Cerebellar Infarction After PEA Arrest: A Post-Resuscitation Diagnostic Pitfall

A 59-year-old woman with end-stage heart failure with reduced ejection fraction (EF approximately 10%), coronary artery disease, chronic obstructive pulmonary disease, and HIV on antiretroviral therapy presented with acute hypoxic respiratory failure from decompensated systolic heart failure. Her HIV viral load was undetectable but CD4 count remained at 136 cells/µL — in the AIDS range — indicating persistent immune dysfunction. She had a documented history of cocaine use disorder with repeated positive urine toxicology extending through the months prior to admission. On presentation she had severe anasarca, bilateral pleural effusions, and a markedly elevated BNP of 2,107 pg/mL.

During her hospitalization she became increasingly agitated, repeatedly removed supplemental oxygen, and refused non-invasive ventilation — behavior likely reflecting evolving hypoxia and hypercapnia from decompensated heart failure rather than primary neurological injury. She was subsequently found pulseless with pulseless electrical activity (PEA) arrest. Advanced cardiac life support was initiated, with return of spontaneous circulation (ROSC) achieved after approximately 16 minutes. She was emergently intubated, central access was placed via the right femoral vein, and norepinephrine was initiated for hypotension. She was transferred to the ICU in cardiogenic shock requiring norepinephrine and milrinone.

Neurological examination off sedation demonstrated lethargy, inability to follow commands, minimal pupillary reactivity, preserved brainstem reflexes, and withdrawal to noxious stimulation without purposeful movement. EEG showed moderate generalized slowing without epileptiform activity — an indeterminate prognostic pattern. Non-contrast CT head performed approximately nine hours after ROSC revealed a focal finding that changed the clinical course.

Figure 1

Non-Contrast CT Brain: Left Cerebellar Infarction Nine Hours Post-ROSC

An approximately 3-cm hypodense lesion in the left cerebellar hemisphere (arrow) is consistent with acute to subacute infarction. Critically, there is no diffuse cerebral edema — a finding that distinguishes this focal ischemic stroke from global hypoxic-ischemic injury, which typically produces diffuse loss of gray-white differentiation. The posterior fossa location increases vulnerability to false-negative MRI on subsequent imaging.

CT angiography of the head and neck demonstrated patent posterior circulation without large-vessel occlusion. MRI of the brain performed approximately four days after ROSC — delayed because hemodynamic instability required vasopressor support before safe transport was feasible — demonstrated no acute diffusion restriction and no acute territorial infarct.

Figure 2

MRI Brain Four Days After ROSC: No Acute Diffusion Restriction

The blue arrow corresponds to the same left cerebellar region identified on early CT (Figure 1). No corresponding lesion is visible on this follow-up MRI — a classic example of CT-MRI discordance in posterior circulation ischemia. This may reflect timing-related diffusion normalization ("DWI reversal"), where acute diffusion restriction fades after the initial ischemic injury phase. The "acute to subacute" characterization on CT suggests the diffusion abnormality may have already begun normalizing by the time MRI was obtained at day 4.

These imaging findings — early CT demonstrating focal cerebellar infarction while delayed MRI showed no acute lesion — were incorporated into multidisciplinary goals-of-care discussions with the family. The patient's clinical course was ultimately dominated by refractory cardiogenic shock and multisystem organ failure despite maximal supportive care.

Discussion

The central clinical lesson from this case is that neurological deterioration after cardiac arrest is not always global hypoxic-ischemic injury — focal ischemic stroke can occur concurrently and may be missed if early CT is not obtained. In this patient, early CT was decisive: the focal left cerebellar infarction would not have been captured on delayed MRI obtained four days later, where diffusion-weighted imaging was negative. This CT-MRI discordance in posterior circulation ischemia is well-described and reflects both technical limitations of posterior fossa imaging and the phenomenon of DWI reversal, in which the apparent diffusion coefficient normalizes as membrane pumps recover or as vasogenic edema displaces the initial cytotoxic pattern. The "acute to subacute" CT description supports this interpretation — the lesion was not hours old when imaged, suggesting diffusion changes may have already begun resolving. Clinicians should recognize that a negative MRI in this setting does not negate an earlier CT finding.

Multiple factors converged to increase this patient's stroke risk beyond the cardiac arrest itself: end-stage HFrEF with EF of approximately 10% (promoting low-flow cerebral perfusion), cocaine use (associated with vasoconstriction and arrhythmogenesis), and persistent immune dysregulation from HIV despite virologic suppression (associated with accelerated endothelial dysfunction and elevated cerebrovascular risk). Isolated cerebellar infarction would not fully explain the depth of her encephalopathy — her neurological impairment was multifactorial, combining focal ischemia with global hypoxia during the 16-minute arrest, cardiogenic shock, metabolic derangements, and sedation. Identifying the focal lesion early nonetheless served a crucial function: it prevented premature attribution of all neurological findings to irreversible hypoxic-ischemic injury and ensured a broader differential was maintained for the family's goals-of-care discussions.