefully controlled research model in hypothyroid patients who had little functional thyroid tissue, Lansing and Trunne1l3) deprived patients of thyroid replacement and obtained serial EEGs. These investigators found slowing of dominant alpha rhythms, but were unable to document significant changes in amplitude. When thyroid replacment was reinstituted, the EEG abnormalities disappeared. New research by Whybrow and Prange36 .37 focusing on the thyroid axis and catecholamine interaction suggests that thyroid function plays a role in the expression of certain affective disorders: JANUARY 1983· VOL 24 • NO I

A lack of thyroid hormones can lower the threshold for depression; an excess can contribute to a state of tense dysphoria. Thyroid function in some persons also appears to influence the course of affective disorders. Adequate mobilization of thyroid hormones favors recovery from depression; excess mobilization increases the risk of mania in vulnerable individualsY

These authors, in reviewing available information, propose that thyroid hormones modulate the activity of central ,B-adrenergic re-

Discontinuation of therapy by the patient typicaUy leads to a return ofsymptoms within a short period oftime. ceptors in their response to the presence of catecholamines. They suggest that thyroid hormone increases the ability of these central fJ-adrenergic receptors to receive stimulation from norepinephrine. Thyroid hormone, by modulating catecholamine neurotransmission in the CNS, would therefore serve as a mechanism for physiologic adjustment and "defense" during times of adaptive demand. This hypothesis is important, since it explains a wide variety of clinical findings and suggests important new areas of research. Differential diagnosis As stated earlier, psychiatric symptoms may be the earliest or most prominent signs or symptoms reported by the hypothyroid patient. The essential diagnostic features are shown in Table I. Hypothyroidism should be considered in the differential diagnosis of patients who appear neurasthenic and/or

have unexplained menstrual disorders, weight gain, or macrocytic anemia. The condition should also be included in the differential diagnosis of unexplained ascites, refractory heart failure, and idiopathic hyperlipemia. Various effusions, all of which have high protein content, may occur in hypothyroid patients. The hypothyroid patient's thick tongue may suggest amyloidosis. Hypothyroidism should also be considered in patients who present with what appear to be myasthenic or rheumatic syndromes. The clinician should remember that cerebrospinal fluid protein levels are high in myxedematous patients. The major complications of the disease are cardiac in nature, and occasionally a patient may develop refractory hyponatremia resulting from inappropriate secretion of antidiuretic hormone. The clinician should also remember that myxedematous patients are unusually sensitive to opiates and that the administration of average doses of these drugs may prove fata(.38 Treatment Following appropriate diagnosis, thyroid replacement treatment should be initiated cautiously. If the myxedema is severe, if myxedematous heart disease exists, or if the patient is elderly, the clinician should begin treatment with c:xtreme caution, as rapid physiologic changes in thyroid levels may be associated with worsening of cardiac symptoms or the development of a mania-like or organic psychosis. If replacement therapy is used, doses in the range of 8 to 15 mg/d for a week, then increased by 15 mg/d up to a total of 100 to 200 mg/d, are usually effective. Levothyroxine sodium given in

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Thyroid hormone disturbance

the range of 0.15 to 0.3 mg/ d is probably the medication of choice for the majority of hypothyroid patients because of its predictable action. Dosage should be adjusted upward until the T4 rises to high normal levels. When a rapid response is necessary, the clinician may wish to consider liothyronine sodium (TJ). Lower doses, beginning in the 5-p.g range, should be used because of this agent's rapidity of action. The level should be increased slowly. New medications

that represent a mixture of T4 and TJ in 4-to-1 ratio (liotrix) are thought by some to represent a more "complete and balanced" product for replacement. J8 Course following treatment If treatment is initiated slowly and the patient is followed carefully, most mental and physical symptoms abate over a period of days to months. Some physicians have the mistaken belief that if psychological symptoms have not abated

Table 1-Dlagnostlc Features of Hypothyroidism· Symptoms Weakness Fatigue Mental slowing Cold intolerance Constipation Confusion Depression Agitated paranoia Menorrhagia or amenorrhea

Hoarseness Pathological fatigue (ie, made worse by sleep) Lethargy Headache Joint pain Nervousness Weight gain Decreased taste and smell Schizophreniform or mania-like psychoses Signs

Skin-dry, cold, puffy, pale yellowish SCant eyebrows Coarse, brittle hair Thick tongue

Bradycardia Delayed return of deep tendon reflexes "Water bottle" heart Thin, brittle nails

Laboratory findings T4 less than 3.5 p.g/1 OOmL Radioiodine uptake below 10% in 24 hours T3 uptake usually low Plasma cholesterol elevated In primary hypothyroidism Macrocytic anemia possibly present 17-ketosteroids may be low Thyroid-stimulating hormone (TSH) radioassay elevated in primary hypothyroidism Adapted With permISSion Irom Current MedICal D,agnOSIS and TI a/ment. 1978. pp 670·672 (Kolb F()J8)

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within five days following treatment, an underlying thought disorder must be present. In fact, many behavioral and mental symptoms may persist for considerable periods after resolution of the physical complaints. It is not unusual for patients to report that from two to six months elapsed before they felt that their mental function had fully returned to normal. Sleep and consequently human-growth-hormone release during sleep may remain disturbed for several weeks to months following replacement of thyroid hormone. Patients who have been psychotic usually experience the disappearance of delusions and hallucinations within the first week. This is particularly true if antipsychotics are added when thyroid hormone replacement is begun. Gradually, over the next week to ten days. the patient becomes more alert and the physical signs of myxedema begin to resolve. J9 Kales and associates4° have shown that improvement in clinical condition tends to parallel restoration of normal sleep patterns and. in fact. suggested that the return of normal sleep may be an excellent predictor of treatment outcome. Discontinuation of therapy by the patient typically leads to a return of symptoms within a short period. JJ If the patient is taking T4 or a mixed TJ plus T4 preparation. psychotic symptoms usually reappear over four to seven days. Psychosis may reappear within 12 to 18 hours when T3 is discontinued. Some patients become worse following initiation of treatment. Mason 41 suggests tha t small changes in thyroid levels produce dramatic effects on brain function. If mental symptoms are worsened PSYCHOSOMATICS

by treatment, the reinstitution of therapy at lower dosages is recommended. Phenothiazines (chlorpromazine or thioridazine) are useful in moderate dosages (100 to 300 mg/d) for the treatment of myxedematous psychosis. HYPERTHYROIDISM History In 1918, Woodbury'2 described the manifestations of Graves' disease as involving fatigue, irritability, intolerance to cold, fine tremor, restlessness, insomnia, excitability, labile emotional disposition, nervousness, weight loss, palpitations, doubts, and fears. Amburg and Lunde43 later depicted the hyperthyroid patient as "characterized by hyperexcitability, irritability, restlessness, increased sexual motivation, exaggerated response to environmental stimuli, emotional instability and ultimately psychosis." There seems to be a consensus in the literature concerning the occurrence of fatigue, irritability, and instability of personality, but psychosis associated with hyperthyroidism remains a much less common finding. The prevalence of psychosis in severe hyperthyroid states has been reported to range between 1% and 20%. In 1928, Johnson 44 studied 2,286 patients with operative goiter and found only 24 cases of psychosis. However, many clinicians believe that the incidence of psychosis in hyperthyroid states is considerably higher. Lidz and Whitehorn,24 Kleinschmidt and associates,45 and Deutsch 46 stated that the rate of psychosis in hyperthyroid patients approximated 20%. Bursten 47 reported an 18.5% rate of psychosis among hospitalized hyperthyroid patients, but noted that this was a selected population. In another

studt7of 8,000 psychotic and 2,500 schizophrenic patients, he found an overall incidence of hyperthyroidism of less than 1%; these figures are in fundamental agreement with findings by Bluestone.48 It is interesting to note that the majority of the existing literature concerning the mental effects of hyperthyroidism explores possible psychogenic etiologies for this syndrome, rather than defining clearcut mental changes of the type that occur with hypothyroidism. In reviewing the literature, one is left

The prevalence ofpsychosis in severe hyperthyroidism is between 1% and 2fRo. with the impression that psychotic mental changes in the hyperthyroid state are not only less common but less extreme in their manifestation than those occurring with hypothyroidism. Ettigi and Brown49 note that hyperthyroidism is "almost inevitably associated with mental changes." The most common presenting symptoms include nervousness, manifested as apprehension, restlessness, and inability to concentrate; marked emotional lability; and hyperkinesia. 50 Psychosis The "typical" psychosis of hyperthyroidism is reported by most authors4 2.44 to simulate a manic-depressive psychosis. Other presentations reported in the literature24.44-47.49 include simple, catatonic, and paranoid schizophrenia; psychotic depression; "functional psychosis"; organic brain syndrome; and psychoses of undetermined type. Reports are available of psycho-

sis occurring in hyperthyroid states, which were subsequently reversed by surgery. Rulison and associates51 describe a case characterized by psychosis with hallucinations and delusions that cleared following thyroidectomy. Bluestone48 reported on three cases "each of which responded to thyroidectomy with abrupt cessation of psychotic symptoms." Greer and Parsons52 described a hyperthyroid patient who presented as a paranoid schizophrenic. Consistent agreement can be found in the literature that fatigue, irritability, emotional instability, and excitability are all common features of the hyperthyroid state, as are episodes of severe and often disabling anxiety. No clear picture, however, exists concerning any fixed psychotic constellation of symptoms or progression of psychiatric disease. Some individuals become delirious, while others experience periods of hyperexcitability simulating mania that alternate with periods of exhaustion and depression. Other symptoms The most frequent office presentation of hyperthyroidism is a hyperactive individual complaining of anxiety and nervousness. Often a fine generalized tremor is present, and the patient will report feeling shaky or jittery. Family members often remark about personality changes and marked increases in both irritability and emotional lability. Jefferson and Marshall s3 point out that this "nervousness" is dissimilar to that seen in the patient with anxiety neurosis, in that it is "characterized by restlessness, shortness of attention span, and a need to move about." Popkin and Mackenzie 2 state that the behavioral changes of hy(continued)

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perthyroidism are numerous and frequently suggest a diagnosis of either anxiety neurosis or neurasthenia. Hyperthyroidism can be differentiated from these latter conditions by the following findings: "In thyroid dysfunction, sleeping pulse will remain accelerated; sedated pulse will exceed 80; palms will be dry and warm, not cool and clammy; fatigue will be accompanied by a desire to be active; and cognitive dysfunction is more prominent than in neurasthenia." Restlessness, increased work activity, and emotional explosiveness occur fairly frequently, as does marked emotional lability with unexpected tearfulness and crying, which often produce a sense of shame and bewilderment in the patient. When questioned, patients report that they are unaware of why they are crying. Often they describe diminished frustration tolerance, and although their work energy seems increased, their actual ability to complete tasks is diminished owing to shortened attention span and heightened distractibility. Subtle cognitive changes are clearly demonstrable in the hyperthyroid patient. 54 Cognitive disorders present on testing disappear as thyroid levels return to normal. Wilson and associates 55 were able to show that the experimental administration ofT3 to II normal volunteers, simulating an acute hyperthyroid state, produced marked changes in interpersonal functioning and caused dysphoria, depression, jitteriness, and decreased friendliness. Several investigators45 .56 have reported depression to be associated with the hyperthyroid state. When depression does occur in the hyperthyroid patient, it is qualitatively JANUARY 1983 • VOL 24 • NO I

and quantitatively less severe than depression in hypothyroid patients. Most patients with hyperthyroidism do not report significant depression. When it does occur, it is more likely to be of the agitated type rather than the retarded type, and to be associated with marked variability of mood rather than consistently depressed mood. Apathetic hyperthyroidism, described by Lackey'7 in 1931 (and also referred to as "silent or masked" thyrotoxicosis because these patients do not appear to be

The behavioral changes of hyperthyroidism are many and often simulate anxiety neurosis or neurasthenia. in a hypermetabolic state), may present as retarded or stuporous depression or apathetic dementia. This presentation is most frequent in the elderly. Initially the patient may complain of confusion, fatigue, weakness, profound weight loss, and cardiovascular complications. Later, depressive features become more marked. The depression deriving from apathetic hyperthyroidism simulates that seen in some cases of hypothyroidism. Often these patients appear to have advanced psychomotor retardation and to be totally detached and disinterested in any attempt to reach them. 58 While hypothyroidism frequently coexists with major psychiatric symptoms in hospitalized mental patients, hyperthyroidism does not seem to be particularly prevalent in this population. Bursten47 reported only ten cases of thyrotoxicosis in 8,000 overtly psychotic patients, while Bluestone48 was able to find

only one hyperthyroid patient in a group of 1,000 patients at a large public mental institution. Although there is no characteristic, single psychosis associated with hyperthyroidism, paranoid symptoms, suspiciousness, and maniclike states are most frequently reported. Whybrow and associates59 report that both the schizophrenia and paranoia scales of the MMPI are consistently elevated in hyperthyroid patients with psychosis. These authors stress that the mental changes encountered clear quickly following treatment, suggesting that the behavioral manifestations of hyperthyroidism are toxic phenomena rather than some form of liberated "latent psychosis." These findings are supported by the work of MacCrimmon and associates,60 who demonstrated MMPI scale deviations in hyperthyroid patients suggestive of hysterical somatization. These patterns returned rapidly to normal following treatment. This study indicates that the behavioral, neurotic, and psychotic manifestations of hyperthyroidism are related more to the biochemical abnormalities associated with the disease than they are to the patient's previous personality pattern. Physical diagnosis Physical signs and symptoms th.at occur in 70% or more of hyperthyroid patients include tachycardia, goiter, nervousness, soft moist skin, fine tremor, hyperhidrosis, heat hypersensitivity, exophthalmos, stare, dyspnea, weight loss, bruit over the thyroid, palpitations, fatigue, muscular weakness, and loose stools. The disease has its highest incidence in women between the ages of 20 and 40. When hyperthyroidism is associated with a diffuse 15

Thyroid hormone disturbance

goiter and ocular signs, the condition is termed Graves' disease. Clinicians should remember that spider angiomas and gynecomastia, which might otherwise suggest hepatic disease or alcoholism, occur commonly in hyperthyroid patients. Other physical signs that the clinician may not routinely associate with the condition, but which in fact are common, include a harsh pulmonary systolic (Means') murmur,lymphadenopathy, and splenomegaly. Osteoporosis also occurs commonly in patients with longstanding disease. Additional skin signs include pretibial myxedema (a localized, non pitting, hard, bilateral swelling over the tibia), and an infiltrative dermopathy with similar infiltrations over the dorsum of the feet. Clubbing and swelling of the fingers may also occur (see Table 2).

Laboratory diagnosis Laboratory findings characteristic of the disease include elevated radio-T3 resin uptake, and elevated T4 and radioiodine uptake. The radioiodine uptake characteristicalIy cannot be suppressed by TJ administration. An unusual condition called TJ toxicosis evidences normal T4 levels with elevated serum T3. Serum cholesterol may be low and postprandial glucosuria may be present. Urinary creatinine levels are usually increased. Lymphocytosis is generally present. Hypokalemia may also occur. Thyroid-stimulating hormone (TSH) levels are usually low, while longacting thyroid stimulator (LATS) and thyroid stimulating immunoglobulin (TSI) are elevated. JX Differential diagnosis The major psychiatric differentials include manic-depressive psycho16

sis, manic phase; anxiety neurosis, particularly in menopausal women; schizoaffective disorders; and drug abuse (stimulants, amphetamines, cocaine, phencyclidine). Other medical problems that should be included in the differential diagnosis are acute and subacute thyroiditis, pituitary tumor, and other conditions associated

with a hypermetabolic state such as leukemia, polycythemia vera, and severe anemias. Pheochromocytoma and acromegaly may be associated with hypermetabolism and an enlarged thyroid gland.o l

Treatment Controversy stilI exists as to the most efficacious treatment for a

Table 2-Dlagnostic Features of Hyperthyroidismo

f

Symptoms Heat intolerance Restlessness Easy fatigability Increased appetite Speech quickened

Weakness Irritability Nervousness Personality change Anxiety states Loose stools

Signs Sweating Weight loss TaChycardia Skin-soft, moist, warm, thin Tremor Stare Exophthalmos Goiter BrUIt over thyroid Clubbing of fingers Infiltrative dermopathy Dyspnea Palpitations

Pretibial myxedema Periorbital edema Lid lag Lack of pupillary accommodation Hair fine and silky Spider angiomas Gynecomastia Means' murmur Splenomegaly Lymphadenopathy Muscle wasting Osteoporosis

.

Laboratory findings Elevated T4 Elevated radlo- T3 resin uptake Radioiodine uptake elevated (Failure of suppression by T3 administration). Serum cholesterol usually low Urinary creatine Increased Postprandial glycosuria may occur Lymphocytosis Urinary and serum calcium may be elevated TSH can be low while LATS and TSI are elevated Adapted With permISSIon trom CUff 0, camargo CAlI)

nr MedIcal DiagnoSIs and Trearment,

1960, pp 667·694 (Kolb

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PSYCHOSOMATICS

particular patient. The literature today suggests an increased tendency toward long-term medical treatment. followed by radioiodine therapy. rather than surgical thyroidectomy. Medical treatment is performed with drugs of the thiouracil type. often combined with iodine. In addition. particularly for patients being prepared for surgery. the use of propranolol in doses of 80 to 240 mgt d seems an effective and rapid way of reversing the toxic manifestations of the disease. Because propranolol merely controls the symptoms rather than reversing the hypermetabolic state, escape and thyroid storm may occur. Radioactive iodine has provided excellent results in the treatment of diffuse or toxic nodular goiter. The clinician needs to remember that lithium, which acts as a colloid trap, is effective in reducing the severity of hyperthyroidism. This is particularly imponant in psychiatry, since one of the most frequent psychiatric misdiagnoses is that of manic-depressive disorder. If this diagnosis is accepted in a hyperthyroid patient without appropriate study, lithium administration often produces dramatic shortterm results and thereby erroneously confirms in the clinician's mind the diagnosis of mania. The dilemma with lithium therapy is

that it is only an adjunctive treatment for hyperthyroidism, and misdiagnosis may predispose the patient to the subsequent development of thyroid storm. If a hyperthyroid patient develops psychotic symptoms, these can often be controlled with either reserpine or chlorpromazine. b' Haloperidol has also been reponed b2 to be effective in treating psychosis associated with thyrotoxicosis that is unresponsive to chlorpromazine. However. several case reportsbJ •bb indicate that there may be increased neurotoxicity associated with haloperidol in hyperthyroid patients. Finally. several reponsb7 .b8 exist of non psychotic hypenhyroid patients developing what appears to be either a schizophreniform psychosis or an agitated organic psychosis following the initiation of treatment with antithyroid drugs. Consequently. vigilance is needed during the treatment phase. Thyroid screening in psychiatric patients Gold and associatesb9 recently demonstrated the value of endocrine screening in psychiatric patients. In their study of 250 consecutive patients admitted to a psychiatric hospital with the diagnosis of depression and anergia. endocrine diseases were a frequent finding.

Twenty of these patients were determined to be hypothyroid. The thyrotropin-releasing hormone test was the most useful in establishing the proper diagnosis. In a study of 480 newly admitted psychiatric patients. conducted at the Yale-New Haven Psychiatric Evaluation Unit. Cohen and Swigar70 demonstrated elevations in effective free thyroxin (EFT) in 43 patients (9%). Twenty-seven of these patients were thought to be suffering from "acute stress hyperthyroidism." The EFT levels of this group spontaneously reverted to normal within two weeks following admission. In addition, the EFT level was diminished in 42 patients admitted to the unit (9%). In 16 of these patients the EFT level subsequently had returned to normal. A presumptive diagnosis of secondary hypothyroidism was made in eight patients. An additional nine patients with known thyroid disease were found to be taking inadequate or excessive replacement therapy. Cohen and Swigar70 concluded that thyroid function tests are of value in psychiatric patients, but they caution that diagnosis and treatment should not be based on a single laboratory value. Rather, careful physical and laboratory examination is necessary to ensure proper diagnosis and treatment. 0

adult life In women. Trans Cltn Soc London 7180-185.1874. 5. Ord WM: On myxedema. R Med Chirg Soc Trans 6"57-58.1878. 6. Report on myxedema. Trans Cltn Soc London 21 (suppl):31. 1888. 7. Von Juaregg JW: Myxodem und Kretlnismus. in: Aschaffenburg'S Handbuch der Psychia. tf/e. part 2. section I. Leipzig. Halite. 1912. 8 Hayward EP. Woods AH: Mental derangements In hypothyroidism JAMA 97:64.1931. 9 Ziegler LH: PsyctlOsis associated with myx· edema. J Neurol PsychOpathol tl:20-27. 1930. 10. Whybrow PC. Prange JR. Treadway CA.

Mental changes accompanying thyroid gland dysfunction. Arch Gen PsyChiatry 20:48-63. 1969 11 Jain VK: Affective disturbance in hypothy· rOldlsm Br J Psychiatry 119:279-289. 1971. 12. Clower CG. Young AG. Kepas 0: PsychOfic states resultlng from disorders of thyroid function. Johns Hopkins Med J t24:305-310. 1969 13. Akelaitis AJ: PsyChiatric aspects of myxedema. J Nerv Ment Dis 83:22·36.1936. 14. Savage GH: Myxedema and its nervous symptoms. J Ment Sci 25:517-519.1980. 15 Tonks CM: Mental illness in hypothyroid patients Br J Psychiatry 110:706-710. 1964.

REFERENCES 1 Hall RCW. Gardner ER. Popkin MK. et al' Unrecognozed phYSical illness prompting psychiatric admission: A prospective study. Am J Psychiatry 138:629-635. 1981. 2. Popkin MK. Mackenzie TB: PsychiatriC presentations of endocrine dysfunction. In Hall RCW (ed): Psychiatric PresentatIons of Medica/ Illness New York. Spectrum Books. 1980. pp 142-143 3. Lavis VA. PsychiatriC manifestations of endocrine disease In the elderly. in Levenson AF. Hall RCW (eds) Aging. vol 14: Neuropsychiatf/c Disease in the Elderly. New York. Raven Press. 1981. pp 59-81 . 4. Gull W: On a cretinoid state supervening in

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