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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

Lovely Chhabra1, Vinod K Chaubey1, Saurabh Joshi1, Jayant Phadke2,  
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

Correspondence Address:
Lovely Chhabra
Department of Internal Medicine, Saint Vincent Hospital, University of Massachusetts Medical School, Worcester, MA 01608
USA




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;61:671-673


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 2021 Dec 8 ];61:671-673
Available from: https://www.neurologyindia.com/text.asp?2013/61/6/671/125370


Full Text

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}{Figure 2}

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

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