Update: Spinal intramedullary tuberculosis

Spinal intramedullary tuberculosis

First reported by Cascino and Dibble 1).

Epidemiology

Intramedullary spinal tuberculosis is rare and constitute only 0.2-5% of all CNS tuberculoma2) 3). The combination of intramedullary and intracranial tuberculomas is extremely rare and only few cases have been reported in the literature so far 4) 5) 6) 7) 8).

Clinical features

Clinical presentation of spinal intramedullary tuberculosis (SIMT) is similar to intramedullary spinal cord tumor, with a characteristic subacute myelopathy, with slowly progressive paraplegia, sensory deficits, and/or bowel and bladder dysfunction.

Diagnosis

Diagnosis is strongly suspected with a clinical history of known tuberculosis in conjunction with characteristic findings on magnetic resonance imaging.
The MRI is a sensitive and non-invasive tool for diagnosing and localizing intramedullary as well as brain tuberculomas. The lesion appears as an isointense or hyperintense ring on the T1-weighted images and as an isointense or hypointense lesion on the T2-weighted images. MRI will also delineate the extent of surrounding edema. MRI also helps in determining the stage of tuberculoma formation. Presence of a bright central spot in the granuloma (target sign) is indicative of central caseation (rich foci).
Gd-DTPA enhancement MRI is more sensitive than MRI without enhancement in demonstrating the lesions of tuberculoma and arachnoiditis. In early stages of brain tuberculoma contrast MRI will show homogeneous enhancement representing the early tuberculoma stage, which may later evolve to ring enhancement with hypointense center. 9) 10) 11).
Jaiswal et al. suggest that MRI of the brain should be performed in all case of intramedullary spinal tuberculoma because of the possible presence of early asymptomatic/mild symptomatic intracranial tuberculomas 12).

Treatment

Management involves multiagent antitubercular chemotherapy without or with operative intervention.
Conservative treatment with antituberculosis medications and a short course of injectable steroids offers an effective, inexpensive, safe, and feasible option for treating intra-medullary tuberculoma, especially in developing countries 13).
Role of steroid is largely unproven. However, in patients with peri-lesional edema short-term steroids may be helpful 14). Usually, the conservative treatment is successful in achieving complete clinical neurological recovery over a period of 1 year, which is also accompanied by resolution of the tuberculomas 15).
Surgery is reserved for the patients with large lesions causing significant compression, patients who do not respond to or deteriorates during conservative treatment 16) 17) 18) 19) 20) 21) 22) 23) 24).

Case series

2009

Fifteen patients were analyzed. Mean age of presentation was 31 years (range: 18-45 years), with average duration at presentation being 11 months (2-24 months). Common locations: dorsal region: 7 cases, cervical: 5 cases, cervicodorsal: 2 cases and dorsolumbar region: 1 case. Sensori-motor involvement was noted in fourteen patients. Bowel and bladder involvement was seen in ten patients while one patient had respiratory distress. Only 40% of patients had secondary involvement of spine while the rest of the cases were having primary spinal intramedullary tuberculosis. Three patients had previous history of tubercular meningitis, while one patient had old pulmonary tuberculosis. There were one case each of cervical node involvement and intracranial granuloma. Twelve patients underwent surgery while others were conservatively managed, all patients received antitubercular therapy for 18 months. Nine of the twelve operated patients showed improvement in motor power, while two of the conservatively managed patients improved. Patients presenting late had a poorer outcome.
Spinal intramedullary tuberculosis is a non-malignant, treatable lesion giving a good outcome on management. Surgically managed patients showed a better outcome 25).

2002

During a period of 16 years (1985-2000), ten cases of intramedullary tuberculomas were diagnosed in All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India. Of these, eight cases were histologically proven intramedullary tuberculomas. The clinical profile, radiological data and histological slides were reviewed.
Age ranged from 18 to 45 years (mean 29.7 years) and there was slight male preponderance (six men, four women). Duration of symptom varied from 3 to 20 months (mean 11.5 months). All of them presented with motor weakness and sensory impairment. Most common site of involvement was dorsal cord followed by cervical, cervicodorsal and dorsolumbar regions. Three patients had associated involvement of lungs, cervical lymphnodes, and brain, and one patient had past history of tuberculous meningitis. Two patients were treated conservatively but surgical excision was done in eight cases followed by medical treatment.
Radiologically, intramedullary tuberculomas should be differentiated from other space occupying lesions (SOL) to avoid unnecessary surgery especially in those patients with tuberculosis of the other organs. The incidence of intramedullary tuberculomas is likely to increase with a rise in the incidence of AIDS 26).

Case reports

2017

A case of concurrent occurrence of intramedullary tuberculoma with multiple intracranial tuberculomas in a young 16-year-old boy, who presented with two weeks history of paresthesias and weakness of the lower limbs and diminution of vision in left eye, who had been treated for pulmonary tuberculosis. Magnetic resonance imaging (MRI) spine showed a well-circumscribed lesion opposite L1, which was diagnosed as intramedullary tuberculoma. As for vision complaint, on cranial imaging, he was found to have multiple round contrast enhancing lesions, which were diagnosed as intracranial tuberculomas based on their typical MRI findings. He had complete recovery with conventional treatment of anti-tubercular therapy and steroids, without any surgical intervention.
They suggest that MRI of the brain should be performed in all case of intramedullary spinal tuberculoma because of the possible presence of early asymptomatic/mild symptomatic intracranial tuberculomas 27).


A 9 month old boy with a retrospectively-recognized history of pulmonary TB presenting with fever and back tenderness found to have lower extremity hypertonia and clonus. Imaging revealed concurrent intracranial and spinal intramedullary tuberculomas. The patient was treated for hydrocephalus with external ventricular drainage followed by T8-10 laminectomy, drainage of abscess, and duraplasty. Parietal lobe biopsies proved the tuberculous etiology of intracranial lesions 28).


Varghese et al. report the case of a 49-year-old female with dull aching pain of both upper limbs of 1-week duration. On examination, she had no motor deficits. All the deep tendon reflexes were normal. The plantar responses were flexor bilaterally. Cervical spine imaging favored intramedullary tumor. She had partial relief of symptoms with steroid treatment. Repeat imaging done 1 month later revealed mild interval enlargement of the intramedullary lesions and multiple enlarged mediastinal and hilar nodes. Endoscopic ultrasound-guided fine-needle aspiration cytology of mediastinal nodes was suggestive of granulomatous inflammation. Hence, SIMT was considered as the probable diagnosis. The patient was started on antituberculosis therapy 29).

2015

A 25-year-old male who presented with a history of progressive paraparesis. Initial diagnosis was made as an intramedullary tumor by magnetic resonance imaging (MRI). The treatment of the patient involved is complete surgical excision of intramedullary lesion followed by appropriate antituberculous therapy. Postoperatively, his neurological symptoms were dramatically improved. With combination of both surgical and medical treatments, excellent clinical outcome was obtained.
This case illustrates the risk of misdiagnosis and the importance of histological confirmation of a pathological lesion as spinal cord tuberculoma prior to surgical therapy, which should be kept in mind as a differential diagnosis of the intramedullary spinal cord tumors 30).

2012

A patient with dorsal intramedullary tuberculoma who improved clinically as well as radiologically with antituberculous treatment and steroids 31).

References

1)

Cascino J, Dibble JB. Tuberculoma of spinal cord. JAMA. 1956;162(5):461–462.
2) , 16)

Citow JS, Ammirati M. Intramedullary tuberculoma of the spinal cord: Case report. Neurosurgery. 1994;35:327–30.
3) , 17)

Süzer T, Coşkun E, Tahta K, Bayramoǧlu H, Düzcan E. Intramedullary spinal tuberculoma presenting as a conus tumor: A case report and review of the literature. Eur Spine J. 1998;7:168–71.
4) , 14)

Huang CR, Lui CC, Chang WN, Wu HS, Chen HJ. Neuroimages of disseminated neurotuberculosis: Report of one case. Clin Imaging. 1999;23:218–22.
5) , 9)

Lin SK, Wu T, Wai YY. Intramedullary spinal tuberculomas during treatment of tuberculous meningitis. Clin Neurol Neurosurg. 1994;96:71–8.
6) , 18)

Shen WC, Cheng TY, Lee SK, Ho YJ, Lee KR. Disseminated tuberculomas in spinal cord and brain demonstrated by MRI with gadolinium-DTPA. Neuroradiology. 1993;35:213–5.
7) , 10) , 13) , 15)

Thacker MM, Puri AI. Concurrent intra-medullary and intra-cranial tuberculomas. J Postgrad Med. 2004;50:107–9.
8) , 19)

Yen HL, Lee RJ, Lin JW, Chen HJ. Multiple tuberculomas in the brain and spinal cord: A case report. Spine (Phila Pa 1976) 2003;28:E499–502.
11) , 20)

Shaharao VB, Pawar M, Agarwal R, Bavdekar SB. Intra-medullary tuberculoma occurring during treatment of tuberculous meningitis. Indian J Pediatr. 2004;71:107–8.
12) , 27)

Jaiswal M, Gandhi A, Purohit D, Mittal RS. Concurrent multiple intracranial and intramedullary conus tuberculoma: A rare case report. Asian J Neurosurg. 2017 Apr-Jun;12(2):331-333. doi: 10.4103/1793-5482.143461. PubMed PMID: 28484568; PubMed Central PMCID: PMC5409404.
21)

Gupta VK, Sharma BS, Khosla VK. Intramedullary tuberculoma: Report of two cases with MRI findings. Surg Neurol. 1995;44:241–3.
22)

Kayaoglu CR, Tuzun Y, Boga Z, Erdogan F, Gorguner M, Aydin IH. Intramedullary spinal tuberculoma: A case report. Spine (Phila Pa 1976) 2000;25:2265–8.
23)

Kumar R, Jain R, Kaur A, Chhabra DK. Brain stem tuberculosis in children. Br J Neurosurg. 2000;14:356–61.
24)

Rhoton EL, Ballinger WE, Jr, Quisling R, Sypert GW. Intramedullary spinal tuberculoma. Neurosurgery. 1988;22:733–6
25)

Ramdurg SR, Gupta DK, Suri A, Sharma BS, Mahapatra AK. Spinal intramedullary tuberculosis: a series of 15 cases. Clin Neurol Neurosurg. 2009 Feb;111(2):115-8. doi: 10.1016/j.clineuro.2008.09.029. Epub 2008 Dec 5. PubMed PMID: 19058910.
26)

Sharma MC, Arora R, Deol PS, Mahapatra AK, Sinha AK, Sarkar C. Intramedullary tuberculoma of the spinal cord: a series of 10 cases. Clin Neurol Neurosurg. 2002 Sep;104(4):279-84. PubMed PMID: 12140088.
28)

Ghali MGZ, Srinivasan VM, Kim CJ, Malik A. Spinal intramedullary tuberculosis with concurrent supra- and infratentorial intracranial disease in a 9 month old boy: case report and review of the literature. World Neurosurg. 2017 May 19. pii: S1878-8750(17)30768-4. doi: 10.1016/j.wneu.2017.05.069. [Epub ahead of print] Review. PubMed PMID: 28532916.
29)

Varghese P, Abdul Jalal MJ, Kandathil JC, Mathew IL. Spinal Intramedullary Tuberculosis. Surg J (N Y). 2017 Mar 30;3(2):e53-e57. doi: 10.1055/s-0037-1599823. eCollection 2017 Apr. PubMed PMID: 28825021; PubMed Central PMCID: PMC5553513.
30)

Mishra SS, Das D, Das S, Mohanta I, Tripathy SR. Spinal cord compression due to primary intramedullary tuberculoma of the spinal cord presenting as paraplegia: A case report and literature review. Surg Neurol Int. 2015 Mar 23;6:42. doi: 10.4103/2152-7806.153844. eCollection 2015. PubMed PMID: 25883834; PubMed Central PMCID: PMC4392528.
31)

Thirunavukarasu SC, Ramachandrappa A. A rare case of intramedullary tuberculoma: Complete resolution after medical treatment and role of magnetic resonance imaging in diagnosis and follow-up. Asian J Neurosurg. 2012 Oct;7(4):223-6. doi: 10.4103/1793-5482.106661. PubMed PMID: 23559994; PubMed Central PMCID: PMC3613649.

Tuberculosis espinal

Percival Pott fue la primera persona que hizo la descripción clásica de la tuberculosis espinal (TB) en 1779, de ahí, que la tuberculosis espinal se denomine Enfermedad de Pott 1) 2) 3). 4).

Epidemiología

Es más frecuente en el tercer mundo.
Por empeoramiento de la epidemia de tuberculosis pulmonar (TB), la incidencia de la tuberculosis espinal se ha incrementado en los últimos años.
Representa el 2% de todos los casos de tuberculosis, 15% de los casos de tuberculosis extrapulmonar y el 50% de los casos de tuberculosis esquelética.
En la columna vertebral, principalmente en la zona tóracolumbar.

Etiología

Es generalmente resultado de la diseminación hematógena del Mycobacterium tuberculosis a la densa vascularización del hueso esponjoso de los cuerpos vertebrales. El sitio de la infección primaria es o bien un foco pulmonar o de otros focos extraóseos tales como los ganglios linfáticos, gastrointestinal, o cualquier otra víscera 5) 6).

Anatomía patológica

Se localiza en el cuerpo vertebral o disco intervertebral.

Clínica

La aparición de los síntomas suele ser insidioso y la progresión de la enfermedad es lenta.
La duración de los síntomas antes del diagnóstico oscila entre 2 semanas a varios años. Históricamente, este intervalo era al menos 12 meses en promedio, bajando a entre 3 y 6 meses en la época reciente.
La presentación depende de la etapa de la enfermedad, sitio de la enfermedad, la presencia de complicaciones, tales como déficit neurológico, abscesos o fístulas y síntomas constitucionales, como debilidad, pérdida de apetito, pérdida de peso, aumento de la temperatura por la noche, y sudores nocturnos.
Los hallazgos clínicos incluyen dolor de espalda, paraparesia, cifosis, alteraciones sensoriales y disfunción intestinal y vesical 7).
Su diagnóstico a menudo se retrasa debido a estos síntomas inespecíficos, lo que conduce a complicaciones graves.
El déficit neurológico puede desarrollarse en un 10-47 % de los pacientes, debido a inflamación medular o radicular.
La infección rara vez se extiende al canal espinal.

Diagnóstico

La afectación se produce en varios niveles generalmente a nivel tóracolumbar, sobre todo del cuerpo vertebral.

Resonancia

En RM T1W1 señal hipointensa en cuerpos vertebrales y espacio discal.
Se debe de completar con secuencias T2 (T2W), y STIR en axial, sagital y coronal, seguido de secuencias T1W con contraste
En T2 la señal es hiperintensa con realce heterogéneo del cuerpo vertebral.
Las secuencias STIR son útiles para diferenciar el fluido de componente graso en secuencias sin contraste. Los hallazgos característicos incluyen la destrucción de dos cuerpos vertebrales adyacentes y las platillos; destrucción discal; edema de cuerpo vertebral, y aparición de abscesos prevertebral, paravertebrales, y epidural.

Importante alteración en la intensidad de señal con hiperintensidad en STIR e hipointensidad en T1 del cuerpo vertebral L4 y la mitad inferior del cuerpo vertebral L3 y con hiperintensidad discal a este nivel, con marcado componente de partes blandas rodeando estos cuerpos vertebrales de predominio en la porción anterior y lateral, con irregularidad del platillo superior en la parte posterior del cuerpo L3.
El disco intervertebral presenta una herniación posterior parcialmente extruida dirigida en dirección caudal. Además se aprecian varias colecciones en ambos músculos psoas, de mayor tamaño en el lado izquierdo donde se extiende hasta la pélvis con alteración de la intensidad de señal intramuscular. Tras la administración de contraste se aprecia una marcada captación de ambos cuerpos vertebrales mencionados y de las partes blandas alrededor de esto con componente intracanal de predominio más evidente a nivel L4 disminuyendo de forma marcada el diámetro ánteroposterior del canal vertebral. Llama la atención la ausencia de captación del disco intervertebral L3-L4.
Se aprecian otros dos focos de captaciones en la articulación facetaria derecha L5-S1 y en el canal sacro a la altura S2, esta última de aspecto quístico con realce parietal.

Gammagrafía

La gammagrafía puede dar falsos positivos por cambios degenerativos, cirugía reciente o fractura.
En la radiografía simple los cambios se producen a las 2-8 semanas del inicio de la infección y los cambios se traducen en pérdida de los márgenes de los platillos y pérdida de la altura del espacio discal.
El diagnóstico definitivo se establece tras identificar bacilos ácido-alcohol resistentes cuya muestra se puede obterner por vía percutánea.

Complicaciones

Absceso epidural espinal hasta el 25 % de estas lo son por tuberculosis.
Osteomielitis vertebral
Absceso del psoas

Tratamiento

La aparición de cepas resistentes pueden conducir al fracaso del tratamiento.
La medicación no consigue evitar en muchas ocasiones la aparición de cifosis por fallo mecánico de la columna anterior, lo que obliga a un tratamiento quirúrgico asociado que permita reconstruir el perfil sagital.
El tratamiento quirúrgico está indicado ante la ausencia de diagnóstico, la falta de respuesta al tratamiento farmacológico, en la prevención de la cifosis por fallo mecánico en casos de extenso defecto óseo, en presencia de grandes abscesos que no puedan ser drenados por punción dirigida por tomografía computarizada (TC) o cuando aparece déficit neurológico por absceso epidural o compresión anterior por cifosis.

Técnicas

Curetaje discovertebral, evacuación del absceso, fusión intersomática con hueso autólogo y fusión posterolateral en un segundo tiempo, con o sin material de osteosíntesis a distancia del foco séptico para evitar la colonización del material de osteosíntesis y su aflojamiento séptico es la técnica habitual incluso en pacientes de edad avanzada 8).
La pérdida de gran número de niveles vertebrales funcionales aconseja utilizar técnicas que reduzcan tanto el número de segmentos vertebrales fusionados como la pérdida de balance articular y recuperen el perfil sagital.
La artrodesis intersomática instrumentada sobre los cuerpos vertebrales afectados, con aporte de hueso corticoesponjoso para solucionar el defecto estructural anterior y restablecer el perfil fisiológico, puede cumplir estos objetivos.
Cuando la inestabilidad estructural lo aconseja, se asocia a la fusión anterior una artrodesis posterolateral transpedicular (fusión circunferencial de 360°).
Desafortunadamente , los materiales existentes no han cumplido completamente los requisitos para la reconstrucción, por lo tanto , hay una necesidad urgente de desarrollar nuevos implantes.
Poli -DL -láctico ( PDLLA ) y nano- hidroxiapatita (NHA ) son dos sistemas de administración de fármacos prometedores lo que nos podría ayudar a superar las dificultades en la reconstrucción en el futuro 9).

Cervical

Desbridamiento anterior, descompresión, injerto óseo, y la instrumentación son métodos seguros y eficaces en el tratamiento quirúrgico de la tuberculosis de la columna cervical inferior 10).
La tuberculosis aislada del coxis es extremadamente rara, pero su existencia pone de relieve la importancia de considerar la tuberculosis como un diagnóstico a pesar de que existan sitios inusuales 11).

Bibliografía

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11) Kim, Do Un, Seok Won Kim, and Chang Il Ju. 2012. “Isolated Coccygeal Tuberculosis.” Journal of Korean Neurosurgical Society 52 (5) (November): 495–497. doi:10.3340/jkns.2012.52.5.495.