Letters to Editor
3. 4.
5. 6. 7.
Pilomyxoid astrocytoma of the spinal cord: Report of three cases. Neurosurgery 2005;56:191. Arulrajah S, Huisman TA. Pilomyxoid astrocytoma of the spinal cord with cerebrospinal fluid and peritoneal metastasis. Neuropediatrics 2008;39:243‑5. Matsuzaki K, Kageji T, Watanabe H, Hirose T, Nagahiro S. Pilomyxoid astrocytoma of the cervical spinal cord successfully treated with chemotherapy: Case report. Neurol Med Chir (Tokyo) 2010;50:939‑42. Mendiratta‑Lala M, Kader Ellika S, Gutierrez JA, Patel SC, Jain R. Spinal cord pilomyxoid astrocytoma: An unusual tumor. J Neuroimaging 2007;17:371‑4. Tsugu H, Oshiro S, Yanai F, Komatsu F, Abe H, Fukushima T, et al. Management of pilomyxoid astrocytomas: Our experience. Anticancer Res 2009;29:919‑26. Paraskevopoulos D, Patsalas I, Karkavelas G, Foroglou N, Magras I, Selviaridis P. Pilomyxoid astrocytoma of the cervical spinal cord in a child with rapid progression into glioblastoma: Case report and literature review. Childs Nerv Syst 2011;27:313‑21. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125376
Received: 09‑07‑2013 Review completed: 05‑08‑2013 Accepted: 18‑12‑2013
sequences. With a diagnosis of right parasagittal cavernoma the patient was taken up for right parasagittal craniotomy and total excision of the cavernoma was done. The diagnosis of cavernoma was confirmed on histopathological examination. The post‑operative period was uneventful. At three months follow‑up she regained the normal strength of ankle dorsiflexion. Lesions of the parietal lobe, in the parasagittal region near the foot homunculus of the motor strip may produce foot drop.[4] Although rare and underappreciated, many cerebral lesions such as glioma, [1] meningioma, [1,2,4] abscess,[1] head injury,[1] metastasis,[3,5] cerebral hemorrhage and demyelination plaques[1] can present with foot drop. Review of the literature revealed twenty four cases of foot drop of cerebral origin. The most common causes identified were glioma followed by meningioma and trauma. However, cerebral cavernoma presenting with foot drop has not been reported, probably our patient may be first such case. Most previous reported cases had accompanying upper motor neuron signs or symptoms such as hyperreflexia, ankle clonus and Babinski signs similar to our patient.[1,2] Good results[1,5] were achieved in most of the cerebral causes of foot drop as seen in our patient. Central causes of foot drop should be considered in the differential diagnosis of foot drop when associated with upper motor neuron signs.
Foot drop caused by cerebral cavernous angioma Sir, Foot drop is defined as loss of dorsiflexion of ankle and is commonly due to lesions of the peroneal nerve or fifth lumbar nerve root.[1,2] Rarely it can be due to cerebral lesions and the most common causes are tumors,[1‑5] trauma[2] and demyelination plaques.[1] Foot drop due to cerebral cavernoma has not been reported. A 35‑year‑old woman presented with a history of focal seizures and weakness of the left lower limb of 10 days duration. Neurological examination revealed spasticity of the left lower limb and extensor plantar response and weakness of ankle dorsiflexion (grade 2/5). Brain computed tomography revealed a hyperdense lesion in the right parasagittal parietal region [Figure 1a] and brain magnetic resonance imaging revealed a heterogeneous, altered signal intensity lesion in the right parasagittal parietal region, which was hypointense with hyperintense foci and no contrast enhancement in T1W images [Figure 1b, e and f].The lesion was hyperintense with hypointense peripheral rim on T2W [Figure 1c] and fluid‑attenuated inversion recovery [Figure 1d] Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
a
b
c
d
e
f Figure 1: Imaging of the cavernoma
679
Letters to Editor
B. C. M. Prasad, V. V. Ramesh Chandra, V. Jayachandar Department of Neurosurgery, SVIMS, Tirupati, Andhra Pradesh, India E‑mail: [email protected]
References 1. 2. 3. 4 5.
Eskandary H, Hamzei A, Yasamy MT. Foot drop following brain lesion. Surg Neurol 1995;43:89‑90. Baysefer A, Erdoğan E, Sali A, Sirin S, Seber N. Foot drop following brain tumors: Case reports. Minim Invasive Neurosurg 1998;41:97‑8. Chatterjee A, Orbach D. Isolated foot weakness caused by a parasagittal metastatic parotid adenocarcinoma. Neurol India 2004;52:286‑7. Ozdemir N, Citak G, Acar UD. Spastic foot drop caused by a brain tumour: A case report. Br J Neurosurg 2004;18:314‑5. Westhout FD, Paré LS, Linskey ME. Central causes of foot drop: Rare and underappreciated differential diagnoses. J Spinal Cord Med 2007;30:62‑6. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125378
Received: 01‑08‑2013 Review completed: 02-08-2013 Accepted: 03-12-2013
Single, small, spontaneous, accessory, closed type, frontal sinus pericranii in a child: Favorable outcome with surgical excision
5 cm × 4 cm × 3 cm soft, fluctuant, compressible and completely reducible on standing erect [Figure 1a]. With cough, on lying down and bending forward the lesion would become tense. There was no bruit. Non‑contrast computed tomography scan of head revealed a large homogenous isodense soft‑tissue collection (5 cm × 4 cm × 3 cm) in the right frontal region [Figure 1b]. Bone window revealed defect in diploe [Figure 1b]. Contrast magnetic resonance imaging brain [Figure 1c and d] and percutaneous direct puncture venogram [Figure 1e] confirmed the diagnosis of closed type (non‑drainer) sinus pericranii. Patient was electively operated after informed consent from parents. Patient was taken up for surgery and intra‑operatively there were trans‑diploic dilated venous channels with communication between cortical draining veins into superior sagittal sinus and extracranial subgaleal and periosteal vessels [Figure 2a]. Sinus pericranii was completely excised and communication with intracranial vessels was truncated at the dura mater. Bone defect was covered using split thickness autologous bone grafting [Figure 2b]. Surgery went uneventful with minimal blood loss and he was discharged in stable condition with no residual lesion [Figure 2c] or new onset sensorimotor deficits. Biopsy confirmed presence of vascular endothelium in specimen sent. At 3‑month follow‑up visit, he had surgical outcome with acceptable cosmesis and no recurrence or fresh neurologic deficits. First described as “varix spurious circumscriptus venae diploicae frontalis” by Hecker in 1845, [4] and later as “Sinus Pericranii” by Stromeyer in 1850,[5] is an anomalous trans‑diploic communication between intra‑cranial and trans‑cranial vessels through dilated emissary veins. It is classified as congenital, spontaneous or traumatic.[6] Recent evidence suggests
Sir, Sinus pericranii is a vascular anomaly presenting mostly in childhood It is a well‑circumscribed, soft compressible mass consisting of venous malformation with abnormal communication between intracranial and extra‑cranial venous channels though a precise calvarial defect, usually located in midline over frontal, parietal or occipital bone along sagittal sinus and very rarely reported in temporal bone or along transverse sinus.[1‑3] We describe one such a rare case. A 9‑year‑old boy presented with gradually progressive swelling over forehead 6 cm above glabella with no history of trauma. The swelling was non‑pulsatile 680
Figure 1a: Clinical lateral profile of patient with head bending downwards showing subgalleal swelling (arrow)
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
3. 4.
5. 6. 7.
Pilomyxoid astrocytoma of the spinal cord: Report of three cases. Neurosurgery 2005;56:191. Arulrajah S, Huisman TA. Pilomyxoid astrocytoma of the spinal cord with cerebrospinal fluid and peritoneal metastasis. Neuropediatrics 2008;39:243‑5. Matsuzaki K, Kageji T, Watanabe H, Hirose T, Nagahiro S. Pilomyxoid astrocytoma of the cervical spinal cord successfully treated with chemotherapy: Case report. Neurol Med Chir (Tokyo) 2010;50:939‑42. Mendiratta‑Lala M, Kader Ellika S, Gutierrez JA, Patel SC, Jain R. Spinal cord pilomyxoid astrocytoma: An unusual tumor. J Neuroimaging 2007;17:371‑4. Tsugu H, Oshiro S, Yanai F, Komatsu F, Abe H, Fukushima T, et al. Management of pilomyxoid astrocytomas: Our experience. Anticancer Res 2009;29:919‑26. Paraskevopoulos D, Patsalas I, Karkavelas G, Foroglou N, Magras I, Selviaridis P. Pilomyxoid astrocytoma of the cervical spinal cord in a child with rapid progression into glioblastoma: Case report and literature review. Childs Nerv Syst 2011;27:313‑21. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125376
Received: 09‑07‑2013 Review completed: 05‑08‑2013 Accepted: 18‑12‑2013
sequences. With a diagnosis of right parasagittal cavernoma the patient was taken up for right parasagittal craniotomy and total excision of the cavernoma was done. The diagnosis of cavernoma was confirmed on histopathological examination. The post‑operative period was uneventful. At three months follow‑up she regained the normal strength of ankle dorsiflexion. Lesions of the parietal lobe, in the parasagittal region near the foot homunculus of the motor strip may produce foot drop.[4] Although rare and underappreciated, many cerebral lesions such as glioma, [1] meningioma, [1,2,4] abscess,[1] head injury,[1] metastasis,[3,5] cerebral hemorrhage and demyelination plaques[1] can present with foot drop. Review of the literature revealed twenty four cases of foot drop of cerebral origin. The most common causes identified were glioma followed by meningioma and trauma. However, cerebral cavernoma presenting with foot drop has not been reported, probably our patient may be first such case. Most previous reported cases had accompanying upper motor neuron signs or symptoms such as hyperreflexia, ankle clonus and Babinski signs similar to our patient.[1,2] Good results[1,5] were achieved in most of the cerebral causes of foot drop as seen in our patient. Central causes of foot drop should be considered in the differential diagnosis of foot drop when associated with upper motor neuron signs.
Foot drop caused by cerebral cavernous angioma Sir, Foot drop is defined as loss of dorsiflexion of ankle and is commonly due to lesions of the peroneal nerve or fifth lumbar nerve root.[1,2] Rarely it can be due to cerebral lesions and the most common causes are tumors,[1‑5] trauma[2] and demyelination plaques.[1] Foot drop due to cerebral cavernoma has not been reported. A 35‑year‑old woman presented with a history of focal seizures and weakness of the left lower limb of 10 days duration. Neurological examination revealed spasticity of the left lower limb and extensor plantar response and weakness of ankle dorsiflexion (grade 2/5). Brain computed tomography revealed a hyperdense lesion in the right parasagittal parietal region [Figure 1a] and brain magnetic resonance imaging revealed a heterogeneous, altered signal intensity lesion in the right parasagittal parietal region, which was hypointense with hyperintense foci and no contrast enhancement in T1W images [Figure 1b, e and f].The lesion was hyperintense with hypointense peripheral rim on T2W [Figure 1c] and fluid‑attenuated inversion recovery [Figure 1d] Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
a
b
c
d
e
f Figure 1: Imaging of the cavernoma
679
Letters to Editor
B. C. M. Prasad, V. V. Ramesh Chandra, V. Jayachandar Department of Neurosurgery, SVIMS, Tirupati, Andhra Pradesh, India E‑mail: [email protected]
References 1. 2. 3. 4 5.
Eskandary H, Hamzei A, Yasamy MT. Foot drop following brain lesion. Surg Neurol 1995;43:89‑90. Baysefer A, Erdoğan E, Sali A, Sirin S, Seber N. Foot drop following brain tumors: Case reports. Minim Invasive Neurosurg 1998;41:97‑8. Chatterjee A, Orbach D. Isolated foot weakness caused by a parasagittal metastatic parotid adenocarcinoma. Neurol India 2004;52:286‑7. Ozdemir N, Citak G, Acar UD. Spastic foot drop caused by a brain tumour: A case report. Br J Neurosurg 2004;18:314‑5. Westhout FD, Paré LS, Linskey ME. Central causes of foot drop: Rare and underappreciated differential diagnoses. J Spinal Cord Med 2007;30:62‑6. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125378
Received: 01‑08‑2013 Review completed: 02-08-2013 Accepted: 03-12-2013
Single, small, spontaneous, accessory, closed type, frontal sinus pericranii in a child: Favorable outcome with surgical excision
5 cm × 4 cm × 3 cm soft, fluctuant, compressible and completely reducible on standing erect [Figure 1a]. With cough, on lying down and bending forward the lesion would become tense. There was no bruit. Non‑contrast computed tomography scan of head revealed a large homogenous isodense soft‑tissue collection (5 cm × 4 cm × 3 cm) in the right frontal region [Figure 1b]. Bone window revealed defect in diploe [Figure 1b]. Contrast magnetic resonance imaging brain [Figure 1c and d] and percutaneous direct puncture venogram [Figure 1e] confirmed the diagnosis of closed type (non‑drainer) sinus pericranii. Patient was electively operated after informed consent from parents. Patient was taken up for surgery and intra‑operatively there were trans‑diploic dilated venous channels with communication between cortical draining veins into superior sagittal sinus and extracranial subgaleal and periosteal vessels [Figure 2a]. Sinus pericranii was completely excised and communication with intracranial vessels was truncated at the dura mater. Bone defect was covered using split thickness autologous bone grafting [Figure 2b]. Surgery went uneventful with minimal blood loss and he was discharged in stable condition with no residual lesion [Figure 2c] or new onset sensorimotor deficits. Biopsy confirmed presence of vascular endothelium in specimen sent. At 3‑month follow‑up visit, he had surgical outcome with acceptable cosmesis and no recurrence or fresh neurologic deficits. First described as “varix spurious circumscriptus venae diploicae frontalis” by Hecker in 1845, [4] and later as “Sinus Pericranii” by Stromeyer in 1850,[5] is an anomalous trans‑diploic communication between intra‑cranial and trans‑cranial vessels through dilated emissary veins. It is classified as congenital, spontaneous or traumatic.[6] Recent evidence suggests
Sir, Sinus pericranii is a vascular anomaly presenting mostly in childhood It is a well‑circumscribed, soft compressible mass consisting of venous malformation with abnormal communication between intracranial and extra‑cranial venous channels though a precise calvarial defect, usually located in midline over frontal, parietal or occipital bone along sagittal sinus and very rarely reported in temporal bone or along transverse sinus.[1‑3] We describe one such a rare case. A 9‑year‑old boy presented with gradually progressive swelling over forehead 6 cm above glabella with no history of trauma. The swelling was non‑pulsatile 680
Figure 1a: Clinical lateral profile of patient with head bending downwards showing subgalleal swelling (arrow)
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
