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Table of Contents    
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1712-1713

Ruptured Intracranial Dermoid Cyst – Unusual Cause of Obstructive Hydrocephalus

Department of Radiodiagnosis, VMMC and Safdarjung Hospital, New Delhi, India

Date of Submission21-May-2020
Date of Decision17-Aug-2020
Date of Acceptance27-Sep-2021
Date of Web Publication30-Aug-2022

Correspondence Address:
Ankita Aggarwal
Department of Radiodiagnosis, VMMC and Safdarjung Hospital, Ansari Nagar East, Near AIIMS Metro Station, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.355165

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How to cite this article:
Jain P, Aggarwal A, Jain SG, Jain S. Ruptured Intracranial Dermoid Cyst – Unusual Cause of Obstructive Hydrocephalus. Neurol India 2022;70:1712-3

How to cite this URL:
Jain P, Aggarwal A, Jain SG, Jain S. Ruptured Intracranial Dermoid Cyst – Unusual Cause of Obstructive Hydrocephalus. Neurol India [serial online] 2022 [cited 2022 Oct 2];70:1712-3. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1712/355165


A 35-year-old gentleman presented to the ER with complaints of seizures and loss of consciousness. Past history of headaches and memory loss was present. Noncontrast CT Brain revealed a well-circumscribed fat attenuation lesion measuring 3 × 4.7 × 3 cm3 (AP × TR × CC) in the left anterior temporal extra-axial space with focal wall calcifications [Figure 1]a. Additionally, multiple such fat attenuating and calcific foci were seen in bilateral subarachnoid cisternal and sulcal spaces [Figure 1]b and [Figure 1]c. Gross obstructive hydrocephalus was seen with transition at foramen at Monro and fat-CSF levels in both lateral ventricles [Figure 1]d. Features of raised intracranial pressure, including diffuse effacement of sulcal spaces and cisterns, and bilateral uncal herniations were seen [Figure 1]e and [Figure 1]f. Final diagnosis of “ruptured dermoid cyst (DC) causing acute obstructive hydrocephalus with raised intracranial pressure” was given. The patient underwent emergency ventriculoperitoneal (VP) shunt surgery for CSF diversion and the postoperative period was uneventful.
Figure 1: NCCT-Brain Axial image (a) Fat attenuation lesion in left anterior temporal extra-axial space with wall calcifications (red arrow) causing scalloping of the temporal bone (yellow arrow). MinIP-Axial image (b) Subarachnoid extension of fat foci with fat-CSF levels in lateral ventricles. Coronal image (c) Fat foci with calcifications in bilateral periventricular regions (yellow-arrows) Mid-sagittal image (d) Narrowing at the level of the foramen of Monro with inferior descent of pineal gland (red arrow). Axial sections (e and f) Effacement of sulci and cisterns and bilateral uncal herniations (red arrowheads)

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Intracranial DCs are rare, benign, slow-growing lesions derived from the inclusion of ectodermally committed cells during neural tube closure. DCs are much less common than epidermoids and occur in a younger age group, around the second and third decades.[1],[2],[3] They are usually extra-axial midline lesions, with common intracranial sites being the suprasellar cistern, posterior fossa, and frontonasal region.[1],[3],[4] Lumbosacral region is the most common site for spinal DCs.[3] Most remain asymptomatic until rupture,[1],[2] with symptoms arising due to its irritative or compressive effects.[3] DC rupture commonly results in chemical meningitis causing communicating hydrocephalus.[1],[3],[4] Other complications include vasospasm, infarction, and even death.[1],[2],[3]

On CT, DCs appear intensely hypodense with predominant fat attenuation due to lipid content.[1],[2],[3],[4] Presence of hair, calcification, and debris can cause heterogeneity. Approximately 20% of cases show calcifications in capsule.[1],[2] Cyst rupture dissemination of fat droplets is seen in the cortical and cisternal subarachnoid spaces and as fat-CSF levels in the ventricles.[1],[2],[4]

On MRI, DCs are hyperintense on T1WI, with signal intensity on T2WI varying depending on cyst contents.[1],[2],[3],[4] Signal heterogeneity with linear or striated laminations may represent the presence of hair within the cyst. Ruptured DCs demonstrate sulcal FLAIR hyperintensity and bloom on GRE/SWI sequences.[1]

Most DCs do not enhance,[1],[3],[4] though leptomeningeal enhancement may be seen with ruptured DCs.[1],[2]

Close differentials include epidermoid, lipoma, teratoma, and craniopharyngioma.[1],[2]

Complete surgical resection of the cyst is the goal as recurrence rates are low.[1],[2],[3]

Presentation of obstructive hydrocephalus in our case is highly unusual as ruptured DCs more commonly present with communicating hydrocephalus secondary to chemical meningitis.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Osborn AG, Hedlund GL, Salzman KL. Nonneoplastic Cysts. Osborn's Brain: Imaging, Pathology, and Anatomy. 2nd ed. Salt Lake City, Utah: Elsevier; 2018. p. 877-9.  Back to cited text no. 1
Jacków J, Tse G, Martin A, Sąsiadek M, Romanowski C. Ruptured intracranial dermoid cysts: A pictorial review. Pol J Radiol 2018;83:465-70.  Back to cited text no. 2
Prasad GL, Sinha S, Krishna G. Rupture of spinal dermoid cyst with intracranial dissemination: Report of a case and review of the literature. Neurol India 2018;66:1195-9.  Back to cited text no. 3
[PUBMED]  [Full text]  
Rai SP. Ruptured intracranial dermoid cyst. Neurol India 2009;57:98-9.  Back to cited text no. 4
[PUBMED]  [Full text]  


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