Symptoms include cerebellar ataxia, spasticity, optic atrophy, epilepsy,[1] loss of motor functions, irritability, vomiting, coma,[2] and even fever has been tied to VWM.

Symptoms generally appear in young children or infants who were previously developing fairly normally.

[3] A unique characteristic of VWM is that only oligodendrocytes and astrocytes are negatively affected while other glial cells and neurons seem to be unaffected.

However through an intensive survey, it was determined that even if an individual has premature ovarian failure, she does not necessarily have VWM.

Rarefaction of the white matter is seen through light microscopy and the small number of axons and U-fibers that were affected can also be seen.

These foamy oligodendrocytes tend to have increased cytoplasmic structures, a greater number of irregular mitochondria and a higher rate of apoptosis.

[3] Common signs to look for include chronic progressive neurological deterioration with cerebellar ataxia, spasticity, mental decline, decline of vision, mild epilepsy, hand tremor, the ability to chew and swallow food becomes difficult, rapid deterioration and fibrile infections following head trauma or fright, loss of motor functions, irritability, behavioural changes, vomiting, and even coma.

He noticed sexual impotency, social isolation, unexplained aggression and sadness, loss of motivation, inert laughs, auditory hallucinations, thought insertion, delusions, and imperative commenting.

[4] Over time, the MRI is excellent at showing rarefaction and cystic degeneration of the white matter as it is replaced by fluid.

To show this change, displaying white matter as a high signal (T2-weighted), proton density, and Fluid attenuated inversion recovery (FLAIR) images are the best approach.

To view the remaining tissue, and get perspective on the damage done (also helpful in determining the rate of deterioration) (T1-weighted), proton density, and FLAIR images are ideal as they show radiating stripe patterns in the degenerating white matter.

A failure of MRI images is their ineffectiveness and difficulty in interpretation in infants since the brain has not fully developed yet.

A potentially similar appearance of MRI with white matter abnormalities and cystic changes may be seen in some patients with hypomelanosis of Ito, some forms of Lowe's (oculocerebrorenal) disease, or some of the mucopolysaccharidoses.

[4] The characteristics of the brain upon autopsy are often very similar to atypical diffuse sclerosis, such as the presence of fibrillary astrocytes and scant sudanophilic lipids.

[11] Common misdiagnosis from misinterpreting the MRI include asphyxia, congenital infections, metabolic diseases.

[2] Multiple sclerosis is often a misdiagnosis, but only in children due to its neurological characteristics, onset in early years, and MRI abnormalities.

[2] Melatonin has been shown to provide cytoprotective traits to glial cells exposed to stressors such as excitotoxicity and oxidative stress.

Throughout the duration of her life, she experienced chronic episodes with extensive deterioration of her brain following minor physical trauma.

Upon death, autopsy was performed in which the cerebral white matter displayed dispersed cystic areas.

These areas were surrounded by a dense net of oligodendrocytes in which only mild fibrillary astrocytes and scant sudanophilic lipids were found.

The key factor which allowed them to connect these patients together was the results of the magnetic-resonance spectroscopy in which the normal white matter signals were gone and often replaced with resonances indicative of lactate and glucose.