The spread of mucormycosis to CNS is amongst the most severe manifestations of this fungal infection causing high mortality and residual functional damage. The spread is most commonly direct through the paranasal sinuses and orbit in about 70% of the cases. The rest of the cases can be infected through the hematogenous route or as an isolated CNS infection in intravenous drug abusers [17]. Patients may present with focal seizures, hemiparesis, focal deficit, or altered sensorium.
The intracranial spread can be direct from the nasosinal cavities, through the ophthalmic arteries or the cribriform plate to the frontal lobes, or the cavernous sinus by orbital apex [18] One of the recent case reports also suggests intracranial extension through the olfactory tracts [19]. Initially, there may be an extradural invasion of the mucormycosis resulting in enhancing soft tissue in the extradural space of basifrontal regions or medial temporal lobe. It will have an associated enhancement of the overlying dura.
As the infection spreads further, there may be a parenchymal invasion of the brain which will appear as T1 hypointense and T2 iso to mildly hyperintense soft tissue with diffusion restriction and post gadolinium enhancement (Fig. 10). Few blooming foci may also be appreciated.
There can be fungal abscesses with an irregular inner wall and T2 W hypointense contents. There shall be peripheral diffusion restriction due to the presence of fungal hyphae. Marked surrounding edema with mass effect may be seen. Trehalose peak on MR spectroscopy further authenticates the diagnosis of a fungal abscess [20].
At times, the fungal infiltration into the cerebral parenchyma may mimic a brain tumor [21] having a mass effect with increased cerebral blood volume and may require a histopathological diagnosis for confirmation.
Isolated involvement of the CNS is highly uncommon. This is seen in a few case reports in patients of intravenous drug abuse [22].
As the fungus is angioinvasive, it infests the blood vessels at the base of the brain resulting in infarction of the deep grey matter like basal ganglia [23]. Initially, it is unilateral with rapid progression to the other side basal ganglia. Cerebro Spinal fluid (CSF) examination does not yield the fungus in 50% of the cases and thus a high index of suspicion is advisable when isolated basal ganglia involvement is seen in intravenous drug abusers [24].
In advanced disease, there may be a leptomeningeal enhancement. Rarely there may also be excessive thickening of the dura appearing as T2 iso to hypointense thickening with enhancement on post gadolinium images. This may be confused with meningioma. However, an appropriate clinical setting with regression on initiation of antifungal would support the diagnosis of fungal pachymeningeal hypertrophy [25] (Fig. 11).
Less commonly, there may be involvement of the bones of the calvarium resulting in osteomyelitis. On CT, this will appear as expansion, sclerosis, erosion, and irregular lytic lesions of the bone [26].