[Downloaded free from http://www.neurologyindia.com on Thursday, March 13, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor organ involvement, primary lung infection may be subclinical.[2] Some authors hold that lung nodules on imaging in a setting of CNA represent pulmonary involvement.[1] Joung et al.[1] have described an immunocompetent patient who had concurrent pulmonary aspergillosis and CNA. They also reported the co-existence of both pathologies in the immunocompromised. However in their case, the diagnosis of cerebral nocardiosis preceded that of pulmonary aspergillosis. In our patient there was a preceding history of pulmonary aspergillosis that led to initiation of empirical antifungal treatment. At the time of diagnosis of pulmonary aspergillosis, the possibility of pulmonary nocardiosis was not kept in mind it would thus not be possible to say if the brain abscesses in this patient were a delayed manifestation of systemic nocardial infection. She was on steroids for interstitial lung disease but this was tapered off as soon as the diagnosis of nocardial cerebral abscess was established. The standard regime[4] of trimethoprim and sulfamethoxazole was given to our patient with gratifying results. CNA have high morbidity and mortality (30%)[2,5] as compared to 10% for other abscesses.[2] This is said to be highest among all cerebral abscesses.[3] Mortality is greater in immunocompromised (55%) as compared to immunocompetent (20%) patients.[1] Hence early aggressive treatment needs to be instituted and the possibility of nocardiosis should be considered in all brain abscesses. Serological tests are not useful[2] and only cultures can establish a diagnosis of nocardial abscess. Antimicrobial drug sensitivity testing is not standardized[6] and empirical sulfonamides are the backbone of treatment. [5] Various other antibiotics such as linezolid, amoxicillin/clavulanate, imipenem, minocycline etc., have also been described.[2] Due to high relapse rate,[6] prolonged therapy (several months)[2,5,6] is advocated. Prasad Krishnan, Rohit Mishra, Rajaraman Kartikueyan, Eswara Rao Thamatapu Department of Neurosurgery, National Neurosciences Centre, Kolkata, West Bengal, India E-mail: prasad.krishnan@rediffmail.com References 1. 2. 3. Joung MK, Kong DS, Song JH, Peck KR. Concurrent Nocardia related brain abscess and semi-invasive pulmonary aspergillosis in an immunocompetent patient. J Korean Neurosurg Soc 2011;49:305-7. Tamarit M, Poveda P, Barón M, Del Pozo JM. Four cases of nocardial brain abscess. Surg Neurol Int 2012;3:88. Patil A, Cherian A, Iype T, Sandeep P. Nocardial brain abscess in an immunocompetent individual. Neurol India 2011;59:779-82. Neurology India | Jan-Feb 2014 | Vol 62 | Issue 1 4. 5. 6. Mathisen GE, Johnson JP. Brain abscess. Clin Infect Dis 1997;25:763-79. Dias M, Nagarathna S, Mahadevan A, Chandramouli BA, Chandramuki A. Nocardial brain abscess in an immunocompetent host. Indian J Med Microbiol 2008;26:274-7. Sabuncuoğlu H, Cibali Açikgo Z Z, Caydere M, Ustün H, Semih Keskil I. Nocardia farcinica brain abscess: A case report and review of the literature. Neurocirugia (Astur) 2004;15:600-3. Access this article online Quick Response Code: Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.128359 Received: 22-10-2013 Review completed: 29-12-2013 Accepted: 29-01-2014 Rapidly progressive dementia, Parkinsonism and myoclonus: An unusual presentation of dural arteriovenous fistula Sir, Dural arteriovenous fistulas (DAVFs) consist of arteriovenous shunts between meningeal arteries and veins within the dura and account for 10-15% of cerebrovascular malformations. [1-3] The clinical presentation is heterogeneous headache , pulsatile tinnitus, proptosis, dementia, parkinsonism and intracranial hemorrhage.[3-7] The presenting feature of DAVFs is related to the location and pattern of venous drainage.[3] Untreated aggressive DAVF have an annual event rate of 15% and an annual mortality rate of 10.4%.[8] We report an untreated aggressive DAVF presenting with dementia, parkinsonism and myoclonus. A 73-year-old female patient presented with 3 months history of progressive cognitive decline, gait difficulty and myoclonic jerks. Her initial symptom was cognitive decline in the form of memory impairment, disorientation to time and visuospatial disorientation which rapidly progressed over 2 months to complete inability to comprehend and attend to her routine activities. About 3 weeks into her illness, she developed tremulousness of the hands and stiffness of all limbs with slowness of gait. She also developed frequent jerking movements of her limbs after 1 month. Her illness progressed rapidly and she became bedridden and dependent for all activities of daily living by 2½ months. She had a past 107 [Downloaded free from http://www.neurologyindia.com on Thursday, March 13, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor history of long standing diabetes mellitus and systemic hypertension. Neurological examination at presentation revealed significant and diffuse cognitive impairment with impaired comprehension and poor attention. She had moderate rigidity of all limbs with normal deep tendon reflexes and flexor plantar responses. She had stimulus sensitive multifocal myoclonus of upper limbs. Computed tomography (CT) brain showed prominent and hyperdense transverse sigmoid junction with a few calcific foci raising the suspicion of a DAVF fistula [Figure 1]. Magnetic resonance imaging (MRI) brain showed bilateral DAVFs involving transverse sinus-sigmoid sinus junctions with prominent draining vein and hypertrophied feeders from extracranial arteries bilaterally [Figure 2]. Ill-defined white matter hyperintensities were also seen in bilateral cerebral hemispheres. During the course of evaluation, she had worsening of lower respiratory tract infection, developed sepsis which progressed to multiorgan failure with hypotension, because of which confirmatory digital substraction angiography could not be done. She expired within 1 week of admission. DAVFs most commonly develop in the region of the transverse and sigmoid sinuses[3,4] and comprise more than 60% of all DAVFs.[2] The exact pathogenesis of DAVF is unknown and it has been postulated that thrombosis of the dural venous sinuses may be the initial triggering event in the development of DAVFs.[9] As a sequelae to sinus thrombosis or large amounts of flow through the DAVF there is an increase in pressure within the dural sinuses, resulting in venous hypertension. The retrograde transmission of venous pressure may occur into the superior sagittal sinus, straight sinus and cortical veins.[4,9] The major risk factor for aggressive behavior of DAVFs, including intracranial hemorrhage is the retrograde transmission of pressure causing enlargement of cortical veins.[10,11] The increased venous pressure results in venous a b hypertension, congestion and impaired parenchymal venous drainage resulting in ischemia, leading to progressive encephalopathy with dementia.[11,12] In addition to cognitive deterioration, nonspecific clinical picture may delay detection of the responsible lesion, permitting further deterioration in the absence of treatment, as in our patient. Progressive headache and cranial bruit in a patient with dementia should raise suspicion of an underlying vascular lesion. In a large series of DAVFs, 3-12% of patients with DAVFs presented with predominantly progressive cognitive deficits with or without decreased level of consciousness or lateralizing findings.[11,13] The MRI abnormalities in our patients arose as a consequence of venous outflow obstruction and correlate well with the potential for aggressive behavior from these high-flow DAVFs. Gradient or susceptibility weighted imaging may be helpful in the diagnosis of DAVF even before angiogram. Angiography is imaging of choice for the diagnosis of a DAVF and also provides a route for endovascular therapy.[11] CT or MR studies most often show minimal or no abnormalities in the case of DAVFs venous outflow obstruction, and and a high degree of suspicion is required to make the diagnosis.[14] MRI may show diffuse white matter hyperintensities, hemorrhage, dilated vessels, vascular enhancement and flow-voids. MR angiograms may identify DAVF with sufficiently high flow with widespread venous hypertension and generalized cognitive dysfunction.[14] The presence of non-specific parenchymal abnormalities in patients with DAVFs helps in excluding other more common causes of cognitive decline.[11] Arterial embolization is usually successful in decreasing fl ow through a DAVF, with cognitive improvement in most of the cases. [13] Additional arterial embolization may be required if there is recurrence of cognitive decline, in order to decrease flow and venous hypertension. c Figure 1: Non contrast computed tomography head (a) prominent right transverse-sigmoid sinus junction with focal calcification. (b) Prominent left transverse-sigmoid sinus junction. (c) Right parahippocampal calcification 108 Neurology India | Jan-Feb 2014 | Vol 62 | Issue 1 [Downloaded free from http://www.neurologyindia.com on Thursday, March 13, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor a b d c e Figure 2: T2-weighted axial images (a-c) and susceptibility weighted imaging images (d) and (e) reveal presence of dural arteriovenous fistula at bilateral transverse sinus – sigmoid sinus junction (thick arrow) with prominent cortical veins in that region (thin arrow) with hypertrophied feeders from extracranial arteries bilaterally (hallow arrow) A combined endovascular - surgical approach is considered in many centers. The potential for recurrent and possibly permanent ischemic damage emphasizes the need for an aggressive approach to closure of these lesions to relieve excessive venous pressure. Our patient presented with rapidly progressive dementia, Parkinsonism and myoclonus and succumbed to her illness before definitive treatment could be administered underlining the need for maintaining a high index of clinical suspicion for this condition. In patients with rapidly progressive dementia, Parkinsonism and myoclonus; venous hypertensive encephalopathy secondary to DAVFs should be considered as a rare but reversible differential diagnosis. Delay in diagnosis and treatment will result in irreversible neuronal damage due to venous ischemia. Departments of Neurology, and 1Imaging Sciences and Intervention Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India E-mail: sujitjagtap@gmail.com References 1. 2. 3. 4. 5. 6. 7. Sujit Abajirao Jagtap, Sruthi S. Nair, Narendra Jain1, M. D. Nair Neurology India | Jan-Feb 2014 | Vol 62 | Issue 1 8. Obrador S, Soto M, Silvela J. Clinical syndromes of arteriovenous malformations of the transverse-sigmoid sinus. J Neurol Neurosurg Psychiatry 1975;38:436-51. Awad IA, Little JR, Akarawi WP, Ahl J. Intracranial dural arteriovenous malformations: Factors predisposing to an aggressive neurological course. J Neurosurg 1990;72:839-50. Lasjaunias P, Chiu M, ter Brugge K, Tolia A, Hurth M, Bernstein M. Neurological manifestations of intracranial dural arteriovenous malformations. J Neurosurg 1986;64:724-30. Viñuela F, Fox AJ, Pelz DM, Drake CG. Unusual clinical manifestations of dural arteriovenous malformations. J Neurosurg 1986;64:554-8. Malik GM, Pearce JE, Ausman JI, Mehta B. Dural arteriovenous malformations and intracranial hemorrhage. Neurosurgery 1984;15:332-9. Lee PH, Lee JS, Shin DH, Kim BM, Huh K. Parkinsonism as an initial manifestation of dural arteriovenous fistula. Eur J Neurol 2005;12:403-6. Kajitani M, Yagura H, Kawahara M, Hirano M, Ueno S, Fujimoto K, et al. Treatable fluctuating Parkinsonism and dementia in a patient with a dural arteriovenous fistula. Mov Disord 2007;22:437-9. van Dijk JM, terBrugge KG, Willinsky RA, Wallace MC. Clinical course 109 [Downloaded free from http://www.neurologyindia.com on Thursday, March 13, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor 9. 10. 11. 12. 13. 14. of cranial dural arteriovenous fistulas with long-term persistent cortical venous reflux. Stroke 2002;33:1233-6. Chaudhary MY, Sachdev VP, Cho SH, Weitzner I Jr, Puljic S, Huang YP. Dural arteriovenous malformation of the major venous sinuses: An acquired lesion. AJNR Am J Neuroradiol 1982;3:13-9. Cognard C, Gobin YP, Pierot L, Bailly AL, Houdart E, Casasco A, et al. Cerebral dural arteriovenous fistulas: Clinical and angiographic correlation with a revised classification of venous drainage. Radiology 1995;194:671-80. Hurst RW, Bagley LJ, Galetta S, Glosser G, Lieberman AP, Trojanowski J, et al. Dementia resulting from dural arteriovenous fistulas: The pathologic findings of venous hypertensive encephalopathy. AJNR Am J Neuroradiol 1998;19:1267-73. Hirono N, Yamadori A, Komiyama M. Dural arteriovenous fistula: A cause of hypoperfusion-induced intellectual impairment. Eur Neurol 1993;33:5-8. Dehdashti AR, Matouk CC, Terbrugge K, Wallace MC, Willinsky RA. Clues to dural arteriovenous fistulas in patients with progressive dementia. Can J Neurol Sci 2010;37:532-4. De Marco JK, Dillon WP, Halback VV, Tsuruda JS. Dural arteriovenous fistulas: Evaluation with MR imaging. Radiology 1990;175:193-9. Beuy Joob, Viroj Wiwanitkit1,2,3 Sanitation 1 Medical Academic Center, Bangkok, Thailand, 1 Hainan Medical University, China, 2 Faculty of Medicine, University of Nis, Serbia, 3 Joseph Ayobabalola University, Nigeria E-mail: beuyjoob@hotmail.com References 1. 2. 3. Verma R, Anand KS, Sharma BB, Garg J. Neurocysticercosis presenting as Parkinsonism. Neurol India 2013;61:656-7. Cavalcanti CE. Calcified cysticerci in basal ganglia and Parkinson’s syndrome: Report of a case. Arq Neuropsiquiatr 1984;42:183-6. Cosentino C, Velez M, Torres L, Garcia HH, Cysticercosis Working Group in Perú. Cysticercosis lesions in basal ganglia are common but clinically silent. Clin Neurol Neurosurg 2002;104:57-60. Access this article online Quick Response Code: Website: www.neurologyindia.com Access this article online Quick Response Code: PMID: *** Website: www.neurologyindia.com DOI: 10.4103/0028-3886.128361 PMID: *** DOI: 10.4103/0028-3886.128360 Received: 29-10-2013 Review completed: 18-12-2013 Accepted: 02-02-2014 Comment on: Neurocysticercosis presenting as Parkinsonism Sir, The recent report on “neurocysticercosis presenting as Parkinsonism” is very interesting.[1] A study by Verma et al. noted that their report is probably the first case series in which anatomically symmetric cysticercal lesions within basal ganglia were associated with a clinical syndrome of parkinsonism.[1] Indeed, neurocysticercosis at basal ganglion is not rare. It is apparently that the present case is not the fi rst case of basal ganglia neurocysticercosis with Parkinsonism. At least, another case was previously reported by Cavalcanti.[2] In addition, Cosentino et al. noted that basal ganglia localization is common in neurocysticercosis but it is rarely associated with clinical manifestations.[3] Therefore, it is questionable whether the present cases are only accidental concomitant findings or not. 110 Received: 21-01-2014 Review completed: 27-01-2014 Accepted: 03-02-2014 Authors’ Reply Sir, We have already mentioned in the article that neurocysticercosis (NCC) associated with Parkinsonism has been previously reported and its presence in basal ganglia is not rare. However, the concomitant presence of NCC in basal ganglia associated with Parkinsonism has been reported previously once as a single case report and not series of cases.[1,3] Moreover, we are not sure whether the previously reported case had anatomically symmetrical NCC. And as we have mentioned in the letter, the location of lesion itself appears insufficient to cause any precise changes as it has been observed that NCC affects brain regions that are distant from location of the cysticerci.[4] Finally, subsequent improvement in one of the case with only cysticidal therapy further supports our stance of NCC presenting as Parkinsonism in our case. Rohit Verma, Kuljeet Singh Anand1, B. B. Sharma2, Jyoti Garg1 Department of Psychiatry, Lady Hardinge Medical College and Smt. S. K. Hospital, Departments of 1Neurology, and 2Radiodiagnosis, Post Graduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi, India E-mail: Rohit.aiims@gmail.com Neurology India | Jan-Feb 2014 | Vol 62 | Issue 1 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. 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