Types of Muscular Dystrophy
Myopathies
1. Are Myopathies also known by other names?Yes, some of the myopathies are known by alternative names:
Disorder
Central Core Disorder
Congenital Fibre Type Disproportion Myopathy
Hyperkalemic Periodic Paralysis
Myotubular Myopathy
Nemaline Myopathy
Minicore Myopathy
Myotonia Congenita
Paramyotonia Congenita
Alternative Name(s)
Central Core Myopathy
Adynamia Episodica Hereditaria
Centronuclear Myopathy
Rod Body Disease
Multicore Myopathy
Thomson's Disease
Eulenberg's Disease
2. What is a myopathy?
The term myopathy is derived from the Greek and it means muscle disorder (myo = muscle and pathy = disorder). It includes congenital -, metabolic -, endocrine - and inflammatory myopathies.
Congenital myopathies:
Central core disease
Congenital fibre type disproportion
Minicore disease
Myopathies with abnormalities of other subcellular organelles
Myotubular myopathy
Nemaline myopathy
Non-specific congenital myopathies Metabolic myopathies: Glycogenoses
Lipid disorders
Mitochondrial disorders
Ion channel disorders:
Myotonia congenital Hyperkalemic periodic paralysis
Hypokalemic periodic paralysis
Paramyotonia congenita
Malignant hyperthermia
Endocrine myopathies:
Hypothyroidism
Hyperthyroidism Inflamatory myopahties:
Bacterial, parasitic, viral
Dermatomyositis/Polymiositis
3. What is a Congenital Myopathy?
"Congenital” refers to the onset at birth. In general symptoms of a congenital myopathy are non-progressive, present at birth but may not be recognised until later on in childhood or even in adult life. The congenital myopathies are a group of conditions that cause weakness and hypotonia. There are exceptions of rapid progression of weakness.
4. What are the 10 major types of myopathy?
The eight inheritable myopathies are:
Central Core disorder, Myotonia Congenita (see separate fact sheet for more information), Paramyotonia Congenita (see Myotonia Congenita fact sheet), Myotubular Myopathy, Nemaline Myopathy, Hypokalemic Periodic Paralysis, Hyperkalemic Periodic Paralysis and Normokalemic Periodic Paralysis. Two myopathies are caused by endocrine abnormalities: myopathy associated with hyperthyroidism and hypothyroidism.
5. What are the different myopathies?
Central Core Disease (CCD):
It is a non-progressive disorder of voluntary muscle (those muscles necessary for movement) and is disabling but not life threatening. The name “central core” was first suggested in 1956 and refers to the abnormal central part of the affected muscle fibre which is occupied by one or several “cores” or abnormal areas, running along its length.
Fibre Type Disproportion Myopathy:
The name “fibre type disproportion” was first suggested in 1973 and refers to the difference in size of the muscle fibres. When normal muscle is looked at under the microscope, two types of muscle fibres (type 1 and 2) are seen, both of which are needed for the proper functioning of the muscle. The size of type 1 and type 2 fibres in the muscles of most young children is roughly similar. However, in congenital fibre type disproportion, type 1 fibres are smaller than type 2.
Minicore (or Multicore) Myopathy:
The name “multicore myopathy” was first suggested in 1971, but a few years later in 1974 the name “minicore myopathy” became the preferred name for this condition. Both names refer to the abnormal structures of “minicores” which are seen in the affected muscle fibres when looked at under the microscope.
Myotubular (or Centronuclear) Myopathy:
The name “myotubular myopathy” was suggested in 1966 and refers to the appearance of the affected muscle fibres that look like myotubes (muscle cells found only during fetal development when the fetus is between 12 and 20 weeks old). The condition is also known as “centronuclear myopathy” because the nuclei of affected muscle cells are found in the centre of each cell instead of the periphery (as occurs in healthy muscle cells).
Nemaline Myopathy:
The name “nemaline myopathy” was suggested in 1963 and refers to the tiny rod-like structures seen in the affected muscle fibres, which look like tiny threads (the name “nemaline” comes from the Greek word “nema” which means thread).
Periodic Paralysis:
There are three distinct forms of periodic paralysis, although the three forms might be related. These myopathies are non-lethal disorders of voluntary muscle. All three forms of periodic paralyses are characterised by intermittent attacks of weakness, during which affected muscles become slack, weak and unable to contract. However, between the attacks the affected muscles function normally. The names of the three different forms are derived from the level of potassium (kalemic) in the blood during an attack. The three different forms are:
Hypokalemic periodic paralysis:
Indicating that potassium levels decrease during an attack.
Normokalemic periodic paralysis:
Potassium levels remain normal during an attack.
Hyperkalemic periodic paralysis:
Potassium levels rise during an attack.
6. What causes a Congenital Myopathy?
Central Core Disorder (CCD):
Different defects in the same gene on chromosome 19 lead to Central Core Myopathy and Malignant Hyperthermia. The usual mode of inheritance Central Core Disorder is autosomal dominant. This means that one (either) of the two parents is affected, may be only very mildly so, but carries the abnormal gene, and each child (of any sex) of that affected parent has a 50% (1 in 2) chance of being affected. In the remaining cases there does not appear to be a clear pattern of inheritance and these are described as “sporadic” cases which means they occur randomly, in other words as a one-off situation with very little risk of other children in the family being affected. However, each child of a person who has a sporadic mutation will have a 50% risk of being affected.
Fibre Type Disproportion Myopathy:
The exact cause is unknown, but it is an inherited disorder.
Minicore (or Multicore) Myopathy:
This relatively benign muscle disorder with mild weakness and relatively non-progressive weakness is an inherited disorder and the specific gene has not been identified.
Myotubular (or Centronuclear) Myopathy:
It is a genetic disorder with different patterns of inheritance. Nemaline Myopathy: Nemaline myopathy is an inherited muscle disorder with different patterns of inheritance. An abnormal gene on chromosome 1 has been identified in some families.
Periodic Paralysis:
Mutations in ion channel genes have been associated with some of the forms of periodic paralysis.
7. What are the symptoms and which muscles are affected?
Central Core Disorder (CCD):
Most cases of central core myopathy present as a delay in walking or with muscle weakness. In rare cases newborn babies may have symptoms of hypotonia (floppiness), swallowing and breathing difficulties, facial weakness, or with dislocation of the hip and foot deformities. Later on, the child may show delayed motor development (crawling, standing and walking), and continue to show either non-progressive or slowly-progressive muscle weakness, affecting the facial muscles and the “proximal” musculature (muscles near the trunk, such as shoulders and thigh muscles), which cannot function as well as normal muscles. Because of this weakness children may have a variety of symptoms ranging from drooping of the eyelids, drooling, swallowing difficulties, weakness of the limbs and the trunk and may develop a curvature of the spine. Some children also suffer from constipation and this may be as a direct result of the muscles in the gut being affected, caused by lack of exercise and insufficient mobility. Hearing, vision and intelligence are usually not affected. In some cases the muscle weakness is so mild that an affected parent may have a “life-long” history of weakness that may be accepted as normal, or simply be unaware of any weakness and the diagnosis of the parent is only made after their child has been diagnosed. The severity of muscle involvement may vary from one affected person to another within the same family.
Fibre Type Disproportion Myopathy:
A number of cases of congenital fibre type disproportion have an onset in infancy, and may even present at birth with hypotonia (floppiness), swallowing and breathing difficulties, joint contractures (limitation of joint movement) or dislocation of the hips. In other cases the child may show delayed motor development (ie. slow to crawl, stand or walk). The muscle weakness is usually non-progressive or very slowly-progressive after the age of two years. In some cases the condition may actually improve after that time, although the degree of muscle weakness is variable. It involves the muscles of the trunk and limbs, with more “proximal” involvement (proximal muscles are those that are near the trunk such as shoulder and thigh muscles).Because of this weakness children may have a variety of symptoms ranging from recurrent chest infections, drooping of the eyelids, drooling, swallowing difficulties, and weakness of the limbs and the trunk. Children with this condition are usually shorter than other children and in addition may develop curvature of the spine. Some children also suffer from constipation and this may be as a direct result of the muscles in the gut being affected, or caused by lack of exercise and insufficient mobility. Hearing, vision and intelligence are usually unaffected. As the child grows older, usually after the age of 2 years, the disorder becomes static or improvement may take place.
Minicore (or Multicore) Myopathy:
Most cases of minicore myopathy have an onset in infancy and very rarely the disorder may present at birth with symptoms of hypotonia (floppiness), swallowing and breathing difficulties, and facial weakness. Later on the child may show delayed motor development (crawling, standing and walking), and then continue to show either non-progressive muscle weakness, affecting the facial muscles, and the “proximal” musculature (muscles near the trunk such as shoulder and thigh muscles).Because of this weakness children may have a variety of symptoms ranging from drooping of the eyelids, drooling, swallowing difficulties, and weakness of the limbs and the trunk. Some children also suffer from constipation and this may be as a direct result of the muscles in the gut being affected, or caused by lack of exercise and insufficient mobility. Hearing, vision and intelligence are usually unaffected. In some cases the muscle weakness is so mild that the affected parent may have a life-long history of weakness which has been accepted as normal, or is simply unaware of any weakness. The diagnosis in the parent is sometimes only made after the diagnosis has been made in the child. Some cases may manifest with sleep disturbances and early morning headaches or drowsiness. This may be the result of insufficient breathing during the night.
Myotubular (or Centronuclear) Myopathy:
There are different forms of this condition, with the severest form presenting at birth or even antenatally (before birth, during pregnancy), in contrast to the four milder forms which present later or in childhood. A mother may notice a reduction in fetal movements during the pregnancy, or the doctors might have mentioned that there was too much fluid (water) around the baby. The symptoms seen at birth are hypotonia (floppiness), swallowing and breathing difficulties and facial weakness. Sometimes in very severely affected individuals, the baby may not survive more than a few days. In others, there appears to be slow progressive muscle weakness that not only affects the face, but also the arms and legs and muscles involved in breathing. The affected muscles are weak and cannot function as well as normal (unaffected) muscles.Because of this weakness children may have a variety of symptoms which range from drooping of the eyelids, drooling, swallowing difficulties, foot drop, and weakness of limbs and trunk. Some children are constipated and this may be as a direct result of the muscles in the gut being affected or caused by lack of exercise and insufficient mobility. Hearing, vision and intelligence are usually unaffected.
Nemaline Myopathy:
Like many other congenital myopathies, nemaline myopathy occurs in two main forms, with the severest form presenting at birth or even antenatally (before birth, during pregnancy), in contrast to the milder form which presents later on in childhood. A mother may notice a reduction in fetal movements during the pregnancy, or the doctors might have said that there was too much fluid (water) around the baby. At birth the baby may be very floppy (hypotonic) and weak and may have swallowing and breathing difficulties, facial weakness (myopathic face) and a high arched palate. In this form, the baby may not survive more than a few weeks or months of life, and may need immediate resuscitation at birth.In patients who present later in either childhood or adult life there may be only slow progression or even no progression of the muscle weakness which not only affects the face but also the arms and legs and those muscles involved in breathing. The affected muscles are thin and weak, and cannot function as well as normal muscles. Because of this weakness children may have a variety of symptoms; these range from drooping of the eyelids, drooling, swallowing difficulties, foot drop, and weakness of limbs and trunk. They are at increased risk of serious respiratory infections. Some children suffer from constipation, which may be as a direct result of the muscles in the gut being affected, or caused by lack of exercise and insufficient mobility. Hearing, vision and intelligence are usually unaffected. Other reported clinical features are skeletal abnormalities, difficulty with breathing, especially at night, tremor of the hands, and weak heart muscles.
Periodic Paralysis:
Symptoms and muscles affected. Intermittent attacks of weakness, during which the affected muscles become weak, slack and unable to contract. Affected muscles are function normally between attacks. Intervals between attacks vary from days, to months, and even years. Periodic paralysis can cause progressive weakness, but the number of attacks and their severity tend to decrease with age and the attacks may disappear altogether, especially in women. The three forms differ from one another in the age of onset, precipitating factors, symptoms and response to therapy.
Hypokalemic Periodic Paralysis:
Initially the muscles of the back, shoulder and thigh are affected, then spreading to the arms, neck and lower legs. Speech and breathing are also affected, although generally not drastically.
Normokalemic Periodic Paralysis:
Attacks are generally more severe and last longer than those of either hypokalemic or hyperkalemic periodic paralysis. Exercise and a number of different drugs may trigger these attacks. The symptoms are often similar to those of the hyperkalemic form.
Hyperkalemic Periodic Paralysis:
Myotonia is often experienced - the inability to immediately relax a contracted muscle. However, this myotonia is neither muscle-wasting nor progressive, as it is in myotonic dystrophy, nor does it affect all muscle groups as does myotonia congenita. Attacks are usually triggered by strenuous exercise, administration of potassium or by exposure to cold. Such attacks may induce myotonia, paralysis or a mixture of both. They frequently begin with pain, numbness and a tingling sensation in the legs. While the consequent weakness may be felt in all parts of the body, the muscles of the arms and the legs are primarily involved. Attacks are typically more frequent but shorter in duration than those of hypokalemic periodic paralysis.
8. How is a Congenital Myopathy inherited?
Central Core Disorder (CCD):
Different defects in the same gene on chromosome 19 may lead to central core myopathy. The usual mode of inheritance is autosomal dominant. This means that one (either) of the two parents is affected, may be only very mildly so, but carries the abnormal gene, and each child (of any sex) of that affected parent has a 50% (1 in 2) chance of being affected. In the remaining cases there does not appear to be a clear pattern of inheritance and these are described as “sporadic” cases which means they occur randomly, in other words as a one-off situation with very little risk of other children in the family being affected. However, people who are themselves sporadic cases will be at risk of passing the disorder on to their children. Fibre Type Disproportion Myopathy: It is usually an inherited disorder. Although the exact genetic cause is unknown, different patterns of inheritance are recognised; these are known as autosomal recessive and autosomal dominant. In the remaining cases there does not appear to be a clear pattern of inheritance and these are described as “sporadic” cases which means they occur randomly, or as a one-off, with very little risk of other children in the family being affected. However, individuals who are themselves sporadic cases will be at risk or passing the condition on to their children.In the autosomal dominant type of inheritance one (either) of the two parents is affected, may be only very mildly so, but carries the abnormal gene, and each child (of either sex) of that affected parent has a 50% (1 in 2) chance of being affected. The autosomal recessive type may be clinically difficult to separate from the autosomal dominant form, although onset is generally earlier, and the condition may present as a ‘floppy infant’, or later on with severe muscle weakness. In the recessive form both parents are carriers of the condition, and the risk of a child of either sex being affected is 25% (1 in 4).
Minicore (or Multicore) Myopathy:
It is usually an inherited disorder. Although the exact genetic cause is unknown, different patterns of inheritance are recognised; these are known as autosomal recessive and autosomal dominant. In the remaining cases there does not appear to be a clear pattern of inheritance and these are described as “sporadic” cases which means they occur randomly, or as a one-off, with very little risk of other children in the family being affected. However, individuals who are themselves sporadic cases will be at risk or passing the condition on to their children.In the autosomal dominant type of inheritance one (either) of the two parents is affected, may be only very mildly so, but carries the abnormal gene, and each child (of either sex) of that affected parent has a 50% (1 in 2) chance of being affected. The autosomal recessive type may not be very different from the autosomal dominant form, although onset is generally earlier, and the condition may present as a ‘floppy infant’, or later on with severe muscle weakness. In the recessive form both parents are carriers of the condition, and the risk of a child of either sex being affected is 25% (1 in 4).
Myotubular (or Centronuclear) Myopathy:
This is an inherited disorder. Although the exact genetic cause is unknown, different patterns of inheritance are recognised; these are known as X-linked recessive, autosomal recessive and autosomal dominant. In the remaining cases there does not appear to be a clear pattern of inheritance and these are described as “sporadic”, which means they occur randomly, or as a one-off, with very little risk of other children in the family being affected. However, individuals who are themselves sporadic cases will be at risk of passing on the condition to their children.In the X-linked recessive type, which is the most severe form of the disorder and presents early in life, the abnormality lies on the X-chromosome. In these cases the mother is usually the carrier in which case only boys are affected. There is a 50% chance (1 in 2) that any of her sons may have inherited the condition.The autosomal dominant type of inheritance is slightly more common than the autosomal recessive one. The age of onset is usually older (late childhood or adult life) but may be earlier. The weakness and wasting is mainly proximal (involving muscles near the trunk such as the shoulders and thighs) and slowly progressive. In this type of dominant inheritance, one (either) of the two parents is affected, may be only mildly so, but carries the abnormal gene, and each child of (either sex) of that affected parent has a 50% (1 in 2) chance of being affected. The autosomal recessive type may be clinically difficult to separate from the autosomal dominant form, although onset is generally earlier, and the condition may present as a “floppy infant”, or later on with severe muscle weakness. In the recessive form both parents are carriers of the condition, and the risk of a child of either sex being affected in 25% (1 in 4).
Nemaline Myopathy:
Nemaline myopathy is usually inherited. Although the exact cause is unknown, different patterns of inheritance are recognised; these are known as autosomal recessive and autosomal dominant, and some cases are thought to be sporadic, ie. a one-off with little risk of other children in the family being affected. However, individuals who are themselves sporadic cases will be at risk of passing on the condition to their children.The most severe form of the disorder that presents in the first days or months of life is thought to be of autosomal recessive inheritance. In this form both parents need to be carriers of the condition, and the risk of a child of any sex being affected is 25% (1 in 4). The autosomal recessive type may not be very different from the autosomal dominant form, although onset is generally earlier, and the condition may present as a ‘floppy infant’, or later on with severe muscle weakness.The most likely pattern of inheritance is by a dominant gene that is slightly more common than the autosomal recessive one. The age of onset is usually older (late childhood or adult life) but may be earlier. The weakness and wasting is mainly proximal (muscles near the trunk such as the shoulders and thighs) and slowly progressive. In this type of dominant inheritance, one (either) of the two parents is affected, may be only very mildly so, but carries the abnormal gene, and each child (of any sex) of that affected parent has a 50% (1 in 2) chance of being affected.
Periodic Paralysis:
These myopathies are generally inherited in an autosomal dominant manner, with different ages of onset.
Hypokalemic Periodic Paralysis:
Age of onset is adolescence to young adulthood.
Normokalemic Periodic Paralysis:
Age of onset is during infancy to early childhood.
Hyperkalemic Periodic Paralysis:
Age of onset is during infancy to early childhood.
As these are genetic conditions, genetic counselling is strongly recommended. Genetic counselling provides information on the inheritance pattern, risks to other family members, prognosis, psycho-social support, as well as information about diagnostic testing, carrier testing, preclinical and prenatal testing (where available).
9. How is Congenital Myopathy diagnosed?
The diagnosis of a myopathy is usually suspected from the affected individual’s medical and family history, and from physical examination. A specific diagnosis of the different myopathies can be made by looking at a piece of muscle (muscle biopsy) under the microscope. The specific patterns seen within the biopsy will lead to the diagnosis of the specific myopathy. A blood test which measures the level of a muscle enzyme (creatine kinase or CK level), which can be slightly elevated may also be performed - but is not specific to a particular myopathy. Another test which may be done is an electrical test of the muscles and the nerves supplying the muscle; it involves the placing of a fine needle into the muscle which then measures the electrical activity arising from that muscle. Although this test may be able to show a ‘myopathic’ pattern of abnormal muscle activity (seen in any myopathy) it is not able to define the exact type.
Central Core Disease (CCD):
The specific diagnosis of central core myopathy is nearly always made by looking at a piece of muscle (muscle biopsy). The muscle biopsy will confirm the diagnosis and in this condition show abnormal ‘cores’ or fibrils which are usually found in the centre of the muscle fibre.
Fibre Type Disproportion Myopathy:
The specific diagnosis of congenital fibre type disproportion is nearly always made via a muscle biopsy. The muscle biopsy in this condition characteristically shows smaller type 1 than type 2 fibres within the muscle.
Minicore (or Multicore) Myopathy:
The specific diagnosis of minicore myopathy is nearly always made by a muscle biopsy. The muscle in this condition shows evidence of abnormal “minicores” which are scattered randomly in the muscle.
Myotubular (or Centronuclear) Myopathy:
The specific diagnosis of myotubular myopathy is nearly always made by a muscle biopsy. The muscle in this condition shows evidence of abnormal central nuclei in a proportion of muscle fibres (centronuclear or myotubular myopathy).
Nemaline Myopathy:
The specific diagnosis of nemaline myopathy is nearly always made on a muscle biopsy. The muscle biopsy is therefore the important test which will make the diagnosis and will show the thread or rod-line structures within the muscle fibres. These rods may be numerous, filling almost the whole fibre, or may be much less, being seen in only a few muscle fibres.
Periodic Paralysis:
These forms of congenital myopathies are generally diagnosed on a clinical level, via a thorough examination, the measurement of potassium levels during an attack and the history of the family.
Hypokalemic Periodic Paralysis:
This form has been linked to a calcium channel gene.
Hyperkalemic Periodic Paralysis:
Mutations in a sodium channel gene on chromosome 17 are associated with this form of periodic paralysis.
10. Is there a cure?
Central Core Disorder, Fibre Type Disproportion, Myotubular (Centronuclear) and Nemaline Myopathy:
At the moment, there is no cure, nor any drug treatment for central core and fibre type disproportion myopathy. However, other very helpful measures can be taken such as physiotherapy, the use of antibiotics to treat chest infections, or nasogastric tube feeding when necessary.
Minicore (or Multicore) Myopathy:
At the moment, there is no cure, nor any drug treatment for minicore myopathy. However, other very helpful measures can be taken such as physiotherapy (see below), the use of antibiotics to treat chest infections, or nasogastric tube feeding when necessary. Nocturnal nasal mask ventilation may be an option in patients with nocturnal hyperventilation. Periodic Paralysis: There are no permanent cures for the periodic paralyses, although some forms disappear with age.
Hypokalemic Periodic Paralysis:
The administration of potassium during an attack may relieve symptoms. However, long-term use of potassium to prevent attacks often has no effect.
11. Is there any treatment?
Myopathies:
Physiotherapy is one of the main forms of treatment. An initial physiotherapy assessment at the time of the diagnosis should be followed by an exercise programme and regular check-ups. The main aim of physiotherapy is to keep the muscles as active as possible to prevent the formation of ‘contractures’ (muscle tendon tightness causing restriction in the range of joint movement). It is also important to provide good seating and to ensure a proper sitting and standing posture to prevent scoliosis (curvature of the spine). The other role of physiotherapy is to help with provision of appliances, such as splints, callipers, standing frames (mechanical aids helping to keep affected individuals on their feet) and wheel chairs where necessary. Affected individuals are encouraged to remain as active as possible and ensure that they do not become overweight to limit the strain imposed on their weak muscles. Swimming is a particularly good form of exercise.
Nemaline Myopathy:
Affected individuals with breathing problems may benefit from night-time ventilation.
Periodic Paralysis:
No permanent treatment is available.
Hypokalemic Periodic Paralysis:
The administration of potassium during an attack may relieve symptoms. However, long-term use of potassium to prevent attacks often has no effect.
12. Is there a risk during anaesthesia?
There is a definite risk for individuals affected by any myopathy to develop malignant hyperthermia during anaesthesia. Malignant hyperthermia develops when susceptible individuals are exposed to certain anaesthetic agents such as succinyl choline and halothane. An MH crisis is treated by the administration of dantrolene. It is always recommended that the presence of a muscular disorder be mentioned to your doctor.
13. Has research been conducted on Congenital Myopathies in South Africa?
Research is conducted on congenital fibre type disproportion myopathy at the Red Cross Childrens Hospital in Cape Town. Central Core Disorder is genetically related to Malignant Hyperthermia, on which extensive research has been conducted in South Africa - in the past at the University of Cape Town, and the University of the Witwatersrand, and currently at the University of Pretoria.
14. The role of the Muscular Dystrophy Foundation in South Africa
The MDF supports individuals affected by muscular dystrophy and their families by offering emotional support, information - including a series of fact sheets, referrals to genetic counselling and other clinics, formation of support groups, assistance with special equipment, when possible, as well as financial support for research projects in muscular dystrophy in South Africa. Creating public awareness for muscular dystrophy is also an important aspect of our work, since the MDF relies solely on contributions from its members and other donors to provide an on-going support service. Through our newsletter members are kept informed of all the activities and receive national and international research updates. Please contact any office of the MDF if you require information about any of our activities or programmes.
15. Support group or contact person
Fairuze Simons (053) 861-4572
If you are unable to contact any of this individual, please contact the MDF.
16. Where can we find assistance?
Please contact your local MDF office for further information:
Special Equipment: Phone either ILC or DIC for information on where to get special equipment.
MDF Website: Please visit our MDF website (www.mdsa.org.za) for muscular dystrophy news updates.
17. Please note
The treatments and drugs mentioned in this fact sheet are for information purposes ONLY. Please consult your physician or other health care specialist for information regarding the use of any of the above. The MDF encourages duplication of this fact sheet, under the following condition: that it is duplicated in its entirety - including the MDF logo and full text. Only individuals authorised by the MDF may make changes to this fact sheet (the information "updated by" and "last update" should be completed). Alterations to this fact sheet by any other party are strictly prohibited.
This fact sheet was adapted from the following source(s): Fact sheet(s) of the Muscular Dystrophy Group of Great Britain and Northern Ireland.
Compiled by: MDF-Gauteng Branch
Updated by: MDF-Gauteng Branch
Approved and Released by: National Office of the MDF
Last update: 30 May 2000
