Home Cure for Chronic Fatigue Syndrome
Symptoms of chronic fatigue may antedate or appear after the onset of illness severity of underlying medical disorder may not parallel the severity of fatigue symptoms fatigue may persist after apparent clinical recovery in many cases Anaemia (all causes) sharing symptoms of CFS-type fatigue suggests a dysfunction of the dopamine-dependent neostri-atal-dorsolateral prefrontal network as the final pathway in the genesis of chronic fatigue symptoms.
Obviously, adaptive immune-mediated depression-like syndrome should be transient and restricted to the time period in which the organism is sick. Indeed, many factors have been documented to tightly regulate and limit the behavioral, neural and neuroendocrine effects of cytokines, including glucocorticoids, vasopressin, and a-melanocyte stimulating hormone (a-MSH) (Dantzer et al., 1996). Disruption of these regulatory factors might lead to impairment in shutting off the immune and neural mechanisms underlying sickness behavior, thus resulting in maladaptive depressive symptomatology. This process may underlie the Chronic Fatigue Syndrome (CFS) and the Post-Viral Fatigue Syndrome (PVFS). Both syndromes are associated with psychological changes that persist long after recuperation from viral infection (Komaroff, Fagioli, Geiger, Doolittle, Lee, Kornish, Gleit, & Guerriero, 1996). They are mainly characterized by fatigue, which reduces patients' level of everyday activity by at least 50...
More subtle than the histologically identifiable alterations in cell distribution are the biochemical changes that indicate a low level of chronic inflammation. Alterations in measures of oxidative stress have been observed in several hypersensitivity disorders, such as fibromylagia64 and chronic fatigue syndrome,65 and form a basis for sensory changes in the absence of histological changes. Use of antioxidant micronutrient therapies (e.g. vitamins C and E, selenium) has had reported utility in the treatment of painful visceral disorders, such as chronic pan-creatitis.66
Intracellular antiviral pathways.37 While 'active' intracellular bacterial infections, e.g. Lyme disease and tuberculosis, can certainly cause chronic fatigue as one of the common symptoms of systemic infections (secondary or symptomatic CFS), the patient with an active bacterial infection does not have CFS by definition, since a confident diagnosis of CFS can only be made after exclusion of all systemic medical causes (Table 15.2). However, unlike antiviral therapy in CFS (although newer antivirals such as pleconaril have not been tested), there has been anecdotal evidence of improvement in a small proportion of CFS patients treated with specific macrolide antibiotics (typically doxycycline, erythromycin or clarithromycin). During the outbreaks of neuromyasthenia in the 1960s, chloram-phenicol, another macrolide antibiotic, was believed to be effective in some patients.38 We do not yet know if this antibiotic-responsive CFS population represents a true cohort of 'chronically'...
Our current understanding of CFS is that the mechanism of fatigue is central, possibly related to the dysfunction of the neostriatal-prefrontal cortical network as a consequence of altered neurotransmit-ter balance and channelopathy that appear to be related to antecedent viral infections, stress and cytokine effect. There is no known therapy at present, either pharmacological, or behavioural, that is effective in curing CFS. Understanding the mechanism of fatigue, the hallmark of CFS, is crucial to the successful development of any treatment strategy. Any therapeutic claims in CFS at present have to be interpreted cautiously and must be tested by well-designed, multicentre, placebo-controlled, randomized trials before recommendations for use in all or a subgroup of CFS patients. Since the symptoms and severity of fatigue in CFS fluctuate, carefully planned treatment designs will be necessary to avoid bias in favour of the treatment due to the phenomenon of regression to mean. There...
Basal ganglia are considered to be the neural integrator for the motor and motivational aspects of higher cortical and limbic activities.46 Dyfunction of the dopamine-dependent neostriatal-thalamic-prefrontal circuit is currently proposed as the neuroanatomical model of the physical and mental fatigue in CFS, while the fluctuations in symptom severity are considered to be the effects of ion channelopathy Indeed, the structure of the ion channels (e.g. voltage-gated potassium channel) has been remarkably conserved throughout evolution, and their functions in the excitable tissues can be influenced by viral infections and cell injury.48 Certain acquired ion channelopathies share identical fatigue symptoms and neuroendocrine changes with CFS, e.g. chronic fatigue after ciguatera fish poisoning (ciguatera toxin chronically inactivates sodium channels in an open mode) and Isaac's syndrome (acquired neuromyotonia, often associated with antibodies to the voltage-gated potassium channels)....
There are a group of disorders that have been termed affective spectrum disorders'' which frequently coexist with one another. These include fibromyalgia, but also irritable bowel syndrome, chronic fatigue syndrome, depression and anxiety disorders, and migraine. These are all associated with psychological distress. It had been thought that depression may lead to the development of widespread pain, and although it is commonly reported in fibromyalgia (in 20-30 percent of patients) it is more likely that it in fact occurs the other way round (the pain results in depression) as the majority of patients do not suffer from any psychiatric illness and, when present, the depression can be treated without improving the pain state.
Some evidence suggests that other stress-related neuropsychiatric conditions may be associated with immune activation, although these conditions are less well characterized than major depression. These disorders include posttraumatic stress disorder (PTSD), chronic fatigue syndrome (CFS), seasonal affective disorder (SAD), and fibromyalgia. Patients with combat-related PTSD have been reported to demonstrate increased plasma concentrations of IL-1 and increased CSF concentrations of IL-6 (Baker et al. 2001 Spivak et al. 1997). PTSD following civilian disasters appears to be associated with elevated plasma concentrations of IL-6 and its soluble receptor (Maes et al. 1999c). Although not found consistently (Maes et al. 1999c), both severity of symptoms and duration of illness have been reported to correlate positively with indices of immune activation in PTSD (Miller et al. 2001 Spivak et al. 1997).
The accumulated research evidence in CFS at present clearly points to a central role of fatigue. We currently believe that basal ganglia pathways are involved in the mechanism of the chronic fatigue that comprises symptoms of both physical and mental fatigue. Basal ganglia are exquisitely sensitive to pro-inflammatory cytokines and also to direct viral invasion (e.g. HIV, various encephalitis viruses, influenza A virus).45 Post-viral modification of functions affecting the receptors or the neurotrans-mitter release will induce critical changes in the excitable tissues and affect the facilitatory striato-thalamic input to the prefrontal cortex that may play an important role in the fatigue symptoms in CFS.
Superior to fluoxetine, and both duloxetine and venlafaxine also may be effective) fibromyalgia peptic ulcer and irritable bowel syndrome hot flashes of menopause chronic fatigue cataplexy tics migraine and sleep apnea. These disorders may have some psychobiological relationship to mood or anxiety disorders.
The prevalence of other functional somatic syndromes such as chronic fatigue syndrome or irritable bowel symptoms has been reported as 30-80 , depending on the setting and the diagnostic methods used 33 . The frequent aggregation of functional somatic syn-droms suggests a common pathophysiology 17 .
The etiology of fibromyalgia is unclear, but evidence suggests that it is a heritable disorder. The etiology of fibromyalgia is now thought to be due to a combination of several factors associated with the presence of both chronic pain and affective disorders, similar to those postulated in irritable bowel syndrome, chronic fatigue syndrome, major depressive disorder, temperomandibular joint disorder, and tension and migraine headaches. The factors include genetic factors, aberrant pain processing in the central nervous system, abnormalities in the neuroendocrine system, and specific triggers in the environment.
Caffeine is a potent CNS and metabolic stimulant, and is used both recreationally and medically to reduce physical fatigue, and to restore mental alertness. It stimulates the CNS first at the higher levels, resulting in increased alertness and wakefulness, faster and clearer flow of thought, increased focus, and better general body coordination, and later at the spinal cord level at higher doses. Caffeine is used in combination with a number of painkillers. Caffeine is also used with ergotamine in the treatment of migraine and cluster headaches as well as to overcome the drowsiness caused by antihistamines.
Fatigue is a common symptom in MS patients, being present in about one-third of patients,2-4 and for many of them fatigue is the more disabling symptom.5. However, this high prevalence is influenced by the frequent occurrence in MS patients of motor problems, painful syndromes and mood abnormalities.6 Fatigue may occur at any stage of MS, even if it is more frequent and severe in primary and secondary progressive patients than in relapsing remitting patients.7,8 Occasionally, fatigue may be the onset symptom of MS and may occur weeks or months before the first attack. Fatigue may be a transient phenomenon, frequently associated with or preceding clinical relapses,9,10 or chronic, being present all the time. It is unclear whether transitory and chronic fatigue are different types of fatigue or if they share a common pathophysiology. There is no clear correlation between disability and fatigue in MS nevertheless, fatigue has a tremendous impact on the activities of daily living,...
Finally, oxidation of membrane lipids could cause membrane changes that affect Ca2+ movement. This idea is supported by the observation that muscle from patients with chronic fatigue syndrome is under oxidative stress. Muscle from these patients has altered membrane fluidity and fatty acid composition (Fulle et al, 2000 Fulle et al., 2003).
Chronic Fatigue Syndrome Solution Official Download Page
Chronic Fatigue Syndrome Solution will be instantly available for you to download right after your purchase. No shipping fees, no delays, no waiting to get started.