2024 ICD-10-CM Diagnosis Code R27.0

Approximate Synonyms

The following clinical terms are approximate synonyms or lay terms that might be used to identify the correct diagnosis code:

• Abetalipoproteinemia
• Acquired ataxia
• Acquired ataxia
• Acquired ataxia
• Acquired ataxia
• Acute cerebellar ataxia due to varicella
• Arms ataxic
• Ataxia
• Ataxia co-occurrent and due to abetalipoproteinemia
• Ataxia co-occurrent and due to phytanic acid storage disease
• Ataxia due to cerebrotendinous xanthomatosis
• Ataxia due to chronic infection of central nervous system
• Ataxia due to disorder of immune function
• Ataxia due to multiple system atrophy, cerebellar variant
• Ataxia due to subpial siderosis
• Ataxia of bilateral upper limbs
• Ataxia with vitamin E deficiency
• Ataxic hemiparesis
• Benign paroxysmal tonic upgaze of childhood with ataxia
• Bilateral lower limb ataxia
• Drug-induced cerebellar ataxia
• HSMN IV
• Hypermetria
• Hypometria
• Intermittent ataxia
• Legs ataxic
• Motor ataxia
• Muscular atrophy, ataxia, retinitis pigmentosa, and diabetes mellitus
• Neurogenic muscle weakness, ataxia and retinitis pigmentosa
• Nutritional ataxic neuropathy
• Oral motor ataxia
• Postinfectious ataxia
• Progressive myoclonus epilepsy with ataxia
• Secondary cerebellar degeneration
• Secondary cerebellar degeneration
• Sensory ataxia
• Single limb ataxia
• Static ataxia
• Toxin-induced ataxia
• Truncal ataxia

Clinical Information

• Ataxia

  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.

• Ataxia Telangiectasia

  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).

• Ataxia Telangiectasia Mutated Proteins

  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.

• Ataxins

  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.

• Cerebellar Ataxia

  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)

• Feline Panleukopenia

  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.

• 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)

• Gait Ataxia

  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.

• Machado-Joseph Disease

  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)

• Myoclonic Cerebellar Dyssynergia

  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)

• Myoclonic Epilepsies, Progressive

  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.

• Nijmegen Breakage 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.

• Olivopontocerebellar Atrophies

  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)

• Pyruvate Carboxylase Deficiency Disease

  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)

• Pyruvate Dehydrogenase Complex Deficiency Disease

  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.

• Spinocerebellar Ataxias

  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)

• Spinocerebellar Degenerations

  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.

• Swayback

  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)

• Tabes Dorsalis

  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)

• Abetalipoproteinemia

  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.

• Hypobetalipoproteinemia, Familial, Apolipoprotein B

  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.

• Abetalipoproteinemia

  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.

Convert R27.0 to ICD-9-CM

• ICD-9-CM Code: 781.3 - Lack of coordination
  Approximate Flag - The approximate mapping means there is not an exact match between the ICD-10 and ICD-9 codes and the mapped code is not a precise representation of the original code.

Patient Education

Movement Disorders

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

• Increased movement that can be voluntary (intentional) or involuntary (unintended)
• Decreased or slow voluntary movement

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

• Ataxia, the loss of muscle coordination
• Dystonia, in which involuntary contractions of your muscles cause twisting and repetitive movements. The movements can be painful.
• Huntington's disease, an inherited disease that causes nerve cells in certain parts of the brain to waste away. This includes the nerve cells that help to control voluntary movement.
• Parkinson's disease, which is disorder that slowly gets worse over time. It causes tremors, slowness of movement, and trouble walking.
• Tourette syndrome, a condition which causes people to make sudden twitches, movements, or sounds (tics)
• Tremor and essential tremor, which cause involuntary trembling or shaking movements. The movements may be in one or more parts of your body.

Causes of movement disorders include:

• Genetics
• Infections
• Medicines
• Damage to the brain, spinal cord, or peripheral nerves
• Metabolic disorders
• Stroke and vascular diseases
• Toxins

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.

Code History

• FY 2024 - No Change, effective from 10/1/2023 through 9/30/2024
• FY 2023 - No Change, effective from 10/1/2022 through 9/30/2023
• FY 2022 - No Change, effective from 10/1/2021 through 9/30/2022
• FY 2021 - No Change, effective from 10/1/2020 through 9/30/2021
• FY 2020 - No Change, effective from 10/1/2019 through 9/30/2020
• FY 2019 - No Change, effective from 10/1/2018 through 9/30/2019
• FY 2018 - No Change, effective from 10/1/2017 through 9/30/2018
• FY 2017 - No Change, effective from 10/1/2016 through 9/30/2017
• FY 2016 - New Code, effective from 10/1/2015 through 9/30/2016. This was the first year ICD-10-CM was implemented into the HIPAA code set.