Memory impairment caused by cerebral hematoma in the left medial temporal lobe due to ruptured posterior cerebral artery aneurysm

Cognitive disorders, such as memory disturbances, are often observed following a subarachnoid hemorrhage. Basal forebrain amnesia due to aneurysm rupture of the anterior communicating artery was reported more than 50 years ago [1, 2]. Anatomically, the basal forebrain is a region consisting of the external and internal septal nuclei, the basal nucleus of Mynert, and the diagonal band of Broca. It is believed that cholinergic neurons that regulate cerebral blood flow by projecting to the cerebral cortex, hippocampus, and amygdala are present in this structure. It has also been reported that damage to the lower branch of the corpus callosum, which is a penetrating branch from the anterior communicating artery, may cause amnestic syndrome with spontaneous confabulation or impaired attention [3‐6]. Moreover, memory disturbances are seen after surgery on cerebral aneurysm of the basilar tip. It is believed that the primary cause of this is damage to the hippocampus, hippocampal gyrus, amygdala, fornix, etc., which form the perfusion region of the posterior cerebral artery. This damage may result in a circulatory disorder, or occlusion of the paramedian thalamic artery and thalamogeniculate artery bifurcating from the posterior cerebral artery that sends blood to the diencephalon, or occlusion of the polar artery bifurcating from the posterior communicating artery [7‐9]. Aneurysm rupture of the middle cerebral artery, in cases where a hematoma is formed in the cerebral parenchyma, can result in persistent neurological symptoms such as motor paralysis. However, there are hardly any reports of only memory disturbance. Here, we report a case of amnestic syndrome and formation of a hematoma inside the left temporal lobe due to a dissecting aneurysm rupture of the distal portion of posterior cerebral artery.

A 56-year-old, right-handed man, with a formal education history of 16 years and company employees (office work in an insurance company) was admitted to our hospital because of a consciousness disturbance on 3^rd January, 2011. He did not have any history of medication. On that day, he lost consciousness immediately after going to the toilet and his family requested emergency treatment. Subarachnoid hemorrhage due to an aneurysm rupture of the left posterior cerebral artery was diagnosed, and coil embolization was performed on the same day. After interventional surgery, the case was referred to our department for rehabilitation.

Amnestic syndromes are conditions in which memory functions are disproportionately impaired compared to other cognitive functions in otherwise alert patients [8, 9]. In the 1950s, research conducted on memory impairment due to hippocampal lesions was mainly after resection in patients with serious mental disorders or temporary lobe epilepsy. Scoville et al. [10] studied memory impairment after resection of the mesial temporal lobe, and reported that memory impairment is found only when there is invasion on both sides of the hippocampus. Moreover, Penfield [11] suggested that occurrence of memory disturbances on one side is due to a cryptic lesion on the opposite side, and he emphasized that lesions on either side can cause memory impairment. Thereafter, it was reported that relatively mild memory disturbances may be observed due to unilateral lesion, and that mainly verbal memory is impaired due to a left-sided lesion, while non-verbal memory is impaired due to a right-sided lesion; however, temporary memory loss is seen in most cases of unilateral lesion [12, 13]. In recent years, cases of not only verbal memory impairment, but also visual memory impairment and prolonged amnesia due to unilateral lesion have also been reported. In the present case of unilateral lesion of the left side, verbal memory, as well as non-verbal memory, was impaired [14]. This supports the hypothesis that there may be individual variation in verbal and non-verbal lateralization related to memory.

With regard to neural circuits related to memory, the Papez circuit that consists of the hippocampus, a group of anterior thalamic nuclei, the medial nucleus of the mammillary body, and the hippocampal gyrus, and the Yakovlev circuit that consists of the amygdala, medial nucleus of thalamus, and interior surface of the frontal cortex have been implicated. Although these circuits are independent, they have a strong mutual relationship [15]. The damage limited to bilateral hippocampus causes anterograde amnesia, but it does not necessarily cause retrograde amnesia [16]. Severe retrograde amnesia was caused by damage to both of parahippocampal gyri with hippocampus. A widely distributed network of regions underlies the retrieval of past memories, and that the extent of lateral temporal damage appears to be critical to the emergence of severe remote memory impairment was discussed [17]. Since retrograde amnesia was mild and remote memory was maintained, we supposed that the pathological lesion of our case was limited to the unilateral hippocampus and parahippocampal gyri.

In stroke patients, cerebral infarction is the most frequent cause of memory impairment [7, 9, 14], and in many cases it occurs as the result of a thalamic or hippocampal lesion. Moreover, with regard to the site of cerebral hemorrhage, pathology of the caudate nucleus, the anterior region of the thalamus, or the anterior part of the splenium of the corpus callosum, have also been reported. On the other hand, memory impairment due to subarachnoid hemorrhage may be caused by several factors such as diffuse brain damage due to the subarachnoid hemorrhage itself, intracerebral hematoma, an invasive surgical procedure, or the effect of cerebral vasospasm and hydrocephalus.

As postoperative complications following cerebral aneurysm of the posterior circulation system, damage to the hippocampus, hippocampal gyrus, amygdala, fornix, etc., which forms the perfusion region of the posterior cerebral artery, causes circulatory disorder due to occlusion of the initial portion. Additionally, the paramedian thalamic artery from the posterior cerebral artery P1 section, the thalamogeniculate artery from the P2 section, or the polar artery from the posterior communicating artery sends blood to the diencephalon after branching, and particularly when approached infratemporally, there is risk that penetrating branches or the posterior cerebral artery will be obstructed [18, 19]. In the present case, coil embolization was performed. However occlusion of the posterior cerebral artery or cerebral embolism of its penetrating branches was not found in the postoperative MRI. Moreover, during the treatment course, symptomatic cerebral vasospasm or hydrocephalus was not observed, and overall cognitive function such as immediate recall and intelligence remained consistent. In addition, in SPECT images, diffuse brain damage was not observed, and functional lesions were restricted to the left medial temporal lobe where the hematoma was present. Rather than storage of memory or memory retrieval, the hippocampus is an important site for encoding the memory, and it is involved in fixation of the memory in a specific time in the past [20]. Therefore, when the hippocampus is damaged, retrograde amnesia is not so severe (in most of the cases it is restricted to a few years before the onset of symptoms), and remote memory remains intact. Accordingly, in the present case, retrograde amnesia was restricted to a few weeks before the onset of symptoms, and remote memory was intact. Moreover, spontaneous confabulation or attention disorders, often seen in basal forebrain amnesia [6], were absent.

This was a very rare case where rupture of a posterior cerebral artery aneurysm caused restricted damage to the hippocampus unilaterally, and caused memory disturbances. We believe that this is an important case for confirming the role of the hippocampus in memory.