- Email: [email protected]
Spontaneous third ventriculostomy
Case Report / Journal of Clinical Neuroscience 15 (2008) 587–590
haemorrhage associated with sinus thrombosis, so all four criteria were fulfilled and a diagnosis of idiopathic HES was made. Although the pathogenesis of idiopathic HES is unclear, it appears that a hypersensitivity reaction may trigger dysregulation of eosinophil production. Direct damage to tissues and hypercoagulability are caused by infiltration of eosinophils into organs. Involvement of the cardiovascular system is the main source of morbidity and mortality.3 Neurological manifestations are often observed, and comprise three types.2 The first type is caused by thromboemboli (either of cardiac origin or locally produced), and multiple recurrent embolic strokes may occur. The second type comprises central nervous dysfunction with distinct encephalopathy. The third type comprises peripheral neuropathies, which occur in half of all HES patients. Alfaham et al. reported that three out of 19 children with idiopathic HES exhibited neurological complications and died. Postmortem examinations revealed brain swelling and thrombosis in the cerebral arteries and veins.4 A case of cerebral haemorrhage in idiopathic HES was reported by Roche et al.5 In that case, haemorrhage was observed in both temporal lobes and cerebellar hemispheres.5 Although angiograms were not obtained and indirect signs, such as the cord sign or empty delta sign, were not observed, it is possible that the double haemorrhage was associated with sinus thrombosis. Schulman et al. reported a paediatric case of idiopathic HES, which was suspected to be nonhaemorrhagic sinus thrombosis on the basis of the classic CT empty delta sign and cord sign in the straight sinus, but not on the basis of angiogram findings.6 The cord sign is a significant sign of thrombosis, but spontaneous density in the straight sinus can also be observed in normal subjects.7 Furthermore, the empty delta sign may represent normal anatomic variation, such as high splitting of the superior sagittal sinus.8 Visualization on angiography, in addition to these signs in the CT scan, is essential for the diagnosis of sinus thrombosis. Our case is the first in which direct evidence of sinus thrombosis has been found in idiopathic HES. Compared with digital subtraction angiography and MR venography, CT venography more sensitively depicts the cerebral veins and dural sinuses.9,10 CT venography
has the added advantage that it can be used in the emergent setting. In our case, the cord sign was seen in the left transverse sinus (Fig. 1), and CT angiography showed a filling defect in the left transverse and sigmoid sinuses. These two findings were consistent with thrombosis of the transverse and sigmoid sinuses, which explains the lobar haemorrhage (haemorrhagic infarction) in the temporal lobe. Also, we speculate that hypercoagulability caused by the effects of eosinophils initiated this thrombosis. Repeated haemorrhage in the short term caused the death from sinus thrombosis in this case. Use of lowmolecular-weight heparin after the emergent surgery or precautionary craniectomy may have prevented this death. References 1. Weaver DF, Heffernan LP, Purdy RA, et al. Eosinophil-induced neurotoxicity: axonal neuropathy, cerebral infarction, and dementia. Neurology 1988;38:144–6. 2. Moore PM, Harley JB, Fauci AS. Neurologic dysfunction in the idiopathic hypereosinophilic syndrome. Ann Intern Med 1985;102: 109–14. 3. Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994;83:2759–79. 4. Alfaham MA, Ferguson SD, Sihra B, et al. The idiopathic hypereosinophilic syndrome. Arch Dis Child 1987;62:601–13. 5. Roche S, Cross S, Kaufman B. Intracranial haemorrhages occurring in the idiopathic hypereosinophilic syndrome. J Neurol Neurosurg Psychiatry 1990;53:440–1. 6. Schulman H, Hertzog L, Zirkin H, et al. Cerebral sinovenous thrombosis in the idiopathic hypereosinophilic syndrome in childhood. Pediatr Radiol 1999;29:595–7. 7. Segall HD, Ahmadi J, McComb JG, et al. Computed tomographic observations pertinent to intracranial venous thrombotic and occlusive disease in childhood. State of the art, some new data, and hypotheses. Radiology 1982;143:441–9. 8. Casey SO, Alberico RA, Patel M, et al. Cerebral CT venography. Radiology 1996;198:163–70. 9. Wetzel SG, Kirsch E, Stock KW, et al. Cerebral veins: comparative study of CT venography with intraarterial digital subtraction angiography. AJNR Am J Neuroradiol 1999;20:249–55. 10. Ozsvath RR, Casey SO, Lustrin ES, et al. Cerebral venography: comparison of CT and MR projection venography. AJR Am J Roentgenol 1997;169:1699–707.
doi:10.1016/j.jocn.2006.12.021
Spontaneous third ventriculostomy Alex Yuen a, Kristian J. Bulluss a,b, Nicholas Trost c, Michael A. Murphy a,b,* a
Department of Neurosurgery, St Vincent’s Hospital, 41 Victoria Parade, Fitzroy 3065, Victoria, Australia b Department of Surgery, University of Melbourne, Parkville, Victoria, Australia c Department of Radiology, St Vincent’s Hospital, Fitzroy, Victoria, Australia Received 17 January 2007; accepted 22 May 2007
*
Corresponding author. Tel.: +61 3 92883341; fax: +61 3 9288 3350. E-mail addresses: [email protected] (M.A. Murphy).
587
588
Case Report / Journal of Clinical Neuroscience 15 (2008) 587–590
Abstract Spontaneous ventriculostomy (SV) is a rare condition where there is a spontaneous communication between the ventricle and the subarachnoid space as a result of hydrocephalus. Only four cases of SV through the floor of the third ventricle have been previously reported. Two further cases are presented and the literature reviewed. Ó 2008 Published by Elsevier Ltd. Keywords: Spontaneous ventriculostomy; Third ventricle; Hydrocephalus
1. Introduction Spontaneous ventriculostomy (SV) is a rare condition. We report two cases of SV in the floor of the third ventricle. Previously only four cases have been reported. The clinical and radiological features are discussed and the literature reviewed. 2. Case report 1 An 18-year-old previously well female was admitted to our institution for investigation of recurrent dizzy spells and loss of weight. She had no symptoms of raised intracranial pressure. A CT scan revealed a 2.5 cm lesion of slightly higher density than cerebrospinal fluid, centered in the pineal cistern. The third and lateral ventricles were moderately dilated. An MRI confirmed a simple cystic lesion of the pineal gland compressing the tectum and obstructing the aquaduct (Fig. 1). The third and lateral ventricles were dilated, but there was no subependymal oedema and a flow artifact was demonstrated in the foramen of Munro, third ventricle and suprasellar cistern, on the fluid attenuated inversion recovery (FLAIR) sequence. A defect in the floor of the
third ventricle, posterior to the infundibulum, was evident on sagittal sequences (Fig. 2). This communication was confirmed by a flow-sensitive phase contrast cine MR study performed on follow-up (Fig. 3). The patient underwent a frameless stereotactic posterior fossa craniotomy and biopsy of the lesion. Histopathology was consistent with a simple pineal cyst. There was no postoperative complication. Her presenting symptoms resolved, although it was not felt that they were secondary to her intracranial pathology. 3. Case report 2 A 68-year-old man presented with a 3-month history of increasing confusion and rapid deterioration in his gait. He had a past history of a low-grade glioma having been resected from his right temporal lobe 47 years ago. He had no symptoms of raised intracranial pressure. A CT scan revealed severe hydrocephalus involving the lateral and third ventricles; the fourth ventricle was not dilated. A subsequent MRI revealed a 2.5 cm lesion centered in the left of the midbrain (Fig. 4). It involved the tectum extending to the left cerebral peduncle and thalamus, and it compressed the aqueduct; the third and lateral ventricles
Fig. 1. A series of three T2-weighted axial MRIs demonstrate the pineal cyst (short arrow) and dilated lateral ventricles. Reduced signal in the cerebrospinal fluid (CSF) of the third ventricle and suprasellar cistern (long arrows) is flow artifact from the CSF jet through the defect.
Case Report / Journal of Clinical Neuroscience 15 (2008) 587–590
589
4. Discussion
Fig. 2. Midsagittal T1-weighted MRI demonstrates the defect in the floor of the third ventricle dorsal to the tuber cinerum (long arrow) with subtle flow artefact. Pineal cyst (short arrow) and narrowed aqueduct are demonstrated.
were dilated. There was no subependymal edema but a flow artefact was seen in the foramen of Munro, third ventricle and suprasellar cistern, on the FLAIR sequence. A defect in the floor of the third ventricle, posterior to the infundibulum, was evident on sagittal sequences (Fig. 5). Following review by the neurologists in our institution, a lumbar puncture was performed with an opening pressure of 22 mmH2O. In the context of his clinical condition, a ventriculoperitoneal shunt was inserted to treat the hydrocephalus. The patient made a good postoperative recovery. His symptoms gradually resolved over the next few months.
We report two further cases of a SV through the floor of the third ventricle. SV has previously been reported involving the trigone of the lateral ventricle, the lamina terminalis, the suprapineal recess or the infrapineal recess of the third ventricle.1,2 This rare communication between the ventricles and the subarachnoid space occurs with rupture of the thinnest part of the third ventricular floor found between the median eminence of the tuber cinereum and the mamillary bodies.3,4 This segment of the floor is used to perform endoscopic ventriculostomy in obstructive hydrocephalus.5 In all previously reported cases, SV has been associated with chronic hydrocephalus secondary to aqueduct stenosis.1,6 It has been hypothesized that spontaneous communication is not seen in acute hydrocephalus as the elasticity of the ventricular walls prevents potential rupture when there is a rapid increase in intraventricular pressure.1 Radiological evidence of hydrocephalus is seen in all reported cases of SV involving the floor of the third ventricle.1,6 It usually consists of dilatation of the lateral and third ventricle but no periventricular oedema which is consistent with chronic hydrocephalus. Patients usually have minimal or no symptoms or signs of increased intracranial pressure. The diagnosis of SV in the third ventricle is a difficult radiological diagnosis to make with either CT scan or MRI. In fact, all previously reported cases were diagnosed with flow-sensitive phase contrast cine MRI or ventriculography.1,6 In our cases, the diagnosis was made on a routine MRI study. A defect in the floor of the third ventricle was clearly seen on coronal and sagittal T1-weighted images. A flow artifact from the third ventricle into the suprasellar cistern was found on T2-weighted and FLAIR sequences. These findings were confirmed with flow-sensitive phasecontrast cine MRI. It showed no CSF wave across the aqueduct and a pulsatile wave through the opening in the floor of the third ventricle.
Fig. 3. Preoperative temporal image of the cerebrospinal fluid (CSF) flow study (left) obtained in the midsagittal plane demonstrates flow between the third ventricle and basal cistern (arrow). Nine months postoperative image with further improvement in CSF flow study (right).
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Case Report / Journal of Clinical Neuroscience 15 (2008) 587–590
Fig. 4. Axial T2-weighted MRIs demonstrate the tectal mass (short arrow), dilated lateral and third ventricle, and flow artifact in the third ventricle and suprasellar cistern (long arrow).
In conclusion, spontaneous third ventriculostomy is a rare condition associated with chronic hydrocephalus. All reported cases have followed a benign course. It is difficult to diagnose and is often missed on routine imaging. As a result, the actual incidence of the condition may be underestimated. References
Fig. 5. Midsagittal T1-weighted MRI demonstrates the defect in the floor of the third ventricle (long arrow) and mass (short arrow).
The clinical presentation of SV in other locations within the ventricular system is different from that through the floor of the third ventricle. All cases of SV found other than through the floor of the third ventricle have all been reported in babies younger than 6 months.2,7 This compares to all six cases of third ventriculostomy which have occurred in adult patients. Moreover, all reported cases of ventriculostomy in other locations were associated with symptoms and signs of acute intracranial hypertension, and in some cases resulted in death of the patient. In addition to radiological evidence of acute hydrocephalus, ventricular diverticulum is also commonly seen and they occur at the same sites as the SV.2,7–10 doi:10.1016/j.jocn.2007.05.015
1. Rovira A, Capellades J, Grive E, et al. Spontaneous ventriculostomy: report of three cases revealed by flow-sensitive phase-contrast cine MR imaging. AJNR Am J Neuroradiol 1999;20:1647–52. 2. Zilkha A. Spontaneous ventriculostomy. Report of two cases demonstrated by Pantopaque ventriculography. Radiology 1974;111: 633–7. 3. Rosenbaum AE, Hawkins RL, Newton TH. Normal third ventricle. In: Newton TH, Potts DG, editors. Radiology of the Skull and Brain. Ventricles and Cisterns. St Louis, MO: Mosby; 1978. p. 3398–439. 4. Berry MM, Standring SM, Bannister LH. Nervous system. In: Williams PL, editor. Gray’s Anatomy. New York: Churchill-Livingstone; 1995. p. 1094–107. 5. Drake JM. Ventriculostomy for treatment of hydrocephalus. Neurosurg Clin N Am 1993;4:657–66. 6. Miyasaka Y, Morii S, Takagi H, et al. A case of spontaneous 3rd ventriculostomy. No Shinkei Geka 1977;5:81–7. 7. Alonso A, Taboada D, Alvarez JA, et al. Spontaneous ventriculostomy and ventricular diverticulum. Radiology 1979;133: 651–4. 8. Dyke CG. Acquired subtentorial pressure diverticulum of the cerebral lateral ventricle. Radiology 1942;39:167–74. 9. Lavender JP, Du Boulay GH. Aqueduct stenosis and cystic expansion of the suprapineal recess. Clin Radiol 1965;16:330–3. 10. Macfarlane WV, Falconer MA. Diverticulum of the lateral ventricle extending into the posterior cranial fossa: report of a case successfully relieved by operation. J Neurol Neurosurg Psychiatry 1947;10:101–6.
haemorrhage associated with sinus thrombosis, so all four criteria were fulfilled and a diagnosis of idiopathic HES was made. Although the pathogenesis of idiopathic HES is unclear, it appears that a hypersensitivity reaction may trigger dysregulation of eosinophil production. Direct damage to tissues and hypercoagulability are caused by infiltration of eosinophils into organs. Involvement of the cardiovascular system is the main source of morbidity and mortality.3 Neurological manifestations are often observed, and comprise three types.2 The first type is caused by thromboemboli (either of cardiac origin or locally produced), and multiple recurrent embolic strokes may occur. The second type comprises central nervous dysfunction with distinct encephalopathy. The third type comprises peripheral neuropathies, which occur in half of all HES patients. Alfaham et al. reported that three out of 19 children with idiopathic HES exhibited neurological complications and died. Postmortem examinations revealed brain swelling and thrombosis in the cerebral arteries and veins.4 A case of cerebral haemorrhage in idiopathic HES was reported by Roche et al.5 In that case, haemorrhage was observed in both temporal lobes and cerebellar hemispheres.5 Although angiograms were not obtained and indirect signs, such as the cord sign or empty delta sign, were not observed, it is possible that the double haemorrhage was associated with sinus thrombosis. Schulman et al. reported a paediatric case of idiopathic HES, which was suspected to be nonhaemorrhagic sinus thrombosis on the basis of the classic CT empty delta sign and cord sign in the straight sinus, but not on the basis of angiogram findings.6 The cord sign is a significant sign of thrombosis, but spontaneous density in the straight sinus can also be observed in normal subjects.7 Furthermore, the empty delta sign may represent normal anatomic variation, such as high splitting of the superior sagittal sinus.8 Visualization on angiography, in addition to these signs in the CT scan, is essential for the diagnosis of sinus thrombosis. Our case is the first in which direct evidence of sinus thrombosis has been found in idiopathic HES. Compared with digital subtraction angiography and MR venography, CT venography more sensitively depicts the cerebral veins and dural sinuses.9,10 CT venography
has the added advantage that it can be used in the emergent setting. In our case, the cord sign was seen in the left transverse sinus (Fig. 1), and CT angiography showed a filling defect in the left transverse and sigmoid sinuses. These two findings were consistent with thrombosis of the transverse and sigmoid sinuses, which explains the lobar haemorrhage (haemorrhagic infarction) in the temporal lobe. Also, we speculate that hypercoagulability caused by the effects of eosinophils initiated this thrombosis. Repeated haemorrhage in the short term caused the death from sinus thrombosis in this case. Use of lowmolecular-weight heparin after the emergent surgery or precautionary craniectomy may have prevented this death. References 1. Weaver DF, Heffernan LP, Purdy RA, et al. Eosinophil-induced neurotoxicity: axonal neuropathy, cerebral infarction, and dementia. Neurology 1988;38:144–6. 2. Moore PM, Harley JB, Fauci AS. Neurologic dysfunction in the idiopathic hypereosinophilic syndrome. Ann Intern Med 1985;102: 109–14. 3. Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994;83:2759–79. 4. Alfaham MA, Ferguson SD, Sihra B, et al. The idiopathic hypereosinophilic syndrome. Arch Dis Child 1987;62:601–13. 5. Roche S, Cross S, Kaufman B. Intracranial haemorrhages occurring in the idiopathic hypereosinophilic syndrome. J Neurol Neurosurg Psychiatry 1990;53:440–1. 6. Schulman H, Hertzog L, Zirkin H, et al. Cerebral sinovenous thrombosis in the idiopathic hypereosinophilic syndrome in childhood. Pediatr Radiol 1999;29:595–7. 7. Segall HD, Ahmadi J, McComb JG, et al. Computed tomographic observations pertinent to intracranial venous thrombotic and occlusive disease in childhood. State of the art, some new data, and hypotheses. Radiology 1982;143:441–9. 8. Casey SO, Alberico RA, Patel M, et al. Cerebral CT venography. Radiology 1996;198:163–70. 9. Wetzel SG, Kirsch E, Stock KW, et al. Cerebral veins: comparative study of CT venography with intraarterial digital subtraction angiography. AJNR Am J Neuroradiol 1999;20:249–55. 10. Ozsvath RR, Casey SO, Lustrin ES, et al. Cerebral venography: comparison of CT and MR projection venography. AJR Am J Roentgenol 1997;169:1699–707.
doi:10.1016/j.jocn.2006.12.021
Spontaneous third ventriculostomy Alex Yuen a, Kristian J. Bulluss a,b, Nicholas Trost c, Michael A. Murphy a,b,* a
Department of Neurosurgery, St Vincent’s Hospital, 41 Victoria Parade, Fitzroy 3065, Victoria, Australia b Department of Surgery, University of Melbourne, Parkville, Victoria, Australia c Department of Radiology, St Vincent’s Hospital, Fitzroy, Victoria, Australia Received 17 January 2007; accepted 22 May 2007
*
Corresponding author. Tel.: +61 3 92883341; fax: +61 3 9288 3350. E-mail addresses: [email protected] (M.A. Murphy).
587
588
Case Report / Journal of Clinical Neuroscience 15 (2008) 587–590
Abstract Spontaneous ventriculostomy (SV) is a rare condition where there is a spontaneous communication between the ventricle and the subarachnoid space as a result of hydrocephalus. Only four cases of SV through the floor of the third ventricle have been previously reported. Two further cases are presented and the literature reviewed. Ó 2008 Published by Elsevier Ltd. Keywords: Spontaneous ventriculostomy; Third ventricle; Hydrocephalus
1. Introduction Spontaneous ventriculostomy (SV) is a rare condition. We report two cases of SV in the floor of the third ventricle. Previously only four cases have been reported. The clinical and radiological features are discussed and the literature reviewed. 2. Case report 1 An 18-year-old previously well female was admitted to our institution for investigation of recurrent dizzy spells and loss of weight. She had no symptoms of raised intracranial pressure. A CT scan revealed a 2.5 cm lesion of slightly higher density than cerebrospinal fluid, centered in the pineal cistern. The third and lateral ventricles were moderately dilated. An MRI confirmed a simple cystic lesion of the pineal gland compressing the tectum and obstructing the aquaduct (Fig. 1). The third and lateral ventricles were dilated, but there was no subependymal oedema and a flow artifact was demonstrated in the foramen of Munro, third ventricle and suprasellar cistern, on the fluid attenuated inversion recovery (FLAIR) sequence. A defect in the floor of the
third ventricle, posterior to the infundibulum, was evident on sagittal sequences (Fig. 2). This communication was confirmed by a flow-sensitive phase contrast cine MR study performed on follow-up (Fig. 3). The patient underwent a frameless stereotactic posterior fossa craniotomy and biopsy of the lesion. Histopathology was consistent with a simple pineal cyst. There was no postoperative complication. Her presenting symptoms resolved, although it was not felt that they were secondary to her intracranial pathology. 3. Case report 2 A 68-year-old man presented with a 3-month history of increasing confusion and rapid deterioration in his gait. He had a past history of a low-grade glioma having been resected from his right temporal lobe 47 years ago. He had no symptoms of raised intracranial pressure. A CT scan revealed severe hydrocephalus involving the lateral and third ventricles; the fourth ventricle was not dilated. A subsequent MRI revealed a 2.5 cm lesion centered in the left of the midbrain (Fig. 4). It involved the tectum extending to the left cerebral peduncle and thalamus, and it compressed the aqueduct; the third and lateral ventricles
Fig. 1. A series of three T2-weighted axial MRIs demonstrate the pineal cyst (short arrow) and dilated lateral ventricles. Reduced signal in the cerebrospinal fluid (CSF) of the third ventricle and suprasellar cistern (long arrows) is flow artifact from the CSF jet through the defect.
Case Report / Journal of Clinical Neuroscience 15 (2008) 587–590
589
4. Discussion
Fig. 2. Midsagittal T1-weighted MRI demonstrates the defect in the floor of the third ventricle dorsal to the tuber cinerum (long arrow) with subtle flow artefact. Pineal cyst (short arrow) and narrowed aqueduct are demonstrated.
were dilated. There was no subependymal edema but a flow artefact was seen in the foramen of Munro, third ventricle and suprasellar cistern, on the FLAIR sequence. A defect in the floor of the third ventricle, posterior to the infundibulum, was evident on sagittal sequences (Fig. 5). Following review by the neurologists in our institution, a lumbar puncture was performed with an opening pressure of 22 mmH2O. In the context of his clinical condition, a ventriculoperitoneal shunt was inserted to treat the hydrocephalus. The patient made a good postoperative recovery. His symptoms gradually resolved over the next few months.
We report two further cases of a SV through the floor of the third ventricle. SV has previously been reported involving the trigone of the lateral ventricle, the lamina terminalis, the suprapineal recess or the infrapineal recess of the third ventricle.1,2 This rare communication between the ventricles and the subarachnoid space occurs with rupture of the thinnest part of the third ventricular floor found between the median eminence of the tuber cinereum and the mamillary bodies.3,4 This segment of the floor is used to perform endoscopic ventriculostomy in obstructive hydrocephalus.5 In all previously reported cases, SV has been associated with chronic hydrocephalus secondary to aqueduct stenosis.1,6 It has been hypothesized that spontaneous communication is not seen in acute hydrocephalus as the elasticity of the ventricular walls prevents potential rupture when there is a rapid increase in intraventricular pressure.1 Radiological evidence of hydrocephalus is seen in all reported cases of SV involving the floor of the third ventricle.1,6 It usually consists of dilatation of the lateral and third ventricle but no periventricular oedema which is consistent with chronic hydrocephalus. Patients usually have minimal or no symptoms or signs of increased intracranial pressure. The diagnosis of SV in the third ventricle is a difficult radiological diagnosis to make with either CT scan or MRI. In fact, all previously reported cases were diagnosed with flow-sensitive phase contrast cine MRI or ventriculography.1,6 In our cases, the diagnosis was made on a routine MRI study. A defect in the floor of the third ventricle was clearly seen on coronal and sagittal T1-weighted images. A flow artifact from the third ventricle into the suprasellar cistern was found on T2-weighted and FLAIR sequences. These findings were confirmed with flow-sensitive phasecontrast cine MRI. It showed no CSF wave across the aqueduct and a pulsatile wave through the opening in the floor of the third ventricle.
Fig. 3. Preoperative temporal image of the cerebrospinal fluid (CSF) flow study (left) obtained in the midsagittal plane demonstrates flow between the third ventricle and basal cistern (arrow). Nine months postoperative image with further improvement in CSF flow study (right).
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Case Report / Journal of Clinical Neuroscience 15 (2008) 587–590
Fig. 4. Axial T2-weighted MRIs demonstrate the tectal mass (short arrow), dilated lateral and third ventricle, and flow artifact in the third ventricle and suprasellar cistern (long arrow).
In conclusion, spontaneous third ventriculostomy is a rare condition associated with chronic hydrocephalus. All reported cases have followed a benign course. It is difficult to diagnose and is often missed on routine imaging. As a result, the actual incidence of the condition may be underestimated. References
Fig. 5. Midsagittal T1-weighted MRI demonstrates the defect in the floor of the third ventricle (long arrow) and mass (short arrow).
The clinical presentation of SV in other locations within the ventricular system is different from that through the floor of the third ventricle. All cases of SV found other than through the floor of the third ventricle have all been reported in babies younger than 6 months.2,7 This compares to all six cases of third ventriculostomy which have occurred in adult patients. Moreover, all reported cases of ventriculostomy in other locations were associated with symptoms and signs of acute intracranial hypertension, and in some cases resulted in death of the patient. In addition to radiological evidence of acute hydrocephalus, ventricular diverticulum is also commonly seen and they occur at the same sites as the SV.2,7–10 doi:10.1016/j.jocn.2007.05.015
1. Rovira A, Capellades J, Grive E, et al. Spontaneous ventriculostomy: report of three cases revealed by flow-sensitive phase-contrast cine MR imaging. AJNR Am J Neuroradiol 1999;20:1647–52. 2. Zilkha A. Spontaneous ventriculostomy. Report of two cases demonstrated by Pantopaque ventriculography. Radiology 1974;111: 633–7. 3. Rosenbaum AE, Hawkins RL, Newton TH. Normal third ventricle. In: Newton TH, Potts DG, editors. Radiology of the Skull and Brain. Ventricles and Cisterns. St Louis, MO: Mosby; 1978. p. 3398–439. 4. Berry MM, Standring SM, Bannister LH. Nervous system. In: Williams PL, editor. Gray’s Anatomy. New York: Churchill-Livingstone; 1995. p. 1094–107. 5. Drake JM. Ventriculostomy for treatment of hydrocephalus. Neurosurg Clin N Am 1993;4:657–66. 6. Miyasaka Y, Morii S, Takagi H, et al. A case of spontaneous 3rd ventriculostomy. No Shinkei Geka 1977;5:81–7. 7. Alonso A, Taboada D, Alvarez JA, et al. Spontaneous ventriculostomy and ventricular diverticulum. Radiology 1979;133: 651–4. 8. Dyke CG. Acquired subtentorial pressure diverticulum of the cerebral lateral ventricle. Radiology 1942;39:167–74. 9. Lavender JP, Du Boulay GH. Aqueduct stenosis and cystic expansion of the suprapineal recess. Clin Radiol 1965;16:330–3. 10. Macfarlane WV, Falconer MA. Diverticulum of the lateral ventricle extending into the posterior cranial fossa: report of a case successfully relieved by operation. J Neurol Neurosurg Psychiatry 1947;10:101–6.