Article Figures & Data
Figures
- Fig 1.
CNS VZV–IRIS. A 37-year-old HIV+ woman with a herpes zoster rash with a T7 dermatome was treated with acyclovir 6 weeks prior to admission (PTA). Four weeks PTA, the patient developed leg numbness and tingling. HAART was initiated 2 weeks PTA. Double vision was followed by severe weakness in her legs 1–2 days PTA. Initial MR imaging of the thoracic spine with fast spin-echo axial (A) and sagittal (B) views shows scattered patchy extensive high-signal lesions in the spinal cord, which enhance on contrast sagittal (C) and axial (D) contrast T1WI and are associated with leptomeningeal enhancement, indicating an inflammatory VZV meningitis and myelitis.
- Fig 2.
CNS VZV–IRIS (same patient as in Fig 1). When the patient developed a right third-nerve palsy and a left hemiparesis, initial brain MR imaging shows, on axial FLAIR (A and B), hyperintense signal in the subarachnoid spaces diffusely compatible with meningitis and focal high signal in the right midbrain along with a mild communicating hydrocephalus. Restricted diffusion is demonstrated in the midbrain on DWI (C) and ADC maps (D), indicative of an acute infarct. Contrast T1WI in sagittal projection (E) reveals leptomeningeal enhancement in the interpeduncular fossa and prepontine cisterns. CSF PCR was positive for varicella zoster virus. Her CD4 count was 140 cells/μL. Intravenous acyclovir was started and HAART was stopped. Three weeks later progression to paraplegia and right upper extremity weakness occurred, several days after completion of the acyclovir therapy. CNS VZV-IRIS (same patient as in Fig. 1). Follow-up MR imaging shows new high signal on FLAIR (F) in the pons along with restricted diffusion on DWI (G) and ADC maps (latter not shown), compatible with another acute infarct. Contrast T1WI in axial (H and I) views reveals leptomeningeal enhancement along with focal enhancement at multiple sites, including in the left Sylvian fissure, which conventional angiography demonstrates is due to a vasculitis with vessel beading, narrowing, and aneurysms (J) as seen on lateral view of the left carotid injection. Acyclovir was restarted, and steroids were added.
- Fig 3.
CNS VZV–IRIS. A 51-year-old woman who, 3 weeks prior to admission at an outside hospital, was newly diagnosed with seizures and HIV and was started on HAART. She was also treated with antibiotics for a leg cellulitis. Altered mental status and tonic-clonic seizure prompted a new hospital admission 3 weeks later where herpes zoster lesions of her left foot were seen, and acyclovir was begun. Absolute CD4 count was 283 cells/μL. CSF cultures and PCR were negative. Fat-saturated contrast sagittal (A) and axial (B) images show enhancement of the entire course of the left S1 nerve root, compatible with a radiculitis, and enhancement and enlargement of the left dorsal root ganglia. Some thoracolumbar leptomeningeal enhancement is also seen indicating meningitis.
- Fig 4.
CNS VZV–IRIS (same patient as in Fig 3). Initial MR imaging of the brain shows, on axial FLAIR (A and B) and contrast T1WI (C and D), bilateral hyperintense signal abnormalities without restricted diffusion in the cortical and subcortical regions of the occipital, temporal, frontal, and parietal lobes with leptomeningeal and some patchy adjacent parenchymal enhancement with mild sulcal compression and no MRA (not shown) abnormalities. She was restarted on HAART and finished a 3-week course of acyclovir followed by suppressive therapy. Follow-up MR imaging 1 year later (E–H) shows a marked decrease in FLAIR (E and F) high-signal abnormalities with concomitant atrophy and near resolution of the leptomeningeal and parenchymal areas of enhancement, shown on axial contrast images (G and H).
- Fig 5.
CNS TB. A 28-year-old man presented with headache and vomiting for 3–4 weeks and meningeal irritation. The first MR imaging reveals, on axial FLAIR (A), a communicating hydrocephalus with transexudation of CSF and, on contrast axial T1WI (B), avid and diffuse enhancement of the leptomeningeal spaces compatible with meningitis. On routine CSF examination, PCR for TB was consistent with TB meningitis. The patient was kept on antitubercular treatment and showed clinical signs of deterioration after 8 weeks of therapy. Follow-up axial FLAIR (C) and contrast T1WI (D) reveal a marked increase in edema, evidenced by the diffuse hypertense signal in the brain parenchyma (C), persistent hydrocephalus, and new enhancing parenchymal lesions (D), compatible with tuberculomas. However, the basal meningeal enhancement showed improvement. After 6 months of therapy (E and F), there is MR imaging improvement associated with clinical improvement. Axial FLAIR (E) reveals a marked decrease in edema and in the ventricular size and resolution of the tuberculomas. While this patient was not HIV-infected and was not on HAART, the imaging appearance is similar to that seen in CNS TB–IRIS.
- Fig 6.
Chronic CNS-IRIS without coinfection. Two years following the institution of HAART, this HIV-positive patient developed a chronic relapsing and remitting meningitis without detectable organisms. Initial MR imaging on axial FLAIR (A) shows bilateral diffuse deep and subcortical white matter hyperintensities with no atrophy and with high signal in the subarachnoid spaces, while on axial contrast T1WI (B), leptomeningeal enhancement is seen. Minimal brain stem high FLAIR signal is also demonstrated (not shown). Two years later at the time of greatest neurologic impairment, axial FLAIR MR imaging (C) reveals mild mass effect and progression of the supratentorial and brain stem lesions. No organism was detected by CSF analysis. Following brain biopsy and steroid administration, there was symptom resolution. A follow-up MR imaging on axial FLAIR (D) reveals resolution of mass effect and a decrease in white matter lesions. Figures A, C, and D reproduced with permission from Costello et al.77
