Recent research suggests that specific social difficulties may be a result of impaired face processing. The unusual social behavior in childhood often resembles that of an autism spectrum disorder.Other characteristics sometimes associated with callosal disorders include seizures, spasticity, early feeding difficulties and/or gastric reflux, hearing impairments, abnormal head and facial features, and intellectual disability. Associated brain anomalies
Brain anomalies that can sometimes occur in syndromes that cause callosal disorders include:
Aplasia of the cerebellar vermis
Chiari malformation
Colpocephaly
Dandy–Walker syndrome
Holoprosencephaly
Hydrocephalus
Neuronal migration disorders such as grey matter heterotopia
Schizencephaly

Associated syndromes and conditions
Some syndromes that frequently include ACC are:
Acrocallosal syndrome
Aicardi syndrome
Andermann syndrome
Donnai–Barrow syndrome
Dwarfism
FG syndrome
L1CAM syndrome
Microcephalic osteodysplastic primordial dwarfism type II
Mowat–Wilson syndrome
Oculocerebrocutaneous syndrome
Saal Bulas syndrome
Septo-optic dysplasia (optic nerve hypoplasia)
Shapiro syndrome
Vici syndromeSome conditions that can sometimes be associated with ACC or other callosal disorders include:
1p36 deletion syndrome
13q deletion syndrome
CDK13-related disorder
Craniofacial abnormalities and other oral and maxillofacial pathologies
Fetal alcohol syndrome
Fetal warfarin syndrome
Genitopatellar syndrome
Gomez-Lopez-Hernandez syndrome
Joubert syndrome
Lujan–Fryns syndrome
Marden–Walker syndrome
Maternal nutritional deficiencies or infections
Metabolic disorders
Okamoto syndrome
Opitz G/BBB syndrome
Pascual-Castroviejo syndrome
Pitt–Hopkins syndrome
Sensenbrenner syndrome
Strømme syndrome
Triploid syndrome
Trisomy 9
Xia-Gibbs syndrome

Causes
Agenesis of the corpus callosum is caused by disruption to development of the fetal brain between the 3rd and 12th weeks of pregnancy. In most cases, it is not possible to know what caused an individual to have ACC or another callosal disorder. However, research suggests that some possible causes may include chromosome errors, inherited genetic factors, prenatal infections or injuries, prenatal toxic exposures, structural blockage by cysts or other brain abnormalities and metabolic disorders.
Examination checks for sensory differences between the affected leg and the other leg.Differentiation of meralgia paraesthetica from a second lumbar root lesion remains the greatest problem in diagnosis and relies on the careful delineation of the paraesthetic area, the degree of numbness and a negative MR scan of the lumbar spine. Although the L2 area and the area supplied by the lateral cutaneous nerve correspond well laterally, the second root also contributes to the innervation of the groin and the inner aspect of the thigh. Furthermore, in L2 root lesions the analgesia is very slight because of the overlap between L2 and L3, whereas in lesions of the lateral cutaneous nerve, there is
almost full anaesthesia, with a clear-cut border.Accurate diagnosis may require an abdominal and pelvic examination to exclude problems in those areas.Electromyographic (EMG) nerve-conduction studies may be required.X-rays may be needed to exclude bone abnormalities that might put pressure on the nerve; likewise CT or MRI scans to exclude soft tissue causes such as a tumor. Treatment
Treatment varies. In most cases, the best treatment is to remove the cause of compression by modifying patient behavior, in combination with medical treatment to relieve inflammation and pain. Whatever the cause, typical treatment takes several weeks to months—depending on the degree of nerve damage. Typical treatment options include:
Active Release Technique (ART) soft tissue treatment
Wearing looser clothing and suspenders rather than belts
Weight loss if obesity is present
Non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammatory pain if pain level limits motion and prevents sleep
Reducing physical activity in relation to pain level.