From OMIM
Leukoencephalopathy with vanishing white matter is an autosomal recessive neurologic disorder characterized by variable neurologic features, including progressive cerebellar ataxia, spasticity, and cognitive impairment associated with white matter lesions on brain imaging. Age at onset ranges from early infancy to adulthood. Rapid neurologic deterioration can occur following minor head trauma. Female mutation carriers may additionally develop ovarian failure, manifest as primary amenorrhea or as secondary amenorrhea lasting more than 6 months, associated with elevated gonadotropin levels at age less than 40 years (summary by Van der Knaap et al., 1998 and Schiffmann et al., 1997). The association of vanishing white matter leukodystrophy with ovarian failure had been referred to as 'ovarioleukodystrophy.' Genetic Heterogeneity of Leukoencephalopathy with Vanishing White Matter Leukoencephalopathy with vanishing white matter may be caused by mutations in any of the 5 genes encoding the subunits of the eukaryotic translation factor initiation factor 2B. VWM2 (620312) is caused by mutation in the EIF2B2 gene (606454) on chromosome 14q24; VWM3 (620313) is caused by mutation in the EIF2B3 gene (606273) on chromosome 1p34; VWM4 (620314) is caused by mutation in the EIF2B4 gene (606687) on chromosome 2p23; and VWM5 (620315) is caused by mutation in the EIF2B5 gene (603945) on chromosome 3q27.  http://www.omim.org/entry/603896

From MedlinePlus Genetics
Leukoencephalopathy with vanishing white matter is a progressive disorder that mainly affects the brain and spinal cord (central nervous system). This disorder causes deterioration of the central nervous system's white matter, which consists of nerve fibers covered by myelin. Myelin is the fatty substance that insulates and protects nerves.

In most cases, people with leukoencephalopathy with vanishing white matter show no signs or symptoms of the disorder at birth. Affected children may have slightly delayed development of motor skills such as crawling or walking. During early childhood, most affected individuals begin to develop motor symptoms, including abnormal muscle stiffness (spasticity) and difficulty with coordinating movements (ataxia). There may also be some deterioration of mental functioning, but this is not usually as pronounced as the motor symptoms. Some affected females may have abnormal development of the ovaries (ovarian dysgenesis). Specific changes in the brain as seen using magnetic resonance imaging (MRI) are characteristic of leukoencephalopathy with vanishing white matter, and may be visible before the onset of symptoms.

While childhood onset is the most common form of leukoencephalopathy with vanishing white matter, some severe forms are apparent at birth. A severe, early-onset form seen among the Cree and Chippewayan populations of Quebec and Manitoba is called Cree leukoencephalopathy. Milder forms may not become evident until adolescence or adulthood, when behavioral or psychiatric problems may be the first signs of the disease. Some females with milder forms of leukoencephalopathy with vanishing white matter who survive to adolescence exhibit ovarian dysfunction. This variant of the disorder is called ovarioleukodystrophy.

Progression of leukoencephalopathy with vanishing white matter is generally uneven, with periods of relative stability interrupted by episodes of rapid decline. People with this disorder are particularly vulnerable to stresses such as infection, mild head trauma or other injury, or even extreme fright. These stresses may trigger the first symptoms of the condition or worsen existing symptoms, and can cause affected individuals to become lethargic or comatose.  https://medlineplus.gov/genetics/condition/leukoencephalopathy-with-vanishing-white-matter