and returns to its normal resting state." "...The child with low tone has muscles that are slow to initiate a muscle contraction, contract very slowly in response to a stimulus, and cannot maintain a contraction for as long as his 'normal' peers. Because these low-toned muscles do not fully contract before they again relax (muscle accommodates to the stimulus and so shuts down again), they remain loose and very stretchy, never realizing their full potential of maintaining a muscle contraction over time. " Cause The most common cause of central hypotonia in newborns is hypoxic ischemic encephalopathy. Brain malformations and inborn errors of metabolism account for 13% and 3% respectively. Causes that affects the central nervous systems are: chromosomal disorders, inborn errors of metabolism, cerebral dysgenesis, and trauma to the brain and spinal cord. Metabolic causes includes: glycogen storage disease type II, pyruvate dehydrogenase deficiency, mitochondrial disease, Zellweger syndrome, Smith–Lemli–Opitz syndrome, and congenital disorder of glycosylation. Metabolic disorders in infants are usually presented with various other features such as dysmorphic feature, seizures, encephalopathy, biochemistry profile apart from hypotonia. Some conditions known to cause hypotonia include: Congenital – i.e. disease a person is born with (including genetic disorders presenting within 6 months) Genetic disorders are the most common cause 22q13 deletion syndrome a.k.a. Phelan–McDermid syndrome 3-Methylcrotonyl-CoA carboxylase deficiency Achondroplasia Aicardi syndrome Autism spectrum disorders Canavan disease Centronuclear myopathy (including myotubular myopathy) Central core disease CHARGE syndrome Cohen syndrome Costello syndrome Dejerine–Sottas disease (HMSN Type III) Down syndrome a.k.a. trisomy 21 — most common Ehlers–Danlos syndrome Familial dysautonomia (Riley–Day syndrome) FG syndrome Fragile X syndrome Griscelli syndrome Type 1 (Elejalde syndrome) Holocarboxylase synthetase deficiency / Multiple carboxylase deficiency Krabbe disease Leigh's disease Lesch–Nyhan syndrome Marfan's syndrome Menkes syndrome Methylmalonic acidemia Myotonic dystrophy Niemann–Pick disease Nonketotic hyperglycinemia (NKH) or Glycine encephalopathy (GCE) Noonan syndrome Neurofibromatosis Patau syndrome a.k.a. trisomy 13 Pituitary dwarfism/growth hormone deficiency(in adults) Prader–Willi syndrome Rett syndrome Septo-optic dysplasia (de Morsier syndrome) Snyder–Robinson syndrome (SRS) Spinal muscular atrophy (SMA) Succinic semialdehyde dehydrogenase deficiency (SSADH) Tay–Sachs disease Werdnig–Hoffmann syndrome – Spinal muscular atrophy with congenital degeneration of anterior horns of spinal cord. Autosomal recessive Wiedemann–Steiner syndrome Williams syndrome Zellweger syndrome a.k.a. cerebrohepatorenal syndrome Developmental disability Cerebellar ataxia (congenital) Sensory processing disorder Developmental coordination disorder Hypothyroidism (congenital) Hypotonic cerebral palsy Teratogenesis from in utero exposure to Benzodiazepines Acquired Acquired – i.e. onset occurs after birth Genetic Muscular dystrophy (including Myotonic dystrophy) – most