Schneckenbecken dysplasia is a rare pre-natally fatal hereditary autosomal recessive condition which affects the bones and pre-natal growth. Signs and symptoms
Fetuses with the condition typically have a hypoplastic iliac bone which resembles a snail, short ribs, short neck, shortened and widened (dysplastic) fibula bones, premature ossification of the tarsus, shortened and broadened long bones which resemble a dumbbell, hypoplastia and flattening vertebrae, macrocephaly, dolichocephaly, toenail hypoplasia, flattening of the malar prominence, and micromelic (short-limbed) dwarfism. Complications
Fetuses homozygous for this condition typically die before being born, and because of this they dont usually live to experience the complications of the disease. Genetics
This condition is typically caused by loss-of-function mutations in the SLC35D1 gene, located in chromosome 1. These mutations are inherited in an autosomal recessive manner. Diagnosis
This condition can be diagnosed through the following methods:

Ultrasound (due to its prenatally fatal nature)
Whole genome sequencing
Physical examination
Post-mortem autopsy

Treatment
There is no cure for this disorder, and attempted treatment will always be ineffective due to this conditions lethal nature. Prevalence
According to OrphaNet, less than 20 cases have been reported. History
This condition was first discovered in 1986 by Knowles et al. when they described 5 fetuses born to a consanguineous, first-cousin Asian couple. The couple in question went through 13 pregnancies, these pregnancies consisted of 4 successful pregnancies which resulted in healthy children, 5 pregnancies which resulted in dead dwarf babies, 3 pregnancies which ended in miscarriage, and 1 pregnancy which was clinically aborted after the pre-natal detection of dwarfism.
It is caused by a defect in the glycine cleavage system (GCS), which is made up of four protein subunits. Each of these four subunits is encoded by a separate gene. Defects in three of these four genes have been linked to glycine encephalopathy. : 790 
There is a fourth unit in the complex, dihydrolipoamide dehydrogenase or GCSL. However, to date there have been no mutations in GCSL found to be associated with glycine encephalopathy. A small percentage of affected individuals do not have detectable mutations in any of the three genes (listed above) that are typically associated with the disease. However, they still show defective glycine-cleavage enzymatic activity. It is thought that these patients may have mutations in the genes encoding one of the cofactors associated with the GCS complex.Defects in the GCS proteins can prevent the complex from functioning properly or can prevent the GCS complex from forming entirely. When the complex is unable to metabolize glycine properly, this causes excess glycine to build up to toxic levels in the bodys organs and tissues. Damage caused by elevated levels of glycine in the brain and cerebrospinal fluid is responsible for the characteristic seizures, breathing difficulties, movement disorders, and intellectual disability.This disorder is inherited in an autosomal recessive pattern. The term "autosomal" signifies that the gene associated with the disorder is located on an autosome. In an autosomal recessive inheritance pattern, two defective copies of the gene (one inherited from each parent) are required in order for a child to be born with the disorder.