Presentation
Giddiness for one day with sudden loss of consciousness.
Patient Data
Ill-defined hypodensity is seen at left cerebellum with loss of grey-white matter differentiation. Associated with mass effect onto the fourth ventricles and effacement of left cerebellar folia and adjacent basal cisterns.
Bilateral lateral and third ventricles are dilated in keeping with acute hydrocephalus.
No intracranial haemorrhage. No midline shift.
Encephalomalacia is seen at the right temporo-occipito-parietal and left frontal regions, likely secondary to previous insult.
Ill-defined T1 hypointense and T2/FLAIR hyperintense signal with patchy enhancement and restricted diffusion is seen at the left cerebellum involving the left cerebellar vermis. Associated with mass effect onto fourth ventricle, adjacent basal cisterns and effacement of the adjacent left cerebellar folia. Inferior descent of the cerebellar tonsils below foramen magnum.
Blooming artefact on SWI sequence is noted within left cerebellar lesion and right parieto-temporo-occipital region, likely haemosiderin deposits.
No significant midline shift. Bilateral lateral and third ventricles are dilated in keeping with acute hydrocephalus.
Area of T1 low signal intensity and T2 high signal with almost signal suppression on FLAIR sequence and no enhancement is seen at right parieto-temporo-occipital region in keeping with encephalomalacia. No restricted diffusion.
T1 hypointense and T2/ FLAIR hyperintense gliosis with no enhancement and no restricted diffusion is observed at the left frontal lobe.
Subtle T1 hypointense and T2/ FLAIR hyperintense lesion with no enhancement and no restricted diffusion is seen at the right sided medulla oblongata.
Case Discussion
This is an unusual case of acute left cerebellar infarct with obstructive hydrocephalus.
Initial CT features was interpreted as cerebellitis or posterior fossa tumour in view of left cerebellar hypodensity showed mass effect and hydrocephalus.
However, clinical history of sudden onset giddiness and loss of consciousness raised the suspicion of acute cerebellar infarct. MRI was done, DWI/ ADC map revealed restricted diffusion and confirmed the diagnosis of recent infarct. Differential diagnosis includes acute cerebellitis with cytotoxic oedema.
Blood culture and sensitivity showed no growth.
Patient was referred to neurosurgical team and underwent decompressive craniectomy to relieve raised intracranial pressure (ICP). Patient survived after operation, recovered and was discharged.
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