| Ataxia spinipennis | |
|---|---|
Scientific classification  | |
| Domain: | Eukaryota |
| Kingdom: | Animalia |
| Phylum: | Arthropoda |
| Class: | Insecta |
| Order: | Coleoptera |
| Infraorder: | Cucujiformia |
| Family: | Cerambycidae |
| Subfamily: | Lamiinae |
| Tribe: | Pteropliini |
| Genus: | Ataxia |
| Species: | A. spinipennis |
| Binomial name | |
| Ataxia spinipennis Chevrolat, 1862 | |
| Synonyms | |
| |
Ataxia spinipennis is a species of beetle in the family Cerambycidae. It was described by Louis Alexandre Auguste Chevrolat in 1862. It is known from Puerto Rico and Cuba. [1]
Ataxia is a neurological sign consisting of lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements, that indicates dysfunction of parts of the nervous system that coordinate movement, such as the cerebellum.
Ataxia–telangiectasia, also referred to as ataxia–telangiectasia syndrome or Louis–Bar syndrome, is a rare, neurodegenerative, autosomal recessive disease causing severe disability. Ataxia refers to poor coordination and telangiectasia to small dilated blood vessels, both of which are hallmarks of the disease. A–T affects many parts of the body:
Olivopontocerebellar atrophy (OPCA) is the degeneration of neurons in specific areas of the brain – the cerebellum, pons, and inferior olivary nucleus. OPCA is present in several neurodegenerative syndromes, including inherited and non-inherited forms of ataxia and multiple system atrophy (MSA), with which it is primarily associated.
Friedreich's ataxia is an autosomal-recessive genetic disease that causes difficulty walking, a loss of coordination in the arms and legs, and impaired speech that worsens over time. Symptoms generally start between 5 and 20 years of age. Many develop hypertrophic cardiomyopathy and require a mobility aid such as a cane, walker, or wheelchair in their teens. As the disease progresses, some affected people lose their sight and hearing. Other complications may include scoliosis and diabetes mellitus.
Spinocerebellar ataxia (SCA) is a progressive, degenerative, genetic disease with multiple types, each of which could be considered a neurological condition in its own right. An estimated 150,000 people in the United States have a diagnosis of spinocerebellar ataxia at any given time. SCA is hereditary, progressive, degenerative, and often fatal. There is no known effective treatment or cure. SCA can affect anyone of any age. The disease is caused by either a recessive or dominant gene. In many cases people are not aware that they carry a relevant gene until they have children who begin to show signs of having the disorder.
Purkinje cells, or Purkinje neurons, are a class of GABAergic inhibitory neurons located in the cerebellum. They are named after their discoverer, Czech anatomist Jan Evangelista Purkyně, who characterized the cells in 1839.
Sensory ataxia is both a symptom and a sign in neurology. It is a form of ataxia caused not by cerebellar dysfunction but by loss of sensory input into the control of movement.
Cerebellar ataxia is a form of ataxia originating in the cerebellum. Non-progressive congenital ataxia (NPCA) is a classical presentation of cerebral ataxias.
Spinocerebellar ataxia type 6 (SCA6) is a rare, late-onset, autosomal dominant disorder, which, like other types of SCA, is characterized by dysarthria, oculomotor disorders, peripheral neuropathy, and ataxia of the gait, stance, and limbs due to cerebellar dysfunction. Unlike other types, SCA 6 is not fatal. This cerebellar function is permanent and progressive, differentiating it from episodic ataxia type 2 (EA2) where said dysfunction is episodic. In some SCA6 families, some members show these classic signs of SCA6 while others show signs more similar to EA2, suggesting that there is some phenotypic overlap between the two disorders. SCA6 is caused by mutations in CACNA1A, a gene encoding a calcium channel α subunit. These mutations tend to be trinucleotide repeats of CAG, leading to the production of mutant proteins containing stretches of 20 or more consecutive glutamine residues; these proteins have an increased tendency to form intracellular agglomerations. Unlike many other polyglutamine expansion disorders expansion length is not a determining factor for the age that symptoms present.
Episodic ataxia (EA) is an autosomal dominant disorder characterized by sporadic bouts of ataxia with or without myokymia. There are seven types recognized but the majority are due to two recognized entities. Ataxia can be provoked by psychological stress or startle, or heavy exertion, including exercise. Symptoms can first appear in infancy. There are at least six loci for EA, of which 4 are known genes. Some patients with EA also have migraine or progressive cerebellar degenerative disorders, symptomatic of either familial hemiplegic migraine or spinocerebellar ataxia. Some patients respond to acetazolamide though others do not.
Ataxia, described by Haldeman in 1847, is an American genus of longhorn beetles of the subfamily Lamiinae, tribe Pteropliini.
Cav2.1, also called the P/Q voltage-dependent calcium channel, is a calcium channel found mainly in the brain. Specifically, it is found on the presynaptic terminals of neurons in the brain and cerebellum. Cav2.1 plays an important role in controlling the release of neurotransmitters between neurons. It is composed of multiple subunits, including alpha-1, beta, alpha-2/delta, and gamma subunits. The alpha-1 subunit is the pore-forming subunit, meaning that the calcium ions flow through it. Different kinds of calcium channels have different isoforms (versions) of the alpha-1 subunit. Cav2.1 has the alpha-1A subunit, which is encoded by the CACNA1A gene. Mutations in CACNA1A have been associated with various neurologic disorders, including familial hemiplegic migraine, episodic ataxia type 2, and spinocerebellar ataxia type 6.
Potassium voltage-gated channel, Shaw-related subfamily, member 3 also known as KCNC3 or Kv3.3 is a protein that in humans is encoded by the KCNC3.
Ataxia is the sixth studio album released by alternative / psychedelic-rock band Circus Devils on October 31, 2008. All songs on Ataxia were written and performed by Robert Pollard, Todd Tobias, and Tim Tobias.
Hadramphus, commonly known as knobbled weevils, is a genus of flightless molytine weevils from the family Curculionidae. It is endemic to New Zealand and consists of four species.
Para triathlon is a variant of the triathlon for athletes with a physical disability. The sport is governed by World Triathlon, and was first held as a Paralympic event at the 2016 Summer Paralympics in Rio de Janeiro, Brazil.
Acetergamine is an organic chemical compound; specifically it is a derivative of ergoline, making it a member of the ergotamine family of compounds. Acetergamine currently has no mainstream uses, however its potential as an alpha-1 blocker and vasodilator has led to it being covered in several patents concerning therapies for erectile dysfunction. It has also been investigated as a treatment for cerebellar ataxia.
Hadramphus spinipennis, commonly called the coxella weevil, is a large, nocturnal, flightless weevil only found on Mangere and Rangatira Islands in the Chatham Islands, New Zealand.
Brimus spinipennis is a species of beetle in the family Cerambycidae. It was described by Francis Polkinghorne Pascoe in 1858. It is known from the South African Republic.
Truncal ataxia is a wide-based "drunken sailor" gait characterised by uncertain starts and stops, lateral deviations and unequal steps. It is an instability of the trunk and often seen during sitting. It is most visible when shifting position or walking heel-to-toe.