A rare cause of cerebral venous thrombosis: cryptococcal meningoencephalitis

Şenadım, Songül; Baslo, Sezin Alpaydın; Güveli, Betül Tekin; Daryan, Metin Dedei; Kantaroglu, Elif; Ozturk, Oya; Atakli, Dilek

doi:10.1007/s10072-016-2550-9

Cited by 9 publications

(6 citation statements)

References 17 publications

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“…Together with the fact that the main venous sinuses were patent (Fig. 2 ) and that venules were widely congested, the massive cerebellar edema may be predominantly due to occlusion of small veins at the subarachnoid space rather than due to occlusion of large veins such as sinuses [ 10 ]. The findings on autopsy indicated that the unique progression of the ischemic and edematous lesion on MRI reflected the invasion of the fungi and aggressive fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Subarachnoid small vein occlusion due to inflammatory fibrosis—a possible mechanism for cerebellar infarction in cryptococcal meningoencephalitis: a case report

et al. 2017

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BackgroundCryptococcal meningoencephalitis (CM) causes cerebral infarction, typically, lacunar infarction in the basal ganglia. However, massive cerebral infarction leading to death is rare and its pathophysiology is unclear. We report a case of CM causing massive cerebellar infarction, which led to cerebral herniation and death.Case presentationA 56-year-old man who suffered from dizziness and gait disturbance for one month was admitted to our hospital and subsequently diagnosed with a cerebellar infarction. He had a past medical history of hepatitis type B virus infection and hepatic failure. Although the findings on magnetic resonance imaging (MRI) imitated an arterial infarction of the posterior inferior cerebellar artery, an accompanying irregular peripheral edema was observed. The ischemic lesion progressed, subsequently exerting a mass effect and leading to impaired consciousness. External and internal decompression surgeries were performed. Cryptococcus neoformans was confirmed in the surgical specimen, and the patient was diagnosed with CM. In addition, venule congestion in the parenchyma was observed with extensive fibrosis and compressed veins in the subarachnoid space. The patient died 26 days after admission. Autopsy revealed that pathological changes were localized in the cerebellum.Conclusion C. neoformans can induce extensive fibrosis of the subarachnoid space, which may compress small veins mechanically inducing venule congestion and massive cerebral infarction. In such cases, the clinical course can be severe and even rapidly fatal. An atypical pattern of infarction on MRI should alert clinicians to the possibility of C. neoformans infection.

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Section: Discussionmentioning

confidence: 99%

Subarachnoid small vein occlusion due to inflammatory fibrosis—a possible mechanism for cerebellar infarction in cryptococcal meningoencephalitis: a case report

et al. 2017

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“…Subsequently, fingolimod administration has been associated with cryptococcal infections of various types, including meningoencephalitis [ 3 ], cutaneous cryptococcosis [ 4 ], and disseminated cryptococcosis [ 5 ]. Cryptococcus has been rarely identified as a cause of cerebral venous thrombosis; one such case has been described in a patient without an apparent immunodeficiency [ 6 ]. We report a case of cerebral venous thrombosis secondary to cryptococcus in a patient receiving fingolimod.…”

Section: Introductionmentioning

confidence: 99%

Cerebral Venous Thrombosis due to Cryptococcus in a Multiple Sclerosis Patient on Fingolimod

Kammeyer

Lehmann²

2022

Case Rep Neurol

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Fingolimod is a disease-modifying treatment utilized in the treatment of relapsing-remitting multiple sclerosis. Fingolimod has been associated with an increased risk in herpes simplex and varicella infection in clinical trials. We report a case of cerebral venous thrombosis secondary to cryptococcus in a patient receiving fingolimod. A 61-year-old male with multiple sclerosis treated with fingolimod presented with a 2-week history of headache, chills, and night sweats. An MRI of the brain revealed a left transverse and sigmoid sinus thrombosis. Two blood cultures revealed <i>Cryptococcus neoformans</i>; a serum cryptococcal antigen was also positive. HIV testing was negative. A lumbar puncture was deferred as the patient was placed on heparin and, subsequently, warfarin for the cerebral venous thrombosis. The patient received antifungal therapy for 14 days with liposomal amphotericin B and flucytosine, followed by oral fluconazole for 8 weeks. He was subsequently readmitted 60 days later with bilateral papilledema; his anticoagulation was reversed, and a lumbar puncture revealed a negative cryptococcal antigen and an intracranial pressure of 20. A repeat MRI revealed worsening superior sagittal sinus thrombosis, thought to be the cause of the papilledema; his anticoagulation was reinitiated. He received a brief course of intravenous methylprednisolone, but as his multiple sclerosis was well-controlled, further therapy was deferred. His symptoms had resolved at a 3-month follow-up appointment. This is the first report of a multiple sclerosis patient treated with fingolimod to develop cerebral venous thrombosis secondary to cryptococcal fungemia. The risks of opportunistic infections should be considered in patients managed with fingolimod.

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“…Cerebral venous sinus thrombosis (CVST) is easily misdiagnosed, thus resulting in treatment delay and subsequent poor outcomes, regarding its variable and non-specific clinical manifestations [1]. Recently, some special or complex causes of CVST are emerging, which may display more intricate clinical presentations and require customized management [2,3], although the mainstay treatment still focuses on anticoagulation [4].…”

Section: Introductionmentioning

confidence: 99%

Methylmalonic Aciduria may be an Innegligible Etiology of Cerebral Venous Sinus Thrombosis

Zhou¹,

Wu²,

Ding³

et al. 2018

Neuropsychiatry

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This paper analyzed a case of Methylmalonic Aciduria (MMA) in combination with Patent Foramen Ovale (PFO), presenting as cerebral venous sinus thrombosis (CVST) and cerebral venous infarctions coexisted with fresh arterial infarctions located at bilateral cerebella. From the aspects including clinical manifestations, physical examination, final diagnosis confirmation, comprehensive therapy, and clinical outcomes, this paper will be a very useful reference to clinicians.

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A rare cause of cerebral venous thrombosis: cryptococcal meningoencephalitis

Cited by 9 publications

References 17 publications

Subarachnoid small vein occlusion due to inflammatory fibrosis—a possible mechanism for cerebellar infarction in cryptococcal meningoencephalitis: a case report

Subarachnoid small vein occlusion due to inflammatory fibrosis—a possible mechanism for cerebellar infarction in cryptococcal meningoencephalitis: a case report

Cerebral Venous Thrombosis due to Cryptococcus in a Multiple Sclerosis Patient on Fingolimod

Methylmalonic Aciduria may be an Innegligible Etiology of Cerebral Venous Sinus Thrombosis

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