The nervous system originates as a tiny, simple open tube called the neural tube;  the front of this tube develops into the brain (and retinas of the eye), while the spinal cord develops from the very back end. Neurons begin to form early, but most of them become structural rather than active nerve cells. The brain generally forms from the inside-out, especially in the case of the neocortex. The difficulties arising from this are readily apparent, as each successive layer of cells must travel through the previous layer to reach its destination. Therefore, nervous tissue develops ladders made of radial glial cells that neurons climb, through the previous layers, to reach their proper destination. Some destinations, such as the cerebral cortex, even have "placeholder" neurons that travel up the ladder to form a structure;  when the final neurons germinate, they find a correct placeholder and then the placeholder cell dies. Heterotopia
The complexity of neural development makes it fraught with opportunities for error. Grey matter heterotopia is such an example. It is believed that gray matter heterotopia are caused by arrested migration of neurons to the cerebral cortex; that is, when neurons that are supposed to form part of the cerebral cortex. fail to climb to the end of their ladder correctly and are permanently situated in the wrong location. Gray matter heterotopia are common malformations of cortical development classed as neuronal migration disorders. Heterotopias are classed in two groups: nodular and diffuse. Nodular types are subependymal and subcortical; diffuse types are termed band heterotopias.
The highest incidence of glycogen storage disease type III is in the Faroe Islands where it occurs in 1 out of every 3,600 births, probably due to a founder effect. There seem to be two mutations in exon 3 (c.17_18delAG) being one of them, which are linked to the subtype IIIb.The amylo-alpha-1, 6-glucosidase, 4-alpha-glucanotransferase gene and mutations to it, are at the root of this condition. The gene is responsible for creating glycogen debranching enzyme, which in turn helps in glycogen decomposition. Diagnosis
In terms of the diagnosis for glycogen storage disease type III, the following tests/exams are carried out to determine if the individual has the condition:
Biopsy (muscle or liver)
CBC
Ultrasound
DNA mutation analysis (helps ascertain GSD III subtype)

Differential diagnosis
The differential diagnosis of glycogen storage disease type III includes GSD I, GSD IX and GSD VI. This however does not mean other glycogen storage diseases should not be distinguished as well. Classification
Clinical manifestations of glycogen storage disease type III are divided into four classes:
GSD IIIa, is the most common, (along with GSD IIIb) and which clinically includes muscle and liver involvement
GSD IIIb, which clinically has liver involvement but no muscle involvement
GSD IIIc  which clinically affects liver and muscle. GSD IV affects liver only (not muscle)

Treatment
Treatment for glycogen storage disease type III may involve a high-protein diet, in order to facilitate gluconeogenesis. Additionally the individual may need:
IV glucose (if oral route is inadvisable)
Nutritional specialist
Vitamin D (for osteoporosis/secondary complication)
Hepatic transplant (if complication occurs)

References
Further reading
Mayorandan, Sebene; Meyer, Uta; Hartmann, Hans; Das, Anibh Martin (1 January 2014).