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| LETTER TO EDITOR |
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| Year : 2020 | Volume
: 68
| Issue : 1 | Page : 219-221 |
Acute Herpes Zoster Followed by Cerebral Venous Sinus Thrombosis
Rending Zhu, Chuanqin Fang, Juanjuan Wang, Xiaolu He
Department of Neurology, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China
| Date of Web Publication | 28-Feb-2020 |
Correspondence Address:
Dr. Chuanqin Fang
The Second Affiliated Hospital of Anhui Medical University, Anhui Medical University, 678 Fu Rong Road, Hefei, Anhui Province . 230601
People's Republic of China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.279658
How to cite this article:
Zhu R, Fang C, Wang J, He X. Acute Herpes Zoster Followed by Cerebral Venous Sinus Thrombosis. Neurol India 2020;68:219-21 |
Sir,
Cerebral venous sinus thrombosis (CVST) is a rare disease and a potentially disabling or lethal one at that.[1] Patients with CVST more often have multiple risk factors such as infection, neoplasm, systemic diseases, coagulopathies, and so on. When the infection is the causative factor for CVST, it can have bacterial and viral components.[2] There were several reports about CVST associated with primary varicella zoster virus and herpes sine zoster infection in earlier literature.[3],[4],[5] This paper reports a rare case of CVST with an initial manifestation of acute herpes zoster with headache.
A 73-year-old man presented with a 15-day history of left temporal pain, characterized by recurrent paroxysms of lancinating pain, and sleep interruption. A local doctor diagnosed him with trigeminal neuralgia. He was treated with carbamazepine and pregabalin at doses of 200 and 75mg respectively twice a day. Following this, his pain was duly relieved. On the seventh day, herpetic rash occurred on the left forehead region, along with pruritis and paralysis. He denied having any kind of headache or family history of headache in the past. Three days before his presentation, he had complained of dizziness, nausea, vomiting and fever. Two days later, he was brought to the emergency department of our hospital because of progressively worsening pain and dizziness accompanied by chills. His past medical history was notable only for Type 2 diabetes.
Computed tomography (CT) [Figure 1]a images of the brain showed multiple flake-shaped shadows in the right basal ganglia and left parietal lobes. The CT scan of his chest revealed some scattered patchy and cord-like shadows of the pulmonary lobe both sides. Brain magnetic resonance imaging (MRI) [Figure 1]b, [Figure 1]c, [Figure 1]d showed multiple spots of longer T1 and T2 signals in the bilateral frontal-parietal lobes and lateral ventricles. Fluid-attenuated inversion recovery sequence showed high signals. | Figure 1: Computed tomography showed some scattered ischemia in the right parietal lobe and right basal ganglia (a). Brain magnetic resonance imaging showed multiple ischemia in the bilateral frontal-parietal lobes and lateral ventricles, and softening lesion of the left parietal lobe (b-d)
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He had a normal sinus rhythm on electrocardiography. On examination, we found that rashes on his left forehead were crusting [Figure 2]. His vital signs were temperature 38.8°C, pulse rate 71 beats/minute, respiratory rate 20/minute, and blood pressure 158/92 mm Hg. He had no neck rigidity or any extremity weakness. At the same time, his chest, abdomen and legs were normal. Kernig and Brudzinski signs were negative, central nervous system examination revealed no abnormalities. A diagnosis of acute herpes zoster was made by the emergency department, and he was duly transferred to our institution. Blood routine examination indicated a slightly elevated neutrophil percentage 80.6% (reference range, 40.0-75.0%) and reduced platelet count of 104 × 109/L (reference range, 125-150 × 109/L). Fasting blood-glucose was 13.17 mmol/L (normal range, 3.90-6.10 mmol/L), electrolytes showed that sodium was 132.0 mmol/L. Other laboratory tests such liver function tests, renal function tests, immune function tests, homocysteine, blood culture and indexes of tumor were within normal limits. Analysis of his serum rheumatism antibody profile, antinuclear antibody series, anticardiolipin antibody were all negative. Serum analysis was negative for human immunodeficiency virus (HIV), hepatitis B and C antigen or antibody profile, and fluorescent treponema antibody absorption examination. C-reactive protein was 123 mg/L (0–4.0 mg/L); coagulation parameters were normal except for fibrinogen degradation products at 10.3 μg/mL (reference range, 0.0-5.0 μgm/L), D-dimer was 2.47 μg/mL (reference range, 0.00-0.5 μgm/L).
We had a treatment for him including antiviral, antalgic, and body temperature control. Over the next three days, the patients experienced a new onset of progressively worsening bifrontal headache. Neurological examination was unremarkable. Lumbar puncture with cerebrospinal fluid (CSF) was clear and the opening pressure was above 300 mmH2O. CSF report showed glucose 3.97 mmol/L (2.20-3.90 mmol/L), chloride 115.0 mmol/L. CSF-Protein level, white blood cell count, and percentage of monocytes were normal. CSF-toxoplasma, rubella virus, cytomegalovirus, and herpes simplex virus antibody were not detected. Gram staining, acid-fast staining, cryptococcal antigen test results were negative. CSF did not grow any bacteria, fungus, or acid-fast bacillus as culture. In consideration of possible venous sinus thrombosis, a magnetic resonance venogram (MRV) of brain was done. Brain MRV [Figure 3] showed that the left sigmoid sinus and transverse sinus were slender, showing disruption and blurring. | Figure 3: Brain MRV disclosed thrombosis of the left sigmoid sinus and transverse sinus (a and b)
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He was diagnosed as acute herpes zoster as well as cerebral venous sinus thrombosis. The patient was treated with anticoagulation measures of low-molecular-weight heparin calcium (4000 IU, subcutaneous injection, once every 12 hours). Dehydration and supportive therapeutic measures were taken simultaneously. Five days later, the patient's headache was relieved. Within ten days of the treatment, low-molecular-weight heparin calcium was replaced with warfarin. Discharge instruction was to continue to take warfarin oral medication, and he was asked to follow-up with with coagulation parameter monitoring.
Varicella-zoster virus (VZV) is a human herpes virus that produces varicella on primary infection then becomes latent in ganglionic neurons. Under the influence of some factors, VZV reactivates to cause zoster.[6] Diagnosis of herpes zoster is often based on clinical manifestations of rash. In a lesion affected by herpes zoster, a unilateral rash may present and the patients may feel pain and paresthesia. Localized areas of pain and paresthesia are also common before the appearance of rashes.[7] This patient started with left forehead pain, followed by rashes. According to previous study, CVST can cause headache, and headache is about 90% of all initial and major symptoms in all CVST cases.[8] When pain in the head area is a major clinical manifestations of herpes zoster patients, it may lead to delayed diagnosis. However, the headache range of CVST is notable in that it is usually diffused, and its severity usually develops gradually due o increased intracranial pressure.[8] A study by Anuradha Mehta et al.[4] reported that herpes zoster could cause neurological complications such as stroke and cerebral venous thrombosis. Previous reports indicate that activated varicella could infect the meninges and cerebral vein and sinus through transcranial movement. The mechanism of cerebrovascular events following VZV infection may be vasculitis,[3] but the pathogenesis of VZV vascular disease remains controversial.[4] In our patient, cerebral venous sinus thrombosis could be attributed to acute herpes zoster (after VZV reactivation). He had no other risk factors. CVST is a challenging disease due to its confusing clinical manifestations. Clinicians should identify its predisposing factors as early as possible for early diagnosis and treatment.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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| 3. | Sada S, Kammineni A, Kaniikannan MA, Afshan J. Cerebral sinus venous thrombosis: A rare complication of primary Varicella virus. Neuro India 2012;60:645-6. |
| 4. | Mehta A, Arora A, Sharma M, Malik R, Porwal YC. Hemorrhagic stroke and cerebral venous thrombosis: Rare neurological sequelae of chickenpox infection. Ann Indian Acad Neurol 2018;21:228-32. [ PUBMED] [Full text] |
| 5. | Chan J, Bergstrom RT, Lanza DC, Oas JG. Lateral sinus thrombosis associated with zoster sine herpete. Am J Otolaryngol 2004;25:357-60. |
| 6. | Gershon AA, Breuer J, Cohen JI, Cohrs RJ, Gershon MD, Gilden D, et al. Varicella zoster virus infection. Nat Rev Dis Primers 2015;1:15016. |
| 7. | Johnson RW, Whitton TL. Management of herpes zoster (shingles) and postherpetic neuralgia. Expert Opin Pharmacother 2004;5:551-9. |
| 8. | Einhäupl K, Stam J, Bousser MG, De Bruijn SF, Ferro JM, Martinelli I, et al. EFNS guideline on the treatment of cerebral venous and sinus thrombosis in adult patients. Eur J Neurol 2010;17:1229-35. |
[Figure 1], [Figure 2], [Figure 3]
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