Letters to Editor
However, immediate improvement in syringomyelia and relatively short history indicate congenital predisposition aggravated by growth spurt. Tension related to tethering of the bottom or middle of the spinal cord probably leads to stretch injury that can obstruct the flow of fluid within the central canal or produce fluid cavitation per se. This type of syrinx is unlikely to benefit from foramen magnum decompression, and best treated with surgery to untether the spinal cord. The remarkable improvement in clinical symptoms and radiology indicates the magnitude of tension within the whole of cord, with re‑establishment of CSF dynamics. Though there have been isolated reports of sectioning of filum terminale benefitting Chiari or syringomyelia,[4] holocord syringomyelia improving after detethering of cord has not been reported previously. Holocord syringomyelia with tethered cord indicates caudal traction as the primary etiology, and so requires mere detethering of cord. Foramen magnum decompression is not needed even in presence of tonsillar descent. However, individual cases need to be evaluated carefully before deciding treatment.
Ankur Kapoor, Sivashanmugam Dhandapani, Paramjeet Singh1 Departments of Neurosurgery, and 1Radiology, Post Graduate Institute of Medical Education and Research, Chandigarh, India E‑mail: [email protected]
References 1. 2.
3. 4.
Erkan K, Unal F, Kiris T. Terminal syringomyelia in association with the tethered cord syndrome. Neurosurgery 1999;45:1351‑9. Dhandapani S, Mehta VS, Sharma BS. “Horseshoe cord terminus” sans filum around a bone spur: A rare composite of faulty gastrulation with agenesis of secondary neurulation: Case report. J Neurosurg Pediatr 2013;12:411‑3. Roth M. Cranio‑cervical growth collision: Another explanation of the Arnold‑Chiari malformation and of basilar impression. Neuroradiology 1986;28:187‑94. Royo‑Salvador MB, Solé‑Llenas J, Doménech JM, González‑Adrtio R. Results of the section of the filum terminale in 20 patients with syringomyelia, scoliosis and Chiari malformation. Acta Neurochir (Wien) 2005;147:515‑23. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149450
Received: 06‑11‑2014 Review completed: 01‑12‑2014 Accepted: 17‑12‑2014 Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
Virchow–Robin spaces producing visual field defect Sir, Virchow–Robin spaces (VRS) are perivascular, fluid‑filled canals that surround perforating arteries and veins in the parenchyma of the brain.[1] They may be enlarged to a diameter of five millimeters in healthy humans and are usually harmless. When enlarged, they can disrupt the function of the brain regions into which they project.[1] There is no case report in literature where these spaces had increased in size to produce visual field defects. We report a case of dilated atypical VRS affecting the optic radiations producing changes in visual field. An 83‑year‑old man came to the neuro‑ophthalmology clinic for a routine eye examination. His best corrected visual acuity (BCVA) was 6/9 in right eye and 6/6 in left eye, with refractive error of + 3.5/‑1.5 × 90o in both eyes. Pupils were normal in size and reacting briskly to light in both eyes. Slit lamp evaluation showed grade II nuclear sclerotic changes in both the lens. Intraocular pressure (IOP) by applanation tonometry was 12 mm of Hg in both eyes. On fundus, disc measured 2.2 mm with cup to disc ratio (CDR) of 0.7 in both eyes with healthy neuroretinal rim. Humphrey’s visual field analyzer (24‑2 program) revealed right superior quadrantanopia [Figure 1a and b]. Contrast magnetic resonance imaging (MRI) of brain showed multiple perivascular non‑enhancing empty spaces [Figure 2a and b] in left temporal lobe, largest measuring approximately 2.6 × 1.4 centimeters [Figure 2c and d], without associated mass effect correlating with the field defect. They were hypointense on T1 and fluid‑attenuated inversion‑recovery (FLAIR) sequence, hyperintense on T2 consistent with diagnosis of VRS. The appearance of VRS was first noted in 1843 by Durand Fardel.[2] These spaces are gaps containing interstitial fluid that span between blood vessels and the brain matter which they penetrate.[3] Use of the scanning electron microscope has determined that VRS surrounding blood vessels in the subarachnoid space are not continuous with the subarachnoid space because of the presence of pia mater cells joined by desmosomes.[1] VRS are best seen on T2‑weighted MRI due to their characteristic appearance of distinct round or oval entities with signal intensity equivalent to that of cerebrospinal fluid in the subarachnoid space.[2,4] Normally, VRS are seen in every subject using high‑resolution three‑dimensional MRI with one‑third of them having a size of 3 mm.[5] Normally, a VRS has no mass effect and is located along the blood vessel around 709
Letters to Editor
a
b Figure 1: Automated visual field on Humphrey’s visual field analyzer (24-2 program) of right eye (a) and (b) left eye showing right superior quadrantanopia (pie in the sky)
a
b
c
d
Figure 2: Magentic resonance imaging of brain with intravenous contrast showing multiple non-enhancing CSF density lesions in left temporal lobe (green arrow) that are (a) hyperintense on axial T2 weighted image and (b) hypointense on axial FLAIR image obtained at the same level and showing the largest lesion measuring 2.6 × 1.4 centimeters without associated mass effect in medial temporal lobe (green arrow) that is (c) hyperintense on axial T2 weighted image and (d) hypointense on axial FLAIR image
which it forms.[4] They are most commonly located in the basal ganglia, thalamus, midbrain, cerebellum, hippocampus, white matter of cerebrum and along the optic tract.[6] With advancing age, VRS are found with increasing frequency and of larger size. VRS may be enlarged to a diameter of five millimeters in healthy humans without causing any harm. With further enlargement, they can disrupt the function of the brain regions into which they project.[1] Dilatation can occur on one or both sides of the brain.[2] Extreme dilation has been associated with several specific clinical symptoms. In cases of severe dilation in only one hemisphere, symptoms reported include a non‑specific fainting attack, hypertension, positional vertigo, headache, early recall disturbances, and hemifacial tics. Symptoms associated with severe bilateral dilation include ear pain, dementia and seizures.[6] Other general symptoms associated with dilated VRS (dVRS) include headaches, 710
dizziness, memory impairment, poor concentration, dementia, visual changes, oculomotor abnormality, tremors, seizures, limb weakness, and ataxia.[1] The only reported neuro‑ophthalmologic sign caused by dVRS was the presence of papilledema.[7‑10] Papayannis et al.,[7] reported a patient with a large dVRS in the midbrain inducing an acute obstructive hydrocephalus due to compression of aqueduct of Sylvius while Salzman et al.,[9] and Kanamalla et al.,[10] published similar reports of giant VRS producing mass effect and papilledema. The MR images of dVRS must be distinguished from those of other neurological illnesses like cystic neoplasms, lacunar infarctions, cystic periventricular leukomalacia, cryptococcosis, multiple sclerosis, mucopolysaccharidoses, neurocysticercosis and arachnoid cysts.[2] In our case, atypical VRS (clusters of type II enlarged VR spaces that may be predominantly involving one hemisphere)[2] were found in the left temporal lobe that were dilated to a size of 2.6 × 1.4 centimeters, producing the characteristic defect in the superior visual field (pie in the sky). As per literature search, this is the first report of dVRS causing visual field defect. A judgement on whether dVRS in an individual patient is a normal variant or part of a disease process can be made by taking into account the mass effect on the adjacent tissues on MRI with clinical correlation.[6]
Jyoti H. Matalia, Vimal Krishna Rajput, Bhujang K. Shetty Department of Pediatric Ophthalmology and Neuro‑Ophthalmology, Narayana Nethralaya‑2, Bommasandra, Bangalore, Karnataka, India E‑mail: [email protected]
References 1.
Pollock H, Hutchings M, Weller RO, Zhang ET. Perivascular spaces in the basal ganglia of the human Brain: Their relationship to lacunes. J Anat 1997;191:337‑46. 2. Kwee RM, Kwee TC. Virchow‑Robin Spaces at MR Imaging. Radiographics 2007;27:1071‑86. 3. Fayeye O, Pettorini BL, Foster K, Rodrigues D. Mesencephalic enlarged Virchow–Robin spaces in a 6‑year‑old boy: A case‑based update. Childs Nerv Syst 2010;26:1155‑60. 4. Ogawa T, Okudera T, Fukasawa H, Hashimoto M, Inugami A, Fujita H, et al. Unusual Widening of Virchow–Robin Spaces: MR Appearance. AJNR Am J Neuroradiol 1995;16:1238‑42. 5. Zhu YC, Dufouil C, Mazoyer B, Soumare A, Ricolfi F, Tzourio C, et al. Frequency and location of dilated Virchow‑Robin spaces in elderly people: A population‑based 3D MR imaging study. AJNR Am J Neuroradiol 2011;32:709‑13. 6. Mills S, Cain J, Purandare N, Jackson A. Biomarkers of cerebrovascular disease in dementia. Br J Radiol 2007;80:S128‑45. 7. Papayannis CE, Saidon P, Rugilo CA, Hess D, Rodriguez G, Sica RE, et al. Expanding Virchow Robin spaces in the midbrain causing hydrocephalus. AJNR Am J Neuroradiol 2003;24:1399‑40. 8. House P, Salzman KL, Osborn AG, MacDonald JD, Jenson RL, Couldwell WT. Surgical considerations regarding giant dilations of the perivascular spaces. J Neurosurg 2004;100:820‑4. Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
Letters to Editor
9.
Salzman KL, Osborn AG, House P, Jinkins JR, Ditchfield A, Cooper JA, et al. Giant tumefactive perivascular spaces. AJNR Am J Neuroradiol 2005;26:298‑305. 10. Kanamalla US, Calabro F, Jinkins JR. Cavernous dilatation of mesencephalic Virchow‑Robin spaces with obstructive hydrocephalus. Neuroradiology 2000;42:881‑4.
Access this article online Quick Response Code:
DOI: 10.4103/0028-3886.149452
Received: 12-12-2014 Review completed: 14-12-2014 Accepted: 17-12-2014
Vertebral artery dissection and stroke after scuba diving Sir, A 27‑year‑old man without past medical history developed vertigo and gait imbalance two hours after diving in cold water. The magnetic resonance imaging revealed ischemic lesion in the right side of medulla oblongata in the area of right posterior inferior artery (PICA). Computerized tomography‑angiography (CTA) showed right vertebral artery (VA) dissection [Figure 1a and b]. Six months later patient had no symptoms and the neurological examination was normal. The follow‑up magnetic resonance examination showed partial regression of the previous ischemic lesion and the CTA revealed normal right VA [Figure 1c and d]. The association
c
Justyna Chojdak‑Łukasiewicz, Edyta Dziadkowiak, Joanna Bladowska1, Bogusław Paradowski Departments of Neurology and 1General Radiology, Interventional Radiology and Neuroradiology, Wroclaw Medical University, Wroclaw, Poland E‑mail: [email protected]
Website: www.neurologyindia.com PMID: ***
a
between scuba diving and cerebral arterial dissection is known but rare.[1,2]
b
d
Figure 1: Brain MR shows an ischemic lesion (arrow) in the right side of the medulla oblongata (a). CT angiography (b), reveals dissection of the right vertebral artery (VA) at the level of C2-C3. The follow-up MR (c) Regression of the lesion, the CT angiography (d) Demonstrates the normal right VA
Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
References 1. Konno K, Kurita H, Ito N, Shiokawa Y, Saito I. Extracranial vertebral artery dissection caused by scuba diving. J Neurol 2001;248:816‑7. 2. Brajkovic S, Riboldi G, Govoni A, Corti S, Bresolin N, Comi GP. Growing evidence about the relationship between vessel dissection and scuba diving. Case Rep Neurol 2013;12:155‑61. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149455
Received: 24-08-2014 Review completed: 25-08-2014 Accepted: 09-10-2014
An unusual cause of low backache: Lumbar interspinous bursitis Sir, A 52‑year‑old male presented with low back pain of considerable intensity. Pain was essentially localized to lower lumbar region and got exaggerated on spinal extension. There was no history suggestive of radiculopathy or claudication. Magnetic resonance imaging (MRI) of lumbo‑sacral spine revealed inflammatory fluid‑like hyperintense signal in the interspinous ligaments at L3‑4 and L4‑5 levels on short tau inversion recovery (STIR) images [Figures 1a and b]; consistent with interspinous bursitis. Lumbar interspinous bursitis, also called Baastrup disease, is characterized by close approximation and contact of adjacent spinous processes (kissing spine) with resultant enlargement, flattening, reactive sclerosis of apposing interspinous surfaces forming neo‑articulation. [1,2] Repetitive strain on the interspinous ligaments is thought 711
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.
However, immediate improvement in syringomyelia and relatively short history indicate congenital predisposition aggravated by growth spurt. Tension related to tethering of the bottom or middle of the spinal cord probably leads to stretch injury that can obstruct the flow of fluid within the central canal or produce fluid cavitation per se. This type of syrinx is unlikely to benefit from foramen magnum decompression, and best treated with surgery to untether the spinal cord. The remarkable improvement in clinical symptoms and radiology indicates the magnitude of tension within the whole of cord, with re‑establishment of CSF dynamics. Though there have been isolated reports of sectioning of filum terminale benefitting Chiari or syringomyelia,[4] holocord syringomyelia improving after detethering of cord has not been reported previously. Holocord syringomyelia with tethered cord indicates caudal traction as the primary etiology, and so requires mere detethering of cord. Foramen magnum decompression is not needed even in presence of tonsillar descent. However, individual cases need to be evaluated carefully before deciding treatment.
Ankur Kapoor, Sivashanmugam Dhandapani, Paramjeet Singh1 Departments of Neurosurgery, and 1Radiology, Post Graduate Institute of Medical Education and Research, Chandigarh, India E‑mail: [email protected]
References 1. 2.
3. 4.
Erkan K, Unal F, Kiris T. Terminal syringomyelia in association with the tethered cord syndrome. Neurosurgery 1999;45:1351‑9. Dhandapani S, Mehta VS, Sharma BS. “Horseshoe cord terminus” sans filum around a bone spur: A rare composite of faulty gastrulation with agenesis of secondary neurulation: Case report. J Neurosurg Pediatr 2013;12:411‑3. Roth M. Cranio‑cervical growth collision: Another explanation of the Arnold‑Chiari malformation and of basilar impression. Neuroradiology 1986;28:187‑94. Royo‑Salvador MB, Solé‑Llenas J, Doménech JM, González‑Adrtio R. Results of the section of the filum terminale in 20 patients with syringomyelia, scoliosis and Chiari malformation. Acta Neurochir (Wien) 2005;147:515‑23. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149450
Received: 06‑11‑2014 Review completed: 01‑12‑2014 Accepted: 17‑12‑2014 Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
Virchow–Robin spaces producing visual field defect Sir, Virchow–Robin spaces (VRS) are perivascular, fluid‑filled canals that surround perforating arteries and veins in the parenchyma of the brain.[1] They may be enlarged to a diameter of five millimeters in healthy humans and are usually harmless. When enlarged, they can disrupt the function of the brain regions into which they project.[1] There is no case report in literature where these spaces had increased in size to produce visual field defects. We report a case of dilated atypical VRS affecting the optic radiations producing changes in visual field. An 83‑year‑old man came to the neuro‑ophthalmology clinic for a routine eye examination. His best corrected visual acuity (BCVA) was 6/9 in right eye and 6/6 in left eye, with refractive error of + 3.5/‑1.5 × 90o in both eyes. Pupils were normal in size and reacting briskly to light in both eyes. Slit lamp evaluation showed grade II nuclear sclerotic changes in both the lens. Intraocular pressure (IOP) by applanation tonometry was 12 mm of Hg in both eyes. On fundus, disc measured 2.2 mm with cup to disc ratio (CDR) of 0.7 in both eyes with healthy neuroretinal rim. Humphrey’s visual field analyzer (24‑2 program) revealed right superior quadrantanopia [Figure 1a and b]. Contrast magnetic resonance imaging (MRI) of brain showed multiple perivascular non‑enhancing empty spaces [Figure 2a and b] in left temporal lobe, largest measuring approximately 2.6 × 1.4 centimeters [Figure 2c and d], without associated mass effect correlating with the field defect. They were hypointense on T1 and fluid‑attenuated inversion‑recovery (FLAIR) sequence, hyperintense on T2 consistent with diagnosis of VRS. The appearance of VRS was first noted in 1843 by Durand Fardel.[2] These spaces are gaps containing interstitial fluid that span between blood vessels and the brain matter which they penetrate.[3] Use of the scanning electron microscope has determined that VRS surrounding blood vessels in the subarachnoid space are not continuous with the subarachnoid space because of the presence of pia mater cells joined by desmosomes.[1] VRS are best seen on T2‑weighted MRI due to their characteristic appearance of distinct round or oval entities with signal intensity equivalent to that of cerebrospinal fluid in the subarachnoid space.[2,4] Normally, VRS are seen in every subject using high‑resolution three‑dimensional MRI with one‑third of them having a size of 3 mm.[5] Normally, a VRS has no mass effect and is located along the blood vessel around 709
Letters to Editor
a
b Figure 1: Automated visual field on Humphrey’s visual field analyzer (24-2 program) of right eye (a) and (b) left eye showing right superior quadrantanopia (pie in the sky)
a
b
c
d
Figure 2: Magentic resonance imaging of brain with intravenous contrast showing multiple non-enhancing CSF density lesions in left temporal lobe (green arrow) that are (a) hyperintense on axial T2 weighted image and (b) hypointense on axial FLAIR image obtained at the same level and showing the largest lesion measuring 2.6 × 1.4 centimeters without associated mass effect in medial temporal lobe (green arrow) that is (c) hyperintense on axial T2 weighted image and (d) hypointense on axial FLAIR image
which it forms.[4] They are most commonly located in the basal ganglia, thalamus, midbrain, cerebellum, hippocampus, white matter of cerebrum and along the optic tract.[6] With advancing age, VRS are found with increasing frequency and of larger size. VRS may be enlarged to a diameter of five millimeters in healthy humans without causing any harm. With further enlargement, they can disrupt the function of the brain regions into which they project.[1] Dilatation can occur on one or both sides of the brain.[2] Extreme dilation has been associated with several specific clinical symptoms. In cases of severe dilation in only one hemisphere, symptoms reported include a non‑specific fainting attack, hypertension, positional vertigo, headache, early recall disturbances, and hemifacial tics. Symptoms associated with severe bilateral dilation include ear pain, dementia and seizures.[6] Other general symptoms associated with dilated VRS (dVRS) include headaches, 710
dizziness, memory impairment, poor concentration, dementia, visual changes, oculomotor abnormality, tremors, seizures, limb weakness, and ataxia.[1] The only reported neuro‑ophthalmologic sign caused by dVRS was the presence of papilledema.[7‑10] Papayannis et al.,[7] reported a patient with a large dVRS in the midbrain inducing an acute obstructive hydrocephalus due to compression of aqueduct of Sylvius while Salzman et al.,[9] and Kanamalla et al.,[10] published similar reports of giant VRS producing mass effect and papilledema. The MR images of dVRS must be distinguished from those of other neurological illnesses like cystic neoplasms, lacunar infarctions, cystic periventricular leukomalacia, cryptococcosis, multiple sclerosis, mucopolysaccharidoses, neurocysticercosis and arachnoid cysts.[2] In our case, atypical VRS (clusters of type II enlarged VR spaces that may be predominantly involving one hemisphere)[2] were found in the left temporal lobe that were dilated to a size of 2.6 × 1.4 centimeters, producing the characteristic defect in the superior visual field (pie in the sky). As per literature search, this is the first report of dVRS causing visual field defect. A judgement on whether dVRS in an individual patient is a normal variant or part of a disease process can be made by taking into account the mass effect on the adjacent tissues on MRI with clinical correlation.[6]
Jyoti H. Matalia, Vimal Krishna Rajput, Bhujang K. Shetty Department of Pediatric Ophthalmology and Neuro‑Ophthalmology, Narayana Nethralaya‑2, Bommasandra, Bangalore, Karnataka, India E‑mail: [email protected]
References 1.
Pollock H, Hutchings M, Weller RO, Zhang ET. Perivascular spaces in the basal ganglia of the human Brain: Their relationship to lacunes. J Anat 1997;191:337‑46. 2. Kwee RM, Kwee TC. Virchow‑Robin Spaces at MR Imaging. Radiographics 2007;27:1071‑86. 3. Fayeye O, Pettorini BL, Foster K, Rodrigues D. Mesencephalic enlarged Virchow–Robin spaces in a 6‑year‑old boy: A case‑based update. Childs Nerv Syst 2010;26:1155‑60. 4. Ogawa T, Okudera T, Fukasawa H, Hashimoto M, Inugami A, Fujita H, et al. Unusual Widening of Virchow–Robin Spaces: MR Appearance. AJNR Am J Neuroradiol 1995;16:1238‑42. 5. Zhu YC, Dufouil C, Mazoyer B, Soumare A, Ricolfi F, Tzourio C, et al. Frequency and location of dilated Virchow‑Robin spaces in elderly people: A population‑based 3D MR imaging study. AJNR Am J Neuroradiol 2011;32:709‑13. 6. Mills S, Cain J, Purandare N, Jackson A. Biomarkers of cerebrovascular disease in dementia. Br J Radiol 2007;80:S128‑45. 7. Papayannis CE, Saidon P, Rugilo CA, Hess D, Rodriguez G, Sica RE, et al. Expanding Virchow Robin spaces in the midbrain causing hydrocephalus. AJNR Am J Neuroradiol 2003;24:1399‑40. 8. House P, Salzman KL, Osborn AG, MacDonald JD, Jenson RL, Couldwell WT. Surgical considerations regarding giant dilations of the perivascular spaces. J Neurosurg 2004;100:820‑4. Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
Letters to Editor
9.
Salzman KL, Osborn AG, House P, Jinkins JR, Ditchfield A, Cooper JA, et al. Giant tumefactive perivascular spaces. AJNR Am J Neuroradiol 2005;26:298‑305. 10. Kanamalla US, Calabro F, Jinkins JR. Cavernous dilatation of mesencephalic Virchow‑Robin spaces with obstructive hydrocephalus. Neuroradiology 2000;42:881‑4.
Access this article online Quick Response Code:
DOI: 10.4103/0028-3886.149452
Received: 12-12-2014 Review completed: 14-12-2014 Accepted: 17-12-2014
Vertebral artery dissection and stroke after scuba diving Sir, A 27‑year‑old man without past medical history developed vertigo and gait imbalance two hours after diving in cold water. The magnetic resonance imaging revealed ischemic lesion in the right side of medulla oblongata in the area of right posterior inferior artery (PICA). Computerized tomography‑angiography (CTA) showed right vertebral artery (VA) dissection [Figure 1a and b]. Six months later patient had no symptoms and the neurological examination was normal. The follow‑up magnetic resonance examination showed partial regression of the previous ischemic lesion and the CTA revealed normal right VA [Figure 1c and d]. The association
c
Justyna Chojdak‑Łukasiewicz, Edyta Dziadkowiak, Joanna Bladowska1, Bogusław Paradowski Departments of Neurology and 1General Radiology, Interventional Radiology and Neuroradiology, Wroclaw Medical University, Wroclaw, Poland E‑mail: [email protected]
Website: www.neurologyindia.com PMID: ***
a
between scuba diving and cerebral arterial dissection is known but rare.[1,2]
b
d
Figure 1: Brain MR shows an ischemic lesion (arrow) in the right side of the medulla oblongata (a). CT angiography (b), reveals dissection of the right vertebral artery (VA) at the level of C2-C3. The follow-up MR (c) Regression of the lesion, the CT angiography (d) Demonstrates the normal right VA
Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
References 1. Konno K, Kurita H, Ito N, Shiokawa Y, Saito I. Extracranial vertebral artery dissection caused by scuba diving. J Neurol 2001;248:816‑7. 2. Brajkovic S, Riboldi G, Govoni A, Corti S, Bresolin N, Comi GP. Growing evidence about the relationship between vessel dissection and scuba diving. Case Rep Neurol 2013;12:155‑61. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149455
Received: 24-08-2014 Review completed: 25-08-2014 Accepted: 09-10-2014
An unusual cause of low backache: Lumbar interspinous bursitis Sir, A 52‑year‑old male presented with low back pain of considerable intensity. Pain was essentially localized to lower lumbar region and got exaggerated on spinal extension. There was no history suggestive of radiculopathy or claudication. Magnetic resonance imaging (MRI) of lumbo‑sacral spine revealed inflammatory fluid‑like hyperintense signal in the interspinous ligaments at L3‑4 and L4‑5 levels on short tau inversion recovery (STIR) images [Figures 1a and b]; consistent with interspinous bursitis. Lumbar interspinous bursitis, also called Baastrup disease, is characterized by close approximation and contact of adjacent spinous processes (kissing spine) with resultant enlargement, flattening, reactive sclerosis of apposing interspinous surfaces forming neo‑articulation. [1,2] Repetitive strain on the interspinous ligaments is thought 711
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.
