Some conditions known to cause hypotonia include:

Congenital - i.e. disease a person is born with

Hypotonia, commonly known as floppy baby syndrome, is a state of low muscle tone (the amount of tension or resistance to stretch in a muscle), often involving reduced muscle strength. Hypotonia is not a specific medical disorder, but a potential manifestation of many different diseases and disorders that affect motor nerve control by the brain or muscle strength. Hypotonia is resistance to passive movement, whereas muscle weakness results in impaired active movement. Central hypotonia originates from the central nervous system, while peripheral hypotonia is related to problems within the spinal cord, peripheral nerves and/or skeletal muscles. Recognizing hypotonia, even in early infancy, is usually relatively straightforward, but diagnosing the underlying cause can be difficult and often unsuccessful. The long-term effects of hypotonia on a child's development and later life depend primarily on the severity of the muscle weakness and the nature of the cause. Some disorders have a specific treatment but the principal treatment for most hypotonia of idiopathic or neurologic cause is physical therapy, occupational therapy for remediation, and/or music therapy.

Hypotonia is thought to be associated with the disruption of input from stretch receptors and/or lack of the cerebellum’s facilitatory efferent influence on the fusimotor system, the system that innervates intrafusal muscle fibers thereby controlling muscle spindle sensitivity. On examination a diminished resistance to passive movement will be noted and muscles may feel abnormally soft and limp on palpation. Diminished deep tendon reflexes also may be noted. Hypotonia is a condition that can be helped with early intervention.

The prevalence rate has been estimated to be less than 1/1,000,000 worldwide. However, it is much more common in the French-Canadian population of the Saguenay and Lac-St-Jean regions of Quebec, Canada, where it has a frequency of about 1 in 2100 in live births, and a carrier rate of 1 in 23.

In utero exposure to cocaine and other street drugs can lead to agenesis of corpus callosum.

The prognosis is poor. Patients are usually wheelchair bound by their 20s and die by their 30s.

Flaccid dysarthria is caused when damage occurs to the motor unit (one or more cranial or spinal nerves). Processes that can cause this include:

- Congenital disorders

- Demyelinating disorders

- Infectious/Inflammatory

- Degenerative disorders

- Metabolic

- Neoplastic

- Traumatic

- Vascular Diseases

- Flaccid Paralysis

Several people with distal 18q- have been diagnosed with low IgA levels, resulting in an increased incidence of infections.

Until recently, the medical literature did not indicate a connection among many genetic disorders, both genetic syndromes and genetic diseases, that are now being found to be related. As a result of new genetic research, some of these are, in fact, highly related in their root cause despite the widely varying symptoms apparent on clinical examination. Agenesis of the corpus callosum is one such disease, part of an emerging class of diseases called ciliopathies. The underlying cause may be a dysfunctional molecular mechanism in the primary cilia structures of the cell organelles that are present in many cellular types throughout the human body. The cilia defects adversely affect "numerous critical developmental signaling pathways" essential to cellular development and thus offer a plausible hypothesis for the often multi-symptom nature of a large set of syndromes and diseases. Known ciliopathies include primary ciliary dyskinesia, Bardet–Biedl syndrome, polycystic kidney and liver disease, nephronophthisis, Alström syndrome, Meckel–Gruber syndrome, and some forms of retinal degeneration.

Hypothyroidism has been reported in some people with distal 18q-.

The prognosis for children with lissencephaly varies depending on the malformation. Many individuals remain in a 3–5 month developmental level. Some children with lissencephaly will be able to roll over, sit, reach for objects, and smile socially. Aspiration and respiratory disease are the most common causes of illness or death. In the past, life expectancy was said to be around two years of age. However, with advances in seizure control, and treatments for respiratory illness, most children live well beyond that age. With other advances in therapy, and the broader availability of services and equipment, some children with lissencephaly are able to walk with varying degrees of assistance and to perform other functions once thought too advanced.

18p- is a genetic condition caused by a deletion of all or part of the short arm (the p arm) of chromosome 18. It occurs in about 1 of every 50,000 births.

The collecting system is the structure that collects urine directly from the kidney tissue and routes it by way of the ureter to the bladder. Structural renal abnormalities are rare in both sexes.

1p36 deletion syndrome (also known as monosomy 1p36) is a congenital genetic disorder characterized by moderate to severe intellectual disability, delayed growth, hypotonia, seizures, limited speech ability, malformations, hearing and vision impairment, and distinct facial features. The symptoms may vary, depending on the exact location of the chromosomal deletion.

The condition is caused by a genetic deletion (loss of a segment of DNA) on the outermost band on the short arm (p) of chromosome 1. It is one of the most common deletion syndromes. It is estimated that the syndrome occurs in one in every 5,000 to 10,000 births. Knowledge of the disorder has increased a great deal over the last decade, mainly because more patients have been accurately diagnosed and described in international medical literature.

Most common causes of lower motor neuron injuries are trauma to peripheral nerves that serve the axons – a virus that selectively attacks ventral horn cells.

Disuse atrophy of the muscle occurs i.e., shrinkage of muscle fibre finally replaced by fibrous tissue (fibrous muscle)

Other causes include Guillain–Barré syndrome, "C. botulism", polio, and cauda equina syndrome; another common cause of lower motor neuron degeneration is amyotrophic lateral sclerosis.

Prognosis varies widely depending on severity of symptoms, degree of intellectual impairment, and associated complications. Because the syndrome is rare and so newly identified, there are no long term studies.

About 10-15% of individuals with 18p- have holoprosencephaly.

Approximately 10% of people with 18p- have a congenital heart anomaly. There does not appear to be a specific type of heart defect associated with a deletion of the short arm of chromosome 18. Septal defects, tetralogy of Fallot, dextrocardia, and coarctation of the aorta have all been reported in infants with 18p-.

Mosaic mutations in PIK3CA have been found to be the genetic cause of M-CM. Genetic testing for the mutation is currently only available on a research basis. Other overgrowth conditions with distinct phenotypes have also been found to be caused by mosaic mutations in PIK3CA. How different mutations in this gene result in a variety of defined clinical syndromes is still being clarified. Mutations in PIK3CA have not been found in a non-mosaic state in any of these disorders, so it is unlikely that the conditions could be inherited.

Flaccid dysarthria is a motor speech disorder resulting from damage to peripheral nervous system (cranial or spinal nerves) or lower motor neuron system. Depending on which nerves are damaged, flaccid dysarthria affects respiration, phonation, resonance, and articulation. It also causes weakness, hypotonia (low-muscle tone), and diminished reflexes., Perceptual effects of flaccid dysarthria can include hypernasality, imprecise consonant productions, breathiness of voice, and affected nasal emission.

The lateral meningocele syndrome is a very rare skeletal disorder with facial anomalies, hypotonia and meningocele-related neurologic dysfunction.

Causes of lissencephaly can include viral infections of the uterus or the fetus during the first trimester, or insufficient blood supply to the fetal brain early in pregnancy. There are also a number of genetic causes of lissencephaly, including mutation of the reelin gene (on chromosome 7), as well as other genes on the X chromosome and on chromosome 17. Genetic counseling is usually offered if there is a risk of lissencephaly, coupled with genetic testing.

Pitt–Hopkins syndrome is a rare genetic disorder characterized by developmental delay, a wide mouth, distinctive facial features, and intermittent hyperventilation followed by apnea. It is associated with an abnormality within chromosome 18: specifically, it is caused by an insufficient expression of the TCF4 gene.

Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms. Myoclonus and seizures may be treated with drugs like valproate.

Some have described this condition as difficult to characterize.

Qazi–Markouizos syndrome is a rare hereditary condition characterized by non-progressive, congenital hypotonia, severe intellectual disability, an increased proportion of type 2 muscle fibers, which additionally exhibited increased size, as well as dysharmonic skeletal maturation. To date, the molecular mechanism of Qazi–Markouizos syndrome, which is also known as Puerto Rican infant hypotonia syndrome, remains unknown.

This syndrome appears to be inherited in an autosomal dominant fashion.

Molecular analyses suggest that the causative mutations cause a truncation of the protein. These mutations result in the loss of PEST sequence in the protein. This loss is associated with a prolonged half life of the protein.

Mutations in Notch 3 were found to be associated with this syndrome.

Al-Raqad syndrome (ARS) is a congenital autosomal recessive syndrome discovered by Jordanian physician Mohammad Al-Raqad.

It's characterized by:

- microcephaly

- growth delay

- Psycho-motor developmental delay

- congenital hypotonia.

Al-Raqad syndrome is caused by mutation of DCPS gene.