However, for some MdDS sufferers there maybe have been a correlation between migraine and some pathophysiological overlap or even some other precipitating illness.The condition may be masked by a return to motion such as in a car, train, plane, or boat; however, once the motion ceases, the symptoms rebound or return, often at much higher levels than when the journey first commenced.The symptoms of MdDS may be extremely debilitating and fluctuate high and low on a daily basis; it greatly affects the daily life and working capacity of sufferers with many having to relinquish work; it also limits most other daily and social activities. Sufferers can have low quality of life in both the physical and emotional realms, comparable to people who have multiple sclerosis with many symptoms being of a similar nature. High levels of disequilibrium can contribute to suffers not being able to drive a car or walk far and this can create varying levels of anxiety in some or possibly depression due to the significant level of disability. Diagnosis
MdDS is diagnosed several ways, one being by the symptoms: in particular, the "constant rocking, swaying feeling" and the abatement of this feeling when in motion again and as a matter of exclusion. There are no definitive tests that confirm MdDS, only tests that rule out other conditions. Tests include hearing and balance, and MdDS is generally diagnosed by either a neurologist or an ear, nose, and throat specialist.
Each lesion—a damaged section of DNA—must be snipped out and the DNA repaired to preserve its normal function. Unrepaired DNA can lose its ability to code for proteins. Mutations also can result. These mutations can activate oncogenes or silence tumor suppressor genes. According to research, oxidative damage to active genes is not preferentially repaired, and in the most severe cases, the repair is slowed throughout the whole genome. The resulting accumulation of oxidative damage could impair the normal functions of the DNA and may even result in triggering a program of cell death (apoptosis). The children with this disease do not repair the active genes where oxidative damage occurs. Normally, oxidative damage repair is faster in the active genes (which make up less than five percent of the genome) than in inactive regions of the DNA. The resulting accumulation of oxidative damage could impair the normal functions of the DNA and may even result in triggering a program of cell death (apoptosis). Genetics
Cockayne syndrome is classified genetically as follows:
Mutations in the ERCC8 (also known as CSA) gene or the ERCC6 (also known as CSB) gene are the cause of Cockayne syndrome. Mutations in the ERCC6 gene mutation makes up ~70% of cases. The proteins made by these genes are involved in repairing damaged DNA via the  transcription-coupled repair mechanism, particularly the DNA in active genes. DNA damage is caused by ultraviolet rays from sunlight, radiation, or free radicals in the body. A normal cell can repair DNA damage before it accumulates.