Brain and Nerve最新文献

Learning is classified into two types: "classical conditioning," which modifies simple reflexes, and "operant conditioning," which modifies complex voluntary behaviors. The neural circuits underlying these two types differ significantly. During the learning process of operant conditioning tasks, various changes in firing rate and firing synchrony of neurons can be observed across multiple brain regions. Additionally, neuronal firing rate and synchrony in several brain regions can be voluntarily controlled through operant conditioning. Consequently, it is evident that neurons in widespread brain regions have the potential for plastic changes to facilitate learning. It may be suggested that the learning of complex voluntary behaviors is underlined by widespread dynamic changes in neural activity and is not restricted to only a few brain regions.

Based on a recent review by Krohn et al, the respiratory center and its regulatory mechanisms are described. Although the respiratory control centers in the medulla and pons ensure rhythmic respiration, maintaining and regulating respiration involves a complex network of peripheral chemoreceptors, vagal nerves, and central chemoreceptors. This review discusses the pathophysiology of respiratory disorders in neuromuscular diseases and evaluation and treatment methods based on the anatomy of the respiratory network.

Endocrine dysfunction can considerably impact the nervous system. Various nonspecific neurological symptoms can manifest, including headache, muscle weakness, involuntary movements, and impaired consciousness. Because of their lack of specificity, endocrine abnormalities underlying neurological symptoms may not be recognized and making the diagnosis may be challenging. It is essential that clinicians not overlook endocrine disorders when diagnosing neurological symptoms, as prompt and appropriate treatment, such as hormone replacement therapy, can improve a patient's general condition and neurological symptoms.

The kidneys filter the blood to excrete waste products and excess salt from the body as urine, while reabsorbing what the body needs and keeping it in the body. For this reason, when the function of the kidneys deteriorates, urine cannot be produced, and homeostasis of electrolytes and acid-bases cannot be maintained. As a result, waste products accumulate in the body, resulting in uremia and the need for dialysis induction or kidney transplant. This paper provides an overview of the neurological complications that appear in kidney disease and their treatment.

Idiopathic normal pressure hydrocephalus (iNPH), a syndrome characterized by cognitive impairment, gait abnormalities, and urinary incontinence attributable to cerebrospinal fluid circulatory insufficiency, is associated with an obscure etiology. Several methodologies and imaging analysis techniques, including visualization of cerebral hemodynamics and diffusion tensor imaging have emerged in recent years to determine functional alterations in cases of iNPH. These advancements have led to more comprehensive understanding of the pathophysiological mechanisms underlying iNPH. In this article, we discuss the historical evolution of imaging modalities for iNPH and contemporaneous imaging techniques designed to acquire deeper insight into this disease.

Idiopathic normal pressure hydrocephalus causes a triad of gait disturbance, dementia, and urinary incontinence in the elderly. All these symptoms may manifest as age-related functional decline or from neurological and non-neurological diseases common in the elderly. In idiopathic normal pressure hydrocephalus, characterized by ataxic-ataxic gait, subcortical dementia, and urge urinary incontinence, it is clinically important to consider these characteristic features. This overview describes the symptomatology of idiopathic normal pressure hydrocephalus.

Although the pathophysiology of idiopathic normal pressure hydrocephalus (iNPH) remain largely unknown, it is well acknowledged that iNPH causes ventricular enlargement due to decreased cerebrospinal fluid (CSF) absorption. Pathophysiologically, it is supposed that the excretion of waste proteins is impaired along with CSF. Hence, they tend to aggregate, and in many neurodegenerative diseases, abnormal aggregation and accumulation of such proteins are deeply involved in the pathogenesis of disease. Biomarkers (BMs) contribute to diagnosis by identifying comorbid neurodegenerative diseases that may affect the prognosis of treatment, as well as exploring the pathogenetic mechanisms of iNPH. In addition, BMs can be an important prognostic test for shunt therapy.

According to a cohort study in a Japanese rural area, the prevalence of idiopathic normal pressure hydrocephalus (iNPH) in the 80s was 7.7% among the older inhabitants, despite only a small percentage of the population seeking consultation. The 16-year observation of the cohort revealed that people were in the state of asymptomatic ventriculomegaly with features of iNPH on magnetic resonance imaging or asymptomatic ventricular enlargement several years before presenting symptoms and intracranial changes of iNPH. SFMBT1 was found to be a risk gene for iNPH, and investigating these risk genes will further the study of iNPH pathophysiology.

Cerebrospinal fluid shunting, including ventriculo-abdominal/atrial and lumbar-abdominal shunts, is the only treatment available for idiopathic normal pressure hydrocephalus (iNPH). Hybrid valves that combine a programmable pressure valve and an antisiphon device are being widely used for treatment of iNPH, which has significantly minimized surgical complications, such as shunt revision and subdural hematomas associated with overdrainage. Development of novel technologies that can maintain a more physiological intracranial environment after shunting presents a challenge for future research.

Idiopathic normal pressure hydrocephalus (iNPH) is a clinical condition characterized by symptoms of gait disturbance, cognitive dysfunction, and urinary disturbance. In contrast, progressive supranuclear palsy (PSP) is a progressive neurodegenerative disease characterized by supranuclear gaze palsy, akinetic rigidity, gait disturbance, and dementia. PSP manifests various clinical phenotypes that mimic other diseases and occasionally present iNPH-like presentations. Our previous publication showed that PSP develops iNPH-like magnetic resonance imaging (MRI) features more frequently than other neurodegenerative diseases. It is thus sometimes challenging to distinguish iNPH from PSP. Recently, we showed that patients with PSP, particularly those with iNPH-like MRI findings, often demonstrate amelioration of their gait disturbance following a spinal tap or shunt operation. Moreover, our study revealed that both patients with iNPH and PSP often manifest a placebo effect that can be evaluated by implementing a sham spinal tap. Therefore, although a positive response to a spinal tap has been thought of as a distinct feature of iNPH, it may not be useful in differentiating iNPH and PSP. However, in clinical practice, comparing the response to a spinal tap with that of a sham spinal tap may help accurately specify patients with iNPH or PSP who definitively respond to the shunt operation.