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CASE REPORT
Year : 2014  |  Volume : 41  |  Issue : 3  |  Page : 192-194

Acute cerebral venous sinus thrombosis: A rare complication of binge drinking


Department of Radiology, NM Medical, Pune, Maharashtra, India

Date of Web Publication19-Sep-2014

Correspondence Address:
Chandrashekhar A Sohoni
B-5, Common Wealth Hsg. Soc., Opposite Bund Garden, Pune - 411 001, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-5009.141228

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  Abstract 

The association of alcoholism with stroke is known. However, acute cerebral venous sinus thrombosis (CVST) presenting as a complication of binge drinking is rare. Two such rare cases are presented here. Since, there is an overlap of symptoms between veisalgia and CVST, the diagnosis of CVST may be missed or delayed in alcoholic patients. It is important to keep a rare possibility of acute CVST in mind while dealing with patients who present with neurological symptoms following binge drinking. Imaging plays a vital role in making an early and specific diagnosis, thus preventing complications.

Keywords: Acute cerebral venous sinus thrombosis, alcoholism, binge drinking, computed tomography, magnetic resonance imaging


How to cite this article:
Sohoni CA. Acute cerebral venous sinus thrombosis: A rare complication of binge drinking . J Sci Soc 2014;41:192-4

How to cite this URL:
Sohoni CA. Acute cerebral venous sinus thrombosis: A rare complication of binge drinking . J Sci Soc [serial online] 2014 [cited 2020 Jul 10];41:192-4. Available from: http://www.jscisociety.com/text.asp?2014/41/3/192/141228


  Introduction Top


Alcoholics are predisposed to cerebrovascular accidents. Symptoms such as headache, nausea and drowsiness following binge drinking are commonly attributed to veisalgia. Unless a clinician keeps a high index of suspicion, the diagnosis of cerebral venous sinus thrombosis (CVST) may be missed in such cases due to non-specificity of symptoms. Imaging plays a very important role in early diagnosis of CVST and thus helps in preventing neurological complications.


  Case ReportS Top


0Case 1

The first case is about a 40-year-old male patient who presented with the complaints of severe headache, nausea and vomiting since 24 h. He had a history of regular moderate alcohol consumption since past 10 years and had been binge drinking the previous night. There was no history of seizures, weakness or loss of consciousness. There was no other significant past medical history. The history and general physical examination did not suggest alcohol related malnutrition. The patient was conscious, oriented, afebrile and anicteric. Pulse was 106/min and blood pressure was 130/90 mm Hg. There was no motor or sensory deficit. The pupils were equally reacting to light and extensor plantar response was not elicited. Ultrasonography of abdomen was normal. Since, the patient had already received symptomatic treatment in the form of non-steroidal anti-inflammatory drugs without much response, a computed tomography (CT) scan of brain was performed. The CT revealed abnormal hyperdensity in the posterior portion of superior sagittal sinus [Figure 1]a] and bilateral transverse sinuses [Figure 1]b] suggestive of acute thrombosis. The magnetic resonance imaging (MRI) revealed abnormal hyperintensity in the posterior portion of superior sagittal sinus on T1W images [Figure 1]c], however, it did not reveal an acute infarct or hemorrhage. Non-contrast magnetic resonance venography (MRV) confirmed the acute thrombotic process in posterior portion of superior sagittal sinus [Figure 1]d] and bilateral transverse sinuses [Figure 1]e]. The patient was admitted to the hospital and treatment with subcutaneous enoxaparin (40 mg twice a day) and intravenous normal saline initiated. The liver function tests revealed mildly elevated serum glutamic-oxaloacetic transaminase (73 U/L) and serum glutamate-pyruvate transaminase (61 U/L) levels. Rest of the laboratory parameters were within the normal limits, including normal platelet count, erythrocyte sedimentation rate and serum vitamin B12 level. The patient's headache had subsided significantly on day 4 of admission. At the time of discharge on day 7, the patient was asymptomatic and oral anticoagulation with warfarin (5 mg daily) for 3 months was prescribed. Decision regarding the period of continuation of oral warfarin was to be made after 3 months. Patient was advised against alcohol intake. Serum homocysteine, anti-phospholipid antibody, protein C and S, anti-thrombin III and factor V Leiden levels assessed 8 weeks later were normal.
Figure 1: The computed tomography images reveal abnormal hyperdensity in the posterior portion of superior sagi�� al sinus (a) and bilateral transverse sinuses. (b) The magnetic resonance imaging image shows abnormal hyperintense signal in the superior sagittal sinus on T1W sequence. (c) The magnetic resonance venography images reveal non-visualization of the posterior portion of superior sagittal sinus (d) and bilateral transverse sinuses (e), suggestive of thrombosis

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Figure 2: The magnetic resonance imaging reveals mild hyperintense signal in the left transverse sinus (a) and left sigmoid sinus (b) on T1W images. The magnetic resonance venography shows non-visualization of left transverse and sigmoid sinuses, suggestive of thrombosis (c)

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Case 2

The second case report is about a 41-year-old hypertensive male was brought to the out-patient clinic with symptoms of headache and giddiness since 2 days and a seizure 2 h ago. The patient, who was otherwise an occasional drinker, had developed the symptoms immediately following an episode of binge drinking 2 days ago. Despite the routine analgesics, the symptoms of headache and giddiness had worsened. The patient was being treated for hypertension with amlodipine 5 mg daily for past 5 years. There was no other underlying comorbid condition. On examination, he was conscious but slightly confused. He was afebrile, pulse was 90/min and blood pressure was 150/100 mm Hg. Neurological examination was unremarkable. Fundoscopy was normal. MRI of brain revealed mildly hyperintense signal in the left transverse [Figure 2]a] and sigmoid [Figure 2]b] sinuses suspicious for acute thrombosis. No evidence of acute infarct or hemorrhage was detected. The non-contrast MRV showed non-visualization of the left transverse and sigmoid sinuses suggestive of thrombosis [Figure 2c]. Treatment with subcutaneous enoxaparin (40 mg twice daily) and intravenous normal saline resulted in significant symptomatic improvement by the 3 rd day of admission. The patient's blood pressure was managed with oral amlodipine and telmisartan. Phenytoin (300 mg per oral daily) was administered during hospital stay for seizure prophylaxis. The laboratory parameters were within normal limits, including normal platelet count, erythrocyte sedimentation rate and serum vitamin B12 level. Enoxaparin was continued until day 7 and oral warfarin (5 mg daily) was prescribed for 3 months. Decision regarding the period of continuation of oral warfarin was to be made after 3 months. Patient was advised against alcohol consumption. Evaluation of serum homocysteine, anti-phospholipid antibody, protein C and S, anti-thrombin III and factor V Leiden levels performed 8 weeks later was normal.


  Discussion Top


Heavy alcohol consumption has been associated with increased risk of stroke. [1] Meta-analysis of 35 studies suggests that heavy alcohol consumption increases the relative risk of stroke, whereas light or moderate intake may reduce the overall risk of stroke. [2] Though the pathophysiology of alcohol consumption causing stroke has not been completely explained, various mechanisms such as induction of cardiac arrhythmias and cardiac wall motion abnormalities, induction of hypertension, enhancement of platelet aggregation and activation of the clotting cascade and reduction of cerebral blood flow by stimulation of cerebral vascular smooth muscle contraction have been proposed. [1] Addressing cerebral venous thrombosis in males specifically, some studies suggest dehydration and resultant hyperviscosity of blood induced by heavy alcohol consumption as a possible mechanism for thrombosis. [3],[4] In the absence of any other predisposing condition, an interplay of these physiological changes caused by binge drinking may be able to explain the CVST in the patients described above. The usual predisposing conditions for CVST are oral contraceptives, pregnancy and purperium, prothrombotic conditions, ear-nose-throat infections, central nervous system infections, other infections, central nervous system disorders, cancer, vasculitis and other systemic diseases. [5]

The clinical manifestations of CVST are non-specific and hence it is a diagnostic challenge. Symptoms such as headache, nausea, vomiting and drowsiness are common to veisalgia and CVST and hence the diagnosis of CVST may be easily missed in alcoholic patients. Persistence of symptoms and appearance of new signs and symptoms such as seizure, altered sensorium, paresis or focal neurological deficit should raise the suspicion of CVST in alcoholic patients. [5],[6]

CT and MRI are extremely useful modalities in making an early and specific diagnosis of CVST. Whereas CT shows hyperdensity, MRI shows hyperintensity on T1W sequence in acutely thrombosed sinuses. MRV is the non-invasive modality of choice for diagnosing CVST. [7],[8] In acute clinical setting, non-contrast MRV is fairly accurate for diagnosis of CVST. [7],[8] Contrast enhanced MRV may be required to overcome some of the diagnostic limitations of non-contrast MRV which may arise in cases of anatomic variants, thrombus signal variability and imaging artefacts. [7] In both the cases described above, non-contrast MRV provided accurate diagnosis. A specific diagnosis achieved by imaging facilitates early initiation of treatment with low molecular weight heparin, thus enabling complete recovery without complications.

 
  References Top

1.Gorelick PB. Alcohol and stroke. Stroke 1987;18:268-71.  Back to cited text no. 1
[PUBMED]    
2.Reynolds K, Lewis B, Nolen JD, Kinney GL, Sathya B, He J. Alcohol consumption and risk of stroke: A meta-analysis. JAMA 2003;289:579-88.  Back to cited text no. 2
    
3.Mehta SR, Muthukrishnan MJ, Varadarajulu R, Gupta MA. Cerebral venous sinus thrombosis: A great masquerader. Med J Armed Forces India 2004;60:299-300.  Back to cited text no. 3
    
4.Singh H, Paulomi T, Ray S, Gupta V. A rare presentation of acute alcohol intoxication, subarachnoid haemorrhage and cortical venous thrombosis. J Neurol Res 2012;2:62-4.  Back to cited text no. 4
    
5.Canhao P, Bousseur MG, Barinagarrementeria F, Stam J, Ferro JM; The ISCVT Collaborators. Predisposing conditions for cerebral vein and dural sinus thrombosis. Available from: http://www.iscvt.com/index.htm. [Last cited on 2013 Dec 20].  Back to cited text no. 5
    
6.Mehndiratta MM, Garg S, Gurnani M. Cerebral venous thrombosis - Clinical presentations. J Pak Med Assoc 2006;56:513-6.  Back to cited text no. 6
    
7.Tsai FY, Wang AM, Matovich VB, Lavin M, Berberian B, Simonson TM, et al. MR staging of acute dural sinus thrombosis: Correlation with venous pressure measurements and implications for treatment and prognosis. AJNR Am J Neuroradiol 1995;16:1021-9.  Back to cited text no. 7
    
8.Saposnik G, Barinagarrementeria F, Brown RD Jr, Bushnell CD, Cucchiara B, Cushman M, et al. Diagnosis and management of cerebral venous thrombosis: A statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2011;42:1158-92.  Back to cited text no. 8
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