Weakness or asthenia is a symptom of a number of different conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis.

Muscle cells work by detecting a flow of electrical impulses from the brain, which signals them to contract through the release of calcium by the sarcoplasmic reticulum. Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This makes less calcium available for the muscle cell. In addition, the Columbia researchers propose that an enzyme activated by this released calcium eats away at muscle fibers.

Substrates within the muscle generally serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesn't actually cause the burning sensation we feel when we exhaust our oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver, which is known as the Cori cycle.

Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so.

Muscle weakness or myasthenia (my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness") is a lack of muscle strength. The causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Muscle weakness can also be caused by low levels of potassium and other electrolytes within muscle cells. It can be temporary or long-lasting (from seconds or minutes to months or years).

Muscle weakness can be classified as either "true" or "perceived" based on its cause.

- True muscle weakness (or neuromuscular weakness) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy.

- Perceived muscle weakness (or non-neuromuscular weakness) describes a condition where a person feels more effort than normal is required to exert a given amount of force but actual muscle strength is normal, for example chronic fatigue syndrome.

In some conditions, such as myasthenia gravis, muscle strength is normal when resting, but "true" weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions.

The exact mechanism in which these diseases cause cachexia is poorly understood, but there is probably a role for inflammatory cytokines, such as tumor necrosis factor-alpha (which is also nicknamed 'cachexin' or 'cachectin'), interferon gamma and interleukin 6, as well as the tumor-secreted proteolysis-inducing factor.

Related syndromes include kwashiorkor and marasmus, although these do not always have an underlying causative illness and are most often symptomatic of severe malnutrition.

Those suffering from the eating disorder anorexia nervosa appear to have high plasma levels of ghrelin. Ghrelin levels are also high in patients who have cancer-induced cachexia.

The World Health Organization classifies this condition as a somatoform autonomic dysfunction (a type of psychosomatic disorder) in their ICD-10 coding system. In their ICD-9 system, it was classified under non-psychotic mental disorders. The syndrome is also frequently interpreted as one of a number of imprecisely characterized "postwar syndromes".

There are many names for the syndrome, which has variously been called cardiac neurosis, chronic asthenia, effort syndrome, functional cardiovascular disease, neurocirculatory asthenia, primary neurasthenia, and subacute asthenia. Da Costa himself called it "irritable heart" and the term "soldier's heart" was in common use both before and after his paper. Most authors use these terms interchangeably, but some authors draw a distinction between the different manifestations of this condition, preferring to use different labels to highlight the predominance of psychiatric or non-psychiatric complaints. For example, Oglesby Paul writes that "Not all patients with neurocirculatory asthenia have a cardiac neurosis, and not all patients with cardiac neurosis have neurocirculatory asthenia." None of these terms have widespread use.

Although it is listed in the ICD-10 under "somatoform autonomic dysfunction", the term is no longer in common use by any medical agencies and has generally been superseded by more specific diagnoses.

The orthostatic intolerance observed by Da Costa has since also been found in patients diagnosed with chronic fatigue syndrome, postural orthostatic tachycardia syndrome (POTS) and mitral valve prolapse syndrome. In the 21st century, this intolerance is classified as a neurological condition. Exercise intolerance has since been found in many organic diseases.

Cachexia is often seen in end-stage cancer, and in that context is called "cancer cachexia". Patients with congestive heart failure can have a cachectic syndrome. Also, a cachexia comorbidity is seen in patients who have any of the range of illnesses classified as chronic obstructive pulmonary disease. Cachexia is also associated with advanced stages of chronic kidney disease, cystic fibrosis, multiple sclerosis, motor neuron disease, Parkinson's disease, dementia, HIV/AIDS and other progressive illnesses.

Hereditary motor and sensory neuropathy with proximal dominance (HMSN-P) is an autosomal dominant neurodegenerative disorder that is defined by extensive involuntary and spontaneous muscle contractions, asthenia, and atrophy with distal sensory involvement following. The disease starts presenting typically in the 40s and is succeeded by a slow and continuous onslaught. Muscle spasms and muscle contractions large in number are noted, especially in the earliest stages. The presentation of HMSN-P is quite similar to amyotrophic lateral sclerosis and has common neuropathological findings. Sensory loss happens as the disease progresses, but the amount of sensation lost varies from case to case. There have been other symptoms of HMSN-P reported such as urinary disturbances and a dry cough.

Two large families in Japan have been identified with the disease locus to chromosome 3q. From descendants of Japan, HMSN-P was brought to Brazil, from there it is a pretty isolated disease. Through clinical studies, researchers identified that TFG mutations on chromosome 3q13.2 causes HMSN-P. "The presence of TFG/ubiquitin- and/or TDP-43-immunopositive cytoplasmic inclusions in motor neurons and cytosolic aggregation composed of TDP-43 in cultured cells expressing mutant TFG indicate a novel pathway of motor neuron death"

Up to now, prevalence studies investigating rates of dysphonia on a large-scale level have been limited. According to a large sample of 55 million patients seeking health-care treatment in the United States, dysphonia can be found in approximately 1% of the population. Higher rates are reported in females and elderly adults, however, dysphonia can be found in both sexes and across age groups. It is proposed that higher rates in females are due to anatomical differences of the vocal mechanism.

Certain occupational groups may be more prone to developing voice disorders, namely dysphonia. Occupations that require extensive use of voice may be at a greater risk such as teachers and singers. However, the evidence is highly variable and must be interpreted carefully.

A variety of different cause, which result in abnormal vibrations of the vocal folds, can cause dysphonia. These causes can range from vocal abuse and misuse to systemic diseases. Causes of dysphonia can be divided into five basic categories, although overlap may occur between categories. (Note that this list is not exhaustive):

From 1869, neurasthenia became a "popular" diagnosis, expanding to include such symptoms as weakness, dizziness and fainting, and a common treatment was the rest cure, especially for women, who were the gender primarily diagnosed with this condition at that time. Recent analysis, however, of data from this period gleaned from the Annual Reports of Queen Square Hospital, London, indicates that the diagnosis was more evenly balanced between the sexes than is commonly thought. Virginia Woolf was known to have been forced to have rest cures, which she describes in her book "On Being Ill". Charlotte Perkins Gilman's protagonist in "The Yellow Wallpaper" also suffers under the auspices of rest cure doctors, much as Gilman herself did. Marcel Proust was said to suffer from neurasthenia. To capitalize on this epidemic, the Rexall drug company introduced a medication called 'Americanitis Elixir' which claimed to be a soother for any bouts related to Neurasthenia.

Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms. Myoclonus and seizures may be treated with drugs like valproate.

Some have described this condition as difficult to characterize.

The condition was explained as being a result of exhaustion of the central nervous system's energy reserves, which Beard attributed to modern civilization. Physicians in the Beard school of thought associated neurasthenia with the stresses of urbanization and with stress suffered as a result of the increasingly competitive business environment. Typically, it was associated with upper class people and with professionals working in sedentary occupations, but really can apply to anyone who lives within the monetary system.

Freud included a variety of physical symptoms in this category, including fatigue, dyspepsia with flatulence, and indications of intra-cranial pressure and spinal irritation. In common with some other people of the time, he believed this condition to be due to "non-completed coitus" or the non-completion of the higher cultural correlate thereof, or to "infrequency of emissions" or the infrequent practice of the higher cultural correlate thereof. Later, Freud formulated that in cases of coitus interruptus as well as in cases of masturbation, there was "an insufficient libidinal discharge" that had a poisoning effect on the organism, in other words, neurasthenia was the result of (auto-)intoxication. Eventually he separated it from anxiety neurosis, though he believed that a combination of the two conditions existed in many cases.

RHS type 1 is caused by the impairment of a regulatory mechanism between cerebellar and brainstem nuclei and has been associated with a wide range of diseases, including Lafora disease, dentatorubropallidoluysian atrophy, and celiac disease.

Many individuals have mild symptoms, which recur infrequently, while others may have persistent problems that become debilitating or life-threatening.

Psycho-organic syndrome is typically diagnosed in individuals following 5–10 years of consistent exposure to chemicals like xylene, toluene, and styrene, which are generally found in paint, plastic and degreasing products.

Patients work and environmental history must be evaluated for exposure to organic chemicals. A traumatic brain injury may also lead to POS.

Consistent intoxication (ie excess use of alcohol and drugs) may also cause a lesion in the brain, eventually leading to POS.

Lyme diseae, the great "new imitator", has been known to mimick depression, scizophreania, depersonazlization disorder, and obsessive-complsive disorder.

Although the cause varies by each individual case, localization of the atrophy in the brain can occur due to aging and without external causes, linked to hereditary.

Prevention includes proper and regular use of Preventive Personal Equipment (PPE) in work environments that involve organic chemicals and limiting alcohol and drug substance intake.

Relapsing polychondritis is an autoimmune disease in which the body's immune system begins to attack and destroy the cartilage tissues in the body. It has been postulated that both cell-mediated immunity and humoral immunity are responsible.

Reasons for disease onset are not known, but there is no evidence of a genetic predisposition to developing relapsing polychondritis. However, there are cases where multiple members of the same family have been diagnosed with this illness. Studies indicate that some genetic contribution to susceptibility is likely.

Psychoorganic syndrome is a combination of various symptoms that are caused by organic changes in the brain. The exact component of the solvents that causes the neurological disorder is difficult to isolate due to worker generally being exposed to mixtures of various grades, compositions, and purity of solvents.

At the initial stage, asthenia is prevalent and the progress of the disorder is slow. Acute onset can be diagnosed when a large amount of psychological symptoms surface. The final stage of the disorder is made up of numerous disorders, including demntia, Korsakov's syndrome, and includes severe personality change such as depression, anxiety, memory loss, and drastic change in intellect. Level of kindness, happiness, and insight are greatly affect in the final stage.

The disorder stems from a defect in brain tissue, usually atrophy from another neurological disorder." In pathological findings, focal or diffuse signs of atrophy without inflammation or severe vascular insufficiency are present. Basic clinical picture depends on the localization of atrophy in brain."Although the exact mechanism that solvents have on the nervous system are not fully understood, the metabolism of the solvents in the body that turn them into toxic intermediates are important. Some evidence shows that genetic polymorphisms affect the activity of metabolic enzymes that metabolize foreign chemicals.

The incidence of diarrhea with bicalutamide monotherapy in the trial was comparable to placebo (6.3% vs. 6.4%, respectively). In phase III studies of bicalutamide monotherapy for , the rates of diarrhea for bicalutamide and castration were 6.4% and 12.5%, respectively, the rates of constipation were 13.7% and 14.4%, respectively, and the rates of abdominal pain were 10.5% and 5.6%, respectively.

In the trial, at 7.4 years follow-up, the rate of hot flashes was 9.2% for bicalutamide relative to 5.4% for placebo, which was regarded as relatively low. In the subgroup of the trial, the rate of hot flashes with bicalutamide was 13.1% (relative to 50.0% for castration).

The treatment of nephrotic syndrome can be symptomatic or can directly address the injuries caused to the kidney.

The prognosis for nephrotic syndrome under treatment is generally good although this depends on the underlying cause, the age of the patient and their response to treatment. It is usually good in children, because minimal change disease responds very well to steroids and does not cause chronic renal failure. Any relapses that occur become less frequent over time; the opposite occurs with mesangiocapillary glomerulonephritis, in which the kidney fails within three years of the disease developing, making dialysis necessary and subsequent kidney transplant. In addition children under the age of 5 generally have a poorer prognosis than prepubescents, as do adults older than 30 years of age as they have a greater risk of kidney failure.

Other causes such as focal segmental glomerulosclerosis frequently lead to end stage renal disease. Factors associated with a poorer prognosis in these cases include level of proteinuria, blood pressure control and kidney function (GFR).

Without treatment nephrotic syndrome has a very bad prognosis especially "rapidly progressing glomerulonephritis", which leads to acute kidney failure after a few months.

Management of symptoms for patients within this subgroup of the GERD spectrum is difficult. Once these patients are identified, behavioural and dietary changes are advised. Dietary modifications may include limiting the intake of chocolate, caffeine, acidic food and liquids, gaseous beverages and foods high in fat. Behavioral changes may include weight loss, cessation of smoking, limiting alcohol consumption and avoiding the ingestion of food shortly before bed. Lifestyle changes in children diagnosed with LPR include dietary modifications to avoid foods that will aggravate reflux (e.g., chocolate or acidic and spicy food), altering positioning (e.g., sleeping on your side), modifying the textures of foods (e.g., thickening feeds to heighten awareness of the passing bolus), and eliminating the intake of food before bed.

Proton pump inhibitors (PPIs) are the leading pharmaceutical intervention chosen for the relief and reduction of LPR and are typically recommended for ongoing use twice a day for a period of 3–6 months. PPIs have been shown to be ineffective in very young children and are of uncertain efficacy in older children, for whom their use has been discouraged. While PPIs may provide limited clinical benefits in some adults, there is insufficient evidence to support routine use. Many studies show that PPIs are not more effective than placebos in treating LPR.

When medical management fails, Nissen fundoplication can be offered. However, patients should be advised that surgery may not result in complete elimination of LPR symptoms and even with immediate success, recurrence of symptoms later on is still possible.

One way to assess treatment outcomes for LPR is through the use of voice quality measures. Both subjective and objective measures of voice quality can be used to assess treatment outcomes. Subjective measures include scales such as the Grade, Roughness, Breathiness, Asthenia, Strain Scale (GRBAS); the Reflux Symptom Index; the Voice Handicap Index (VHI); and a voice symptom scale. Objective measures often rely on acoustic parameters such as jitter, shimmer, signal-to-noise ratio, and fundamental frequency, among others. Aerodynamic measures such as vital capacity and maximum phonation time (MPT) have also been used as an objective measure. However, there is not yet a consensus on how best to use the measures or which measures are best to assess treatment outcomes for LPR.

LPR is often regarded as a subtype of GERD that occurs when stomach contents flow upward through the esophagus and reach the level of the larynx and pharynx. However, LPR is associated with a distinct presentation of symptoms. LPR and GERD frequently differ in the relative prevalence of heartburn and throat clearing. While heartburn is present in over 80% of GERD cases, it occurs in only 20% of LPR cases. Throat clearing shows the opposite prevalence pattern, occurring in approximately 87% of LPR cases and in fewer than 5% of GERD cases. Unlike GERD, LPR also poses a risk for bronchitis or pneumonitis as reflux of stomach acid to the level of the larynx can result in aspiration. LPR is also commonly associated with erythema, or redness, as well as edema in the tissues of the larynx that are exposed to gastric contents. In contrast, most cases of GERD are nonerosive, with no apparent injury to the mucosal lining of the esophageal tissue exposed to the refluxed material.

Differences in the molecular structure of the epithelial tissue lining the laryngopharyngeal region may be partly responsible for the different symptomatic manifestations of LPR in comparison to GERD. In contrast to the resistant stratified squamous epithelium lining the esophagus, the larynx is lined by ciliated respiratory epithelium, which is more fragile and susceptible to damage. While the epithelium lining the esophagus is capable of withstanding as many as 50 instances of exposure to gastric contents each day, which is the uppermost estimate considered to be within the range of normal physiologic functioning, injury to laryngeal epithelium can occur following exposure to only small amounts of acidic gastric contents.