Its tendon runs between those of the soleus and gastrocnemius and is embedded in the medial end of the calcaneus tendon.In the deep layer, the tibialis posterior has its origin on the interosseus membrane and the neighbouring bone areas and runs down behind the medial malleolus. Under the foot it splits into a thick medial part attached to the navicular bone and a slightly weaker lateral part inserted to the three cuneiform bones. The muscle produces simultaneous plantar flexion and supination in the non-weight-bearing leg, and approximates the heel to the calf of the leg. The flexor hallucis longus arises distally on the fibula and on the interosseus membrane from where its relatively thick muscle belly extends far distally. Its tendon extends beneath the flexor retinaculum to the sole of the foot and finally attaches on the base of the last phalanx of the hallux. It plantarflexes the hallux and assists in supination. The flexor digitorum longus, finally, has its origin on the upper part of the tibia. Its tendon runs to the sole of the foot where it forks into four terminal tendon attached to the last phalanges of the four lateral toes. It crosses the tendon of the tibialis posterior distally on the tibia, and the tendon of the flexor hallucis longus in the sole. Distally to its division, the quadratus plantae radiates into it and near the middle phalanges its tendons penetrate the tendons of the flexor digitorum brevis. In the non-weight-bearing leg, it plantar flexes the toes and foot and supinates.
Hypervalinemia is a rare autosomal recessive metabolic disorder in which urinary and serum levels of the branched-chain amino acid valine are elevated, without related elevation of the branched-chain amino acids leucine and isoleucine. It is caused by a deficiency of the enzyme valine transaminase. Presentation
Presenting in infancy, symptoms include lack of appetite, vomiting, dehydration, hypotonia and failure to thrive. Genetics
Hypervalinemia is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. Diagnosis
See also
Isovaleric acidemia
Maple syrup urine disease
Propionic acidemia

References


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