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A 45-year-old woman suddenly became comatose several days after a renal transplantation. On examination, her systolic blood pressure had reached 260 mm Hg and her pulse was 28 beats per min. She had a left-sided, wide, light-fixed pupil. She localised to a pain stimulus but required intubation for airway protection. CT scan of head showed a large acute subdural haematoma, with shift of the midline structures and crowding of the basal cisterns and a pontine hyperdensity after craniotomy (figure 1 upper row). After evacuation of the subdural haematoma, she remained stuporous and was left with a complete left-sided ptosis, anisocoria, horizontal ophthalmoplegia, left decorticate motor response, but with the ability to signal with the right hand. MRI showed haemorrhage into the pons and a peduncular lesion. There was no clinical improvement (figure 1 lower row) and she eventually succumbed in a severely disabled state.
The focus here is on classic observations that remain important in the understanding of the pathophysiology of coma involving physiological and neuropathological changes associated with an acute mass effect in the brain. Jonathan Hutchinson (1828–1913) is credited with first describing a dilated pupil after a traumatic head injury.1 In 1867, he documented clinicopathological correlations in two cases and noted that the third nerve was compressed, explaining the pupillary dilatation. Harvey Cushing (1869–1939) noted that when the intracranial pressure rises rapidly, ‘Kussmaul–Tenner’ spasms (extensor rigidity), bladder and bowel incontinence, apnoea and a ‘prominent vagus effect’ – referring to bradycardia and asystole – would occur.2 Henri Duret (1849–1921) hypothesised that a shock wave in the cerebrospinal fluid was augmented in the aqueduct of sylvius, causing haemorrhage under the fourth ventricle.3 James Kernohan (1897–1981) published one of the first comprehensive pathological studies showing that a groove of the shifted crus cerebri occurred on the side contralateral to a brain tumour. This finding explained the development of ipsilateral hemiplegia accompanying expanding cerebral mass lesions.4
This case illustrates each of these four seminal observations. It is rare to see these iconic features on MRI. Moreover, compression of the posterior cerebral artery at the uncinate convolution and tethering of the basilar artery resulted in involvement of the thalamoperforators and posterior cerebral artery, eventually leading to a thalamic and occipital lobe infarction, figure 1: lower row. These secondary acute brain lesions are telltale signs of brainstem displacement due to suddenly increased intracranial pressure.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed. This paper was reviewed by Joe Anderson, Cardiff, UK.