There exist five types of Hanhart syndrome, with the severity and nature of the condition ranging widely on a case-by-case basis.

[2][3] Due to the wide range of symptoms presented in Hanhart syndrome, the disorder has received many different names throughout its diagnostic history.

[2][1] Hanhart syndrome is characterized by an underdeveloped tongue (hypoglossia), small mouth (microstomia), smaller than average jaw size (micrognathia), clefting or abnormal attachment of the tongue, missing teeth (mandibular hypodontia), cleft palate, cranial nerve palsies including Möbius syndrome, broad nose, increased distance between the eyes (telecanthus), defects in the lower eyelids, and facial asymmetry.

[6] Ultrasound examination of the cranial and abdominal regions in patients has found that internal structures are unaffected by Hanhart syndrome.

[9] Hanhart syndrome follows an autosomal dominant inheritance pattern, has a population prevalence of <1/1,000,000, and due to its rarity has been classified as a rare disease.

[5] The prevalence of Hanhart syndrome within consanguineous patients lead to an early hypothesis that a mutation in an autosomal recessive gene led to the condition.

[7] In 1973, a hypothesis that hemorrhagic lesions or blood clots during prenatal development were the cause of Hanhart syndrome was proposed.

[11] Interactions between the ectodermal and mesodermal germ layers,[4] and the use of meclizine hydrochloride during pregnancy have been proposed as a potential causes.

When CVS is used during the early stages of pregnancy, specifically during the first 10 weeks of amenorrhoea, there is an increased correlation with risk of the fetus developing Hanhart syndrome.