Asthenia (Greek: "ἀσθένεια", lit "lack of strength" but also "disease") is a medical term referring to a condition in which the body lacks or has lost strength either as a whole or in any of its parts. It denotes symptoms of physical weakness and loss of strength. General asthenia occurs in many chronic wasting diseases (such as tuberculosis and cancer), sleep disorders or chronic disorders of the heart, lungs or kidneys, and is probably most marked in diseases of the adrenal gland. Asthenia may be limited to certain organs or systems of organs, as in asthenopia, characterized by ready fatiguability. Asthenia is also a side effect of some medications and treatments, such as Ritonavir (a protease inhibitor used in HIV treatment), vaccines such as the HPV vaccine Gardasil and fentanyl patches (an opioid used to treat pain).

Differentiating psychogenic (perceived) asthenia and true asthenia from myasthenia is often difficult, and in time apparent psychogenic asthenia accompanying many chronic disorders is seen to progress into a primary weakness.

Myasthenia (my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness"), or simply muscle 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 diseases, such as myasthenia gravis.

Muscle fatigue can be central, neuromuscular, or peripheral muscular. Central muscle fatigue manifests as an overall sense of energy deprivation, and peripheral muscle weakness manifests as a local, muscle-specific inability to do work. Neuromuscular fatigue can be either central or peripheral.

Muscle weakness can also be classified as either "proximal" or "distal" based on the location of the muscles that it affects. Proximal muscle weakness affects muscles closest to the body's midline, while distal muscle weakness affects muscles further out on the limbs.

Proximal muscle weakness can be seen in Cushing's syndrome and hyperthyroidism.

The severity of muscle weakness can be classified into different "grades" based on the following criteria:

- Grade 0: No contraction or muscle movement.

- Grade 1: Trace of contraction, but no movement at the joint.

- Grade 2: Movement at the joint with gravity eliminated.

- Grade 3: Movement against gravity, but not against added resistance.

- Grade 4: Movement against external resistance with less strength than usual.

- Grade 5: Normal strength.

Symptoms of Da Costa's syndrome include fatigue upon exertion, shortness of breath, palpitations, sweating, and chest pain. Physical examination reveals no physical abnormalities causing the symptoms.

Da Costa's syndrome is generally considered a physical manifestation of an anxiety disorder.

About 50% of all cancer patients suffer from cachexia. Those with upper gastrointestinal and pancreatic cancers have the highest frequency of developing a cachexic symptom. This figure rises to 80% in terminal cancer patients. In addition to increasing morbidity and mortality, aggravating the side effects of chemotherapy, and reducing quality of life, cachexia is considered the immediate cause of death of a large proportion of cancer patients, ranging from 22% to 40% of the patients.

Symptoms of cancer cachexia include progressive weight loss and depletion of host reserves of adipose tissue and skeletal muscle. Cachexia should be suspected if involuntary weight loss of greater than 5% of premorbid weight occurs within a six-month period. Traditional treatment approaches, such as appetite stimulants, 5-HT antagonists, nutrient supplementation, and COX-2 inhibitor, have failed to demonstrate success in reversing the metabolic abnormalities seen in cancer cachexia.

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"

Dysphonia is a broad clinical term which refers to abnormal functioning of the voice. More specifically, a voice can be classified as “dysphonic” when there are abnormalities or impairments in one or more of the following parameters of voice: pitch, loudness, quality, and variability. For example, abnormal pitch can be characterized by a voice that is too high or low whereas abnormal loudness can be characterized by a voice that is too weak or loud. Similarly, a voice that has frequent, inappropriate breaks characterizes abnormal quality while a voice that is monotone (i.e., very flat) or inappropriately fluctuates characterizes abnormal variability. While hoarseness is used interchangeably with the term dysphonia, it is important to note that the two are not synonymous. Hoarseness is merely a subjective term to explain the perceptual quality (or sound) of a dysphonic voice. While hoarseness is a common symptom (or complaint) of dysphonia, there are several other signs and symptoms that can be present such as: breathiness, roughness, and dryness. Furthermore, a voice can be classified as dysphonic when it poses problems in the functional or occupational needs of the individual or is inappropriate for their age or sex.

Voice disorders can be divided into 2 broad categories: organic and functional. The distinction between these broad classes stems from their cause, whereby organic dysphonia results from some sort of physiological change in one of the subsystems of speech (for voice, usually respiration, laryngeal anatomy, and/or other parts of the vocal tract are affected). Conversely, functional dysphonia refers to hoarseness resulting from vocal use (i.e. overuse/abuse). Furthermore, according to ASHA, organic dysphonia can be subdivided into structural and neurogenic; neurogenic dysphonia is defined as impacted functioning of the vocal structure due to a neurological problem (in the central nervous system or peripheral nervous system); in contrast, structural dysphonia is defined as impacted functioning of the vocal mechanism that is caused by some sort of physical change (e.g. a lesion on the vocal folds). Notably, an additional subcategory of functional dysphonia recognized by professionals is psychogenic dysphonia, which can be defined as a type of voice disorder that has no known cause and can be presumed to be a product of some sort of psychological stressors in one’s environment. It is important to note that these types are not mutually exclusive and much overlap occurs. For example, Muscle Tension Dysphonia (MTD) has been found to be a result of many different causes including the following: MTD in the presence of an organic pathology (i.e. organic type), MTD stemming from vocal use (i.e. functional type), and MTD as a result of personality and/or psychological factors (i.e. psychogenic type).

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.

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.

Onset of symptoms usually occur in early adulthood and is characterized by intention tremor, progressive ataxia, convulsions, and myoclonic epileptic jerks.

Tremors usually affect one extremity, primarily the upper limb, and eventually involve the entire voluntary motor system. Overall, the lower extremity is usually disturbed less often than the upper extremity.

Additional features of the syndrome include: an unsteady gait, seizures, muscular hypotonia, reduced muscular coordination, asthenia, adiadochokinesia and errors with estimating range, direction, and force of voluntary movements. Mental deterioration can occur, however it is rare.

Ramsay Hunt syndrome (RHS) type 1 is a rare, degenerative, neurological disorder characterized by myoclonus epilepsy, intention tremor, progressive ataxia and occasionally cognitive impairment

It has also been alternatively called "dyssynergia cerebellaris myoclonica", "dyssynergia cerebellaris progressiva", dentatorubral degeneration, or Ramsay Hunt cerebellar syndrome.

Inflammation occurs in the laryngeal, tracheal and bronchial cartilages. Both of these sites are involved in 10% of persons with RP at presentation and 50% over the course of this autoimmune disease, and is more common among females.

The involvement of the laryngotracheobronchial cartilages may be severe and life-threatening; it causes one-third of all deaths among persons with RP.

Laryngeal chondritis is manifested as pain above the thyroid gland and, more importantly, as dysphonia with a hoarse voice or transient aphonia. Because this disease is relapsing, recurrent laryngeal inflammation may result in laryngomalacia or permanent laryngeal stenosis with inspiratory dyspnea that may require emergency tracheotomy as a temporary or permanent measure.

Tracheobronchial involvement may or may not be accompanied with laryngeal chondritis and is potentially the most severe manifestation of RP.

The symptoms consist of dyspnea, wheezing, a nonproductive cough, and recurrent, sometimes severe, lower respiratory tract infections.

Obstructive respiratory failure may develop as the result of either permanent tracheal or bronchial narrowing or chondromalacia with expiratory collapse of the tracheobronchial tree. Endoscopy, intubation, or tracheotomy has been shown to hasten death.

Involvement of the rib cartilages results in costochondritis. Symptoms include chest wall pain or, less often, swelling of the involved cartilage. The involvement of the ribs is seen in 35% of persons with RP but is rarely the first symptom.

Patients with psychoorganic syndrome often complain about headaches, dizziness, unsteadiness when walking, poor tolerance to the heat, stuffiness, atmospheric pressure changes, loud sounds, neurological symptoms.

The common reported psychological symptoms include:

- loss of memory and concentration

- emotional liability

- Clinical fatigue

- long term major depression

- severe anxiety

- reduced intellectual ability

The cognitive and behavioral symptoms are chronic and have little response to treatment.

Depending on lesion location, some patients may experience visual complications.

Psychoorganic syndrome (POS) is a progressive disease comparable to presenile dementia. It consists of psychopathological complex of symptoms that are caused by organic brain disorders that involve a reduction in memory and intellect. Psychoorganic syndrome is often accompanied by asthenia.

Psychoorganic syndrome occurs during atrophy of the brain, most commonly during presenile and senile age (e.g. Alzheimer's disease, senile dementia). There are many causes, including cerebrovascular diseases, CNS damages to traumatic brain injury, intoxication, exposure to organic solvents such as toluene, chronic metabolic disorders, tumors and abscesses of the brain, encephalitis, and can also be found in cases of diseases accompanied by convulsive seizures. Psychoorganic syndrome may occur at any age but is most pronounced in elderly and senile age.

Depending on the nosological entity, the main symptoms of psychoorganic syndrome are expressed differently. For example, in atrophic cases such as Alzheimer's disease, the symptoms are more geared towards a memory disorder, while in Pick 's disease, mental disorders are more commonly expressed.

Extraesophageal symptoms result from exposure of the upper aerodigestive tract to gastric contents. This causes a variety of symptoms, including hoarseness, postnasal drip, sore throat, difficulty swallowing, indigestion, chronic cough, wheezing, globus pharyngeus, and chronic throat-clearing. Some people with LPR have heartburn, while others have little to no heartburn as refluxed stomach contents do not remain in the esophagus long enough to irritate the surrounding tissue. Individuals with more severe forms of LPR may experience abrasion of tooth enamel due to intermittent presence of gastric contents in the oral cavity.

Additionally, LPR can cause inflammation in the vocal tract which results in the symptom of dysphonia or hoarseness. Hoarseness is considered to be one of the primary symptoms of LPR and is associated with complaints such as strain, vocal fatigue, muskuloskeletal tension, and hard glottal attacks, all of which can reduce a person's ability to communicate effectively. Moreover, LPR patients may try to compensate for their hoarseness by increasing muscular tension in their vocal tract. This hyper-functional technique adopted in response to the inflammation caused by LPR can lead to a condition called muscle tension dysphonia and may persist even after the hoarseness and inflammation has disappeared. A speech-language pathologist will often need to be involved to help resolve this maladaptive, compensatory pattern through the implementation of voice therapy.

LPR presents as a chronic and intermittent disease in children. LPR in children and infants tends to manifest with a unique set of symptoms. Symptoms seen in children with LPR include a cough, hoarseness, stridor, sore throat, asthma, vomiting, globus sensation, wheezing, aspiration and recurrent pneumonia. Common symptoms of LPR in infants include wheezing, stridor, persistent or recurrent cough, apnea, feeding difficulties, aspiration, regurgitation, and failure to thrive. Moreover, LPR in children is commonly concomitant with laryngeal disorders such as laryngomalacia, subglottic stenosis, and laryngeal papillomatosis.

This article is about the side effect profile of bicalutamide, a nonsteroidal antiandrogen (NSAA), including its frequent and rare side effects.

Laryngopharyngeal reflux (LPR), also known as extraesophageal reflux disease (EERD),silent reflux, and supra-esophageal reflux, is the retrograde flow of gastric contents into the larynx, oropharynx and/or the nasopharynx. LPR causes respiratory symptoms such as cough and wheezing and is often associated with head and neck complaints such as dysphonia, globus pharyngeus, and dysphagia. LPR may play a role in other diseases such as sinusitis, otitis media, and rhinitis, and can be a comorbidity of asthma. While LPR is commonly used interchangeably with gastroesophageal reflux disease (GERD), it presents with a different pathophysiology.

LPR reportedly affects approximately 30% of the U.S. population. However, LPR occurs in as many as 50% of individuals with voice disorders.

Some symptoms that are present in nephrotic syndrome, such as edema and proteinuria, also appear in other illnesses. Therefore, other pathologies need to be excluded in order to arrive at a definitive diagnosis.

- Edema: in addition to nephrotic syndrome there are two other disorders that often present with edema; these are heart failure and liver failure. Congestive heart failure can cause liquid retention in tissues as a consequence of the decrease in the strength of ventricular contractions. The liquid is initially concentrated in the ankles but it subsequently becomes generalized and is called anasarca. Patients with congestive heart failure also experience an abnormal swelling of the heart cardiomegaly, which aids in making a correct diagnosis. Jugular venous pressure can also be elevated and it might be possible to hear heart murmurs. An echocardiogram is the preferred investigation method for these symptoms. Liver failure caused by cirrhosis, hepatitis and other conditions such as alcoholism, IV drug use or some hereditary diseases can lead to swelling in the lower extremities and the abdominal cavity. Other accompanying symptoms include jaundice, dilated veins over umbilicus (caput medusae), scratch marks (due to widespread itching, known as pruritus), enlarged spleen, spider angiomata, encephalopathy, bruising, nodular liver and anomalies in the liver function tests. Less frequently symptoms associated with the administration of certain pharmaceutical drugs have to be discounted. These drugs promote the retention of liquid in the extremities such as occurs with NSAIs, some antihypertensive drugs, the adrenal corticosteroids and sex hormones.

Acute fluid overload can cause edema in someone with kidney failure. These people are known to have kidney failure, and have either drunk too much or missed their dialysis. In addition, when Metastatic cancer spreads to the lungs or abdomen it causes effusions and fluid accumulation due to obstruction of lymphatic vessels and veins, as well as serous exudation.

- Proteinuria: the loss of proteins from the urine is caused by many pathological agents and infection by these agents has to be ruled out before it can be certain that a patient has nephrotic syndrome. Multiple myeloma can cause a proteinuria that is not accompanied by hypoalbuminemia, which is an important aid in making a differential diagnosis; other potential causes of proteinuria include asthenia, weight loss or bone pain. In diabetes mellitus there is an association between increases in glycated hemoglobin levels and the appearance of proteinuria. Other causes are amyloidosis and certain other allergic and infectious diseases.

Patients typically have no symptoms until the third or fourth decade of life. In most cases, the disease is discovered incidentally on routine chest Xray. The most common symptoms include the following:

- dyspnea

- dry cough

- chest pain

- sporadic hemoptysis

- asthenia

- pneumothoraces

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.