Neuroimaging

Central nervous system (CNS) involvement in Chagas disease (CD) is an uncommon complication that can result from direct involvement of the parasite or from thromboembolic phenomena. Direct involvement of CNS can occur in both acute and chronic forms of CD, and can also be secondary to reactivation. Reactivation of CD generally occurs in immunosuppressed patients such as those with human immunodeficiency infection or malignancies being rarely described in patients without apparent immunosuppression. We report a case of a patient living for many years in a nonendemic area for CD that presented to the emergency department with sudden onset of neurological symptoms as a result of reactivation of the disease. The microorganism was isolated from cerebrospinal fluid, and despite appropriate use of benznidazole, the patient died of sepsis after 22 days of treatment. Further investigation did not show any apparent cause of immunosuppression. This case report shows the importance of consideri...

Resumen La tomografía por emisión de positrones con metionina carbono 11 (11 C-metionina PET/TC) se utiliza en la evaluación de los tumores primarios del sistema nervioso central. Describimos nuestra expe-riencia sobre los primeros 4 pacientes con tumores de la serie glial estudiados con 11 C-metionina PET/TC. Este es un estudio descriptivo, observacional y prospectivo. Se presentan 4 pacientes entre 38-50 años de edad con diagnóstico de gliomas (clasificación de la OMS). A todos se les realizó RM y 11 C-metionina PET/TC para evaluar actividad tumoral y diferenciar progresión tumoral de pseudoprogresión. Caso 1, gliomatosis cerebri grado II posradioterapia. Caso 2, glioblastoma grado IV postratamiento RT + temozolomida. Caso 3, oligodendroglioma grado II posradioterapia en 1993. Caso 4, oligoastrocitoma anaplásico grado III postratamiento RT + temozolo-mida. El patrón de captación de la 11 C-metionina comparativamente con la RM, demostró progresión tumoral en los casos 1, 3 y 4; en el caso 2 mostró captación aunque el diagnóstico final fue pseudoprogresión. A diferencia del PET con 18 fluordeoxiglucosa, la captación de 11 C-metionina en el tejido cerebral normal y en la pseudopro-gresión es baja, y los gliomas se visualizan como áreas metabólicamente activas. En los casos presentados, el 11 C-metionina PET/TC proveyó información valiosa sobre el comportamiento y extensión de la lesión, aunque en uno de los casos presentados no diferenció progresión tumoral de pseudoprogresión. El 11 C-metionina PET/ TC sería una herramienta útil en el estudio y seguimiento de los pacientes con gliomas. Abstract Utility of 11 C-methionine PET/CT in neuro-oncology. Positron emission tomography (PET) with 11 C-methionine (11 C-methionine PET/CT) is a new technique used to evaluate primary central nervous system (CNS) tumors. We describe our experience regarding the first 4 patients with glial tumors and 11 C-methionine PET/CT. This is a descriptive, observational and prospective study of 4 patients between 38-50 years of age, with different gliomas (WHO classification). MRI and 11 C-methionine PET/CT were performed in all cases. Case 1, gliomatosis cerebri grade II post-radiotherapy. Case 2, oligodendroglioma grade II diagnosed and treated with radiotherapy in 1993. Case 3, glioblastoma grade IV post-radiotherapy + temozolomide. Case 4, anaplastic oligoastrocytoma grade III post-radiotherapy + temozolomide. The pattern of 11 C-methionine uptake compared with MRI showed tumor progression in cases 1, 3 and 4, and in case 2 showed uptake although the final diagnosis was pseudoprogression. Unlike 18 fluordeoxiglucose PET/TC, 11 C-methionine uptake in normal brain tissue and pseudoprogression is low, and gliomas are displayed as metabolically active areas. The 11 C-methionine PET/CT provided valuable information on the tumoral behavior and extension, although in one case presented did not differentiate tumor progression from pseudoprogression. 11 C-methionine PET/CT could be a useful tool in the study and follow-up to patients with gliomas.

Memories become labile when recalled. In humans and rodents alike, reactivated fear memories can be attenuated by disrupting reconsolidation with extinction training. Using functional brain imaging, we found that, after a conditioned fear memory was formed, reactivation and reconsolidation left a memory trace in the basolateral amygdala that predicted subsequent fear expression and was tightly coupled to activity in the fear circuit of the brain. In contrast, reactivation followed by disrupted reconsolidation suppressed fear, abolished the memory trace, and attenuated fear-circuit connectivity. Thus, as previously demonstrated in rodents, fear memory suppression resulting from behavioral disruption of reconsolidation is amygdala-dependent also in humans, which supports an evolutionarily conserved memory-update mechanism.