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LETTER TO EDITOR  
Year : 2018  |  Volume : 60  |  Issue : 3  |  Page : 367-369
Olfactory groove meningioma masquerading as psychiatric disturbances


1 Department of Radiology, St. John's Medical College, Bengaluru, Karnataka, India
2 Department of Anatomy, St. John's Medical College, Bengaluru, Karnataka, India

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Date of Web Publication16-Oct-2018
 

How to cite this article:
Ravikanth R, Pinto DS, Mathew S. Olfactory groove meningioma masquerading as psychiatric disturbances. Indian J Psychiatry 2018;60:367-9

How to cite this URL:
Ravikanth R, Pinto DS, Mathew S. Olfactory groove meningioma masquerading as psychiatric disturbances. Indian J Psychiatry [serial online] 2018 [cited 2018 Nov 17];60:367-9. Available from: http://www.indianjpsychiatry.org/text.asp?2018/60/3/367/243383




Sir,

A 69-year-old male was brought by the family to the emergency department with a 10-month history of morning headaches, loss of smell bilaterally, memory loss, personality changes, and urinary incontinence. Blood investigations were normal. Magnetic resonance imaging (MRI) revealed 5.0 cm × 5.2 cm × 5.0 cm (AP × ML × CC) T1 isointense extra-axial lesion in the anterior cranial fossa showing diffusion restriction [Figure 1] and vivid contrast enhancement [Figures 2], [Figures 3], [Figures 4] arising from the olfactory groove with involvement of the nasal cavity and ethmoidal sinuses. A significant mass effect with cortical buckling and lateral displacement of the medial aspects of the frontal lobes with posterior displacement of the genu of the corpus callosum was noted. The frontal horns of the lateral ventricles were splayed by the mass. Computed tomography revealed white matter hypodensity in the frontal lobes representing vasogenic edema [Figure 5]. Imaging features were favoring olfactory groove meningioma (OGM). The patient was transferred to the neurosurgery department, where he underwent uneventful resection of the mass lesion through the bifrontal approach. Histopathological examination of the resected tissue showed moderately hypercellular meningioma with a well-developed syncytial architecture. Tumor cells had uniform nuclear features with no mitotic figures or areas of necrosis. There was broad attachment to the dura mater. The pathological diagnosis was confirmed as OGM. After the patient was discharged, he was given regular group and individual psychotherapy. Repeat brain MRI performed after 10 months of follow-up showed no recurrence of the tumor and all psychiatric symptoms had resolved.
Figure 1: Axial diffusion-weighted magnetic resonance imaging showing marked diffusion restriction of the mass lesion in the anterior cranial fossa

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Figure 2: Axial T1-weighted gadolinium-enhanced magnetic resonance imaging demonstrating an extra-axial mass in the anterior cranial fossa within the interhemispheric fissure, resulting in marked indentation of the medial aspect of the frontal lobes

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Figure 3: Coronal T1-weighted gadolinium-enhanced magnetic resonance imaging demonstrating a large, midline, and extra-axial lesion within the low frontal region, showing vivid contrast enhancement

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Figure 4: Sagittal T1-weighted gadolinium-enhanced magnetic resonance imaging showing tumor growth inferiorly through the cribriform plate into the ethmoid sinuses, posteriorly to involve the anterior clinoids and anterior to the tuberculum sellae

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Figure 5: Axial plain computed tomography image showing a well-defined lesion in the anterior cranial fossa with white matter hypodensity in bilateral frontal lobes representing vasogenic edema

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Meningiomas are the most common benign brain tumors accounting for 13%–26% of intracranial tumors.[1] The reported incidence is low because most meningiomas are asymptomatic. Meningiomas that compress the frontal lobes are notoriously “silent,” and are thus likely to be misdiagnosed or overlooked. Meningiomas originate from the arachnoid cap cells present intracranially in varying sites. OGMs comprise 4%–10% of the intracranial meningiomas.[2] OGMs arise in the midline over the cribriform plate and frontosphenoidal suture between the crista galli and the tuberculum sellae. They are diagnosed when they cause mental disturbances and visual field defects because of its great size.[3] MRI is the modality of choice for the investigation of meningiomas, providing superior contrast differentiation and the ability to differentiate between intra-axial and extra-axial lesions. The frequent invasion of the paranasal sinuses, the possibility of cerebrospinal fluid leak, and infections are the major challenges for their surgical treatment. The goal of OGM surgery should be radical resection. Hyperostotic bone and sinus invasion are not limitations. The extent of resection of tumor invading the cranial base is associated with the recurrence rate. The recurrence rate of OGMs ranges from 5% to 41%.[4]

Frontal tumors may produce incontinence of urine and feces, to which the patient may be indifferent as part of his general self-neglect; however, at an earlier stage, they may result in frequency and precipitancy of micturition.[5] Brain tumors can cause any type of psychiatric symptoms. Rarely, brain tumors can present with psychiatric symptoms without any localizing signs. It is important for clinicians to have an index of suspicion of brain tumor in patients with new-onset psychiatric symptoms, atypical presentations, and treatment resistance.[6] Psychiatric symptoms may be the only clue to the presence of a brain tumor. Benign tumors, such as meningiomas that compress the frontal lobes from the outside, may not produce any symptoms other than progressive change of personality and intellect until they are large. It is important to conduct a detailed physical, neurologic, and psychiatric examination. Patients with such tumors are often referred first to psychiatrists, and the correct diagnosis may emerge only when the tumor has grown large and has begun to displace the brain. Patients who present with these features should be screened using computed tomography or MRI to detect possible intracranial lesions (e.g., tumors, subdural hematomas, and hydrocephalus) or diseases (e.g., cerebrovascular disease) that may cause or contribute to frontal lobe syndrome.[7]

Anatomical location of the tumor is an important factor in determining the nature and severity of neuropsychiatric symptoms. When a patient with no history of psychiatric disease develops a slow and progressive psychological change or atypical psychiatric presentations, organic brain lesion should be considered in the diagnosis, and brain imaging should be considered further.

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.
Maurice-Williams RS, Dunwoody G. Late diagnosis of frontal meningiomas presenting with psychiatric symptoms. Br Med J (Clin Res Ed) 1988;296:1785-6.  Back to cited text no. 1
    
2.
Babu R, Barton A, Kasoff SS. Resection of olfactory groove meningiomas: Technical note revisited. Surg Neurol 1995;44:567-72.  Back to cited text no. 2
    
3.
Cushing H, Eisenhardt L, editors. The olfactory groove meningiomas with primary anosmia. In: Meningiomas. Springfield, IL: Charles C Thomas; 1938. p. 250-82.  Back to cited text no. 3
    
4.
Mirimanoff RO, Dosoretz DE, Linggood RM, Ojemann RG, Martuza RL. Meningioma: Analysis of recurrence and progression following neurosurgical resection. J Neurosurg 1985;62:18-24.  Back to cited text no. 4
    
5.
Gupta RK, Kumar R. Benign brain tumours and psychiatric morbidity: A 5-years retrospective data analysis. Aust N Z J Psychiatry 2004;38:316-9.  Back to cited text no. 5
    
6.
Butler C, Zeman AZ. Neurological syndromes which can be mistaken for psychiatric conditions. J Neurol Neurosurg Psychiatry 2005;76 Suppl 1:i31-8.  Back to cited text no. 6
    
7.
Oude Elberink AM, Oudijn MS, Kwa VI, Van HL. 'Histrionic personality disorder with regression and conversion': A meningioma. Tijdschr Psychiatr 2011;53:371-6.  Back to cited text no. 7
    

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Correspondence Address:
Reddy Ravikanth
Department of Radiology, St. John's Medical College, Bengaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/psychiatry.IndianJPsychiatry_267_17

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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