Acta Neurol Belg DOI 10.1007/s13760-014-0330-y
LETTER TO THE EDITOR
Treatment of patients with suspected brain tuberculoma before or without bacteriologic confirmation in endemic places: report of two cases Sasannejad Payam • Moghadam-Ahmadi Amir • Shahsavari Sasan • Pourrashidi-Boshrabadi Ahmad Tafakhori Zahra • Sharifi-Razavi Athena
•
Received: 20 April 2014 / Accepted: 29 June 2014 Ó Belgian Neurological Society 2014
Tuberculosis (TB) is the most important infectious disease in the world, and it can produce disease in nearly every organ system, as in the central nervous system (CNS). Neurological involvement is found in approximately 1 % of TB infections, and presents with complications such as tuberculosis meningitis, intracerebral tuberculoma or tuberculosis involvement of the spine with myelopathy (pott’s disease) [19]. Generally, patients declare with headache, seizures, fever, focal neurological deficit and aspects of elevated intracranial pressure. Presentation of infratentorial tuberculoma may be with brainstem syndromes, cerebellar symptoms and multiple cranial nerve palsy [2].
Intramedullary tuberculomas are not routine patterns of CNS TB and figure only 8 % of all the lesions. These lesions can be treated by anti-tuberculosis chemotherapy likewise microsurgical excision [3]. Neurological TB may develop during primary infection or may become reactive as a consequence of immunosuppression. Neurological manifestations of CNS tuberculosis are headache, nausea and vomiting, meningeal irritation, altered mental status and cranial nerve palsies. Untreated disease progresses with decreased level of consciousness, seizures, focal neurological deficits, and ultimately death [4]. We describe two patients with normal immunity, presented with symptoms suggesting focal lesions in the brain, and multiple tuberculomas were detected in several places in their brain, including cerebral hemispheres, cerebellum and brainstem.
S. Payam Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran
Case presentation
Introduction
M.-A. Amir (&) Department of Neurology, Clinical Research and Development Center, Rafsanjan University of Medical Sciences, Ali-EbnAbitaleb Hospital, Rafsanjan, Iran e-mail: [email protected] S. Sasan P.-B. Ahmad Faculty of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran T. Zahra Department of Oromaxillofacial Radiology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran S.-R. Athena Department of Neurology, Mazandaran University of Medical Sciences, Mazandaran, Iran
Case 1 The first patient was a 25-year-old woman who presented with mild subacute progressive headache associated with occasional low-grade fever and sweating, mild weight loss, nausea and vomiting. In neurological examination, she had mild right hemiparesis. Brain CT scan showed multiple hypodense lesions with surrounding edema (Fig. 1). Brain MRI with gadolinium demonstrated more than 100 intracranial ring enhancing lesions, involving almost every part of the brain, such as cerebral hemispheres, cerebellum and brainstem (Fig. 2). Radiological examination of the chest revealed multiple 1-2 mm lesions with miliary pattern infiltration.
123
Acta Neurol Belg Fig. 1 Brain CT scan demonstrates multiple hypodense lesions with surrounding edema in different areas of the brain
Laboratory findings revealed mild leukocytosis, positive C-reactive protein (CRP = ?3) and elevated erythrocyte sedimentation rate (ESR = 55). An intradermal tuberculin test and several blood cultures yielded negative results. Other conditions such as toxoplasmosis, HIV infection and brucellosis were ruled out by appropriate tests. Echocardiography and ultrasonography of the abdomen and pelvis were normal. Examination of the cerebrospinal fluid (CSF) demonstrated low sugar (2 mg/dl), pleocytosis (WBC = 95 with 70 % polymorphonuclear leukocytes), and high protein (80 mg/dl). After a while, polymerase chain reactin (PCR) test for TB in the CSF, bronchoalveolar lavage (BAL) and CSF culture for mycobacterium tuberculosis yielded positive results. Considering the diagnosis of CNS-TB (i.e., brain tuberculoma), the patient was treated with anti-TB drugs (isoniazide, rifampin, ethambutol and pyrazinamide) before PCR and culture results became available. During the treatment course, the patient’s level of consciousness was decreased. Brain CT scan revealed obstructive hydrocephaly; hence, urgent ventriculostomy was performed that was successful and she became fully conscious and alert during the next days. The patient improved
123
gradually in about 10 days, and finally, she was discharged with antituberculosis drugs and phenytoin, while she had no signs or symptoms. Brain lesions were completely eliminated on follow-up radiologic examination. Case 2 The second patient was a 19-year-old man from Afghanistan, with recent-onset episodes of focal seizures in the right upper limb (with occasional secondary generalization). He did not have any complaints of constitutional disturbances such as fever, weight loss and sweating, or a precise history of close contact with a known-case of Mycobacterium tuberculosis infection. Neurological examination revealed no abnormal findings such as papilledema or focal neurological deficits. Axial brain CT scan showed multiple hypodense lesions with surrounding edema, and a thin hyperdense ring around some of them, giving a ‘‘target-appearance’’. After administration of contrast, multiple ring enhancing lesions appeared in all parts of the brain in cerebellum, brainstem, basal ganglia, internal capsule and bilateral frontal, temporal and parietal lobes, with surrounding edema but
Acta Neurol Belg
Fig. 2 Brain MRI with gadolinium demonstrates a lot of intracranial ring enhancing lesions, involving almost every part of the brain including cerebral hemispheres, cerebellum and brainstem
without significant mass effect or hydrocephaly (Fig. 3). Chest radiographic evaluation revealed milliary pattern infiltration.
Despite the absence of a history of close contact with a known case of TB infection, and of course regarding his low socioeconomic status that limited further evaluation,
123
Acta Neurol Belg
Fig. 3 Axial brain CT scan with contrast shows multiple ring enhancing lesions in all parts of the brain in cerebellum, brainstem, basal ganglia, internal capsule and bilateral frontal, temporal and parietal lobes, with surrounding edema but without significant mass effect or hydrocephaly
empiric treatment for TB was initiated with a high-degree of suspicion to brain tuberculoma, considering the fact that he came from Afghanistan, which is an endemic place for TB infection. The patient’s seizures were completely controlled after a while (about 3 weeks after starting the anti-tuberculous regimen), and the patient returned to Afghanistan without any neurological symptoms or signs. So we could not do post-treatment radiologic evaluation.
Discussion Tuberculosis is an airborne disease caused by Mycobacterium tuberculosis. Meningo-encephalitis and granuloma formation are two pathologic forms of CNS-TB [5]. It is a chronic bacterial infection identified by the formation of granulomas in the infected tissues [6]. Recent studies report the incidence of tuberculous infection at 11.1 per 100,000 population in Western countries, and neuro-tuberculosis involves 0.5–2 % of extrapulmonary tuberculous infection in the general tuberculosis prevalence [7, 8]. The incidence of CNS-TB depends on the incidence of tuberculosis and socioeconomic condition of the country. Brain tuberculoma
123
is responsible for 5–8 % of intracerebral space-occupying lesions in developing countries such as Iran and Afghanistan. Intracerebral tuberculoma occur quite frequently in association with tuberculous meningitis [7, 9, 10, 19]. Iran is a country with a relative high prevalence of TB infection. Cerebromeningeal involvement is a potentially lethal complication of brain tuberculomas in developing countries [12]. A past history of active tuberculosis in other parts of the body is seen in about 30-70 % of the cases of brain tuberculomas [12, 13]. Hematogenous spread from tuberculous disease elsewhere in the body develops brain tuberculomas; however, only few reports [14, 15] show miliary tuberculosis presenting with brain tuberculomas. According to the Rich’s hypothesis, small tuberculous lesions occur in CNS during the hematogenous distribution. The CSF invasion is seen after years [17]. However, in our cases, brain tuberculomas occurred in association with miliary tuberculosis apparently. The brain tuberculomas clinically present with paroxysmal onset of headache, occasionaly followed by dizziness, seizures, altered mentation and focal neurological signs [16]. As in the first patient, the investigation of CSF usually shows pleocytosis (mononuclear cells are predominant) with low glucose
Acta Neurol Belg
level and high protein content, and also positive culture for Mycobacterium tuberculosis in more than half of the cases but may take 6–8 weeks to become positive; however, patients with miliary TB or CNS tuberculomas may have a normal CSF initially. Multiple tuberculomas of the brain is generally seen in immunodeficient patient, especially HIV- seropositive patients. Neither of our patients had evidences of immunodeficiencies, diabetes, malnutrition, cancer or history of immunosuppressive treatment. [18]. Appearance of tuberculomas on brain CT scan is in three forms: iso-, hypo- or hyperdense lesions with 1.5–7 cm in diameter and a ring enhancement after injection of contrast [15]. One of the interesting facts about the first patient is the presence of more than 100 ring-enhancing lesions, spread in all parts of the brain, which is the most abundant brain tuberculomas that has been reported in the literature heretofore. It is remarkable in our patients that they had many lesions in the cerebrum, basal ganglia, cerebellum and brainstem; however, they did not have immune deficiency and underlying diseases such as infection with HIV, and there was no evidence of a close contact with a known case of tuberculosis. The course of antituberculous therapy in patients with CNS TB is longer (12–30 months) than other forms of TB. Instance of a new brain tuberculoma, or instance of developing existing lesions, is not an indication for changing the anti-tuberculous regimen [19???]. If the treatment period of brain tuberculoma keeps in recommended course, the death rate will be approximately 10 %, while 50 % of patients recover completely [19, 20???]. Both of the reported cases improved with appropriate treatment quite well, so that after a period, they did not have any neurological complaints or neurological findings on examination.
Conclusion In developing countries and high prevalence areas for TB infection such as Iran and especially Afghanistan, one should keep in mind the possibility of tuberculous infection of the CNS in patients presenting with neurological symptoms such as weakness, fatigue, subacute to chronic progressive headache, and fever, in order to perform immediate and appropriate diagnostic tests and start the treatment, hence decrease the morbidity and mortality of this serious, but potentially treatable, infection. Although open or stereotactic biopsy of the suspected tuberculomas may be necessary if definitive diagnosis of TB cannot be made at an extraneural site, in regions with a high prevalence of TB, the decision to initiate anti-TB therapy may be made even without histological confirmation.
Conflict of interest of interest.
The authors declare that there are no conflicts
References 1. Bradley WG, Daroff RB, Fenichel GM, Jankovic J (2008) (eds) Neurology in clinical practice. 5th ed, Elsevier, Philadelphia, 1434–1438 2. Algahtani HA, Aldarmahi AA, Algahtani AY, Al-Rabia MW, Samkari AM (2013) Tumour-like presentation of central nervous system tuberculosis: a retrospective study in Kingdom of Saudi Arabia. J Taibah Univ Med Sci. doi:10.1016/j.jtumed.2013.11. 002 (Article in press) 3. Deogaonkar M, Das Sh (2006) Isolated spinal intramedullary tuberculoma in a healthy immunocompetent adult. Int J Infect Dis 10(3):266–267 (Epub 2006 Jan 9) 4. Katti MK (2004) Pathogenesis, diagnosis, treatment, and outcome aspects of cerebral tuberculosis. Med Sci Monit 10:215–229 5. Dastur DK, Manghani DK, Udani PM (1995) Pathology and pathogenetic mechanisms in neurotuberculosis. Radiol Clin North Am 33:733–752 6. Hosoglu S (1998) Tuberculous meningitis in adults: an elevenyear review. Int J Tuberc Lung Dis 2:553–557 7. Dehoux E (1996) Urinary retention revealing a tuberculoma of conus medullaris in a patient with intracranial tuberculosis: case report. Spinal Cord 34:630–632 8. Choksey MSA, conus A (1989) Tuberculoma mimicking an intramedullary tumor: a case report and review of the literature. Br J Neurosurg 3:117–122 9. Rhoton EL (1988) Intramedullary spinal tuberculoma. Neurosurgery 22:733–736 10. Compton JS (1984) Intradural extramedullary tuberculoma of cervical spine. case report. J Neurosurg 60:200–203 11. Kalita J (1999) Intramedullary cervical tuberculoma. Spinal Cord 37:297–298 12. Udani PM, Parekh UC, Dastur DK (1971) Neurological and related syndromes in CNS tuberculosis. Clinical features and pathogenesis. J Neurol Sci 14(3):341–357 13. Draouat S, Abdenabi B, Ghanem M, Bourjat P (1987) Computed tomography of cerebral tuberculoma. J Comput Assist Tomogr 11(4):594–597 14. Ramachandran R, Kalyanram S, Prabhakar R (1993) A rare presentation of miliary tuberculosis. Ind J Tub 40:205 15. Traub M, Colchester CF, Kinsley DPE, Swash M (1984) Tuberculosis of central nervous system. Q J Med 53(209):81–100 16. Labhard N, Bicold L, Zellweger JP (1994) Cerebral tuberculosis in the immunocompetent host: 8 cases observed in Switzerland. Tuber Lung Dis 75(6):454–459 17. Adams JH, Chia LG, Shen WC (1992) Locations of cerebral infections in tuberculous meningitis. Neuroradiology 34:197 18. Patel NH, Sathvara P, Patel J, Vaghela D (2013) Disseminated tuberculosis with paradoxical miliary tuberculomas of brain in a child with rickets. J Pediatr Neurosci 8(3):228–231. doi:10.4103/ 1817-1745.123687 19. Hejazi N, Hassler W (1997) Multiple intracranial tuberculomas with atypical response to tuberculostatic chemotherapy: literature review and a case report. Acta Neurochir (Wien) 139(3):194–202 (Review) 20. Pagnoux C, Genereau T, Lafitte F, Congy F, Chiras J, Herson S (2000) Brain tuberculomas. Ann Med Intern (Paris) 151(6):448–455
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LETTER TO THE EDITOR
Treatment of patients with suspected brain tuberculoma before or without bacteriologic confirmation in endemic places: report of two cases Sasannejad Payam • Moghadam-Ahmadi Amir • Shahsavari Sasan • Pourrashidi-Boshrabadi Ahmad Tafakhori Zahra • Sharifi-Razavi Athena
•
Received: 20 April 2014 / Accepted: 29 June 2014 Ó Belgian Neurological Society 2014
Tuberculosis (TB) is the most important infectious disease in the world, and it can produce disease in nearly every organ system, as in the central nervous system (CNS). Neurological involvement is found in approximately 1 % of TB infections, and presents with complications such as tuberculosis meningitis, intracerebral tuberculoma or tuberculosis involvement of the spine with myelopathy (pott’s disease) [19]. Generally, patients declare with headache, seizures, fever, focal neurological deficit and aspects of elevated intracranial pressure. Presentation of infratentorial tuberculoma may be with brainstem syndromes, cerebellar symptoms and multiple cranial nerve palsy [2].
Intramedullary tuberculomas are not routine patterns of CNS TB and figure only 8 % of all the lesions. These lesions can be treated by anti-tuberculosis chemotherapy likewise microsurgical excision [3]. Neurological TB may develop during primary infection or may become reactive as a consequence of immunosuppression. Neurological manifestations of CNS tuberculosis are headache, nausea and vomiting, meningeal irritation, altered mental status and cranial nerve palsies. Untreated disease progresses with decreased level of consciousness, seizures, focal neurological deficits, and ultimately death [4]. We describe two patients with normal immunity, presented with symptoms suggesting focal lesions in the brain, and multiple tuberculomas were detected in several places in their brain, including cerebral hemispheres, cerebellum and brainstem.
S. Payam Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran
Case presentation
Introduction
M.-A. Amir (&) Department of Neurology, Clinical Research and Development Center, Rafsanjan University of Medical Sciences, Ali-EbnAbitaleb Hospital, Rafsanjan, Iran e-mail: [email protected] S. Sasan P.-B. Ahmad Faculty of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran T. Zahra Department of Oromaxillofacial Radiology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran S.-R. Athena Department of Neurology, Mazandaran University of Medical Sciences, Mazandaran, Iran
Case 1 The first patient was a 25-year-old woman who presented with mild subacute progressive headache associated with occasional low-grade fever and sweating, mild weight loss, nausea and vomiting. In neurological examination, she had mild right hemiparesis. Brain CT scan showed multiple hypodense lesions with surrounding edema (Fig. 1). Brain MRI with gadolinium demonstrated more than 100 intracranial ring enhancing lesions, involving almost every part of the brain, such as cerebral hemispheres, cerebellum and brainstem (Fig. 2). Radiological examination of the chest revealed multiple 1-2 mm lesions with miliary pattern infiltration.
123
Acta Neurol Belg Fig. 1 Brain CT scan demonstrates multiple hypodense lesions with surrounding edema in different areas of the brain
Laboratory findings revealed mild leukocytosis, positive C-reactive protein (CRP = ?3) and elevated erythrocyte sedimentation rate (ESR = 55). An intradermal tuberculin test and several blood cultures yielded negative results. Other conditions such as toxoplasmosis, HIV infection and brucellosis were ruled out by appropriate tests. Echocardiography and ultrasonography of the abdomen and pelvis were normal. Examination of the cerebrospinal fluid (CSF) demonstrated low sugar (2 mg/dl), pleocytosis (WBC = 95 with 70 % polymorphonuclear leukocytes), and high protein (80 mg/dl). After a while, polymerase chain reactin (PCR) test for TB in the CSF, bronchoalveolar lavage (BAL) and CSF culture for mycobacterium tuberculosis yielded positive results. Considering the diagnosis of CNS-TB (i.e., brain tuberculoma), the patient was treated with anti-TB drugs (isoniazide, rifampin, ethambutol and pyrazinamide) before PCR and culture results became available. During the treatment course, the patient’s level of consciousness was decreased. Brain CT scan revealed obstructive hydrocephaly; hence, urgent ventriculostomy was performed that was successful and she became fully conscious and alert during the next days. The patient improved
123
gradually in about 10 days, and finally, she was discharged with antituberculosis drugs and phenytoin, while she had no signs or symptoms. Brain lesions were completely eliminated on follow-up radiologic examination. Case 2 The second patient was a 19-year-old man from Afghanistan, with recent-onset episodes of focal seizures in the right upper limb (with occasional secondary generalization). He did not have any complaints of constitutional disturbances such as fever, weight loss and sweating, or a precise history of close contact with a known-case of Mycobacterium tuberculosis infection. Neurological examination revealed no abnormal findings such as papilledema or focal neurological deficits. Axial brain CT scan showed multiple hypodense lesions with surrounding edema, and a thin hyperdense ring around some of them, giving a ‘‘target-appearance’’. After administration of contrast, multiple ring enhancing lesions appeared in all parts of the brain in cerebellum, brainstem, basal ganglia, internal capsule and bilateral frontal, temporal and parietal lobes, with surrounding edema but
Acta Neurol Belg
Fig. 2 Brain MRI with gadolinium demonstrates a lot of intracranial ring enhancing lesions, involving almost every part of the brain including cerebral hemispheres, cerebellum and brainstem
without significant mass effect or hydrocephaly (Fig. 3). Chest radiographic evaluation revealed milliary pattern infiltration.
Despite the absence of a history of close contact with a known case of TB infection, and of course regarding his low socioeconomic status that limited further evaluation,
123
Acta Neurol Belg
Fig. 3 Axial brain CT scan with contrast shows multiple ring enhancing lesions in all parts of the brain in cerebellum, brainstem, basal ganglia, internal capsule and bilateral frontal, temporal and parietal lobes, with surrounding edema but without significant mass effect or hydrocephaly
empiric treatment for TB was initiated with a high-degree of suspicion to brain tuberculoma, considering the fact that he came from Afghanistan, which is an endemic place for TB infection. The patient’s seizures were completely controlled after a while (about 3 weeks after starting the anti-tuberculous regimen), and the patient returned to Afghanistan without any neurological symptoms or signs. So we could not do post-treatment radiologic evaluation.
Discussion Tuberculosis is an airborne disease caused by Mycobacterium tuberculosis. Meningo-encephalitis and granuloma formation are two pathologic forms of CNS-TB [5]. It is a chronic bacterial infection identified by the formation of granulomas in the infected tissues [6]. Recent studies report the incidence of tuberculous infection at 11.1 per 100,000 population in Western countries, and neuro-tuberculosis involves 0.5–2 % of extrapulmonary tuberculous infection in the general tuberculosis prevalence [7, 8]. The incidence of CNS-TB depends on the incidence of tuberculosis and socioeconomic condition of the country. Brain tuberculoma
123
is responsible for 5–8 % of intracerebral space-occupying lesions in developing countries such as Iran and Afghanistan. Intracerebral tuberculoma occur quite frequently in association with tuberculous meningitis [7, 9, 10, 19]. Iran is a country with a relative high prevalence of TB infection. Cerebromeningeal involvement is a potentially lethal complication of brain tuberculomas in developing countries [12]. A past history of active tuberculosis in other parts of the body is seen in about 30-70 % of the cases of brain tuberculomas [12, 13]. Hematogenous spread from tuberculous disease elsewhere in the body develops brain tuberculomas; however, only few reports [14, 15] show miliary tuberculosis presenting with brain tuberculomas. According to the Rich’s hypothesis, small tuberculous lesions occur in CNS during the hematogenous distribution. The CSF invasion is seen after years [17]. However, in our cases, brain tuberculomas occurred in association with miliary tuberculosis apparently. The brain tuberculomas clinically present with paroxysmal onset of headache, occasionaly followed by dizziness, seizures, altered mentation and focal neurological signs [16]. As in the first patient, the investigation of CSF usually shows pleocytosis (mononuclear cells are predominant) with low glucose
Acta Neurol Belg
level and high protein content, and also positive culture for Mycobacterium tuberculosis in more than half of the cases but may take 6–8 weeks to become positive; however, patients with miliary TB or CNS tuberculomas may have a normal CSF initially. Multiple tuberculomas of the brain is generally seen in immunodeficient patient, especially HIV- seropositive patients. Neither of our patients had evidences of immunodeficiencies, diabetes, malnutrition, cancer or history of immunosuppressive treatment. [18]. Appearance of tuberculomas on brain CT scan is in three forms: iso-, hypo- or hyperdense lesions with 1.5–7 cm in diameter and a ring enhancement after injection of contrast [15]. One of the interesting facts about the first patient is the presence of more than 100 ring-enhancing lesions, spread in all parts of the brain, which is the most abundant brain tuberculomas that has been reported in the literature heretofore. It is remarkable in our patients that they had many lesions in the cerebrum, basal ganglia, cerebellum and brainstem; however, they did not have immune deficiency and underlying diseases such as infection with HIV, and there was no evidence of a close contact with a known case of tuberculosis. The course of antituberculous therapy in patients with CNS TB is longer (12–30 months) than other forms of TB. Instance of a new brain tuberculoma, or instance of developing existing lesions, is not an indication for changing the anti-tuberculous regimen [19???]. If the treatment period of brain tuberculoma keeps in recommended course, the death rate will be approximately 10 %, while 50 % of patients recover completely [19, 20???]. Both of the reported cases improved with appropriate treatment quite well, so that after a period, they did not have any neurological complaints or neurological findings on examination.
Conclusion In developing countries and high prevalence areas for TB infection such as Iran and especially Afghanistan, one should keep in mind the possibility of tuberculous infection of the CNS in patients presenting with neurological symptoms such as weakness, fatigue, subacute to chronic progressive headache, and fever, in order to perform immediate and appropriate diagnostic tests and start the treatment, hence decrease the morbidity and mortality of this serious, but potentially treatable, infection. Although open or stereotactic biopsy of the suspected tuberculomas may be necessary if definitive diagnosis of TB cannot be made at an extraneural site, in regions with a high prevalence of TB, the decision to initiate anti-TB therapy may be made even without histological confirmation.
Conflict of interest of interest.
The authors declare that there are no conflicts
References 1. Bradley WG, Daroff RB, Fenichel GM, Jankovic J (2008) (eds) Neurology in clinical practice. 5th ed, Elsevier, Philadelphia, 1434–1438 2. Algahtani HA, Aldarmahi AA, Algahtani AY, Al-Rabia MW, Samkari AM (2013) Tumour-like presentation of central nervous system tuberculosis: a retrospective study in Kingdom of Saudi Arabia. J Taibah Univ Med Sci. doi:10.1016/j.jtumed.2013.11. 002 (Article in press) 3. Deogaonkar M, Das Sh (2006) Isolated spinal intramedullary tuberculoma in a healthy immunocompetent adult. Int J Infect Dis 10(3):266–267 (Epub 2006 Jan 9) 4. Katti MK (2004) Pathogenesis, diagnosis, treatment, and outcome aspects of cerebral tuberculosis. Med Sci Monit 10:215–229 5. Dastur DK, Manghani DK, Udani PM (1995) Pathology and pathogenetic mechanisms in neurotuberculosis. Radiol Clin North Am 33:733–752 6. Hosoglu S (1998) Tuberculous meningitis in adults: an elevenyear review. Int J Tuberc Lung Dis 2:553–557 7. Dehoux E (1996) Urinary retention revealing a tuberculoma of conus medullaris in a patient with intracranial tuberculosis: case report. Spinal Cord 34:630–632 8. Choksey MSA, conus A (1989) Tuberculoma mimicking an intramedullary tumor: a case report and review of the literature. Br J Neurosurg 3:117–122 9. Rhoton EL (1988) Intramedullary spinal tuberculoma. Neurosurgery 22:733–736 10. Compton JS (1984) Intradural extramedullary tuberculoma of cervical spine. case report. J Neurosurg 60:200–203 11. Kalita J (1999) Intramedullary cervical tuberculoma. Spinal Cord 37:297–298 12. Udani PM, Parekh UC, Dastur DK (1971) Neurological and related syndromes in CNS tuberculosis. Clinical features and pathogenesis. J Neurol Sci 14(3):341–357 13. Draouat S, Abdenabi B, Ghanem M, Bourjat P (1987) Computed tomography of cerebral tuberculoma. J Comput Assist Tomogr 11(4):594–597 14. Ramachandran R, Kalyanram S, Prabhakar R (1993) A rare presentation of miliary tuberculosis. Ind J Tub 40:205 15. Traub M, Colchester CF, Kinsley DPE, Swash M (1984) Tuberculosis of central nervous system. Q J Med 53(209):81–100 16. Labhard N, Bicold L, Zellweger JP (1994) Cerebral tuberculosis in the immunocompetent host: 8 cases observed in Switzerland. Tuber Lung Dis 75(6):454–459 17. Adams JH, Chia LG, Shen WC (1992) Locations of cerebral infections in tuberculous meningitis. Neuroradiology 34:197 18. Patel NH, Sathvara P, Patel J, Vaghela D (2013) Disseminated tuberculosis with paradoxical miliary tuberculomas of brain in a child with rickets. J Pediatr Neurosci 8(3):228–231. doi:10.4103/ 1817-1745.123687 19. Hejazi N, Hassler W (1997) Multiple intracranial tuberculomas with atypical response to tuberculostatic chemotherapy: literature review and a case report. Acta Neurochir (Wien) 139(3):194–202 (Review) 20. Pagnoux C, Genereau T, Lafitte F, Congy F, Chiras J, Herson S (2000) Brain tuberculomas. Ann Med Intern (Paris) 151(6):448–455
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