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nerve. Since the afferent fibers of the lingual nerve travel in the hypoglossal nerve,[3] there is a possibility that they may also possess connections with the C2 spinal nerve roots. The greater and lesser occipital nerve also arise from the second spinal nerve. The steroid block for the occipital neuralgia stabilized the transmission of impulses within the related interconnected nerves including the occipital nerve, the C2 spinal nerve root, the hypoglossal and the lingual nerve (the latter containing the afferent fibers from the chorda tympani nerve that carry taste sensations from the anterior two‑thirds of the tongue) leading to improvement in dysgeusia.[3,8] Post‑traumatic misdirectional regeneration of facial nerve fibers can result in a cross‑talk between the facial nerve and the cervical plexus (and the occipital nerve in particular).[8] Suppression of these direct interneural connections by an occipital block could have resulted in the recovery of the dysgeusia. In conclusion, occipital nerve block may be effective in the resolution of traumatic dysgeusia; however, the mechanism of action is unclear. Further in‑depth studies are required to assess the role of occipital nerve block in the amelioration of dysgeusia.
Acknowledgments We would like to extend our appreciation to the patient for allowing us to carry out this work and to all those who participated in her interdisciplinary care.
Vaibhav Rastogi, Atish Patel, Abhishek D. Lunagariya, Vishnumurthy Shushrutha Hedna Department of Neurology, University of Florida, Florida, United States E‑mail: [email protected]
References 1. 2.
3. 4. 5. 6. 7.
8.
260
Spielman AI. Chemosensory function and dysfunction. Crit Rev Oral Biol Med 1998;9:267‑91. Morris GK, Michael S. Occipital nerve block. Comprehensive treatment of chronic pain by medical, interventional, and integrative approaches. New York: Springer; 2013. p. 309‑17. Borody C. Neck‑tongue syndrome. J Manipulative Physiol Ther 2004;27:e8. Frank ME. Taste‑responsive neurons of the glossopharyngeal nerve of the rat. J Neurophysiol 1991;65:1452‑63. Strauss L, Loder E, Rizzoli P. Transient facial nerve palsy after occipital nerve block: A case report. Headache 2014;54:1651‑5. Elston JS. Traumatic third nerve palsy. Br J Ophthalmol 1984;68:538‑43. de Ruiter GC, Spinner RJ, Verhaagen J, Malessy MJ. Misdirection and guidance of regenerating axons after experimental nerve injury and repair. J Neurosurg 2014;120:493‑501. Chen JM, Bodmer D, Khetani JD, Lin VV. Tactile dysgeusia: A new clinical observation of middle ear and skull base surgery. Laryngoscope 2008;118:99‑103.
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Meningeal melanocytoma of the middle cranial fossa (the Meckel’s cave) Sir, Primary meningeal melanocytoma of the middle cranial fossa is extremely rare. A 29‑year‑old lady presented with a 3‑year history of headache associated with a 4‑month history of diplopia and left facial numbness. On neurological examination, she had impairment of sensations in the entire left trigeminal nerve distribution, loss of corneal reflex, left masseteric weakness, and left VIth nerve palsy. On magnetic resonance imaging (MRI), a dumbbell mass was detected invading the left middle cranial fossa reaching upto the ipsilateral cavernous sinus and extending posteriorly into the cerebellopontine angle (CPA) compressing the brain‑stem. The tumor was demonstrated as a hyperintense lesion on T1‑weighted imaging (T1WI) and a hypointense lesion on T2‑weighted imaging (T2WI) [Figure 1] with no perilesional edema. The contrast‑enhanced MRI scan showed that the lesion was heterogeneously enhancing. A temporal craniotomy and a subtemporal approach was performed for tumor excision. A well‑circumscribed lesion with a gritty texture was located at the base of the middle cranial fossa, sandwiched between the two layers of dura [Figure 2]. The entire left Meckel's cave was covered by a dark pigmented material tightly adherent to the trigeminal ganglion and was difficult to peel off from it.The majority of the tumor was removed and a small portion densely adherent to the dura left in situ. A subsequent physical examination did not reveal any other cutaneous melanoma. On immunohistochemistry, a few tumor cells were found surrounded by numerous dark pigmented granules [Figure 3]. The melanocytic feature, Melan‑A and S‑100 protein
Neurology India / March 2015 / Volume 63 / Issue 2
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Letters to Editor
diplopia and left facial numbness still persisted at a follow up of one‑and‑a‑half years.
Figure 1: The lesion was demonstrated as a hypointense mass on T2 weighted imaging (T2WI)
Figure 2: Intraoperative photographs showing a well-circumscribed lesion with gritty texture located at the base of middle cranial fossa, sandwiched between the two layers of dura
Primary meningeal melanocytoma is a slow‑growing benign tumor of the central nervous system, which was first defined by Limas and Tio in 1972. [1] The tumor occurs in about 1 person per 10 million with a female predominance.[2] Although the number of cases is limited, there is a predilection of meningeal melanocytomas to occur in the spinal cord, especially the thoracic cord.[3] Primary meningeal melanocytoma occuring in the middle cranial fossa is extremely rare, and only a few cases have been reported in the literature. When occurring at atypical sites, the tumor is often misdiagnosed on radiology as a meningioma. In this case, the tumor was initially diagnosed as a trigeminal neurinoma. Although a meningeal melanocytoma is a benign neoplasm, its frequent relapse and malignant transition have often been described in the literature. In 2011, Wang reported a malignant transformation in a supratentorial meningeal melanocytoma that recurred after 3 years as a malignant melanoma. [4] Due to the possibility of its malignant transformation into a melanoma, meningeal melanocytoma should be subjected to total excision, if feasible. Radiotherapy is considered as a vital adjunctive therapy. Yanming Ren, Anqi Xiao, Xia Wu1, Yuekang Zhang Departments of Neurosurgery, and 1Pathology, West China Hosptial, China E‑mail: [email protected]
References 1.
2. 3.
4. Figure 3: Haematoxylin and eosin, ×40: A few tumor cells with abundant pigmented granules
were positive, while epithelial membrane antigen (EMA), calretinin (CR) and D2‑40 were negative. Cellular proliferation was assessed by evaluating the Ki‑67 which appeared weakly positive (less than 1%). Based on the pathological results, the tumor was adjudged as World Health Organization (WHO) grade I (low grade) tumor. After surgery, the patient received radiation therapy. The postoperative magnetic resonance imaging after six months revealed no tumor recurrence. The
Limas C, Tio FO. Meningeal melanocytoma (“melanotic meningioma”). Its melanocytic origin as revealed by electron microscopy. Cancer 1972;30:1286‑94. Liubinas SV, Maartens N, Drummond KJ. Primary melanocytic neoplasms of the central nervous system. J Clin Neurosci 2010;17:1227‑32. Aimar E, Debernardi A, Tancioni F, Di Leva A, Bossi P, Gaetani P, et al. Meningeal melanocytoma of the temporal lobe. An uncommon tumor in an unusual location. Case report. J Clin Neurosci 2003;47:211‑14 Wang F, Qiao G, Lou X, Song X, Chen W. Malignant transformation of intracranial meningeal melanocytoma. Case report and review of the literature. Neuropathology 2011;31:414‑20.
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www.neurologyindia.com DOI: 10.4103/0028-3886.156300 PMID: xxxxx
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Letters to Editor
nerve. Since the afferent fibers of the lingual nerve travel in the hypoglossal nerve,[3] there is a possibility that they may also possess connections with the C2 spinal nerve roots. The greater and lesser occipital nerve also arise from the second spinal nerve. The steroid block for the occipital neuralgia stabilized the transmission of impulses within the related interconnected nerves including the occipital nerve, the C2 spinal nerve root, the hypoglossal and the lingual nerve (the latter containing the afferent fibers from the chorda tympani nerve that carry taste sensations from the anterior two‑thirds of the tongue) leading to improvement in dysgeusia.[3,8] Post‑traumatic misdirectional regeneration of facial nerve fibers can result in a cross‑talk between the facial nerve and the cervical plexus (and the occipital nerve in particular).[8] Suppression of these direct interneural connections by an occipital block could have resulted in the recovery of the dysgeusia. In conclusion, occipital nerve block may be effective in the resolution of traumatic dysgeusia; however, the mechanism of action is unclear. Further in‑depth studies are required to assess the role of occipital nerve block in the amelioration of dysgeusia.
Acknowledgments We would like to extend our appreciation to the patient for allowing us to carry out this work and to all those who participated in her interdisciplinary care.
Vaibhav Rastogi, Atish Patel, Abhishek D. Lunagariya, Vishnumurthy Shushrutha Hedna Department of Neurology, University of Florida, Florida, United States E‑mail: [email protected]
References 1. 2.
3. 4. 5. 6. 7.
8.
260
Spielman AI. Chemosensory function and dysfunction. Crit Rev Oral Biol Med 1998;9:267‑91. Morris GK, Michael S. Occipital nerve block. Comprehensive treatment of chronic pain by medical, interventional, and integrative approaches. New York: Springer; 2013. p. 309‑17. Borody C. Neck‑tongue syndrome. J Manipulative Physiol Ther 2004;27:e8. Frank ME. Taste‑responsive neurons of the glossopharyngeal nerve of the rat. J Neurophysiol 1991;65:1452‑63. Strauss L, Loder E, Rizzoli P. Transient facial nerve palsy after occipital nerve block: A case report. Headache 2014;54:1651‑5. Elston JS. Traumatic third nerve palsy. Br J Ophthalmol 1984;68:538‑43. de Ruiter GC, Spinner RJ, Verhaagen J, Malessy MJ. Misdirection and guidance of regenerating axons after experimental nerve injury and repair. J Neurosurg 2014;120:493‑501. Chen JM, Bodmer D, Khetani JD, Lin VV. Tactile dysgeusia: A new clinical observation of middle ear and skull base surgery. Laryngoscope 2008;118:99‑103.
Access this article online Website:
Quick Response Code
www.neurologyindia.com DOI: 10.4103/0028-3886.156298 PMID: xxxxx
Meningeal melanocytoma of the middle cranial fossa (the Meckel’s cave) Sir, Primary meningeal melanocytoma of the middle cranial fossa is extremely rare. A 29‑year‑old lady presented with a 3‑year history of headache associated with a 4‑month history of diplopia and left facial numbness. On neurological examination, she had impairment of sensations in the entire left trigeminal nerve distribution, loss of corneal reflex, left masseteric weakness, and left VIth nerve palsy. On magnetic resonance imaging (MRI), a dumbbell mass was detected invading the left middle cranial fossa reaching upto the ipsilateral cavernous sinus and extending posteriorly into the cerebellopontine angle (CPA) compressing the brain‑stem. The tumor was demonstrated as a hyperintense lesion on T1‑weighted imaging (T1WI) and a hypointense lesion on T2‑weighted imaging (T2WI) [Figure 1] with no perilesional edema. The contrast‑enhanced MRI scan showed that the lesion was heterogeneously enhancing. A temporal craniotomy and a subtemporal approach was performed for tumor excision. A well‑circumscribed lesion with a gritty texture was located at the base of the middle cranial fossa, sandwiched between the two layers of dura [Figure 2]. The entire left Meckel's cave was covered by a dark pigmented material tightly adherent to the trigeminal ganglion and was difficult to peel off from it.The majority of the tumor was removed and a small portion densely adherent to the dura left in situ. A subsequent physical examination did not reveal any other cutaneous melanoma. On immunohistochemistry, a few tumor cells were found surrounded by numerous dark pigmented granules [Figure 3]. The melanocytic feature, Melan‑A and S‑100 protein
Neurology India / March 2015 / Volume 63 / Issue 2
[Downloaded free from http://www.neurologyindia.com on Thursday, May 07, 2015, IP: 61.16.135.116]
Letters to Editor
diplopia and left facial numbness still persisted at a follow up of one‑and‑a‑half years.
Figure 1: The lesion was demonstrated as a hypointense mass on T2 weighted imaging (T2WI)
Figure 2: Intraoperative photographs showing a well-circumscribed lesion with gritty texture located at the base of middle cranial fossa, sandwiched between the two layers of dura
Primary meningeal melanocytoma is a slow‑growing benign tumor of the central nervous system, which was first defined by Limas and Tio in 1972. [1] The tumor occurs in about 1 person per 10 million with a female predominance.[2] Although the number of cases is limited, there is a predilection of meningeal melanocytomas to occur in the spinal cord, especially the thoracic cord.[3] Primary meningeal melanocytoma occuring in the middle cranial fossa is extremely rare, and only a few cases have been reported in the literature. When occurring at atypical sites, the tumor is often misdiagnosed on radiology as a meningioma. In this case, the tumor was initially diagnosed as a trigeminal neurinoma. Although a meningeal melanocytoma is a benign neoplasm, its frequent relapse and malignant transition have often been described in the literature. In 2011, Wang reported a malignant transformation in a supratentorial meningeal melanocytoma that recurred after 3 years as a malignant melanoma. [4] Due to the possibility of its malignant transformation into a melanoma, meningeal melanocytoma should be subjected to total excision, if feasible. Radiotherapy is considered as a vital adjunctive therapy. Yanming Ren, Anqi Xiao, Xia Wu1, Yuekang Zhang Departments of Neurosurgery, and 1Pathology, West China Hosptial, China E‑mail: [email protected]
References 1.
2. 3.
4. Figure 3: Haematoxylin and eosin, ×40: A few tumor cells with abundant pigmented granules
were positive, while epithelial membrane antigen (EMA), calretinin (CR) and D2‑40 were negative. Cellular proliferation was assessed by evaluating the Ki‑67 which appeared weakly positive (less than 1%). Based on the pathological results, the tumor was adjudged as World Health Organization (WHO) grade I (low grade) tumor. After surgery, the patient received radiation therapy. The postoperative magnetic resonance imaging after six months revealed no tumor recurrence. The
Limas C, Tio FO. Meningeal melanocytoma (“melanotic meningioma”). Its melanocytic origin as revealed by electron microscopy. Cancer 1972;30:1286‑94. Liubinas SV, Maartens N, Drummond KJ. Primary melanocytic neoplasms of the central nervous system. J Clin Neurosci 2010;17:1227‑32. Aimar E, Debernardi A, Tancioni F, Di Leva A, Bossi P, Gaetani P, et al. Meningeal melanocytoma of the temporal lobe. An uncommon tumor in an unusual location. Case report. J Clin Neurosci 2003;47:211‑14 Wang F, Qiao G, Lou X, Song X, Chen W. Malignant transformation of intracranial meningeal melanocytoma. Case report and review of the literature. Neuropathology 2011;31:414‑20.
Access this article online Website:
Quick Response Code
www.neurologyindia.com DOI: 10.4103/0028-3886.156300 PMID: xxxxx
Neurology India / March 2015 / Volume 63 / Issue 2
261
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
