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Abstract. Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare complication of hyperthyroidism and an uncommon form of hypokalemic periodic paralysis. Its differentiation of more common forms of periodic paralysis is important because aggressive treatment can place the patient at risk for rebound hyperkalemia. Treatment of the underlying thyroid dysfunction cures the muscle symptoms. Here we describe a 37-year-old Turkish male with THPP whose paralysis attack recurred soon after administration of radioactive iodine. THYROTOXIC hypokalemic periodic paralysis (THPP) is a rare complication of hyperthyroidism in the Western population. It occurs primarily in males of Asian descent, including patients of Japanese, Chinese, Vietnamese, Korean, Filipino, American Indian, and Hispanic ancestry [1][2][3][4][5][6][7][8][9][10]. Although the association of thyrotoxicosis and periodic paralysis has been wellknown since 1931 [11] it is not reported from Turkey in English literature, most probably because of unfamiliarity with the disorder. We herein report a 37-year-old Turkish male patient with THPP who also experienced a paralysis attack ten days after the administration of radioiodine despite the treatment with propranolol. Case reportA 37-year-old Turkish male patient presented with the complaint of approximately ten episodes of muscle weakness for 2 years. These attacks occurred in all but one episode at night, following exertion or consumption of large carbohydrate meals. He was usually awakened from sleep in the early hours with difficulty of ambulation due to muscle weakness of extremities mainly in his legs. There were no prodromal symptom and no seasonal variation of the attacks. The duration of paralysis attacks ranged from four to 24 hours. He didn't seek medical attention for the paralysis attacks and they all resolved spontaneously. There was no family history of neuromuscular and endocrine abnormality.He was diagnosed as having hyperthyroidism based on the clinical symptoms of occasional palpitation and nervousness and the suppressed thyroid stimulating hormone (TSH) of 0.01 mU/mL (normal, 0.35-4.5 mU/ mL) five months ago. Then he was put on carbimazole therapy (20 mg daily). After the cessation of therapy by his own decision approximately one month ago, he experienced another attack. He denied any weight loss, heat intolerance, or diarrhea. The physical examination including muscle strength and tendon reflexes was unremarkable.His free thyroxine (FT 4 ) level was 5.26 ng/dL (normal, 0.8-1.9 ng/dL) and TSH level was <0.002 mU/mL (normal, 0.4-5.0 mU/mL). The TSH-receptor-stimulating antibody level was 135 U/L (normal, 0-9 U/L). Thyroid scan revealed diffuse uptake in a normal sized gland with a 24-hour radioactive iodine uptake of 52.1%. These findings were found to be most con-

Attention deficit hyperactivity disorder (ADHD) is a developmental, neurobehavioral syndrome with an onset in childhood. The aim of this study was to investigate the existence of regional perfusion changes in ADHD by means of Tc-99m HMPAO brain SPECT. Thirteen children with a diagnosis of ADHD and 7 healthy, age-matched controls were included in this study. Hypoperfusion was observed on the right temporal cortex in 9, and on the left temporal cortex in 3 children. The distribution of the lesions showed right lateral temporal cortex involvement in 3, right medial temporal cortex in 9 and left medial temporal cortex in 8 children. Asymmetric perfusion was seen on the caudate nucleus in 4, on the thalamus in 3 and on the frontal cortex in 6 children. There was a significant difference between children with ADHD and controls in right medial temporal cortex: cerebellum and right lateral temporal cortex: cerebellum ratios. Hypoperfusion in the right medial temporal cortex was significantly and inversely correlated with Du Paul teachers' questionnaire rating scale (r = -0.71, p = 0.006). It has been postulated that difficulty in self regulating response to stimuli in ADHD is mediated by underfunctioning of the orbital frontal cortex and subsequent connection to the limbic system. Decreased temporal cortex perfusion may dysfunction of the limbic system or the orbito-frontal-limbic axis.