Fukuyama congenital muscular dystrophy has a poor prognosis. Most children with FCMD reach a maximum mobility at sitting upright and sliding. Due to the compounded effects of continually worsening heart problems, impaired mental development, problems swallowing and additional complications, children with FCMD rarely live through adolescence, the disorder proves fatal by age 20.

The disease is found across 5 continents (30 countries) and is frequently seen in French Canadians, with a prevalence 1:1000. OPMD affects males and females equally, and affected individuals have been found in Europe (France), Jewish Ashkenazi, and Spanish Americans.

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. The prevalence may be as high as 1 in 500 in regions such as Quebec, possibly due to the founder effect. In most populations, DM1 appears to be more common than DM2. However, recent studies suggest that type 2 may be as common as type 1 among people in Germany and Finland.

The incidence of congenital myotonic dystrophy is thought to be about 1:20,000. DM occurs in about 1 per 7,000–8,000 people and has been described in people from all over the world. It affects males and females approximately equally. About 30,000 people in the United States are affected.

Facioscapulohumeral muscular dystrophy (FSHMD, FSHD or FSH)—originally named Landouzy-Dejerine—is a usually autosomal dominant inherited form of muscular dystrophy (MD) that initially affects the skeletal muscles of the face (facio), scapula (scapulo) and upper arms (humeral). FSHD is the third most common genetic disease of skeletal muscle. Orpha.net lists the prevalence as 4/100,000 while a 2014 population-based study in the Netherlands reported a significantly higher prevalence of 12 in 100,000.

Symptoms may develop in early childhood and are usually noticeable in the teenage years, with 95% of affected individuals manifesting disease by age 20 years. A progressive skeletal muscle weakness usually develops in other areas of the body as well; often the weakness is asymmetrical. Life expectancy can be threatened by respiratory insufficiency, and up to 20% of affected individuals become severely disabled, requiring use of a wheel chair or mobility scooter. In a Dutch study, approximately 1% of patients required (nocturnal or diurnal) ventilatory support. Non-muscular symptoms frequently associated with FSHD include subclinical sensorineural hearing loss and retinal telangiectasia.

In more than 95% of known cases, the disease is associated with contraction of the D4Z4 repeat in the 4q35 subtelomeric region of Chromosome 4. Seminal research published in August 2010 now shows the disease requires a second mechanism, which for the first time provides a unifying theory for its underlying genetics. The second mechanism is a "toxic gain of function" of the DUX4 gene, which is the first time in genetic research that a "dead gene" has been found to "wake up" and cause disease.

Building on the 2010 unified theory of FSHD, researchers in 2014 published the first proposed pathophysiology definition of the disease and four viable therapeutic targets for possible intervention points.

In 2007 the FSHD Global Research Foundation was established to increase the amount of funding available to research bodies. The Foundation has identified 13 priority areas of interest for FSHD research.

The genetics of congenital muscular dystrophy are autosomal recessive which means two copies of an abnormal gene must be present

for the disease or trait to happen. In the case of collagen VI-deficient, it is autosomal dominant, which means a child could inherit the disease from only one copy of a gene present in only one parent.

The prevalence for congenital muscular dystrophy seems to be between 2.6-4.5 in 10,000 according to Reed, 2009. MDCIA, for example is due to a mutation in the LAMA-2 gene and is involved with the 6q2 chromosome.

Fukuyama congenital muscular dystrophy (FCMD) is a rare, autosomal recessive form of muscular dystrophy (weakness and breakdown of muscular tissue) mainly described in Japan but also identified in Turkish and Ashkenazi Jewish patients, fifteen cases were first described on 1960 by Fukuyama.

FCMD mainly affects the brain, eyes, and muscles, in particular, the disorder affects development of the skeletal muscles leading to weakness and deformed appearances, and brain development is blunted affecting cognitive functioning as well as social skills. In 1995, the disorder was linked to mutations in a gene coding for the protein fukutin (the "FCMD" gene). Fukuyama congenital muscular dystrophy is the second most prevalent form of muscular dystrophy in Japan. One out of every 90 people in Japan is a heterozygous carrier.

The prognosis of this sub-type of MD indicates that the affected individual may eventually have feeding difficulties. Surgery, at some point, might be an option for scoliosis.

Scoliosis which is a sideways curve of the persons vertebrate, is determined by a variety of factors, including the degree (mild or severe), in which case if possible a brace might be used by the individual

Emery–Dreifuss muscular dystrophy is a condition that mainly affects muscles used for movement, such as skeletal muscles and also affects the cardiac muscle, it is named after Alan Eglin H. Emery and Fritz E. Dreifuss.

In northern Scandinavia, the prevalence of myotonia congenita has been estimated at 1:10,000.

Myotonia congenita is estimated to affect 1 in 1,000,000 people worldwide.

Ullrich congenital muscular dystrophy is a form of congenital muscular dystrophy.It is associated with variants of type VI collagen, it is commonly associated with muscle weakness and respiratory problems, though cardiac issues are not associated with this type of CMD. It is named after Otto Ullrich, who is also known for the Ullrich-Turner syndrome.

Distal muscular dystrophy (or distal myopathy) is a group of disorders characterized by onset in the hands or feet. Many types involve dysferlin, but it has been suggested that not all cases do.

Types include:

DYSF is also associated with limb-girdle muscular dystrophy type 2B.

Distal muscular dystrophy is a type of muscular dystrophy that affects the muscles of the extremities, the hands, feet, lower arms, or lower legs. The cause of this dystrophy is very hard to determine because it can be a mutation in any of at least eight genes and not all are known yet. These mutations can be inherited from one parent, autosomal dominant, or from both parents, autosomal recessive. Along with being able to inherit the mutated gene, distal muscular dystrophy has slow progress therefore the patient may not know that they have it until they are in their late 40’s or 50’s. There are eight known types of distal muscular dystrophy. They are Welander’s distal myopathy, Finnish (tibial) distal myopathy, Miyoshi distal myopathy, Nonaka distal myopathy, Gowers–Laing distal myopathy, hereditary inclusion-body myositis type 1, distal myopathy with vocal cord and pharyngeal weakness, and ZASP-related myopathy. All of these affect different regions of the extremities and can show up as early as 5 years of age to as late as 50 years old. Doctors are still trying to determine what causes these mutations along with effective treatments.

Oculopharyngeal muscular dystrophy (OPMD) is a rare form of muscular dystrophy with symptoms generally starting when an individual is 40 to 50 years old. It can be autosomal dominant neuromuscular disease or autosomal recessive. The most common inheritance of OPMD is autosomal dominant, which means only one copy of the mutated gene needs to be present in each cell. Children of an affected parent have a 50% chance of inheriting the mutant gene.

Autosomal dominant inheritance is the most common form of inheritance. Less commonly, OPMD can be inherited in an autosomal recessive pattern, which means that two copies of the mutated gene need to be present in each cell, both parents need to be carriers of the mutated gene, and usually show no signs or symptoms. The PABPN1 mutation contains a GCG trinucleotide repeat at the 5' end of the coding region, and expansion of this repeat which then leads to autosomal dominant oculopharyngeal muscular dystrophy (OPMD) disease.

Parents of a proband

- The parents of an affected individual are obligate heterozygotes and therefore carry one mutant allele.

- Heterozygotes (carriers) are asymptomatic.

Sibs of a proband

- At conception, each sibling of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier.

- Once an at-risk sibling is known to be unaffected, the risk of his/her being a carrier is 2/3.

- Heterozygotes (carriers) are asymptomatic.

Offspring of a proband

- Offspring of a proband are obligate heterozygotes and will therefore carry one mutant allele.

- In populations with a high rate of consanguinity, the offspring of a person with GPR56-related BFPP and a reproductive partner who is a carrier of GPR56-related BFPP have a 50% chance of inheriting two GPR56 disease-causing alleles and having BFPP and a 50% chance of being carriers.

Other family members of a proband.

- Each sibling of the proband's parents is at a 50% risk of being a carrier

Possible complications associated with MD are cardiac arrhythmias.(BMD) Becker muscular dystrophy also demonstrates the following:

- Mental impairment (less common in BMD than it is in DMD.)

- Pulmonary failure

- Pneumonia

Becker muscular dystrophy is an X-linked recessive inherited disorder characterized by slowly progressive muscle weakness of the legs and pelvis. It is a type of dystrophinopathy. This is caused by mutations in the dystrophin gene, which encodes the protein dystrophin. Becker muscular dystrophy is related to Duchenne muscular dystrophy in that both result from a mutation in the "dystrophin" gene.

Bethlem myopathy is an autosomal dominant myopathy, classified as a congenital form of muscular dystrophy, that is caused by a mutation in one of the three genes coding for type VI collagen. These include COL6A1, COL6A2, and COL6A3.

Duchenne muscular dystrophy is a rare progressive disease which eventually affects all voluntary muscles and involves the heart and breathing muscles in later stages. As of 2013, the life expectancy is estimated to be around 25, but this varies. With excellent medical care males are often living into their 30s.

In rare cases, people with DMD have been seen to survive into their forties or early fifties, with proper positioning in wheelchairs and beds, and the use of ventilator support (via tracheostomy or mouthpiece), airway clearance, and heart medications. Early planning of the required supports for later-life care has shown greater longevity for people with DMD.

Curiously, in the mdx mouse model of Duchenne muscular dystrophy, the lack of dystrophin is associated with increased calcium levels and skeletal muscle myonecrosis. The intrinsic laryngeal muscles (ILMs) are protected and do not undergo myonecrosis. ILMs have a calcium regulation system profile suggestive of a better ability to handle calcium changes in comparison to other muscles, and this may provide a mechanistic insight for their unique pathophysiological properties. The ILM may facilitate the development of novel strategies for the prevention and treatment of muscle wasting in a variety of clinical scenarios.

In terms of the mechanism of congenital muscular dystrophy, one finds that though there are many types of CMD the glycosylation of α-dystroglycan and alterations in those genes that are involved are an important part of this conditions pathophysiology

In terms of the genetics LGMD is an inherited disorder, though it may be inherited as a dominant or recessive genetic defect. The result of the defect is that the muscles cannot properly form certain proteins needed for normal muscle function. Several different proteins can be affected, and the specific protein that is absent or defective identifies the specific type of muscular dystrophy. Among the proteins affected in LGMD are α, β, γ and δ sarcoglycans. The sarcoglycanopathies could be possibly amenable to gene therapy.

Zaspopathy, also called ZASP-related myofibril myopathy, is a novel autosomal dominant form of progressive muscular dystrophy, first described in 2005.

The disease encompasses multiple forms of both distal and proximal myopathies, and is caused by mutations in the gene referred to as ZASP.

Limb-girdle muscular dystrophy (LGMD) or Erb's muscular dystrophy is a genetically and clinically heterogeneous group of rare muscular dystrophies. It is characterised by progressive muscle wasting which affects predominantly hip and shoulder muscles. LGMD has an autosomal pattern of inheritance and currently has no known cure.

Myotonic dystrophy is a genetic condition which is inherited in an autosomal dominant pattern and thus will be passed along to 50% of a carrier's offspring, on average. Myotonic dystrophy is one of several known trinucleotide repeat disorders. Certain areas of DNA have repeated sequences of two or three nucleotides.

Myotonic dystrophy (DM) is an inherited disease. A severe form of DM, congenital myotonic dystrophy, may appear in newborns of mothers who have DM. Congenital myotonic dystrophy can also be inherited via the paternal gene, although it is said to be relatively rare. Congenital means that the condition is present from birth.

Several gene mutations have been identified in patients with camptocormia. These include the RYR1 gene in axial myopathy, the DMPK gene in myotonic dystrophy, and genes related to dysferlinopathy and Parkinson’s disease. These genes could serve as targets for gene therapy to treat the condition in the years to come.

Sodium channel myotonias (SCN4A)

- Potassium-aggravated myotonia (acetazolamide responsive myotonia)

- Paramyotonia congenita

- Hyperkalemic periodic paralysis

Dystrophies

- Myotonic dystrophy (myotonic muscular dystrophy: Type 1 and Type 2)

Potassium channel disorders (KCNJ2)

- Andersen-Tawil syndrome

Other disorders

- Thyroid disorders

- Neuromyotonia (Isaacs Syndrome)

- Stiff person syndrome

- Brody myopathy (Brody Disease, Brody's Disease, Brody's Myopathy)