PICA infarction

Case contribution: Dr Radhiana Hassan

Clinical:

  • A 58 years old female with underlying diabetes and hypertension
  • Presented with lethargy, headache, vomiting for the past 1 week.
  • Headache was throbbing in nature with pain score 3/10 and is associated with neck stiffness and photophobia.
  • No limb weakness no fever. No constitutional symptoms.
  • Clinical examination shows GCS E4V5M6. Pupils 3/3 reactive
  • CVS/lung/abdomen examination normal.
  • Breast examination – no mass palpable
  • Power left upper and lower limb 4/5
  • Cerebellar sign positive. Dysdiadochokinesia positive over right side
  • No pass pointing. No intention tremors
  • FBC/RP/Coagulation profile normal.
CT brain in axial planes soft tissue window; non-contrast (upper row) and post contrast (lower row).

CT scan findings:

  • There is an ill-defined hypodensity at the left cerebellum (yellow arrows)
  • No enhancement seen post contrast
  • No hyperdense area to suggest acute hemorrhage
  • Mass effect with compression and narrowing of the fourth ventricle (red arrow)
  • There is obstructive hydrocephalus (white arrows)
  • Cerebral oedema is also noted.
MRI brain in axial planes at the level of cerebellum

MRI brain in sagittal and coronal plane T1-weighted image post contrast

MRI findings (3 weeks after CT scan)

  • A T2/FLAIR hyperintensity seen in the left cerebellum
  • Post contrast study shows gyriform enhancement at posterior and medial part of left cerebellum which shows territorial distribution
  • Areas of restricted diffusion seen within the same region
  • No mass effect. No surrounding oedema.

Diagnosis : PICA (posterior inferior cerebellar artery) infarction

Discussion:

  • Cerebellar infarction is a relatively uncommon subtype of ischaemic stroke
  • It accounts for about 2% of all cerebral infarctions
  • On acute stage it is seen as hyperintense area on DWI
  • Cerebral oedema peaks about 3 days
  • Parenchymal contrast enhancement may be visible 2-4 months after infarction
  • Mortality rate is higher due to concomitant brainstem infarction or compressive hydrocephalus rather than cerebellar infarction itself.

Progress of patient:

  • Patient underwent Right EVD insertion. Post operative, patient is able to extubate and GCS was E4V5M6.
  • Post operative D5, EVD was removed from patient and patient was discharge from ward with early MRI brain appointment.
  •  Patient is improving and EVD is able to wean off
Author: radhianahassan