Temporal lobe epilepsy is known to present with various cognitive impairments, among which memory deficits are frequently reported by patients. Memory deficits can be classified into two types: classical hippocampal amnesia, which is characterized by abnormalities detected in neuropsychological assessments, and atypical memory deficits, such as accelerated long-term amnesia and autobiographical memory impairment, which cannot be identified using standard testing methods. These deficits are believed to arise from a complex interplay among structural brain abnormalities, interictal epileptic discharges, pharmacological factors, and psychological states. While fundamental treatments are limited, there are opportunities for interventions such as environmental adjustments and rehabilitation. This review article aims to provide a comprehensive overview of the types, underlying pathophysiology, and intervention methods for memory disorders observed in patients with temporal lobe epilepsy.

A workshop of the Special Committee on Measures for Transition from Pediatric to Adult Health Care, the Japanese Society of Neurology was held to discuss various issues and practices involved in healthcare transition. The following points were addressed: (1) the history of, and issues involved in, promoting support for patients requiring medical care, (2) cooperation between pediatric medical centers and university hospitals, (3) collaboration between pediatrics and neurology in medical and rehabilitation facilities, and (4) a questionnaire survey of members of the Japanese Society of Neurology. The reasons for extreme difficulties in pediatric-adult healthcare transition for patients with neurological diseases, especially those who require continuous intensive medical care over a long period of time, include the difference in the operating systems of pediatric and adult departments, in addition to the difference in the diseases treated during childhood and adulthood. For holistic transition support, it is necessary to strengthen cooperation not only among medical professionals, but also among multiple professions, as well as between local communities and government.

Migraine is a disease that is difficult to be recognized by those around the patients, even though it causes significant hindrances. In this study, we conducted an exploratory comparison of the perceptions on migraine among patients, family members living with them, and physicians treating migraine patients. Patients and family members shared a common understanding on the pain of migraine, and hoped to spend more/better time together as a family. However, although family members felt compassion for the patients, lack of understanding by and patients’ concern for the surroundings led to feelings of resignation and endurance on the side of patients. Regarding physicians’ medical care, our results suggested the importance to understand the wishes and obstacles of each patient and to propose treatment accordingly. In order to reduce the burden of migraine, it is necessary to create an environment and raise awareness that allows people around the patients to understand and support the pain and hopes that each patient feels.

A 21-year-old man who was diagnosed with Ollier disease at the age of 1 year developed incidental multiple gliomas at the age of 15 years. Subsequently, the multiple gliomas enlarged and the patient underwent three surgical removals. Genetic analysis revealed the IDH1 p.R132C mutation in the gliomas, and histopathology showed malignant transformation. Despite multimodality treatment, the gliomas could not be controlled, and the patient died at the age of 23 years. Ollier disease is a rare disease with IDH1/2 mutations and is often associated with gliomas. However, there are very few reports on genetic analysis of IDH1/2 mutations and long-term follow-up in Ollier disease-related gliomas. Genetic analysis of IDH mutations may contribute to the elucidation of its pathogenesis. The cross-departmental collaboration is required for long-term follow-up of Ollier disease-related gliomas.

A 44-year-old woman with autism spectrum disorder developed bulbar symptoms and generalized muscle weakness 7 months before referral. Six months before, she was administered glucocorticoid for liver involvement. During the course, while she presented alopecia, skin ulcers, and poikiloderma, hyperCKemia was observed only twice. Due to complications including cardiac involvement and hearing loss as well, we suspected mitochondrial disease and performed a muscle biopsy. The muscle pathology showed sarcoplasmic myxovirus resistance A (MxA) expression with scattered pattern. Since anti-melanoma differentiation-associated gene 5 (MDA5) antibody was detected, we diagnosed the patient with anti-MDA5 antibody-positive dermatomyositis (DM). We reinforced immunosuppressive therapy, and her clinical symptoms and liver involvement were improved. When we diagnose a case of anti-MDA5 antibody-positive DM who is difficult to make clinical diagnosis, it may be valuable to evaluate sarcoplasmic MxA expression on muscle pathology.

An 82-year-old woman developed a droopy right eyelid with ipsilateral hemiparesis. Her ocular symptom was caused by weakness of the right frontalis, which is usually seen in patients with peripheral facial nerve palsy. However, head MRI showed acute cerebral infarction of the left lenticulostriate artery, and electroneurography did not detect damage to the right facial nerve. To explain the pathophysiology in this patient, asymmetrical bilateral cortex innervation to the right upper face was hypothesized. This case suggested that patients with some hemispheric strokes could develop upper facial weakness mimicking facial nerve palsy, and clinicians should pay attention to this potential pitfall in the differential diagnosis of facial nerve palsy.

A 43-year-old man was admitted to our department due to fever and headache. The cerebrospinal fluid analysis confirmed bacterial meningitis. Campylobacter species were isolated from blood cultures on the third day of admission. The patient was treated with meropenem (MEPM) and discharged on the 17th day. However, he experienced a recurrence of meningitis and was readmitted on the 68th day, initiating MEPM therapy. Campylobacter fetus was isolated from cerebrospinal fluid cultures on the 74th day. MEPM was continued until the 81st day, followed by one month of minocycline (MINO) therapy. The patient had an uneventful recovery without further recurrence. This case highlights the potential for recurrence of Campylobacter fetus meningitis approximately two months after the resolution of the initial infection. In addition to carbapenem therapy for at least two weeks, the adjunctive administration of MINO may be beneficial.