Isolated bilateral fornix anterior columns infarction with acute amnesia and fiber tracts damage, a case report.

Isolated fornix anterior column infarction has rarely been described and is difficult to assess accurately using conventional magnetic resonance imaging (MRI). We report the case of a 75-year-old female who experienced acute anterograde amnesia. MRI performed within 24 h after amnesia onset showed an isolated infarction of the bilateral anterior columns of the fornix on diffusion-weighted imaging (DWI). Her symptoms persisted for up to 50 days, and diffusion tensor imaging (DTI) showed disruption of the fiber tracts of the fornix. when acute amnesia syndrome onset, fornix anterior column infarction should be considered, and optimized DWI and DTI methods are needed to study the fornix in vivo in future research.

A Teenager With Acute Anterograde Amnesia.

Isolated amnesia is an uncommon presenting complaint in the pediatric age group. We report the case of an 18-year-old woman who presented with the acute onset of memory difficulty and an otherwise normal neurologic examination. Brain magnetic resonance imaging demonstrated inflammation in the bilateral temporal lobes. Serum and cerebrospinal fluid testing ultimately revealed a diagnosis of autoimmune encephalitis. Although rare, the acute onset of isolated amnesia deserves a prompt, comprehensive evaluation.

Pure topographical disorientation in novel environments without anterograde amnesia: a case study.

Topographical disorientation (TD) in novel environments is considered to be a part of anterograde amnesia. A 56-year-old woman presented with pure TD only in novel environments following limbic encephalitis. She could not remember directions inside the hospital on weekly outpatient visits; however, her verbal and visual anterograde memories were normal. In the test of learning photographs of scenes, faces, and objects, only her scores for landscapes were worse than those in healthy controls. These findings suggested that her TD specific to landscapes and directions in novel environments was caused by category-specific memory impairment related to bilateral hippocampal and parahippocampal dysfunction.

Persistent anterograde amnesia due to the artery of Percheron occlusion: a case report.

Bilateral thalamic infarction involving the artery of Percheron (AOP) can cause diagnostic difficulties due to the varying clinical presentations. AOP infarcts presented with isolated memory impairment are not common and the factors affecting the persistence of memory disorders are still unknown. A 41-year-old male patient was hospitalized with acute unconsciousness. MRI disclosed bilateral paramedian thalamic infarction The patient had isolated memory deficit and his anterograde amnesia continued without any change in the past decade. More cases might answer the questions concerning the intra- and extra-thalamic structures responsible for the amnesic syndrome and the factors affecting the persistence of the symptoms.

Human herpes virus-6 encephalitis causing severe anterograde amnesia associated with rituximab, azathioprine and prednisolone combination therapy for dermatomyositis.

Human herpes virus-6 (HHV-6) reactivation is a well-recognised complication following haematological stem cell transplantation, but it is novel in the context of combination immunomodulatory therapy for autoimmune disease. We report a case of severe anterograde amnesia caused by HHV-6 encephalitis in a young female patient on rituximab, azathioprine and prednisolone for dermatomyositis (DM). The use of targeted biologic treatments for systemic autoimmune connective tissue diseases (CTDs) is increasing, particularly when refractory to conventional management. The anti-CD20 B cell depleting monoclonal antibody, rituximab is now increasingly used, often in combination with conventional immunomodulatory treatments, in certain autoimmune neurological conditions and systemic CTDs including DM. Physicians should be aware of the possibility of HHV-6 in those who develop encephalitis while CD20 B cell deplete, especially in the presence of additional immunomodulatory therapies. Prompt diagnosis and treatment of HHV-6 encephalitis with evidence-based anti-viral therapy may help reduce the extent of irreversible morbidity such as amnesia.

Profound anterograde amnesia following routine anesthetic and dental procedure: a new classification of amnesia characterized by intermediate-to-late-stage consolidation failure?

Anterograde amnesia caused by bilateral hippocampal or diencephalon damage manifests in characteristic symptoms of preserved intellect and implicit learning, and short span of awareness with complete and rapid forgetting of episodic material. A new case, WO, 38-year-old male with anterograde amnesia, in the absence of structural brain changes or psychological explanation is presented, along with four comparison cases from the extant literature that share commonalities between them including preserved intellect, span of awareness greater than working memory, and complete forgetting within hours or days following successful learning, including notably for both explicit and implicit material. WO's amnesia onset coincided with anesthetic injection and root canal procedure, with extended vasovagal-like incident. The commonalities between the five cases presented may suggest a shared biological mechanism involving the breakdown of intermediate-to-late-stage consolidation that does not depend on the structural integrity of the hippocampi. Speculation on the mechanism of consolidation breakdown and diagnostic implications are discussed.

Autobiographical age awareness disturbance syndrome in autoimmune limbic encephalitis: two case reports.

BACKGROUND: Autobiographical memory is a form of episodic memory characterized by a sense of time and consciousness that enables an individual to subjectively re-experience his or her past. As part of this mental re-enactment, the past is recognized relative to the present. Dysfunction of this memory system may lead to confusion regarding the present perception of time. CASE PRESENTATION: Two Japanese women (42 and 55 years old) temporarily believed they were living in their past during a course of autoimmune limbic encephalitis. Their autobiographical memories and behaviour reflected their self-estimated age, and they could not recall memories experienced beyond that age. More surprisingly, their subjective age estimations and autobiographical memories were transiently corrected when they were made aware of their true age. Disorientation, anterograde amnesia, and retrograde amnesia were common additional symptoms. Neuroimaging suggested disturbances in medial temporal and orbitofrontal brain regions in both cases. CONCLUSIONS: This syndrome is characterized by three elements: 1) failure to subjectively recognize the present; 2) inability to suppress irrelevant past memories; and 3) transient restitution of awareness of the present through realization of the individual's true age. We defined this syndrome as 'autobiographical age awareness disturbance', and focused our investigation on the role of age self-awareness. If recall of relevant and suppression of irrelevant past memories are both necessary to subjectively recognize the present relative to the past, dysfunction of medial temporal and orbitofrontal brain regions is predicted to lead to abnormal subjective placement in time. However, the subjective experience of age tends to be an important informational component for retrieving remote autobiographical memories. This suggests that correct age awareness is essential for the proper recognition of the remote past in relation to the present. This is the first report to focus on the relationship between subjective temporal orientation and age self-awareness. While the role of age awareness in this process is still unclear, investigating autobiographical age awareness disturbance as a part of subjective temporal awareness dysfunction can be useful in understanding the processes underlying human time recognition.

Memory impairment following right cerebellar infarction: a case study.

We reported a patient with a right cerebellar infarction who showed anterograde amnesia. Cognitive dysfunction caused by cerebellar lesions was called cerebellar cognitive affective syndrome, and deactivation of the contralateral prefrontal cortex function due to disconnections of cerebello-cerebral fiber tracts have been hypothesized as mechanism underlying the syndrome. The episodic memory impairment, however, could not be supported by the same mechanism because the prefrontal lesions cannot cause amnesia syndrome. The feature of the impairment of our patient was similar to that of diencephalic amnesia, and a single photon emission computed tomography study showed a relative hypoperfusion in the right cerebellar hemisphere and left anterior thalamus. We considered that the memory deficit was caused by the dysfunction of the thalamus, which is a relay center of the cerebello-cerebral connectivity network.

Impaired picture recognition in transient epileptic amnesia.

Transient epileptic amnesia (TEA) is an epileptic syndrome characterized by recurrent, brief episodes of amnesia. Transient epileptic amnesia is often associated with the rapid decline in recall of new information over hours to days (accelerated long-term forgetting - 'ALF'). It remains unknown how recognition memory is affected in TEA over time. Here, we report a systematic study of picture recognition in patients with TEA over the course of one week. Sixteen patients with TEA and 16 matched controls were presented with 300 photos of everyday life scenes. Yes/no picture recognition was tested 5min, 2.5h, 7.5h, 24h, and 1week after picture presentation using a subset of target pictures as well as similar and different foils. Picture recognition was impaired in the patient group at all test times, including the 5-minute test, but it declined normally over the course of 1week. This impairment was associated predominantly with an increased false alarm rate, especially for similar foils. High performance on a control test indicates that this impairment was not associated with perceptual or discrimination deficits. Our findings suggest that, at least in some TEA patients with ALF in verbal recall, picture recognition does not decline more rapidly than in controls over 1week. However, our findings of an early picture recognition deficit suggest that new visual memories are impoverished after minutes in TEA. This could be the result of deficient encoding or impaired early consolidation. The early picture recognition deficit observed could reflect either the early stages of the process that leads to ALF or a separable deficit of anterograde memory in TEA. Lastly, our study suggests that at least some patients with TEA are prone to falsely recognizing new everyday visual information that they have not in fact seen previously. This deficit, alongside their ALF in free recall, likely affects everyday memory performance.

A sinister cause of anterograde amnesia: painless aortic dissection.

Aortic dissection is a frequently devastating diagnosis classically associated with severe chest pain.We present a case of painless aortic dissection with anterograde amnesia. An 84-year-old man was brought to the emergency department by ambulance, when his wife noted that he developed acute onset complete loss of short-term memory. Medical history was notable for a 4.5-cm fusiform thoracic aortic root aneurysm. On arrival,he denied pain or syncope.On examination, he was mildly hypotensive(110/59 mm Hg); and there were no murmurs, pulse deficits, or focal neurologic deficits. During his stay, he developed left flank pain. Chest radiography demonstrated subtle mediastinal widening and obscuration of the aortic knob compared with previous films. Computed tomography revealed an extensive intimal flap consistent with an aortic dissection involving the sinus of Valsalva and left renal artery. The patient subsequently developed acute onset chest pain after which he became unresponsive. Echocardiography demonstrated tamponade physiology.The family decided to transition to comfort care measures, and the patient died soon after.We identified 7 other cases in the literature of aortic dissection cases with presentations consistent with transient global amnesia,5 of which without neurologic deficits and 3 of which without pain. This case highlights the imperative of a thorough history and high index of suspicion for this catastrophic diagnosis in patients with transient global amnesia who otherwise might be expected to have an excellent prognosis and little need for diagnostic work-up.

Neuropsychiatric Manifestations of Colloid Cysts: a review of the literature.

Colloid cysts account for approximately 2% of primary brain tumours and the majority of cases are identified in the fourth and fifth decade. They are small, gelatinous neoplasms lined by a single layer of mucin-secreting columnar epithelium that are thought to arise from errors in folding of the primitive neuroepithelium. They develop in the rostral aspect of the third ventricle in the foramen of Monro in 99% of cases and despite their benign histology carry a poor prognosis, with a mortality greater than 10% in symptomatic cases. The location of colloid cysts within the ventricular system results in obstruction of the foramen of Monro as the cyst grows, disrupting the circulation of cerebrospinal fluid (CSF) and causing hydrocephalus. This is the mechanism behind the most common presenting symptoms of postural headache, nausea and vomiting - a clinical picture synonymous with hydrocephalus and intracranial pathology. In addition to these classical neurological symptoms, there is a high prevalence of psychiatric symptoms in the patient population, with symptoms ranging from anterograde amnesia to gustatory hallucination. These symptoms can occur with or without the presence of hydrocephalus, and are thought to be secondary to compression of connecting pathways between the mesocortices and subcortical limbic regions. These symptoms have been shown to be comparative in frequency to the classical symptoms, yet are rarely the reason for referral to a neurological or neurosurgical service for investigation.

Retrosplenial amnesia without topographic disorientation caused by a lesion in the nondominant hemisphere.

We report the case of a 68-year-old right-handed man who was admitted to our hospital because of sudden onset of headache. On admission, he presented with left homonymous hemianopsia, disorientation, and recent memory disturbance; however, he had normal remote memory and digit span. He was able to recall the room layout of his house and describe the route from the nearest station to his home on a map. However, at the hospital, he sometimes lost his way because of amnesia. Computed tomography (CT) and magnetic resonance imaging revealed a subcortical hematoma in the right occipital forceps and the parietal lobe, involving the cingulate isthmus. Single-photon emission CT imaging showed reduced perfusion not only in the retrosplenial region but also in the right thalamus. These findings suggested that the retrosplenial amnesia might have been caused by the interruption of hippocampal input into the anterior thalamus.

Pure amnestic seizure: A clinico-intracranial EEG study.

OBJECTIVE: Enduring anterograde amnesia is caused by lesions in bilateral mesial temporal lobes. However, whether transient dysfunction of bilateral mesial temporal regions induces reversible amnesia has not been proven. We investigated this association in patients with epilepsy and analyzed the electroclinical correlation during pure amnestic seizures (PAS). PAS are defined as seizures with anterograde amnesia as the only ictal manifestation, accompanied by preserved responsiveness and other cognitive functions. METHODS: We retrospectively searched our intracranial EEG database to find PAS. Pure ictal amnesia was confirmed by immediate and comprehensive ictal examinations. RESULTS: Among 401 patients who underwent intracranial EEG recording, three patients with temporal lobe epilepsy (TLE) manifesting PAS were identified. The patients talked and behaved normally during seizure but did not remember the episodes afterwards. Ictal discharges were confined to bilateral mesial temporal regions, with no or mild involvement of surrounding structures. Spread of low-voltage fast activities to bilateral mesial temporal regions corresponded to onset of ictal anterograde amnesia. Two patients underwent unilateral mesial temporal resection and became seizure-free with improvement in cognitive functions. SIGNIFICANCE: PAS is a rare ictal semiology in TLE. Bilateral mesial temporal regions that play a critical role in memory encoding are presumably the symptomatogenic zones for PAS.

Hypoxia/reoxygenation impairs memory formation via adenosine-dependent activation of caspase 1.

After hypoxia, a critical adverse outcome is the inability to create new memories. How anterograde amnesia develops or resolves remains elusive, but a link to brain-based IL-1 is suggested due to the vital role of IL-1 in both learning and brain injury. We examined memory formation in mice exposed to acute hypoxia. After reoxygenation, memory recall recovered faster than memory formation, impacting novel object recognition and cued fear conditioning but not spatially cued Y-maze performance. The ability of mice to form new memories after hypoxia/reoxygenation was accelerated in IL-1 receptor 1 knockout (IL-1R1 KO) mice, in mice receiving IL-1 receptor antagonist (IL-1RA), and in mice given the caspase 1 inhibitor Ac-YVAD-CMK. Mechanistically, hypoxia/reoxygenation more than doubled caspase 1 activity in the brain, which was localized to the amygdala compared to the hippocampus. This reoxygenation-dependent activation of caspase 1 was prevented by broad-spectrum adenosine receptor (AR) antagonism with caffeine and by targeted A1/A2A AR antagonism with 8-cyclopentyl-1,3-dipropylxanthine plus 3,7-dimethyl-1-propargylxanthine. Additionally, perfusion of adenosine activated caspase 1 in the brain, while caffeine blocked this action by adenosine. Finally, resolution of anterograde amnesia was improved by both caffeine and by targeted A1/A2A AR antagonism. These findings indicate that amygdala-based anterograde amnesia after hypoxia/reoxygenation is sustained by IL-1ß generated through adenosine-dependent activation of caspase 1 after reoxygenation.

Episodic memory in frontotemporal dementia: a critical review.

This review offers a critical appraisal of the literature on episodic memory performance in frontotemporal dementia. Historically, description of patients diagnosed with what was then known as Pick's disease included the presence of memory deficits and an underlying amnestic syndrome was noted in some of these patients. Over the last 20 years, however, the clinical view has been that episodic memory processing is relatively intact in the frontotemporal dementia syndrome. In particular, patients with the subtypes of behavioural variant frontotemporal dementia and progressive non-fluent aphasia are reported to perform within normal limits on standard memory tests. In the third clinical presentation of frontotemporal dementia, semantic dementia, relatively intact episodic memory against a significantly impaired semantic memory was regarded as the hallmark. This position was instrumental in the development of clinical diagnostic criteria for frontotemporal dementia in which amnesia was explicitly listed as an exclusion criterion for the disease. The relative intactness of episodic memory, therefore, appeared to be a useful diagnostic marker to distinguish early frontotemporal dementia from Alzheimer's disease, in which early episodic memory disturbance remains the most common clinical feature. We argue that recent evidence questions the validity of preserved episodic memory in frontotemporal dementia, particularly in behavioural variant frontotemporal dementia. In semantic dementia, a complex picture emerges with preservation of some components of episodic memory, notably recognition-based visual memory and recall of recent autobiographical events. We propose a critical synthesis of recent neuropsychological evidence on retrograde and anterograde memory in light of neuroimaging and neuropathological findings, demonstrating involvement of medial temporal structures in frontotemporal dementia, structures known to be critical for episodic memory processing. We further argue that the multifactorial nature of most memory tests commonly used clinically fail to capture the memory deficits in frontotemporal dementia and that sensitive assessment tools of memory are needed. Together, recent clinical and experimental findings and the historical evidence represent a strong case for a re-evaluation of the importance of memory disturbance in the clinical diagnosis of frontotemporal dementia.

A double-blind, placebo-controlled study of the impact of galantamine on anterograde memory impairment during electroconvulsive therapy.

BACKGROUND: Electroconvulsive therapy (ECT) continues to be an effective treatment option for patients who fail to respond to pharmacological interventions, are unable to tolerate medications, and show a suboptimal response to behavioral and psychotherapeutic treatments. However, risks for cognitive impairment may contribute to some patients' refusal of ECT. METHODS: The present study examined galantamine as a pharmacological intervention to reduce cognitive adverse effects from ECT. Thirty-nine inpatients diagnosed with major depressive disorder; bipolar disorder, depressed type; or schizoaffective disorder, depressed type and admitted for ECT were randomized to galantamine or placebo. Study drugs were initiated 24 to 48 hours before starting ECT and continued throughout the course of ECT. A neuropsychological test battery was administered at baseline and 24 to 48 hours after completing a course of ECT treatments. Depression severity was monitored using the 17-item Hamilton Rating Scale for Depression and Clinical Global Impression Scale at baseline, weekly, and end point. Self-rated adverse effects were monitored weekly. RESULTS: Thirty participants (12 patients in the galantamine group, 18 patients in the placebo group) had both pretreatment and posttreatment neuropsychological ratings. Those in the galantamine group scored significantly higher at discharge for delayed memory (t28 = 2.44, P < 0.05). Hierarchical regressions examined if treatment condition predicted changes in delayed memory scores from baseline to discharge. Inclusion of the treatment condition in the final model made a significant incremental improvement in prediction (ΔR = 0.12, F1,27 change = 4.65, P < 0.05; ß = 0.37, t = 2.16, P < 0.05). Galantamine was well tolerated with no clinically significant bradycardia or prolonged paralysis when administered with ECT. CONCLUSIONS: Galantamine may be protective against impairment in retention of new learning. Galantamine exhibited minimal adverse effects and was safe when administered during ECT. The present findings require replication by future researchers using larger samples before broad conclusions can be drawn.