Diagnosis
Classification
A few SCAs remain unspecified and can not be precisely diagnosed, but in the last decade genetic testing has allowed precise identification of dozens of different SCAs  and more tests are being added each year. In 2008, a genetic ataxia blood test developed to test for 12 types of SCA, Friedreichs ataxia, and several others. However, since not every SCA has been genetically identified some SCAs are still diagnosed  by neurological examination, which  may include a physical exam, family history, MRI scanning of the brain and spine, and spinal tap.Many SCAs below fall under the category of polyglutamine diseases, which are caused when a disease-associated protein (i.e., ataxin-1, ataxin-3, etc.) contains a large number of repeats of glutamine residues, termed a polyQ sequence or a "CAG trinucleotide repeat" disease for either the one-letter designation or codon for glutamine respectively. The threshold for symptoms in most forms of SCA is around 35, though for SCA3 it extends beyond 50. Most polyglutamine diseases are dominant due to the interactions of resulting polyQ tail.The first ataxia gene was identified in 1993 and called "Spinocerebellar ataxia type 1" (SCA1); later genes were called SCA2, SCA3, etc. Usually, the "type" number of "SCA" refers to the order in which the gene was found. At this time, there are at least 29 different gene mutations that have been found.The following is a list of some of the many types of Spinocerebellar ataxia. Others include SCA18, SCA20, SCA21, SCA23, SCA26, SCA28, and SCA29.
Hypocapnia (from the Greek words υπό meaning below normal and καπνός kapnós meaning smoke), also known as hypocarbia, sometimes incorrectly called acapnia, is a state of reduced carbon dioxide in the blood. Hypocapnia usually results from deep or rapid breathing, known as hyperventilation. Hypocapnia is the opposite of hypercapnia. Effects
Even when marked, hypocapnia is normally well tolerated. Symptoms include tingling sensation (usually in the limbs), abnormal heartbeat, painful muscle cramps, and seizures. Acute hypocapnia causes hypocapnic alkalosis, which causes cerebral vasoconstriction leading to cerebral hypoxia, and this can cause transient dizziness, fainting, and anxiety. A low partial pressure of carbon dioxide in the blood also causes alkalosis (because CO2 is acidic in solution), leading to lowered plasma calcium ions (Hypocalcaemia), causing increased nerve and muscle excitability. This explains the other common symptoms of hyperventilation—pins and needles, muscle cramps and tetany in the extremities, especially hands and feet.Because the brain stem regulates breathing by monitoring the level of blood CO2 instead of O2, hypocapnia can suppress breathing to the point of blackout from cerebral hypoxia, as exhibited in shallow water blackout. Hypocapnia also results in bronchoconstriction in order to decrease ventilation. This mechanism is meant to counteract hyperventilation, and decrease the amount of oxygen coming into the lungs. The bodys "goal" is to have a relatively even ratio of the partial pressure of oxygen to the partial pressure of carbon dioxide. Chemoreceptors in the body sense a change in partial pressures and pH (hydrogen ion concentration) in the blood.