We herein report a case of subarachnoid hemorrhage caused by the rupture of a cerebral aneurysm that was treated by clipping surgery. The patient was a right-handed woman in her 40s who presented with attention disorder and transient Gerstmann syndrome, including left-right disorientation, finger agnosia, acalculia, and agraphia, associated with brain retraction injury in the left inferior frontal gyrus and perforating branch infarction of the horizontal segment of the left anterior cerebral artery. Diffusion tensor tractography was performed to investigate the underlying pathophysiological mechanism of transient Gerstmann syndrome. White matter fibers connecting the frontal lobe to the other lobes such as the left superior longitudinal fasciculus/arcuate fasciculus (SLF/AF), inferior fronto-occipital fasciculus (IFOF), and uncinate fasciculus were compressed by vasogenic and cytotoxic edema without evidence of disconnection. The left thalamic-prefrontal peduncle (TPP), connecting the thalamus and inferior frontal gyrus, was not visualized, whereas left parietal angular-to-supramarginal U-fibers were preserved. These findings suggested that connectional diaschisis involving SLF/AF and IFOF, together with TPP damage, contributed to the development of transient Gerstmann syndrome. Early clinical improvement was expected due to the preservation of multiple association fibers from the frontal lobe to the other lobes without definite disconnection. (Received February 20, 2026; Accepted June 30, 2026; Published October 1, 2026).

Mice use ultrasonic vocalizations beyond the range of human hearing to achieve social communication. This review summarizes the behavioral features of mouse ultrasonic vocalizations, including pup calls, male courtship vocalizations, and vocalizations emitted during female-female and male-male interactions. It also compares mouse vocalizations with rat ultrasonic calls and bird songs. Finally, this review discusses male courtship vocalizations as an index of sexual motivation and emotional expression, and outlines their neuroendocrine regulation through sex hormones and neural circuits centered on the medial preoptic area.

Transthyretin (TTR) amyloidosis, particularly the wild-type form (ATTRwt), is an age-related systemic disease characterized by the deposition of misfolded TTR in tendons and ligaments. Patients therefore frequently present initially to orthopaedic or hand surgeons with carpal tunnel syndrome (CTS) or lumbar spinal stenosis (LSS) rather than to cardiologists or neurologists. These musculoskeletal manifestations may precede ATTR cardiomyopathy (ATTR-CM) by several years to more than a decade, serving as "red flags" that provide an opportunity for early diagnosis, particularly now that disease-modifying therapies (the TTR stabilizers tafamidis and acoramidis and the silencer vutrisiran) are available and are most effective when initiated early. Amyloid is detectable in the flexor tenosynovium or transverse carpal ligament in approximately 10% of unselected patients with CTS and up to approximately 30% of routinely biopsied patients with CTS, and in the ligamentum flavum in approximately half of patients undergoing surgery for LSS, predominantly as ATTRwt. This review summarizes, from the perspective of orthopaedic-neurology collaboration, when to suspect amyloidosis in patients with CTS and LSS and how to proceed with the diagnostic work-up, including intraoperative tissue biopsy with Congo red staining and typing, mandatory exclusion of AL amyloidosis, bone scintigraphy using non-biopsy diagnostic criteria, and TTR genotyping with genetic counseling. The review incorporates recent evidence and our institutional experience.

Surgical indications for lumbar spine disorders should not be determined solely based on degenerative or stenotic magnetic resonance imaging findings. This article discusses how orthopedic spine surgeons evaluate lumbar pathology in collaboration with neurologists. The central issue is whether the patient's symptoms, neurological findings, and imaging abnormalities can be used to identify the responsible lesion that is likely to improve after surgery. Differential diagnoses, including cervical or thoracic myelopathy, peripheral neuropathy, motor neuron disease, vascular claudication, hip disease, tumors, and infection, must be considered, particularly in older patients with multiple coexisting disorders. The article also outlines orthopedic perspectives that influence surgical decision-making, including spinal instability, sagittal and coronal alignment, bone quality, frailty, sarcopenia, walking ability, and postoperative activities of daily living. The choice between decompression alone and decompression with fusion was reviewed together with perioperative management, rehabilitation, patient explanation, and shared decision-making. Complementary collaboration between orthopedic surgeons and neurologists may help clarify the responsible lesion, optimize referral timing, and avoid undertreatment and overtreatment.

Lower-limb numbness, pain, and weakness are common clinical complaints that require differentiation between cauda equina or radicular lesions associated with lumbar spinal disease and peripheral nerve disorders. Because degenerative findings on lumbar imaging are common, particularly among older adults, the responsible lesion should not be determined based on imaging findings alone. In this context, neurological examination contributes to anatomical localization and is central to the differential diagnosis. Particular emphasis is placed on interpreting muscle weakness and sensory disturbance according to myotomal, dermatomal, and peripheral nerve distributions. Other neurological findings, including gait disturbance, neurogenic claudication, bladder or bowel dysfunction, nerve stretch signs, and reflex changes, also provide important clues for localization. This review further addresses common diagnostic challenges encountered in daily practice, including differentiation of L5 radiculopathy from fibular neuropathy in patients with foot drop, distinction between cauda equina lesions and polyneuropathy, recognition of immune-mediated polyradiculoneuropathies, and identification of amyotrophic lateral sclerosis when it mimics lumbar spinal disease. Ancillary tests such as nerve conduction studies, needle electromyography, somatosensory evoked potentials, nerve ultrasound, and imaging should be interpreted in relation to the lesion localization suggested by neurological examination.

In patients presenting with numbness, sensory disturbances, or motor deficits in the upper extremities, it is important to differentiate between cervical spinal cord or nerve root disorders and peripheral neuropathies. This article discusses the key points for distinguishing C8 spinal cord segment and nerve root disorders from peripheral neuropathies, particularly ulnar neuropathy and posterior interosseous nerve palsy. A comprehensive evaluation of the patterns of muscle weakness, distribution of sensory disturbances, and electrophysiological findings is essential, with careful consideration also given to the coexistence of cervical spine lesions and peripheral neuropathies. Furthermore, when the preoperative diagnosis does not correspond with the postoperative course, inflammatory or neoplastic diseases of the spinal nerves and other conditions should also be considered in the differential diagnosis, and collaboration with a neurologist is recommended.

Accurate lesion localization is a fundamental component of neurological diagnosis. This review describes how neurological examination can be used to differentiate cervical spinal cord lesions, cervical radiculopathy, brachial plexopathy, and peripheral nerve disorders in patients presenting with upper-limb sensory and motor symptoms. Particular attention is given to the distribution of sensory impairment, tendon reflex abnormalities, and patterns of muscle weakness. The characteristic clinical features of cervical spondylotic myelopathy, cervical radiculopathy, brachial plexus disorders, and entrapment neuropathies are summarized, together with practical considerations for anatomical localization. Common clinical scenarios, including wrist drop, finger drop, dorsal interosseous muscle atrophy, and radial or ulnar-sided hand numbness, are discussed to illustrate the diagnostic approach. Neurological examination remains essential for lesion localization and should be integrated with electrophysiological and imaging studies to achieve an accurate diagnosis.

Orthopedic surgeons and neurologists manage many of the same clinical manifestations, including sensory disturbances and muscle weakness in the upper and lower limbs, and gait impairment, and both emphasize anatomical diagnosis. However, their respective diagnostic processes differ. Orthopedic surgeons identify the responsible anatomical structures and interpret symptoms based on physical examination maneuvers and imaging findings. In contrast, neurologists map neurological findings onto neural pathways, proceeding from localization of the lesion to characterization of the clinical pattern and underlying etiology. In this article, the similarities and differences between the diagnostic reasoning processes used in these two specialties are reviewed, the clinical situations in which their diagnoses may diverge are discussed, and key considerations for mutual referral are outlined. Ongoing efforts to quantify assessment of muscle strength, as a common clinical language in orthopedic surgery and neurology, are described.

Case report A 31-year-old previously healthy man who had sex with men presented with a two-day history of acute-onset dizziness, nausea, and vomiting. On admission, he was afebrile with generalized lymphadenopathy and a truncal and lower-limb rash. Neurological examination revealed no motor weakness or hyperreflexia, but he could not walk unassisted due to dizziness. Brain MRI diffusion-weighted imaging (DWI) showed characteristic V-shaped hyperintense lesions in the bilateral medial medulla (Fig. 1A) and at the pontomedullary junction (Fig. 1B). MR angiography (MRA) showed no stenosis or dissection of the basilar or vertebral arteries (VA) (Fig. 1C).

The distribution of amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) in the Kii Peninsula of Japan exhibits regional variations, with ALS/PDC in the Hohara focus closely resembling that in Guam and ALS in the Kozagawa focus. Recent structural analysis using cryo-electron microscopy revealed that the tau filaments in patients with ALS/PDC in Kii have a chronic traumatic encephalopathy (CTE) fold, confirming the disease's distinct pathological identity and commonality with the Guam focus. While the exact causal genes remain unidentified, research utilizing patient-derived induced pluripotent stem cells and proteomic analysis has uncovered endogenous mitochondrial dysfunction, specifically involving decreased expression of CHCHD2 and SSBP1. The presence of migrant cases further suggests that ALS/PDC is a multifactorial disorder triggered by environmental factors that influence genetic vulnerability. Although the incidence of ALS in Kozagawa and Hohara districtst has declined, new cases with PDC continue to emerge in Hohara. Identifying these modifiable environmental triggers is crucial for preventing and eradicating neurological disorders.

Difficulty walking is a common complaint in neurological practice which may arise from a wide range of disorders of the central nervous system, peripheral nerves, or musculoskeletal system. Because human gait requires the complex integration of multiple neural and biomechanical processes, careful clinical assessment is essential to achieve accurate diagnosis. In this review, we outlined a practical approach for patients presenting with walking difficulties. Emphasis is placed on the importance of detailed history-taking and neurological examination, including observation of gait, posture, gait initiation, and turning. We further summarize the key clinical features of the major organic causes of gait disturbance, such as lower limb weakness, pyramidal tract disorders, and Parkinsonian syndromes. Functional gait disorder is an important and increasingly recognized cause of gait disturbance. Recognizing the positive clinical signs and characteristic variability in symptoms is essential for appropriate diagnosis and management. Careful clinical evaluation remains the cornerstone for assessing gait disorders, and diagnostic tests should be used to confirm the clinical diagnosis based on the history and neurological examination.

When diagnosing dementia disorders, obtaining a detailed medical history and identifying relevant findings on physical and neurological examinations are fundamental. It is essential to assess cognitive function, neurological symptoms and signs, and dementia severity; conduct additional tests; and establish a differential diagnosis. With the widespread use of anti-amyloid antibody therapies, mild cognitive impairment (MCI) due to Alzheimer's disease (AD) and early-stage AD must not be overlooked. When evaluating patients with dementia who present with diverse symptoms, clinicians must consider neurological signs, findings from diagnostic tests, and the clinical course to establish an accurate diagnosis and guide appropriate treatment.

In the examination of patients with "lack of strength", abnormalities in motor units (α motor neurons, myelinated fibers, neuromuscular junctions, and muscle fibers), spinal cord-mediated neurons, projections that descend the spinal cord to control motor units (corticospinal tract, corticoreticular tract, and reticulospinal tract), and autonomic nerves, are considered, and physiological changes, diseases, and external factors are investigated. Appropriate assessment of muscle strength, investigations for pyramidal tract signs, appropriate expression of pathology, blood sampling, needle electromyography, and magnetic resonance imaging/magnetic resonance angiography of the head, are desirable.

Trembling/shaking is among the most common complaints encountered in general or neurological clinics. The differential diagnosis of this symptom is important as it can be caused by various conditions and neurological diseases. Essential tremor (ET) is a dominantly inherited disorder that manifests as a bilateral fine (>8Hz) postural tremor. Physiological tremor can develop in patients with sympathetically activated conditions, such as hyperthyroidism, fever, anxiety, and muscle fatigue, in addition to being induced by many drugs. Patients with Parkinson's disease may demonstrate lateralized, moderately fast (4-6Hz) resting and postural tremors. Rubral (midbrain) tremors in the arms with low frequency (3Hz) oscillation or palatal myoclonus may suggest lesions within the Guillain-Mollaret's triangle, which comprises the contralateral midbrain rubral nucleus, contralateral medullary inferior olivary nucleus, and ipsilateral cerebellar dentate nucleus. Intension (terminal) tremor is defined as an action tremor showing an amplitude increases towards the end of the movement to touch a target, as in the finger-nose-finger test. Orthostatic tremor (also termed shaky legs syndrome) is a variant of ET involving the legs observed only in the standing still position. In conclusion, a precise diagnosis of symptoms allows the management of the condition according to its causal mechanism.

This review provides a practical approach to evaluating and managing patients presenting with numbness and pain in the extremities. It emphasizes that careful history-taking and neurological examination remain the foundation of anatomic localization before imaging or electrophysiological studies are considered. The review summarizes the epidemiology, differential diagnosis, appropriate laboratory testing and neurophysiological investigations, indications for specialist referral, and current treatment strategies. Particular attention is given to distinguishing among nociceptive pain, neuropathic pain, and the recently recognized category of nociplastic pain because each requires a different therapeutic approach. The review also discusses chronic sensory symptoms frequently encountered in older adults, including patients with idiopathic distal sensory polyneuropathy and small-fiber neuropathy, in whom conventional investigations may be inconclusive. The review places these conditions within the spectrum of age-related peripheral nerve dysfunction while acknowledging emerging evidence for previously unrecognized etiologies. The review concludes that neurologists should focus not only on identifying serious neurological disorders but also on recognizing and validating patients' subjective sensory symptoms. A systematic clinical approach, combined with appropriate referral and individualized management, can substantially improve diagnostic accuracy and patient care in routine neurological practice.