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Muscular Dystrophy Diagnosis and Treatment in Hyderabad: From the Child Who Falls Too Often to the Adult With Shoulders That Cannot Lift — Accurate Genetic Diagnosis Is the Starting Point for Everything
Expert diagnosis and management of Duchenne, Becker, Limb-Girdle, FSHD, EDMD, and other muscular dystrophies at KIMS Neuroscience, Secunderabad, Hyderabad.
The muscular dystrophies are a large family of distinct inherited conditions causing progressive muscle degeneration from a genetic defect in a muscle structural or regulatory protein. They share a final common pathway (progressive muscle loss) but differ in their gene, inheritance pattern, age of onset, distribution of weakness, cardiac/respiratory involvement, and treatment. The six main types at KIMS: (1) Duchenne Muscular Dystrophy (DMD): X-linked recessive, boys, most severe, dystrophin absent, CK 50-200x normal, walking lost ~10-12 years untreated, dilated cardiomyopathy by teens; (2) Becker MD (BMD): same dystrophin gene but in-frame deletion (partial dystrophin preserved), milder, cardiac may dominate; (3) Limb-Girdle MD (LGMD): >30 subtypes, autosomal recessive (higher prevalence in Telangana/AP from consanguinity) or dominant; (4) Facioscapulohumeral MD (FSHD): D4Z4 repeat contraction, autosomal dominant, face + scapula + asymmetric; (5) Emery-Dreifuss MD (EDMD): EMD/LMNA mutations, triad of contractures + humeroperoneal weakness + life-threatening cardiac conduction disease; (6) Oculopharyngeal MD (OPMD): PABPN1 GCN repeat expansion, ptosis + dysphagia from 40s-60s. Diagnosis: serum CK + EMG + MLPA/gene panel + muscle biopsy (when required).
- Gower's sign — the clinical key to DMD
- Gower's sign: the child cannot rise from the floor without using both hands to push sequentially up the legs (climbing up the body). This occurs because the proximal hip extensor muscles (glutei) are too weak to straighten the body from a bent position. In a boy aged 2-5 who is falling frequently and cannot keep up with peers, Gower's sign is Duchenne Muscular Dystrophy until proven otherwise. Serum CK is the first investigation: in DMD, CK is 50-200 times normal — a finding so dramatic it virtually confirms muscle disease instantly.
- South Indian DMD mutation spectrum — exon-specific therapies
- In a South Indian study of 250 DMD patients: 63% had exon deletion mutations (predominantly distal hotspot, exons 45-53); 21% had duplications (predominantly proximal, exons 3-25); 6% had point mutations. The most common single exon deletions were exon 45 (16%) and exon 44 (10.7%). This mutation map is clinically relevant because exon-specific therapy eligibility is mutation-dependent: casimersen targets exon 45 skipping (16% of the South Indian cohort potentially eligible); golodirsen/viltolarsen target exon 53 (approximately 8-10% eligible). Precise genetic diagnosis determines eligibility.
- Corticosteroids in DMD — standard of care that is still not reaching all patients
- Prednisolone (0.75 mg/kg/day) or deflazacort (0.9 mg/kg/day) extend independent walking by an average of 2-3 years, delay respiratory decline, reduce scoliosis rate, and improve survival. Both are inexpensive and available in India. Yet many DMD patients in Telangana and AP are not receiving them — because diagnosis is delayed, families are not counselled on the evidence, or follow-up is not maintained. At KIMS, steroid initiation is a priority discussion at the first appointment after diagnosis in any ambulatory child aged 4-8 years.
- EDMD — the cardiac emergency in disguise
- Emery-Dreifuss MD (LMNA form) can cause sudden cardiac death in patients with only mild skeletal muscle weakness. The cardiac conduction disease of EDMD does not wait for muscle disease to become severe. Pacemaker implantation for significant conduction disease and ICD implantation for ventricular arrhythmia risk must be performed at KIMS before symptomatic events occur. Sudden death as the first cardiac presentation has been documented in EDMD. Immediate cardiology referral for electrophysiological assessment at the time of EDMD diagnosis.
- FSHD — scapular winging and the surgical option
- Facioscapulohumeral Muscular Dystrophy: the shoulder blades wing away from the chest wall when the patient pushes against a wall (serratus anterior weakness). In patients with significant functional limitation from scapular winging — inability to raise the arm above head level, difficulty with daily activities — scapular fixation surgery (scapulothoracic fusion) significantly improves arm elevation. This procedure is available at KIMS for carefully selected FSHD patients. Characteristic asymmetry: FSHD consistently affects one side more than the other.
- BMD cardiac dominance — the important misconception
- In Becker Muscular Dystrophy, the degree of skeletal muscle weakness does NOT predict the degree of cardiac involvement. A BMD patient who walks well and works normally may simultaneously be developing severe dilated cardiomyopathy. Annual echocardiography is mandatory in ALL BMD patients regardless of walking ability. ACE inhibitors are started prophylactically from a defined age (or when LV dysfunction is detected) to delay cardiomyopathy progression, regardless of cardiac symptoms.
- New therapies — honest assessment for Indian families
- Eteplirsen (exon 51), golodirsen/viltolarsen (exon 53), casimersen (exon 45), ELEVIDYS (AAV gene therapy, FDA June 2024 for ambulatory DMD aged 4+), givinostat (non-steroidal, FDA March 2024 for DMD aged 6+) — none are CDSCO-approved in India as of 2025. Named patient programme applications guided at KIMS. DART India (Duchenne Action Research Trust India) patient organisation connected. The honest assessment: the standard of care at KIMS for DMD remains corticosteroids + comprehensive multi-system monitoring, supplemented by named patient access where achievable.
About This Condition
A Family of Conditions, Not a Single Disease
A 4-year-old boy in Hyderabad has been falling more than his peers since he started walking. His parents were told he is clumsy. At nursery school, his teacher notices that he cannot climb the steps to the slide and that when he falls, he takes much longer than the other children to get back up — pushing himself up from the floor using his hands on his thighs. His serum CK (creatine kinase) is 15,000 U/L — more than 50 times the normal upper limit.
At KIMS Neuroscience, this combination — a boy, early walking difficulties, the characteristic Gower's sign, and a dramatically elevated CK — means one thing until proven otherwise: Duchenne Muscular Dystrophy. The genetic test is sent that day.
A 28-year-old woman in Secunderabad presents with a different story. For the past three years she has found it increasingly difficult to raise her arms above her head. She cannot brush her hair without resting her arms. Her shoulder blades have started to protrude abnormally from her back when she tries to push against a wall. She has no family history she is aware of. A serum CK is mildly elevated. Her EMG shows a myopathic pattern.
This clinical picture — scapulohumeral weakness with winging in a young adult — is consistent with a muscular dystrophy but is not specific to any single condition. Facioscapulohumeral Muscular Dystrophy (FSHD) is among the leading differentials, but LGMD and other neuromuscular conditions must be systematically excluded. The specific diagnosis requires genetic testing at KIMS — management pathway, genetic risk, and prognosis all depend on which condition is confirmed.
The muscular dystrophies are not one disease. They are a large family of distinct genetic conditions, each caused by a mutation in a different gene, each producing a different clinical profile, and each requiring a different diagnostic and management pathway. What they share is the final common pathway: progressive muscle degeneration from a genetic defect in a muscle structural or regulatory protein. Getting the specific diagnosis right is not just academically important — it changes what you do next, what the family's genetic risk is, and whether new therapies are available.
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The Main Types Treated at KIMS
Each muscular dystrophy is described with its key features, India-specific context, and management approach. Each is caused by a mutation in a different gene, and each has a distinct inheritance pattern, age of onset, clinical course, and management plan.
Duchenne Muscular Dystrophy (DMD)
X-linked recessive · boys · most severe. DMD gene (Xp21) mutations cause complete absence of dystrophin. Deletions account for ~63% of Indian DMD mutations; duplications 21%; point mutations the remainder. Affects boys almost exclusively, ~1 in 5,000–6,000 male births. Presentation: developmental motor delay, toe-walking, frequent falls, Gower's sign at age 2–5. CK 50–200 times normal at diagnosis. Walking is lost at an average of 9.5 years in untreated patients; corticosteroids extend this by 2–3 years on average. Dilated cardiomyopathy develops in virtually all patients by the late teens. KIMS management: MLPA genetic confirmation, early corticosteroid initiation, annual echocardiogram or cardiac MRI from diagnosis, ACE inhibitor prophylaxis for cardiomyopathy started early, respiratory monitoring, physiotherapy, orthotic support, scoliosis monitoring, and family counselling.
Becker Muscular Dystrophy (BMD)
X-linked recessive · boys/men · milder than DMD. Same DMD gene but with an in-frame deletion that allows production of a shortened but partially functional dystrophin protein. Phenotype is significantly milder — walking is typically maintained into adulthood, sometimes into the 40s or 50s. Proximal weakness presenting in teens or early adulthood, exercise-related muscle pain and cramps, elevated CK. Cardiomyopathy is prominent and can be the dominant or presenting feature — some patients have severe cardiac disease with relatively mild skeletal weakness. Annual echocardiography is mandatory. KIMS management: MLPA + sequencing, cardiac monitoring with early ACE inhibitor/beta-blocker, physiotherapy, ICD where indicated.
Limb-Girdle Muscular Dystrophies (LGMD)
Autosomal recessive or dominant · both sexes · highly variable. A large family of conditions (over 30 subtypes — LGMD R1–R26 recessive, LGMD D1–D5 dominant) causing progressive weakness of the shoulder and hip girdle muscles, with relative sparing of the face. The autosomal recessive forms are significantly more common in populations with higher rates of consanguineous marriage — as in Telangana and Andhra Pradesh. Important Indian subtypes: LGMD R1 (calpain-3), LGMD R2 (dysferlin / Miyoshi myopathy), LGMD R5/R6 (sarcoglycanopathies — cardiac involvement). KIMS management: comprehensive LGMD gene panel, cardiac screening for relevant subtypes, respiratory monitoring, family counselling and carrier testing.
Facioscapulohumeral Muscular Dystrophy (FSHD)
Autosomal dominant · both sexes · slowly progressive. Caused by contraction of the D4Z4 repeat array on chromosome 4q35, leading to inappropriate expression of the DUX4 transcription factor in muscle. Onset typically in teens to 20s. The name describes the muscles affected: face (difficulty closing eyes, whistling), scapular muscles (winging of the scapulae), and upper arm/shoulder muscles. Asymmetry is characteristic — FSHD typically affects one side more than the other. Extra-muscular features: retinal vasculopathy, high-frequency hearing loss. Cardiac and respiratory involvement uncommon. KIMS management: D4Z4 repeat sizing, scapular fixation surgery, ankle-foot orthoses for foot drop, annual ophthalmology in severe cases.
Emery-Dreifuss Muscular Dystrophy (EDMD)
X-linked or autosomal dominant/recessive · high cardiac risk. Genes: EMD (emerin, X-linked), LMNA (lamin A/C, autosomal). Distinctive triad: (1) early joint contractures at elbows, ankles, and posterior neck — occurring before significant weakness; (2) slowly progressive humeroperoneal weakness; (3) life-threatening cardiac conduction disease — heart block, arrhythmias, sudden death. Cardiac complications are the dominant life-threatening feature, particularly the LMNA form, where sudden cardiac death can occur in patients with only mild muscular weakness. Pacemaker and ICD implantation is frequently required. KIMS management: emerin staining + sequencing, immediate cardiac referral for electrophysiological assessment, contracture physiotherapy, cascade testing.
Oculopharyngeal Muscular Dystrophy (OPMD)
Autosomal dominant · late onset · ptosis + swallowing. PABPN1 gene — a GCN trinucleotide repeat expansion. Typically presents in the 40s–60s, both sexes equally. Ptosis and dysphagia as the dominant symptoms, often mistaken for Myasthenia Gravis or motor neuron disease. Proximal limb weakness develops later. Distinguishing from MG: ptosis and dysphagia are slowly progressive over years (not fluctuating), do not respond to pyridostigmine, AChR antibodies are negative, repetitive nerve stimulation is normal. KIMS management: genetic confirmation, eyelid (ptosis) surgery when vision is impaired, cricopharyngeal myotomy or dilatation for severe dysphagia, nutritional support.
Comparison at a Glance
A reference for clinicians and informed patients — the key distinguishing features of the major muscular dystrophies seen at KIMS, including inheritance, age of onset, key features, and cardiac risk.
DMD — X-linked, early childhood (2–5y)
Rapid progression, loss of walking ~10–12y, very high CK. Cardiac risk: high — dilated cardiomyopathy by late teens; ACE inhibitor prophylaxis initiated early.
BMD — X-linked, teens to adulthood
Milder, walking maintained; cardiac may dominate. Cardiac risk: high — cardiomyopathy can precede skeletal weakness.
LGMD (recessive) — autosomal recessive, teens–30s
Hip and shoulder girdle weakness; many subtypes; high prevalence in South India due to consanguinity. Cardiac risk: variable by subtype.
FSHD — autosomal dominant, teens–20s
Face + scapular winging + asymmetry. Cardiac risk: low (most cases).
EDMD — X-linked or AD/AR, childhood–teens
Contractures + humeroperoneal weakness + cardiac conduction disease. Cardiac risk: very high — sudden cardiac death risk.
OPMD — autosomal dominant, 40–60s
Ptosis + dysphagia; mimics MG. Cardiac risk: low.
Myotonic dystrophy — autosomal dominant, variable onset
Myotonia + distal weakness + multi-system. Cardiac risk: high — arrhythmias, sudden cardiac death.
The India-Specific Context — Why Local Genetic and Treatment Patterns Matter
The muscular dystrophies present a different epidemiological and access picture in India than in Western countries. DMD molecular testing is the second most common genetic test performed in India after beta-thalassemia testing — reflecting the significant burden of the disease in Indian families. The autosomal recessive Limb-Girdle Muscular Dystrophies are significantly more common in Telangana and Andhra Pradesh because of consanguineous marriage traditions. And new therapies are emerging at pace internationally — but accessibility in India remains the question that defines what families can actually do next.
At KIMS Neuroscience, every muscular dystrophy patient is given an honest assessment of where standard-of-care management ends and where access barriers to emerging therapies begin — so families plan against the reality, not the headline.
DMD genetic testing in India
DMD molecular testing — MLPA for deletions/duplications of the 79-exon dystrophin gene — is the second most common genetic test performed in India after beta-thalassemia testing. In a South Indian study of 250 DMD patients, 63% had exon deletion mutations (predominantly in the distal hotspot region, exons 45–53), 21% had duplications (predominantly proximal, exons 3–25), and 6% had point mutations. The most common single exon deletions were exon 45 (16%) and exon 44 (10.7%). This mutation spectrum is relevant because exon-specific therapies (where available) are mutation-dependent.
The steroid access gap
Corticosteroids — prednisolone and deflazacort — are the established standard of care in DMD and have been shown to extend independent walking, preserve respiratory function, and improve survival. In India, these medications are inexpensive and available. Yet many DMD patients in Telangana and Andhra Pradesh are still not receiving them — either because diagnosis is delayed beyond the optimal treatment window, families are not counselled on the evidence, or follow-up is not maintained. At KIMS, steroid initiation is a priority discussion at the first appointment after diagnosis.
LGMD and consanguinity in South India
The autosomal recessive Limb-Girdle Muscular Dystrophies are significantly more common in Telangana and Andhra Pradesh than in populations without consanguineous marriage traditions. A child of a consanguineous couple who presents with proximal muscle weakness — difficulty climbing stairs, waddling gait, difficulty rising from the floor — must have LGMD in the differential, even if the presentation is mild. Specific LGMD subtype can only be determined by gene panel testing. At KIMS, NGS-based gene panels covering all known LGMD genes are available.
The New Therapy Landscape — What Is Accessible in India
Exon-skipping therapies and gene therapy — what families in India need to know: Several mutation-specific therapies for DMD have received accelerated approval in the USA: eteplirsen (exon 51 skipping), golodirsen and viltolarsen (exon 53 skipping), casimersen (exon 45 skipping) — together applicable to approximately 30% of DMD patients. Delandistrogene moxeparvovec (ELEVIDYS) — an AAV-based micro-dystrophin gene therapy — received FDA approval in June 2024 for ambulatory DMD patients aged 4 and older. Givinostat (Duvyzat) — the first non-steroidal anti-inflammatory drug for DMD regardless of mutation — received FDA approval in March 2024 for patients aged 6 and older. As of 2025, none of these therapies have received CDSCO (Indian regulatory) approval or are routinely accessible in India outside of named patient programmes. At KIMS, families are informed about the current access landscape, connected with DART (Duchenne Action Research Trust India) and similar patient organisations, and guided through named patient programme applications where applicable. The standard of care at KIMS for DMD remains corticosteroids plus comprehensive multi-system monitoring.
Diagnosis at KIMS — The Pathway
Serum CK — the first and fastest signal
Creatine kinase (CK) leaks from damaged muscle fibres into the bloodstream. In DMD, CK is typically 50–200 times the normal upper limit — a finding so dramatic that it virtually confirms significant muscle disease the moment it is reported. In LGMD and BMD, CK is elevated 5–50 times normal. In FSHD and EDMD, CK may be only mildly elevated. At KIMS, CK is measured in every patient presenting with muscle weakness as the first investigation.
EMG and nerve conduction studies
EMG confirms the myopathic pattern of muscle disease — small, brief motor unit potentials on voluntary contraction — and excludes neuropathic conditions and anterior horn cell disease (SMA, MND) that can produce similar weakness. This is an essential early step at KIMS to direct the subsequent genetic workup.
Genetic testing — the definitive answer
For suspected DMD/BMD: MLPA is the first-line test, identifying deletions and duplications with high sensitivity. If MLPA is normal in a convincing clinical picture, full gene sequencing detects point mutations and small indels. For suspected LGMD: a comprehensive gene panel covering all known LGMD genes is sent from a single blood sample, with results in 4–6 weeks. For FSHD: D4Z4 repeat sizing on chromosome 4q35. For EDMD: emerin immunostaining on muscle biopsy + genetic sequencing of EMD and LMNA.
Muscle biopsy (where indicated)
Muscle biopsy remains essential when genetic testing does not yield a definitive diagnosis, or when characterising pathological severity to guide treatment. At KIMS, muscle biopsy is performed under local anaesthesia from a moderately affected muscle. Immunohistochemistry with antibodies to dystrophin, sarcoglycans, dysferlin, calpain-3, emerin, and other proteins provides a protein-level diagnosis that complements genetic findings.
Multi-system baseline assessment
On diagnosis of any muscular dystrophy with cardiac or respiratory risk: echocardiogram, pulmonary function tests, and — in ambulatory children — six-minute walk test (6MWT) as a functional baseline. Spine X-ray for scoliosis assessment in non-ambulant patients. Ophthalmology and audiology review for FSHD. Genetic counselling for all confirmed cases.
Management at KIMS — Treating Every System, Not Just the Muscle
Cardiac surveillance and therapy at KIMS
DMD/BMD: Annual echocardiogram or cardiac MRI from diagnosis; ACE inhibitors (enalapril, ramipril) started prophylactically early — before cardiomyopathy develops — evidence shows they delay onset of LV dysfunction; beta-blockers added when LV function declines; ICD considered in severe LV dysfunction or arrhythmia
EDMD: Immediate electrophysiological assessment; pacemaker for significant conduction disease; ICD for ventricular arrhythmia risk — this cannot wait for symptoms, since sudden death is the first presentation in some EDMD patients
LGMD subtypes with cardiac risk: Annual echo for sarcoglycanopathies (R5, R6) and LMNA-related LGMD
Respiratory monitoring and support at KIMS
Annual spirometry (FVC) from the time of diagnosis or from age 6 in DMD
Cough assist device (mechanical insufflator-exsufflator) when peak cough flow falls — essential for managing chest infections in DMD without escalating to hospital
Non-invasive ventilation (BiPAP) when nocturnal hypoventilation is detected on overnight oximetry or sleep study, or when FVC falls below 50% predicted
Pneumococcal and annual influenza vaccination — chest infections are the leading cause of acute crisis and hospitalisation in DMD patients in India
In advanced DMD: planning and counselling for long-term ventilatory support, gastrostomy (PEG), and palliative care decisions in collaboration with the family
Physiotherapy and orthotics
• Daily passive stretching of ankles, knees, hips, and elbows — to delay contracture development • Ankle-foot orthoses (AFOs) to prevent equinus deformity and extend walking duration • Powered wheelchair planning — transition from walking aids to manual to powered wheelchair as strength declines • Scoliosis surveillance — spinal X-ray annually when non-ambulant. Spinal stabilisation surgery (posterior spinal fusion) when scoliosis exceeds 20–25 degrees and respiratory function is adequate for anaesthesia — preserves sitting balance and slows respiratory decline • For FSHD: scapular stabilisation surgery — surgical fixation of the scapula to the chest wall — significantly improves arm elevation and function in carefully selected patients
Genetic Counselling and Reproductive Planning
At KIMS, genetic counselling is offered to the family of every confirmed muscular dystrophy patient: • DMD/BMD — X-linked: Mother carrier testing (obligate carrier if she has an affected son and an affected brother/maternal uncle; otherwise carrier probability requires genetic testing). 50% risk to future sons; 50% risk to daughters of being carriers. Prenatal diagnosis by CVS at 11–13 weeks. Pre-implantation genetic diagnosis (PGD) available. • LGMD recessive: Both parents are typically carriers (unaffected). 25% recurrence risk per pregnancy. Sibling carrier testing. Prenatal diagnosis and PGD available. • FSHD, EDMD (LMNA), OPMD — autosomal dominant: 50% risk per child of an affected parent. Genetic testing of at-risk family members to identify presymptomatic carriers who require cardiac monitoring (EDMD) or surveillance.
Corticosteroids in DMD — the most important intervention
Prednisolone (0.75 mg/kg/day) or deflazacort (0.9 mg/kg/day) are the standard-of-care pharmacological treatments for DMD. The evidence is robust: • Extends independent walking by an average of 2–3 years • Delays onset of respiratory decline and need for ventilatory support • Reduces the rate of scoliosis development • Improves muscle strength and function scores during the ambulatory phase • Long-term prospective data shows improved survival At KIMS, steroids are started as soon as the diagnosis is confirmed in a child who is in the plateau or early decline phase of motor function — typically age 4–8. The decision on dosing schedule (daily vs weekend-only) is individualised based on age, weight, family preferences, and side-effect tolerance. Side effects managed at KIMS include: weight gain and Cushingoid features, blood pressure monitoring, blood glucose monitoring, bone density assessment with Vitamin D and calcium supplementation, and cataract surveillance.
Related Conditions
Muscular Dystrophy belongs to the family of neuromuscular disorders managed at KIMS Neuroscience:
FAQs
Frequently Asked Questions
| Fact | Details |
|---|---|
| DMD: first-line workup | Serum CK (50-200x normal) · EMG · MLPA: first-line genetic test for deletions/duplications · Sequencing for point mutations if MLPA normal · Diagnosis same week at KIMS |
| Steroids in DMD | Prednisolone (0.75 mg/kg/day) or deflazacort (0.9 mg/kg/day) · Start 4-8 years (ambulatory plateau phase) · Extends walking by 2-3 years · Delays cardiac/respiratory decline · Inexpensive in India but underused |
| Cardiac monitoring | DMD/BMD: annual echo or cardiac MRI from diagnosis · ACE inhibitor prophylaxis started early · EDMD: immediate EP study, pacemaker/ICD before symptoms · LGMD sarcoglycanopathies: annual echo |
| LGMD in South India | Autosomal recessive forms more common in Telangana/AP (consanguinity) · >30 subtypes · NGS gene panel covers all known LGMD genes · Specific subtype determines cardiac risk |
| FSHD | D4Z4 repeat contraction (chromosome 4q35) · Asymmetric face + scapula + shoulder · Autosomal dominant · Scapular fixation surgery at KIMS for selected cases · Retinal vasculopathy screen |
| Emerging therapies (India 2025) | None CDSCO-approved as of 2025 · Named patient programme guided at KIMS · DART India patient organisation · Steroids + multi-system monitoring remain standard of care |
| Genetic counselling | DMD/BMD: X-linked, mother carrier testing, 50% risk to sons, PGD available · LGMD recessive: 25% recurrence risk · FSHD/EDMD/OPMD dominant: 50% risk per child of affected parent |
A boy who falls too often. A child who cannot climb stairs. A young woman whose shoulders have stopped lifting. A father with a heart that is failing faster than his legs. Muscular dystrophy presents in many ways — but the path through it starts with one thing: a precise genetic diagnosis.
At KIMS Neuroscience, Secunderabad, Hyderabad, every patient presenting with suspected muscular dystrophy receives the complete diagnostic pathway: serum CK, EMG, MLPA or gene panel genetic testing, muscle biopsy where indicated, and a full multi-system baseline assessment. The diagnosis determines the treatment, the monitoring plan, the family's genetic risk, and — increasingly — eligibility for emerging therapies. We do not manage symptoms. We manage the specific disease — because muscular dystrophy is not one disease.
International enquiries: info@kimsneurosciences.com