The average lifespan for children with type B is up to 7 years of age. These symptoms are seen in CS type 2 children. Cockayne syndrome type C (CSC) appears later in childhood with milder symptoms than the other types and a slower progression of the disorder. People with this type of Cockayne syndrome live into adulthood, with an average lifespan of 40 to 50 years. These symptoms are seen in CS type 3. Epidemiology
Cockayne syndrome is rare worldwide. No racial predilection is reported for Cockayne syndrome. No sexual predilection is described for Cockayne syndrome; the male-to-female ratio is equal. Cockayne syndrome I (CS-A) manifests in childhood. Cockayne syndrome II (CS-B) manifests at birth or in infancy, and it has a worse prognosis. Recent research
The recent research on Jan 2018 mentions different CS features that are seen globally with similarities and differences:
CS has an incidence of 1 in 250,000 live births, and a prevalence of approximately 1 per 2.5 million, which is remarkably consistent across various regions globally:

See also
Accelerated aging disease
Biogerontology
Degenerative disease
Genetic disorder
CAMFAK syndrome — thought to be a form (or subset) of Cockayne syndrome

References
External links
This article incorporates some public domain text from The U.S. National Library of Medicine
Dietary needs must be closely managed.Mutations in both copies of the PCCA or PCCB genes cause propionic acidemia. These genes contain instructions to form alpha- and beta-subunits of PCC, the enzyme called propionyl-CoA carboxylase. PCC is required for the normal breakdown of the essential amino acids valine, isoleucine, threonine, and methionine, as well as certain odd-chained fatty-acids. Mutations in the PCCA or PCCB genes disrupt the function of the enzyme, preventing these acids from being metabolized. As a result, propionyl-CoA, propionic acid, ketones, ammonia, and other toxic compounds accumulate in the blood, causing the signs and symptoms of propionic acidemia. Hyperammonemia develops due to the inhibitory effects of propionyl-CoA on N-Acetylglutamate synthase, indirectly resulting in slowing of the urea cycle. Diagnosis
Elevated metabolites of propionic acid (for example, 3-hydroxypropionate, methylcitrate, tiglylglycine, propionylglycine) found in blood and urine along with normal biotinidase levels. Management
Patients with propionic acidemia should be started as early as possible on a low protein diet. In addition to a protein mixture that is devoid of methionine, threonine, valine, and isoleucine, the patient should also receive L-carnitine treatment and should be given antibiotics 10 days per month in order to remove the intestinal propiogenic flora. The patient should have diet protocols prepared for them with a “well day diet” with low protein content, a “half emergency diet” containing half of the protein requirements, and an “emergency diet” with no protein content.