Higher TSH Values Research Articles

Prevalence and follow‐up of abnormal thyrotrophin (TSH) concentrations in the elderly in the United Kingdom

Increasing use of assays for TSH with improved sensitivity as a first-line test of thyroid function has raised questions regarding prevalence and clinical significance of abnormal results, especially values below normal. We have assessed the thyroid status of 1210 patients aged over 60 registered with a single general practice by measurement of serum TSH using a sensitive assay. High TSH values were more common in females (11.6%) than males (2.9%). TSH values below normal were present in 6.3% of females and 5.5% of males, with values below the limit of detection of the assay present in 1.5% of females and 1.4% of males. Anti-thyroid antibodies were found in 60% of those with high TSH but only 5.6% of those with subnormal TSH. Eighteen patients were hypothyroid (high TSH, low free thyroxine) and one thyrotoxic (low TSH, raised free thyroxine) at initial testing. Seventy-three patients with elevated TSH but normal free T4 were followed for 12 months; 13 (17.8%) developed low free T4 levels and commenced thyroxine, TSH returned to normal in four (5.5%) and 56 (76.7%) continued to have high TSH values. Sixty-six patients with TSH results below normal were followed. Of the 50 subjects with low but detectable TSH at initial testing, 38 (76%) returned to normal at 12 months; of those 16 with undetectable TSH followed, 14 (87.5%) remained low at 12 months. Only one subject (who had an undetectable TSH) developed thyrotoxicosis. In view of the marked prevalence of thyroid dysfunction in the elderly, we suggest that screening of all patients over 60 should be considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Thyroid function in down syndrome

The thyroid function of 181 patients with Down syndrome was investigated. When compared with a control group of 163 children we found T4 and FT4 levels to be significantly lower and T3 and TSH levels to be significantly higher in the Down syndrome population. Of the 181 patients with Down syndrome, 29 (16%) showed evidence of either uncompensated or compensated hypothyroidism: 11 (6%) had both low T4 and high TSH levels, 14 (8%) had only high TSH values, and 4 (2%) had only low T4 values. One of the patients with Down syndrome had a significantly elevated T4 level. Studying different age groups, we observed a decline of the mean T4, FT4, T3, FT3, and TBG values with advancing age. T4, T3, and TSH blood levels obtained in 1988 were slightly but not significantly lower when compared with values from 1985. Because thyroid dysfunctions in patients with Down syndrome are more common than in the general population, periodic thyroid hormone function tests should be performed in persons with Down syndrome in particular as they advance in age. Thus, individuals with significantly abnormal results can be identified early before clinical symptoms become manifest. If patients with Down syndrome are found to have a thyroid hormone disorder, appropriate treatment should be forthcoming, which in turn will enhance their quality of life.

Serum thyrotropin in hospitalized psychiatric patients: Evidence for hyperthyrotropinemia as measured by an ultrasensitive thyrotropin assay

In order to gather further insight into the basis for high serum T4 and/or T3 of psychiatric illnesses, we studied thyroid function in 84 consecutive newly hospitalized psychiatric patients (HPP) in a 12-week period. Serum T4 and T3 were measured by immunoassay and thyrotropin (thyroid-stimulating hormone [TSH]) by an ultrasensitive immunoradiometric assay. Serum T4 was in the normal range in 64 (76%) and elevated in 20 (24%); free T4 index was elevated in 13 of 75 (16%), total T3 in 12 of 60 (20%), free T3 index in seven of 56 (13%), and TSH in 14 of 84 (17%) cases so studied. Serum TSH was subnormal in only one case (1%). Among the 14 patients with elevated serum TSH, serum free T4 index was normal in 12 and elevated in two. High serum T4 (or free T4 index) and high serum TSH were not correlated significantly by χ 2 analysis. None of the patients with elevated TSH demonstrated goiter or antithyroglobulin or antimicrosomal antibodies. On repeat testing 7 to 21 days after admission, serum TSH (and/or T4) normalized in the three of five patients studied. Serum TSH response to 500 μg intravenous (IV) thyrotropin-releasing hormone (TRH) was normal (serum TSH post-TRH, 8 to 28 μU/mL) in two patients with elevated TSH and T4, one patient with normal TSH and high T4, and one patient with normal TSH and T4. One patient with suppressed serum TSH (0.1 μU/mL) had elevated serum T4 (16.9 μg/dL, normal 4.8 to 11.5). In conclusion, in HPP (1) elevated serum T4 (or free T4 index) is mainly associated with normal or elevated serum TSH; TSH is suppressed in only 1%; (2) the transiency of high TSH (and T4) and absence of goiter and antithyroid antibodies suggest that high TSH (and T4) values are a result of a central abnormality in the central nervous system (CNS)-hypothalamothyrotropic axic.

Autoimmune thyroid disease in the puerperium. Predictive value of thyroid enlargement and related hormonal changes occurring during pregnancy

The incidence of goiter detected during pregnancy and its significance as an indicator of autoimmune thyroid disease after delivery was investigated in a sample of 707 pregnant women (81% in their 2nd trimester of gestation). Goiter was detected in 106 subjects (15%). Blood T4, T3, TSH, free T4 index (FT4I), antimicrosomal antibodies (AMA) and urinary iodine excretion were measured in these women and in a control group of gravidas without goiter. These measurements were repeated at 1 and 3 months after delivery. Compared with controls during pregnancy, subjects with goiter had lower FT4I values (11.0 +/- 2.8 vs 9.0 +/- 1.8; p less than 0.01) and higher TSH values (2.9 +/- 0.6 microU/ml vs 4.2 +/- 2.1 microU/ml; p less than 0.01). In contrast, T4, T3, AMA and urinary iodine excretion values were similar in both groups. In subjects with goiter FT4I values increased over pregnancy levels at 1 month (11.2 +/- 2.0; p less than 0.05) and 3 months (14.0 +/- 3.0; p less than 0.05) after delivery; in 29% a biochemical hyperthyroidism (FT4I greater than 13.5) was detected. During the same period TSH values decreased significantly (1 month: 1.9 +/- 0.7 microU/ml; p less than 0.05; 3 months: 2.7 +/- 3.0 microU/ml; p less than 0.05). Frequency of positive AMA increased from 8.6% during pregnancy up to 32.1% in the post-delivery period (p less than 0.01). In the control group no variation in the FT4I, TSH or AMA were observed after delivery. These results indicate that goiter during pregnancy is common in Chilean gravidas and that it has predictive value for the appearance of autoimmune thyroid disease after delivery.

Specificity of sensitive assays of thyrotropin (TSH) used to screen for thyroid disease in hospitalized patients.

Thyrotropin (TSH) concentrations were measured in 1580 hospitalized patients and 109 normal persons. Using the mean +/- 3 SD limits of the log values for the controls (0.35-6.7 milli-int. units/L), the proportion of abnormal TSH results in the hospitalized patients was 17.2%. TSH was undetectable (less than 0.1 milli-int. unit/L) in 3.1% of patients, suggesting hyperthyroidism, and high (greater than 20 milli-int. units/L) in 1.6%, suggesting hypothyroidism. On follow-up of 329 patients, 62% with abnormal TSH (less than 0.35 or greater than 6.7 milli-int. units/L) and 38% with normal TSH concentrations, only 24% of those with undetectable TSH had thyroid disease: 36% of them were being treated with glucocorticoids and 40% had nonthyroidal illness (NTI). Although half the patients with TSH greater than 20 milli-int. units/L had thyroid disease, 45% of patients had high TSH values associated with NTI. TSH concentrations usually returned towards normal when patients' therapy with glucocorticoids was discontinued or they recovered from NTI. TSH test sensitivity appeared good when the mean +/- 3 SD limits of the reference population were used, i.e., no cases of hyper- or hypothyroidism, as identified by free thyroxin index (FT4I), were missed. However, TSH test specificity was inferior to that of the FT4I test (90.7% vs 92.3%), although specificity could be improved to 97.0% if the wider TSH reference limits of 0.1 to 20 milli-int. units/L were used--limits considered pathological if applied to outpatients. Evidently, different reference intervals for TSH are needed for hospitalized and nonhospitalized patients. We conclude that a "sensitive TSH assay" is not a cost-effective thyroid screening test for hospitalized patients as compared with the FT4I.

847 THYROID DYSFUNCTION IN DOWN SYNDROME

We investigated the thyroid function of 151 children with Down syndrome. Compared with a control group of 89 siblings nearest in age to their brother or sister with Down syndrome the mean TSH value was significantly higher in children with Down syndrome than in the non-Down syndrome children (8.49 μU/ml vs. 3.55 μU/ml). However, the mean T4, levels in both groups were nearly the same (8.36 μg/dl and 8.60 μg/dl). In the Down syndrome group there was a trend for TSH values to increase and for T4 values to decrease with advancing age. Of the 151 patients with Down syndrome, 10 had both significantly elevated TSH levels ( > 9.5 μU/ml) and significantly decreased T4 levels (< 5.5 μg/dl) 21 had abnormally high TSH values (>9.5 μU/ml), 7 had markedly increased T4 levels (> 12.0 μg/dl), and 3 had significantly decreased T4 levels (< 5.5 μg/dl). The intellectual functioning of children with both abnormal TSH and T4 levels was significantly lower (mean IQ 41.7) than that of Down syndrome children with only increased TSH values (mean IQ 53.8) and that of Down syndrome children with normal thyroid function (mean IQ 55.3).This study provides evidence that there is an increased prevalence of thyroid dysfunction in children with Down syndrome. Therefore, children with Down syndrome should have thyroid function studies performed at regular intervals and prompt treatment should be instituted if thyroid dysfunction has been identified.

Transient impairment of thyroid function in newborn from an area of endemic goiter.

Thyroid function was studied in newborn from 3 areas of Sicily in which iodine intake is normal (area A), moderately decreased (area B), and severely decreased (area C). In the latter 2 areas, there is a high incidence of goiter and in area C endemic cretinism is present. TSH and T4 were measured in the cord serum of 5673 newborn from area A, 2096 from area B, and 184 from area C. The mean TSH value was significantly higher in areas C (P less than 0.001) and B (P less than 0.005) when compared to area A; moreover, in both endemic goiter areas the mean cord serum T4 was significantly reduced (P less than 0.01). All infants with cord serum TSH levels above 50 microU/ml were recalled because of the suspicion of congenital hypothyroidism. Such values were found in 41 of the 7953 infants (0.52%) with an increasing frequency from area A (9:5673 = 0.16%) to area B (14:2096 = 0.67%) to area C (18:184 = 9.78%). At the time of the recall examination [mean age, 32 +/- 8 (SD) days], 3 of the 41 recalled infants had died. Of the remaining 38 infants, 3 patterns evolved: 1) 23 had normal serum TSH and T4 values and were not studied further (false positives). 2) Eleven had elevated serum TSH and normal T4 values. They were reevaluated again after 3-6 weeks: all had normal values (transient hyperthyropinemia ). 3) Four infants had both high serum TSH and low serum T4 values (2 from area A and 2 from area C). They were diagnosed as having congenital hypothyroidism and treated with T4. At 10-13 months of age, after treatment withdrawal, the 2 infants from area A had permanent congenital hypothyroidism due to thyroid agenesis whereas the 2 infants from area C were euthyroid (transient congenital hypothyroidism). The present studies indicate, therefore, that in newborn from areas of iodine deficiency there is a higher frequency of elevated TSH levels and low T4 values than is found in areas where iodine intake is normal. This frequency is correlated to the degree of the iodine deficiency. The data suggest that the impairment of thyroid function at birth may be a transient phenomenon. The duration and the severity of the transient neonatal hypothyroidism, however, is greatly variable and its evolution unpredictable.

Defective thyroidal iodine concentration in protein-calorie malnutrition.

Although protein-calorie malnutrition (PCM) is known to result in various abnormalities of thyroid function, the exact relationship between the two is not clearly understood. Therefore, the thyroid function of 10 men, 13-55 yr of age, with severe PCM was studied in a clinical research ward before and 3-4 months after protein-calorie repletion. Before repletion, all subjects had low serum T4 (mean +/- SEM, 5.1 +/- 0.5 micrograms/dl) and T3 (74 +/- 6 ng/dl) concentrations. Eight subjects were chemically euthyroid, and their free T4 (1.5 +/- 0.1 ng/dl) and serum TSH (2.9 +/- 1.4 microU/ml) values were normal. Two subjects were chemically hypothyroid, with low free T4 values and high serum TSH values. After repletion, the 8 euthyroid subjects had significant increases in serum T4 (P less than 0.01) and T3 (P less than 0.005), but TSH did not change. Serum T4 and T3 were still lower (P less than 0.05-0.001) and TSH higher (P less than 0.01) than in 28 normal men of comparable age coming from the same area. After repletion, values remained unchanged in the 2 hypothyroid subjects, except for moderate increases in serum T3 and slight decreases in TSH. In all PCM subjects, values of thyroidal exchangeable iodine (23.1 +/- 7 vs. 42.9 +/- 8 mg; P less than 0.02), estimated thyroidal I per g wet wt (1.05 +/- 0.3 vs. 1.99 +/- 0.36 mg; P less than 0.02), and thyroidal iodide clearance (13.8 +/- 1.6 vs. 19.4 +/- 1.3 ml/min; P less than 0.002) were lower before repletion than after; the protein-bound 131I level (72 h; 0.27% vs. 0.08 dose/liter; P less than 0.05) was higher, but thyroid hormone secretion rates (200 +/- 49 vs. 153 +/- 25 micrograms/day) were not significantly different. Thyroid iodide clearance was lower even though plasma inorganic iodine (6.3 +/- vs. 12.5 +/- 3 micrograms/liter; P less than 0.05) and daily urinary iodine excretion (158 +/- 43 vs. 395 +/- 62 micrograms; P less than 0.01) were lower before than after repletion. In 2 PCM euthyroid subjects, baseline thyroid 131I uptake was lower before than after repletion, and the magnitude of the increase after TSH (10 U, im) stimulation was greater when the malnourished state improved. TSH increased concentrations of serum T4 and T3 both before and after protein repletion. After repletion, one hypothyroid patient failed to respond to TSH; the other had a small increase in 131I uptake but not in serum T4 or T3. The results indicate defective thyroid iodine concentration in human PCM, but adequate hormone secretion. This situation leads to depletion of thyroid iodine stores. This alteration, if extreme, might result in hypothyroidism. Adequate protein-calorie intake tends to reverse these abnormalities.

Alterations of serum thyroxine, triiodothyronine, and thyrotropin in the progeny of hypothyroid rats.

Thyroid function in the progeny of hypothyroid rats was studied from 19 days of gestation until adulthood. Total T4, T3, and TSH were measured by RIA in the sera of control, surgically thyroidectomized (Tx), and GH-treated Tx pregnant rats and their progeny from the late fetal period through adulthood. By the 22nd day of gestation, the fetuses of Tx mothers had T4 and TSH levels significantly above those of their controls. This condition, whereby fetal serum T4 and TSH levels were elevated, was aggravated by GH treatment of the Tx mothers. The progeny of Tx- and Tx and GH-treated mothers also showed alterations in serum T4, T3, and TSH. While the T4 levels of the progeny of Tx mothers were significantly below those of th control progeny only at 30 days of age, T3 levels were significantly depressed at 1, 5, and 30 days of age. These same animals had lower serum TSH levels than the control progeny at 1 and 5 days of age and higher TSH levels at 30 and 75 days of age. Prenatal GH treatment of the mother did not consistently correct thyroid function of the progeny. As adults the progeny of the Tx mothers had normal serum concentrations of T4 and T3 but TSH was high. High serum TSH values were not seen in the progeny of Tx plus GH-treated mothers. These results suggest that maternal hypothyroidism during pregnancy may result in permanent alterations in the thyroidal response to TSH in their progeny.

Passive materno-fetal transfer of a material interfering in the TSH radioimmunoassay : a cause to transitory neonatal hyperthyrotropenemia

Through our screening program for hypothyroidism 16 babies were detected with high TSH at day 5 (83.5 ± 40 uu/ml Blood). They were euthyroid with normal thyroid scintigram (123I) and normal T4 and T3. Plasma radioimmunoassayable TSH (RIA-TSH) gradually decreased to reach normal values at the end of the second month. Mothers were euthyroid with no past history of thyroid diseases and no medication taken during pregnancy. Plasma RIA-TSH was elevated, remained high during 2 months post partum.Although this material exhibited a perfect parralelism in the TSH-RIA with the standard TSH it has a molecular weight of 150.000 (sepharose 6 B chromatography). It is retained by Prot A sepharose column wich indicates that it is an immunoglobulin. Preliminary data show that it binds 125I-TSH and rabbit 125I-IgG. In conclusion High molecular weight TSH like material is passively transfered from mother to fetus leading to false high TSH values in the neonates. Time decay in the neonates, molecular weight and biochemical propertie seems to indicate that it is an immunoglobulin, probably secreted during pregnancy.

Transient hypothyroidism associated with prematurity, sepsis, and respiratory distress.

Serial TSH and T4 determinations were performed in sixty neonates admitted to our hospital for neonatal intensive care within a period of three months. Seven patients (12%) showed transient hypothyroidism on the basis of low T4 and high TSH values. Only one of these patients, who had meconium aspiration and pneumonia, did not have the respiratory distress syndrome. In addition, 4 of these patients had sepsis. All of the patients were born before 37 gestational weeks and had birth weights under 2200 g. In addition, two patients of this gestational age and birth weight group had a progressive fall of T4 to extremely hypothyroid values without simultaneous elevation of TSH. Two of the 5 patients who died had histological studies of their thyroids. These revealed colloid-depleted vesicles, desquamated epithelium, and prominent vascularisation of the thyroid. The results of this study show that early recognition and therapy of transient hypothyroidism may be live saving.

The effect of lithium on the peripheral turnover of thyroxine and triiodothyronine.

The effect of litium on the peripheral turnover of T4 and T3 was investigated in 14 euthyroid subjects using lymphocytes as target cells. Lithium caused a dose-dependent rise in T4 turnover, which did not lead to increased T3 production, but no rise in T3 turnover. A further 3 patients with lithium induced hypothyroidism were studied. Patients with high T4 turnover had high TSH values and in these patients lithium induced a decrease in T4 turnover. This may lead to the conclusion that the demonstrated effect of lithium in the control group did not cause the low T4 in these patients. In 2 patients defective T4 degradation was demonstrated.

Effects of substitution with thyroxine on the thyrotrophin (TSH) response to thyrotrophin-releasing hormone (TRH) in severe primary myxoedema and in mild hypothyroidism following prolonged thyrostatic therapy.

ABSTRACT The evolution of the thyrotrophin (TSH) response after 400 μg thyrotrophin-releasing hormone (TRH) was investigated during recovery of hypothyroidism. In 14 myxoedematous patients, replacement therapy with thyroxine (T4) caused characteristic changes. Before treatment a relatively blunted pattern with mΔTSH1) of 51.2 ± 30.6 mU/1 was found. Two and 4 weeks after treatment an enhanced response was evolved with values for mΔTSH of 87.7 ± 43.4 and 96.0 ± 48.0 mU/1 (P &lt; 0.02 respectively &lt; 0.01). Comparison of the TSH curve showed significant increases in ΔTSH during the first 4 weeks of treatment at 20, 40 and 60 min compared to corresponding measurements in the basal state. In 17 overtreated hyperthyroid patients with mild, mostly chemical hypothyroidism the influence of T4 replacement on TSH responses at different TSH levels was studied. At the stage of mild TSH elevation (3–10 mU/1) mΔTSH before and during substitution were 12.6 ± 6.7 and 25.9 ± 15.3 mU/1, respectively (P &lt; 0.01). Moderate TSH elevation (10–25 mU/1) was accompanied by mΔTSH of 25.4 ± 13.4, respectively 44.5 ± 22.9 mU/1 (P &lt; 0.01) while high TSH values (&gt; 26 mU/1) had responses of 39.1 ± 16.0 and 92.5 ± 22.0 mU/1 (P &lt; 0.001). In these patients the initial blunting of TSH responses could not be attributed to the foregoing toxicosis, since follow up during 6–15 weeks of protracted hypothyroidism did not show any tendency to enhancement of relative release (% mΔTSH). These findings suggest that in the early stage of replacement therapy of hypothyroidism, either pituitary TSH is accumulating or that endogenous TRH is declining.

Transient hypothyroidism in the newborn infant

NEONATAL SCREENING for congenital hypothyroidism is important because of the possibility that mental retardation may be avoided if treatment is started early.' The diagnosis rests on the detection of a high serum level of TSH and low T, during the first few days of life. Whether the presence of these biochemical signs soon after birth necessarily indicates permanent thyroid insufficiency is unknown. Recent data suggest that, in some circumstances, thyroid insufficiency may be transient. Premature infants with respiratory distress have low T4 and T~ levels associated with high TSH levels in cord blood, 2 but these abnormalities revert progressively.:* Furthermore, preliminary data' show a temporary drop in serum T4 values in some premature infants admitted to an intensive care unit. Herein we discuss six infants in whom thyroid insufficiency was detected in the early days of life and disappeared spontaneously after a few weeks. PATIENTS The six infants, five of them premature, were admitted to the neonatal intensive care unit for different serious conditions (Table I). In Patients 2 to 6 abnormal thyroid function was suspected on the basis of high serum TSH values on the fifth day of life) and in Patient 1 because of thyroid hyperplasia detected on the forty-fifth day.

SCREENING FOR CONGENITAL HYPOTHYROIDISM

The early diagnosis of congenital hypothyroidism relies essentially on the biological evidence of the defect. Preliirinary data of a systematic screening of neonates are presented. The values of serum thyroxine (T4) and TSH were determined in the cord blood of 271 infants. In 152 of these children serum TSH was again measured on a finger puncture sample at 5 days of age. Serum T4 was measured by the competitive binding method of Murphy and Patty. Serum TSH was determined by double antibody radioimnunoassay with the TSHk of CEA-IRE-SORIN. Results are as follows : At birth the variability is important for T4 and TSH. On the 5th day the scattering of TSH values is much smaller and the mean is lower than at birth (< 0.001). In agreement with previously reported data we found serum TSH levels of 160 and 500 U/ml in 2 hypothyroid infants younger than 1 month. The striking difference between these high TSH values and the control values observed on the 5th day allow to support the view that this screening procedure is reliable for detecting congenital hypothyr.

Thyrotrophin estimation in diagnosis and treatment of childhood thyroid disorders.

Serum thyrotrophin (TSH) was estimated by double-antibody radioimmunoassay in 200 children aged 2 months to 16 years with normal thyroid function. There was no apparent variation in TSH with age or sex and only 4 children had TSH levels greater than 5 muU/ml. High TSH values were obtained in 9 children with primary hypothyroidism, in 3 children with thyroiditis, and in one girl with a lingual thyroid. Moderately raised TSH was found in 3 girls with thyroiditis, 2 brothers with goitres due to enzyme defect, and a girl with an ectopic thyroid. In one girl with a defect of iodine organification and in 3 boys with thyroxine binding globulin deficiency the TSH levels were normal despite very low serum thyroxine values. Serum TSH was also estimated in 20 children during treatment for primary hypothyroidism. 3 of these children showed slightly raised TSH levels despite apparently adequate replacement therapy with L-thyroxine. One girl showed a very high TSH level 3 weeks after treatment had been temporarily withdrawn.

Plasma thyrotropin response to thyrotropin-releasing hormone in patients with pituitary and hypothalamic disorders.

The plasma TSH response to TRH (200 μg iv) was investigated in a group of normal subjects of both sexes and in 108 patients with hypothalamic-pituitary disorders: 89 had pituitary tumors (49 had acromegaly, 36 had pituitary tumors without recognized hormonal secretion, 8 had craniopharyngioma, 1 had hypothalamic-pituitary metastasis from breast cancer, 1 had a hypothalamic- pituitary vascular tumor), 19 had other hypothalamic-pituitary disorders (1 Sheehan's syndrome, 4 primary empty sella, 12 idiopathic hypopituitarism, 2 idiopathic diabetes insipidus). Seventy-two were euthyroid; 32 had secondary hypothyroidism, 4 were thyrotoxic. The pattern of TSH response to TRH was defined with respect to the magnitude of the increase and to the pattern of the response curve. Three thyrotoxic patients did not respond to TRH, while one patient with high basal TSH values had a poor increase. Most of the other patients (88%) showed positive responses and the percentage of absent responses in euthyroid and hypothyroid patients did not significantly differ. Exaggerated responses were more frequently observed in hypothyroid patients (mostly in nontumorous cases). Regular response curves were observed in 55% of euthyroid and in only 19% of hypothyroid patients in whom there was a higher incidence of either delayed or prolonged response (56% and 37%, respectively). Frequently, prolonged responses were, at the same time, delayed and exaggerated. The incidence of these abnormalities was larger in patients with craniopharyngioma, in patients with pituitary tumors with suprasellar extension and in patients with idiopathic hypopituitarism. Therefore, these abnormalities can be considered quite characteristic of hypothalamic disorders.

ATYPICAL FACIAL NEURALGIA IN THE HYPOTHYROID STATE

Article1 July 1951ATYPICAL FACIAL NEURALGIA IN THE HYPOTHYROID STATEFREDERICK B. WATTS, M.D., F.A.C.P.FREDERICK B. WATTS, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-35-1-186 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA deficiency of the thyroid hormone in the adult may give rise to a syndrome of chronic, recurring pain about the face and neck and recurring headaches, as recently pointed out by Fenichel.1The type and intensity of the pain vary considerably, and may be manifested as a dull aching or throbbing pain in either carotid area, in or about the ear, in the frontal or temporal area, or along the upper or lower jaw or the posterior cervical area. Quite frequently there may be an associated dull pain or sense of constriction over the precordium. The pain may be...Bibliography1. Fenichel NM: Chronic headache due to masked hypothyroidism, Ann. Int. Med. 29: 456, 1948. LinkGoogle Scholar2. Grollman A: Essentials of endocrinology, 1947, J. B. Lippincott Co., Philadelphia, p. 197. Google Scholar3. Seward BP: A clinical study of the mild grades of hypothyroidism, Ann. Int. Med. 9: 178, 1935. LinkGoogle Scholar4. Wechsler IS: A text book of clinical neurology, 1935, W. B. Saunders Co., Philadelphia. Google Scholar5. Gittens TR: Headache and neuralgia; classification and differential diagnosis, Laryngoscope 53: 27-38 (Jan.) 1943. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Detroit, Michigan*Received for publication January 16, 1950. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThyroid disease and the nervous systemLow headache prevalence amongst women with high TSH values. Head-HUNT - a large population-based studyNeurologic Manifestations of MyxedemaNervous and muscular systems in myxedemaFacial Pain: Review of Ætiological Factors 1 July 1951Volume 35, Issue 1Page: 186-193KeywordsThyroid hormones Issue Published: 1 July 1951 PDF downloadLoading ...