Entry - #613869 - MYOPATHY, MYOFIBRILLAR, FATAL INFANTILE HYPERTONIC, ALPHA-B CRYSTALLIN-RELATED - OMIM - (MIRROR)
# 613869

MYOPATHY, MYOFIBRILLAR, FATAL INFANTILE HYPERTONIC, ALPHA-B CRYSTALLIN-RELATED


Alternative titles; symbols

MFM, FATAL INFANTILE HYPERTONIC, ALPHA-B CRYSTALLIN-RELATED


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
11q23.1 Myopathy, myofibrillar, fatal infantile hypertonic, alpha-B crystallin-related 613869 AR 3 CRYAB 123590
Clinical Synopsis
 
Phenotypic Series
 

INHERITANCE
- Autosomal recessive
RESPIRATORY
- Respiratory insufficiency, progressive
- Respiratory failure
- Weak cry
- Apneic episodes
CHEST
- Decreased chest wall compliance due to muscular hypertonicity
SKELETAL
- Contractures (variable)
MUSCLE, SOFT TISSUES
- Muscle hypertonicity
- Rigidity
- Stiffness
- EMG shows increased insertion activity and fibrillation
- Muscle biopsy shows dystrophic changes
- Endomysial fibrosis
- Eosinophilic inclusions
- Z-band streaming
- Granular deposits in the sarcomeres
LABORATORY ABNORMALITIES
- Increased serum creatine kinase
MISCELLANEOUS
- Onset in first 8 weeks of life
- Rapidly progressive
- Death usually in the first 2 years of life
MOLECULAR BASIS
- Caused by mutation in the alpha-B crystallin gene (CRYAB, 123590.0005)

TEXT

A number sign (#) is used with this entry because of evidence that fatal infantile hypertonic myofibrillar myopathy is caused by homozygous mutation in the CRYAB gene (123590) on chromosome 11q23.


Description

Fatal infantile hypertonic myofibrillar myopathy is a severe autosomal recessive muscular dystrophy with onset in the first weeks of life after a normal neonatal period. Affected infants show rapidly progressive muscular rigidity of the trunk and limbs associated with increasing respiratory difficulty resulting in death before age 3 years (summary by Del Bigio et al., 2011).


Clinical Features

Lacson et al. (1994) reported 11 Canadian aboriginal infants of Cree ancestry with a similar form of fatal hypertonic muscular dystrophy. All presented in the first 8 weeks of life with respiratory insufficiency, except 1 who was hypertonic at age 3 weeks and died suddenly at age 6 weeks. The patients developed muscle stiffness and rigidity of the trunk and limb muscles with a progressive inability to ventilate due to decreased chest wall compliance. The hypertonicity did not respond to muscle relaxants or neuromuscular blockade. Cognition appeared normal, and facial muscle were not involved. Variable features included weak cry, apneic spells, anoxic seizures, and contractures. Several infants required continued ventilation, and 2 died suddenly. All died in infancy, except 1 child who survived to age 3 years. Electromyograms showed increased insertion activity and fibrillation potentials, and serum creatine kinase (CK) was increased. Muscle biopsies showed dystrophic changes, including variation in fiber size, eosinophilic inclusions, necrotic fibers, regeneration, and endomysial fibrosis. Electron microscopic studies showed a powdery, granular transformation of the Z-bands with Z-band streaming and granular deposits amid the sarcomeres. All these features were consistent with a myofibrillar myopathy. Cardiac muscle was unaffected. Del Bigio et al. (2011) found that muscle biopsies from affected patients had strong immunoreactivity to desmin (DES; 125660), but absence of staining for the full alpha-B-crystallin protein; however, there was some residual staining for antibodies directed against the first 10 residues of alpha-B-crystallin.


Inheritance

The transmission pattern of fatal infantile hypertonic myofibrillar myopathy in the families reported by Lacson et al. (1994) was consistent with autosomal recessive inheritance.


Molecular Genetics

In 8 patients with fatal infantile hypertonic myofibrillar myopathy, including 3 reported by Lacson et al. (1994), Del Bigio et al. (2011) identified the same homozygous 1-bp deletion in the CRYAB gene (60delC; 123590.0005), resulting in a truncated protein of 44 amino acids, including 23 missense residues. Heterozygous parents were unaffected, although 1 mother had mild myopathic symptoms and normal CK levels. Del Bigio et al. (2011) noted that individuals with heterozygous CRYAB mutations resulting in alpha-B crystallin-related late-onset myofibrillar myopathy (MFM2; 608810) have been observed, and suggested that in the severe infantile disease, the parental phenotype may have been rescued by limited expression of the highly truncated nonfunctional gene product.


REFERENCES

  1. Del Bigio, M. R., Chudley, A. E., Sarnat, H. B., Campbell, C., Goobie, S., Chodirker, B. N., Selcen, D. Infantile muscular dystrophy in Canadian aboriginals is an alpha-B-crystallinopathy. Ann. Neurol. 69: 866-871, 2011. [PubMed: 21337604, images, related citations] [Full Text]

  2. Lacson, A. G., Seshia, S. S., Sarnat, H. B., Anderson, J., DeGroot, W. R., Chudley, A., Adams, C., Darwish, H. Z., Lowry, R. B., Kuhn, S., Lowry, N. J., Ang, L. C., Gibbings, E., Trevenen, C. L., Johnson, E. S., Hoogstraten, J. Autosomal recessive, fatal infantile hypertonic muscular dystrophy among Canadian natives. Can. J. Neurol. Sci. 21: 203-212, 1994. [PubMed: 8000975, related citations] [Full Text]


Creation Date:
Cassandra L. Kniffin : 4/5/2011
carol : 07/18/2016
terry : 6/23/2011
carol : 4/22/2011
terry : 4/18/2011
ckniffin : 4/7/2011
wwang : 4/7/2011
ckniffin : 4/5/2011

# 613869

MYOPATHY, MYOFIBRILLAR, FATAL INFANTILE HYPERTONIC, ALPHA-B CRYSTALLIN-RELATED


Alternative titles; symbols

MFM, FATAL INFANTILE HYPERTONIC, ALPHA-B CRYSTALLIN-RELATED


SNOMEDCT: 782883004;   ORPHA: 280553;   DO: 0080309;  


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
11q23.1 Myopathy, myofibrillar, fatal infantile hypertonic, alpha-B crystallin-related 613869 Autosomal recessive 3 CRYAB 123590

TEXT

A number sign (#) is used with this entry because of evidence that fatal infantile hypertonic myofibrillar myopathy is caused by homozygous mutation in the CRYAB gene (123590) on chromosome 11q23.


Description

Fatal infantile hypertonic myofibrillar myopathy is a severe autosomal recessive muscular dystrophy with onset in the first weeks of life after a normal neonatal period. Affected infants show rapidly progressive muscular rigidity of the trunk and limbs associated with increasing respiratory difficulty resulting in death before age 3 years (summary by Del Bigio et al., 2011).


Clinical Features

Lacson et al. (1994) reported 11 Canadian aboriginal infants of Cree ancestry with a similar form of fatal hypertonic muscular dystrophy. All presented in the first 8 weeks of life with respiratory insufficiency, except 1 who was hypertonic at age 3 weeks and died suddenly at age 6 weeks. The patients developed muscle stiffness and rigidity of the trunk and limb muscles with a progressive inability to ventilate due to decreased chest wall compliance. The hypertonicity did not respond to muscle relaxants or neuromuscular blockade. Cognition appeared normal, and facial muscle were not involved. Variable features included weak cry, apneic spells, anoxic seizures, and contractures. Several infants required continued ventilation, and 2 died suddenly. All died in infancy, except 1 child who survived to age 3 years. Electromyograms showed increased insertion activity and fibrillation potentials, and serum creatine kinase (CK) was increased. Muscle biopsies showed dystrophic changes, including variation in fiber size, eosinophilic inclusions, necrotic fibers, regeneration, and endomysial fibrosis. Electron microscopic studies showed a powdery, granular transformation of the Z-bands with Z-band streaming and granular deposits amid the sarcomeres. All these features were consistent with a myofibrillar myopathy. Cardiac muscle was unaffected. Del Bigio et al. (2011) found that muscle biopsies from affected patients had strong immunoreactivity to desmin (DES; 125660), but absence of staining for the full alpha-B-crystallin protein; however, there was some residual staining for antibodies directed against the first 10 residues of alpha-B-crystallin.


Inheritance

The transmission pattern of fatal infantile hypertonic myofibrillar myopathy in the families reported by Lacson et al. (1994) was consistent with autosomal recessive inheritance.


Molecular Genetics

In 8 patients with fatal infantile hypertonic myofibrillar myopathy, including 3 reported by Lacson et al. (1994), Del Bigio et al. (2011) identified the same homozygous 1-bp deletion in the CRYAB gene (60delC; 123590.0005), resulting in a truncated protein of 44 amino acids, including 23 missense residues. Heterozygous parents were unaffected, although 1 mother had mild myopathic symptoms and normal CK levels. Del Bigio et al. (2011) noted that individuals with heterozygous CRYAB mutations resulting in alpha-B crystallin-related late-onset myofibrillar myopathy (MFM2; 608810) have been observed, and suggested that in the severe infantile disease, the parental phenotype may have been rescued by limited expression of the highly truncated nonfunctional gene product.


REFERENCES

  1. Del Bigio, M. R., Chudley, A. E., Sarnat, H. B., Campbell, C., Goobie, S., Chodirker, B. N., Selcen, D. Infantile muscular dystrophy in Canadian aboriginals is an alpha-B-crystallinopathy. Ann. Neurol. 69: 866-871, 2011. [PubMed: 21337604] [Full Text: https://doi.org/10.1002/ana.22331]

  2. Lacson, A. G., Seshia, S. S., Sarnat, H. B., Anderson, J., DeGroot, W. R., Chudley, A., Adams, C., Darwish, H. Z., Lowry, R. B., Kuhn, S., Lowry, N. J., Ang, L. C., Gibbings, E., Trevenen, C. L., Johnson, E. S., Hoogstraten, J. Autosomal recessive, fatal infantile hypertonic muscular dystrophy among Canadian natives. Can. J. Neurol. Sci. 21: 203-212, 1994. [PubMed: 8000975] [Full Text: https://doi.org/10.1017/s0317167100041172]


Creation Date:
Cassandra L. Kniffin : 4/5/2011

Edit History:
carol : 07/18/2016
terry : 6/23/2011
carol : 4/22/2011
terry : 4/18/2011
ckniffin : 4/7/2011
wwang : 4/7/2011
ckniffin : 4/5/2011