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Table of Contents    
LETTER TO EDITOR
Year : 2013  |  Volume : 61  |  Issue : 6  |  Page : 671-673

Thyrotoxic hypercoagulable state with cerebral venous thrombosis and venous infarction masquerading as epilepsia partialis continua


1 Department of Internal Medicine, Saint Vincent Hospital, University of Massachusetts Medical School, Worcester, MA 01608, USA
2 Department of Neurology, Saint Vincent Hospital, University of Massachusetts Medical School, Worcester, MA 01608, USA

Date of Submission16-Nov-2013
Date of Decision19-Nov-2013
Date of Acceptance05-Dec-2013
Date of Web Publication20-Jan-2014

Correspondence Address:
Lovely Chhabra
Department of Internal Medicine, Saint Vincent Hospital, University of Massachusetts Medical School, Worcester, MA 01608
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.125370

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How to cite this article:
Chhabra L, Chaubey VK, Joshi S, Phadke J. Thyrotoxic hypercoagulable state with cerebral venous thrombosis and venous infarction masquerading as epilepsia partialis continua. Neurol India 2013;61:671-3

How to cite this URL:
Chhabra L, Chaubey VK, Joshi S, Phadke J. Thyrotoxic hypercoagulable state with cerebral venous thrombosis and venous infarction masquerading as epilepsia partialis continua. Neurol India [serial online] 2013 [cited 2019 Dec 12];61:671-3. Available from: http://www.neurologyindia.com/text.asp?2013/61/6/671/125370


Sir,

A 45-year-old woman presented with the "worst headache of her life" and intermittent numbness and weakness of the left-side of her face, arm and leg. Other symptoms included unintentional weight loss of 15 lbs, diarrhea, tremors, palpitations, heat intolerance and heavy menses, for 2 months and worsened a week prior to presentation. Physical examination showed sinus tachycardia (heart rate-115 beats/min), warm clammy skin, left upper extremity weakness of a pyramidal pattern and left-sided facial sensory impairment to touch and pin prick over the V1 and V2 distribution. She also was quite restless and had intermittent confusion. Computerized tomography of brain and cerebrospinal fluid analysis were unremarkable. She subsequently developed continuous focal seizure. Electroencephalography showed epileptiform discharges [Figure 1]. Contrast-enhanced brain magnetic resonance imaging revealed a filling defect in the superior sagittal sinus and a small right frontal hemorrhagic infarct [Figure 2]a and b. Magnetic resonance venography (MRV) of the brain revealed extensive sub-acute superior sagittal and transverse sinus thrombosis [Figure 2]c and d. Endocrinological work-up revealed severe thyrotoxicosis (undetectable thyroid stimulating hormone <0.005 mIU/L, high T3 at 209 ng/dL [N = 58-159 ng/dL], high free T3 at 17.6 pg/mL [N = 2-4.4 pg/mL] and high free T4 at 18.6 μg/dL [N = 4.5-12.0 μg/dL]). Thyroid stimulating immunoglobulins were elevated at 497% (N = 0-139%). A comprehensive hypercoagulable screening including anti-phospholipid antibodies, antithrombin III deficiency, protein C and S, activated protein C resistances, hyperhomocysteinemia, factor V Leiden and prothrombin gene mutation were all unremarkable. There was significantly increased factor VIII activity (367%; normal 50-150%) and mildly elevated fibrinogen levels (448 mg/dL; normal 193-423 mg/dL). Serum protein electrophoresis and work-up for vasculitis was unremarkable.
Figure 1: Electroencephalography revealing focal epileptiform abnormality, consistent with epilepsia partialis

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Figure 2: (a) Contrast-enhanced magnetic resonance imaging of the brain reveals a filling defect in the superior sagittal sinus consistent with superior sagittal venous thrombosis; (b) Contrast-enhanced magnetic resonance imaging of the brain reveals a small area of right frontal hemorrhagic infarction resulting from venous thrombosis; (c) Magnetic resonance venography of the brain reveals transverse venous sinus thrombosis. Left transverse sinus narrowing represents a congenital anomaly; (d) Magnetic resonance venography of the brain reveals extensive sub acute superior saggital venous sinus thrombosis; (e and f) Repeat magnetic resonance venography 5 months later shows a complete recannalisation of the sagittal and transverse sinuses

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She was treated with oral methimazole, iodine drops and propranolol for the thyrotoxic storm. Weight-based intravenous heparin (without bolus), followed by oral warfarin were initiated for the cerebral venous thrombosis (CVT) and the epilepsia partialis continua only resolved after initiating phenobarbital followed by intravenous levetiracetam. She made remarkable clinical recovery and 8 weeks later, she was euthyroid. Repeat MRV 5 months later showed complete recanalization of the sagittal and transverse sinuses [Figure 2]e and f.

There have been sparse reports of the association of hyperthyroidism and CVT. [1],[2],[3] Thyrotoxicosis produces a hypercoagulable state by increasing the activity of factor VIII and fibrinogen levels. [4],[5] Generalized seizures and rarely partial seizures have been previously reported in association with severe thyrotoxicosis although its causal relationship has not been clearly established. [6] To the best of our knowledge, focal motor status in the setting of thyrotoxic CVT has not been previously reported, making our case probably the first such report in the literature. Focal motor status indeed occurred as a result of the CVT, which in turn was an outcome of thyrotoxic hypercoagulable state. Our case reiterates the need for evaluation for hyperthyroidism in patients with CVT. It also illustrates an important point that focal motor status or new onset partial or complex partial seizures may occur in the setting of thyrotoxicosis and should lead one to look for cerebral venous sinus thrombosis as one of the possible underlying mechanisms leading to venous infarction as early aggressive therapy may result in excellent clinical outcomes.

 
  References Top

1.Hwang JU, Kwon KY, Hur JW, Lee JW, Lee HK. The role of hyperthyroidism as the predisposing factor for superior sagittal sinus thrombosis. J Cerebrovasc Endovasc Neurosurg 2012;14:251-4.  Back to cited text no. 1
[PUBMED]    
2.Hermans E, Mariën P, De Deyn PP. Sinus sigmoideus thrombosis secondary to graves› disease: A case description. Case Rep Neurol 2011;3:203-9.  Back to cited text no. 2
    
3.Dai A, Wasay M, Dubey N, Giglio P, Bakshi R. Superior sagittal sinus thrombosis secondary to hyperthyroidism. J Stroke Cerebrovasc Dis 2000;9:89-90.  Back to cited text no. 3
[PUBMED]    
4.Erem C, Ersoz HO, Karti SS, Ukinç K, Hacihasanoglu A, Deðer O, et al . Blood coagulation and fibrinolysis in patients with hyperthyroidism. J Endocrinol Invest 2002;25:345-50.  Back to cited text no. 4
    
5.Rogers JS 2 nd , Shane SR, Jencks FS. Factor VIII activity and thyroid function. Ann Intern Med 1982;97:713-6.  Back to cited text no. 5
    
6.Song TJ, Kim SJ, Kim GS, Choi YC, Kim WJ. The prevalence of thyrotoxicosis-related seizures. Thyroid 2010;20:955-8.  Back to cited text no. 6
[PUBMED]    


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