ICD-10-CM Diagnosis Code R27.0 - Ataxia, unspecified (original) (raw)

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Ataxia, unspecified

ICD-10-CM Code:

R27.0

ICD-10 Code for:

Ataxia, unspecified

Is Billable?

Yes - Valid for Submission

Chronic Condition Indicator: [1]

Not chronic

Code Navigator:

R27.0 is a billable diagnosis code used to specify a medical diagnosis of ataxia, unspecified. The code is valid during the current fiscal year for the submission of HIPAA-covered transactions from October 01, 2025 through September 30, 2026.

Unspecified diagnosis codes like R27.0 are acceptable when clinical information is unknown or not available about a particular condition. Although a more specific code is preferable, unspecified codes should be used when such codes most accurately reflect what is known about a patient's condition. Specific diagnosis codes should not be used if not supported by the patient's medical record.

According to ICD-10-CM guidelines this code should not to be used as a principal diagnosis code when a related definitive diagnosis has been established.

  1. Code Information
  2. Approximate Synonyms
  3. Clinical Classification
  4. Clinical Information
  5. Tabular List of Diseases and Injuries
  6. Index to Diseases and Injuries References
  8. Convert to ICD-9 Code
  9. Patient Education
  10. Other Codes Used Similar Conditions
  11. Code History

The following list of clinical terms are approximate synonyms, alternative descriptions, or common phrases that might be used by patients, healthcare providers, or medical coders to describe the same condition. These synonyms and related diagnosis terms are often used when searching for an ICD-10 code, especially when the exact medical terminology is unclear. Whether you're looking for lay terms, similar diagnosis names, or common language alternatives, this list can help guide you to the correct ICD-10 classification.

Clinical Classifications group individual ICD-10-CM diagnosis codes into broader, clinically meaningful categories. These categories help simplify complex data by organizing related conditions under common clinical themes.

They are especially useful for data analysis, reporting, and clinical decision-making. Even when diagnosis codes differ, similar conditions can be grouped together based on their clinical relevance. Each category is assigned a unique CCSR code that represents a specific clinical concept, often tied to a body system or medical specialty.

CCSR Code: SYM010

Inpatient Default: Y - Yes, default inpatient assignment for principal diagnosis or first-listed diagnosis.

Outpatient Default: Y - Yes, default outpatient assignment for principal diagnosis or first-listed diagnosis.

impairment of the ability to perform smoothly coordinated voluntary movements. this condition may affect the limbs, trunk, eyes, pharynx, larynx, and other structures. ataxia may result from impaired sensory or motor function. sensory ataxia may result from posterior column injury or peripheral nerve diseases. motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions.

an autosomal recessive inherited disorder characterized by choreoathetosis beginning in childhood, progressive cerebellar ataxia; telangiectasis of conjunctiva and skin; dysarthria; b- and t-cell immunodeficiency, and radiosensitivity to ionizing radiation. affected individuals are prone to recurrent sinobronchopulmonary infections, lymphoreticular neoplasms, and other malignancies. serum alpha-fetoproteins are usually elevated. (menkes, textbook of child neurology, 5th ed, p688) the gene for this disorder (atm) encodes a cell cycle checkpoint protein kinase and has been mapped to chromosome 11 (11q22-q23).

a group of protein serine-threonine kinases which activate critical signaling cascades in double strand breaks, apoptosis, and genotoxic stress such as ionizing ultraviolet a light, thereby acting as a dna damage sensor. these proteins play a role in a wide range of signaling mechanisms in cell cycle control.

a family of predominantly nuclear proteins that regulate gene transcription and protein degradation. the expansion of cag trinucleotide repeats in genes that encode ataxins is associated with spinocerebellar ataxias (sca). in sca patients, the number of cag repeats correlates with the severity of disease and inversely correlates with the age of disease onset.

incoordination of voluntary movements that occur as a manifestation of cerebellar diseases. characteristic features include a tendency for limb movements to overshoot or undershoot a target (dysmetria), a tremor that occurs during attempted movements (intention tremor), impaired force and rhythm of diadochokinesis (rapidly alternating movements), and gait ataxia. (from adams et al., principles of neurology, 6th ed, p90)

a highly contagious dna virus infection of the cat family, characterized by fever, enteritis and bone marrow changes. it is also called feline ataxia, feline agranulocytosis, feline infectious enteritis, cat fever, cat plague, and show fever. it is caused by feline panleukopenia virus or the closely related mink enteritis virus or canine parvovirus.

a protein involved in the transfer of iron and sulfur to iron-sulfur cluster (isc) assembly complex for de novo synthesis of a [2fe-2s] cluster, the first step of the mitochondrial iron-sulfur protein biogenesis. deficiency leads to the neurodegenerative disease friedreich ataxia.

an autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts. clinical manifestations include gait ataxia, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin. (from adams et al., principles of neurology, 6th ed, p1081; n engl j med 1996 oct 17;335(16):1169-75) the severity of friedreich ataxia associated with expansion of gaa repeats in the first intron of the frataxin gene correlates with the number of trinucleotide repeats. (from durr et al, n engl j med 1996 oct 17;335(16):1169-75)

impairment of the ability to coordinate the movements required for normal ambulation (walking) which may result from impairments of motor function or sensory feedback. this condition may be associated with brain diseases (including cerebellar diseases and basal ganglia diseases); spinal cord diseases; or peripheral nervous system diseases.

a dominantly-inherited ataxia first described in people of azorean and portuguese descent, and subsequently identified in brazil, japan, china, and australia. this disorder is classified as one of the spinocerebellar ataxias (type 3) and has been associated with a mutation of the mjd1 gene on chromosome 14. clinical features include progressive ataxia, dysarthria, postural instability, nystagmus, eyelid retraction, and facial fasciculations. dystonia is prominent in younger patients (referred to as type i machado-joseph disease). type ii features ataxia and ocular signs; type iii features muscular atrophy and a sensorimotor neuropathy; and type iv features extrapyramidal signs combined with a sensorimotor neuropathy. (from clin neurosci 1995;3(1):17-22; ann neurol 1998 mar;43(3):288-96)

a condition marked by progressive cerebellar ataxia combined with myoclonus usually presenting in the third decade of life or later. additional clinical features may include generalized and focal seizures, spasticity, and dyskinesias. autosomal recessive and autosomal dominant patterns of inheritance have been reported. pathologically, the dentate nucleus and brachium conjunctivum of the cerebellum are atrophic, with variable involvement of the spinal cord, cerebellar cortex, and basal ganglia. (from joynt, clinical neurology, 1991, ch37, pp60-1)

a heterogeneous group of primarily familial epilepsy disorders characterized by myoclonic seizures, tonic-clonic seizures, ataxia, progressive intellectual deterioration, and neuronal degeneration. these include lafora disease; merrf syndrome; neuronal ceroid-lipofuscinosis; sialidosis (see mucolipidoses), and unverricht-lundborg syndrome.

a chromosome instability syndrome resulting from a defective response to dna double-strand breaks. in addition to characteristic facies and microcephaly, patients have a range of findings including radiosensitivity, immunodeficiency, increased cancer risk, and growth retardation. causative mutations occur in the nbs1 gene, located on human chromosome 8q21. nbs1 codes for nibrin, the key regulator protein of the r/m/n (rad50/mre11/nbs1) protein complex which senses and mediates cellular response to dna damage caused by ionizing radiation.

a group of inherited and sporadic disorders which share progressive ataxia in combination with atrophy of the cerebellum; pons; and inferior olivary nuclei. additional clinical features may include muscle rigidity; nystagmus, pathologic; retinal degeneration; muscle spasticity; dementia; urinary incontinence; and ophthalmoplegia. the familial form has an earlier onset (second decade) and may feature spinal cord atrophy. the sporadic form tends to present in the fifth or sixth decade, and is considered a clinical subtype of multiple system atrophy. (from adams et al., principles of neurology, 6th ed, p1085)

an autosomal recessive metabolic disorder caused by absent or decreased pyruvate carboxylase activity, the enzyme that regulates gluconeogenesis, lipogenesis, and neurotransmitter synthesis. clinical manifestations include lactic acidosis, seizures, respiratory distress, marked psychomotor delay, periodic hypoglycemia, and hypotonia. the clinical course may be similar to leigh disease. (from am j hum genet 1998 jun;62(6):1312-9)

an inherited metabolic disorder caused by deficient enzyme activity in the pyruvate dehydrogenase complex, resulting in deficiency of acetyl coa and reduced synthesis of acetylcholine. two clinical forms are recognized: neonatal and juvenile. the neonatal form is a relatively common cause of lactic acidosis in the first weeks of life and may also feature an erythematous rash. the juvenile form presents with lactic acidosis, alopecia, intermittent ataxia; seizures; and an erythematous rash. (from j inherit metab dis 1996;19(4):452-62) autosomal recessive and x-linked forms are caused by mutations in the genes for the three different enzyme components of this multisubunit pyruvate dehydrogenase complex. one of the mutations at xp22.2-p22.1 in the gene for the e1 alpha component of the complex leads to leigh disease.

a group of predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. progressive ataxia is a central feature of these conditions, and in certain subtypes polyneuropathy; dysarthria; visual loss; and other disorders may develop. (from joynt, clinical neurology, 1997, ch65, pp 12-17; j neuropathol exp neurol 1998 jun;57(6):531-43)

a heterogenous group of degenerative syndromes marked by progressive cerebellar dysfunction either in isolation or combined with other neurologic manifestations. sporadic and inherited subtypes occur. inheritance patterns include autosomal dominant, autosomal recessive, and x-linked.

congenital locomotor ataxia of lambs, thought to be associated with copper deficiency. it is characterized clinically by progressive incoordination of the hind limbs and pathologically by disruption of neuron and myelin development in the central nervous system. it is caused by a deficiency of metabolizable copper in the ewe during the last half of her pregnancy. (dorland, 28th ed; stedman, 26th ed)

parenchymatous neurosyphilis marked by slowly progressive degeneration of the posterior columns, posterior roots, and ganglia of the spinal cord. the condition tends to present 15 to 20 years after the initial infection and is characterized by lightening-like pains in the lower extremities, urinary incontinence; ataxia; severely impaired position and vibratory sense, abnormal gait (see gait disorders, neurologic), optic atrophy; argyll-robertson pupils, hypotonia, hyperreflexia, and trophic joint degeneration (charcot's joint; see arthropathy, neurogenic). (from adams et al., principles of neurology, 6th ed, p726)

an autosomal recessive disorder of lipid metabolism. it is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (triglycerides; cholesterol esters; phospholipids) and is required in the secretion of beta-lipoproteins (low density lipoproteins or ldl). features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent ldl.

an autosomal dominant disorder of lipid metabolism. it is caused by mutations of apolipoproteins b, main components of chylomicrons and beta-lipoproteins (low density lipoproteins or ldl). features include abnormally low ldl, normal triglyceride level, and dietary fat malabsorption.

an autosomal recessive disorder characterized by defective absorption of dietary fat, cholesterol and fat-soluble vitamins. it results in multiple vitamin deficiencies. signs and symptoms include failure to thrive, diarrhea, steatorrhea, acanthocytosis and ataxia.

The following annotation back-references for this diagnosis code are found in the injuries and diseases index. The Index to Diseases and Injuries is an alphabetical listing of medical terms, with each term mapped to one or more ICD-10-CM code(s).

References found for this diagnosis code in the External Cause of Injuries Index:

Below are the ICD-9 codes that most closely match this ICD-10 code, based on the General Equivalence Mappings (GEMs). This ICD-10 to ICD-9 crosswalk tool is helpful for coders who need to reference legacy diagnosis codes for audits, historical claims, or approximate code comparisons.

ICD-9-CM: 781.3

Approximate Flag - The approximate mapping means this ICD-10 code does not have an exact ICD-9 equivalent. The matched code is the closest available option, but it may not fully capture the original diagnosis or clinical intent.

Movement Disorders

Movement disorders are neurologic conditions that cause problems with movement, such as:

There are many different movement disorders. Some of the more common types include:

Causes of movement disorders include:

Treatment varies by disorder. Medicines can cure some disorders. Others get better when an underlying disease is treated. Often, however, there is no cure. In that case, the goal of treatment is to improve symptoms and relieve pain.

[Learn More in MedlinePlus]