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In chronic hepatitis type C fatigue, depression and neuropsychiatric complications of interferon treatment are more frequently reported than in the other parenchymal liver diseases. It contributes to a significant reduction of health related quality of life (HRQL) in those patients. It is believed that psychiatric disorders are the result of brain dysfunction caused by the virus. The hypothesis of neurotropic character of HCV infection is supported by the detection of HCV-RNA in brain tissue, identification of brain-specific quasispecies variants of hepatitis C virus, specific detection of negative-strand viral RNA in the astroglia of patients with acquired-immunodeficiency syndrome and demonstration of metabolic changes resembling HIV-1 encephalopathy in the basal ganglia of patients with chronic hepatitis C. On the other hand there is good evidence that decreased HRQL is directly related to the consciousness of infection and hence, is not of the organic nature. Some authors suggest that patient's worry and anxiety, aggravated by some mass-media and the lack of knowledge, may be a strong determinant of psychological status. Given the complex nature of symptoms in chronic hepatitis C therapy should include education on the natural history of HCV infection and results of treatment, psychotherapy and medical treatment of depression and anxiety. Moreover, antiviral therapy should be considered in highly motivated patients despite lack of clear clinical indications for treatment.
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PMID:[Chronic HCV infection--disease of body or disease of soul?]. 1619 May 74

The clinical presentation of acute liver failure and hepatic encephalopathy (HE) in patients with cirrhosis differs significantly. The most serious neurological complication of acute liver failure is the development of devastating brain oedema. Therefore, intracranial pressure monitoring is urgently needed in these patients. Brain oedema is amplified by hypoglycemia, hypoxia and seizures, which are also frequent complications of acute liver failure. Therefore, these parameters must also be monitored. In contrast to acute liver failure in which cerebral dysfunction progresses rapidly, cognitive decline may be clinically undetectable for a long time in cirrhotic patients, until clinically overt symptoms such as psychomotor slowing, disorientation, confusion, extrapyramidal and cerebellar symptoms or a decrease in consciousness occur. Clinically, overt HE is preceded by minimal alterations of cerebral function that can only be detected by neuropsychological or neurophysiological measures, but which nevertheless interfere with the patient's daily living. Rapidly progressing spastic paraparesis (hepatic myelopathy) is a rare complication of cirrhosis. In contrast to HE, it does not respond to blood ammonia lowering therapies but must be considered as an indication for urgent liver transplantation. Cognitive dysfunction has recently been detected in hepatitis C virus (HCV)-infected patients with normal liver function. The patients presented with severe fatigue, cognitive dysfunction and mood disorders. Alterations in brain metabolites, as detected by magnetic resonance spectroscopy, indicated central nervous system alteration in these patients. In contrast to patients with HE, HCV-infected patients did not show motor symptoms or deficits in visual perception, but considerable deficits in attention and concentration ability.
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PMID:Neurological and neuropsychiatric syndromes associated with liver disease. 1625 35

We review here aggression-related human psychopathologies and propose that human aggressiveness is mainly due to three major factors: (i) brain dysfunction affecting aggression-controlling brain centers (e.g. in certain types of brain lesions, epilepsy, Alzheimer disease, etc.); (ii) hypoarousal associated with chronically low plasma glucocorticoids, which foster violence by diminishing emotional barriers that limit such behaviors (e.g. in conduct disorder and antisocial personality disorder); (iii) hyperarousal which leads to irritability and outbursts (e.g. in depression, intermittent explosive disorder, chronic fatigue, etc.). Different disorders are associated with different types of aggressiveness; e.g. hypoarousal is often associated with instrumental aggression, whereas hyperarousal is associated with uncontrollable outbursts. Many psychological disorders have been simulated in laboratory models, which were used to assess aggressiveness. Little effort was invested, however, in assessing the abnormal dimension of such aggressiveness. We present here three models that appear especially suitable to assess abnormal aspects of rodent aggression: (i) abnormal attack targeting (head, throat, and belly) that is induced by hypoarousal in rats and models violence in hypoarousal-driven human aggression (ii) 'escalated' aggression (increased aggressive response due to frustration or instigation), which models irritability and hyperarousal-driven aggressiveness; and (iii) context-independent attacks induced by hypothalamic stimulation or genetic manipulations. These three models address different aspects of abnormal aggressiveness, and can become extremely useful in three areas: in evaluating and assessing models of human psychopathologies, in studying transgenic animals, and in developing new treatment strategies. Research based on these or similar models do not address aggressiveness in quantitative terms, but follows the development of abnormal aspects, and the possibilities of their specific treatment.
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PMID:Normal and abnormal aggression: human disorders and novel laboratory models. 1648 89

Impairment after stroke may have acute and long-lasting psychological implications. Additionally, organic brain dysfunction also appears to play an important role in poststroke affective modifications. Emotional state is multidetermined and can be specifically modified by alteration of some brain networks. This article illustrates a certain number of acute and more chronic emotional disturbances after stroke, such as mood disorders, emotional dyscontrol, and modification of emotional experiences. Some neural mechanisms implicated in these modifications are discussed. The main modifications described are depression anxiety, psychosis, modification of emotional experience, and fatigue.
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PMID:Emotional disturbances after stroke. 1683 30

The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain. As any other organ, the brain is elaborated from substances present in the diet (sometimes exclusively, for vitamins, minerals, essential amino-acids and essential fatty acids, including omega- 3 polyunsaturated fatty acids). However, for long it was not fully accepted that food can have an influence on brain structure, and thus on its function, including cognitive and intellectuals. In fact, most micronutrients (vitamins and trace-elements) have been directly evaluated in the setting of cerebral functioning. For instance, to produce energy, the use of glucose by nervous tissue implies the presence of vitamin B1; this vitamin modulates cognitive performance, especially in the elderly. Vitamin B9 preserves brain during its development and memory during ageing. Vitamin B6 is likely to benefit in treating premenstrual depression. Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters. Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), provided it is administered in a precise clinical timing window, before the onset of the first symptoms. Supplementation with cobalamin improves cerebral and cognitive functions in the elderly; it frequently improves the functioning of factors related to the frontal lobe, as well as the language function of those with cognitive disorders. Adolescents who have a borderline level of vitamin B12 develop signs of cognitive changes. In the brain, the nerve endings contain the highest concentrations of vitamin C in the human body (after the suprarenal glands). Vitamin D (or certain of its analogues) could be of interest in the prevention of various aspects of neurodegenerative or neuroimmune diseases. Among the various vitamin E components (tocopherols and tocotrienols), only alpha-tocopherol is actively uptaken by the brain and is directly involved in nervous membranes protection. Even vitamin K has been involved in nervous tissue biochemistry. Iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxidase), and for the synthesis of neurotransmitters and myelin; iron deficiency is found in children with attention-deficit/hyperactivity disorder. Iron concentrations in the umbilical artery are critical during the development of the foetus, and in relation with the IQ in the child; infantile anaemia with its associated iron deficiency is linked to perturbation of the development of cognitive functions. Iron deficiency anaemia is common, particularly in women, and is associated, for instance, with apathy, depression and rapid fatigue when exercising. Lithium importance, at least in psychiatry, is known for a long time. Magnesium plays important roles in all the major metabolisms: in oxidation-reduction and in ionic regulation, among others. Zinc participates among others in the perception of taste. An unbalanced copper metabolism homeostasis (due to dietary deficiency) could be linked to Alzheimer disease. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells; the dietary reduction of iodine during pregnancy induces severe cerebral dysfunction, actually leading to cretinism. Among many mechanisms, manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. More specifically, the full genetic potential of the child for physical growth ad mental development may be compromised due to deficiency (even subclinical) of micronutrients. Children and adolescents with poor nutritional status are exposed to alterations of mental and behavioural functions that can be corrected by dietary measures, but only to certain extend. Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects, beneficial or adverse. Brain diseases during aging can also be due to failure for protective mechanism, due to dietary deficiencies, for instance in anti-oxidants and nutrients (trace elements, vitamins, non essential micronutrients such as polyphenols) related with protection against free radicals. Macronutrients are presented in the accompanying paper.
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PMID:Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. 1706 9

Chronic fatigue syndrome (CFS) is an operational concept proposed by Centers for Disease Control and Prevention to clarify the unknown etiology of the syndrome characterized by the sensation of abnormally prolonged fatigue. Lots of investigators reported various abnormalities such as virus infection, immune abnormalities, HPA axis abnormalities, metabolic abnormalities, etc., but there are a few abnormalities common to vast majority cases of CFS. Therefore, lots of people as well as medical doctors are still skeptical about the presence of CFS. However, recent studies reveal that CFS can be understood to be a special condition based on the abnormality of neuroendocrine-immunologic system caused by the psycho-social stress and some genetic components. Under these conditions, a reactivation of various kinds of herpes virus infections and/or chronic infections might occur as a result of immune dysfunction, causing the abnormal production of several cytokines. A distinctive feature of CFS is thought to be the secondary brain dysfunction caused by the abnormal production of several cytokines. In this paper, I show the overview of CFS focusing around prevalence, economic impact and diagnostic criteria in Japan.
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PMID:[Overview of chronic fatigue syndrome focusing on prevalence and diagnostic criteria]. 1756 86

Though patients with chronic fatigue syndrome (CFS) have lots of complaints, abnormal findings cannot be detected by biochemical screening tests. However, some specialized blood tests have revealed neuroendocrine immune axis abnormalities, which is closely associated with each other. Recent studies indicate that CFS can be understood as a special condition based on abnormality of the psycho-neuro-endocrino-immunological system, with the distinguishing feature of CFS seeming to be the secondary brain dysfunction caused by several cytokines and/or autoantibodies. In this paper, we summarize these abnormalities found in CFS and show the neuro-molecular mechanism leading to chronic fatigue.
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PMID:[Chronic fatigue syndrome: biochemical examination of blood]. 1756 99

Mild traumatic brain injury (TBI) is common but accurate diagnosis and defining criteria for mild TBI and its clinical consequences have been problematic. Mild TBI causes transient neurophysiologic brain dysfunction, sometimes with structural axonal and neuronal damage. Biomarkers, such as newer imaging technologies and protein markers, are promising indicators of brain injury but are not ready for clinical use. Diagnosis relies on clinical criteria regarding depth and duration of impaired consciousness and amnesia. These criteria are particularly difficult to confirm at the least severe end of the mild TBI continuum, especially when relying on subjective, retrospective accounts. The postconcussive syndrome is a controversial concept because of varying criteria, inconsistent symptom clusters and the evidence that similar symptom profiles occur with other disorders, and even in a proportion of healthy individuals. The clinical consequences of mild TBI can be conceptualized as two multidimensional disorders: (1) a constellation of acute symptoms that might be termed early phase post-traumatic disorder (e.g., headache, dizziness, imbalance, fatigue, sleep disruption, impaired cognition), that typically resolve in days to weeks and are largely related to brain trauma and concomitant injuries; (2) a later set of symptoms, a late phase post-traumatic disorder, evolving out of the early phase in a minority of patients, with a more prolonged (months to years), sometimes worsening set of somatic, emotional, and cognitive symptoms. The later phase disorder is highly influenced by a variety of psychosocial factors and has little specificity for brain injury, although a history of multiple concussions seems to increase the risk of more severe and longer duration symptoms. Effective early phase management may prevent or limit the later phase disorder and should include education about symptoms and expectations for recovery, as well as recommendations for activity modifications. Later phase treatment should be informed by thoughtful differential diagnosis and the multiplicity of premorbid and comorbid conditions that may influence symptoms. Treatment should incorporate a hierarchical, sequential approach to symptom management, prioritizing problems with significant functional impact and effective, available interventions (e.g., headache, depression, anxiety, insomnia, vertigo).
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PMID:Mild traumatic brain injury. 2570 14

"Cutis Marmorata" skin symptoms after diving, most frequently in the form of an itching or painful cutaneous red-bluish discoloration are commonly regarded as a mild form of decompression sickness (DCS), and treated with oxygen inhalation without reverting to hyperbaric recompression treatment. It has been observed that the occurrence of Cutis Marmorata is frequently associated with the presence of a Patent Foramen Ovale (PFO) of the heart, and indeed, with a properly executed contrast echocardiographic technique, these patients have an almost 100% prevalence of PFO. Only occasionally, Cutis Marmorata is accompanied by other symptoms of DCS. These symptoms usually are in the form of visual distortions, vertigo, or mild, vague but generalized cerebral dysfunction (such as abnormal fatigue, clumsiness, concentration problems). The pathogenesis of these other manifestations is clearly emboligenic, and we hypothesize that Cutis Marmorata is also a manifestation of gas bubbles embolizing the brain stem: the site of autonomic nervous system regulation of skin blood vessel dilation and constriction. The consequences of this hypothesis are that Cutis Marmorata skin decompression sickness should no longer be considered a mild, innocuous form but rather a serious, neurological form and treated accordingly.
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PMID:Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles. 2643 31

Hepatitis C virus (HCV) infection may induce chronic fatigue and cognitive dysfunction. Virus replication was proven within the brain and HCV-positive cells were identified as microglia and astrocytes. We hypothesized that cerebral dysfunction in HCV-afflicted patients is associated with microglia activation. Microglia activation was assessed in vivo in 22 patients with chronic HCV infection compared to six healthy controls using [(11) C]-PK11195 Positron Emission Tomography (PET) combined with magnetic resonance tomography for anatomical localization. Patients were subdivided with regard to their PCR status, Fatigue Impact Scale score (FIS) and attention test sum score (ATS). A total of 12 patients (54.5%) were HCV PCR positive [of which 7 (58.3%) had an abnormal FIS and 7 (58.3%) an abnormal ATS], 10 patients (45.5%) were HCV PCR negative (5 (50%) each with an abnormal FIS or ATS). Patients without attention deficits showed a significantly higher accumulation of [(11) C]-PK11195 in the putamen (P = 0.05), caudate nucleus (P = 0.03) and thalamus (P = 0.04) compared to controls. Patients with and without fatigue did not differ significantly with regard to their specific tracer binding in positron emission tomography. Preserved cognitive function was associated with significantly increased microglia activation with predominance in the basal ganglia. This indicates a probably neuroprotective effect of microglia activation in HCV-infected patients.
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PMID:Cerebral microglia activation in hepatitis C virus infection correlates to cognitive dysfunction. 2676 55


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