Entry - #612067 - DYSTONIA 16; DYT16 - OMIM - (MIRROR)
# 612067

DYSTONIA 16; DYT16


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
2q31.2 Dystonia 16 612067 AR 3 PRKRA 603424
Clinical Synopsis
 
Phenotypic Series
 

INHERITANCE
- Autosomal recessive
HEAD & NECK
Face
- Oromandibular dyskinesia
- Grimacing
Neck
- Torticollis
- Retrocollis
ABDOMEN
Gastrointestinal
- Dysphagia
NEUROLOGIC
Central Nervous System
- Dystonia
- Gait abnormalities
- Fine motor task disruption
- Lower limb pain
- Involuntary movements
- Upper limb dystonia
- Pyramidal signs
- Dysarthria
- Opisthotonic posturing
- Bradykinesia
- Postural tremor
- Parkinsonism
- Hyperreflexia
- Delayed motor development (in some patients)
- Delayed speech development (in some patients)
- Cognitive impairment (in 1 patient)
VOICE
- Spasmodic dysphonia
MISCELLANEOUS
- Onset between 7 and 18 years
- Progressive disorder
- Some patients become wheelchair-bound
- Four unrelated families have been reported (last curated February 2015)
MOLECULAR BASIS
- Caused by mutation in the protein kinase, interferon-inducible double-stranded RNA-dependent activator gene (PRKRA, 603424.0001)
Dystonia - PS128100 - 37 Entries
Location Phenotype Inheritance Phenotype
mapping key
Phenotype
MIM number
Gene/Locus Gene/Locus
MIM number
1p36.32-p36.13 Dystonia 13, torsion AD 2 607671 DYT13 607671
1p35.3 Dystonia, childhood-onset, with optic atrophy and basal ganglia abnormalities AR 3 617282 MECR 608205
1p35.1 Dystonia 2, torsion, autosomal recessive AR 3 224500 HPCA 142622
1p34.2 GLUT1 deficiency syndrome 2, childhood onset AD 3 612126 SLC2A1 138140
1p34.2 Dystonia 9 AD 3 601042 SLC2A1 138140
2p22.2 Dystonia 33 AD, AR 3 619687 EIF2AK2 176871
2q14.3-q21.3 Dystonia 21 AD 2 614588 DYT21 614588
2q31 Paroxysmal nonkinesigenic dyskinesia 2 AD 2 611147 PNKD2 611147
2q31.2 Dystonia 16 AR 3 612067 PRKRA 603424
2q35 Paroxysmal nonkinesigenic dyskinesia 1 AD 3 118800 PNKD 609023
2q37.3 Dystonia 27 AR 3 616411 COL6A3 120250
3p13 ?Dystonia 35, childhood-onset AR 3 619921 SHQ1 613663
4q21.1 Dystonia 37, early-onset, with striatal lesions AR 3 620427 NUP54 607607
5q22.3 ?Dystonia 34, myoclonic AD 3 619724 KCNN2 605879
7q21.3 Dystonia-11, myoclonic AD 3 159900 SGCE 604149
8p11.21 Dystonia 6, torsion AD 3 602629 THAP1 609520
9q22.32 Dystonia 31 AR 3 619565 AOPEP 619600
9q34 Dystonia 23 AD 2 614860 DYT23 614860
9q34.11 Dystonia-1, torsion AD 3 128100 TOR1A 605204
11p14.3-p14.2 Dystonia 24 AD 3 615034 ANO3 610110
11q13.2 Episodic kinesigenic dyskinesia 3 AD 3 620245 TMEM151A 620108
11q23.3 ?Dystonia 32 AR 3 619637 VPS11 608549
14q22.2 Dystonia, DOPA-responsive AD, AR 3 128230 GCH1 600225
16p11.2 Episodic kinesigenic dyskinesia 1 AD 3 128200 PRRT2 614386
16q13-q22.1 Episodic kinesigenic dyskinesia 2 AD 2 611031 EKD2 611031
17q22 ?Dystonia 22, adult-onset AR 3 620456 TSPOAP1 610764
17q22 Dystonia 22, juvenile-onset AR 3 620453 TSPOAP1 610764
18p11 Dystonia-15, myoclonic AD 2 607488 DYT15 607488
18p Dystonia-7, torsion AD 2 602124 DYT7 602124
18p11.21 Dystonia 25 AD 3 615073 GNAL 139312
19p13.3 Dystonia 4, torsion, autosomal dominant AD 3 128101 TUBB4A 602662
19q13.12 Dystonia 28, childhood-onset AD 3 617284 KMT2B 606834
19q13.2 Dystonia-12 AD 3 128235 ATP1A3 182350
20p13 Dystonia 30 AD 3 619291 VPS16 608550
20p11.2-q13.12 Dystonia-17, primary torsion AR 2 612406 DYT17 612406
22q12.3 Dystonia 26, myoclonic AD 3 616398 KCTD17 616386
Xq13.1 Dystonia-Parkinsonism, X-linked XLR 3 314250 TAF1 313650

TEXT

A number sign (#) is used with this entry because of evidence that dystonia-16 (DYT16) is caused by homozygous mutation in the PRKRA gene (603424) on chromosome 2q31.


Clinical Features

Camargos et al. (2008) reported 2 unrelated consanguineous families from Brazil in which a total of 6 individuals had early-onset dystonia-parkinsonism. Patients had onset of gait abnormalities and leg pain around age 12 years, followed by dysphagia, spasmodic dysphonia generalized dystonia, torticollis, upper limb dystonia, and opisthotonic posturing. Orofacial dystonia and facial grimacing were prominent features. Four patients had bradykinesia, 1 of whom also had tremor. Two patients had delayed development, and several had speech and language impairment.

Zech et al. (2014) reported 2 adult brothers of Polish descent who developed limb dystonia at ages 16 and 11 years, respectively. The disorder was slowly progressive in both patients, resulting in difficulties in fine motor tasks, walking, and speech. The symptoms were not responsive to medication. Cognition was unaffected in 1 patient at age 58 years. The other patient, who was more severely affected, underwent pallidotomy and later had a severe ischemic stroke resulting in complete loss of walking ability. This patient also had significant cognitive deficits at age 64 years. Both patients had mild parkinsonian features, including akinesia and rigidity.


Inheritance

The transmission pattern of DYT16 in the families reported by Camargos et al. (2008) and Zech et al. (2014) was consistent with autosomal recessive inheritance.


Mapping

By genomewide linkage analysis of 2 Brazilian families with early-onset dystonia, Camargos et al. (2008) identified a locus, designated DYT16, on chromosome 2q31.2.


Molecular Genetics

In affected members of 2 unrelated Brazilian families with early-onset dystonia-16, Camargos et al. (2008) identified a homozygous mutation in the PRKRA gene (P222L; 603424.0001). The mutation was found by linkage analysis and candidate gene sequencing. Haplotype analysis suggested a founder effect.

Seibler et al. (2008) identified a heterozygous 2-bp deletion in the PRKRA gene (603424.0002) in a 9-year-old German boy with early-onset dystonia of the legs that spread gradually over a few years. There was no family history of movement disorders. Although a second pathogenic PRKRA mutation was not identified, Seibler et al. (2008) postulated that there may be a mutation in noncoding gene regions or that there may be a gene dosage effect. Alternatively, the heterozygous mutation may be pathogenic in itself.

Zech et al. (2014) identified a homozygous P222L mutation in the PRKRA gene in 2 Polish brothers with DYT16. The mutation, which was found by whole-exome sequencing, segregated with the disorder in the family. Haplotype analysis indicated identity by state with the Brazilian patients who carried this mutation (Camargos et al., 2008), consistent with a founder effect. Functional studies of the variant were not performed. No additional PRKRA mutations were found in 10 German patients with generalized dystonia. Three heterozygous variants (T34S, N102S, and c.-14A-G) in the PRKRA gene were found in 3 of 329 patients with mainly adult-onset focal or segmental dystonia, but the pathogenicity of these heterozygous variants was unclear.


REFERENCES

  1. Camargos, S., Scholz, S., Simon-Sanchez, J., Paisan-Ruiz, C., Lewis, P., Hernandez, D., Ding, J., Gibbs, J. R., Cookson, M. R., Bras, J., Guerreiro, R., Oliveira, C. R., Lees, A., Hardy, J., Cardoso, F., Singleton, A. B. DYT16, a novel young-onset dystonia-parkinsonism disorder: identification of a segregating mutation in the stress-response protein PRKRA. Lancet Neurol. 7: 207-215, 2008. [PubMed: 18243799, related citations] [Full Text]

  2. Seibler, P., Djarmati, A., Langpap, B., Hagenah, J., Schmidt, A., Bruggemann, N., Siebner, H., Jabusch, H.-C., Altenmuller, E., Munchau, A., Lohmann, K., Klein, C. A heterozygous frameshift mutation in PRKRA (DYT16) associated with generalised dystonia in a German patient. Lancet Neurol. 7: 380-381, 2008. [PubMed: 18420150, related citations] [Full Text]

  3. Zech, M., Castrop, F., Schormair, B., Jochim, A., Wieland, T., Gross, N., Lichtner, P., Peters, A., Gieger, C., Meitinger, T., Strom, T. M., Oexle, K., Haslinger, B., Winkelmann, J. DYT16 revisited: exome sequencing identifies PRKRA mutations in a European dystonia family. Mov. Disord. 29: 1504-1510, 2014. [PubMed: 25142429, related citations] [Full Text]


Contributors:
Cassandra L. Kniffin - updated : 2/12/2015
Creation Date:
Cassandra L. Kniffin : 5/19/2008
carol : 07/07/2017
carol : 02/18/2015
mcolton : 2/18/2015
ckniffin : 2/12/2015
carol : 9/2/2014
wwang : 5/23/2008
ckniffin : 5/19/2008

# 612067

DYSTONIA 16; DYT16


SNOMEDCT: 722435003;   ORPHA: 210571;   DO: 0090048;  


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
2q31.2 Dystonia 16 612067 Autosomal recessive 3 PRKRA 603424

TEXT

A number sign (#) is used with this entry because of evidence that dystonia-16 (DYT16) is caused by homozygous mutation in the PRKRA gene (603424) on chromosome 2q31.


Clinical Features

Camargos et al. (2008) reported 2 unrelated consanguineous families from Brazil in which a total of 6 individuals had early-onset dystonia-parkinsonism. Patients had onset of gait abnormalities and leg pain around age 12 years, followed by dysphagia, spasmodic dysphonia generalized dystonia, torticollis, upper limb dystonia, and opisthotonic posturing. Orofacial dystonia and facial grimacing were prominent features. Four patients had bradykinesia, 1 of whom also had tremor. Two patients had delayed development, and several had speech and language impairment.

Zech et al. (2014) reported 2 adult brothers of Polish descent who developed limb dystonia at ages 16 and 11 years, respectively. The disorder was slowly progressive in both patients, resulting in difficulties in fine motor tasks, walking, and speech. The symptoms were not responsive to medication. Cognition was unaffected in 1 patient at age 58 years. The other patient, who was more severely affected, underwent pallidotomy and later had a severe ischemic stroke resulting in complete loss of walking ability. This patient also had significant cognitive deficits at age 64 years. Both patients had mild parkinsonian features, including akinesia and rigidity.


Inheritance

The transmission pattern of DYT16 in the families reported by Camargos et al. (2008) and Zech et al. (2014) was consistent with autosomal recessive inheritance.


Mapping

By genomewide linkage analysis of 2 Brazilian families with early-onset dystonia, Camargos et al. (2008) identified a locus, designated DYT16, on chromosome 2q31.2.


Molecular Genetics

In affected members of 2 unrelated Brazilian families with early-onset dystonia-16, Camargos et al. (2008) identified a homozygous mutation in the PRKRA gene (P222L; 603424.0001). The mutation was found by linkage analysis and candidate gene sequencing. Haplotype analysis suggested a founder effect.

Seibler et al. (2008) identified a heterozygous 2-bp deletion in the PRKRA gene (603424.0002) in a 9-year-old German boy with early-onset dystonia of the legs that spread gradually over a few years. There was no family history of movement disorders. Although a second pathogenic PRKRA mutation was not identified, Seibler et al. (2008) postulated that there may be a mutation in noncoding gene regions or that there may be a gene dosage effect. Alternatively, the heterozygous mutation may be pathogenic in itself.

Zech et al. (2014) identified a homozygous P222L mutation in the PRKRA gene in 2 Polish brothers with DYT16. The mutation, which was found by whole-exome sequencing, segregated with the disorder in the family. Haplotype analysis indicated identity by state with the Brazilian patients who carried this mutation (Camargos et al., 2008), consistent with a founder effect. Functional studies of the variant were not performed. No additional PRKRA mutations were found in 10 German patients with generalized dystonia. Three heterozygous variants (T34S, N102S, and c.-14A-G) in the PRKRA gene were found in 3 of 329 patients with mainly adult-onset focal or segmental dystonia, but the pathogenicity of these heterozygous variants was unclear.


REFERENCES

  1. Camargos, S., Scholz, S., Simon-Sanchez, J., Paisan-Ruiz, C., Lewis, P., Hernandez, D., Ding, J., Gibbs, J. R., Cookson, M. R., Bras, J., Guerreiro, R., Oliveira, C. R., Lees, A., Hardy, J., Cardoso, F., Singleton, A. B. DYT16, a novel young-onset dystonia-parkinsonism disorder: identification of a segregating mutation in the stress-response protein PRKRA. Lancet Neurol. 7: 207-215, 2008. [PubMed: 18243799] [Full Text: https://doi.org/10.1016/S1474-4422(08)70022-X]

  2. Seibler, P., Djarmati, A., Langpap, B., Hagenah, J., Schmidt, A., Bruggemann, N., Siebner, H., Jabusch, H.-C., Altenmuller, E., Munchau, A., Lohmann, K., Klein, C. A heterozygous frameshift mutation in PRKRA (DYT16) associated with generalised dystonia in a German patient. Lancet Neurol. 7: 380-381, 2008. [PubMed: 18420150] [Full Text: https://doi.org/10.1016/S1474-4422(08)70075-9]

  3. Zech, M., Castrop, F., Schormair, B., Jochim, A., Wieland, T., Gross, N., Lichtner, P., Peters, A., Gieger, C., Meitinger, T., Strom, T. M., Oexle, K., Haslinger, B., Winkelmann, J. DYT16 revisited: exome sequencing identifies PRKRA mutations in a European dystonia family. Mov. Disord. 29: 1504-1510, 2014. [PubMed: 25142429] [Full Text: https://doi.org/10.1002/mds.25981]


Contributors:
Cassandra L. Kniffin - updated : 2/12/2015

Creation Date:
Cassandra L. Kniffin : 5/19/2008

Edit History:
carol : 07/07/2017
carol : 02/18/2015
mcolton : 2/18/2015
ckniffin : 2/12/2015
carol : 9/2/2014
wwang : 5/23/2008
ckniffin : 5/19/2008