A 43-year-old male patient was brought with complaints of speech disturbances and altered mental behaviour for 15 days. He had a HIV seropositive diagnosis 2 years before but was not on any treatment. On admission, his CD4 count was 98 cells/μL.
Gadolinium enhanced T1W MRI brain showed multiple ring enhancing lesions of varying sizes (most of them are small 2-3 cm) with few of them showing eccentric nodular enhancement (Eccentric target sign) at the grey-white matter junction of both cerebral hemispheres, bilateral basal ganglia, both thalami and pons with marked perilesional oedema.
These lesions were hypointense on T1 and were of mixed intensity on T2/FLAIR images. The largest lesion was seen in the right frontal lobe. It showed alternating concentric zones of hyper and hypointensities on T2W images.
On DWI, most of these lesions showed diffusion restriction peripherally with corresponding low ADC map values. On SWI, few focal areas of blooming were seen in some of these lesions suggestive of haemorrhage. These lesions showed reduced rCBV on MR perfusion images. MR spectroscopy of eccentric nodule of large lesion in the right frontal lobe showed an increased lipid lactate peak at 1.30 ppm (TE 135ms).
Cerebral toxoplasmosis is caused by the parasite toxoplasma gondii which exists in three forms as oocysts, tachyzoites and bradyzoites. Oocysts occur in cats and infect humans (intermediate hosts) when ingested. Oocysts develop into tachyzoites which are rapidly multiplying, convert to bradyzoites (tissue cysts) when enter CNS or muscle. Toxoplasmosis typically causes necrotizing encephalitis with tissue cysts in the periphery of necrotic areas .
Toxoplasmosis infection in healthy individuals is usually asymptomatic. It is the most common opportunistic CNS infection in HIV/AIDS patients . In most cases, it is due to reactivation of latent infection in patients with CD4 count <200 cells/μL [1, 3]. Patients may present with headache, altered mental status, seizures, fever, visual field defects, speech disturbances, cranial nerve abnormalities, motor weakness and sensory disturbances .
Lesions of cerebral toxoplasmosis are most commonly small (2-3 cm in size) and multiple, frequently involving grey-white matter junction, basal ganglia and thalamus [1, 3]. They can also involve white matter, brainstem and cerebellum [1-3]. Lesions involving corpus callosum may mimic glioblastoma multiforme . On CT, these lesions are hypo to iso attenuating and may show ring or nodular enhancement on contrast injection with perilesional oedema and mass effect [1, 2]. T1W MRI show hypointense lesions with occasional mild peripheral hyperintensity due to haemorrhage or coagulative necrosis . SWI show areas of haemorrhage as blooming which helps in differentiating toxoplasmosis from lymphomas which typically does not haemorrhage before treatment [1, 2]. Toxoplasmosis lesions show high to mixed intensity on T2 and FLAIR images with marked perilesional hyperintensity representing oedema and demyelination [2, 3]. T2W images may also show alternating concentric zones of hyper and hypointensities . Tuberculomas show central T2 hypointensity surrounded by isointense capsule that may mimic toxoplasmic lesion . Contrast-enhanced T1W images show masses with peripheral ring enhancement and in less than 30% of cases they show small eccentric nodular enhancement (eccentric target sign) which is pathognomonic of toxoplasmosis with 95% specificity and 25% sensitivity, representing inflamed leaky vessels entering the lesion through a sulcus histopathologically [1, 3, 4]. DWI show diffusion restriction peripherally with no central restricted diffusion that differentiates it from cerebral abscess which show central diffusion restriction . MRS show elevated lipid lactate peak and pMR show reduced rCBV .
Patients with typical imaging features of toxoplasmosis are treated empirically with multi-drug regimen (pyrimethamine, sulfadiazine and folic acid) . However, as lymphoma can also present with similar imaging appearances as toxoplasmosis, follow-up evaluation is mandatory 2-3 weeks after therapy [1, 2]. Our patient tested positive for anti-toxoplasma antibodies.
Differential Diagnosis List
Primary CNS lymphoma