Diagnostic Dilemma of Central Nervous System Tuberculosis with Neurocysticercosis and Neurosarcoidosis: A Case Report.

Multiple ring-enhancing lesions are commonly encountered abnormalities in neuroimaging. There are many differentials for such lesions as infections, neoplasms, vascular lesions, inflammatory and demyelinating conditions, and granulomatous diseases. In developing countries, tuberculoma and neurocysticercosis are the two important etiologies to be considered. This case report illustrates how multiple ring-enhancing lesions can lead to our management in one direction while the true diagnosis remains elusive. A 53-year-old male who presented with a headache was initially diagnosed and treated as neurocysticercosis, then neurosarcoidosis ultimately turned out to be a case of Central Nervous System Tuberculosis on further evaluation. Consideration of only clinical scenarios and neurological imaging can lead to diagnostic inaccuracy, mismanagement and poor outcome, therefore, other supporting lab investigations should be considered for making a correct diagnosis. Keywords: brain; case reports; neurocysticercosis; sarcoidosis; tuberculoma.

Tumor necrosis factor antagonists for paradoxical inflammatory reactions in the central nervous system tuberculosis: Case report and review.

RATIONALE: Paradoxical reaction/immune reconstitution inflammatory syndrome is common in patients with central nervous system tuberculosis. Management relies on high-dose corticosteroids and surgery when feasible. PATIENT CONCERN: We describe 2 cases of HIV-negative patients with corticosteroid-refractory paradoxical reactions of central nervous system tuberculosis. DIAGNOSES: The 2 patients experienced clinical impairment shortly after starting therapy for TB, and magnetic resonance imaging showed the presence of tuberculomas, leading to the diagnosis of a paradoxical reaction. INTERVENTIONS: We added infliximab, an anti-tumor necrosis factor (TNF)-alpha monoclonal antibody, to the dexamethasone. OUTCOMES: Both patients had favorable outcomes, 1 achieving full recovery but 1 suffering neurologic sequelae. LESSONS: Clinicians should be aware of the risk of paradoxical reactions/immune reconstitution inflammatory syndrome when treating patients with tuberculosis of the central nervous system and should consider the prompt anti-TNF-α agents in cases not responding to corticosteroids.

Central Nervous System Tuberculosis : Etiology, Clinical Manifestations and Neuroradiological Features.

PURPOSE: As a result of multilateral migration and globalization in times of humanitarian crises, western countries face a possible increase in the incidence of central nervous system tuberculosis (CNS TB). The diagnosis of CNS TB is challenging and often delayed due to the manifold and often non-specific presentation of the disease. The aim of this review is to analyze and summarize imaging features and correlated clinical findings of CNS TB. METHODS: The different manifestations of CNS TB are explained and illustrated by characteristic neuroradiological as well as neuropathological findings. An overview on diagnostic and therapeutic approaches is provided. For clarity, tables summarizing the lesion patterns, differential diagnoses and diagnostic hints are added. RESULTS: The CNS TB can be manifested (1) diffuse as tuberculous meningitis (TBM), (2) localized as tuberculoma or (3) tuberculous abscess or (4) in extradural and intradural spinal infections. Information on clinical presentation, underlying pathology and the distinguishing features is demonstrated. The TBM is further described, which may lead to cranial nerve palsy, hydrocephalus and infarction due to associated arteritis of the basal perforators. The differential diagnoses are vast and include other infections, such as bacterial, viral or fungal meningoencephalitis, malignant causes or systemic inflammation with CNS. Complicating factors of diagnosis and treatment are HIV coinfection, multi-drug resistance and TB-associated immune reconstitution inflammatory syndrome (IRIS). CONCLUSIONS: Neurologists and (neuro-)radiologists should be familiar with the neuroradiological presentation and the clinical course of CNS TB to ensure timely diagnosis and treatment.

[Not Available]. / Meningoencefalitis tuberculosa con quistes aracnoideos medulares y siringomielia aguda.

TITLE: Meningoencefalitis tuberculosa con quistes aracnoideos medulares y siringomielia aguda.

DIAGNOSIS OF ENDOCRINE DISEASE: Expanding the cause of hypopituitarism.

Hypopituitarism is defined as one or more pituitary hormone deficits due to a lesion in the hypothalamic-pituitary region. By far, the most common cause of hypopituitarism associated with a sellar mass is a pituitary adenoma. A high index of suspicion is required for diagnosing hypopituitarism in several other conditions such as other massess in the sellar and parasellar region, brain damage caused by radiation and by traumatic brain injury, vascular lesions, infiltrative/immunological/inflammatory diseases (lymphocytic hypophysitis, sarcoidosis and hemochromatosis), infectious diseases and genetic disorders. Hypopituitarism may be permanent and progressive with sequential pattern of hormone deficiencies (radiation-induced hypopituitarism) or transient after traumatic brain injury with possible recovery occurring years from the initial event. In recent years, there is increased reporting of less common and less reported causes of hypopituitarism with its delayed diagnosis. The aim of this review is to summarize the published data and to allow earlier identification of populations at risk of hypopituitarism as optimal hormonal replacement may significantly improve their quality of life and life expectancy.

Worsening of longstanding headaches, dizziness, visual symptoms · Dx?

The clinical presentation and imaging studies of central nervous system tuberculosis are often indistinguishable from those of patients with malignant neoplasms or metastatic disease. Biopsies may be necessary to distinguish tuberculomas from other intracranial lesions such as pyogenic abscesses or necrotic tumors.

Patient taking chemotherapy for a small cell lung cancer: not every cerebral nodule is a metastasis: the tree that hides the forest.

We report the case of a 53- year-old man in whom the diagnosis of small cell lung cancer (SCLC) was made by the biopsy of a mass of the right trapezius muscle. A tumor was revealed on flexible bronchoscopy which pathological study showed tuberculosis (TB). Chest computed tomography (CT) scan revealed findings related to the SCLC associated to micronodules and nodules compatible with pulmonary TB. Cerebral CT scan revealed a nodule of 4.5 mm in diameter presenting enhancement after contrast material injection thought to be a metastasis. The patient was administered antitubercular treatment. Fiveteen days later, the patient started chemoptherapy with etoposid and carboplatin. A control cerebral CT scan realized after the end of the chemotherapy (2 months and a half of antitubercular treatment) revealed numerous cortical and subcortical infracentimetric nodules with contrast enhancement with a tentorial and subtentorial location considered to be in relation with cerebral miliary TB. The nodule discovered on the first cerebral scan was therefore a posteriori considered to have been of tubercular origin. The PS of the patient rapidly worsened. He presented mental confusion and died in some days.

Immune reconstitution inflammatory syndrome in central nervous system tuberculosis.

BACKGROUND: Immune reconstitution inflammatory syndrome (IRIS) related to tuberculosis (TB) is an exacerbation of an inflammatory response that most often occurs in HIV-infected patients but it has also been observed in non-HIV immunocompromised hosts. We describe two cases of TB associated IRIS with CNS involvement, one in a patient diagnosed with HIV infection and the other in a patient with immunosuppression due to anti tumor necrosis factor treatment. CASE REPORT; The first case was a 40-year-old man, newly diagnosed with HIV infection, who developed right hemiplegia and expressive aphasia. Lumbar puncture and MRI sustained the diagnosis of TB meningoencephalitis. He initially improved understandard antituberculous therapy (ATT). After 6 weeks of ATT antiretroviral treatment (ART) was initiated and one week later the patient experienced worsening of his symptoms (left hemiparesis and mixed aphasia), of CSF and MRI changes. He improved after he was starting on corticosteroids in tapering doses, with clinical deterioration at lower doses over a 5-month period. The second case was a 56-year-old male, treated for 3 years with Infliximab for ankylosing spondylitis. He was diagnosed with disseminated TB (CNS tuberculomas and pulmonary TB), histological and bacteriological confirmed the diagnosis. His neurological symptoms improved after starting ATT but after 2 weeks of therapy he presented with diplopia and generalized tonic-clonic seizures. These symptoms improved only after corticosteroids were added (tapering doses during the next 6 months). CONCLUSION: TB-associated IRIS with CNS involvement is potentially life threatening. Corticosteroids should be used to control the IRIS symptoms in those patients. The dosing and duration should be tailored to each patient.

Neurologic diseases in HIV-infected patients.

Since the introduction of highly active antiretroviral therapy there has been an improvement in the quality of life for people with HIV infection. Despite the progress made, about 70% of HIV patients develop neurologic complications. These originate either in the central or the peripheral nervous system (Sacktor, 2002). These neurologic disorders are divided into primary and secondary disorders. The primary disorders result from the direct effects of the virus and include HIV-associated neurocognitive disorder (HAND), HIV-associated vacuolar myelopathy (VM), and distal symmetric polyneuropathy (DSP). Secondary disorders result from marked immunosuppression and include opportunistic infections and primary central nervous system lymphoma (PCNSL). A differential diagnosis which can be accomplished by detailed history, neurologic examination, and by having a good understanding of the role of HIV in various neurologic disorders will help physicians in approaching these problems. The focus of this chapter is to discuss neuropathogenesis of HIV, the various opportunistic infections, primary CNS lymphoma, neurosyphilis, CNS tuberculosis, HIV-associated peripheral neuropathies, HIV-associated neurocognitive disorder (HAND), and vacuolar myelopathy (VM). It also relies on the treatment recommendations and guidelines for the above mentioned neurologic disorders proposed by the US Centers for Disease Control and Prevention (CDC) and the Infectious Diseases Society of America.

Central nervous system tuberculosis presenting as branch retinal vein occlusion.

Branch retinal vein occlusion (BRVO) associated with ocular tuberculosis (TB) is a rare presentation of retinal vasculitis but it can also present in the absence of active uveitis. We present a 39-year-old patient with BRVO who slowly developed bilateral papilloedema due to TB in the central nervous system. To our knowledge, this is the first case of systemic central nervous system TB confirmed by biopsy presenting as a branch retinal vein occlusion and shows the importance of extensive causative investigation of BRVO, especially for young patients.

Isolated homonymous hemianopsia due to presumptive cerebral tubercular abscess as the initial manifestation of human immunodeficiency virus infection.

We report a case of isolated homonymous hemianopsia due to presumptive cerebral tubercular abscess as the initial manifestation of human immunodeficiency virus (HIV) infection. A 30-year-old man presented to our outpatient department with sudden loss of visibility in his left visual field. He had no other systemic symptoms. Perimetry showed left-sided incongruous homonymous hemianopsia denser above the horizontal meridian. Magnetic resonance imaging revealed irregular well-marginated lobulated lesions right temporo-occipital cerebral hemisphere and left high fronto-parietal cerebral hemisphere suggestive of brain tubercular abscess. Serological tests for HIV were reactive, and the patient was started only on anti-tubercular drugs with the presumptive diagnosis of cerebral tubercular abscess. Therapeutic response confirmed the diagnosis. Atypical ophthalmic manifestations may be the initial presenting feature in patients with HIV infection. This highlights the need for increased index of suspicion for HIV infection in young patients with atypical ophthalmic manifestations.

The contribution of a murine CNS-TB model for the understanding of the host-pathogen interactions in the formation of granulomas.

Central nervous system (CNS) tuberculosis (TB) is the most severe form of TB, characterized morphologically by brain granulomas and tuberculous meningitis (TBM). Experimental strategies for the study of the host-pathogen interaction through the analysis of granulomas and its intrinsic molecular mechanisms could provide new insights into the neuropathology of TB. To verify whether cerebellar mycobacterial infection induces the main features of the disease in human CNS and better understand the physiological mechanisms underlying the disease, we injected bacillus Calmette-Guerin (BCG) into the mouse cerebellum. BCG-induced CNS-TB is characterized by the formation of granulomas and TBM, a build up of bacterial loads in these lesions, and microglial recruitment into the lesion sites. In addition, there is an enhanced expression of signaling molecules such as nuclear factor-κB (NF-κB) and there is a presence of inducible nitric oxide synthase (iNOS) in the lesions and surrounding areas. This murine model of cerebellar CNS-TB was characterized by cellular and biochemical immune responses typically found in the human disease. This model could expand our knowledge about granulomas in TB infection of the cerebellum, and help characterize the physiological mechanisms involved with the progression of this serious illness that is responsible for killing millions people every year.

Tuberculoma cerebral en paciente inmunocompetente / Brain tuberculoma in an inmunocompetent patient

Uruguay presenta baja prevalencia de tuberculosis, ubicándose en la etapa de control de la endemia. El tuberculoma cerebral representa el 1% del total de casos de tuberculosis en inmunocompetentes. Se presenta el caso clínico de una mujer, de 45 años, diabética tipo 2, con un cuadro clínico progresivo de paresia e hipoestesia braquial derecha y crisis epilépticas parciales simples. Estudios imagenológicos evidenciaron lesiones frontoparietales izquierdas, la serología para virus de inmunodeficiencia humana (VIH): negativa, la velocidad de eritrosedimentación: 24 mm/h; el PPD: 3 mm. Se realizó biopsia esteroatáxica. La anatomía patológica evidenció granulomas con necrosis caseosa y el cultivo Mycobacterium tuberculosis. Se comenzó tratamiento según pautas nacionales de la Comisión Honoraria de Lucha Antituberculosa, obteniéndose remisión clínica e imagenológica. La literatura revisada muestra que la demora en el diagnóstico en paciente inmunocompetentes es aproximadamente cuatro veces mayor que en inmunodeprimidos. La presentación clínica es inespecífica, siendo frecuentes la cefalea, la crisis epiléptica generalizada y hemiparesia. La RM es el estudio de mayor sensibilidad diagnóstica, no existiendo imágenes patognomónicas de tuberculoma. El tratamiento es médico; el tratamiento neuroquirúrgico se reserva para casos con hipertensión endocraneana y progresión bajo tratamiento médico. La respuesta al tratamiento se monitoriza con la remisión de los síntomas y el control imagenológico, destacándose la lenta resolución imagenológica.

Tuberculous encephalopathy without meningitis: pathology and brain MRI findings.

Tuberculous encephalopathy (TBE) is an established disease entity of diffuse cerebral damage occurring with tuberculosis and an underlying immune pathogenesis. However, the presence of this disease entity remains controversial. We report a 15-year-old boy with seizures and a progressive decline of cognitive function. Brain MRI showed diffuse, hyperintense lesions in the white matter on a T2-weighted image, with gadolinium enhancement on a T1-weighted image. Brain biopsy revealed demyelination and granuloma in the white matter. Ziehl-Neelsen staining showed acid-fast bacilli in the granulomas. Antituberculous medication with concomitant steroid treatment resulted in radiological resolution in addition to clinical improvement. Clinicopathological evidence in this case provides additional convincing evidence of TBE as a disease entity distinct from tuberculous meningitis.

Tuberculous brainstem abscess: case report.

OBJECTIVE: Tuberculous brainstem abscess is a clinically rare condition with potentially high mortality and morbidity. We present this report to draw attention to the importance of early recognition and adequate treatment of tuberculous brainstem abscess. CLINICAL PRESENTATION: A 24-year-old man complained of longstanding fever, headache, and weakness followed by development of progressive slurred speech and hemiparesis of the right extremities. Magnetic resonance imaging revealed a large thick-walled cystic lesion lying within the brainstem. INTERVENTION: The patient demonstrated a remarkable clinical recovery after microsurgery combined with a course of antituberculous therapy. Microbiological and histological findings confirmed the diagnosis of a tuberculous abscess. CONCLUSION: Despite its rarity, the tuberculous brainstem abscess must be considered in the differential diagnosis of cystic brainstem mass lesions in vulnerable patients. When confronted with progressing neurological deterioration and poor response to antituberculous therapy, stereotactic or microsurgical management should be considered. Microsurgical excision combined with a complete course of antituberculous therapy in our patient led to a good outcome.