Incidentally Detected Cerebral Ischemia with Contralateral Muscular “Hemi-Hypometabolism” on FDG PET in a Patient with Incidentally Discovered Internal Carotid Artery Occlusion

A 44-year-old man with monoclonal gammopathy of undetermined significance and worsening anaemia underwent fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) for possible progression to multiple myeloma. Fasting serum glucose was 139 mg/dL before injection of FDG. Although imaging was not concerning for myeloma, maximum intensity projection images [Fig 1a: Arrows] showed striking asymmetrical brain and muscular uptake between the right and left sides of the body. Coronal CT, PET, and fused images [Fig 1b-d: Arrows] and axial fused image [Fig 1e: Arrows] demonstrated low uptake and mild atrophy of several left-sided muscle groups compared to right, for example, the trapezius, rotator cuff muscles, pectoralis muscles, and latissimus dorsi. Axial PET images of the brain demonstrated diffusely decreased uptake in the right cerebral hemisphere, basal ganglia, and thalamus with crossed cerebellar diaschisis with hypometabolism of the left cerebellum [Figure 2a and b: arrows, also seen in fused Fig 2c].

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Fig 1: (a) MIP image PET demonstrating diffuse right cerebral hypo-metabolism (arrow in the right side of the head) and contralateral diffuse muscular hypo-metabolism (arrows in the left shoulder and thigh), (b) coronal CT, (c) fused PET/CT image, (d) coronal PET image and (e) axial fused PET/CT demonstrating hypo-metabolism and atrophic changes compared to right side (arrows in a-e).

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Fig 2: (a) Axial PET diffuse right cerebral hypo-metabolism (arrow). (b) Axial PET left cerebellar hypo-metabolism (arrow). (c) Axial fused PET/CT showing right cerebellar hypo-metabolism similar to axial PET. (d) Axial CT angiogram showing diminished arterial flow in the right cerebral hemisphere (white arrow) and (e) coronal CT angiogram showing occluded right internal carotid artery (arrows comparing two sides).

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The patient reported the onset of left upper extremity weakness approximately 3 years ago, with progressive worsening over the past 8 months. CT angiography of the head and neck revealed scattered calcific atherosclerotic disease and complete occlusion of the cervical segment of the right internal carotid artery [Fig 2d (arrow)]. Diminished flow was demonstrated in the right anterior and middle cerebral arteries, likely from collateral filling via the circle of Willis [Fig 2e (arrow)]. This case highlights the unique imaging features of chronic cerebral ischemia on FDG PET in a patient without a historyof stroke or a transient ischemic attack. Brain metabolism depends on glucose as its primary energy substrate, with characteristically high brain activity on FDG-PET mediated by various glucose transporters.^[1]

Cerebral ischemia interrupts glucose delivery to the brain and, over time, causes neuronal death, resulting in decreased activity of the affected territory on FDG-PET.^[2] However, this decreased FDG activity has been shown to be reversible to an extent following revascularisation, suggesting that chronic ischemia may result in neurons entering a state of low metabolic activity but remaining viable, similar to hibernating myocardium.^[3] In addition, seen in this case was crossed cerebellar diaschisis, a well-recognised phenomenon following cerebral infarction that is postulated to occur due to interruption of the corticopontocerebellar tract, producing functional inhibition and vasoconstriction at the contralateral cerebellar hemisphere.^[4] Decreased FDG uptake in muscles on the contralateral side of cerebral ischemia was most likely due to long-standing stroke-induced denervation and amyotrophy.^[5] Of note, prior reports suggest differences in metabolic activity of affected muscles in patients with flaccid versus spastic hemiparesis,^[6,7] and this case supports the notion that wider impairment of the motor circuit predicts development of flaccid, as opposed to spastic, muscle weakness.^[8]