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 Table of Contents  
Year : 2021  |  Volume : 9  |  Issue : 2  |  Page : 81-84

Asymptomatic diffuse cerebritis presenting as middle cerebral artery infarct: A case report and review of literature

Department of Neurosurgery & Spine Surgery, St. Johns' Hospital, Bangalore, India

Date of Submission30-Dec-2020
Date of Decision19-Jan-2021
Date of Acceptance25-Mar-2021
Date of Web Publication11-Jun-2021

Correspondence Address:
Dr. Sibhi Ganapathy
Assistant Professor, Department of Neurosurgery and Spine Surgery, St. John's Medical Collage and Hospital, Bangalore, Karnataka State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mjhs.mjhs_33_20

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Diffuse cerebritis is a devastating disease presenting with features of raised intracranial tension, deficits, and features of meningeal and neural irritation. The most common feature is seizures which may persist despite normal antiepileptic medication. We present a patient with diffuse cerebritis who presented as a subacute middle cerebral artery (MCA) territory infarct without any symptoms of meningeal irritation or infection. The patient once admitted deteriorated with pupillary asymmetry and loss of consciousness. A computerized tomography scan revealed a massive increase in cerebral edema of the infarcted brain with midline shift and mass effect. In view of the serious threat to life, a decompressive craniectomy was done. Once the dura was opened, pus was seen subpially oozing into the subdural space. This was sampled for analysis and the scalp flap was closed with a drain. The patient improved well post surgically and was gradually extubated. His pus was found to grow Klebsiella pneumoniae sensitive to amikacin and gentamicin. A prolonged course of antibiotics was started. An angiogram done to determine the cause of the infarct showed only distal MCA branches (M4) occluded. The patient later deteriorated with venous thrombosis and succumbed to his illness later. We present a discussion on the etiology of the patient's condition and possible treatment options when faced with such situations.

Keywords: Diffuse cerebritis, middle cerebral artery territory infarct, raised intracranial tension, seizures

How to cite this article:
Ganapathy S, Adesh J, Bysani P, Pandya J, Raykar RR. Asymptomatic diffuse cerebritis presenting as middle cerebral artery infarct: A case report and review of literature. MRIMS J Health Sci 2021;9:81-4

How to cite this URL:
Ganapathy S, Adesh J, Bysani P, Pandya J, Raykar RR. Asymptomatic diffuse cerebritis presenting as middle cerebral artery infarct: A case report and review of literature. MRIMS J Health Sci [serial online] 2021 [cited 2023 Mar 23];9:81-4. Available from: http://www.mrimsjournal.com/text.asp?2021/9/2/81/318153

  Introduction Top

Cerebritis is the inflammation of the brain in the setting of infection. Malignant middle cerebral artery (MCA) territory infarct requiring decompressive craniectomy in the presence of cerebritis is a lesser-known affair. We present a case with a similar presentation and try to analyze and understand this relationship between cerebritis and infarction. We also try to explain the dogma as to which is the cause and which is the effect in the presence of both.

  Case Report Top

A 67-year-old farmer presented to the emergency unconscious with complete paralysis of the right half of his body coupled and difficulty breathing. On eliciting a history, he was diagnosed to have a large MCA territory infarct a week ago in a peripheral hospital and advised treatment. He was a known diabetic who had stopped medications himself against the advice of doctors and relatives a month ago. During the evaluation, then he was found to be partially conscious, then with hemiparesis. The relatives refused treatment and took the patient home, fed him through the mouth, and neglected him for a week until he completely lost consciousness.

On arrival, he was found to have a Glasgow Coma Scale (GCS) of E1M4V2 with pupils bilaterally equal but sluggishly reacting to light. He had a dense left hemiplegia with increased but no meningeal signs of irritation. He had severe aspiration pneumonia with diabetic ketoacidosis and had not passed urine for the last 3 days as well. His blood investigations showed severe infection with a total blood cell count of 20,000 with 90% neutrophils, coupled with high creatinine, and blood sugar levels above 300 g/dl. He was intubated and shifted to the intensive care unit (ICU) where his metabolic parameters were attended to. A computerized tomography (CT) scan of the brain showed a large MCA infarct without mass effect or midline shift. Thus, it was decided to wait and observe putting him on decongestants, while the rest of his metabolic syndrome was tackled. He was dialyzed on the 2nd day of admission and his renal and blood parameters resolved. The aspiration pneumonia however worsened, resulting in septicemia. His blood culture grew Staphylococcus aureus which was aggressively treated with intravenous antibiotics.

On day 3 after admission, he developed pupillary asymmetry with a sudden drop in GCS. The scan done showed an increase in edema with midline shift and impending uncal herniation [Figure 1]. Decompressive craniectomy was immediately done and the pupillary asymmetry was brought back to normal. The surface of the brain viewed after the opening of the dura was full of subpial pus oozing through rents into the subdural space. The pus was taken for culture and analysis [Figure 2]. Post decompression, his GCS improved to E2M5Vt. Pus culture was shown to grow Klebsiella pneumoniae sensitive to common antibiotics. This was started immediately. A CT angiogram was also done to ascertain the cause of infarct [Figure 3], the angiogram showed peripheral branches of the MCA (M4) occluded with the trunk and proximal branches patent.
Figure 1: Coronal computerized tomography of the brain (plain) showing a large middle cerebral artery territory infarct in the right side compressing the lateral ventricle and pushing the midline towards the opposite side

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Figure 2: Intraoperative photograph showing pus in the subpial space exuding into the subarachnoid and subdural space following decompressive craniectomy and durotomy

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Figure 3: Computerized tomography angiogram of the patient showing absence of patent vasculature over the distal middle cerebral artery territory on the right side

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The patient was carefully monitored in the ICU. On postoperative day 4, he suddenly deteriorated again. His CT scan showed [Figure 4] hemorrhagic transformation worsening the uncal herniation and midline shift. The pattern of hemorrhage suggested possible cortical venous infarction secondary to cerebritis. At this stage, further surgical intervention was not possible due to derailment of other metabolic parameters. He was also found to have deep-venous thrombosis of the right common femoral vein and the entire right lower limb venous vasculature. Despite the best efforts of all concerned, the patient succumbed to the disease on the 7th day after admission.
Figure 4: Hemorrhagic transformation of the infarct with worsening of the mass effect and midline shift despite decompressive craniectomy

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  Discussion Top

The acute presentation of a stroke with CT imaging support tends to be a monochromatic affair, with well-established protocols in place for efficient management.[1] The problem arises when there is a deviation from the normal leading to speculation and discussion. Once the diagnosis of cerebritis was made postdecompressive craniectomy, a retrospective analysis was conducted to analyze the causes. We found ourselves to be in a chicken and egg situation where one is at difficulty to determine which pathology came first, thereby influencing the development of the other. For example, if cerebritis was the first disease, aided by diabetes in poor control, then it is possible that the infection led to an endarteritis obliterans which resulted in the infarct.[2],[3],[4],[5],[6] This is supported by the fact that the angiogram showed only superficial occlusion of the M4 branches of the MCA as opposed to the truncal occlusion often seen with entire MCA terror infarcts. Against this theory is the fact that the patient did not suffer any symptoms of infection prior to the presentation of stroke nor can it be explained how he developed a de novo cerebritis as opposed to other organ system infections leading to a septicemia and eventual brain seeding.[3] The lack of meningeal infection is also difficult to explain.

Another theory is that the infarct came first. This led to the destruction of the blood–brain barrier and cell membranes of the neurons and glia presenting their content as fertile culture media to any bacterial organism around.[4],[5] The home management with aspiration coupled with uncontrolled diabetes in a debilitated old man could have led to a septicemia from the infected lungs which could then have seeded this infarcted brain leading to the cerebritis. This is supported by the fact that the blood counts, inflammatory markers, and signs of infection came later after the onset of the hemiparesis and obtundation. Against this is the fact that the MCA stem is patent with only distal M4 branches occluded. This can be explained by the fact that the patient was imaged after a week of the onset of occlusive symptoms, thereby giving enough time for spontaneous thrombolysis to occur without affecting the status of the infarcted brain.[6],[7] Early CT or magnetic resonance imaging (MRI) of the brain was not done in this case due to the unstable condition of the patient which needed urgent attention. Neither was he stable to tolerate an MRI nor could he tolerate IV contrast for a CT angiogram due to his renal failure. Hence, this aspect of our discussion although documented in literature is speculative.

Liquefactive necrosis often seen to resemble the appearance of pus was also considered.[8]

After the infarct is established, treatment options are limited. After decompressive craniotomy, supportive intensive care was provided. Despite the best antibiotic therapy, progression of the infection was seen. What could be perplexing is the nondevelopment of an abscess which is the usual step after a diffuse cerebritis. Brain abscess develops when a diffuse cerebritis changes to a focal inflammation and is eventually walled off into an abscess. The process usually takes 2–4 weeks. This was probably not seen in our patient due to extreme virulence of the organism coupled with uncontrolled diabetes and debilitation of the patient which led to a violent spread and prostration of the patient before such an abscess could be formed. The lack of inflammatory response also implies a degree of immunosuppression which can be explained due to the comorbidities listed above.[7],[8]

  Conclusion Top

Infective infarcts, although not common, are an increasingly difficult to detect in time resulting in major morbidity and mortality to the patient. Aggressive decompression coupled with antibiotic therapy ideally should help retard the progression and minimize the severity of the infection. In reality, however, multiple comorbidities coupled with moribund patients make brain parenchyma salvage a daunting prospect.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Wintermark M. Imaging recommendations for acute stroke and transient ischemic attack patients: A joint statement by the American Society of Neuroradiology, the American College of Radiology, and the Society of NeuroInterventional Surgery. AJNR Am J Neuroradiol 2013;34.11:E117-27.  Back to cited text no. 1
Mischel PS, Vinters HV. Coccidioidomycosis of the central nervous system: Neuropathological and vasculopathic manifestations and clinical correlates. Clini Infect Dis 1995;20:400-5.  Back to cited text no. 2
Torres-Miranda D, Al-Saffar F, Ibrahim S, Diaz-Font S. Rapid progressive seeding of a community acquired pathogen in an immune-competent host: End organ damage from head to bone. Infect Dis Rep 2015;7:5849.  Back to cited text no. 3
Carod-Artal FJ. Stroke in central nervous system infections. Ann Indian Acad Neurol 2008;11 Suppl S1:64-78.  Back to cited text no. 4
Chamorro A, Urra X, Planas AM. Infection after acute ischemic stroke: A manifestation of brain-induced immunodepression. Stroke 2007;38:1097-103.  Back to cited text no. 5
Hayes L, Malhotra P. Central nervous system infections masquerading as cerebrovascular accidents: Case series and review of literature. IDCases 2014;1:74-7.  Back to cited text no. 6
Kassem-Moussa H, Graffagnino C. Nonocclusion and spontaneous recanalization rates in acute ischemic stroke: A review of cerebral angiography studies. Arch Neurol 2002;59:1870-3.  Back to cited text no. 7
Adigun R, Basit H, Murray J. Cell Liquefactive Necrosis. In: Stat Pearls. Treasure Island (FL): Stat Pearls Publishing; 2020. https://www.ncbi.nlm.nih.gov/books/NBK430935/ [Last updated on 2020 Aug 10].  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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