Humans ; Nervous System ; physiopathology ; Schizophrenia ; physiopathology

AIMVarious forms of social adversity have been implicated in the development and emergence of psychosis. However, how and when these events exert their influences are not clear. In this paper, we attempt to examine these putative psychosocial factors and place them in a temporal context and propose a neurobiological mechanism linking these factors.

METHODSMedline databases were searched between 1966 and 2007 followed by the cross-checking of references using the following keywords: psychosocial, stress, stressors, life events, psychological, combined with psychosis and schizophrenia.

RESULTSWhile some findings are conflicting, there are a number of positive studies which suggest that factors like prenatal stress, urban birth and childhood trauma accentuate the vulnerability for schizophrenia and other psychoses while other factors like life events, migration particularly being a minority group, and high expressed emotions, which occur later in the vulnerable individual may move the individual towards the tipping point for psychosis.

CONCLUSIONOverall, there is evidence to implicate psychosocial factors in the pathophysiology of schizophrenia. These factors may act via a common pathway, which involves stress-induced dysregulation of the HPA axis and the dopaminergic systems. To establish the causal relationship of the various factors would require prospective studies that are adequately powered.

Humans ; Nervous System ; physiopathology ; Schizophrenia ; physiopathology

The physiological and pathological phenomenon along the running courses of meridians such as enrichment of small charged molecular, low-resistance, isotope migration, electromyography phenomenon, acoustical conductivity, thermal radiation, magnetic phenomenon and optical-electrical characteristics, etc. are explored in this article. And based on the above mentioned studies, it is concluded that as a physiological sensation along meridians, propagated sensation could only be the result of the reflection of nerve excitation. The direct stimulator of the neural electrical activities of the propagated sensation is the enrichment of charged small biological molecular at the corresponding site of the organism. The root cause of the enrichment is the unique electrophysiological mechanism and distribution discipline of the human nerve fiber, which formed an electric field of biological source for the concentration of the small molecular. Thus, it is concluded that the electric field along the running courses of meridians is an isopotential balanced line formed by multiple neural bioelectrical activities in different spaces closed to meridians.
Electrophysiological Phenomena ; Humans ; Meridians ; Nervous System ; physiopathology

Autonomic Nervous System Diseases ; physiopathology ; Humans ; Liver Cirrhosis ; physiopathology

Animals ; Autonomic Nervous System ; physiology ; Humans ; Parasympathetic Nervous System ; physiology ; Sepsis ; etiology ; physiopathology ; Sympathetic Nervous System ; physiology

Central Nervous System ; pathology ; Humans ; Infant ; Leigh Disease ; pathology ; physiopathology

Synapsins serve as flagships among the presynaptic proteins due to their abundance on synaptic vesicles and contribution to synaptic communication. Several studies have emphasized the importance of this multi-gene family of neuron-specific phosphoproteins in maintaining brain physiology. In the recent times, increasing evidence has established the relevance of alterations in synapsins as a major determinant in many neurological disorders. Here, we give a comprehensive description of the diverse roles of the synapsin family and the underlying molecular mechanisms that contribute to several neurological disorders. These physiologically important roles of synapsins associated with neurological disorders are just beginning to be understood. A detailed understanding of the diversified expression of synapsins may serve to strategize novel therapeutic approaches for these debilitating neurological disorders.
Animals ; Central Nervous System Diseases ; physiopathology ; Humans ; Synapsins ; physiology

Peripheral nerve injury frequently leads to neuropathic pain like hyperalgesia, spontaneous pain, mechanical allodynia, thermal allodynia. It is uncertain where the neuropathic pain originates and how it is transmitted to the central nervous system. This study was performed in order to determine which peripheral component may lead to the symptoms of neuropathic pain. Under halothane anesthesia, male Sprague-Dawley rats were subjected to neuropathic surgery by tightly ligating and cutting the tibial and sural nerves and leaving the common peroneal nerve intact. Behavioral tests for mechanical allodynia, thermal allodynia, and spontaneous pain were performed for 2 weeks postoperatively. Subsequently, second operation was performed as follows: in experiment 1, the neuroma was removed; in experiment 2, the dorsal roots of the L4-L6 spinal segments were cut; in experiment 3, the dorsal roots of the L2-L6 spinal segments were cut. Behavioral tests were performed for 4 weeks after the second operation. Following the removal of the neuroma, neuropathic pain remained in experiment 1. After the cutting of the L4-L6 or L2-L6 dorsal roots, neuropathic pain was reduced in experiments 2 and 3. The most remarkable relief was seen after the cutting of the L2-L6 dorsal roots in experiment 3. According to the fact that the sciatic nerve is composed of the L4-L6 spinal nerves and the femoral nerve is composed of the L2-L4 spinal nerves, neuropathic pain is transmitted to the central nervous system via not only the injured nerves but also adjacent intact nerves. These results also suggest that the dorsal root ganglion is very important in the development of neuropathic pain syndrome.
Animal ; Ganglia, Spinal/physiopathology ; Male ; Nervous System Diseases/physiopathology* ; Nervous System Diseases/complications ; Pain/physiopathology* ; Pain/etiology ; Rats ; Rats, Sprague-Dawley ; Spinal Nerve Roots/physiopathology ; Spinal Nerves/physiopathology

The autonomic nervous system consists of the sympathetic nervous system and the parasympathetic nervous system. These two systems control the heart and work in a reciprocal fashion to modulate myocardial energy metabolism, heart rate as well as blood pressure. Multiple cardiac pathological conditions are accompanied by autonomic imbalance, characterized by sympathetic overactivation and parasympathetic inhibition. Studies have shown that overactive sympathetic nervous system leads to increased cardiac inflammatory reaction. Orchestrated inflammatory response serves to clear dead cardiac tissue and activate reparative process, whereas excessive inflammation may result in pathological cardiac remodeling. Since the discovery of the α7 nicotinic acetylcholine receptor (α7nAChR)-mediated cholinergic anti-inflammatory pathway (CAP), the protective effects of the parasympathetic nervous system in cardiac inflammation have attracted more attention recently. In this review, we summarized the role and underlying mechanisms of the sympathetic and parasympathetic nervous systems in cardiac inflammation, in order to provide new insight into cardiac inflammatory response in cardiovascular diseases.
Autonomic Nervous System ; physiology ; Heart ; physiopathology ; Humans ; Inflammation ; physiopathology ; Parasympathetic Nervous System ; physiology ; alpha7 Nicotinic Acetylcholine Receptor ; physiology