The presence of brain atrophy in patients with non-A IDS may be related to the fact that MR of brain tissue can accurately show enlarged VR gaps and gelatinous pseudocapsules, and MR can show significant abnormalities when CT shows normal, which is consistent with the literature. The enlarged VR gap is common in all patients in this group, and all patients in this group showed this on MR examination. Cryptococcal cells can be seen on smear examination or culture. This is followed by gelatinous pseudocysts, which appear as multiple well-defined oval cysts on MR, mostly in the basal ganglia or thalamus, and may accumulate in clusters of cysts with a soap bubble shape, which is characteristic and strongly suggests cryptococcal infection. Hydrocephalus is seen in both groups and both are traffic hydrocephalus, which is eventually caused by exudation from acute meningitis and meningeal adhesions or impaired function of the arachnoid villi during the infection. The causes of cerebral atrophy formation are not identical, and foreign literature reports that patients with A IDS-related CM are associated with HIV virus infection. Wang Jin et al. found that Cryptococcus neoformans is a conditionally pathogenic bacterium, and most of them are associated with degeneration and necrosis after respiratory inhalation. Non-A IDS-associated novel Cryptococcus meningoencephalitis produces a transient pneumonia in which the fungus is phagocytosed by alveolar phagocytes and is transmitted through the bloodstream as foci of intracerebral reinforcing nodules with limited cerebral edema, which is disseminated to the brain in non-A IDS patients. Because the cerebrospinal fluid lacks the complement contained in normal serum the degree of meningeal strengthening is significantly higher than in the A IDS group, which may be related to the non-A IDS body, and the dopamine in the cerebrospinal fluid favors the growth of Cryptococcus novelis, Cryptococcus novelis has a high affinity for the CNS. Cryptococcal meningoencephalitis occurs mainly in immunocompromised patients with chronic underlying diseases, such as A IDS, diabetes mellitus, malignancy, and chronic kidney disease, but nearly 30% of patients do not have underlying diseases, and the disease has a poor prognosis and a high mortality rate. The incidence of CM in patients with A IDS has increased significantly in recent years, mainly because cellular immunity plays a major role in preventing novel cryptococcal infections, and the immune function of the body in patients with A IDS is severely defective. The incidence rate of A IDS patients is significantly higher than that of non-A IDS patients. There was no significant difference in the age of prevalence between A IDS and non-A IDS patients with Cryptococcal meningitis.
The main imaging findings of CM were: enlarged VR gaps, gelatinous pseudocapsules, nodular granulomas, limited hydrocephalus, hydrocephalus, cerebral atrophy, and meningeal enhancement. The first four are intracerebral parenchymal lesions, preferably in the basal ganglia, temporal lobe, midbrain and subcortical areas on both sides. Restricted hydrocephalus, nodular granuloma and meningeal enhancement often represent the inflammatory response of the body to cryptococcal invasion. Previously, there are few reports comparing the imaging of A IDS and non-A IDS related CM. The author found that the common features of the imaging of A IDS and non-A IDS related CM patients are: compared to CT, most of the patients in the group have normal immunity and obvious inflammatory response, so inflammatory edema, enhanced inflammatory granulomas and significantly enhanced meninges are seen. In contrast, patients with A IDS were immunocompromised, lacked an inflammatory response, had mildly enhanced meninges, and did not show restricted cerebral edema or granulomas.
The CT and MRI manifestations of novel cryptococcal meningoencephalitis are mainly gelatinous pseudocapsules, hydrocephalus, brain atrophy and meningeal enhancement formed by enlarged VR gaps in the brain parenchyma. The detection rate of MRI is significantly higher than that of CT and provides more information, so it should be the technique of choice. Compared to non-A IDS, patients with A IDS are less likely to be diagnosed because of the milder inflammatory response and less obvious imaging than non-A IDS. For patients with confirmed treatment, laboratory tests can only provide information on the presence of novel cryptococci in the cerebrospinal fluid, but not on the invasion of brain tissue by the pathogen, so imaging, especially MRI, can provide detailed changes in the brain tissue of CM and provide accurate guidance for further clinical treatment. The imaging manifestation of some CM still lacks specificity, and coupled with the fact that its imaging manifestation is not necessarily related to the clinical manifestation, severity of lesions and regression, the imaging diagnosis of CM should be closely combined with clinical data and laboratory tests.