Cerebral folate deficiency results from folate is either deficient in transport to the central nervous system or as a result of high turnover in folate in the central nervous system. Active folate, also referred to as vitamin B9, is acquired from leafy greens. Deficient folic acid has been linked to poor neural development and management. As maternal parents we were required to take a synthetic form of folic acid during pregnancy. (Please note: synthetic folic acid is not as effective as the active form of folate which is best acquired through leafy greens).
Clinically folate deficiency can present as early as in the infant stage and as late as teen years and manifests in one third of children as epilepsy. The types of epilepsy are not limited to a “type” or a “syndrome”. Although certain early signs of cerebral folate deficiency may include unrest, irritability, deceleration of head growth at 4 months of age and visual and hearing disturbances around age 3, many children have gone undiagnosed.
Treatment is utilizing an active form of folate referred to as 5 methyl tetrahydrafolate. Some gene expressions of MTHFRC677T heterozygous or homozygous may be an indicator. More importantly low cerebrospinal fluid of folate (my son was never “offered” a lumbar puncture), and disturbances in methionine and homocysteine may indicate the deficiency.
The earlier cerebral folate deficiency is identified the greater the chance of improvements.
http://www.ncbi.nlm.nih.gov/pubmed/15581159
Be well,
Lynn
