Similar to the muscular manifestations above, in the mouth, poor tongue control may be observed. Skin
Skin signs and symptoms in Noonan syndrome include lymphedema (lymph swelling of the extremities), keloid formation, excessive scar formation, hyperkeratosis (overdevelopment of outer skin layer), pigmented nevi (darkly pigmented skin spots), and connective tissue disease. Musculoskeletal
Abnormalities in the limbs and extremities may occur in Noonan syndrome. This may manifest as bluntly ended fingers, extra padding on fingers and toes, edema of the back of hands and tops of feet, and cubitus valgus (wide carrying angle of the elbows). For short stature, growth hormone is sometimes combined with IGF-1 (or as an alternative, IGF-1 as a stand-alone) can be used to achieve an increased height/final height quicker. The final adult height of individuals with Noonan syndrome is about 161–167 cm in males and 150–155 cm in females, which approaches the lower limit of normal.Spinal abnormalities may be present up to 30% of the time and this may require surgery to correct in over 60% of these cases. Other musculoskeletal manifestations in Noonan syndrome are associated with undifferentiated connective-tissue disorders which can be associated with joint contractures (tightness) or joint hypermobility (looseness). Additional factors may present in the form of winging of the scapula, scoliosis, breast bone prominence (pectus carinatum), breast bone depression (pectus excavatum). Muscle abnormalities may present as hypotonia (low muscle tone), which may lead to lordosis (increased hollow in the back) due to poor abdominal muscle tone. Heart
Noonan syndrome is the second most common syndromic cause of congenital heart disease.
The blood received by the parasitic twin has already been used by the normal fetus, and as such is already de-oxygenated, leaving little developmental nutrients for the acardiac twin. Because it is pumping blood for both itself and its acardiac twin, this causes extreme stress on the normal fetus heart. Many T.R.A.P. pregnancies result in heart failure for the healthy twin. This twinning condition usually occurs very early in pregnancy. A rare variant of the acardiac fetus is the acardius acormus where the head is well developed but the heart and the rest of the body are rudimentary. While it is thought that the classical T.R.A.P./Acardius sequence is due to a retrograde flow from the umbilical arteries of the pump twin to the iliac arteries of the acardiac twin resulting in preferential caudal perfusion, acardius acormus is thought to be a result of an early embryopathy. Images of parasitic twins
Human
Animals
See also
Dipygus
Frank Lentini
Lakshmi Tatma
Lazarus and Joannes Baptista Colloredo
Rudy Santos
Vestigial twin

References
Further reading
Lebel, Robert Roger; Carlos Mock; Jeannette Israel; William Senica (June 1994). "Twin reversed arterial perfusion syndrome, acephalic presenting at full term". TheFetus.net. Retrieved 18 February 2013.