Paradoxical giftedness and memory decline after anterior communicating artery aneurysm clipping: A high-resolution MRI case report

INTRODUCTION

Amnesia or memory impairment is a well-recognized complication following surgical repair of anterior communicating artery (ACoA) aneurysms.^[1-5] Among the perforating vessels most vulnerable during surgery, the subcallosal artery and the recurrent artery of Heubner (RAH) are of particular relevance.^[6] The subcallosal artery, typically unpaired, originates from the posterior aspect of the ACoA and supplies the bilateral columns of the fornix (FxCo) and adjacent basal forebrain regions.^[7,8] Because it is unpaired, injury to the subcallosal artery commonly results in bilateral infarction. In contrast, the RAH arises bilaterally from the A1 to A2 junction of the anterior cerebral artery and supplies the medial basal ganglia but is more often injured unilaterally during surgery.^[9] Their detailed anatomy is illustrated in Figure 1 (panels A and B, reproduced with permission from Mugikura et al.^[9] and panel C reproduced with permission from Takahashi et al.^[10])

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Figure 1:

Anatomy of the subcallosal and recurrent arteries of Heubner. (A) A schematic illustration, viewed sagittally, demonstrates the course and territory of the subcallosal artery. Originating from the posterosuperior aspect of the anterior communicating artery (ACoA), the subcallosal artery (white arrow heads) ascends dorsally through the lamina terminalis (LT) cistern. It follows a characteristic S-shaped curve to supply eight distinct regions: the preoptic area (POpA), paraterminal gyrus (PTG), subcallosal area, anterior commissure (AC), columns of the fornix (FxCo), rostrum (CCr) and genu (CCg) of the corpus callosum, and the anterior cingulate gyrus (CGa). (FM, foramen of Monro; MB, mammillary body; OC, optic chiasm; SP, septum pellucidum; 3V, third ventricle). (B) A posterior view of a methacrylic resin cast of the ACoA complex shows the origin of the subcallosal artery (white arrow heads) from the ACoA. The A1 and A2 segments of the anterior cerebral arteries and the bilateral recurrent arteries of Heubner (RAH) are also visible. (C) A coronal microangiogram displays the single, unpaired subcallosal artery (blue arrowhead) arising from the ACoA (yellow arrow) and the bilateral RAH (red arrows). The subcallosal artery predominantly perfuses the medial basal forebrain and periventricular regions, whereas the RAH supplies the more lateral basal forebrain and striatal regions. The cisternal course of the RAH curves alongside the A1 segment of the anterior cerebral artery (white small arrows). Importantly, the superior aspect of the caudate head is typically supplied by lateral striate arteries (LSA) rather than the RAH. The vessels seen overlying the RAH at the upper aspect of the caudate nucleus represent terminal branches of the LSA (white long arrow). The RAH and LSA often show a complementary perfusion pattern, with one predominating when the other is diminutive.

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High-resolution 3D MRI has improved the detection of infarctions in these territories. Subcallosal artery infarction is a principal cause of postoperative amnesia due to disruption of the Papez memory circuit.^[9] When accompanied by RAH infarction, patients may also exhibit slowed processing speed and executive dysfunction, likely reflecting fronto-striatal involvement.^[11]

Here, we present the case of a 63-year-old man who exhibited a paradoxical cognitive profile following surgical clipping of a ruptured ACoA aneurysm. Despite gifted-level intellectual ability, formal neuropsychological testing revealed selective impairments in memory and processing speed. 3D MR imaging performed 10 months postoperatively demonstrated small but anatomically significant infarctions in the subcallosal artery and RAH territory. These findings directly corresponded to the patient’s dissociative cognitive pattern. This report aims to demonstrate the clinical value of combining advanced neuroimaging with detailed neuropsychological assessment to detect functionally important deficits that may be masked by high cognitive reserve. It also provides compelling support for the dual-circuit model of cognitive impairment involving infarctions in both the subcallosal artery and RAH ^[11] as clearly illustrated by this paradoxical case of giftedness and memory decline.

CASE REPORT

A 63-year-old right-handed male, a former computer programmer, underwent surgical clipping of a ruptured ACoA aneurysm. During post-operative follow-up, he reported persistent subjective memory concerns.

High-resolution 3D MR imaging, including 3D T1-weighted and T2-weighted sequences optimized for structural delineation, was obtained approximately 10 months after surgery and analyzed using multiplanar reconstruction techniques. Anatomical segmentation of the basal forebrain followed vascular territories as described in prior literature.^[9] Regions of interest were classified into eight subcallosal artery territories per hemisphere, six RAH territories, and three additional basal forebrain regions. Lesions outside these vascular areas, such as orbitofrontal and temporal tip infarctions, were recorded separately. A comprehensive summary of infarcted and preserved regions has been presented in Table 1.

3D MR imaging revealed a pattern of infarction consistent with the dual-vascular territory model. First, bilateral infarctions were identified in the subcallosal artery territory, involving the FxCo, paraterminal gyrus (PTG), and subcallosal areas. However, infarction was not observed in three distal subcallosal artery territories: The rostral cingulate cortex, genu of the corpus callosum, and anterior cingulate gyrus (CGa), as summarized in Table 1. These regions are located more distally along the subcallosal artery distribution and may have been spared presumably due to collateral flow from the A2 segment of the anterior cerebral artery [Figure 1].^[9] Second, a right-sided infarction was identified within the territory of the RAH, involving the nucleus accumbens (NAc), anteroinferior portion of the anterior limb of the internal capsule (ICa), globus pallidus (Gp), and putamen (Pt). The head of the caudate nucleus (Cd) was preserved by infarction [Table 1 and Figure 2]. An infarct in the right temporal tip was likely attributable to surgical manipulation through the right Sylvian fissure approach. Additional infarctions were observed in the bilateral orbitofrontal cortices, but extended more on the right side. A complete summary of infarct locations and abbreviations has been provided in Table 1.

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Figure 2:

High-resolution MRI of the basal forebrain and infarction sites in subcallosal and Heubner artery territories. A 63-year-old male, a former computer programmer, underwent surgical clipping of a ruptured anterior communicating artery (ACoA) aneurysm. During postoperative follow-up, he reported persistent subjective memory concerns, and high-resolution 3D MR imaging obtained 10 months after surgery revealed small infarctions in the subcallosal artery and recurrent artery of Heubner (RAH) territories. (A and B) Anatomical reference images. Multiplanar reconstructions from a high-resolution 3D T1-weighted image (3D-T1WI) are shown in coronal (A) and axial (B) planes through the paraterminal gyrus (PTG). The most medial basal forebrain, corresponding to the subcallosal artery territory, includes the columns of the fornix (FxCo, black arrow in panel B), paraterminal gyrus (PTG), and the rostrum (CCr) and genu (CCg) of the corpus callosum (panel B). The lateral basal forebrain and striatal structures, supplied by the RAH, include the anteroinferior head of the caudate nucleus (Cd), nucleus accumbens (NAc), putamen (Pt), globus pallidus (Gp), and the anterior limb of the internal capsule (ICa). Unspecified periventricular regions in this plane also include the diagonal band of Broca (DBB) and the bed nucleus of the stria terminalis (BNST, white arrow in panel A). This anatomical mapping illustrates the medial subcallosal artery territory versus the more lateral RAH territory, as seen on high-resolution MR imaging. (C-F) images from the present case. (C) An axial high-resolution T2-weighted image (T2WI) obtained 10 months after surgery shows bilateral subcallosal artery territory infarctions, evidenced by hyperintense signals in the columns of the fornix (FxCo, red arrows) and atrophy of the paraterminal gyri (PTG, blue arrows). (D) A coronal high-resolution T2WI demonstrates an infarction in the right-sided RAH territory, involving the nucleus accumbens (NAc), anteroinferior part of the anterior limb of the internal capsule (ICa), putamen (Pt), and globus pallidus (GP). The head of the caudate nucleus (#) remains unaffected. The asterisk (*) indicates a signal-loss artifact from the surgical clip. Infarction in the lower part of the PTG (blue arrows) is also seen, bilaterally. (E) An axial high-resolution T1WI confirms the bilateral subcallosal artery territory infarction, showing volume loss in the FxCo (red arrows) and PTG (blue arrows). (F) A magnified view of the region outlined in (E). This image reveals that both FxCo (red arrows) have evolved into cavity-like structures secondary to infarction, and the upper part of PTG (blue arrows) appears severely atrophic.

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Approximately 5 years after clipping, a formal neuropsychological evaluation, including the Wechsler Adult Intelligence Scale, third edition, and the Wechsler Memory Scale-Revised,^[12-14] revealed the paradoxical cognitive profile. As shown in Table 2, the results confirmed exceptionally high intellectual functioning, with a Full-Scale IQ of 144 (Very superior/Gifted) and a Verbal IQ of 156 (Very superior/Exceptionally gifted). In stark contrast, the general memory quotient (General MQ) of 115 and the processing speed index (PSI) of 110 fell within the high-average range. Although these memory and processing scores were above average, they were markedly lower than expected given his intellectual potential. The discrepancies between Full-Scale IQ and General MQ (29 points) and between Full-Scale IQ and PSI (34 points) were clinically meaningful. This paradoxical dissociation between gifted intelligence and diminished memory and processing speed aligns with the distribution of infarcts and supports a dual circuit model of cognitive dysfunction. According to this model, subcallosal artery infarction impairs memory through disruption of the Papez circuit, whereas infarction in the RAH contributes to slowed processing through fronto-striatal disconnection.

DISCUSSION

This case provides strong support for our previously proposed dual-circuit model of cognitive impairment as a complication of ACoA aneurysm repair.^[11] Retrospective analysis confirmed that the patient’s paradoxical neuropsychological dissociation was consistent with the anatomical distribution of vascular injuries identified on high-resolution 3D-MR imaging. Bilateral infarctions in the subcallosal artery territory likely disrupted the Papez circuit, leading to memory decline, while an RAH infarction on either side contributed to slowed processing through frontostriatal disconnection.

The most notable feature of this case is the paradoxical dissociation between the patient’s gifted-level intelligence and his selective deficits in memory and processing speed, which might have gone undetected without reference to his elevated intelligence baseline. This dissociation was quantitatively evident in the 29-point gap between his Full-Scale IQ (144) and General MQ (115), and the 34-point gap between his Full-Scale IQ and PSI (110), both exceeding conventional clinical thresholds for significant intra-individual discrepancy.

The bilateral columns of the fornix, revealed as infarcted on high-resolution 3D MR imaging, are core components of the Papez circuit and critical for memory retrieval. Our previous study of ACoA aneurysm patients with postoperative amnesia has consistently shown that injury to these structures is a primary cause of memory impairment.^[9,15] Notably, a prior SPECT study reported that ACoA post-operative amnesia was associated with hypoperfusion in both the subcallosal gyrus in the basal forebrain and the anterior cingulate gyrus (CGa).^[16] In our case, the CGa remained structurally intact, which likely supported the patient’s preservation of high-average memory function, even in the presence of bilateral infarctions affecting the columns of the fornix and basal forebrain.

Infarctions were also observed in regions typically supplied by the RAH, including the anterior limb of the anterior limb of the internal capsule (ICa), nucleus accumbens (NAc), globus pallidus (Gp), and putamen (Pt), while the caudate nucleus was notably spared. In our previous study, unilateral RAH infarction often co-occurred with subcallosal artery infarction and was linked to reduced processing speed, especially when both territories were involved.^[9,11] This pattern, together with the complementary vascular supply from the RAH and lateral striate arteries,^[17] likely supported residual fronto-striatal function and mitigated the severity of the patient’s processing speed deficits.

Regarding the clinical sequelae of these vascular injuries, we fully acknowledge that cognitive deficits, which include memory decline, are well-known complications of ruptured ACoA aneurysms.^[18,19] Cognitive outcomes are often anticipated in cases where large hematomas involving the basal forebrain are evident on computed tomography^[1] or when infarctions in the subcallosal artery or RAH territories are clearly visualized on acute diffusion-weighted MR imaging (DWI).^[9] However, diagnostic difficulty arises when such overt imaging indicators are absent or cannot be obtained in the acute phase, and neuropsychological deficits emerge only in the chronic stage, despite the well-established vulnerability of these perforators to ischemic injury.

Conventionally, the etiology of decline in higher cortical function is usually related to the severity of vasospasm, and management has primarily focused on this critical factor due to its association with high mortality and morbidity.^[20] Indeed, vasospasm frequently leads to ischemia or infarction in the subcallosal artery and RAH territories. Digital subtraction angiography remains the gold standard for assessing vascular patency, and a prior case report by Kannath et al. demonstrated that the subcallosal artery, initially not visualized, reappeared following vasodilator therapy, indicating that localized vasospasm can cause reversible occlusion that may progress to infarction.^[21] This underscores the importance of recognizing vasospasm, rather than surgical manipulation alone, as a potential cause of perforator infarction.^[5]

In the present case, high-resolution 3D MRI obtained in the chronic phase revealed concomitant infarctions in both the subcallosal artery and RAH territories, highlighting the susceptibility of these perforators to selective ischemic injury. Importantly, the patient’s preserved gifted-level general intelligence strongly argues against diffuse cerebral ischemia from severe generalized vasospasm. This suggests that the ischemic event was highly focal, affecting primarily the perforator territories rather than the brain globally. Thus, the clinical relevance lies in the structural consequence: 3D MRI successfully delineated the specific dual-territory infarctions that account for the patient’s paradoxical “gifted yet amnesic” profile. This case illustrates how even small, strategically located infarcts can yield disproportionate cognitive effects, particularly in individuals with high cognitive reserve.

Several limitations of this case report should be noted. First, as a single case, the findings may not be fully generalizable to all ACoA aneurysm patients; however, the discrete vascular pathology provides a clear example of the dual-circuit model. Second, although the structural-functional correlation is strong, other factors, such as the initial impact of subarachnoid hemorrhage or psychological factors, could theoretically contribute to the cognitive profile. Nevertheless, the distinct dissociation in cognitive scores aligned with the anatomical findings offers compelling evidence for the structural basis of the deficits.

CONCLUSION

This case demonstrates that even small, strategically located infarcts in the subcallosal artery and RAH territories can result in paradoxical dissociation in cognitively gifted individuals. High-resolution MRI combined with a detailed neuropsychological assessment is essential for detecting such subtle deficits that might otherwise go unrecognized even in the chronic phase.