Ataxia in the context of "Huntington's disease"

Alcohol intoxication, commonly described in higher doses as drunkenness or inebriation, and known in overdose as alcohol poisoning, is the behavior and physical effects caused by recent consumption of alcohol. The technical term intoxication in common speech may suggest that a large amount of alcohol has been consumed, leading to accompanying physical symptoms and deleterious health effects. Mild intoxication is mostly referred to by slang terms such as tipsy or buzzed. In addition to the toxicity of ethanol, the main psychoactive component of alcoholic beverages, other physiological symptoms may arise from the activity of acetaldehyde, a metabolite of alcohol. These effects may not arise until hours after ingestion and may contribute to a condition colloquially known as a hangover.

Symptoms of intoxication at lower doses may include mild sedation and poor coordination. At higher doses, there may be slurred speech, trouble walking, impaired vision, mood swings and vomiting. Extreme doses may result in a respiratory depression, coma, or death. Complications may include seizures, aspiration pneumonia, low blood sugar, and injuries or self-harm such as suicide. Alcohol intoxication can lead to alcohol-related crime, with perpetrators more likely to be intoxicated than victims.

Wernicke–Korsakoff syndrome (WKS), colloquially referred to as wet brain syndrome, is the combined presence of Wernicke encephalopathy (WE) and Korsakoff syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome. It mainly causes vision changes, ataxia and impaired memory.

The cause of the disorder is thiamine (vitamin B₁) deficiency. This can occur due to eating disorders, malnutrition, and alcohol abuse. These disorders may manifest together or separately. WKS is usually secondary to prolonged alcohol abuse.

Multiple system atrophy (MSA) is a rare neurodegenerative disorder characterized by tremors, slow movement, muscle rigidity, postural instability (collectively known as parkinsonism), autonomic dysfunction and ataxia. This is caused by progressive degeneration of neurons in several parts of the brain including the basal ganglia, inferior olivary nucleus, and cerebellum. MSA was first described in 1960 by Milton Shy and Glen Drager and was then known as Shy–Drager syndrome.

Many people affected by MSA experience dysfunction of the autonomic nervous system, which commonly manifests as orthostatic hypotension, impotence, loss of sweating, dry mouth and urinary retention and incontinence. Palsy of the vocal cords is an important and sometimes initial clinical manifestation of the disorder.

Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a group of progressive, incurable, and invariably fatal conditions that are associated with the degeneration of the nervous system in many animals, including humans, cattle, and sheep. Strong evidence supports the once unorthodox hypothesis that prion diseases are transmitted by abnormally shaped protein molecules known as prions. Prions consist of a protein called the prion protein (PrP). Misshapen PrP (often referred to as PrP) conveys its abnormal structure to naive PrP molecules by a crystallization-like seeding process. Because the abnormal proteins stick to each other, and because PrP is continuously produced by cells, PrP accumulates in the brain, harming neurons and eventually causing clinical disease.

Prion diseases are marked by mental and physical deterioration that worsens over time. A defining pathologic characteristic of prion diseases is the appearance of small vacuoles in various parts of the central nervous system that create a sponge-like appearance when brain tissue obtained at autopsy is examined under a microscope. Other changes in affected regions include the buildup of PrP, gliosis, and the loss of neurons.

Minamata disease (Japanese: 水俣病, Hepburn: Minamata-byō) is a neurological disease caused by severe mercury poisoning. Signs and symptoms include ataxia, numbness in the hands and feet, general muscle weakness, loss of peripheral vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A congenital form of the disease affects fetuses, causing microcephaly, extensive cerebral damage, and symptoms similar to those seen in cerebral palsy.

Minamata disease was first discovered in the city of Minamata, Kumamoto Prefecture, Japan, in 1956. It was caused by the release of methylmercury in the industrial wastewater from a chemical factory owned by the Chisso Corporation, which continued from 1932 to 1968. It has also been suggested that some of the mercury sulfate in the wastewater was also metabolized to methylmercury by bacteria in the sediment. This highly toxic chemical bioaccumulated and biomagnified in shellfish and fish in Minamata Bay and the Shiranui Sea, which, when eaten by the local population, resulted in mercury poisoning. The poisoning and resulting deaths of both humans and animals continued for 36 years, while Chisso and the Kumamoto prefectural government did little to prevent the epidemic. The animal effects were severe enough in cats that they came to be named as having "dancing cat fever."

Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a group of progressive, incurable, and invariably fatal conditions that are associated with the degeneration of the nervous system in many animals, including humans, cattle, and sheep. Strong evidence supports the once unorthodox hypothesis that prion diseases are transmitted by abnormally shaped protein molecules known as prions. Prions consist of a protein called the prion protein (PrP). Misshapen PrP (often referred to as PrP) conveys its abnormal structure to native PrP molecules by a crystallization-like seeding process. Because the abnormal proteins stick to each other, and because PrP is continuously produced by cells, PrP accumulates in the brain, harming neurons and eventually causing clinical disease.

Prion diseases are marked by mental and physical deterioration that worsens over time. A defining pathologic characteristic of prion diseases is the appearance of small vacuoles in various parts of the central nervous system that create a sponge-like appearance when brain tissue obtained at autopsy is examined under a microscope. Other changes in affected regions include the buildup of PrP, gliosis, and the loss of neurons.