Objective. Examining the prevalence of laryngeal sensory neuropathy (LSN) in goiter patients versus a control group. Study Design. Cross-sectional study. Methods. 33 Goiter patients were enrolled versus 25 age-matched controls. TSH levels, size of thyroid gland, and presence or absence of thyroid nodules were reported. Subjects were asked about the presence or absence of any of the following symptoms: cough, globus pharyngeus, and/or throat clearing that persistented for more than 6 weeks. The presence of one or more of these symptoms for at least six weeks in the absence of LPRD, allergy, asthma, ACE inhibitor intake, and psychogenic disorder was defined as LSN. Results. For goitrous patients mean age (years) was ( ) versus ( ) for controls. 82% goitrous patients had known nodules and 27% carried a simultaneous diagnosis of hypothyroidism. Among those with documented size (61%), mean total thyroid volume was ？cm3, with a range from 9.430 to 67.022？cm3. The overall prevalence of LSN among goitrous patients was 42% versus 12% among controls ( ). There was no correlation between LSN, size of thyroid gland, and TSH level. Conclusion. The prevalence of LSN in goitrous patients is significantly higher than that in a nongoitrous population. 1. Introduction Goiter is the most prevalent endocrine condition in the world affecting over 500 million with prevalence rates reaching up to 30% [1, 2]. It is believed to result from an interaction between genetics and environmental factors, namely, iodine deficiency. It has long been established that adequate iodine uptake is crucial, as low iodine levels lead to hypothyroidism which in turn increases blood levels of thyroid stimulating hormone (TSH) resulting in glandular hypertrophy [3]. Thus, certain conditions that exacerbate iodine deficiency, such as smoking or increased parity, can be considered risk factors for goiter [4]. While the exact contribution of each factor remains unclear, genetic predisposition to goiter also plays a crucial role in goitrogenesis [5]. Patients with goiter may complain of cosmetic disfigurement attributed to the visibly enlarged thyroid gland, of symptoms of hyper or hypothyroidism secondary to the altered levels of thyroid hormones, and last but not the least of compressive neck symptoms. These include respiratory discomfort, stridor, and change in voice quality, globus pharyngeus, dysphagia, and others. The neck and throat symptoms in patients with goiter have been invariably attributed to the glandular hypertrophy of the thyroid and its mass effect on the laryngotracheal framework.
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