Concurrent Graves' disease and intracranial arterial stenosis/occlusion: Special considerations regarding the state of thyroid function, etiology, and treatment

Shigeo Ohba, Toru Nakagawa, Hideki Murakami

研究成果: Article

24 引用 (Scopus)

抄録

Several studies have shown the relation between Graves' disease and stenosis/occlusion of intracranial arteries. To our knowledge, only 31 cases, including our case, of concurrent Graves' disease and moyamoya syndrome or intracranial arterial stenosis/occlusion have been described. The patients were predominantly women, and their ages ranged from 10 to 54 years (mean, 29.3 years). Transient ischemic attacks and cerebral infarction were the common symptoms in these patients. Except one previous case and the present case, all cases showed thyrotoxicity when the cerebral ischemic event occurred. Among the 29 cases, in which the treatment regimen was known, antithyroid therapy was administered in 25 cases, and surgical treatment for cerebral vessel diseases was performed in 11 cases. Most of the patients eventually recovered from the neurological symptoms after medical and/or surgical treatment; one of the patients died, and one patient's condition worsened. Although the mechanism underlying intracranial arterial occlusion or stenosis in patients with Graves' disease has not been elucidated, several hypotheses have been described. Thyroid hormones may augment vascular sensitivity to the sympathetic nervous system and induce pathological changes in the arterial walls. An immune-mediated mechanism may play a role in the pathogenesis of these diseases. Atherosclerosis may be associated with these disorders. Vasculitis induced by antithyroid drugs may cause changes in the intracranial arteries. Finally, the possibility of a mere coincidence of Graves' disease and these vascular changes should also be considered. Cerebrovascular hemodynamic changes induced by thyrotoxicosis were considered to be responsible for the cerebral ischemic events. Excessive thyroid hormone production is considered to increase the cerebral metabolism and oxygen consumption. In addition, thyrotoxicosis-induced hypercoagulability may influence ischemic events. Therefore, the possibility of thyrotoxicosis should be considered when patients with Graves' disease show exacerbation of cerebral ischemic symptoms at follow-up. The necessity of surgery in addition to antithyroid therapy might be dependent on the mechanisms of the vascular changes and symptoms. If hyperthyroidism is associated with vascular changes and symptoms, antithyroid therapy may be adequate. However, if immune-mediated mechanisms or coincidences are considered to be associated with vascular changes and symptoms, like our case, surgical procedures might be needed.

元の言語English
ページ(範囲)297-304
ページ数8
ジャーナルNeurosurgical Review
34
発行部数3
DOI
出版物ステータスPublished - 01-07-2011
外部発表Yes

Fingerprint

Graves Disease
Thyroid Gland
Pathologic Constriction
Blood Vessels
Thyrotoxicosis
Thyroid Hormones
Therapeutics
Arteries
Moyamoya Disease
Antithyroid Agents
Thrombophilia
Transient Ischemic Attack
Sympathetic Nervous System
Cerebral Infarction
Hyperthyroidism
Vasculitis
Oxygen Consumption
Disease Progression
Atherosclerosis
Hemodynamics

All Science Journal Classification (ASJC) codes

  • Surgery
  • Clinical Neurology

これを引用

@article{c190db88d90442058d080cbb2dda15bd,
title = "Concurrent Graves' disease and intracranial arterial stenosis/occlusion: Special considerations regarding the state of thyroid function, etiology, and treatment",
abstract = "Several studies have shown the relation between Graves' disease and stenosis/occlusion of intracranial arteries. To our knowledge, only 31 cases, including our case, of concurrent Graves' disease and moyamoya syndrome or intracranial arterial stenosis/occlusion have been described. The patients were predominantly women, and their ages ranged from 10 to 54 years (mean, 29.3 years). Transient ischemic attacks and cerebral infarction were the common symptoms in these patients. Except one previous case and the present case, all cases showed thyrotoxicity when the cerebral ischemic event occurred. Among the 29 cases, in which the treatment regimen was known, antithyroid therapy was administered in 25 cases, and surgical treatment for cerebral vessel diseases was performed in 11 cases. Most of the patients eventually recovered from the neurological symptoms after medical and/or surgical treatment; one of the patients died, and one patient's condition worsened. Although the mechanism underlying intracranial arterial occlusion or stenosis in patients with Graves' disease has not been elucidated, several hypotheses have been described. Thyroid hormones may augment vascular sensitivity to the sympathetic nervous system and induce pathological changes in the arterial walls. An immune-mediated mechanism may play a role in the pathogenesis of these diseases. Atherosclerosis may be associated with these disorders. Vasculitis induced by antithyroid drugs may cause changes in the intracranial arteries. Finally, the possibility of a mere coincidence of Graves' disease and these vascular changes should also be considered. Cerebrovascular hemodynamic changes induced by thyrotoxicosis were considered to be responsible for the cerebral ischemic events. Excessive thyroid hormone production is considered to increase the cerebral metabolism and oxygen consumption. In addition, thyrotoxicosis-induced hypercoagulability may influence ischemic events. Therefore, the possibility of thyrotoxicosis should be considered when patients with Graves' disease show exacerbation of cerebral ischemic symptoms at follow-up. The necessity of surgery in addition to antithyroid therapy might be dependent on the mechanisms of the vascular changes and symptoms. If hyperthyroidism is associated with vascular changes and symptoms, antithyroid therapy may be adequate. However, if immune-mediated mechanisms or coincidences are considered to be associated with vascular changes and symptoms, like our case, surgical procedures might be needed.",
author = "Shigeo Ohba and Toru Nakagawa and Hideki Murakami",
year = "2011",
month = "7",
day = "1",
doi = "10.1007/s10143-011-0311-z",
language = "English",
volume = "34",
pages = "297--304",
journal = "Neurosurgical Review",
issn = "0344-5607",
publisher = "Springer Verlag",
number = "3",

}

TY - JOUR

T1 - Concurrent Graves' disease and intracranial arterial stenosis/occlusion

T2 - Special considerations regarding the state of thyroid function, etiology, and treatment

AU - Ohba, Shigeo

AU - Nakagawa, Toru

AU - Murakami, Hideki

PY - 2011/7/1

Y1 - 2011/7/1

N2 - Several studies have shown the relation between Graves' disease and stenosis/occlusion of intracranial arteries. To our knowledge, only 31 cases, including our case, of concurrent Graves' disease and moyamoya syndrome or intracranial arterial stenosis/occlusion have been described. The patients were predominantly women, and their ages ranged from 10 to 54 years (mean, 29.3 years). Transient ischemic attacks and cerebral infarction were the common symptoms in these patients. Except one previous case and the present case, all cases showed thyrotoxicity when the cerebral ischemic event occurred. Among the 29 cases, in which the treatment regimen was known, antithyroid therapy was administered in 25 cases, and surgical treatment for cerebral vessel diseases was performed in 11 cases. Most of the patients eventually recovered from the neurological symptoms after medical and/or surgical treatment; one of the patients died, and one patient's condition worsened. Although the mechanism underlying intracranial arterial occlusion or stenosis in patients with Graves' disease has not been elucidated, several hypotheses have been described. Thyroid hormones may augment vascular sensitivity to the sympathetic nervous system and induce pathological changes in the arterial walls. An immune-mediated mechanism may play a role in the pathogenesis of these diseases. Atherosclerosis may be associated with these disorders. Vasculitis induced by antithyroid drugs may cause changes in the intracranial arteries. Finally, the possibility of a mere coincidence of Graves' disease and these vascular changes should also be considered. Cerebrovascular hemodynamic changes induced by thyrotoxicosis were considered to be responsible for the cerebral ischemic events. Excessive thyroid hormone production is considered to increase the cerebral metabolism and oxygen consumption. In addition, thyrotoxicosis-induced hypercoagulability may influence ischemic events. Therefore, the possibility of thyrotoxicosis should be considered when patients with Graves' disease show exacerbation of cerebral ischemic symptoms at follow-up. The necessity of surgery in addition to antithyroid therapy might be dependent on the mechanisms of the vascular changes and symptoms. If hyperthyroidism is associated with vascular changes and symptoms, antithyroid therapy may be adequate. However, if immune-mediated mechanisms or coincidences are considered to be associated with vascular changes and symptoms, like our case, surgical procedures might be needed.

AB - Several studies have shown the relation between Graves' disease and stenosis/occlusion of intracranial arteries. To our knowledge, only 31 cases, including our case, of concurrent Graves' disease and moyamoya syndrome or intracranial arterial stenosis/occlusion have been described. The patients were predominantly women, and their ages ranged from 10 to 54 years (mean, 29.3 years). Transient ischemic attacks and cerebral infarction were the common symptoms in these patients. Except one previous case and the present case, all cases showed thyrotoxicity when the cerebral ischemic event occurred. Among the 29 cases, in which the treatment regimen was known, antithyroid therapy was administered in 25 cases, and surgical treatment for cerebral vessel diseases was performed in 11 cases. Most of the patients eventually recovered from the neurological symptoms after medical and/or surgical treatment; one of the patients died, and one patient's condition worsened. Although the mechanism underlying intracranial arterial occlusion or stenosis in patients with Graves' disease has not been elucidated, several hypotheses have been described. Thyroid hormones may augment vascular sensitivity to the sympathetic nervous system and induce pathological changes in the arterial walls. An immune-mediated mechanism may play a role in the pathogenesis of these diseases. Atherosclerosis may be associated with these disorders. Vasculitis induced by antithyroid drugs may cause changes in the intracranial arteries. Finally, the possibility of a mere coincidence of Graves' disease and these vascular changes should also be considered. Cerebrovascular hemodynamic changes induced by thyrotoxicosis were considered to be responsible for the cerebral ischemic events. Excessive thyroid hormone production is considered to increase the cerebral metabolism and oxygen consumption. In addition, thyrotoxicosis-induced hypercoagulability may influence ischemic events. Therefore, the possibility of thyrotoxicosis should be considered when patients with Graves' disease show exacerbation of cerebral ischemic symptoms at follow-up. The necessity of surgery in addition to antithyroid therapy might be dependent on the mechanisms of the vascular changes and symptoms. If hyperthyroidism is associated with vascular changes and symptoms, antithyroid therapy may be adequate. However, if immune-mediated mechanisms or coincidences are considered to be associated with vascular changes and symptoms, like our case, surgical procedures might be needed.

UR - http://www.scopus.com/inward/record.url?scp=79959945849&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79959945849&partnerID=8YFLogxK

U2 - 10.1007/s10143-011-0311-z

DO - 10.1007/s10143-011-0311-z

M3 - Article

C2 - 21424208

AN - SCOPUS:79959945849

VL - 34

SP - 297

EP - 304

JO - Neurosurgical Review

JF - Neurosurgical Review

SN - 0344-5607

IS - 3

ER -