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Article ; Online: Diagnosis and new treatments in muscular dystrophies.

Manzur, A Y / Muntoni, F

2009 Volume 85, Issue 1009, Page(s) 622–630

Abstract: Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD) and limb girdle muscular dystrophies (LGMD) represent a significant proportion of paediatric and adult neuromuscular neurology practice. The proactive symptom-based multidisciplinary team ...

Abstract	Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD) and limb girdle muscular dystrophies (LGMD) represent a significant proportion of paediatric and adult neuromuscular neurology practice. The proactive symptom-based multidisciplinary team (MDT) management and access to non-invasive ventilation have enabled improved survival into adulthood. Nevertheless the severe disability imposed by conditions such as DMD poses a challenge for successful transition of care and management for paediatric and adult neurology teams. DMD is discussed in detail as a paradigm illustrating diagnosis, management and role for different pharmacological interventions to improve survival, but also challenges in adulthood care, and cutting-edge therapies. LGMDs are much rarer than DMD and BMD, and in addition there is a significant genetic and clinical heterogeneity, which leads to diagnostic difficulties. The clinical and laboratory diagnostic features of seven LGMD subtypes are summarised, and their allelic "non-limb girdle" phenotypes are tabulated to illustrate the theme of one gene causing multiple clinical phenotypes, with the aim of refining the clinician's diagnostic approach. The lessons learnt from DMD MDT management to improve survival are broadly applicable to LGMDs with severe motor disability/multisystem complications.
Language	English
Publishing date	2009-11-05
Publishing country	England
Document type	Journal Article
ZDB-ID	80325-x
ISSN	1469-0756 ; 0032-5473
ISSN (online)	1469-0756
ISSN	0032-5473
DOI	10.1136/jnnp.2008.158329
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Article ; Online: Diagnosis and new treatments in muscular dystrophies.

Manzur, A Y / Muntoni, F

Journal of neurology, neurosurgery, and psychiatry

2009 Volume 80, Issue 7, Page(s) 706–714

Abstract	Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD) and limb girdle muscular dystrophies (LGMD) represent a significant proportion of paediatric and adult neuromuscular neurology practice. The proactive symptom-based multidisciplinary team (MDT) management and access to non-invasive ventilation have enabled improved survival into adulthood. Nevertheless the severe disability imposed by conditions such as DMD poses a challenge for successful transition of care and management for paediatric and adult neurology teams. DMD is discussed in detail as a paradigm illustrating diagnosis, management and role for different pharmacological interventions to improve survival, but also challenges in adulthood care, and cutting-edge therapies. LGMDs are much rarer than DMD and BMD, and in addition there is a significant genetic and clinical heterogeneity, which leads to diagnostic difficulties. The clinical and laboratory diagnostic features of seven LGMD subtypes are summarised, and their allelic "non-limb girdle" phenotypes are tabulated to illustrate the theme of one gene causing multiple clinical phenotypes, with the aim of refining the clinician's diagnostic approach. The lessons learnt from DMD MDT management to improve survival are broadly applicable to LGMDs with severe motor disability/multisystem complications.
MeSH term(s)	Adrenal Cortex Hormones/therapeutic use ; Adult ; Child ; Humans ; Muscular Dystrophies/complications ; Muscular Dystrophies/diagnosis ; Muscular Dystrophies/genetics ; Muscular Dystrophies/physiopathology ; Muscular Dystrophies/therapy ; Muscular Dystrophies, Limb-Girdle/diagnosis ; Muscular Dystrophies, Limb-Girdle/therapy ; Muscular Dystrophy, Duchenne/diagnosis ; Muscular Dystrophy, Duchenne/therapy ; Physical Therapy Modalities ; Sleep Apnea Syndromes/etiology ; Sleep Apnea Syndromes/therapy ; Treatment Outcome
Chemical Substances	Adrenal Cortex Hormones
Language	English
Publishing date	2009-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3087-9
ISSN	1468-330X ; 0022-3050
ISSN (online)	1468-330X
ISSN	0022-3050
DOI	10.1136/jnnp.2008.158329
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Article ; Online: Update on the management of Duchenne muscular dystrophy.

Manzur, A Y / Kinali, M / Muntoni, F

Archives of disease in childhood

2008 Volume 93, Issue 11, Page(s) 986–990

Abstract: Duchenne muscular dystrophy (DMD) is familiar to paediatricians as the most common childhood muscular dystrophy and leads to severe disability and early death in the late teenage years if untreated. Improvements in general care, glucocorticoid ... ...

Abstract	Duchenne muscular dystrophy (DMD) is familiar to paediatricians as the most common childhood muscular dystrophy and leads to severe disability and early death in the late teenage years if untreated. Improvements in general care, glucocorticoid corticosteroid treatment, non-invasive ventilatory support, and cardiomyopathy and scoliosis management have significantly changed the course of DMD in treated individuals, so that survival into adulthood is now a realistic possibility for most patients. This has important implications for the medical and social sectors involved in the transition to adult medical services and the provision of suitable employment and social care. Multidisciplinary team working for optimal management of DMD-specific multisystem complications is essential, and collaboration in disease specific national clinical networks is recommended. Several curative therapeutic strategies including cell and gene therapy are being pursued but are still at an experimental stage.
MeSH term(s)	Cardiomyopathy, Dilated/etiology ; Cardiomyopathy, Dilated/therapy ; Dystrophin/genetics ; Genetic Therapy/methods ; Glucocorticoids/therapeutic use ; Humans ; Male ; Muscular Dystrophy, Duchenne/complications ; Muscular Dystrophy, Duchenne/diagnosis ; Muscular Dystrophy, Duchenne/genetics ; Muscular Dystrophy, Duchenne/therapy ; Patient Care Team ; Physical Therapy Modalities ; Respiration Disorders/etiology ; Respiration Disorders/therapy ; Scoliosis/etiology ; Scoliosis/therapy
Chemical Substances	Dystrophin ; Glucocorticoids
Language	English
Publishing date	2008-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	524-1
ISSN	1468-2044 ; 0003-9888 ; 1359-2998
ISSN (online)	1468-2044
ISSN	0003-9888 ; 1359-2998
DOI	10.1136/adc.2007.118141
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Article ; Online: Clinical spectrum, treatment and outcome of children with suspected diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy.

Silwal, A / Pitt, M / Phadke, R / Mankad, K / Davison, J E / Rossor, A / DeVile, C / Reilly, M M / Manzur, A Y / Muntoni, F / Munot, P

Neuromuscular disorders : NMD

2018 Volume 28, Issue 9, Page(s) 757–765

Abstract: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a treatable chronic disorder of the peripheral nervous system. We retrospectively studied 30 children with a suspected diagnosis of CIDP. The diagnosis of CIDP was compared against the ... ...

Abstract	Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a treatable chronic disorder of the peripheral nervous system. We retrospectively studied 30 children with a suspected diagnosis of CIDP. The diagnosis of CIDP was compared against the childhood CIDP revised diagnostic criteria 2000. Of the 30 children, five did not meet the criteria and four others met the criteria but subsequently had alternative diagnosis, leaving a total of 21 children (12 male) with CIDP as the final diagnosis. Thirteen children presented with chronic symptom-onset (>8 weeks). The majority presented with gait difficulties or pain in legs (n = 16). 12 children (57%) met the neurophysiological criteria and 18/19 (94%) met the cerebrospinal fluid criteria. Nerve biopsy was suggestive in 3/9 (33%), with magnetic resonance imaging supportive in 9/20 (45%). Twenty-one children received immuno-modulatory treatment at first presentation, of which majority (n = 19, 90%) received IVIG (immunoglobulin) monotherapy with 13 (68%) showing a good response. 8 children received second line treatment with either IVIG or steroids or plasmapharesis (PE) and 4 needed other immune-modulatory agents. During a median follow-up of 3.6 years, 9 (43%) had a monophasic course and 12 (57%) had a relapsing-remitting course. At last paediatric follow up 7 (33%) were off all treatment, 9 (43%) left with no or minimal residual disability and 6 (28%) children were walking with assistance (n = 3) or were non-ambulant (n = 3). Our review highlights challenges in the diagnosis and management of paediatric CIDP. It also confirms that certain metabolic disorders may mimic CIDP.
MeSH term(s)	Adolescent ; Child ; Child, Preschool ; Disease Progression ; Female ; Gait/physiology ; Humans ; Immunoglobulins, Intravenous/therapeutic use ; Immunologic Factors/therapeutic use ; Magnetic Resonance Imaging ; Male ; Neural Conduction/physiology ; Plasmapheresis ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/diagnosis ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/physiopathology ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/therapy ; Retrospective Studies ; Treatment Outcome
Chemical Substances	Immunoglobulins, Intravenous ; Immunologic Factors
Language	English
Publishing date	2018-06-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1077681-3
ISSN	1873-2364 ; 0960-8966
ISSN (online)	1873-2364
ISSN	0960-8966
DOI	10.1016/j.nmd.2018.06.001
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Article: A Large Deletion Affecting TPM3, Causing Severe Nemaline Myopathy.

Kiiski, K / Lehtokari, V-L / Manzur, A Y / Sewry, C / Zaharieva, I / Muntoni, F / Pelin, K / Wallgren-Pettersson, C

Journal of neuromuscular diseases

2015 Volume 2, Issue 4, Page(s) 433–438

Abstract: Background and objectives: Nemaline myopathy may be caused by pathogenic variants in the TPM3 gene and is then called NEM1. All previously identified disease-causing variants are point mutations including missense, nonsense and splice-site variants. The ...

Abstract	Background and objectives: Nemaline myopathy may be caused by pathogenic variants in the TPM3 gene and is then called NEM1. All previously identified disease-causing variants are point mutations including missense, nonsense and splice-site variants. The aim of the study was to identify the disease-causing gene in this patient and verify the NM diagnosis. Methods: Mutation analysis methods include our self-designed nemaline myopathy array, The Nemaline Myopathy Comparative Genomic Hybridisation Array (NM-CGH array), whole-genome array-CGH, dHPLC, Sanger sequencing and whole-exome sequencing. The diagnostic muscle biopsy was investigated further by routine histopathological methods. Results: We present here the first large (17-21 kb) aberration in the α-tropomyosinslow gene (TPM3), identified using the NM-CGH array. This homozygous deletion removes the exons 1a and 2b as well as the promoter of the TPM3 isoform encoding Tpm3.12st. The severe phenotype included paucity of movement, proximal and axial weakness and feeding difficulties requiring nasogastric tube feeding. The infant died at the age of 17.5 months. Muscle biopsy showed variation in fibre size and rods in a population of hypotrophic muscle fibres expressing slow myosin, often with internal nuclei, and abnormal immunolabelling revealing many hybrid fibres. Conclusions: This is the only copy number variation we have identified in any NM gene other than nebulin (NEB), suggesting that large deletions or duplications in these genes are very rare, yet possible, causes of NM.
Language	English
Publishing date	2015-09-21
Publishing country	Netherlands
Document type	Journal Article
ISSN	2214-3599
ISSN	2214-3599
DOI	10.3233/JND-150107
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Article ; Online: The value of cardiac MRI versus echocardiography in the pre-operative assessment of patients with Duchenne muscular dystrophy.

Brunklaus, A / Parish, E / Muntoni, F / Scuplak, S / Tucker, S K / Fenton, M / Hughes, M L / Manzur, A Y

European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society

2015 Volume 19, Issue 4, Page(s) 395–401

Abstract: Background/purpose: Duchenne Mmuscular Ddystrophy (DMD) related cardiomyopathy is associated with significant perioperative mortality. Cardiac MRI (CMR) has not previously been systematically evaluated as pre-operative assessment tool for heart function ...

Abstract	Background/purpose: Duchenne Mmuscular Ddystrophy (DMD) related cardiomyopathy is associated with significant perioperative mortality. Cardiac MRI (CMR) has not previously been systematically evaluated as pre-operative assessment tool for heart function in DMD. Our aim was to establish whether CMR versus echocardiography contributes to pre-operative DMD assessment. Methods: Case records were retrospectively reviewed of 35 consecutive DMD boys who underwent evaluation for surgical procedures between 2010 and 2013. Results: Echocardiography revealed a median left ventricular (LV) shortening fraction (SF) of 29/% (range: 7-44). 37% of boys (13/35) had abnormal SF <25%, 66% (23/35) showed hypokinesia and 26% (9/35) had LV dilatation. CMR revealed a median left ventricular ejection fraction (LVEF) of 52% (range: 27-67%). 57% of boys (20/35) had abnormal LVEF <55%, 71% (25/35) had hypokinesia, and 82% late gadolinium enhancement. Extensive versus minimal late gadolinium enhancement was associated with reduced left ventricular ejection fraction (48% vs 58%; p = 0.003) suggesting more severe cardiomyopathy. Although echocardiography shortening fraction correlated with CMR ejection fraction (rs = 0.67; p < 0.001), three-quarter of echocardiography studies had suboptimal scanning windows and in 26% measurements significantly over- or underestimated left-ventricular function compared to CMR. Conclusion: Our findings clearly demonstrate the added value of CMR versus echocardiography in assessing DMD-cardiomyopathy. Particularly when echocardiographic scanning windows are suboptimal, CMR should be considered to allow accurate pre-operative cardiac assessment.
MeSH term(s)	Cardiomyopathies/etiology ; Cardiomyopathies/surgery ; Child ; Echocardiography/methods ; Humans ; Magnetic Resonance Imaging, Cine/methods ; Male ; Muscular Dystrophy, Duchenne/complications ; Muscular Dystrophy, Duchenne/physiopathology ; Preoperative Care/methods ; Retrospective Studies
Language	English
Publishing date	2015-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1397146-3
ISSN	1532-2130 ; 1090-3798
ISSN (online)	1532-2130
ISSN	1090-3798
DOI	10.1016/j.ejpn.2015.03.008
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Article ; Online: Glucocorticoid corticosteroids for Duchenne muscular dystrophy.

Manzur, A Y / Kuntzer, T / Pike, M / Swan, A

The Cochrane database of systematic reviews

2008 , Issue 1, Page(s) CD003725

MeSH term(s)	Adrenal Cortex Hormones/adverse effects ; Adrenal Cortex Hormones/therapeutic use ; Glucocorticoids/adverse effects ; Glucocorticoids/therapeutic use ; Humans ; Male ; Muscular Dystrophy, Duchenne/drug therapy ; Prednisolone/therapeutic use ; Prednisone/therapeutic use ; Pregnenediones/therapeutic use ; Randomized Controlled Trials as Topic ; Walking
Chemical Substances	Adrenal Cortex Hormones ; Glucocorticoids ; Pregnenediones ; Prednisolone (9PHQ9Y1OLM) ; Prednisone (VB0R961HZT)
Language	English
Publishing date	2008-01-23
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Review
ISSN	1469-493X
ISSN (online)	1469-493X
DOI	10.1002/14651858.CD003725.pub3
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Article ; Online: Glucocorticoid corticosteroids for Duchenne muscular dystrophy.

Manzur, A Y / Kuntzer, T / Pike, M / Swan, A

The Cochrane database of systematic reviews

2004 , Issue 2, Page(s) CD003725

MeSH term(s)	Adrenal Cortex Hormones/adverse effects ; Adrenal Cortex Hormones/therapeutic use ; Glucocorticoids/adverse effects ; Glucocorticoids/therapeutic use ; Humans ; Male ; Muscular Dystrophy, Duchenne/drug therapy ; Prednisolone/therapeutic use ; Prednisone/therapeutic use ; Pregnenediones/therapeutic use ; Randomized Controlled Trials as Topic ; Walking
Chemical Substances	Adrenal Cortex Hormones ; Glucocorticoids ; Pregnenediones ; Prednisolone (9PHQ9Y1OLM) ; deflazacort (KR5YZ6AE4B) ; Prednisone (VB0R961HZT)
Language	English
Publishing date	2004-04-16
Publishing country	England
Document type	Journal Article ; Review ; Systematic Review
ISSN	1469-493X
ISSN (online)	1469-493X
DOI	10.1002/14651858.CD003725.pub2
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Article: Backache in a Duchenne boy.

Kinali, M / Robinson, R / Manzur, A Y / Burren, C P / Robb, S A

Neuromuscular disorders : NMD

2007 Volume 17, Issue 4, Page(s) 346–348

MeSH term(s)	Back Pain/etiology ; Child ; Humans ; Male ; Muscular Dystrophy, Duchenne/pathology ; Muscular Dystrophy, Duchenne/physiopathology ; Radiography ; Scoliosis/diagnostic imaging
Language	English
Publishing date	2007-04
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	1077681-3
ISSN	1873-2364 ; 0960-8966
ISSN (online)	1873-2364
ISSN	0960-8966
DOI	10.1016/j.nmd.2007.01.008
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Article ; Online: Congenital myopathies--clinical features and frequency of individual subtypes diagnosed over a 5-year period in the United Kingdom.

Maggi, L / Scoto, M / Cirak, S / Robb, S A / Klein, A / Lillis, S / Cullup, T / Feng, L / Manzur, A Y / Sewry, C A / Abbs, S / Jungbluth, H / Muntoni, F

Neuromuscular disorders : NMD

2013 Volume 23, Issue 3, Page(s) 195–205

Abstract: The congenital myopathies are a group of inherited neuromuscular disorders mainly defined on the basis of characteristic histopathological features. We analysed 66 patients assessed at a single centre over a 5 year period. Of the 54 patients where muscle ...

Abstract	The congenital myopathies are a group of inherited neuromuscular disorders mainly defined on the basis of characteristic histopathological features. We analysed 66 patients assessed at a single centre over a 5 year period. Of the 54 patients where muscle biopsy was available, 29 (54%) had a core myopathy (central core disease, multi-minicore disease), 9 (17%) had nemaline myopathy, 7 (13%) had myotubular/centronuclear myopathy, 2 (4%) had congenital fibre type disproportion, 6 (11%) had isolated type 1 predominance and 1 (2%) had a mixed core-rod myopathy. Of the 44 patients with a genetic diagnosis, RYR1 was mutated in 26 (59%), ACTA1 in 7 (16%), SEPN1 in 7 (16%), MTM1 in 2 (5%), NEB in 1 (2%) and TPM3 in 1 (2%). Clinically, 77% of patients older than 18 months could walk independently. 35% of all patients required ventilatory support and/or enteral feeding. Clinical course was stable or improved in 57/66 (86%) patients, whilst 4 (6%) got worse and 5 (8%) died. These findings indicate that core myopathies are the most common form of congenital myopathies and that more than half can be attributed to RYR1 mutations. The underlying genetic defect remains to be identified in 1/3 of congenital myopathies cases.
MeSH term(s)	Adolescent ; Age of Onset ; Child ; Child, Preschool ; Disease Progression ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Muscle, Skeletal/pathology ; Muscular Diseases/congenital ; Muscular Diseases/diagnosis ; Muscular Diseases/genetics ; Muscular Diseases/pathology ; Mutation ; United Kingdom
Language	English
Publishing date	2013-02-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1077681-3
ISSN	1873-2364 ; 0960-8966
ISSN (online)	1873-2364
ISSN	0960-8966
DOI	10.1016/j.nmd.2013.01.004
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