HBP: Hypertension, DM: Diabetes mellitus, CAD: Coronary artery disease, HLP: Hyperlipedemia, ... cardiology clinic in Toronto.25 These observations need to ...
Cysticercosis is the most common parasitic disease worldwide; with an estimated prevalence greater than 50 million persons are infected. The life cycle of the pork tapeworm, Taenia solium, begins at the larval stage in pigs. Human tapeworm infection
Cerebral amyloid angiopathy presenting as a ... Clinical recognition of cerebral amyloid angiopathy is important since aggressive antiplatelet or ... formation and reactive inflammation. ... event probably related to cerebral amyloid angiopathy.
dysfunction soon after ingesting aconitine for pain control. ... A patient with aconitine poisoning typically ... indicate a low partial carbon dioxide pressure.
We report here a case of extensive cerebral venous sinus thrombosis involving three ... puncture revealed CSF pressure of 9 cmH2O, .... arteriovenous fistula.
measured using an automated coagulation analyzer. (SYSMEX, CA-7000, Sysmex Co., Kobe, Japan); and homocysteine (Hisens, HBI Inc., Anyang,.
Herpes zoster ophthalmicus commonly presents with vesicular eruptions of skin along a ... of brain showed subacute infarct in left middle cerebral artery territory.
Neurology Asia 2011; 16(2) : 163 â 166. Address ... Neurology Asia. June 2011. 164. Cooling .... role of segment S5 revealed by a novel hyperkalaemic periodic ...
ASD: atrial septum defect; PDA: patent ductus arteriosus; CLS: capillary leak syndrome. Several unique features of infantile SCA7 cases compared to the ...
Neurology Asia 2012; 17(1) : 75 â 78. Address correspondence to: .... Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of ...
1Department of Parasitology and Mycology, 2Department of Community ... toxoplasmosis is one of the main cause's aquired epilepsy in developing countries.
cold-stimulus headache on taking ice cold food after the onset of thalamic hemorrhage. ... It is previously termed âice-cream headacheâ or. âicepick headacheâ.
procedure for well-defined and deep-seated lesions that are difficult to ..... Rev Neurol (Paris) 2002; 158(4):405-11. 16. Dunoyer C ... 2003; 43(2):61-8. 26.
She had a massive hematochezia 5 days earlier and tarry stools until the admission. A colonoscopy showed ulcerative lesions at the ascending colon and ...
Simple partial status epilepticus occurs more rarely than other forms of status epilepticus. This report describes ... born after an uncomplicated pregnancy. Her.
Malaysian patient, of indigenous Bajau ethnicity who presented with recurrent ... A 25-year-old Malaysian man of ethnic Bajau ... Family history was significant.
Moyamoya disease has a high prevalence in Asia, particularly in Japan,. Korea and China. ..... (Refer to the Image Diagnostic Guidelines by MRI and MRA.).
(Korean-Color Word Stroop Test) compared to the patients with CDR 0.5 (Table 2). However, the scores of K-BNT (Korean-Boston naming Test) and Verbal and ...
(2), action or postural tremor of hands (1), rigidity (1), finger taps (1), hand movements (1), rapid alternating movements of hands (1), leg agility (1), and gait (1).
and sequenced directly using a BigDye terminator cycle sequencing kit (Applied Biosystems, Foster. City, USA.) and 3730xl DNA analyzer (Applied. Biosystems) ...
There is also lack of epilepsy knowledge among the professionals, patients, families as well as the public. ... in 1990 and the medical insurance system in. 1994.
named Sysmex KX-21N. Statistical .... dL are classified as borderline, and above 500 .... manual for the State-Trait Anxiety Inventory. ... Palo Alto, CA: Consulting.
Parvaiz A Shah MD DM, G Hussain Bardi MD, Bashir A Naiku MD DM, A Khaliq Dar MD, ... Address correspondence to: Dr. Parvaiz A. Shah, Consultant Neurologist, H. No:35, Momina-bad, ..... Health Organisation MONICA Project (monitoring.
selected. WHAT IS STATUS EPILEPTICUS? ... subtle convulsive movements) from overt SE.2. As subtle .... present not known to be of any benefit and may, in fact .... has become a standard part of treatment algorithms ..... Pohlmann-Eden B, Hoch DB, Coc
Neurology Department, 2Physical Medicine & Rehabilitation Department, 3Neurosurgery Department, Clinical Microbiology & Infectious Disease Department, 5Pathology Department, Faculty of Medicine, Ege University, Bornova, Izmir, Turkey
Abstract This is the report of a 32-year-old man with Behçet’s disease described dizziness, double vision and headache. The cranial MRI demonstrated a ring enhancing nodular lesion in left medial occipital lobe, and T2 hyperintense lesion in diencephalon mimicking abscesses. A stereotactic biopsy was performed. The histology showed features of neuro-Behçet’s disease and an abscess was ruled out. During the procedure till the histopathologic results were gathered he was given ceftriaxone and metronidazole when cerebellar signs appeared. Cranial MRI showed additional symmetrical hyperintensities in bilateral cerebellar dentate nuclei which was attributed to metronidazole toxicity. Repeat MRI performed forty days later showed complete resolution of both dentate hyperintensities and diencephalic and occipital ring enhancing lesions. This is the first case of neuro-Behcet’s disease complicated by metronidazoleinduced encephalopathy. This case also showed that nodular ring enhancing lesions can be seen in neuro-Behçet’s disease and can lead to difficulties in diagnosis and management. INTRODUCTION Behçet’s disease (BD) is a chronic, relapsing multisystem inflammatory disorder first described by the Turkish dermatologist Hulusi Behçet in 1937.1 Inflammatory perivasculitis can arise in almost any tissue. Nervous system involvement is one of the most serious manifestations of BD and has been reported to occur in 5.3%2 up to 59%3 in hospital based series, usually after systemic manifestations from months to years. Two different patterns of Central nervous system (CNS) involvement have been defined: parenchymal and nonparenchymal or vascular.4 Vascular BD can be confirmed by computed tomographic angiography, magnetic resonance angiography, or magnetic resonance venography. Magnetic resonance imaging (MRI) is the examination of choice for the study of parenchymal involvement in BD. Mesodiencephalic junction, cerebellar peduncles, pons, medulla, basal ganglia, internal capsule, and cerebral hemispheres are the commonly involved sites.5 We describe a case of parenchymal BD with nodular abscess-like lesions who was diagnosed with stereotactic brain biopsy. As an infection could not be excluded before the histopathologic examination he was treated with ceftriaxone
and metronidazole which caused metronidazoleinduced encephalopathy. CASE REPORT A 32-year-old man presented with dizziness, double vision and headache that had started four days earlier. BD had been diagnosed 8 years prior with recurring oral and genital ulcers and two previous uveitis attacks. He was on colchicine since then. The medical history was otherwise nonspecific. Other than restriction of the upward gaze, neurological examination was normal. Complete blood count and biochemistry revealed leukocytosis with neutrophilia (17.64 10^3/µL). Sedimentation rate, C-reactive protein levels, thyroid functions were normal. The cranial MRI demonstrated a ring enhancing lesion with internal hypointensity on the left medial occipital lobe next to the interhemispheric fissure on T1-weighted images with gadolinium injection. T2-weighted and FLAIR sequences revealed an additional nodular occipital and a left diencephalic lesion which were hyperintense. Diffusion weighted imaging (DWI) and apparent diffusion coefficient (ADC) map revealed central hyperintensity on
Address correspondence to: Nese Celebisoy, M.D., Ege University Faculty of Medicine, Neurology Department, Ankara Street, 35100, Bornova, Izmir, Turkey. Tel:+905332654508, e-mail:nes‚ [email protected], [email protected]
Figure 1: First cranial MRI: A) Ring enhancing lesion with internal hypointensity on the left medial occipital lobe next to the interhemispheric fissure on T1-weighted magnetic resonance images with gadolinium injection, B-C) T2-weighted and FLAIR sequences revealed another nodular occipital and a left diencephalic lesion, D-E) DWI and ADC map revealed central hyperintensity on DWI B1000 with hipointensity on ADC for occipital lesions.
DWI B1000 with hypointensity on ADC for occipital lesions (Figure 1). Lumbar puncture performed demonstrated normal results. As an infectious etiology could not be ruled out the patient was started on ceftriaxone 2x1g and metronidazole 4x0.5g. A stereotactic biopsy was performed at the left occipital ring enhancing lesion. Biopsy specimen showed a necrotic focus containing
histiocytes and also lymphocytic vasculitis characterized with perivascular lymphocytic infiltration (immunohystochemical staining revealed T lymphocytes (CD3 (+), CD20 (-)) and reactive gliosis (Figure 2). Cultures for bacteria, tuberculosis and viruses were negative. Antibiotic therapy had been continued for 14 days when the patient began to complain increasing imbalance. The neurological examination showed
Figure 2: Biopsy specimen: (HE, X200) foamy histiocytes (arrow) and lymphocytic vasculitis characterized with perivascular lymphocyte infiltration (star) with reactive gliosis.
Figure 3: Cranial MRI performed after development of the cerebellar findings: FLAIR sequences showed hyperintensities in bilateral cerebellar dentate nuclei.
dysarthria, dysmetria and an ataxic wide-based gait. Control cranial MRI showed no decrease in the size of previous lesions. In addition, T2 FLAIR sequence showed hyperintensities in bilateral cerebellar dentate nuclei which was attributed to metronidazole toxicity (Figure 3). The drug was stopped immediately and intravenous
methyl prednisolone 1g/day was given for five days which was followed by oral prednisone 60mg/g daily. Control MRI performed forty days later showed complete resolution of both dentate hyperintensities and diencephalic and ring enhancing lesions (Figure 4).
Figure 4: Control MRI performed forty days later: FLAIR (A), T1 (B), DWI (C) and T2 (D) sequences showed complete resolution of both dentate and diencephalic hyperintensities and also ring enhancing lesions.
DISCUSSION The most common imaging lesion seen in the acute or subacute stage of parenchymal involvement in BD is an asymmetric mesodiencephalic junction lesion, which is hyperintense on T2weighted images often associated with edema and shows contrast enhancement.5-8 Mass-like lesions mimicking cerebral tumors have also been described.9-12 Nodular ring enhancing lesions as it was the case in our patient have been described in just one previous case.13 In another patient with similar imaging features an abscess involving gram-positive cocci has been identified.14 Central hyperintensity on DWI and hypointensity on ADC map is known to be associated with brain abscess due to the impeded water mobility of pus. Necrotic tumors on the other hand are characterized by central hypointensity on DWI and hyperintensity on ADC map.15 Although our patient’s diencephalic involvement supported neuro-Behçet’s disase, occipital lesions made it difficult to rule out an accompanying abscess, therefore antibiotic therapy was started before stereotactic surgery and it was continued till histopathologic results were obtained. The neuropathologic findings of neuroBehçet’s disease in the acute phase involves meningoencephalitis with an intense inflammatory infiltration including polymorphs, eosinophils, lymphocytes and macrophages with areas of necrosis and apoptotic neuronal loss.16,17 It is not a cerebral vasculitis as the blood vessels are not infiltrated; rather it is an inflammatory perivascultis.17 Our patient’s biopsy specimen revealed histopathologic features of neuroBehçet’s disease and an abscess was ruled out. During this period he was on metronidazole for two weeks when cerebellar symptoms and signs appeared. Metronidazole is a commonly used drug against protozoal and anaerobic bacterial infections. Metranidazole toxicity has been reported to induce neurologic side effects including peripheral neuropathy, encephalopathy, cerebellar dysfunction and seizures. 18-21Cumulative doses usually required to elicit cerebellar symptoms has been reported as 25-110 g.18 In our patient, total doses of metronidazole were 28 g. Though the mechanism of metronidazole toxicity remains unclear most lesions show complete resolution.18,19,22 This has been proposed to be associated with acute axonal swelling with increased water content rather than a demyelinating process.18 Symmetric and bilateral T2 hyperintense lesions in the cerebellar dentate
nuclei, typical for metabolic encephalopathy are the most common MRI findings.18,19 After discontinuation of the drug, both the clinical and MRI findings of our patient showed complete resolution. To our knowledge, this is the only reported case with co-existing neuro-Behcet’s disease and metronidazole-induced encephalopathy. Ring enhancing lesions made it difficult to rule out an abscess and metronidazole was initiated after admission to the hospital and was continued till the histopathologic results were gathered which induced cerebellar dysfunction associated with typical MRI findings. Neuro-Behcet’s disease is a serious condition requiring aggressive immunosuppressive treatment to prevent mortality and permanent neurological sequelae. Co-existence of metronidazole toxicity as we report here is a rare but possible complication of treatment and may lead to difficulties in diagnosis and management of this already complicated clinical picture. DISCLOSURE Conflict of interest: None REFERENCES 1. Behçet H. Über residivierende, aphtöse durch ein Virus verursachtes Geschwüre am Mund, am Auge und an der Genitalien. Derm Wschr 1937; 105:1152-7. 2. Serdaroglu P, Yazici H,Özdemir C, Yurdakul S, Bahar S, Aktin E. Neurologic involvement in Behçet’s syndrome, a prospective study.Arch Neurol1989; 46:265-9. 3. Farah S, Al-Shubaili A, Montaser A, et al. Behçet’s syndrome: a report of 41 patients with emphasis on neurological manifestations. J Neurol Neurosurg Psychiatry 1998; 64:382-4. 4. Akman-Demir G, Serdaroglu P, Tasci B. Clinical patterns of neurological involvement in Behcet’s disease: evaluation of 200 patients. The Neuro-Behcet Study Group. Brain 1999; 22:2171-82. 5. Kocer N, Islak C, Siva A, et al. CNS involvement in neuro-Behçet syndrome: An MR study. AJNR 1999; 20:1015-24. 6. Morrisey SP, Miller DH, Hermaszewski R, et al. Magnetic resonance imaging of the central nervous system in Behcet’s disease. Eur Neurol 1993; 33: 287-93. 7. Wechsler B, Dell’sola B, Vidailhet M, et al. MRI in 31 patients with Behçet’s disease and neurological involvement: prospective study with clinical correlation. J Neurol Neurosurg Psychiatry 1993; 56:783-9. 8. Al Kawi MZ, Bohlega S, Banna M. MRI findings in neuro-Behçet’s disease. Neurology 1991; 41:405-8. 9. Tuzgen S, Kaya AH, Erdinçler D, Oguzoglu SA,
10. 11. 12. 13.
16. 17. 18.
19. 20. 21. 22.
Ulu O, Saip S. Two cases of neuro-Behçet’s disease mimicking cerebral tumor. Neurol India 2003; 51:376-8. Park JH, Jung MK, Bang CO, et al. Neuro-Behçet’s disease mimicking a cerebral tumor: A case report. J Korean Med Sci 2002; 17:718-22. Imoto H, Nishizaki T, Nogami K, et al. Neuro-Behçet’s disease manifesting as a neoplasm-like lesion-case report. Neurol Med Chir 2002; 42:406-9. Appenzeller S, de Castro R, de Souza Queiroz L, et al. Brain tumor-like lesion in Behçet disease. Rheumatol Int 2006; 26:577-80. Heo JH, Lee ST, Chu K, Kim M. Neuro-Behçet’s disease mimicking multiple brain tumors: Diffusion weighted MR study and literature review. J Neurol Sci 2008; 264: 177-81. Ganau S, Berenguer J, Pujol T, Mercader JM. An unusual central nervous system manifestation of Behçet’s disease. AJR 2001; 177:721-22. Desprechins B, Stadnik T, Koerts G, Shabana W, Breucq C, Osteaux M. Use of diffusion-weighted MR imaging in differential diagnosis between necrotic tumors and cerebral abscesses. AJNR 1999; 20:1252-7. Hadfield MG, Aydın F, Lippman HR, Sanders KM. Neuro-Behçet’s disease. Clin Neuropathol 1997; 16:55-60. Hirohata S. Histopathology of central nervous system lesions in Behçet’s disease. J Neurol Sci 2008; 267:41-7. Kim H, Kim YW, Kim SR, Park IS, Jo KW. Metronidazole-induced encephalopathy in a patient with infectious colitis: a case report. J Med Case Reports 2011; 5:63-6. Ahmed A, Loes DJ, Bressler EL. Reversible magnetic resonance imaging findings in metronidazole-induced encephalopathy. Neurology 1995; 45:588-9. Coxon A, Pallis CA. Metronidazole neuropathy. J Neurol Neurosurg Psychiatry 1976; 39:403-5. Halloran TJ. Convulsions associated with high cumulative doses of metronidazole. Drug IntellClin Pharm 1982; 16:409. Kwon KY, Lee DK, Lee KH, Cho KH, Lee E, Chung SJ. Two cases of metronidazole-induced neurotoxicity lacking of clinico-radiological correlation. J Korean NeurolAssoc2006; 24:581-4.