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CME QUIZ
Year : 2019  |  Volume : 17  |  Issue : 4  |  Page : 152-154

Status epilepticus secondary to meningioma


Department of Neurology, Federal University of Santa Maria, Santa Maria, Rio Grande Do Sul, Brazil

Date of Submission18-Jan-2019
Date of Decision23-Aug-2019
Date of Acceptance25-Aug-2019
Date of Web Publication11-Dec-2019

Correspondence Address:
Mr. Jamir Pitton Rissardo
Rua Elpídio De Menezes, 195, Santa Maria, Rio Grande Do Sul
Brazil
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_2_19

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How to cite this article:
Rissardo JP, Caprara AL. Status epilepticus secondary to meningioma. Curr Med Issues 2019;17:152-4

How to cite this URL:
Rissardo JP, Caprara AL. Status epilepticus secondary to meningioma. Curr Med Issues [serial online] 2019 [cited 2020 Aug 13];17:152-4. Available from: http://www.cmijournal.org/text.asp?2019/17/4/152/272796




  case Scenario Top


A 73-year-old male with left upper limb shaking was admitted to our hospital with 12 h of onset. His son reported that the patient started having abnormal movement of the left upper limb lasting up to 2 min followed by a 30-min seizure-free interval till the next episode started. However, the son mentioned that the time between the episodes started to shorten, until the time the patient did not recover consciousness and was producing the movements repetitively. The patient worked as a farmer, and his family history was negative for neurological diseases. His comorbid conditions were dyslipidemia and essential hypertension. He was under the use of simvastatin, carvedilol, and amlodipine. The neurological examination is shown in Video 1. Concomitant alterations were left hyperreflexia and plantar extension. A noncontrast cranial computed tomography scan was performed [Figure 1].
Figure 1: Noncontrast cranial computed tomography scan.

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  Questions Top


  1. What are the findings in the noncontrast cranial computed tomography scan?
  2. Describe the findings shown on the neurological examination
  3. What is the most likely diagnosis taking into account this clinical scenario?
  4. What is the management of this condition?
  5. Which differential diagnoses are possible?



  Answers Top


  1. The axial view of noncontrast cranial computed tomography reveals a hyperdense and calcified lesion associated with slight hyperostosis [Figure 2][1]
  2. The neurological examination shows clonic movements in the left upper limb [2]
  3. Status epilepticus (SE) secondary to meningioma.
Figure 2: Arrow points to the meningioma.

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  Pathophysiology Top


Meningioma, the most frequent primary brain tumor, is an extra-axial tumor that originates from arachnoid meningothelial cells.[3],[4] This type of tumor has diverse localization, histology, and molecular biology. In this context, it could be classified according to the World Health Organization's schema, which is based on morphologic features. This system divides meningioma into the following three groups: grade I are benign with a favorable prognosis, Grade II are atypical, and Grade III are malignant.[5] However, an accurate specification of these tumors by genetic and molecular markers is necessary as the clinical value is limited, and there is no optimal interobserver agreement when only morphologic criteria are used.[5]

A seizure is one of the most common symptoms of brain tumors, which occurs probably due to local compression, and it is present in half of the patients.[4] Furthermore, a brain tumor such as a meningioma can present with SE that “is a condition characterized by an epileptic seizure that is sufficiently prolonged or repeated at sufficiently brief intervals so as to produce an unvarying and enduring epileptic condition.”[2],[6]


  Diagnosis and Investigation Top


The diagnosis of SE is based on clinical features. The Commission on Classification and Terminology and the Commission on Epidemiology of the International League Against Epilepsy (ILAE) charged a task force to revise the concepts, definition, and classification of SE in 2015.[2] The ILAE suggested the operational criteria for SE, which is presented in [Table 1].[2] The meningioma is diagnosed definitively with histologic confirmation. However, the association between history, physical examination, laboratory tests, and neuroimaging provides a useful diagnosis for empiric treatment [Table 1].[7]
Table 1: The International League Against Epilepsy task force to revise concepts, definition, and classification of status epilepticus

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4. SE management [7]

First, the initial assessment should stabilize the patient, which is as follows:

  1. General evaluation including vital signs with attention to respiratory and circulatory systems
  2. Attempt intravenous (IV) access and request laboratory tests
  3. Finger-stick glucose.


Second, the initial therapy. A benzodiazepine is the initial therapy of choice. If IV access is available, the choice is lorazepam 0.1 mg/kg or diazepam 0.15 mg/kg. Without IV access, midazolam 10 mg intramuscularly can be administered.

Third, the second therapy. There is no evidence for the second therapy of choice. Choose one among fosphenytoin 20 mg/kg, valproic acid 30 mg/kg, and levetiracetam 60 mg/kg, as proposed by Glauser et al.[7]


  Meningioma Management Top


Factors such as age, comorbidities, and presence of symptoms determine the management of known or presumed benign meningioma. In this context, surgical resection is preferred when the meningioma is an accessible location and is infiltrating, large, symptomatic, or associated with important edema. However, when the tumor is asymptomatic, small, and without edema, a careful observation may be done.[1] In addition, radiation therapy could be used as empiric therapy after surgery or when the meningioma is nonresectable but should be analyzed on a case-by-case basis.[5]

5. The differential diagnosis of SE should include alcohol-related SE, autoimmune disorders, central nervous system infections, cerebral hypoxia or anoxia, cerebrovascular diseases, chromosomal aberrations and genetic abnormalities, cortical dysplasias, head trauma, intoxication, other intracranial tumors, metabolic disorders and disturbances, mitochondrial diseases, neurocutaneous syndromes, neurodegenerative diseases, and withdrawal of or low levels of antiepileptic drugs.[2] It is important to know the differential in order to do the necessary and appropriate investigations.[7]

In [Table 2], the differential diagnosis of meningioma is based on main dural masses, location, and hyperostosis.[1],[3],[5]
Table 2: Differential diagnosis of meningioma

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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

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Chourmouzi D, Potsi S, Moumtzouoglou A, Papadopoulou E, Drevelegas K, Zaraboukas T, et al. Dural lesions mimicking meningiomas: A pictorial essay. World J Radiol 2012;4:75-82.  Back to cited text no. 1
    
2.
Trinka E, Cock H, Hesdorffer D, Rossetti AO, Scheffer IE, Shinnar S, et al. A definition and classification of status epilepticus – report of the ILAE task force on classification of status epilepticus. Epilepsia 2015;56:1515-23.  Back to cited text no. 2
    
3.
Pieper DR, Al-Mefty O, Hanada Y, Buechner D. Hyperostosis associated with meningioma of the cranial base: Secondary changes or tumor invasion. Neurosurgery 1999;44:742-6.  Back to cited text no. 3
    
4.
Cavaliere R, Farace E, Schiff D. Clinical implications of status epilepticus in patients with neoplasms. Arch Neurol 2006;63:1746-9.  Back to cited text no. 4
    
5.
Euskirchen P, Peyre M. Management of meningioma. Presse Med 2018;47:e245-52.  Back to cited text no. 5
    
6.
Annegers JF, Schoenberg BS, Okazaki H, Kurland LT. Epidemiologic study of primary intracranial neoplasms. Arch Neurol 1981;38:217-9.  Back to cited text no. 6
    
7.
Glauser T, Shinnar S, Gloss D, Alldredge B, Arya R, Bainbridge J, et al. Evidence-based guideline: Treatment of convulsive status epilepticus in children and adults: Report of the guideline committee of the American Epilepsy Society. Epilepsy Curr 2016;16:48-61.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2]



 

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