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Sphenoid sinus mucocoele presenting as complete ophthalmoplegia
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Sphenoid sinus mucocoele presenting as complete ophthalmoplegia E. Roufail1, R. Briggs2, B. Tress3, A. H. Kaye1 1 Department of Surgery, Neurosurgery, 2 Otolaryngology and 3 Radiology, Royal Melbourne Hospital, The University of Melbourne, Grattan Street, Parkville, 3052, Victoria, Australia
Summary Sphenoid sinus mucocoeles represent 1% of all paranasal sinus mucocoeles. We describe a case of a sinus mucocoele with an atypical presentation comprising the sudden onset of a complete ophthalmoplegia. There was good recovery following drainage of the mucocoele. © 2001 Harcourt Publishers Ltd Journal of Clinical Neuroscience (2001) 8(4), 372–374 © 2001 Harcourt Publishers Ltd DOI: 10.1054/jocn.2000.0830, available online at http://www.idealibrary.com on
Keywords: mucocoele, sphenoid sinus, ophthalmoplegia Received 21 March 2000 Accepted 8 May 2000 Correspondence to: Prof A. Kaye, Tel.: ;61 3 9347 7067; Fax: ;61 3 9347 7695.
INTRODUCTION Sphenoid sinus mucocoele, first described by Berg (1889),1 represents 1% of all paranasal sinus mucocoeles2 and between 15 and 29% of all cases of sphenoid sinus disease.3,4 Mucocoeles
themselves are epithelial-lined lesions containing inspissated mucus, arising as a result of obstruction of the sinus osteum. The obstruction can be the result of inflammation, trauma, congenital anomalies, previous surgery or tumourous lesions.5,6 The differential diagnosis of lesions in the area of the sphenoid include hypophyseal tumours, craniopharyngioma, meningioma, glioma, chordoma, dysgerminoma and cholesteatoma, as well as neoplastic lesions of the skull base, sinus and nasopharynx.7 The lesions may extend to affect adjacent structures, giving rise to a variety of clinical manifestations including headache, facial pain, anosmia, ocular displacement, ocular palsy, visual failure8 and, rarely, hypopituitarism.9 This report highlights an atypical presentation of sphenoid sinus mucocoele and considers its importance in the differential diagnosis of sudden onset of complete ophthalmoplega. CASE REPORT A 66 year old female with a past history of a two stage craniotomy for excision of a right sided middle cranial fossa meningioma 10 years earlier presented with a 2-day history of severe left frontal and parietal headache for which she was admitted to hospital. Three days after the initial onset of the headache she developed sudden onset of complete left ophthalmoplegia. Examination revealed complete left ptosis, a fixed dilated left pupil and complete failure of any eye movements in the left eye. Visual acuity was 6/36 in the right eye and 6/6 in the left. Visual fields were normal. Fundoscopy showed right optic atrophy related to previous meningioma surgery. There was decreased sensation to all modalities in the right trigeminal nerve distribution and a grade one right lower motor neuron seventh nerve palsy, both of which had been documented as being residual from the earlier two stage craniotomy. There were no other cranial nerve abnormalities and the remainer of the physical examination was normal. A computed
Fig. 1A, B CT scan showing relatively low density soft tissue mass in the right infratemporal fossa with anterior displacement of the posterior wall of the maxillary sinus (A) and similar low density, non-soft tissue within the spheniodal sinus (B).
Journal of Clinical Neuroscience (2001) 8(4)
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Fig. 2A, B Sagittal T1-weighted scans show markedly hyperintense soft tissue filling the enlarged sphenoid sinus (A). Extensive meningioma en plaque is well demonstrated in the contrast enhanced image (small white arrows) (B). The sphenoid sinus contents show no enhancement.
Fig. 3A, B Axial T2-weighted scans (A) showing soft tissue of varying decreased intensity in sphenoidal sinus and right infratemporal fossa. Axial T1-weighted, fat saturated axial images show tissue in both sphenoidal sinuses and infratemporal fossae to be of high signal intensity (B).
tomograph (CT) scan showed a non-enhancing soft tissue mass density material in the sphenoidal sinus and the right infratemporal fossa where it had deformed the posterior margin of the right maxillary sinus (Fig. 1). Magnetic resonance image (MRI) showed that the tissue within the sphenoidal sinus and infratemporal fossa was markedly hyperintense on T1-weighted scans (Fig. 2) and relatively low intensity on T2-weighted scans (Fig. 3). Both CT and MRI showed residual extensive enhancing meningioma en plaque lining the medial aspect of the anterior and right middle cranial fossae. © 2001 Harcourt Publishers Ltd
Endoscopic sphenoethmoidectomy to decompress the mucocoele was undertaken, followed by a revision 6 days later to further decompress the left sphenoid sinus mucocoele. Straw coloured serous fluid was drained at initial operation which grew Gram positive cocci for which the patient received 7 days of intravenous flucloxacillin followed by a week of oral flucloxacillin. Over the ensuing week there was good recovery of eyelid retraction, eye movements and pupil reactivity. Two months after the initial surgery, all left eye functions were normal. Journal of Clinical Neuroscience (2001) 8(4)
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DISCUSSION The clinical manifestations of sphenoid sinus mucocoele are determined by their involvement of surrounding structures. Holt and Rötth (1940)10 suggested the name ‘orbital apex and sphenoidal fissure syndrome’, while Tassman11 in 1947 suggested the term ‘sphenoid fissure-optic canal syndrome with complete ophthalmoplegia’ because the syndrome was considered to be incomplete when the optic nerve or other structures were spared. Proetz (1948)12 identified 13 structures adjacent to the sphenoid sinus that could be involved, including cranial nerves II to VI, dura mater, pituitary, gland, cavernous sinus, internal carotid artery, sphenopalatine ganglion and artery, and pterygoid nerve. Headache, present in 70–80% of cases3,8,13 is the most common clinical symptom. It is typically retro- or supra-orbital, of severe character, radiating to the forehead and occipital regions and lasting from several hours to several days.8 Typically the headaches become more severe and frequent over ensuing months, becoming associated with visual symptoms. The headache probably results from stretching of the dura over the planum sphenoidale.13 Visual disturbance is the second most common group of symptoms, and typically precipitates surgical intervention. Visual disturbances result from involvement of cranial nerves II, III, IV and VI in isolation or combination. The optic nerve is the most frequently involved cranial nerve with reduction in visual acuity in up to 65% of cases.13 The deterioration in visual acuity is usually gradual although sudden blindness may occur.14–16 Up to 25% of cases have bilateral symptoms.16 Palsies of eye movement occur in 30–50% of cases.8,13 The oculomotor nerve is affected more frequently than the trochlear and abducent nerves,17 accounting for 70% of palsies reviewed by Friedmann and Harrison (1970).8 There is often associated optic nerve involvement and isolated oculomotor palsy is rare. Pupil sparing occurs in approximately 50% of cases.18 This case is of interest because a sudden onset of complete ophthalmoplegia associated with sphenoid mucocoele has rarely been reported in the literature. Often, there have only been comments made as to the frequency of individual cranial nerve palsies.8,13 Furthermore, sudden and dramatic onset of signs and symptoms in this case is unusual because typically in this disease the headache is an initial isolated symptom, with a relapsing and remitting course over several months. The increasing intensity and frequency is often later associated with visual symptoms. These features, together with the sparing of the second cranial nerve, highlight that the importance of this presentation of sphenoid sinus mucocoele lies in the differential diagnoses. We emphasise an awareness of sphenoid sinus mucocoele as a cause of complete, sudden onset ophthalmoplegia and its rapid response to prompt surgical intervention and antibiotic treatment. REFERENCES 1.
2. 3. 4. 5. 6. 7.
Berg J. Bidrag till kännedomen om sjukdomarana I näsans biholor samt till läran om cerebro-spinal-vätskas flytning ur näsam. Nordiskt Medicinskt Arkiv 1889; 21: 1–24. Zizmore J, Noyek A. Cysts and benign tumors of the paranasal sinuses. Seminars in Roetgenology 1968; 3: 172–201. Wyllie TW, Kern EB, Djalilian M. Isolated sphenoid sinus lesions. Laryngoscope 1973; 83: 1252–1265. Rothfeild RE, de Vries EJ, Rueger RG. Isolated sphenoid sinus disease. Head Neck 1991; 13: 208–212. Moriyama H, Nakajima T, Honda Y. Studies on mucocoeles of the ethmoid and sphenoid sinuses: Analysis of 47 cases. J Laryngol Otol 1992; 106: 23–27. Natvig K, Larson TE. Mucocoel of the paranasal sinuses. J Laryngol Otol 1992; 92: 107–108. Muneer A, Jones NS. Unilateral abducens nerve palsy: A presenting sing of sphenoid sinus mucocoeles. J Laryngol Otol 1997; 111: 644–646.
Journal of Clinical Neuroscience (2001) 8(4)
9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
Friedmann G, Harrison S. Mucocoele of the sphenoid sinus as a cause of recurrent oculomotor nerve palsy. J Neurol Neurosurg Psychiatry 1970; 33: 172–179. Valvassori GE, Putterman AM. Ophthalmological and radiological findings in sphenoid mucocels. Arch Ophthalmol 1973; 90: 416–419. Holt H, Rötth A. Orbital apex and sphenoid fissure syndrome. Arch Ophthalmol 1940; 24: 731–741. Tassman IS. Complete unilateral ophthalmoplegia due to primary carcinoma of the sphenoid sinus. Arch Ophthalmol 1947; 37: 294–303. Proetz AW. The sphenoid sinus. BMJ 1948; 2: 243–245. Nugent GR, Sprinkle P, Bloor BM. Sphenoid sinus mucocoels. J Neurosurg 1970; 72: 443–451. Blum ME, Larson A. Mucocoels of the sphenoid sinus with sudden blindness. Laryngoscope 1973; 83: 2042–2049. Gore RM, Weinberg PE, Kim KS, et al. Sphenoid sinus mucocoels presenting as intracranial mass on computed tomography. Surg Neurol 1980; 13: 375–379. Wurster CF, Levine TM, Sisson GA. Mucocoel of the sphenoid sinus causing sudden onset blindness. Otolaryngol Head Neck Surg 1986; 94: 257–259. Sethi D, Lau DPC, Chan C. Sphenoid sinus mucocoel presenting with isolated oculomotor nerve palsy. J Laryngol Otol 1997; 111: 471–473. Johnson LN, Hepler RS, Yee RD et al. Sphenoid sinus mucocoel (anterior clinoid variant) mimicking diabetic ophthalmoplegia and retrobulbar neuritis: Am J Ophthalmol 1986; 102: 111–115.
Spinal cord pilocytic astrocytoma with cranial meningeal metastases Ho-Keung Ng1 MD FRCPATH FRCPA FCAP, Clarence H. S. Leung2 MD CHB FRCS (E), Ronald Boet2 MBBS FCA (SA), Wai-Sang Poon2 MB CHB FRCS(G) 1
Department of Anatomical and Cellular Pathology, 2Neurosurgical Unit, Department of Surgery, The Chinese University of Hong Kong, Hong Kong, P.R.China
Summary Dissemination of tumour cells along the cerebrospinal fluid (CSF) pathway has been reported mostly in medulloblastomas, germ cell tumours or high grade gliomas. Juvenile pilocytic astrocytoma (JPA) is usually a benign astrocytoma. However, drop metastases of indolent nature from intracranial tumours to the spinal cord are documented. All of the previously reported cases represent metastases of cerebellar or hypothalamic tumours spreading to the spinal cord. We document in this paper the first report of a spinal cord pilocytic astrocytoma spreading via the CSF to the cerebral meninges. A 9 year old girl had a JPA of C5 to C7 subtotally resected. Two and a half years later she presented with hydrocephalus with radiologically meningeal enhancement. The meninges were biopsied which showed metastatic JPA. The girl was relatively well 4 years after initial surgery with residual tumour. Spinal cord JPA can rarely metastasise to the cranial meninges. Similar to intracranial tumours which spread to the spinal cord, such metastatic lesions are indolent. © 2001 Harcourt Publishers Ltd Journal of Clinical Neuroscience (2001) 8(4), 374–377 © 2001 Harcourt Publishers Ltd DOI: 10.1054/jocn.2000.0762, available online at http://www.idealibrary.com on
Keywords: juveile pilocytic astrocytoma, metastasis, subarachnoid spread Received 21 March 2000 Accepted 4 April 2000 Correspondence to: Dr H. K. Ng, Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, Shatin, Hong Kong. Tel.: 852 2632 3337; Fax: 852 2637 6274; E-mail: [email protected]
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Sphenoid sinus mucocoele presenting as complete ophthalmoplegia E. Roufail1, R. Briggs2, B. Tress3, A. H. Kaye1 1 Department of Surgery, Neurosurgery, 2 Otolaryngology and 3 Radiology, Royal Melbourne Hospital, The University of Melbourne, Grattan Street, Parkville, 3052, Victoria, Australia
Summary Sphenoid sinus mucocoeles represent 1% of all paranasal sinus mucocoeles. We describe a case of a sinus mucocoele with an atypical presentation comprising the sudden onset of a complete ophthalmoplegia. There was good recovery following drainage of the mucocoele. © 2001 Harcourt Publishers Ltd Journal of Clinical Neuroscience (2001) 8(4), 372–374 © 2001 Harcourt Publishers Ltd DOI: 10.1054/jocn.2000.0830, available online at http://www.idealibrary.com on
Keywords: mucocoele, sphenoid sinus, ophthalmoplegia Received 21 March 2000 Accepted 8 May 2000 Correspondence to: Prof A. Kaye, Tel.: ;61 3 9347 7067; Fax: ;61 3 9347 7695.
INTRODUCTION Sphenoid sinus mucocoele, first described by Berg (1889),1 represents 1% of all paranasal sinus mucocoeles2 and between 15 and 29% of all cases of sphenoid sinus disease.3,4 Mucocoeles
themselves are epithelial-lined lesions containing inspissated mucus, arising as a result of obstruction of the sinus osteum. The obstruction can be the result of inflammation, trauma, congenital anomalies, previous surgery or tumourous lesions.5,6 The differential diagnosis of lesions in the area of the sphenoid include hypophyseal tumours, craniopharyngioma, meningioma, glioma, chordoma, dysgerminoma and cholesteatoma, as well as neoplastic lesions of the skull base, sinus and nasopharynx.7 The lesions may extend to affect adjacent structures, giving rise to a variety of clinical manifestations including headache, facial pain, anosmia, ocular displacement, ocular palsy, visual failure8 and, rarely, hypopituitarism.9 This report highlights an atypical presentation of sphenoid sinus mucocoele and considers its importance in the differential diagnosis of sudden onset of complete ophthalmoplega. CASE REPORT A 66 year old female with a past history of a two stage craniotomy for excision of a right sided middle cranial fossa meningioma 10 years earlier presented with a 2-day history of severe left frontal and parietal headache for which she was admitted to hospital. Three days after the initial onset of the headache she developed sudden onset of complete left ophthalmoplegia. Examination revealed complete left ptosis, a fixed dilated left pupil and complete failure of any eye movements in the left eye. Visual acuity was 6/36 in the right eye and 6/6 in the left. Visual fields were normal. Fundoscopy showed right optic atrophy related to previous meningioma surgery. There was decreased sensation to all modalities in the right trigeminal nerve distribution and a grade one right lower motor neuron seventh nerve palsy, both of which had been documented as being residual from the earlier two stage craniotomy. There were no other cranial nerve abnormalities and the remainer of the physical examination was normal. A computed
Fig. 1A, B CT scan showing relatively low density soft tissue mass in the right infratemporal fossa with anterior displacement of the posterior wall of the maxillary sinus (A) and similar low density, non-soft tissue within the spheniodal sinus (B).
Journal of Clinical Neuroscience (2001) 8(4)
© 2001 Harcourt Publishers Ltd
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Fig. 2A, B Sagittal T1-weighted scans show markedly hyperintense soft tissue filling the enlarged sphenoid sinus (A). Extensive meningioma en plaque is well demonstrated in the contrast enhanced image (small white arrows) (B). The sphenoid sinus contents show no enhancement.
Fig. 3A, B Axial T2-weighted scans (A) showing soft tissue of varying decreased intensity in sphenoidal sinus and right infratemporal fossa. Axial T1-weighted, fat saturated axial images show tissue in both sphenoidal sinuses and infratemporal fossae to be of high signal intensity (B).
tomograph (CT) scan showed a non-enhancing soft tissue mass density material in the sphenoidal sinus and the right infratemporal fossa where it had deformed the posterior margin of the right maxillary sinus (Fig. 1). Magnetic resonance image (MRI) showed that the tissue within the sphenoidal sinus and infratemporal fossa was markedly hyperintense on T1-weighted scans (Fig. 2) and relatively low intensity on T2-weighted scans (Fig. 3). Both CT and MRI showed residual extensive enhancing meningioma en plaque lining the medial aspect of the anterior and right middle cranial fossae. © 2001 Harcourt Publishers Ltd
Endoscopic sphenoethmoidectomy to decompress the mucocoele was undertaken, followed by a revision 6 days later to further decompress the left sphenoid sinus mucocoele. Straw coloured serous fluid was drained at initial operation which grew Gram positive cocci for which the patient received 7 days of intravenous flucloxacillin followed by a week of oral flucloxacillin. Over the ensuing week there was good recovery of eyelid retraction, eye movements and pupil reactivity. Two months after the initial surgery, all left eye functions were normal. Journal of Clinical Neuroscience (2001) 8(4)
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8.
DISCUSSION The clinical manifestations of sphenoid sinus mucocoele are determined by their involvement of surrounding structures. Holt and Rötth (1940)10 suggested the name ‘orbital apex and sphenoidal fissure syndrome’, while Tassman11 in 1947 suggested the term ‘sphenoid fissure-optic canal syndrome with complete ophthalmoplegia’ because the syndrome was considered to be incomplete when the optic nerve or other structures were spared. Proetz (1948)12 identified 13 structures adjacent to the sphenoid sinus that could be involved, including cranial nerves II to VI, dura mater, pituitary, gland, cavernous sinus, internal carotid artery, sphenopalatine ganglion and artery, and pterygoid nerve. Headache, present in 70–80% of cases3,8,13 is the most common clinical symptom. It is typically retro- or supra-orbital, of severe character, radiating to the forehead and occipital regions and lasting from several hours to several days.8 Typically the headaches become more severe and frequent over ensuing months, becoming associated with visual symptoms. The headache probably results from stretching of the dura over the planum sphenoidale.13 Visual disturbance is the second most common group of symptoms, and typically precipitates surgical intervention. Visual disturbances result from involvement of cranial nerves II, III, IV and VI in isolation or combination. The optic nerve is the most frequently involved cranial nerve with reduction in visual acuity in up to 65% of cases.13 The deterioration in visual acuity is usually gradual although sudden blindness may occur.14–16 Up to 25% of cases have bilateral symptoms.16 Palsies of eye movement occur in 30–50% of cases.8,13 The oculomotor nerve is affected more frequently than the trochlear and abducent nerves,17 accounting for 70% of palsies reviewed by Friedmann and Harrison (1970).8 There is often associated optic nerve involvement and isolated oculomotor palsy is rare. Pupil sparing occurs in approximately 50% of cases.18 This case is of interest because a sudden onset of complete ophthalmoplegia associated with sphenoid mucocoele has rarely been reported in the literature. Often, there have only been comments made as to the frequency of individual cranial nerve palsies.8,13 Furthermore, sudden and dramatic onset of signs and symptoms in this case is unusual because typically in this disease the headache is an initial isolated symptom, with a relapsing and remitting course over several months. The increasing intensity and frequency is often later associated with visual symptoms. These features, together with the sparing of the second cranial nerve, highlight that the importance of this presentation of sphenoid sinus mucocoele lies in the differential diagnoses. We emphasise an awareness of sphenoid sinus mucocoele as a cause of complete, sudden onset ophthalmoplegia and its rapid response to prompt surgical intervention and antibiotic treatment. REFERENCES 1.
2. 3. 4. 5. 6. 7.
Berg J. Bidrag till kännedomen om sjukdomarana I näsans biholor samt till läran om cerebro-spinal-vätskas flytning ur näsam. Nordiskt Medicinskt Arkiv 1889; 21: 1–24. Zizmore J, Noyek A. Cysts and benign tumors of the paranasal sinuses. Seminars in Roetgenology 1968; 3: 172–201. Wyllie TW, Kern EB, Djalilian M. Isolated sphenoid sinus lesions. Laryngoscope 1973; 83: 1252–1265. Rothfeild RE, de Vries EJ, Rueger RG. Isolated sphenoid sinus disease. Head Neck 1991; 13: 208–212. Moriyama H, Nakajima T, Honda Y. Studies on mucocoeles of the ethmoid and sphenoid sinuses: Analysis of 47 cases. J Laryngol Otol 1992; 106: 23–27. Natvig K, Larson TE. Mucocoel of the paranasal sinuses. J Laryngol Otol 1992; 92: 107–108. Muneer A, Jones NS. Unilateral abducens nerve palsy: A presenting sing of sphenoid sinus mucocoeles. J Laryngol Otol 1997; 111: 644–646.
Journal of Clinical Neuroscience (2001) 8(4)
9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
Friedmann G, Harrison S. Mucocoele of the sphenoid sinus as a cause of recurrent oculomotor nerve palsy. J Neurol Neurosurg Psychiatry 1970; 33: 172–179. Valvassori GE, Putterman AM. Ophthalmological and radiological findings in sphenoid mucocels. Arch Ophthalmol 1973; 90: 416–419. Holt H, Rötth A. Orbital apex and sphenoid fissure syndrome. Arch Ophthalmol 1940; 24: 731–741. Tassman IS. Complete unilateral ophthalmoplegia due to primary carcinoma of the sphenoid sinus. Arch Ophthalmol 1947; 37: 294–303. Proetz AW. The sphenoid sinus. BMJ 1948; 2: 243–245. Nugent GR, Sprinkle P, Bloor BM. Sphenoid sinus mucocoels. J Neurosurg 1970; 72: 443–451. Blum ME, Larson A. Mucocoels of the sphenoid sinus with sudden blindness. Laryngoscope 1973; 83: 2042–2049. Gore RM, Weinberg PE, Kim KS, et al. Sphenoid sinus mucocoels presenting as intracranial mass on computed tomography. Surg Neurol 1980; 13: 375–379. Wurster CF, Levine TM, Sisson GA. Mucocoel of the sphenoid sinus causing sudden onset blindness. Otolaryngol Head Neck Surg 1986; 94: 257–259. Sethi D, Lau DPC, Chan C. Sphenoid sinus mucocoel presenting with isolated oculomotor nerve palsy. J Laryngol Otol 1997; 111: 471–473. Johnson LN, Hepler RS, Yee RD et al. Sphenoid sinus mucocoel (anterior clinoid variant) mimicking diabetic ophthalmoplegia and retrobulbar neuritis: Am J Ophthalmol 1986; 102: 111–115.
Spinal cord pilocytic astrocytoma with cranial meningeal metastases Ho-Keung Ng1 MD FRCPATH FRCPA FCAP, Clarence H. S. Leung2 MD CHB FRCS (E), Ronald Boet2 MBBS FCA (SA), Wai-Sang Poon2 MB CHB FRCS(G) 1
Department of Anatomical and Cellular Pathology, 2Neurosurgical Unit, Department of Surgery, The Chinese University of Hong Kong, Hong Kong, P.R.China
Summary Dissemination of tumour cells along the cerebrospinal fluid (CSF) pathway has been reported mostly in medulloblastomas, germ cell tumours or high grade gliomas. Juvenile pilocytic astrocytoma (JPA) is usually a benign astrocytoma. However, drop metastases of indolent nature from intracranial tumours to the spinal cord are documented. All of the previously reported cases represent metastases of cerebellar or hypothalamic tumours spreading to the spinal cord. We document in this paper the first report of a spinal cord pilocytic astrocytoma spreading via the CSF to the cerebral meninges. A 9 year old girl had a JPA of C5 to C7 subtotally resected. Two and a half years later she presented with hydrocephalus with radiologically meningeal enhancement. The meninges were biopsied which showed metastatic JPA. The girl was relatively well 4 years after initial surgery with residual tumour. Spinal cord JPA can rarely metastasise to the cranial meninges. Similar to intracranial tumours which spread to the spinal cord, such metastatic lesions are indolent. © 2001 Harcourt Publishers Ltd Journal of Clinical Neuroscience (2001) 8(4), 374–377 © 2001 Harcourt Publishers Ltd DOI: 10.1054/jocn.2000.0762, available online at http://www.idealibrary.com on
Keywords: juveile pilocytic astrocytoma, metastasis, subarachnoid spread Received 21 March 2000 Accepted 4 April 2000 Correspondence to: Dr H. K. Ng, Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, Shatin, Hong Kong. Tel.: 852 2632 3337; Fax: 852 2637 6274; E-mail: [email protected]
© 2001 Harcourt Publishers Ltd