Clinical—A 24-year-old female was diagnosed with neuromyelitis optica in March 2014 following an admission under our care for right hemiparesis secondary to relapsing medullary myelitis. She was at the time successfully treated with intravenous methylprednisolone. She presented again in April 2014 with one day of malaise and fevers, a week following commencement of prophylactic azathioprine in the community.On examination, she was tachycardic, tachypnoeic, febrile, and lethargic, with pronounced right hemiparesis and a right tongue deviation. No source of infection could be ascertained clinically. Given recent immunosuppression, sepsis of indeterminate origin was suspected.Azathioprine was withheld, and empiric intravenous ceftriaxone, amoxicillin, and acyclovir were started following a full septic screen, including lumbar puncture, blood cultures, and chest radiograph. Additionally, urgent MRI brain with contrast was ordered to investigate the hemiparesis and rule out progressive multifocal leukoencephalopathy, a rare consequence of immunosuppression in inflammatory neurological disorders.T2 imaging with a fluid attenuated inversion recovery (FLAIR) sequence revealed extension of the previous medullary lesion, with a new left perithalamic focus (Figure 1).Antimicrobial therapy was immediately stopped in place of high-dose intravenous methylprednisolone. Her symptoms resolved within 24 hours, and she was discharged a week later on a tapering course of oral prednisone. The full septic screen done prior to antimicrobial therapy was negative, including all cultures following full period of incubation. There were no complications at follow-up in May 2014. Figure 1. MRI brain showing an (arrowed) inflammatory left parathalamic lesion enhanced on an axial T2 FLAIR slice (left), with a T1 slice (right) at the same level for comparison Discussion—Patients on immunosuppressive therapy are at increased risk of severe infections. The pre-optic and posterior nuclei of the hypothalamus have an important role in thermoregulation. Our case illustrates how a primary inflammatory lesion in or adjacent to this area can masquerade as sepsis. It is important that perithalamic lesions remain in the differential diagnosis when treating the newly febrile immunosuppressed patient with a background of inflammatory neurological disorder.Definitive management may appear counter-intuitive to the infection-like presentation; as with any relapse of autoimmune myelitis, further immunosuppression is indicated.

Clinical—A 24-year-old female was diagnosed with neuromyelitis optica in March 2014 following an admission under our care for right hemiparesis secondary to relapsing medullary myelitis. She was at the time successfully treated with intravenous methylprednisolone. She presented again in April 2014 with one day of malaise and fevers, a week following commencement of prophylactic azathioprine in the community.On examination, she was tachycardic, tachypnoeic, febrile, and lethargic, with pronounced right hemiparesis and a right tongue deviation. No source of infection could be ascertained clinically. Given recent immunosuppression, sepsis of indeterminate origin was suspected.Azathioprine was withheld, and empiric intravenous ceftriaxone, amoxicillin, and acyclovir were started following a full septic screen, including lumbar puncture, blood cultures, and chest radiograph. Additionally, urgent MRI brain with contrast was ordered to investigate the hemiparesis and rule out progressive multifocal leukoencephalopathy, a rare consequence of immunosuppression in inflammatory neurological disorders.T2 imaging with a fluid attenuated inversion recovery (FLAIR) sequence revealed extension of the previous medullary lesion, with a new left perithalamic focus (Figure 1).Antimicrobial therapy was immediately stopped in place of high-dose intravenous methylprednisolone. Her symptoms resolved within 24 hours, and she was discharged a week later on a tapering course of oral prednisone. The full septic screen done prior to antimicrobial therapy was negative, including all cultures following full period of incubation. There were no complications at follow-up in May 2014. Figure 1. MRI brain showing an (arrowed) inflammatory left parathalamic lesion enhanced on an axial T2 FLAIR slice (left), with a T1 slice (right) at the same level for comparison Discussion—Patients on immunosuppressive therapy are at increased risk of severe infections. The pre-optic and posterior nuclei of the hypothalamus have an important role in thermoregulation. Our case illustrates how a primary inflammatory lesion in or adjacent to this area can masquerade as sepsis. It is important that perithalamic lesions remain in the differential diagnosis when treating the newly febrile immunosuppressed patient with a background of inflammatory neurological disorder.Definitive management may appear counter-intuitive to the infection-like presentation; as with any relapse of autoimmune myelitis, further immunosuppression is indicated.