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LETTER TO EDITOR
Year : 2014  |  Volume : 62  |  Issue : 1  |  Page : 104-105

Calcified cavernous malformation of the lower cranial nerves


1 Department of Neurosurgery, Christian Medical College, Vellore, Tamil Nadu, India
2 Department of Neuropathology, Christian Medical College, Vellore, Tamil Nadu, India

Date of Submission18-Jan-2014
Date of Decision24-Jan-2014
Date of Acceptance24-Jan-2014
Date of Web Publication7-Mar-2014

Correspondence Address:
Krishna Prabhu
Department of Neurosurgery, Christian Medical College, Vellore, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.128358

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How to cite this article:
Nair BR, Prabhu K, Chacko G, Chacko AG. Calcified cavernous malformation of the lower cranial nerves. Neurol India 2014;62:104-5

How to cite this URL:
Nair BR, Prabhu K, Chacko G, Chacko AG. Calcified cavernous malformation of the lower cranial nerves. Neurol India [serial online] 2014 [cited 2019 Sep 18];62:104-5. Available from: http://www.neurologyindia.com/text.asp?2014/62/1/104/128358


Sir,

Cavernous malformations (CMs) account for 10-15% of all vascular malformations of central nervous system [1] and mostly supratentorial intraparenchymal lesions. Extra axial cavernomas involving the cranial nerves are extremely rare and are seen mostly seen in relation to optic nerves or VII-VIII nerves. [1] Only two cases involving the lower cranial nerves had been reported in the literature, [2] hence this report.

A 59-year-old male patient presented with hoarseness of voice, difficulty in swallowing with nasal regurgitation for 5 months and mild hearing loss in the right ear for 3 months duration. He had a grade 2 House and Brackman facial paresis, mild sensorineural hearing loss and impaired gag reflex on the right side. A computed tomography scan showed a 16 mm × 15 mm hyperdense lesion in the right cerebellopontine (CP) angle cistern. The lesion was on magnetic resonance imaging hypointense on T2W and hyperintense on T1W sequence and susceptibility weighted imaging sequence showed a hemosiderin staining along the periphery of the lesion [Figure 1]a and b. The lesion abutted 7/8 th nerve roots with no intracanalicular extension and splayed the lower cranial nerves on right side. Angiography ruled out the possibility of a thrombosed aneurysm. With a clinical diagnosis of a CM, he underwent a right retromastoid suboccipital craniectomy and there was a well-defined greyish lesion seen in the CP angle region with xanthochromia of the adjacent cerebellum. There was compression of lower cranial nerves inferiorly by the lesion and was dorsal to the VII/VIII nerve complex [Figure 1]c. The lesion had a capsule and contained dark brownish, firm and old partially calcified clot. After opening the capsule, calcified clot was removed in piecemeal with forceps. Capsule had a good plane with middle cerebellar peduncle and VII/VIII nerve complex. The lesion was totally excised. Histopathologic examination revealed several ectatic closely packed hyalinized blood vessels lined by endothelial cells, containing blood, consistent with diagnosis of a CM. There were foci of calcification within the walls of blood vessels [Figure 1]d. Post-operatively his lower cranial nerve function remained same and was advised to undergo a percutaneous endoscopic gastrostomy for feeding.
Figure 1: Magnetic resonance imaging brain T2W axial image showing a hypointense mass (a) and ring of calcifi cation in susceptibility weighted imaging axial image (b). (c) The cavernoma abutting the lower cranial nerves (arrow). (d) The photomicrograph of the hemangioma highlighting the ectatic vascular channels with foci of calcifi cation (arrow) seen on
biopsy (H and E, ×90)


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CMs are mulberry-like conglomeration of thin walled vascular sinusoids lined by a thin endothelium lacking smooth muscle and elastin, displaying no intervening brain parenchyma, surrounded by hemosiderin deposits and gliosis, which may or may not be thrombosed. [3] There have been reports of CMs involving various cranial nerves [2] such as optic nerve (21 cases), CP-angle (26 cases), oculomotor (4 cases), trochlear (3 cases) and lower cranial nerves (2 cases) Extra-axial CM is generally believed to arise from a capillary plexus associated with the dura mater or the vascular plexus associated with the cranial nerve. [4] Though CP-angle CMs have been reported more frequently, only two cases of lower cranial nerve CMs are reported in the literature, [2] of which one has been a calcified CM. [2] The cranial nerve CMs frequently present with cranial nerve deficits. In our patient, the operative finding of xanthochromia point toward bleed in the past. Though surgical decompression was required in optic nerve CMs, to preserve vision from bleeding, no definite treatment guidelines exist for other cranial nerve CMs. Resection may be required in patients with bleed, increase in size in serial imaging or in those with deficits.

 
  References Top

1.Batra S, Lin D, Recinos PF, Zhang J, Rigamonti D. Cavernous malformations: Natural history, diagnosis and treatment. Nat Rev Neurol 2009;5:659-70.  Back to cited text no. 1
    
2.Albanese A, Sturiale CL, D′Alessandris QG, Capone G, Maira G. Calcified extra-axial cavernoma involving lower cranial nerves: Technical case report. Neurosurgery 2009;64:onsE135-6.  Back to cited text no. 2
    
3.Raychaudhuri R, Batjer HH, Awad IA. Intracranial cavernous angioma: A practical review of clinical and biological aspects. Surg Neurol 2005;63:319-28.  Back to cited text no. 3
    
4.Adachi K, Yoshida K, Akiyama T, Kawase T. Cavernous angioma of the vestibular nerve: Case report and literature review. Surg Neurol 2008;70:82-6.  Back to cited text no. 4
    


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