Epilepsia, 17:33-34,1976
Raven Press, New York
Convulsive Fits in Thyrotoxicosis Amos D. Korczyn and M. Bechar Department of Neurology, Beilinson Medical Center, and Department of Physiology and Pharmacology, Tel Aviv University Medical School, Tel Aviv, Israel (Received November 4,1975) Thyrotoxic patients frequently have brisk tendon reflexes. Frank pyramidal signs which regressed when the thyroid state was controlled have also been reported (Skanse and Nyman, 1956; Ravera et al., 1960). Zondek (1944) has described a state of encephalopathy which he termed coma Basedowicum; others have reported similar cases (Wohl and Shuman, 1957). From the psychiatric point of view, thyrotoxic patients may present with a paranoid or maniacal picture. Epileptic fits related to thyrotoxicosis, however, are extremely rare. We were able to find only 4 such patients in the literature (Chapman and Maloof, 1956; Skanse and Nyman, 1956; Wohl and Shuman, 1957), and we herein report another.
life, and 4 days later he had another attack. On examination he was found to have bilateral exophthalmos and lid-lag. The pulse rate was 100/min. He showed the typical thyrotoxic tremor and his limbs were warm and moist. The only abnormal neurological signs were very brisk symmetrical tendon jerks with nonsustained clonus in both ankles. Abnormal laboratory findings included ESR 69/82 (Westergren), cholesterol 146 and total lipids 366 mgO/o, PBI 11 gamma % and T3 0.73. The iodine uptake was 20% after 2 hr and 40% after 24 hr. A scan showed an enlarged left lobe with hot nodules. Blood count, urea, glucose, electrolytes (including calcium), plasma proteins, and liver function tests as well as examination of the CSF revealed normal results. An electroencephalogram demonstrated a REPORT OF A CASE symmetrical background of rapid alpha and beta frequencies, with occasional bitemporal This patient had first noted a swelling of the tetha waves and sharp waves. neck when he was 25 years old. At the age of The patient was again started on Tapazole, 29 he was started on Tapazole, and a year later 20 mg daily, as well as phenytoin 300 mg daily. subtotal thyroidectomy was performed. The There were no further ictal phenomena and his histology showed nodular goiter. Five years tendon reflexes became less brisk. When exlater the gland again increased in size and amined again 6 weeks later his heart rate was thyrotoxic symptoms first appeared. The 90/min, blood tests demonstrated a euthyroid patient became apprehensive, lost weight de- state, and the EEG had reverted to normal. The spite an increased appetite, and later noted anticonvulsants were withdrawn, and on examitremor of the hands. He was again started on nation 6 months later he was found to have Tapazole (5 mg twice a day) but was referred brisk normal reflexes and a normal EEG. for an iodine uptake test when he failed to improve. He was told to stop medication before the test. One week following withdrawal of the DISCUSSION drug he had a grand ma1 attack, the first in his Key words: Thyrotoxicosis - Hyperthyroidkrn - Epileptic fits
The association of epileptic fits and thyrotoxicosis in this case may have been fortuitous. However, the temporal relationship to the
33
34
A. D. KORCZYN AND M. BECHAR
withdrawal and reinstitution of antithyroid medication suggests a causal connection. Condon et al. (1954) have investigated the EEG records of patients with thyrotoxicosis. In 1 7 of 27 untreated patients the records were abnormal; in most it reverted to normal following treatment. Similar results have been reported by others (Skanse and Nyman, 1956; Wilson and Johnson, 1964). Condon et al. (1954) have noted that “in spite of the great number of definite spike discharges in seven cases, no clinical seizures occurred.” Our case tends to confirm the conclusions drawn by Wohl and Shuman (1957), that the “cerebral type of hyperthyroidism apparently develops in patients having a relatively rapid and progressive toxic process.” The reversibility of the phenomena suggests that the neuronal changes are functional rather than organic in nature. The cerebral metabolic functions of patients with hyperthyroidism have been described as comparable to those of controls in regard to oxygen consumption (Scheinberg, 1950). Contrary to the improvement in most thyrotoxic parameters following treatment with reserpine, the EEG abnormalities increase (Wilson and Johnson, 1964). The cause of these changes is obscure.
SUMMARY
’
A patient with hyperthyroidism is described who developed grand ma1 seizures when antithyroid medication was withdrawn. Pyramidal signs were also present. The EEG reverted to normal and the clinical signs and symptoms disappeared when his thyroid status was again controlled. RESUME On d6crit un patient avec hyperthyroidisme, qui a presente des crises grand mal lorsqu’on a supprim6 son traitement anti-thyroidien. Le sujet presentait aussi des signes pyramidaux. L’EEG est redevenu normal et les sympt6mes cliniques ont disparu lorsque la fonction thyroydienne a 6t6 a nouveau contr616e. (C. A. Tassinari, Marseilles)
RESUMEN Se describe un paciente con hipertiroidismo que desarrollb ataques gran mal cuando se interrumpi6 la medicaci6n antitiroidea. Tambien aparecieron signos piramidales. Los signos y sintomas clinicos, asi como el EEG, se normalizaron cuando se control6 el estado tiroideo. (A. Portera, Madrid)
ZUSAMMENFASSUNG Ein Patient mit Hyperthyreose entwickelte Grand-Mal-Anfalle und zeigte Pyramidenzeichen, als die thyreostatische Behandlung abgesetzt wurde. Das EEG normalisierte sich und die klinischen Symptome verschwanden, sobald die Schilddriisenfunktion wieder unter Kontrolle gelangte. (D. Scheffner, Heidelberg)
REFERENCES Chapman EM and Maloof F. Bizarre clinical manifestations of hyperthyroidism. N Engl J Med 254:l-5, 1956. Condon JV, Becka DR, and Gibbs FA. Electroe n c e p h a l o graphic abnormalities in hypert h y r o i d i s m . J C l i n E n d o c r i n o l Metab 14~1511-1518,1954. Ravera JJ, Cervino JM, and Ferngndez G. Two cases of Grave’s disease with signs of a pyramidal lesion. J Clin Endocrinol Metab 20: 8 7 6-880, 1960. Scheinberg P. Cerebral metabolism in hyperthyroidism and myxedema Fed Proc 9: 113, 1950. Skanse B and Nyman E. Thyrotoxicosis as a cause of cerebral dysrhythmia and convulsive seizures. Acta Endocrinol ( K b h . ) 22:246-263, 1956. Wilson WP and Johnson JE. Thyroid hormone and brain function. Electroencephalogr Clin Neurophysiol 16: 321-328, 1964. Wohl MG and Shuman CR. Atypical syndromes in hyperthyroidism. Ann Intern Med 46:857-867, 1957. Zondek H. The Diseases of the Endocrine Glands. Fourth Edition. Edward Arnold & Co, London, 1944.
Raven Press, New York
Convulsive Fits in Thyrotoxicosis Amos D. Korczyn and M. Bechar Department of Neurology, Beilinson Medical Center, and Department of Physiology and Pharmacology, Tel Aviv University Medical School, Tel Aviv, Israel (Received November 4,1975) Thyrotoxic patients frequently have brisk tendon reflexes. Frank pyramidal signs which regressed when the thyroid state was controlled have also been reported (Skanse and Nyman, 1956; Ravera et al., 1960). Zondek (1944) has described a state of encephalopathy which he termed coma Basedowicum; others have reported similar cases (Wohl and Shuman, 1957). From the psychiatric point of view, thyrotoxic patients may present with a paranoid or maniacal picture. Epileptic fits related to thyrotoxicosis, however, are extremely rare. We were able to find only 4 such patients in the literature (Chapman and Maloof, 1956; Skanse and Nyman, 1956; Wohl and Shuman, 1957), and we herein report another.
life, and 4 days later he had another attack. On examination he was found to have bilateral exophthalmos and lid-lag. The pulse rate was 100/min. He showed the typical thyrotoxic tremor and his limbs were warm and moist. The only abnormal neurological signs were very brisk symmetrical tendon jerks with nonsustained clonus in both ankles. Abnormal laboratory findings included ESR 69/82 (Westergren), cholesterol 146 and total lipids 366 mgO/o, PBI 11 gamma % and T3 0.73. The iodine uptake was 20% after 2 hr and 40% after 24 hr. A scan showed an enlarged left lobe with hot nodules. Blood count, urea, glucose, electrolytes (including calcium), plasma proteins, and liver function tests as well as examination of the CSF revealed normal results. An electroencephalogram demonstrated a REPORT OF A CASE symmetrical background of rapid alpha and beta frequencies, with occasional bitemporal This patient had first noted a swelling of the tetha waves and sharp waves. neck when he was 25 years old. At the age of The patient was again started on Tapazole, 29 he was started on Tapazole, and a year later 20 mg daily, as well as phenytoin 300 mg daily. subtotal thyroidectomy was performed. The There were no further ictal phenomena and his histology showed nodular goiter. Five years tendon reflexes became less brisk. When exlater the gland again increased in size and amined again 6 weeks later his heart rate was thyrotoxic symptoms first appeared. The 90/min, blood tests demonstrated a euthyroid patient became apprehensive, lost weight de- state, and the EEG had reverted to normal. The spite an increased appetite, and later noted anticonvulsants were withdrawn, and on examitremor of the hands. He was again started on nation 6 months later he was found to have Tapazole (5 mg twice a day) but was referred brisk normal reflexes and a normal EEG. for an iodine uptake test when he failed to improve. He was told to stop medication before the test. One week following withdrawal of the DISCUSSION drug he had a grand ma1 attack, the first in his Key words: Thyrotoxicosis - Hyperthyroidkrn - Epileptic fits
The association of epileptic fits and thyrotoxicosis in this case may have been fortuitous. However, the temporal relationship to the
33
34
A. D. KORCZYN AND M. BECHAR
withdrawal and reinstitution of antithyroid medication suggests a causal connection. Condon et al. (1954) have investigated the EEG records of patients with thyrotoxicosis. In 1 7 of 27 untreated patients the records were abnormal; in most it reverted to normal following treatment. Similar results have been reported by others (Skanse and Nyman, 1956; Wilson and Johnson, 1964). Condon et al. (1954) have noted that “in spite of the great number of definite spike discharges in seven cases, no clinical seizures occurred.” Our case tends to confirm the conclusions drawn by Wohl and Shuman (1957), that the “cerebral type of hyperthyroidism apparently develops in patients having a relatively rapid and progressive toxic process.” The reversibility of the phenomena suggests that the neuronal changes are functional rather than organic in nature. The cerebral metabolic functions of patients with hyperthyroidism have been described as comparable to those of controls in regard to oxygen consumption (Scheinberg, 1950). Contrary to the improvement in most thyrotoxic parameters following treatment with reserpine, the EEG abnormalities increase (Wilson and Johnson, 1964). The cause of these changes is obscure.
SUMMARY
’
A patient with hyperthyroidism is described who developed grand ma1 seizures when antithyroid medication was withdrawn. Pyramidal signs were also present. The EEG reverted to normal and the clinical signs and symptoms disappeared when his thyroid status was again controlled. RESUME On d6crit un patient avec hyperthyroidisme, qui a presente des crises grand mal lorsqu’on a supprim6 son traitement anti-thyroidien. Le sujet presentait aussi des signes pyramidaux. L’EEG est redevenu normal et les sympt6mes cliniques ont disparu lorsque la fonction thyroydienne a 6t6 a nouveau contr616e. (C. A. Tassinari, Marseilles)
RESUMEN Se describe un paciente con hipertiroidismo que desarrollb ataques gran mal cuando se interrumpi6 la medicaci6n antitiroidea. Tambien aparecieron signos piramidales. Los signos y sintomas clinicos, asi como el EEG, se normalizaron cuando se control6 el estado tiroideo. (A. Portera, Madrid)
ZUSAMMENFASSUNG Ein Patient mit Hyperthyreose entwickelte Grand-Mal-Anfalle und zeigte Pyramidenzeichen, als die thyreostatische Behandlung abgesetzt wurde. Das EEG normalisierte sich und die klinischen Symptome verschwanden, sobald die Schilddriisenfunktion wieder unter Kontrolle gelangte. (D. Scheffner, Heidelberg)
REFERENCES Chapman EM and Maloof F. Bizarre clinical manifestations of hyperthyroidism. N Engl J Med 254:l-5, 1956. Condon JV, Becka DR, and Gibbs FA. Electroe n c e p h a l o graphic abnormalities in hypert h y r o i d i s m . J C l i n E n d o c r i n o l Metab 14~1511-1518,1954. Ravera JJ, Cervino JM, and Ferngndez G. Two cases of Grave’s disease with signs of a pyramidal lesion. J Clin Endocrinol Metab 20: 8 7 6-880, 1960. Scheinberg P. Cerebral metabolism in hyperthyroidism and myxedema Fed Proc 9: 113, 1950. Skanse B and Nyman E. Thyrotoxicosis as a cause of cerebral dysrhythmia and convulsive seizures. Acta Endocrinol ( K b h . ) 22:246-263, 1956. Wilson WP and Johnson JE. Thyroid hormone and brain function. Electroencephalogr Clin Neurophysiol 16: 321-328, 1964. Wohl MG and Shuman CR. Atypical syndromes in hyperthyroidism. Ann Intern Med 46:857-867, 1957. Zondek H. The Diseases of the Endocrine Glands. Fourth Edition. Edward Arnold & Co, London, 1944.
