- Email: [email protected]
Proximal migration of a lumboperitoneal unishunt system
838 Rodrigues et al.
posterior fossa.8 Of these, 5 were in the cerebellar vermis, 4 in the fourth ventricle and 6 in the cerebellar hemisphere. Westergaard et al reported 2 cases in the posterior fossa amongst 96 cases of oligodendroglioma.9 There have been case reports from Indian centers.2,7,10 The clinical course of oligodendroglioma in the posterior cranial fossa is relatively indolent and symptoms are usually long-standing. Packer et al reported a child with posterior fossa oligodendroglioma who had insertion of ventriculoperitoneal shunt for hydrocephalus 10 years prior to the diagnosis of the tumor.5 The CT scan may show a tumor of varying density. Calcification is unusual and the tumor is more often solid than cystic.4 Hydrocephalus is common and tumors enhance with contrast. Due to the rarity and inconsistent radiological features, it may be difficult to preoperatively differentiate oligodendroglioma from astrocytoma. MRI scan is more sensitive than CT scan in detecting multiple intracranial and/or spinal tumors, particularly in patients with oligodendroglioma, which are potentially malignant and may metastasize. Such a preoperative evaluation may establish the presence of multiple tumors. Our patient did not have an MRI. Oligodendroglioma is treated with surgical extirpation followed by local radiation therapy. Holladay and Fruin reported the tendency of oligodendroglioma to metastasize via the cerebrospinal fluid (CSF).3 They recommend CSF cytology in all cases to determine the need for spinal axis irradiation.3 Packer et al reported four children with a median age of 7.5 years who harbored histologically malignant oligodendrogliomas of the cerebellum.5 Three patients received local radiation therapy and all had recurrent disease at a median of 11 months. The relapse in each case was outside the radiation field, with stable disease at the primary site. One child treated with craniospinal irradiation was disease free 15 months after treatment. From these results, Packer et al concluded that the oligodendroglioma of the posterior fossa should be considered potentially malignant and treated with local as well as prophylactic craniospinal radiotherapy. Survival after treatment of posterior fossa oligodendroglioma may be prolonged. Gittens et al reported a woman with cerebellar oligodendroglioma who required 2 operations and survived 13 years after the first surgery.1 The short and long-term outcome and the exact treatment protocol of posterior fossa oligodendroglioma is yet to be established due to the paucity of cases. The prognosis appears to be good if the tumor is resected early, the histology does not show malignancy and after treatment with craniospinal irradiation. Anaplastic oligodendroglioma with 1p and 19q deletions represent a genetically distinct subset. These tumors are more chemosensitive than tumors in which 1p and 19q are intact.11 Whether loss of 1p and 19q represents a marker of chemosensitivity in low-grade tumors is likely to be addressed in future clinical trials.
REFERENCES 1. Gittens WO, Huestis WS, Sangalang VE. Oligodendroglioma of the cerebellum. Surg Neurol 1980; 13: 237–240. 2. Bhatoe HS, Deshpande GU. Childhood cerebellar vermian oligodendroglioma. Neurol India 1999; 47: 341–342. 3. Holladay FP, Fruin AH. Cerebellar oligodendroglioma in a child. Neurosurgery 1980; 6: 552–554. 4. Kitoh A, Itoh Y, Banno T. Infratentorial oligodendroglioma: report of a case. (Japanese) No Shinkei Geka 1984; 12: 1523–1527. 5. Packer RJ, Sutton LN, Rorke LB, et al. Oligodendroglioma of the posterior fossa in childhood. Cancer 1985; 56: 195–199. 6. Baysefer A, Duz B, Erdogan E, Deveci MS. Pediatric cerebellar cystic oligodendroglioma: case report and literature review. Turk J Pediatr 2004; 46: 95–97. 7. Chitkara N, Chanda R, Thakur AK, Chanda S, Sharma NK. Posterior fossa oligodendroglioma. Indian J Pediatr 2002; 69: 1099–1100.
Journal of Clinical Neuroscience (2005) 12(7)
8. Ernest F, Kernohan JW, Craig W. Oligodendroglioma. A review of two hundred cases. Arch Neurol Psychiatry 1950; 63: 964–976. 9. Westergaard L, Gjerris F, Klinken L. Prognostic factors in oligodendrogliomas. Acta Neurochir (Wien) 1997; 139: 600–605. 10. Dharmarajan S, Reginald J, Arumugum R, Sarasa B. Cerebellar oligodendroglioma. Neurol India 1988; 36: 182. 11. Cairncross JG, Ueki K, Zlatescu MC, et al. Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. J Natl Cancer Inst 1998; 90: 1473–1479.
Proximal migration of a lumboperitoneal unishunt system D Rodrigues1 FRCS, R Nannapaneni1 FRCS (SN), 1 2 S Behari1 MCh MCh DNB, M Prasad MCh MCh, A Herwadkar 1 1 CJ Gerber FRCS (SN), P Mitchell FRCS (SN)
FRCR,
1
Department of Neurosurgery, 2Department of Neuroradiology, Newcastle General Hospital, Newcastle upon Tyne, UK
Summary Proximal migration of a lumboperitoneal (LP) shunt is a rare complication associated with unishunt systems. We report three cases with a hypothesis that raised intra-abdominal pressure may be a factor responsible for the proximal migration of a LP unishunt. A rare case of proximal migration of LP shunt into the quadrigeminal cistern is also reported. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(7), 838–841 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.11.009
Keywords: lumboperitoneal shunt, shunt migration, benign intracranial hypertension Received 16 July 2004 Accepted 15 November 2004 Correspondence to: Desiderio Rodrigues, 93 Gretna Road Newcastle upon Tyne, NE15 7PH UK. Tel.: 44 191 2280896; Fax: +44 191 2280896; E-mail: [email protected]
INTRODUCTION LP shunting is a technically simple and effective procedure for the management of benign intracranial hypertension (BIH).1,2 The LP shunt is usually fixed in place using the fixating tabs provided with the shunt system. The unishunt systems, without a chamber, may however migrate, either distally into the peritoneal cavity or rarely, proximally into the spinal subarachnoid space (SAS), or even into the cranial cavity, as the anchoring sutures may loosen or cut through the fixating tabs.3,4 The migration may be facilitated by the pressure differentials between the peritoneal cavity and the SAS, as well as by the repeated movements of the spine.3,5 We report three cases of proximal migration of an LP shunt. In two cases, the shunt migrated into the dorsal SAS and in one, it migrated into the cranial cavity.
CASE REPORTS Case 1 A 37-year old woman with BIH had complete relief of her symptoms of raised intracranial pressure (ICP) following insertion of an ª 2005 Elsevier Ltd. All rights reserved.
Proximal migration of a system
839
LP unishunt. She had recurrence of her symptoms of headache and poor concentration following a road traffic accident, which involved a sudden decelerating seat-belt injury. Her neurological examination revealed no focal deficits or papilloedema. The plain anteroposterior and lateral radiographs of the dorsolumbar spine revealed proximal migration of the entire shunt into the spinal SAS forming a loop at the D11–D12 level with the abdominal end having migrated to the L4 vertebral level (Fig. 1). The CT scan of the brain was unremarkable. Via an L4 laminectomy, the shunt was withdrawn and a new LP shunt system introduced. The LP shunt was fixed to the lumbar and rectus abdominis fascia by fixating tabs at the proximal and distal ends. At follow-up after 18 months, she remained symptom-free. Case 2 A 26-year old woman had an LP shunt inserted for BIH. She remained symptom-free for 3 years. Six weeks following a fullterm, normal delivery, she had recurrent episodes of severe headache with blurred vision. Neurological examination revealed only bilateral papilloedema. The anteroposterior and lateral plain radiographs of the dorsal spine revealed proximal LP shunt migration to the D10 level. Following the retrieval of the displaced shunt and the re-insertion of a new LP shunt, she had relief of her symptoms. Case 3 A 20-year old woman with BIH had an LP shunt inserted and had remained asymptomatic for 3 years. She subsequently presented with progressively increasing headache of one week duration. A month prior to the recurrence of her headaches, she had had severe
Fig. 2 Lateral X-ray of the skull revealed that the shunt had migrated upwards into the cranial cavity (arrow).
bouts of coughing due to acute bronchitis. Neurological examination revealed no deficits and fundoscopic examination was normal. The plain lateral radiograph of the cervical spine revealed that the shunt had migrated upwards into the cranial cavity while the lower end had remained in the abdominal parieties (Fig. 2). The CT scan of the brain showed that the proximal end of the shunt tube had migrated along the dorsum of the brain stem, through the foramen of Magendie into the IVth ventricle, and through the superior medullary velum into the quadrigeminal cistern just posterior to the pineal calcification (Figs. 3a, b, c). At surgery, the catheter was not removed due to the risk of injuring the brainstem. As the peritoneal end of the shunt tube was not draining cerebrospinal fluid (CSF), it was ligated and sutured to the rectus abdominis fascia. A new LP shunt was inserted. Postoperatively, the patient has remained symptom-free at one-year follow-up. DISCUSSION Proposed mechanisms of proximal LP shunt migration
Fig. 1 Lateral X-ray of the dorsolumbar spine showing proximal migration of the entire shunt into the spinal canal (arrow).
ª 2005 Elsevier Ltd. All rights reserved.
Proximal migration of an LP shunt into the SAS, as in two of our cases, and into the cranial cavity, as illustrated by the third case, is rarely reported.4,6–9 A single-piece shunt system without any intervening reservoirs or valve devices is prone to migration.3 Through inappropriate fixation of the tube, or the slippage or cutting through of the fixating ligature, is the root cause of shunt migration, other mechanisms may facilitate this process.3,4 The consistent findings in all three cases we report were the episodes of increased intra-abdominal pressure, which occurred prior to symptoms of shunt malfunction. It is likely that the road traffic accident suffered by the patient in Case 1 resulted in both a transient increase in intra-abdominal pressure due to the seatbelt, and forced spinal flexion. The direct effect of the increased intraabdominal pressure may displace the shunt from the peritoneal cavity into the SAS.3,5 Normal flexion-extension, rotational movements and lateral bending of the lumbar vertebrae may also predispose to displacement of an LP shunt.9 The CSF flow in the upper SAS has been reported to be downward on the ventral side of the cord and upward on the dorsal side of the cord.10 Such directional CSF flow may also facilitate proximal migration of the shunt tubing lying in the dorsal SAS. Journal of Clinical Neuroscience (2005) 12(7)
840 Rodrigues et al.
Fig. 3 Axial CT scan of the brain showing that the proximal end of the shunt tube had migrated along the dorsum of the brainstem (a), through the foramen of Magendie into the IVth ventricle (b) and through the superior medullary velum into the quadrigeminal cistern just posterior to the pineal calcification (c).
It has been proposed that failure to maintain a straight subcutaneous course for the distal shunt tubing also predisposes to shunt migration.3 With time, a smooth subcutaneous tunnel usually forms around the silastic elastomer tubing of the shunt system through which the shunt can easily slide back and forth. The pulsations of CSF in the SAS,11 recurrent episodes of increased intraabdominal pressure,3,5 and flexion and extension of the lumbar spine facilitate the repeated to-and-fro movements of the shunt tube within this tunnel.9 This may cause the fixation tabs to loosen and the dural aperture at the entry point of the shunt into the SAS to widen. This provides an additional impetus for the shunt to migrate proximally.
Journal of Clinical Neuroscience (2005) 12(7)
The technique of fixation It is imperative to fix the shunt in order to prevent its displacement. Various modifications have been proposed in order to secure the LP shunt position and prevent migration. Incorporating a reservoir or valve; placing an intermediate connector between the peritoneal and lumbar shunt segments of differing diameters; or use of a “T-tube” LP shunt,12 would resist proximal migration. However, theses solutions have the disadvantage of the higher rate of shunt malfunction observed in all multi-component shunt systems, with a higher rate of obstruction or disconnection and migration of one of the ends.4,12 We used a technique of proximal and distal anchoring of the LP shunt proposed for unishunt systems by ª 2005 Elsevier Ltd. All rights reserved.
Hypoglycorrachia and leptomeningeal carcinomatosis
Raimondi et al.13 The fixating tabs at both the ends prevented the tube from both migrating and kinking. Unusual migration Migration of shunts has been reported into various unusual sites. These include the cerebellum, ventricular system, subgaleal space, sphenoid sinus, heart, thorax, hollow abdominal viscus, pelvic viscera, scrotum and abdominal incisions and defects.6,7,9,11,14–17 However, in our third case, the LP shunt passed through the spinal SAS, into the IVth ventricle, through the foramen of Magendie, and penetrated the superior medullary velum to lie just posterior to the pineal calcification in the quadrigeminal cistern. This unusual shunt migration has never been reported before. During shunt revision, forced manipulation may have endangered vital structures within and around the brainstem so the original, migrated shunt tube was left in situ. To conclude, episodic increase in intra-abdominal pressure was closely related to the proximal migration of a unishunt system in our reported cases. Proximal migration into the quadrigeminal cistern through the IVth ventricle and the superior medullary velum has not been previously reported. ACKNOWLEDGEMENT We gratefully acknowledge the kind help of Mr Bill Frew, Librarian, Foster Library, for his help with the scientific material and photographs.
REFERENCES 1. Burgett RA, Purvin VA, Kawasaki A. Lumboperitoneal shunting for pseudotumor cerebri. Neurology 1997; 49: 734–739. 2. Suri A, Pandey P, Mehta VS. Subarachnoid hemorrhage and intracerebral hematoma following lumboperitoneal shunt for pseudotumor cerebri: a rare complication. Neurol India 2002; 50: 508–510. 3. Abou el Nasr HT. Modified method for prophylaxis against unishunt system complications with presentation of total intraventricular migration of unisystem ventriculoperitoneal shunt. Child's Nerv Syst 1998; 4: 116–118. 4. Yoshida S, Masunaga S, Hayase M, Oda Y. Migration of the shunt tube after lumboperitoneal shunt - two case reports. Neurol Med Chir (Tokyo) 2000; 40: 594–596. 5. Eljamel MS, Sharif S, Pidgeon CN. Total intraventricular migration of unisystem venticulo-peritoneal shunt. Acta Neurochir (Wien) 1995; 136: 217–218. 6. Alleyne CH, Shutter LA, Colohan AR. Cranial migration of a lumboperitoneal shunt catheter. South Med J 1996; 89: 634–636. 7. Anthogalidis E-I, Sure U, Hellwig D, Bertalanffy H. Intracranial dislocation of a lumboperitoneal shunt catheter: Case report and review of the literature. Clin Neurol Neurosurg 1999; 101: 203–206. 8. Carroll TA, Jakubowski J. Intrathecal migration of a lumboperitoneal shunt. Br J Neurosurg 2000; 14: 496–497. 9. Satow T, Motoyama Y, Yamazoe N, Isaka F, Higuchi K, Nabeshima S. Migration of a lumboperitoneal shunt catheter into the spinal canal–Case report. Neurol Med Chir (Tokyo) 2001; 41: 97–99. 10. Henry-Feugeas MC, Idy-Peretti I, Blanchet B, Hassine D, Zannoli G, Schouman-Claeys E. Temporal and spatial assessment of normal cerebrospinal fluid dynamics with MR imaging. Magn Reson Imaging 1993; 11: 1107–1118. 11. Chan Y, Datta NN, Chan KY, Rehman SU, Poon CY, Kwok JC. Extrusion of the peritoneal catheter of a VP shunt system through a gastrostomy wound. Surg Neurol 2003; 60: 68–70. 12. Martinez-Lage JF, Poza M, Esteban JA. Mechanical complications of the reservoirs and flushing devices in the ventricular shunt systems. Br J Neurosurg 1992; 6: 321–325. 13. Raimondi AJ, Robinson JS, Kuwamura K. Complications of ventriculoperitoneal shunting and a critical comparison of the three-piece systems. Child's Brain 1977; 3: 321–342. 14. Dominguez CJ, Tyagi A, Hall G, Timothy J, Chumas PD. Sub-galeal coiling of the proximal and distal components of a ventriculo-peritoneal shunt. An unusual complication and proposed mechanism. Child's Nerv Syst 2000; 16: 493–495.
ª 2005 Elsevier Ltd. All rights reserved.
841
15. Li KW, Ciceri E, Lasio G, Solero CL, DiMeco F. Shunt migration into the sphenoid sinus: case report. Neurosurgery 2003; 53: 441–443. 16. Rodriguez-Sanchez JA, Cabezudo-Artero JM, Porras Estrada LF. Unusual migration of the distal catheter of a ventriculoperitoneal shunt into the heart: case report. Neurosurgery 2003; 52: 1510. 17. Wani AA, Ramzan A, Wani MA. Protrusion of a peritoneal catheter through the umbilicus: an unusual complication of a ventriculoperitoneal shunt. Pediatr Surg Int 2002; 18: 171–172.
Isolated hypoglycorrachia: leptomeningeal carcinomatosis causing subacute confusion Peter Kim1 MBBS(HONS), David Ashton2 John D Pollard2 PHD FRACP
MBBS,
1 Department of Neurology, Liverpool Hospital, 2Department of Neurology, Royal Prince Alfred Hospital; Sydney, Australia
Summary We report a 76-year-old caucasian man who presented with a 3-week history of progressive confusion. His past medical history included a left nephro-uretectomy for poorly differentiated transitional cell carcinoma 9 years previously. Besides his confusion, his clinical and neurological examination was unremarkable. Extensive investigation revealed only isolated hypoglycorrachia and mildly elevated CSF protein. Cerebral CT and MRI scans without contrast did not reveal any abnormalities. As his condition continued to decline, an MRI scan of the brain with gadolinium was performed which revealed extensive nodular enhancement of the surface of the cerebellum and brainstem and both temporal lobe convexities. Repeat lumbar puncture showed malignant cells in the CSF and confirmed the diagnosis of leptomeningeal carcinomatosis. This case illustrates that leptomeningeal carcinomatosis should be considered in the differential diagnosis of cognitive decline in the elderly, after other common aetiologies have been excluded. The index of suspicion should be increased in patients with a prior history of cancer. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(7), 841–843 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.11.007
Keywords: confusion
hypoglycorrachia,
leptomeningeal
carcinomatosis,
Received 5 July 2004 Accepted 15 November 2004 Correspondence to: Dr. Peter Kim, Department of Neurology, Liverpool Hospital, Locked bag 7103, Liverpool BC, NSW 1871, Australia. Tel.: +61 2 9828 3646; Fax: +61 2 9828 3846; E-mail: [email protected]
INTRODUCTION Leptomeningeal carcinomatosis (LC) was first reported in 1970 and occurs most commonly in adults with a history of breast carcinoma, lung carcinoma and melanoma.1,2,3 LC has been reported to occur in 2 to 25% of patients with malignancy and typically has a poor prognosis even with aggressive treatment.2,3 We present a case of LC in an elderly patient where the only presenting symptom was cognitive decline associated with isolated hypoglycorrachia as the only CSF abnormality. Journal of Clinical Neuroscience (2005) 12(7)
posterior fossa.8 Of these, 5 were in the cerebellar vermis, 4 in the fourth ventricle and 6 in the cerebellar hemisphere. Westergaard et al reported 2 cases in the posterior fossa amongst 96 cases of oligodendroglioma.9 There have been case reports from Indian centers.2,7,10 The clinical course of oligodendroglioma in the posterior cranial fossa is relatively indolent and symptoms are usually long-standing. Packer et al reported a child with posterior fossa oligodendroglioma who had insertion of ventriculoperitoneal shunt for hydrocephalus 10 years prior to the diagnosis of the tumor.5 The CT scan may show a tumor of varying density. Calcification is unusual and the tumor is more often solid than cystic.4 Hydrocephalus is common and tumors enhance with contrast. Due to the rarity and inconsistent radiological features, it may be difficult to preoperatively differentiate oligodendroglioma from astrocytoma. MRI scan is more sensitive than CT scan in detecting multiple intracranial and/or spinal tumors, particularly in patients with oligodendroglioma, which are potentially malignant and may metastasize. Such a preoperative evaluation may establish the presence of multiple tumors. Our patient did not have an MRI. Oligodendroglioma is treated with surgical extirpation followed by local radiation therapy. Holladay and Fruin reported the tendency of oligodendroglioma to metastasize via the cerebrospinal fluid (CSF).3 They recommend CSF cytology in all cases to determine the need for spinal axis irradiation.3 Packer et al reported four children with a median age of 7.5 years who harbored histologically malignant oligodendrogliomas of the cerebellum.5 Three patients received local radiation therapy and all had recurrent disease at a median of 11 months. The relapse in each case was outside the radiation field, with stable disease at the primary site. One child treated with craniospinal irradiation was disease free 15 months after treatment. From these results, Packer et al concluded that the oligodendroglioma of the posterior fossa should be considered potentially malignant and treated with local as well as prophylactic craniospinal radiotherapy. Survival after treatment of posterior fossa oligodendroglioma may be prolonged. Gittens et al reported a woman with cerebellar oligodendroglioma who required 2 operations and survived 13 years after the first surgery.1 The short and long-term outcome and the exact treatment protocol of posterior fossa oligodendroglioma is yet to be established due to the paucity of cases. The prognosis appears to be good if the tumor is resected early, the histology does not show malignancy and after treatment with craniospinal irradiation. Anaplastic oligodendroglioma with 1p and 19q deletions represent a genetically distinct subset. These tumors are more chemosensitive than tumors in which 1p and 19q are intact.11 Whether loss of 1p and 19q represents a marker of chemosensitivity in low-grade tumors is likely to be addressed in future clinical trials.
REFERENCES 1. Gittens WO, Huestis WS, Sangalang VE. Oligodendroglioma of the cerebellum. Surg Neurol 1980; 13: 237–240. 2. Bhatoe HS, Deshpande GU. Childhood cerebellar vermian oligodendroglioma. Neurol India 1999; 47: 341–342. 3. Holladay FP, Fruin AH. Cerebellar oligodendroglioma in a child. Neurosurgery 1980; 6: 552–554. 4. Kitoh A, Itoh Y, Banno T. Infratentorial oligodendroglioma: report of a case. (Japanese) No Shinkei Geka 1984; 12: 1523–1527. 5. Packer RJ, Sutton LN, Rorke LB, et al. Oligodendroglioma of the posterior fossa in childhood. Cancer 1985; 56: 195–199. 6. Baysefer A, Duz B, Erdogan E, Deveci MS. Pediatric cerebellar cystic oligodendroglioma: case report and literature review. Turk J Pediatr 2004; 46: 95–97. 7. Chitkara N, Chanda R, Thakur AK, Chanda S, Sharma NK. Posterior fossa oligodendroglioma. Indian J Pediatr 2002; 69: 1099–1100.
Journal of Clinical Neuroscience (2005) 12(7)
8. Ernest F, Kernohan JW, Craig W. Oligodendroglioma. A review of two hundred cases. Arch Neurol Psychiatry 1950; 63: 964–976. 9. Westergaard L, Gjerris F, Klinken L. Prognostic factors in oligodendrogliomas. Acta Neurochir (Wien) 1997; 139: 600–605. 10. Dharmarajan S, Reginald J, Arumugum R, Sarasa B. Cerebellar oligodendroglioma. Neurol India 1988; 36: 182. 11. Cairncross JG, Ueki K, Zlatescu MC, et al. Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. J Natl Cancer Inst 1998; 90: 1473–1479.
Proximal migration of a lumboperitoneal unishunt system D Rodrigues1 FRCS, R Nannapaneni1 FRCS (SN), 1 2 S Behari1 MCh MCh DNB, M Prasad MCh MCh, A Herwadkar 1 1 CJ Gerber FRCS (SN), P Mitchell FRCS (SN)
FRCR,
1
Department of Neurosurgery, 2Department of Neuroradiology, Newcastle General Hospital, Newcastle upon Tyne, UK
Summary Proximal migration of a lumboperitoneal (LP) shunt is a rare complication associated with unishunt systems. We report three cases with a hypothesis that raised intra-abdominal pressure may be a factor responsible for the proximal migration of a LP unishunt. A rare case of proximal migration of LP shunt into the quadrigeminal cistern is also reported. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(7), 838–841 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.11.009
Keywords: lumboperitoneal shunt, shunt migration, benign intracranial hypertension Received 16 July 2004 Accepted 15 November 2004 Correspondence to: Desiderio Rodrigues, 93 Gretna Road Newcastle upon Tyne, NE15 7PH UK. Tel.: 44 191 2280896; Fax: +44 191 2280896; E-mail: [email protected]
INTRODUCTION LP shunting is a technically simple and effective procedure for the management of benign intracranial hypertension (BIH).1,2 The LP shunt is usually fixed in place using the fixating tabs provided with the shunt system. The unishunt systems, without a chamber, may however migrate, either distally into the peritoneal cavity or rarely, proximally into the spinal subarachnoid space (SAS), or even into the cranial cavity, as the anchoring sutures may loosen or cut through the fixating tabs.3,4 The migration may be facilitated by the pressure differentials between the peritoneal cavity and the SAS, as well as by the repeated movements of the spine.3,5 We report three cases of proximal migration of an LP shunt. In two cases, the shunt migrated into the dorsal SAS and in one, it migrated into the cranial cavity.
CASE REPORTS Case 1 A 37-year old woman with BIH had complete relief of her symptoms of raised intracranial pressure (ICP) following insertion of an ª 2005 Elsevier Ltd. All rights reserved.
Proximal migration of a system
839
LP unishunt. She had recurrence of her symptoms of headache and poor concentration following a road traffic accident, which involved a sudden decelerating seat-belt injury. Her neurological examination revealed no focal deficits or papilloedema. The plain anteroposterior and lateral radiographs of the dorsolumbar spine revealed proximal migration of the entire shunt into the spinal SAS forming a loop at the D11–D12 level with the abdominal end having migrated to the L4 vertebral level (Fig. 1). The CT scan of the brain was unremarkable. Via an L4 laminectomy, the shunt was withdrawn and a new LP shunt system introduced. The LP shunt was fixed to the lumbar and rectus abdominis fascia by fixating tabs at the proximal and distal ends. At follow-up after 18 months, she remained symptom-free. Case 2 A 26-year old woman had an LP shunt inserted for BIH. She remained symptom-free for 3 years. Six weeks following a fullterm, normal delivery, she had recurrent episodes of severe headache with blurred vision. Neurological examination revealed only bilateral papilloedema. The anteroposterior and lateral plain radiographs of the dorsal spine revealed proximal LP shunt migration to the D10 level. Following the retrieval of the displaced shunt and the re-insertion of a new LP shunt, she had relief of her symptoms. Case 3 A 20-year old woman with BIH had an LP shunt inserted and had remained asymptomatic for 3 years. She subsequently presented with progressively increasing headache of one week duration. A month prior to the recurrence of her headaches, she had had severe
Fig. 2 Lateral X-ray of the skull revealed that the shunt had migrated upwards into the cranial cavity (arrow).
bouts of coughing due to acute bronchitis. Neurological examination revealed no deficits and fundoscopic examination was normal. The plain lateral radiograph of the cervical spine revealed that the shunt had migrated upwards into the cranial cavity while the lower end had remained in the abdominal parieties (Fig. 2). The CT scan of the brain showed that the proximal end of the shunt tube had migrated along the dorsum of the brain stem, through the foramen of Magendie into the IVth ventricle, and through the superior medullary velum into the quadrigeminal cistern just posterior to the pineal calcification (Figs. 3a, b, c). At surgery, the catheter was not removed due to the risk of injuring the brainstem. As the peritoneal end of the shunt tube was not draining cerebrospinal fluid (CSF), it was ligated and sutured to the rectus abdominis fascia. A new LP shunt was inserted. Postoperatively, the patient has remained symptom-free at one-year follow-up. DISCUSSION Proposed mechanisms of proximal LP shunt migration
Fig. 1 Lateral X-ray of the dorsolumbar spine showing proximal migration of the entire shunt into the spinal canal (arrow).
ª 2005 Elsevier Ltd. All rights reserved.
Proximal migration of an LP shunt into the SAS, as in two of our cases, and into the cranial cavity, as illustrated by the third case, is rarely reported.4,6–9 A single-piece shunt system without any intervening reservoirs or valve devices is prone to migration.3 Through inappropriate fixation of the tube, or the slippage or cutting through of the fixating ligature, is the root cause of shunt migration, other mechanisms may facilitate this process.3,4 The consistent findings in all three cases we report were the episodes of increased intra-abdominal pressure, which occurred prior to symptoms of shunt malfunction. It is likely that the road traffic accident suffered by the patient in Case 1 resulted in both a transient increase in intra-abdominal pressure due to the seatbelt, and forced spinal flexion. The direct effect of the increased intraabdominal pressure may displace the shunt from the peritoneal cavity into the SAS.3,5 Normal flexion-extension, rotational movements and lateral bending of the lumbar vertebrae may also predispose to displacement of an LP shunt.9 The CSF flow in the upper SAS has been reported to be downward on the ventral side of the cord and upward on the dorsal side of the cord.10 Such directional CSF flow may also facilitate proximal migration of the shunt tubing lying in the dorsal SAS. Journal of Clinical Neuroscience (2005) 12(7)
840 Rodrigues et al.
Fig. 3 Axial CT scan of the brain showing that the proximal end of the shunt tube had migrated along the dorsum of the brainstem (a), through the foramen of Magendie into the IVth ventricle (b) and through the superior medullary velum into the quadrigeminal cistern just posterior to the pineal calcification (c).
It has been proposed that failure to maintain a straight subcutaneous course for the distal shunt tubing also predisposes to shunt migration.3 With time, a smooth subcutaneous tunnel usually forms around the silastic elastomer tubing of the shunt system through which the shunt can easily slide back and forth. The pulsations of CSF in the SAS,11 recurrent episodes of increased intraabdominal pressure,3,5 and flexion and extension of the lumbar spine facilitate the repeated to-and-fro movements of the shunt tube within this tunnel.9 This may cause the fixation tabs to loosen and the dural aperture at the entry point of the shunt into the SAS to widen. This provides an additional impetus for the shunt to migrate proximally.
Journal of Clinical Neuroscience (2005) 12(7)
The technique of fixation It is imperative to fix the shunt in order to prevent its displacement. Various modifications have been proposed in order to secure the LP shunt position and prevent migration. Incorporating a reservoir or valve; placing an intermediate connector between the peritoneal and lumbar shunt segments of differing diameters; or use of a “T-tube” LP shunt,12 would resist proximal migration. However, theses solutions have the disadvantage of the higher rate of shunt malfunction observed in all multi-component shunt systems, with a higher rate of obstruction or disconnection and migration of one of the ends.4,12 We used a technique of proximal and distal anchoring of the LP shunt proposed for unishunt systems by ª 2005 Elsevier Ltd. All rights reserved.
Hypoglycorrachia and leptomeningeal carcinomatosis
Raimondi et al.13 The fixating tabs at both the ends prevented the tube from both migrating and kinking. Unusual migration Migration of shunts has been reported into various unusual sites. These include the cerebellum, ventricular system, subgaleal space, sphenoid sinus, heart, thorax, hollow abdominal viscus, pelvic viscera, scrotum and abdominal incisions and defects.6,7,9,11,14–17 However, in our third case, the LP shunt passed through the spinal SAS, into the IVth ventricle, through the foramen of Magendie, and penetrated the superior medullary velum to lie just posterior to the pineal calcification in the quadrigeminal cistern. This unusual shunt migration has never been reported before. During shunt revision, forced manipulation may have endangered vital structures within and around the brainstem so the original, migrated shunt tube was left in situ. To conclude, episodic increase in intra-abdominal pressure was closely related to the proximal migration of a unishunt system in our reported cases. Proximal migration into the quadrigeminal cistern through the IVth ventricle and the superior medullary velum has not been previously reported. ACKNOWLEDGEMENT We gratefully acknowledge the kind help of Mr Bill Frew, Librarian, Foster Library, for his help with the scientific material and photographs.
REFERENCES 1. Burgett RA, Purvin VA, Kawasaki A. Lumboperitoneal shunting for pseudotumor cerebri. Neurology 1997; 49: 734–739. 2. Suri A, Pandey P, Mehta VS. Subarachnoid hemorrhage and intracerebral hematoma following lumboperitoneal shunt for pseudotumor cerebri: a rare complication. Neurol India 2002; 50: 508–510. 3. Abou el Nasr HT. Modified method for prophylaxis against unishunt system complications with presentation of total intraventricular migration of unisystem ventriculoperitoneal shunt. Child's Nerv Syst 1998; 4: 116–118. 4. Yoshida S, Masunaga S, Hayase M, Oda Y. Migration of the shunt tube after lumboperitoneal shunt - two case reports. Neurol Med Chir (Tokyo) 2000; 40: 594–596. 5. Eljamel MS, Sharif S, Pidgeon CN. Total intraventricular migration of unisystem venticulo-peritoneal shunt. Acta Neurochir (Wien) 1995; 136: 217–218. 6. Alleyne CH, Shutter LA, Colohan AR. Cranial migration of a lumboperitoneal shunt catheter. South Med J 1996; 89: 634–636. 7. Anthogalidis E-I, Sure U, Hellwig D, Bertalanffy H. Intracranial dislocation of a lumboperitoneal shunt catheter: Case report and review of the literature. Clin Neurol Neurosurg 1999; 101: 203–206. 8. Carroll TA, Jakubowski J. Intrathecal migration of a lumboperitoneal shunt. Br J Neurosurg 2000; 14: 496–497. 9. Satow T, Motoyama Y, Yamazoe N, Isaka F, Higuchi K, Nabeshima S. Migration of a lumboperitoneal shunt catheter into the spinal canal–Case report. Neurol Med Chir (Tokyo) 2001; 41: 97–99. 10. Henry-Feugeas MC, Idy-Peretti I, Blanchet B, Hassine D, Zannoli G, Schouman-Claeys E. Temporal and spatial assessment of normal cerebrospinal fluid dynamics with MR imaging. Magn Reson Imaging 1993; 11: 1107–1118. 11. Chan Y, Datta NN, Chan KY, Rehman SU, Poon CY, Kwok JC. Extrusion of the peritoneal catheter of a VP shunt system through a gastrostomy wound. Surg Neurol 2003; 60: 68–70. 12. Martinez-Lage JF, Poza M, Esteban JA. Mechanical complications of the reservoirs and flushing devices in the ventricular shunt systems. Br J Neurosurg 1992; 6: 321–325. 13. Raimondi AJ, Robinson JS, Kuwamura K. Complications of ventriculoperitoneal shunting and a critical comparison of the three-piece systems. Child's Brain 1977; 3: 321–342. 14. Dominguez CJ, Tyagi A, Hall G, Timothy J, Chumas PD. Sub-galeal coiling of the proximal and distal components of a ventriculo-peritoneal shunt. An unusual complication and proposed mechanism. Child's Nerv Syst 2000; 16: 493–495.
ª 2005 Elsevier Ltd. All rights reserved.
841
15. Li KW, Ciceri E, Lasio G, Solero CL, DiMeco F. Shunt migration into the sphenoid sinus: case report. Neurosurgery 2003; 53: 441–443. 16. Rodriguez-Sanchez JA, Cabezudo-Artero JM, Porras Estrada LF. Unusual migration of the distal catheter of a ventriculoperitoneal shunt into the heart: case report. Neurosurgery 2003; 52: 1510. 17. Wani AA, Ramzan A, Wani MA. Protrusion of a peritoneal catheter through the umbilicus: an unusual complication of a ventriculoperitoneal shunt. Pediatr Surg Int 2002; 18: 171–172.
Isolated hypoglycorrachia: leptomeningeal carcinomatosis causing subacute confusion Peter Kim1 MBBS(HONS), David Ashton2 John D Pollard2 PHD FRACP
MBBS,
1 Department of Neurology, Liverpool Hospital, 2Department of Neurology, Royal Prince Alfred Hospital; Sydney, Australia
Summary We report a 76-year-old caucasian man who presented with a 3-week history of progressive confusion. His past medical history included a left nephro-uretectomy for poorly differentiated transitional cell carcinoma 9 years previously. Besides his confusion, his clinical and neurological examination was unremarkable. Extensive investigation revealed only isolated hypoglycorrachia and mildly elevated CSF protein. Cerebral CT and MRI scans without contrast did not reveal any abnormalities. As his condition continued to decline, an MRI scan of the brain with gadolinium was performed which revealed extensive nodular enhancement of the surface of the cerebellum and brainstem and both temporal lobe convexities. Repeat lumbar puncture showed malignant cells in the CSF and confirmed the diagnosis of leptomeningeal carcinomatosis. This case illustrates that leptomeningeal carcinomatosis should be considered in the differential diagnosis of cognitive decline in the elderly, after other common aetiologies have been excluded. The index of suspicion should be increased in patients with a prior history of cancer. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(7), 841–843 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.11.007
Keywords: confusion
hypoglycorrachia,
leptomeningeal
carcinomatosis,
Received 5 July 2004 Accepted 15 November 2004 Correspondence to: Dr. Peter Kim, Department of Neurology, Liverpool Hospital, Locked bag 7103, Liverpool BC, NSW 1871, Australia. Tel.: +61 2 9828 3646; Fax: +61 2 9828 3846; E-mail: [email protected]
INTRODUCTION Leptomeningeal carcinomatosis (LC) was first reported in 1970 and occurs most commonly in adults with a history of breast carcinoma, lung carcinoma and melanoma.1,2,3 LC has been reported to occur in 2 to 25% of patients with malignancy and typically has a poor prognosis even with aggressive treatment.2,3 We present a case of LC in an elderly patient where the only presenting symptom was cognitive decline associated with isolated hypoglycorrachia as the only CSF abnormality. Journal of Clinical Neuroscience (2005) 12(7)