Description  

An adult Caucasian man with a history of polysubstance abuse was found unresponsive by the nursing staff at his rehabilitation centre and intubated by emergency medical services. On examination, he was stuporous, his eyes did not open to stimulation, his pupils were reactive, localised to pain with bilateral upper extremities and demonstrated triple flexion to noxious stimuli in the bilateral lower extremities. Urine toxicology was positive for cocaine metabolites. A CT scan of the head was performed, which showed possible hypodensities in the bilateral temporal lobes. MRI of the brain was performed to further characterise these hypodensities, and it revealed bilateral middle cerebral artery (MCA) infarction and generalised cerebral oedema (figure 1). CT angiogram of the head at this point was performed, which showed narrowing of both MCAs and possible moyamoya pattern on the left (figure 2). This moyamoya-like vascular change was suggested by narrowing of the left MCA and hypervascular lenticulostriate arteries, likely as a result of chronic changes. An intracranial pressure (ICP) monitor (bolt) was placed, which showed steadily rising pressures. Despite sedative measures, osmotherapy, pharmacological induction of paralysis and maximised treatment for ICP, he continued to develop intractable ICP. A CT scan at this point showed evidence of uncal and tonsillar herniation, and infarcts from compression of the posterior cerebral arteries. After discussion with family, his treatment was transitioned to comfort care and he died shortly after palliative extubation.

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Figure 1

MRI of the brain shows bilateral middle cerebral artery (MCA) territory infarction, and demonstrates bilateral infarction of the MCA territory on (A) diffusion-weighted imaging and (B) apparent diffusion coefficient sequences (arrows).

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Figure 2

CT angiogram of the head with contrast reveals bilateral middle cerebral artery (MCA) narrowing (arrows) and moyamoya appearance on the left. The left proximal MCA segment (M1) is severely narrowed and hypervascular lenticulostriate vessels are seen on (A) axial and (B) coronal reconstructions.

Moyamoya represents a chronic, progressive vasculopathy resulting in decreased intracranial blood flow and secondary development of collateral blood supply to perfuse the area of distal ischaemia.1 Cocaine-induced cerebral vasospasm has been well-described with there being several case reports and series.2 The chronic vascular changes seen in this case differentiate it from the previous reports on strokes related to cerebral vasospasm and cocaine use. Chronic cocaine use can lead to chronic vascular changes, possibly including moyamoya seen in this case.3 The underlying mechanism for these observed chronic changes is unknown but may be related to vasculitic changes similar to that seen with methamphetamine use.3 While the aetiology of moyamoya associated with demise in this patient remains unknown, this case suggests that chronic cerebrovascular pathology can lower the threshold for acute stroke with subsequent cocaine use, as seen in this case.