Acute hypoglycaemia may mimic acute ischaemic stroke on brain imaging, in about 20% of cases reported in the literature, by causing either unilateral cortical and adjacent subcortical tissue hypoattenuation and swelling greater than cortical ischaemic stroke (e.g. Case 1), or lacunar ischaemic stroke (e.g. Figure
b). Usually the diagnosis of hypoglycaemia would be obvious, but in patients with hemiparesis, unilateral imaging findings could be mistaken for ischaemic stroke. Brain imaging changes in acute symptomatic hypoglycaemia are not always diffuse or bilateral. The literature suggests that the less severe episodes of hypoglycaemia are more likely to cause hemiparesis and smaller corticospinal tract lesions on imaging, thus may be more likely to mimic ischaemic stroke. These are also likely to be clinically milder strokes or transient ischaemic attacks (TIAs). Alternatively, it may be that hypoglycaemia can cause lesions in a wide range of brain regions but that only those in the corticospinal tracts cause focal neurological symptoms (hemiparesis or hemisensory loss) sufficient to trigger scanning because of the clinical similarity to stroke. Although T2 changes, restricted diffusion and CT attenuation changes are consistent with ischaemia, the pathology is rather different. Clues to the true diagnosis are that the lesion may not conform strictly to an arterial territory and the slightly different time course to ischaemic stroke, e.g. the persistence of swelling at 14 days in our Case 1, although here the duration of the left-sided weakness was unclear as it was only noticed sometime after the onset of hypoglycaemia and was hard to pinpoint as the patient was in a coma. Cases mimicking lacunar stroke may have lesions that appear identical to acute lacunar infarction on diffusion-weighted MR imaging [25
]. The signal/attenuation changes can disappear rapidly. Therefore, as standard practice, plasma glucose should be measured in all patients with suspected acute ischaemic stroke to ensure correct diagnosis and prompt treatment of hypoglycaemia. Hypoglycaemia should be part of the differential diagnosis of patients presenting with clinical or imaging features of stroke or TIA.
The literature summary indicates that hypoglycaemia duration rather than depth was related to clinical outcome, prolonged hypoglycaemia resulting in poor outcome, in agreement with one prospective study [36
]. In general, the more severe the symptoms, the more extensive the bilateral cortical involvement with persistent long-term brain damage. The less severe the symptoms, the imaged abnormalities were more likely unilateral and distributed along the motor pathway, with resolution of lesions. The new cases that we present fell into the poor outcome group with Case 2 fitting the most frequently described pattern of patchy bilateral cortical abnormality, whilst Case 1 fitted the less typical pattern of unilateral confluent cortical abnormality mimicking cortical ischaemic stroke. The proportion of patients with hypoglycaemia who develop imaging abnormalities, and the proportion of those that mimic ischaemic stroke, are unknown as there are no prospective and complete series of patients with hypoglycaemia all of whom had brain imaging. The largest case series (n=17) [42
], mostly patients with poor outcome, was consistent with the other 40 papers, namely that duration but not degree of hypoglycaemia was related to both clinical outcome and extent of imaging lesions. However, the paucity of patients with mild, transient symptoms or unilateral imaging lesions suggests that their retrospective case identification may have overlooked patients with mild hypoglycaemia, some of whom may masquerade as TIA.