Presentation
Sudden drop in GCS with underlying septic shock secondary to pneumonia.
Patient Data
Initial non-contrasted CT brain performed right after dropping in GCS.
All ventricles appear to be dilated comparing to the cerebral sulci, gyri and CSF containing spaces.
Basal cisterns are not effaced. No brainsterm or subfalcine herniation.
No acute intracranial bleed.
Repeated plain and contrast-enhanced CT brain, two days after the initial CT brain.
Diffuse lower attenuating "lesions" or "collections" (hypodense compared to white/grey matter but hyperdense compared to cerebral spinal fluid CSF) seen in the expected grey matter location at bilateral cerebellar folia, vermis, periphery of pons, periphery of midbrain and grey matters bordering the suprasellar cistern (bilateral mesial temporal lobes, bilateral frontal lobes). These "collections" do not show significant enhancement post contrast, and appear to be located in subpial region, especially well seen surrounding the midbrain and pons. The adjacent quadrigeminal cistern, bilateral Sylvian fissures and ambient cisterns still maintained their darker CSF attenuation compared to the subpial "collections" rather than within the subarachnoid cisterns.
Some of the intermediated density "collections" seen wtihin the right thalamus and right basal ganglia, which are suspicious to be located within the right sided perivascular spaces/Virchow Robbin spaces.
These lesions are also observed in the suprasellar cistern, bilateral Sylvian fissures and extending into perivascular space at the right basal ganglia.
No significant abnormal leptomeningeal enhancement.
The opacified circle of Willis appear to maintain their caliber in the suprasellar cistern without significant stenosis in the contrast-enhanced CT scan.
Hydrocephalus with periventricular lucency which can represent acute transependymal CSF seepage. Basal cisterns are effaced.
No acute intracranial bleed.
Proceeded with lumbar puncture. Repeated plain CT brain 2 weeks after the contrast-enhanced CT brain.
Generalized cerebral edema with complete effacement of cerebral and cerebellar sulci as well as the CSF containing spaces.
Ventricles are slit-like. Basal cisterns are effaced with downward cerebellar tonsillar herniation.
The previously noted cortial and periventricular hypodensities become worsened and larger in size.
Pseudosubarachnoid hemorrhages noted.
Suspicious acute intracranial bleed at the right inferior cerebellum, left sided midbrain and pons.
Case Discussion
Proceeded with a lumbar puncture after day 2 of illness where there was high opening pressure and CSF aspirated was cloudy. The CSF analysis showed low glucose, high protein and lymphocytic pleocytosis.
Low glucose and high protein can be present in both bacterial and fungal CNS infections, but for bacterial meningitis, one would expect neutrophilia whereas for fungal would be lymphocytic pleocytosis as in this case.
CSF and culture yielded Cryptococcus neoformans. This patient is immunocompetent. Antifungal therapy started for the patient.
Cryptococcus neoformans is an encapsulated opportunistic yeast-like fungus that triggers life-threatening meningoencephalitis in both immunocompromised and healthy individuals.The prevalence of cryptococcosis in this population ranges between 0.2 to 5.8%, with a total mortality rate of 20% to 50%1.
Most immunocompetent hosts render C. neoformans dormant in their lungs, but immunosuppression can trigger its replication and dissemination via blood or lymph to other organs, especially the brain.
Repeated CT brain on day 2 of illness showed the unusual imaging features of intermediate density "collections" at the subpial region or involving the grey matters. After confirming the presence of CNS cryptococcosis, this can be explained as ischemic necrosis of grey matter which is well established in recently published pathological journal of CNS cryptococcosis in experimental mouse model2. This ischemic necrosis can represent clear spaces of liquefactive tissue where damaged neurons and tissue are phagocytosed. In that mouse model study, there is noticeable accumulation of cryptococci in liquefactive tissue around the border of brain lesion which can proliferate further.
In the same study, acute subarachnoid hemorrhage, ischemia, meningitis and hydrocephalus are very common in CNS cryptococcosis.
The intermediate collections at right sided basal ganglia and thalamus may represent the known imaging features of gelatinous pseudocysts.
The last plain CT brain showed progressive CNS infection resulting in global hypoxic ischemic encephalopathy.
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