Sleepwalking is a disorder characterized by complex motor behaviors arising from slow wave sleep usually occurring in children. The adult onset of sleepwalking suggests the presence of an external precipitating factor leading to the occurrence of the disorder. Hyperthyroidism has been reported to be the possible cause of sleepwalking in a few cases. We present the case of a 36-year-old man who reported a sudden appearance of nocturnal episodes of sleepwalking. He underwent a complete video polysomnography (VPSG), which showed a polygraphic pattern arising from stage N3 sleep related to the presence of simple motor behaviors. Routine blood tests showed a mild hyperthyroidism. After 4 months of thyrostatic treatment, the patient reported no more sleepwalking events. A VPSG performed at the last follow-up showed the absence of pathological electroclinical events arising from stage N3 sleep. Therefore, we hypothesize that there is a link between sleepwalking and thyroid dysfunction in our patient.
Giuliano L, Fatuzzo D, Mainieri G, La Vignera S, Sofia V, Zappia M. Adult-onset sleepwalking secondary to hyperthyroidism: polygraphic evidence. J Clin Sleep Med. 2018;14(2):285–287.
Sleepwalking is a disorder characterized by complex motor behaviors arising from slow wave sleep. It is classified among the non-rapid eye movement (NREM) parasomnias with confusional arousals, sleep terrors, and sleep-related eating disorders.1 It has been demonstrated that heritable factors can predispose to the development of sleepwalking,2 but the clinical expression of the disorder is influenced by different environmental factors that deepen or fragment sleep.3 In particular, the onset of sleepwalking in adulthood strongly suggests the presence of an external precipitating factor leading to the occurrence of the disorder.
It is well known that other sleep disorders such as sleep apnea or restless legs syndrome can increase the probability to manifest sleepwalking, due to the increased number of arousals from deep sleep and the secondary sleep deprivation; also, for the same reason patients with epilepsy show an increased tendency to manifest sleepwalking.4 The consumption of different drugs5 and alcohol6 has been found to be related to many cases of sleepwalking. However, an ascertained causal link between alcohol and sleepwalking has not been found until recently.6 Furthermore, metabolic changes such as hypoglycemia and hyperthyroidism may be linked to the occurrence of ambulatory behaviors during sleep. In fact, hyperthyroidism has been reported to be the possible cause of a few cases of sleepwalking.7
REPORT OF CASE
A 36-year-old man was admitted to our hospital with a 3-month history of nocturnal episodes characterized by wandering around the house associated with complex behaviors such as turning on the lights or opening the drawers. These episodes began suddenly and repeatedly continued with a monthly frequency. From the same period the patient also complained of insomnia. The patient did not report personal or familiar history of NREM parasomnias. His general and neurological examinations were normal. An electroencephalographic recording and the brain magnetic resonance imaging showed no abnormalities. He underwent a complete video polysomnography (VPSG) which showed an altered sleep macrostructure characterized by a decreased percentage of stage N3 sleep (8%) and frequent short awakenings from sleep, with an increase in amount of wake after sleep onset. During stage N3 sleep, a polygraphic pattern compatible with an episode of an arousal disorder was recorded (Figure 1A). This was related to the presence of simple motor behaviors lasting for about 5 seconds, characterized by opening of the eyes, chewing movements without vocalizations, and an attempt to sit on the bed, using the left arm, and a rapid elevation of the head. Neither apneas nor periodic limb movements or other sleep disorders were found. We performed routine blood tests, which showed high free triiodothyronine (FT3) (6.45 pmol/L; normal values: 3.8–6) and free thyroxine (FT4) (17.8 pmol/L; normal values: 7.9–14.4) and low thyroid-stimulating hormone (TSH) levels (0.01 μUI/mL; normal values: 0.34–4.2). A slight increase in antithyroperoxidase antibodies (155 UI/mL; normal values < 4) was found. A treatment with methimazole at the daily dose of 5 mg was carried out due to the mild hyperthyroidism.
(A) VPSG of the patient demonstrating an electroclinical event compatible with an episode of disorder of arousal, associated with a simple motor behavior during stage N3 sleep. (B) VPSG of the patient after the treatment showing a normal stage N3 sleep epoch. LF = 1.6 Hz, HF = 30 Hz, sweep = 60'', sensitivity = 70 μV/cm, VPSG = video polysomnography.
(A) VPSG of the patient demonstrating an electroclinical event compatible with an episode of disorder of arousal, associated with a simple motor behavior during stage N3 sleep...
After 4 months of treatment, the patient reported no more sleepwalking events. Thyroid function blood tests were performed, and normal values of thyroid hormones were found; the levels of antithyroperoxidase antibodies remained slightly high (93 UI/mL). A VPSG performed at the last follow-up showed a normal sleep macrostructure with an increase of stage N3 sleep percentage (15%) and the absence of pathological electroclinical events arising from stage N3 sleep (Figure 1B).
We describe the case of a patient with new-onset sleepwalking probably due to thyrotoxicosis. Our hypothesis is supported by the fact that we could not find any other cause or precipitating factor at the origin of the disease except for the presence of high levels of thyroid hormones. During the first VPSG recording the patient did not manifest a clear event of sleepwalking but he showed an electroclinical pattern compatible with the presence of an arousal disorder from NREM sleep. The disappearance of the sleepwalking events with the beginning of the thyrostatic treatment and the normalization of thyroid hormones levels strongly supports a causative relationship between the two phenomena. Moreover, the sleep macro-structure recorded during the second VPSG demonstrated a normalization of sleep parameters, supporting the possibility of a previous effect of hyperthyroidism on sleep stability. The effect of thyroid hyperfunction on sleep is already known,8–11 usually manifesting with an increased sleep latency, reduced total sleep time, or with a decreased sleep efficiency, leading to difficulties in falling asleep and in maintaining sleep.8,11 Moreover, hyperthyroidism may have promoting effects on rapid eye movement (REM) sleep with an increased REM density and REM duration as well as shorter REM latency.11 A reduction in slow wave sleep due to hyperthyroidism has been found in some studies11 as well as in our patient. Moreover, we also had polygraphic evidence of altered stage N3 sleep dynamics, including intrusion of arousal activity (ie, posterior alpha rhythm counterbalanced by increased delta activity over the anterior regions), as an exaggerated antiarousal defense mechanism.1,12 These altered dynamics of stage N3 sleep may lead to sleepwalking as an arousal disorder.12 Therefore, it is not difficult to hypothesize a link between thyroid dysfunction that leads to stage N3 sleep instability and sleepwalking. To date there is only one study reporting sleepwalking possibly related to hyperthyroidism7 that showed eight patients with thyrotoxicosis caused by diffuse toxic goiter or Graves disease. However, in this study, at variance with our report, a polysomnography recording of the patients was not obtained and only the anamnestic data of the sleep complaint have been reported. In conclusion, hyperthyroidism may affect sleep stability and may induce sleepwalking, promptly reverting with appropriate treatment. Further studies are needed to establish the role of thyroid hormones in sleepwalking.
All authors have seen and approved the manuscript. The authors declare no financial or other conflicts of interest.