There is only limited evidence for biological parameter abnormalities in subclinical hypothyroidism. The aim of this study was to investigate the impact of varying degrees of thyroid failure on the stapedial reflex as a biological index, and establish its role in the evaluation of the hypothyroid patient. We studied 10 patients with subclinical hypothyroidism, 10 patients with clinical hypothyroidism, and 20 controls. All three parameters of stapedial reflex (amplitude, decay, and threshold) were measured before and after restoration of euthyroidism through thyroxine administration. Data are given as mean +/- SEM. Stapedial reflex maximal amplitudes were different among the groups studied (p < 0.0001), as values in subclinical (4.3 +/- 0.4 mm) and clinical (3.7 +/- 0.3 mm) groups before treatment were lower (p < 0.05) than those of control (5.7 +/- 0.3 mm), and subclinical (6.4 +/- 0.5 mm) and clinical (5.6 +/- 0.4 mm) groups after treatment. Similarly, stapedial reflex decays were different among the groups studied (p < 0.001), as values in subclinical (81 +/- 7 ms) and clinical (89 +/- 4 ms) groups before treatment were higher (p < 0.05) than those in control (65 +/- 2 ms), subclinical (56 +/- 8 ms), and clinical (61 +/- 8 mm) groups after treatment. There was no significant difference among the groups for stapedial reflex threshold or significant correlation between stapedial reflex parameters and thyroid function tests. Stapedial reflex, a biological parameter that reflects neuromuscular status, is abnormal in patients with subclinical and clinical hypothyroidism and returns to normal when clinical and biochemical euthyroidism has been achieved through thyroxine administration.

Evoked vertigo is consistently associated with an increase in steroid serum levels and accompanying decreases in the plasma levels of glutamate, aspartate, and GABA. The possible underlying mechanisms and the functional significance of these findings are discussed.