Treatment
The outcome in any particular case of hypotonia depends largely on the nature of the underlying disease. In some cases, the underlying cause is treatable. But in general, treatment comprises providing supportive care with rehabilitation services, nutritional and respiratory support.Along with normal pediatric care, specialists who may be involved in the care of a child with hypotonia include developmental pediatricians (specialize in child development), neurologists, neonatologists (specialize in the care of newborns), geneticists, occupational therapists, physical therapists, speech therapists, orthopedists, pathologists (conduct and interpret biochemical tests and tissue analysis), and specialized nursing care. If the underlying cause is known, treatment is tailored to the specific disease, followed by symptomatic and supportive therapy for the hypotonia. In very severe cases, treatment may be primarily supportive, such as mechanical assistance with basic life functions like breathing and feeding, physical therapy to prevent muscle atrophy and maintain joint mobility, and measures to try to prevent opportunistic infections such as pneumonia. Treatments to improve neurological status might involve such things as medication for a seizure disorder, medicines or supplements to stabilize a metabolic disorder, or surgery to help relieve the pressure from hydrocephalus (increased fluid in the brain). The National Institute of Neurological Disorders and Stroke states that physical therapy can improve motor control and overall body strength in individuals with hypotonia. This is crucial to maintaining both static and dynamic postural stability, which is important since postural instability is a common problem in people with hypotonia.
Strumpellin is highly expressed in skeletal muscle cells and mutations in it are also associated with spastic paraplegia. Strumpellin is involved in endosomal transport and cell death processes. The mutation occurs at a splice site  and causes a substantial decrease in the amount of strumpellin produced by the cell. The phenotype is similar to 6pter-p24 deletion syndrome and 6p25 deletion syndrome but has a different etiology. Screening for the condition prenatally may be done with ultrasound. First-trimester ultrasounds can detected nuchal abnormalities
Second-trimester ultrasounds can pick up characteristic major structural abnormalities.Prenatal diagnosis is possible through genetic testing. Chorionic villus sampling or chorionic villus biopsy (CVS) in the first-trimester. Amniocentesis in the second-trimester.Because 3C syndrome is an autosomal recessive disorder, parents with one child with the disorder have a 25% chance of having another child with the disorder. Diagnosis
Differential diagnosis
There is an overlap in symptoms between 3C syndrome and Joubert syndrome. Joubert syndrome often manifests with similar cerebellar hypoplasia and its sequelae, including hyperpnea, ataxia, changes in eye movement, and cleft lip and palate. Occasionally, Joubert syndrome will include heart malformations. Brachmann–de Lange syndrome must also be differentiated from 3C syndrome. It presents with similar craniofacial and heart abnormalities and can include Dandy–Walker phenotype, making it difficult to distinguish. Dandy-Walker malformation is also occasionally seen in Ellis–Van Creveld syndrome, which is characterized by heart defects and malformed alveolar ridge. Many disorders include the Dandy–Walker phenotype and thus it is not pathognomonic for 3C syndrome.CHARGE syndrome can also be misdiagnosed.