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Year : 2017  |  Volume : 10  |  Issue : 3  |  Page : 290-292  

Graves' disease and idiopathic intracranial hypertension

1 Department of Medicine, King George's Medical College, Lucknow, Uttar Pradesh, India
2 Department of Radiodiagnosis, King George's Medical College, Lucknow, Uttar Pradesh, India

Date of Web Publication19-May-2017

Correspondence Address:
Manish Gutch
Departments of Medicine, King George's Medical College, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.206574

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Idiopathic intracranial hypertension (IIH) is a central nervous system disorder characterized by raised intracranial pressure with normal cerebrospinal fluid composition and absence of any structural anomaly on neuroimaging. Among all endocrine disorders associated with the development of IIH, the association of hyperthyroidism and IIH is very rare with few cases reported till date. Thyroid disturbances have a unique association with IIH. Hypo- and hyper-thyroidism have been reported in association with this disorder. We present a rare case of a 25-year-old man with Graves' disease with intractable headache that was later investigated and attributed to development of IIH.

Keywords: Graves' disease, hyperthyroidism, idiopathic intracranial hypertension

How to cite this article:
Gutch M, Bhattacharjee A, Kumar S, Pushkar D. Graves' disease and idiopathic intracranial hypertension. Med J DY Patil Univ 2017;10:290-2

How to cite this URL:
Gutch M, Bhattacharjee A, Kumar S, Pushkar D. Graves' disease and idiopathic intracranial hypertension. Med J DY Patil Univ [serial online] 2017 [cited 2023 Mar 24];10:290-2. Available from:

  Introduction Top

Idiopathic intracranial hypertension (IIH) is a disorder characterized by elevated intracranial pressure and its associated signs and symptoms accompanied by a normal cerebrospinal fluid (CSF) biochemical composition and absence of structural anomalies on neuroimaging. IIH can be idiopathic as well as due to secondary causes, the most common being drugs (amiodarone, tetracycline, corticosteroids, indomethacin, phenytoin, Vitamin A) and systemic diseases (anemia, multiple sclerosis, chronic renal disease, sarcoidosis, systemic lupus erythematosus). Although both hypo- and hyper-thyroidism have been reported to cause IHH, there are very few cases mentioning the association of IHH with hyperthyroidism.[1],[2],[3],[4] Here, we describe a rare case of a male patient with Graves' disease presenting with intractable headache which was subsequently identified to be due to IHH.

  Case Report Top

A 25-year-old male presented to the outdoor patient department with complaints of on and off palpitations, anxiety, and tremulousness of his hands while trying to execute any work. These symptoms were initially mild and had gradually progressed in severity over the last 3 months. This was associated with a mild aching, holocranial headache without any diurnal or postural variation. He complained of occasional nausea with a few episodes of vomiting for the last 1 month; there was no history of visual blackouts or tinnitus. Owing to his illness, he had lost a significant amount of weight. There was no history suggestive of any other systemic complaints.

On examination, he looked anxious and pale, with warm, sweaty hands. A fine tremor was evident when he was asked to stretch his hands. His pulse rate was 110/min, hyperdynamic, regular, and bilaterally symmetrical. Blood pressure was 134/80 mm Hg. There were no eye signs or nail bed changes characteristic of Graves' disease. Rest of the general examination, examination of the nervous system and cardiovascular system was within normal limits.

His investigations revealed a normal hemogram, electrocardiogram, and liver and kidney function tests. Thyroid function test was suggestive of primary hyperthyroidism (T3 = 250 ng/dl, T4 = 20 μg/dl, thyroid stimulating hormone [TSH] <0.01 mIU/ml). His follicle stimulating hormone was 5.4 mIU/ml (0.81–8.18) and luteinizing hormone was 4.21 mIU/ml (0.69–7.15). Testosterone was 23.86 ng/dl (280–724) and prolactin level was 9.6 ng/ml (2.80–11.00). Fasting cortisol was 11.2 μg/dl (5–18). We subjected him to technetium 99 isotope scan that revealed diffuse uptake in bilateral thyroid glands, suggestive of Graves' disease [Figure 1]. Subsequently, he was started on methimazole 30 mg OD and propranolol 40 mg OD and was advised to follow-up.
Figure 1: Thyroid scintigraphy showing a diffusely increased radiotracer uptake goiter confirmed the diagnosis of Graves' disease

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Four months later, his thyroid function tests were normalized (T3 = 95 ng/dl, T4 = 10 μg/dl, TSH = 0.7 mIU/ml) and he reported improvement in majority of his symptoms. However, his headache had deteriorated in severity and was persistent throughout the day; besides, he also complained of diminution of vision. Visual acuity was 6/24 in both the eyes. Pupillary reaction to light was normal bilaterally. Ocular fundus examination revealed mild bilateral papilledema. Suspecting an intracranial lesion causing hydrocephalus, we ordered a magnetic resonance imaging study of the brain. It revealed the presence of partial empty sella and prominent CSF sleeve around B/L optic nerves [Figure 2]. CSF routine biochemical and microscopic analysis was also normal, apart from a raised CSF opening pressure; however, a therapeutic lumbar puncture did not relieve his symptoms. Other probable etiologies of headache such as infectious and autoimmune disorders were ruled out. We added acetazolamide 250 mg quater in die to his prescribed medications. His symptoms improved after 2 weeks of therapy; his vision normalized to 6/6 in both eyes. Acetazolamide was gradually discontinued while he continued taking antithyroid medications.
Figure 2: Magnetic resonance imaging brain - partially empty sella and prominent cerebrospinal fluid sleeve around B/L optic nerves

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  Discussion Top

Graves' disease causing hyperthyroidism can result in a constellation of symptoms. Common neurological manifestations include tremor, proximal myopathy, and axonal neuropathy causing sensory abnormalities.[5] Seizures, hyperkinetic disorders, dementia, and encephalopathy may occur rarely.

IHH is a central nervous system disorder characterized by elevated intracranial pressure with signs and symptoms resulting from the same, with a normal CSF composition and no structural anomalies detected on neuroimaging. Symptoms include headache, visual blackouts, tinnitus, back pain, and diplopia. However, none are specific for IHH.

The association of IHH with underlying Grave's disease is indeed a rare one, with only four cases reported till date.[1],[2],[3],[4] The pathogenesis of IHH is still unclear.[6],[7] Thyroxine can alter CSF dynamics as it is an important regulator of sodium transport. Hyperthyroidism results in increased cerebral blood flow [8] which is correlated with increased cerebral blood volume and raised intracranial pressure. There seems to be an insufficiently high driving pressure gradient, resulting in failure of CSF drainage from the subarachnoid space to the venous system. The effect of thyroid hormone raising venous pressure may justify the association between those two entities.

Thus, Graves' disease should be kept in mind while evaluating for the causes of IHH. Timely screening of hyperthyroid patients presenting with headache with ocular fundus examination may detect many asymptomatic cases of IHH and help in preventing visual loss.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Coutinho E, Silva AM, Freitas C, Santos E. Graves' disease presenting as pseudotumor cerebri: A case report. J Med Case Rep 2011;5:68.  Back to cited text no. 1
Dickman MS, Somasundaram M, Brzozowski L. Pseudotumor cerebri and hyperthyroidism. N Y State J Med 1980;80(7 Pt 1):1118-20.  Back to cited text no. 2
Merkenschlager A, Ehrt O, Müller-Felber W, Schmidt H, Bernhard MK. Reversible benign intracranial hypertension in a child with hyperthyroidism. J Pediatr Endocrinol Metab 2008;21:1099-101.  Back to cited text no. 3
Roos RA, van der Blij JF. Pseudotumor cerebri associated with hypovitaminosis A and hyperthyroidism. Dev Med Child Neurol 1985;27:246-8.  Back to cited text no. 4
Braverman LE, Utiger RD, DeLong GR, Adams RD. The neuromuscular system and brain in hypothyroidism. in The thyroid, eds Braverman LE, Utiger RD. Lippincott: New York; 1991. p. 1027-39.  Back to cited text no. 5
Skau M, Brennum J, Gjerris F, Jensen R. What is new about idiopathic intracranial hypertension? An updated review of mechanism and treatment. Cephalalgia 2006;26:384-99.  Back to cited text no. 6
Bateman GA. Arterial inflow and venous outflow in idiopathic intracranial hypertension associated with venous outflow stenoses. J Clin Neurosci 2008;15:402-8.  Back to cited text no. 7
Sokoloff L, Wechsler RL, Mangold R, Balls K, Kety SS. Cerebral blood flow and oxygen consumption in hyperthyroidism before and after treatment. J Clin Invest 1953;32:202-8.  Back to cited text no. 8


  [Figure 1], [Figure 2]

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