However, spastic diplegia is indeed a chronic condition; the symptoms themselves cause compounded effects on the body that are typically just as stressful on the human body as a progressive condition is. Despite this reality and the fact that muscle tightness is the symptom of spastic diplegia and not the cause, symptoms rather than cause are typically seen as the primary area of focus for treatment, especially surgical treatment, except when a selective dorsal rhizotomy is brought into consideration, or when an oral baclofen regimen is attempted.Unlike any other condition that may present with similar effects, spastic diplegia is entirely congenital in origin—that is, it is almost always acquired shortly before or during a babys birth process. Things like exposure to toxins, traumatic brain injury, encephalitis, meningitis, drowning, or suffocation do not tend to lead to spastic diplegia in particular or even cerebral palsy generally. Overall, the most common cause of spastic diplegia is Periventricular leukomalacia, more commonly known as neonatal asphyxia or infant hypoxia—a sudden in-womb shortage of oxygen-delivery through the umbilical cord. This sudden lack of oxygen is also almost always combined with premature birth, a phenomenon that, even by itself, would inherently risk the infant developing some type of CP. On the other hand, the presence of certain maternal infections during pregnancy such as congenital rubella syndrome can also lead to spastic diplegia, since such infections can have similar end results to infant hypoxia.
Seckel syndrome, or microcephalic primordial dwarfism (also known as bird-headed dwarfism, Harpers syndrome, Virchow–Seckel dwarfism and bird-headed dwarf of Seckel) is an extremely rare congenital nanosomic disorder. Inheritance is autosomal recessive. It is characterized by intrauterine growth restriction and postnatal dwarfism with a small head, narrow bird-like face with a beak-like nose, large eyes with down-slanting palpebral fissures, receding mandible and intellectual disability. A mouse model has been developed. This mouse model is characterized by a severe deficiency of ATR protein. These mice have high levels of replicative stress and DNA damage. Adult Seckel mice display accelerated ageing. These findings are consistent with the DNA damage theory of aging. Symptoms and signs
Symptoms include:

intellectual disability (more than half of the patients have an IQ below 50)
microcephaly
sometimes pancytopenia (low blood counts)
cryptorchidism in males
low birth weight
dislocations of pelvis and elbow
unusually large eyes
blindness or visual impairment
large, low-set ears
small chin due to receded lower jaw

Genetics
It is believed to be caused by defects of genes on chromosome 3 and 18. One form of Seckel syndrome can be caused by mutation in the gene encoding the ataxia telangiectasia and Rad3-related protein (ATR) which maps to chromosome 3q22.1-q24. This gene is central in the cells DNA damage response and repair mechanism. Types include:

Diagnosis
Treatment
History
The syndrome was named after German-American physician Helmut Paul George Seckel (1900–1960). The synonym Harpers syndrome was named after Rita G. Harper. See also
Koo-Koo the Bird Girl

References
External links
Seckels syndrome at Who Named It?