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2.
Jao T, Liu HM, Tang SC, Jeng JS. Dissection of the posterior inferior cerebellar artery in a young adult with cerebellar infarct. Acta Neurol Taiwan 2008;17;243-47. 3. Kwak YS, Kang DH, Woo HJ. Simultaneous vertebral artery dissection and contralateral posterior inferior cerebellar artery dissecting aneurysm. J Cerebrovasc Endovasc Neurosurg. 2012;14:228-32. 4. Mizushima H, Sasaki K, Kunii N, Nishino T, Jinbo H, Abe T, et al. Dissecting aneurysm in the proximal region of the posterior inferior cerebellar artery presenting as Wallenberg’s syndrome. Case report. Neuro l Med Chir (Tokyo) 1994;34:307-10. 5. Niijima K. Dissecting aneurysm of the vertebral artery with an accessory posterior inferior cerebellar artery: Successful management with clipping between the two posterior inferior cerebellar arteries. Cerebrovasc Dis 2001;11:138-40. 6. Nussbaum ES, Madison MT, Myers ME, Goddard J, Janjua T. Dissecting aneurysms of the posterior inferior cerebellar artery: Retrospective evaluation of management and extended follow-up review in 6 patients. J Neurosurg 2008;109:23-7. 7. Sedat J, Chau Y, Mahagne MH, Bourg V, Lonjon M, Paquis P. Dissection of the posteroinferior cerebellar artery: Clinical characteristics and longterm follow-up in five cases. Cerebrovasc Dis 2007;24:183-90. 8. Takumi I, Mizunari T, Mishina M, Fukuchi T, Nomura R, Umeoka K, et al. Dissecting posterior inferior cerebellar artery aneurysm presenting with subarachnoid hemorrhage right after anticoagulant and antiplatelet therapy against ischemic event. Surg Neurol 2007;68:103-7. 9. Tawk RG, Bendok BR, Qureshi AI, Getch CC, Srinivasan J, Alberts M, et al. Isolated dissections and dissecting aneurysms of the posterior inferior cerebellar artery: Topic and literature review. Neurosurg Rev 2003;26:180-7. 10. Yamaura A, Isobe K, Karasudani H, Tanaka M, Komiya H. Dissecting aneurysms of the posterior inferior cerebellar artery. Neurosurgery 1991;28:894-8. Access this article online Website:
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www.neurologyindia.com DOI: 10.4103/0028-3886.152669 PMID: xxxxx
An unusual cause for a rare neuropathy: Pudendal nerve entrapment syndrome secondary to obturator internus muscle edema Sir, A rare cause of pudendal neuropathy (PN) due to compression by edematous obturator internus muscle is described. A 34-year-old female patient was admitted complaining of pain in the right perianal, gluteal and vulvar region for the
past year. The pain was exacerbated while sitting. She did not respond to pregabalin or nonsteroidal analgesics, and a pelvic MRI revealed edema of the right obturator internus muscle [Figure 1]. Electromyographic activity of bulbocavernous muscle was normal. The bulbocavernosus reflex latency was 48ms, and pudendal nerve terminal motor latency was 3.5ms on the right side. Her electroneuromyography findings were consistent with PN. A pudendal nerve block with marcaine decreased the pain for only a few hours. Due to the intolerable pain, she was referred to an orthopedic surgeon. The orthopedic surgeon thought that the pain was due to a coccygeal fracture and resected the coccyx. However, her pain increased after this operation. On physical examination, the muscle strength and deep tendon reflexes were preserved. She had no sensory loss. She had reported frequent consensual sexual intercourse (8–10 times/day) during the preceeding months before the symptoms began. In our hospital, suspecting a pudendal neuropathy due to compression by edematous obturator internus muscle (based on the clinical and electrophysiological findings), she was placed on duloxetine 75 mg/day, tramadol 50 mg/day, and diclofenac sodium 75 mg/day. She has been using this regimen for 3 months. She reported 50% pain relief at the last follow-up visit. The main feature of PN is pain in the distribution of the pudendal nerve that is exacerbated on sitting. PN is a diagnosis of exclusion but was made in our patient as he fulfilled Nantes’ criteria, a set of simple diagnostic features.[1] The pelvic MRI documented edema of the obturator internus muscle as the cause of PN. The edema was thought to be due to frequent sexual intercourse. There was no history of trauma or pelvic muscle overuse. Insola et al., presented a similar case that was diagnosed as PN and was associated with obturator
a
b
Figure 1: (a) Contrast-enhanced T1 fat sat coronal image demonstrated enhancement at the inferior part of internal obturator muscle. (b) T2 fat sat coronal image showed edema at the same location
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105
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internus muscle fibrosis.[2] A combination of detailed history, a thorough physical examination, imaging techniques, and neurophysiological tests will aid in an accurate diagnosis. The symptoms may be refractory, and a step-by-step, individualized approach is necessary in each case.
Mehmet Besir Turkmen, Figen Kocyigit1, Ali Kocyigit2 Department of Physical Medicine and Rehabilitation, Norobilim Medical Center, Denizli, 1School of Physical Therapy and Rehabilitation, 2Department of Radiology, Faculty of Medicine, Pamukkale University, Denizli, Turkey E-mail: [email protected]
“Chabbra shunt” was inserted. After 3 months, the patient presented in an altered sensorium with decreased oral intake. The upper and lower ends of the shunt were reexplored, found to be functioning well, and left, in situ. On examination, the head was disproportionately enlarged with a bulging and tense anterior fontanel, engorged scalp veins, and the sunset sign. There was a small pulsatile swelling at the parietal burr hole site. The abdominal scar was puckered. The shunt catheter was not palpable anywhere across the chest wall. A guarded lumbar puncture revealed a normal cerebrospinal fluid (CSF) picture. The shunt catheter was not visible on a plain chest and abdominal radiographs. X-ray skull [Figure 1] and computed tomography (CT) of the head
References 1.
2.
Labat JJ, Riant T, Robert R, Amarenco G, Lefaucheur JP, Rigaud J. Diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment (Nantes criteria). Neurourol Urodyn 2008;27:306-10. Insola A, Granata G, Padua L. Alcock canal syndrome due to obturator muscle fibrosis. Muscle Nerve 2010;42:431-2.
Access this article online Website:
Quick Response Code
www.neurologyindia.com DOI: 10.4103/0028-3886.152671
Figure 1: X-ray skull showing completely migrated and coiled intracranial shunt
PMID: xxxxx
Complete intracranial migration of a ventriculoperitoneal shunt: Rare complication of a common procedure Sir, Clinicians managing patients undergoing a ventriculoperitoneal shunt procedure must be aware of its possible complications and their early recognition. Here, we report a rare case of complete intracranial migration of a ventriculoperitoneal shunt, a potentially fatal complication. A 6-month-old female child presented with gradual enlargement of head and decreased oral intake. The child had a previous history of low birth weight and an occipital encephalocele (she was operated for the later condition). The patient developed hydrocephalus in the post-operative period for which a medium-pressure ventriculoperitoneal 106
Figure 2: Non-contrast CT Head showing the coiled intracranial shunt with hydrocephalus
Neurology India / January 2015 / Volume 63 / Issue 1
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.
2.
Jao T, Liu HM, Tang SC, Jeng JS. Dissection of the posterior inferior cerebellar artery in a young adult with cerebellar infarct. Acta Neurol Taiwan 2008;17;243-47. 3. Kwak YS, Kang DH, Woo HJ. Simultaneous vertebral artery dissection and contralateral posterior inferior cerebellar artery dissecting aneurysm. J Cerebrovasc Endovasc Neurosurg. 2012;14:228-32. 4. Mizushima H, Sasaki K, Kunii N, Nishino T, Jinbo H, Abe T, et al. Dissecting aneurysm in the proximal region of the posterior inferior cerebellar artery presenting as Wallenberg’s syndrome. Case report. Neuro l Med Chir (Tokyo) 1994;34:307-10. 5. Niijima K. Dissecting aneurysm of the vertebral artery with an accessory posterior inferior cerebellar artery: Successful management with clipping between the two posterior inferior cerebellar arteries. Cerebrovasc Dis 2001;11:138-40. 6. Nussbaum ES, Madison MT, Myers ME, Goddard J, Janjua T. Dissecting aneurysms of the posterior inferior cerebellar artery: Retrospective evaluation of management and extended follow-up review in 6 patients. J Neurosurg 2008;109:23-7. 7. Sedat J, Chau Y, Mahagne MH, Bourg V, Lonjon M, Paquis P. Dissection of the posteroinferior cerebellar artery: Clinical characteristics and longterm follow-up in five cases. Cerebrovasc Dis 2007;24:183-90. 8. Takumi I, Mizunari T, Mishina M, Fukuchi T, Nomura R, Umeoka K, et al. Dissecting posterior inferior cerebellar artery aneurysm presenting with subarachnoid hemorrhage right after anticoagulant and antiplatelet therapy against ischemic event. Surg Neurol 2007;68:103-7. 9. Tawk RG, Bendok BR, Qureshi AI, Getch CC, Srinivasan J, Alberts M, et al. Isolated dissections and dissecting aneurysms of the posterior inferior cerebellar artery: Topic and literature review. Neurosurg Rev 2003;26:180-7. 10. Yamaura A, Isobe K, Karasudani H, Tanaka M, Komiya H. Dissecting aneurysms of the posterior inferior cerebellar artery. Neurosurgery 1991;28:894-8. Access this article online Website:
Quick Response Code
www.neurologyindia.com DOI: 10.4103/0028-3886.152669 PMID: xxxxx
An unusual cause for a rare neuropathy: Pudendal nerve entrapment syndrome secondary to obturator internus muscle edema Sir, A rare cause of pudendal neuropathy (PN) due to compression by edematous obturator internus muscle is described. A 34-year-old female patient was admitted complaining of pain in the right perianal, gluteal and vulvar region for the
past year. The pain was exacerbated while sitting. She did not respond to pregabalin or nonsteroidal analgesics, and a pelvic MRI revealed edema of the right obturator internus muscle [Figure 1]. Electromyographic activity of bulbocavernous muscle was normal. The bulbocavernosus reflex latency was 48ms, and pudendal nerve terminal motor latency was 3.5ms on the right side. Her electroneuromyography findings were consistent with PN. A pudendal nerve block with marcaine decreased the pain for only a few hours. Due to the intolerable pain, she was referred to an orthopedic surgeon. The orthopedic surgeon thought that the pain was due to a coccygeal fracture and resected the coccyx. However, her pain increased after this operation. On physical examination, the muscle strength and deep tendon reflexes were preserved. She had no sensory loss. She had reported frequent consensual sexual intercourse (8–10 times/day) during the preceeding months before the symptoms began. In our hospital, suspecting a pudendal neuropathy due to compression by edematous obturator internus muscle (based on the clinical and electrophysiological findings), she was placed on duloxetine 75 mg/day, tramadol 50 mg/day, and diclofenac sodium 75 mg/day. She has been using this regimen for 3 months. She reported 50% pain relief at the last follow-up visit. The main feature of PN is pain in the distribution of the pudendal nerve that is exacerbated on sitting. PN is a diagnosis of exclusion but was made in our patient as he fulfilled Nantes’ criteria, a set of simple diagnostic features.[1] The pelvic MRI documented edema of the obturator internus muscle as the cause of PN. The edema was thought to be due to frequent sexual intercourse. There was no history of trauma or pelvic muscle overuse. Insola et al., presented a similar case that was diagnosed as PN and was associated with obturator
a
b
Figure 1: (a) Contrast-enhanced T1 fat sat coronal image demonstrated enhancement at the inferior part of internal obturator muscle. (b) T2 fat sat coronal image showed edema at the same location
Neurology India / January 2015 / Volume 63 / Issue 1
105
[Downloaded free from http://www.neurologyindia.com on Thursday, March 05, 2015, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
internus muscle fibrosis.[2] A combination of detailed history, a thorough physical examination, imaging techniques, and neurophysiological tests will aid in an accurate diagnosis. The symptoms may be refractory, and a step-by-step, individualized approach is necessary in each case.
Mehmet Besir Turkmen, Figen Kocyigit1, Ali Kocyigit2 Department of Physical Medicine and Rehabilitation, Norobilim Medical Center, Denizli, 1School of Physical Therapy and Rehabilitation, 2Department of Radiology, Faculty of Medicine, Pamukkale University, Denizli, Turkey E-mail: [email protected]
“Chabbra shunt” was inserted. After 3 months, the patient presented in an altered sensorium with decreased oral intake. The upper and lower ends of the shunt were reexplored, found to be functioning well, and left, in situ. On examination, the head was disproportionately enlarged with a bulging and tense anterior fontanel, engorged scalp veins, and the sunset sign. There was a small pulsatile swelling at the parietal burr hole site. The abdominal scar was puckered. The shunt catheter was not palpable anywhere across the chest wall. A guarded lumbar puncture revealed a normal cerebrospinal fluid (CSF) picture. The shunt catheter was not visible on a plain chest and abdominal radiographs. X-ray skull [Figure 1] and computed tomography (CT) of the head
References 1.
2.
Labat JJ, Riant T, Robert R, Amarenco G, Lefaucheur JP, Rigaud J. Diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment (Nantes criteria). Neurourol Urodyn 2008;27:306-10. Insola A, Granata G, Padua L. Alcock canal syndrome due to obturator muscle fibrosis. Muscle Nerve 2010;42:431-2.
Access this article online Website:
Quick Response Code
www.neurologyindia.com DOI: 10.4103/0028-3886.152671
Figure 1: X-ray skull showing completely migrated and coiled intracranial shunt
PMID: xxxxx
Complete intracranial migration of a ventriculoperitoneal shunt: Rare complication of a common procedure Sir, Clinicians managing patients undergoing a ventriculoperitoneal shunt procedure must be aware of its possible complications and their early recognition. Here, we report a rare case of complete intracranial migration of a ventriculoperitoneal shunt, a potentially fatal complication. A 6-month-old female child presented with gradual enlargement of head and decreased oral intake. The child had a previous history of low birth weight and an occipital encephalocele (she was operated for the later condition). The patient developed hydrocephalus in the post-operative period for which a medium-pressure ventriculoperitoneal 106
Figure 2: Non-contrast CT Head showing the coiled intracranial shunt with hydrocephalus
Neurology India / January 2015 / Volume 63 / Issue 1
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.
