A case of acute acquired obstructive hydrocephalus in a cat with suspected ischaemic cerebellar infarct

Raimondi, Francesca; Lourinho, Filipa; Scott, Harry; Shihab, Nadia

Ischaemic infarcts affecting the territory of the RCA are clinically described as resulting in peracute, nonprogressive signs of neurological deficits characterised by ataxia with or without hypermetria, non-ambulatory paresis, head tilt, nystagmus, ventrolateral strabismus, decreased menace response, postural and proprioceptive deficits. [6] [7] [8] [9] These infarcts are the result of severe hypoperfusion of the rostral cerebellum and medulla because of an obstruction caused by a thrombus originating within the RCA or from an embolus migrating from elsewhere in the body. 1, 4 The RCA in cats and dogs arises from the arterial circle and vascularises the rostral cerebellum, with collateral branches directed to the medulla and pons. [9] [10] [11] Ischaemia results in energy deprivation, leading to the development of anaerobic glycolysis, lactic acidosis, inflammation, free radical formation, capillary endothelial damage and blood-brain barrier (BBB) disruption. 1, 4 Two different critical phases are recognised in the pathogenesis of the ischaemic infarct. The first phase is characterised by an intracellular accumulation of water due to failure of the ionic pumps (cytotoxic oedema), which develops a few minutes after the event. 1,4,12 A second phase is characterised by the leakage of water and proteins into the extracellular space from the damaged BBB (vasogenic oedema), which has been reported to develop within a few hours (4-6 h) and can last for 3-5 days. 1, 4 Cerebellar infarcts in 25% of human patients may develop a mass effect. [13] [14] [15] [16] In these cases, the infarcted parenchyma and the surrounding vasogenic oedema behave like a spaceoccupying mass in the caudal fossa, causing brainstem compression, collapse of the fourth ventricle and an obstructive hydrocephalus. [13] [14] [15] [16] In the small animal literature, this complication has been suspected but never documented. 7 The MRI changes reported in this case report are similar to previously reported cerebellar infarcts in the small animal literature. [2] [3] [4] [6] [7] [8] The abnormality on MRI was confined to the specific territory supplied by the RCA, had a sharp demarcation from the surrounding parenchyma, a distribution predominantly in the grey matter and an angular (wedge) shape (Figure 1 ). The presumed infarcted area presented with increased T1 and T2 prolongation time that resulted in low signal intensity (compared with the surrounding parenchyma) in T1W images and high signal intensity in T2W and T2 FLAIR images (Figure 2) . It was possible to appreciate in T2W and FLAIR images a moderate mass effect of the presumed infarcted area on the surrounding brain parenchyma. In T1W post-contrast images it was also possible to appreciate a lack of contrast enhancement probably secondary to the poor vascularisation present in the presumed infarcted area as described in similar cases. 2, 4, 17 MRI findings were consistent with acute obstructive hydrocephalus as described previously, 5 and included the dilatation of the right olfactory recess, flattening of the interthalamic adhesion and diminished suprasellar cistern secondary to the third ventricle expansion, 5 and deformation of the interthalamic adhesion that was not distinctly circular in the midsagittal plane. 5 Additionally, there was a narrowing of the cerebral sulci, obliteration of the subarachnoid space around the dorsal convexity of the cerebral hemisphere, elevation of the corpus callosum and overcrowding