Letters to Editor
of hypothalamus. Most secondary cluster headaches have certain atypical features like blurring of vision, background mild continuous headache that may favor the need to search for secondary causes of cluster headache.
Vikas Kanaujia, Vimal K. Paliwal1, A. Aneez1, Rachna Agarwal Departments of Neuro Ophthalmology and 1Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India E‑mail: [email protected]
References 1.
Read RW, Holland GN, Rao NA, Tabbara KF, Ohno S, Arellanes‑Garcia L, et al. Revised diagnostic criteria for Vogt‑Koyanagi‑Harada disease: Report of an international committee on nomenclature. Am J Ophthalmol 2001;131:647‑52. 2. Tavsanli M, Uluduz D, Saip S, Kendiroglu G. Vogt‑Koyanagi‑Harada disease: Headache as an initial manifestation. J Headache Pain 2008;9:255‑6. 3. Headache classification committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia 2013;33:629‑808. 4. Lee MS, Lesell S. Orbital myositis posing as cluster headache. Arch Neurol 2002;59:635‑6. 5. Harley JS, Ahmad F. Cluster‑like headache heralding inflammatory orbital pseudotumour. Cephalalgia 2008;28:401‑2. 6. Evers S, Sörös P, Brilla R, Gerding H, Husstedt IW. Cluster headache after orbital exenteration. Cephalalgia 1997;17:680‑2. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149407
reactive. Fundus examination was normal. No paucity of limb movements. Plantar response was extensor. Brain magnetic resonance imaging (MRI) showed hyperintense signal changes in basis pontis with patchy signal changes in bilateral thalamus on fluid‑attenuated inversion recovery (FLAIR). There was diffusion restriction in the periphery of basis pontis resembling “reverse moustache” [Figure 1]. The platelet count was 50,000/mm3. Immunoglobulin M (IgM) antibodies and nonstructural protein 1 (NS1) antigen for dengue virus were positive in the serum. Cerebrospinal fluid (CSF) analysis was positive for dengue IgM antibodies. A diagnosis of dengue encephalitis was made. He was treated with intravenous dexamethasone for 3 days and showed improvement in level of consciousness. Dengue fever has a variable clinical spectrum ranging from asymptomatic infection to life‑threatening dengue hemorrhagic fever and dengue shock syndrome. However, neurological complications, in general, are unusual. Dengue encephalopathy is usually secondary to multisystem derangement like shock, hepatitis, coagulopathy, and concurrent bacterial infection. However, in dengue encephalitis, there is direct neuronal infiltration by the dengue virus. Although dengue is classically considered a non‑neurotropic virus,[1] there is increasing evidence for dengue viral neurotropism.[2] In a recent study on the cranial imaging in dengue virus infection, MRI abnormalities were reported in 9 out of 21 serologically confirmed patients with dengue: Lesions in thalamic and basal ganglia in 3, focal cortical areas in 3, white matter in 2, and meningeal enhancement in 3 patients.[3] Extensive lesions involving the midbrain, cerebellum, thalamus, and medial temporal region on both sides of the MRI brain have been reported in a serologically confirmed
Received: 16-10-2014 Review completed: 20-10-2014 Accepted: 24-10-2014
Diffusion restriction in pons resembling “reverse moustache” in dengue encephalitis Sir, A 12‑year‑old boy presented with a history of high‑grade fever and chills of 5 days duration. He had holocranial headache with two episodes of vomiting. He lapsed into altered sensorium on the day of admission. No history of seizures. He was febrile and drowsy, irritable, and not following verbal commands. There was terminal neck stiffness. Pupils were equal and Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
a
b
c Figure 1: Magnetic resonance imaging (MRI) brain fluid-attenuated inversion recovery (FLAIR) sequence axial view showing hyperintense signal change in basis pontis predominantly in the periphery (white arrow) (a); Diffusion-weighted imaging (DWI) showing hyperintense signal (b) and apparent diffusion coefficient (ADC) showing hypointense signal (c) in basis pontis with “reverse moustache” appearance (white arrow)
683
Letters to Editor
patient with dengue.[2] Borawake et al., reported a child with dengue encephalitis with extensive parenchymal hyperintense lesions in the bilateral cerebellar cortex, vermis of the cerebellum, entire pons and midbrain, bilateral medial temporal lobes, and both thalami on MRI.[4] Our patient had serologically confirmed dengue infection with predominant lesions in pons and patchy involvement of thalami. The pattern of diffusion restriction in pons in our patient resembled “reverse moustache”, which is an interesting pattern not reported so far.
Anish Mehta, Rohan R. Mahale, Mahendra Javali, R. Srinivasa Department of Neurology, MS Ramaiah Medical College and Hospital, Bangalore, Karnataka, India E‑mail: [email protected]
References 1. Nathanson N, Cole GA. Immunosuppression and experimental virus infection of the nervous system. Adv Virus Res 1970;16:397‑428. 2. Rao S, Kumar M, Ghosh S, Gadpayle AK. A rare case of dengue encephalitis. BMJ Case Rep 2013;2013. 3. Bhoi SK, Naik S, Kumar S, Phadke RV, Kalita J, Misra UK. Cranial imaging findings in dengue virus infection. J Neurol Sci 2014;342:36‑41. 4. Borawake K, Prayag P, Wagh A, Dole S. Dengue encephalitis. Indian J Crit Care Med 2011;15:190‑3. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149408
Received: 26-10-2014 Review completed: 26-10-2014 Accepted: 26-10-2014
Primary central nervous system histiocytic sarcoma mimicking glioma Sir, Histiocytic sarcoma (HS) is a rare but aggressive hematopoietic tumor, and most patients die of progressive disease within two years.[1] These malignant neoplasms are characterized by the morphological and immunophenotypic features of mature tissue histiocytes. The most common sites for these tumors are lymph nodes and certain extranodal sites.[1] The involvement of the central nervous system (CNS) has rarely been reported. The median survival for CNS HS is even worse at approximately five months.[2] We present a case of 684
primary CNS HS mimicking glioma with a relatively good outcome during the following period. A 52‑year‑old man presented with weakness of left lower limb of 15 days. Neurologic examination revealed motor power of grade 4/5 in the left lower limb. Magnetic resonance imaging (MRI) [Figure 1] revealed an irregular intra‑axial mass in the frontal lobe with significant peri‑lesional edema. The solid part was iso‑intense on both T1‑ and T2‑weighted images. Cystic changes were present. On contrast administration, the lesion enhanced significantly. The solid portion showed slightly restricted diffusion on DWI (b = 1000). MR spectroscopy (MRS) showed increase in Cho/NAA and Cho/Cr, decrease in NAA/Cr and lactic acid. These appearances were consistent with the mass being a glioma. The patient underwent a craniotomy and total excision of the tumor under ultrasonic guidance. The postoperative screening for systemic malignancy, including a whole‑body 18F‑FDG PET scan, was unremarkable. The patient underwent postoperative concomitant chemoradiotherapy. He received temozolomide concomitant with 1.8 Gy of radiotherapy five days a week. The radiotherapy was intensity‑modulated radiation therapy for a total of 30 fractions. MRI performed six months after initial presentation showed no evidence of tumor recurrence. The patient is still in good condition when followed up by telephone interview after 16 months. Microscopically, the tumor was composed of histiocytoid cells of variable size with abundant eosinophilic cytoplasm. These cells showed marked nuclear pleomorphism with prominent nucleoli and coarse chromatin [Figure 2a]. Mitotic figures were identified. A typical pathological feature of CNS HS is an associated prominent inflammatory component.[2‑4] In
a
b
c Figure 1: Gadolinium-enhanced T1-weighted sagittal (a) and T2-weighted coronal (b) MRI. A heterogeneous and irregular intra-axial mass was revealed in the right frontal lobe, and peripheral vasogenic edema was obvious. MR spectroscopy (c) showed increased Cho/NAA, increased Cho/Cr, and decreased NAA/Cr
Neurology India | Nov-Dec 2014 | Vol 62 | 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.
of hypothalamus. Most secondary cluster headaches have certain atypical features like blurring of vision, background mild continuous headache that may favor the need to search for secondary causes of cluster headache.
Vikas Kanaujia, Vimal K. Paliwal1, A. Aneez1, Rachna Agarwal Departments of Neuro Ophthalmology and 1Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India E‑mail: [email protected]
References 1.
Read RW, Holland GN, Rao NA, Tabbara KF, Ohno S, Arellanes‑Garcia L, et al. Revised diagnostic criteria for Vogt‑Koyanagi‑Harada disease: Report of an international committee on nomenclature. Am J Ophthalmol 2001;131:647‑52. 2. Tavsanli M, Uluduz D, Saip S, Kendiroglu G. Vogt‑Koyanagi‑Harada disease: Headache as an initial manifestation. J Headache Pain 2008;9:255‑6. 3. Headache classification committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia 2013;33:629‑808. 4. Lee MS, Lesell S. Orbital myositis posing as cluster headache. Arch Neurol 2002;59:635‑6. 5. Harley JS, Ahmad F. Cluster‑like headache heralding inflammatory orbital pseudotumour. Cephalalgia 2008;28:401‑2. 6. Evers S, Sörös P, Brilla R, Gerding H, Husstedt IW. Cluster headache after orbital exenteration. Cephalalgia 1997;17:680‑2. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149407
reactive. Fundus examination was normal. No paucity of limb movements. Plantar response was extensor. Brain magnetic resonance imaging (MRI) showed hyperintense signal changes in basis pontis with patchy signal changes in bilateral thalamus on fluid‑attenuated inversion recovery (FLAIR). There was diffusion restriction in the periphery of basis pontis resembling “reverse moustache” [Figure 1]. The platelet count was 50,000/mm3. Immunoglobulin M (IgM) antibodies and nonstructural protein 1 (NS1) antigen for dengue virus were positive in the serum. Cerebrospinal fluid (CSF) analysis was positive for dengue IgM antibodies. A diagnosis of dengue encephalitis was made. He was treated with intravenous dexamethasone for 3 days and showed improvement in level of consciousness. Dengue fever has a variable clinical spectrum ranging from asymptomatic infection to life‑threatening dengue hemorrhagic fever and dengue shock syndrome. However, neurological complications, in general, are unusual. Dengue encephalopathy is usually secondary to multisystem derangement like shock, hepatitis, coagulopathy, and concurrent bacterial infection. However, in dengue encephalitis, there is direct neuronal infiltration by the dengue virus. Although dengue is classically considered a non‑neurotropic virus,[1] there is increasing evidence for dengue viral neurotropism.[2] In a recent study on the cranial imaging in dengue virus infection, MRI abnormalities were reported in 9 out of 21 serologically confirmed patients with dengue: Lesions in thalamic and basal ganglia in 3, focal cortical areas in 3, white matter in 2, and meningeal enhancement in 3 patients.[3] Extensive lesions involving the midbrain, cerebellum, thalamus, and medial temporal region on both sides of the MRI brain have been reported in a serologically confirmed
Received: 16-10-2014 Review completed: 20-10-2014 Accepted: 24-10-2014
Diffusion restriction in pons resembling “reverse moustache” in dengue encephalitis Sir, A 12‑year‑old boy presented with a history of high‑grade fever and chills of 5 days duration. He had holocranial headache with two episodes of vomiting. He lapsed into altered sensorium on the day of admission. No history of seizures. He was febrile and drowsy, irritable, and not following verbal commands. There was terminal neck stiffness. Pupils were equal and Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6
a
b
c Figure 1: Magnetic resonance imaging (MRI) brain fluid-attenuated inversion recovery (FLAIR) sequence axial view showing hyperintense signal change in basis pontis predominantly in the periphery (white arrow) (a); Diffusion-weighted imaging (DWI) showing hyperintense signal (b) and apparent diffusion coefficient (ADC) showing hypointense signal (c) in basis pontis with “reverse moustache” appearance (white arrow)
683
Letters to Editor
patient with dengue.[2] Borawake et al., reported a child with dengue encephalitis with extensive parenchymal hyperintense lesions in the bilateral cerebellar cortex, vermis of the cerebellum, entire pons and midbrain, bilateral medial temporal lobes, and both thalami on MRI.[4] Our patient had serologically confirmed dengue infection with predominant lesions in pons and patchy involvement of thalami. The pattern of diffusion restriction in pons in our patient resembled “reverse moustache”, which is an interesting pattern not reported so far.
Anish Mehta, Rohan R. Mahale, Mahendra Javali, R. Srinivasa Department of Neurology, MS Ramaiah Medical College and Hospital, Bangalore, Karnataka, India E‑mail: [email protected]
References 1. Nathanson N, Cole GA. Immunosuppression and experimental virus infection of the nervous system. Adv Virus Res 1970;16:397‑428. 2. Rao S, Kumar M, Ghosh S, Gadpayle AK. A rare case of dengue encephalitis. BMJ Case Rep 2013;2013. 3. Bhoi SK, Naik S, Kumar S, Phadke RV, Kalita J, Misra UK. Cranial imaging findings in dengue virus infection. J Neurol Sci 2014;342:36‑41. 4. Borawake K, Prayag P, Wagh A, Dole S. Dengue encephalitis. Indian J Crit Care Med 2011;15:190‑3. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149408
Received: 26-10-2014 Review completed: 26-10-2014 Accepted: 26-10-2014
Primary central nervous system histiocytic sarcoma mimicking glioma Sir, Histiocytic sarcoma (HS) is a rare but aggressive hematopoietic tumor, and most patients die of progressive disease within two years.[1] These malignant neoplasms are characterized by the morphological and immunophenotypic features of mature tissue histiocytes. The most common sites for these tumors are lymph nodes and certain extranodal sites.[1] The involvement of the central nervous system (CNS) has rarely been reported. The median survival for CNS HS is even worse at approximately five months.[2] We present a case of 684
primary CNS HS mimicking glioma with a relatively good outcome during the following period. A 52‑year‑old man presented with weakness of left lower limb of 15 days. Neurologic examination revealed motor power of grade 4/5 in the left lower limb. Magnetic resonance imaging (MRI) [Figure 1] revealed an irregular intra‑axial mass in the frontal lobe with significant peri‑lesional edema. The solid part was iso‑intense on both T1‑ and T2‑weighted images. Cystic changes were present. On contrast administration, the lesion enhanced significantly. The solid portion showed slightly restricted diffusion on DWI (b = 1000). MR spectroscopy (MRS) showed increase in Cho/NAA and Cho/Cr, decrease in NAA/Cr and lactic acid. These appearances were consistent with the mass being a glioma. The patient underwent a craniotomy and total excision of the tumor under ultrasonic guidance. The postoperative screening for systemic malignancy, including a whole‑body 18F‑FDG PET scan, was unremarkable. The patient underwent postoperative concomitant chemoradiotherapy. He received temozolomide concomitant with 1.8 Gy of radiotherapy five days a week. The radiotherapy was intensity‑modulated radiation therapy for a total of 30 fractions. MRI performed six months after initial presentation showed no evidence of tumor recurrence. The patient is still in good condition when followed up by telephone interview after 16 months. Microscopically, the tumor was composed of histiocytoid cells of variable size with abundant eosinophilic cytoplasm. These cells showed marked nuclear pleomorphism with prominent nucleoli and coarse chromatin [Figure 2a]. Mitotic figures were identified. A typical pathological feature of CNS HS is an associated prominent inflammatory component.[2‑4] In
a
b
c Figure 1: Gadolinium-enhanced T1-weighted sagittal (a) and T2-weighted coronal (b) MRI. A heterogeneous and irregular intra-axial mass was revealed in the right frontal lobe, and peripheral vasogenic edema was obvious. MR spectroscopy (c) showed increased Cho/NAA, increased Cho/Cr, and decreased NAA/Cr
Neurology India | Nov-Dec 2014 | Vol 62 | 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.
