Peripheral neuropathy may first be considered when an individual reports symptoms of numbness, tingling, and pain in feet. After ruling out a lesion in the central nervous system as a cause, diagnosis may be made on the basis of symptoms, laboratory and additional testing, clinical history, and a detailed examination.

During physical examination, specifically a neurological examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, although those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies, such as Guillain–Barré syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Classically, ankle jerk reflex is absent in peripheral neuropathy.

A physical examination will involve testing the deep ankle reflex as well as examining the feet for any ulceration. For large fiber neuropathy, an exam will usually show an abnormally decreased sensation to vibration, which is tested with a 128-Hz tuning fork, and decreased sensation of light touch when touched by a nylon monofilament.

Diagnostic tests include electromyography (EMG) and nerve conduction studies (NCSs), which assess large myelinated nerve fibers. Testing for small-fiber peripheral neuropathies often relates to the autonomic nervous system function of small thinly- and unmyelinated fibers. These tests include a sweat test and a tilt table test. Diagnosis of small fiber involvement in peripheral neuropathy may also involve a skin biopsy in which a 3 mm-thick section of skin is removed from the calf by a punch biopsy, and is used to measure the skin intraepidermal nerve fiber density (IENFD), the density of nerves in the outer layer of the skin. Reduced density of the small nerves in the epidermis supports a diagnosis of small-fiber peripheral neuropathy.

Laboratory tests include blood tests for vitamin B-12 levels, a complete blood count, measurement of thyroid stimulating hormone levels, a comprehensive metabolic panel screening for diabetes and pre-diabetes, and a serum immunofixation test, which tests for antibodies in the blood.

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.

Prevention of the condition requires restoration of blood flow after injury and reduction of compartmental pressure on the muscles. Any splints, bandages, or other devices that might be obstructing circulation must be removed. A fasciotomy may be required to reduce pressure in the muscle compartment. If the contracture occurs, surgery to release the fixed tissues may help with the deformity and function of the hand.

While inclusion criteria for Rud syndrome have varied considerably, the major manifestations includes congenital ichthyosis, hypogonadism, small stature, mental retardation, and epilepsy. Ocular findings were inconsistently reported and included strabismus, blepharoptosis, blepharospasm, glaucoma, cataract, nystagmus, and retinitis pigmentosa. Other systemic includes metabolic, bony, neurologic, and muscular abnormalities.

Rud syndrome is a poorly characterized disorder, probably of X-linked recessive inheritance, named after Einar Rud who described 2 patients with the case in 1927 and 1929. It was argued that all reported cases of Rud syndrome are genetically heterogeneous and significantly differ from the original case reports of Rud and that the designation Rud syndrome should be eliminated and that the patients with such diagnosis should be reassigned to other syndromes, such as Refsum disease and Sjögren-Larsson syndrome.Some consider Rud syndrome and Sjögren-Larsson syndrome the same entity and that Rud syndrome doesn't exist.

In "Acanthamoeba" infections, the diagnosis can be made from microscopic examination of stained smears of biopsy specimens (brain tissue, skin, cornea) or of corneal scrapings, which may detect trophozoites and cysts. Cultivation of the causal organism, and its identification by direct immunofluorescent antibody, may also prove useful. Laboratory workers and physicians often mistake the organisms on wet mount for monocytes and a diagnosis of viral meningitis is mistakenly given if the organisms are not motile. Heating a copper penny with an alcohol lamp and placing it on the wet mount slide will activate sluggish trophozoites and more rapidly make the diagnosis. If the person performing the spinal tap rapidly looks at the heated wet mount slide the trophozoites can be seen to swarm while monocytes do not.

The CDC states that PCR testing from a single blood draw is not sufficiently sensitive for "B." "henselae" testing, and can result in high false negative rates due to a small sample volume and levels below the limit of molecular detection.

"Bartonella" spp. are fastidious, slow-growing bacteria that are difficult to grow using traditional solid agar plate culture methods due to complex nutritional requirements and potentially a low number of circulating bacteria. This conventional method of culturing "Bartonella" spp. from blood inoculates plated directly onto solid agar plates requires an extended incubation period of 21 days due to the slow growth rate.

There is no known cure at the moment but there are several things that can be done to relieve the symptoms. Moisturising products are very helpful to minimize the scaling/cracking, and anti-infective treatments are useful when appropriate because the skin is very susceptible to infection. Extra protein in the diet during childhood is also beneficial, to replace that which is lost through the previously mentioned "leaky" skin.

Steroid and retinoid products have been proven ineffective against Netherton syndrome, and may in fact make things worse for the affected individual.

Intravenous immunoglobulin has become established as the treatment of choice in Netherton's syndrome. This therapy reduces infection; enables improvement and even resolution of the skin and hair abnormalities, and dramatically improves quality of life of the patients; although exactly how it achieves this is not known. Given this; it is possible that the reason Netherton's usually is not very severe at or shortly after birth is due to a protective effect of maternal antibodies; which cross the placenta but wane by four to six months.

There have been cases of improvement in extra-ocular movement with botulinum toxin injection.

Causes of the one and a half syndrome include pontine hemorrhage, ischemia, tumors, infective mass lesions such as tuberculomas, and demyelinating conditions like multiple sclerosis.

"Bartonella" growth rates improve when cultured in an enrichment inoculation step in a liquid insect-based medium such as "Bartonella" α-Proteobacteria Growth Medium (BAPGM) or Schneider’s Drosophila-based insect powder medium. Several studies have optimized the growing conditions of "Bartonella" spp. cultures in these liquid media, with no change in bacterial protein expressions or host interactions "in vitro". Insect-based liquid media supports the growth and co-culturing of at least seven "Bartonella" species, reduces bacterial culturing time and facilitates PCR detection and isolation of "Bartonella" spp. from animal and patient samples. Research shows that DNA may be detected following direct extraction from blood samples and become negative following enrichment culture, thus PCR is recommended after direct sample extraction and also following incubation in enrichment culture. Several studies have successfully optimized sensitivity and specificity by using PCR amplification (pre-enrichment PCR) and enrichment culturing of blood draw samples, followed by PCR (post-enrichment PCR) and DNA sequence identification.

Diagnosis of subacute bacterial endocarditis can be done by collecting three blood culture specimens over a 24-hour period for analysis, also it can usually be indicated by the existence of:

- Osler's nodes

- Roth's spots

- Nail clubbing

Diagnosis of Wernicke–Korsakoff syndrome is by clinical impression and can sometimes be confirmed by a formal neuropsychological assessment. Wernicke's encephalopathy typically presents with ataxia and nystagmus, and Korsakoff's psychosis with anterograde and retrograde amnesia and confabulation upon relevant lines of questioning.

Frequently, secondary to thiamine deficiency and subsequent cytotoxic edema in Wernicke's encephalopathy, patients will have marked degeneration of the mamillary bodies. Thiamine (vitamin B) is an essential coenzyme in carbohydrate metabolism and is also a regulator of osmotic gradient. Its deficiency may cause swelling of the intracellular space and local disruption of the blood-brain barrier. Brain tissue is very sensitive to changes in electrolytes and pressure and edema can be cytotoxic. In Wernicke's this occurs specifically in the mammillary bodies, medial thalami, tectal plate, and periaqueductal areas. Sufferers may also exhibit a dislike for sunlight and so may wish to stay indoors with the lights off. The mechanism of this degeneration is unknown, but it supports the current neurological theory that the mammillary bodies play a role in various "memory circuits" within the brain. An example of a memory circuit is the Papez circuit.

Eye and skin infections caused by "Acanthamoeba spp." are generally treatable. Topical use of 0.1% propamidine isethionate (Brolene) plus neomycin-polymyxin B-gramicidin ophthalmic solution has been a successful approach; keratoplasty is often necessary in severe infections. Although most cases of brain (CNS) infection with "Acanthamoeba" have resulted in death, patients have recovered from the infection with proper treatment.

As described, Korsakoff 's syndrome usually follows or accompanies Wernicke's encephalopathy. If treated quickly, it may be possible to prevent the development of Korsakoff's syndrome with thiamine treatments. This treatment is not guaranteed to be effective and the thiamine needs to be administered adequately in both dose and duration. A study on Wernicke-Korsakoff's syndrome showed that with consistent thiamine treatment there were noticeable improvements in mental status after only 2–3 weeks of therapy. Thus, there is hope that with treatment Wernicke's encephalopathy will not necessarily progress to WKS.

In order to reduce the risk of developing WKS it is important to limit the intake of alcohol or drink in order to ensure that proper nutrition needs are met. A healthy diet is imperative for proper nutrition which, in combination with thiamine supplements, may reduce the chance of developing WKS. This prevention method may specifically help heavy drinkers who refuse to or are unable to quit.

Women with a lifelong epileptic history are also liable to psychoses during labour in the puerperium. Women occasionally develop epilepsy for the first time in relation to their first pregnancy, and psychotic episodes have been described.

Very few risk factors for choanal atresia have been identified. While causes are unknown, both genetic and environmental triggers are suspected. One study suggests that chemicals that act as endocrine disrupters may put an unborn infant at risk. A 2012 epidemiological study looked at atrazine, a commonly used herbicide in the U.S., and found that women who lived in counties in Texas with the highest levels of this chemical being used to treat agricultural crops were 80 times more likely to give birth to infants with choanal atresia or stenosis compared to women who lived in the counties with the lowest levels. Another epidemiological report in 2010 found even higher associations between increased incidents of choanal atresia and exposure to second-hand-smoke, coffee consumption, high maternal zinc and B-12 intake and exposure to anti-infective urinary tract medications.

In medicine, a prodrome is an early sign or symptom (or set of signs and symptoms), which often indicate the onset of a disease before more diagnostically specific signs and symptoms develop. It is derived from the Greek word "prodromos", meaning "running before". Prodromes may be non-specific symptoms or, in a few instances, may clearly indicate a particular disease, such as the prodromal migraine aura.

For example, fever, malaise, headache and lack of appetite frequently occur in the prodrome of many infective disorders. A prodrome can be the early precursor to an episode of a chronic neurological disorder such as a migraine headache or an epileptic seizure, where prodrome symptoms may include euphoria or other changes in mood, insomnia, abdominal sensations, disorientation, aphasia, or photosensitivity. Such a prodrome occurs on a scale of days to an hour before the episode, where an aura occurs more immediate to it.

Prodromal labour, mistakenly called "false labour," refers to the early signs before labour starts.

A prodrome for schizophrenia is the period of decreased cognitive functioning that is postulated to correlate with the onset of psychotic symptoms. The concept has been reconsidered as the pathways to emerging psychosis have been investigated since the mid-1990s. One example of the international paradigms aimed at researching the prodrome is the North American Prodrome Longitudinal Study (NAPLS). This study is concerned with brain development, hormones, and neuropsychological functions that may play a role in risk for and prevention of mental illness in young adulthood. The term at risk mental state is sometimes preferred, as a prodromal period cannot be confirmed unless the emergence of the condition has occurred. (Also see early psychosis.)

Prodrome, or psychosis risk syndrome as it is also known, is a proposed syndrome to be used in the "DSM-5" (2013) of psychiatry. It is also defined as "the aura that precedes a psychotic break by up to two or three years." Patients with this condition "still have 'insight' – a pivotal word in psychiatric literature, indicating that a patient can still recognize an altered worldview as a sign of illness, and not a revelation." Prodrome is also sometimes called "attenuated psychotic symptoms syndrome." Chairman of the DSM-IV Task Force, Allen Frances, has criticised the concept of Psychosis Risk Syndrome on the grounds of a high rate of inaccuracy, the potential to stigmatize young people given this label, the lack of any effective treatment, and the risk of children and adolescents being given dangerous antipsychotic medication.

About one third of patients with prodrome are diagnosed with schizophrenia or other psychosis in a few years. In the North American Prodrome Longitudinal Study, researchers found that 35 percent of "patients had a psychotic break within two and a half years of enrolling at a clinic." 65 percent "found that their symptoms passed or plateaued." A psychotic break is made statistically more likely (43% vs. 35%) if the patient abuses certain drugs.

It is named after Richard von Volkmann (1830 - 1889), the 19th century German doctor who first described it, in a paper on ""non-Infective Ischemic conditions of various fascial compartments in the extremities"". Because the contracture occurred at the same time as the paralysis, he considered a nerve cause to be unlikely.

The standard treatment is with a minimum of four weeks of high-dose intravenous penicillin with an aminoglycoside such as gentamicin.

The use of high-dose antibiotics is largely based upon animal models.

Leo Loewe of Brooklyn Jewish Hospital was the first to successfully treat subacute bacterial endocarditis with penicillin. Loewe reported at the time seven cases of subacute bacterial endocarditis in 1944.

Psychiatric disorders of childbirth are mental disorders developed by the mother related to the delivery process itself. They overlap with the Organic prepartum and postpartum psychoses and other psychiatric conditions associated with having children. ; symptoms include rage, or in rare cases, neonaticide.

There are many distinct forms of psychosis which start during pregnancy (prepartum) or after delivery (postpartum). In Europe and North America, only one – polymorphic psychosis (postpartum psychosis)– is commonly seen. Postpartum bipolar disorder, referred to in the DSM-5 as bipolar, peripartum onset, is a separate condition with no psychotic features. Historically, about one quarter of psychoses after childbirth were 'organic' and would now be classified as a form of delirium. This means that a severe mental disturbance, usually in the form of delirium, develops as a complication of a somatic illness.

Splenic infarction can be induced for the treatment of such conditions as portal hypertension or splenic injury. It can also be used prior to splenectomy for the prevention of blood loss.

The condition may be a sign of various disease states, including but not exclusive to the following:

- Cancers

- Lymphoma

- Leukemia

- Infections

- HIV/AIDS

- Tuberculosis

- Mycobacterium avium-intracellulare infection

- Infectious mononucleosis

- Fungal infections (histoplasmosis, coccidioidomycosis)

- Lung abscess

- Infective endocarditis

- Brucellosis

- Pneumocystis pneumonia (most often - in immunocompromised individuals)

- Endocrine disorders

- Menopause

- Premature ovarian failure

- Hyperthyroidism

- Diabetes mellitus (nocturnal hypoglycemia)

- Endocrine tumors (pheochromocytoma, carcinoid)

- Orchiectomy

- Rheumatic disorders

- Takayasu's arteritis

- Temporal arteritis

- Other

- Obstructive sleep apnea

- Gastroesophageal reflux disease

- Chronic fatigue syndrome

- Fibromyalgia

- Granulomatous disease

- Chronic eosinophilic pneumonia

- Lymphoid hyperplasia

- Diabetes insipidus

- Prinzmetal's angina

- Anxiety

- Pregnancy

- Drugs

- Antipyretics (salicylates, acetaminophen)

- Antihypertensives

- Dinitrophenol - a common side effect

- Phenothiazines

- Drug withdrawal: ethanol, benzodiazepines, heroin (and other opiates),

- Over-bundling

- Autonomic over-activity

- IBD (inflammatory bowel disease) - Crohn's disease/ulcerative colitis

It is normally possible to establish the cause of ear pain based on the history. It is important to exclude cancer where appropriate, particularly with unilateral otalgia in an adult who uses tobacco or alcohol.Often migraines are caused by middle ear infections which can easily be treated with antibiotics. Often using a hot washcloth can temporarily relieve ear pain.