[citation needed] DM1 and DM2 differ in regards to the muscles they affect, age of onset, severity of disease, and extramuscular manifestations.

[citation needed] It slowly progresses to involve other muscle groups, including the heart.

[citation needed] Thus, various diagnostic classifications based on the age of onset/severity of the disease have been proposed, although DM1 manifestations likely lie on a continuum.

[5] Manifestations that can be present at birth include hypotonia, respiratory failure, feeding difficulty, and club foot (talipes equinovarus), any of which tend to resolve over several years.

[5] Gastrointestinal issues can result, which can be severe, manifestations including diarrhea, constipation, and fecal incontinence.

Consequently, the children of individuals with premutations or mutations inherit DMPK alleles that are longer than their parents and therefore are more likely to be affected or display an earlier onset and greater severity of the condition, a phenomenon known as anticipation.

[15] Paternal transmission of the congenital form is uncommon (13%), possibly due to selection pressures against sperm with expanded repeats, but juvenile or adult-onset is equally transmitted from either parent.

[citation needed] The RNA from the expanded trinucleotide repeat region forms intranucleoplasmic hairpin loops due to the extensive hydrogen bonding between C-G base pairs, and it has been demonstrated that these sequester the splicing regulator MBNL1 to form distinctive foci.

[16] A severe form of DM1, congenital myotonic dystrophy, may appear in newborns of mothers who have DM.

[5] Also, repeat expansion likely reduces expression of CNBP, loss of which causes muscle toxicity.

[22][5] As a result, people with multiple symptoms that may be explained by a complex disorder such as DM1 or DM2 will generally be referred by their primary care physician to a neurologist for diagnosis.

Depending on the presentation of symptoms, people may be referred to a number of medical specialists including cardiologists, ophthalmologists, endocrinologists, and rheumatologists.

Though there is presently no cure for DM and management is currently symptom-based, a precise diagnosis is still necessary to anticipate multiple other problems that may develop over time (e.g. cataracts).

Potentially serious anesthetic risks are important to note, so the presence of this disorder should be brought to the attention of all medical providers.

[24] Type 2 (DM2), also known as proximal myotonic myopathy (PROMM), is rarer and generally manifests with milder signs and symptoms than DM1.

[13] One case which was proposed as a candidate for the "DM3" label,[25] was later characterized as an unusual form of inclusion body myopathy associated with Paget's disease and frontotemporal dementia.

This can be done at 10–12 weeks gestation by a procedure called chorionic villus sampling (CVS) that involves removing a tiny piece of the placenta and analyzing DNA from its cells.

Each of these procedures has a small risk of miscarriage associated with it and those who are interested in learning more should check with their doctor or genetic counselor.

There is also another procedure called preimplantation diagnosis that allows a couple to have a child that is unaffected by the genetic condition in their family.

It is possible to test someone who is at risk for developing DM1 before they show symptoms to see whether they inherited an expanded trinucleotide repeat.

[13] Compromised lung function can, in turn, contribute to life-threatening complications during anesthesia and pregnancy.

[citation needed] Cardiac complications are the second leading cause of death in DM1, and commonly no symptoms are present before adverse events.

Improving the quality of life which can be measured using specific questionnaires[28] is also a main objective of medical care.

There is a lack of high-quality evidence to determine the effectiveness and the safety of physical activities for people who have myotonic dystrophy.

[30][29] Aerobic exercise via stationary bicycle with an ergometer may be safe and effective in improving fitness in people with DM1.

[31] Cardiovascular impairments and myotonic sensitivities to exercise and temperature necessitate close monitoring of people and educating people in self-monitoring during exercise via the Borg scale, heart rate monitors, and other physical exertion measurements.

[1] DM1 is the most common form of myotonic muscular dystrophy diagnosed in children, with a prevalence ranging from 1 per 100,000 in Japan to 3–15 per 100,000 in Europe.

Myotonic dystrophy was first described by a German physician, Hans Gustav Wilhelm Steinert, who first published a series of six cases of the condition in 1909.

[13] However, due to the weak evidence and potential side effects such as cardiac arrhythmias, these treatments are rarely used.

A recent study in December 2015 showed that a common FDA-approved antibiotic, erythromycin, reduced myotonia in mice.