Description

A 64-year-old man with a previous medical history of hypertension and non-specific focal seizures was admitted for treatment of recurrent anterior communicating artery aneurysm (ACoA). He had previous treatment of the ACoA twice but the aneurysm recanalised again and had grown in size from 1.8 cm in greatest dimension to 2.6 cm and associated with 6 x 7mm of residual filling (figure 1). He was retreated with stent-assisted coil embolisation.

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Figure 1

Cerebral angiogram anterior–posterior view (A) and lateral view (B) and T1 postcontrast MRI (C) demonstrating residual filling of ACoA prior to endovascular reintervention. ACoA, anterior communicating artery aneurysm.

The day after endovascular intervention, he was disoriented to time and situation, confused and inattentive. He was also agitated with pressured speech, unable to recognise his wife, exhibited intermittent expressive aphasia and poor short-term recall after 5 min. His inpatient medication was not contributory to his new-onset altered mental status, as he remained on his home medication of levetiracetam (750 mg two times per day), metoprolol (50 mg two times per day), methadone (50 mg daily) and topical testosterone gel. Despite undergoing treatment for a urinary tract infection, poor mentation persisted, prompting brain MRI that revealed diffusion-restricted, punctate acute ischaemic foci in the fornix and the left frontal and bilateral parietal lobes (figure 2). Psychological evaluation 7 days into his hospital stay revealed a Montreal Cognitive Assessment score of 16/30 and severe anterograde amnesia with visual memory more preserved than verbal memory. His neurological exam otherwise remained benign. He was ultimately discharged shortly thereafter with minimal improvement.

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Figure 2

Diffusion-weighted (DWI)  (A–C) and their corresponding adjusted diffusion coefficient (ADC) (D–F) MRI-weighted imaging representing acute diffusion restriction of ischaemic foci in left forniceal and left frontotemporal areas post stent-assisted coiling. White concave arrows in both DWI and ADC panels indicate enhanced diffusion restriction, and therefore areas of acute stroke in the fornix.

Outpatient neuropsychiatric evaluation 1 month following endovascular revision revealed abnormalities with complex attention, executive function, and most significantly, anterograde amnesia. Subjectively, the patient described frequent memory loss of conversations, with visitors to his house, or where he had been recently. He completed an outpatient traumatic brain injury clinic cognitive behavioural therapy programme without the need for antipsychotic medication and demonstrated recovery of symptoms over the next few months with almost complete resolution after 9 months.

Amnesia after ACoA coiling is rarely described in prior literature.1 The fornix is supplied by medial central arteries that usually arise from the proximal anterior cerebral artery, but may also originate from the ACoA.2 The subcallosal artery, a major perforator branch off the posterior aspect of the ACoA, is the sole source of perfusion to the anterior columns of the fornix bilaterally.3 The risk of forniceal stroke must be weighed against the potential benefits conferred by endovascular obliteration of wide-necked ACoA.

Occlusion or damage to these perforators leading to infarction of fornix and amnesia can occur after seemingly uneventful endovascular treatment of ACoA.3 Injury to mammillary bodies, hippocampus and thalamic nuclei can also lead to amnesia; however, injury to these structures was not seen in our patient. Hence, fornix infarct was the most likely cause of amnesia in our patient.

It is important to recognise forniceal infarction following ACoA coiling as a cause of amnesia postoperatively, as it can be misdiagnosed as delirium or acute stress reaction and lead to inappropriate medication administration. It is also important to counsel patients on reversibility and excellent prognosis with this complication, although the course may be prolonged.