For Neurology Residents Erin O’Ferrall Neuromuscular fellow Jan 13, 2010

 To describe the classification systems for myopathies

 To describe how to elicit history & physical exam findings of myopathy

 To briefly review the most common or important myopathies in each category

  Classification of Muscle Diseases ◦  Molecular ◦  Phenotype ◦  Etiology

  History   Physical exam   The Myopathies: illustrated with cases ◦  Inflammatory

  IBM, PM, DM ◦  Inherited: Muscular Dystrophies

  LGMDs (Calpain, Dysferlin), Dystrophin, OPMD, FSHD, DM1&2 ◦  Metabolic Myopathies ◦  Channelopathies ◦  Toxic/Drug Myopathies

  Conclusions

  The bad news: ◦ Myopathies cannot be covered in 1 hour! ◦  I will spend more time discussing the approach as

well as key points on the history and physical exam…the rest is up to you!

  The good news: ◦ Myology is a neglected area of Neurology and is

not heavily emphasized on the Royal College Exam! ◦ Myology is cool

  Today I will focus on the adult-onset presentations

 Molecular  Phenotype  Etiology

 Extracellular defects

  Sarcolemmal defects

 Myofibrillar and cytoskeletal defects

 Myonuclear abnormalities

Limb Girdle -LGMD -Inflammatory

Limb Girdle Plus -LGMDs -Inflammatory -Duchenne & Becker

Humeroperoneal -Emery-Dreifuss

Facioscapulohumeral -FSHD

Distal -distal myopathies

Ocluopharyngeal -OPMD

  Proximal/ Limb-Girdle Weakness ◦  Most common pattern for hereditary & acquired myopathies

  Distal weakness ◦  Rule out neuropathy (look for sensory involvement) ◦  DMs, FSHD, OPMD, Emery-Dreifuss, IBM ◦  Miyoshi (dysferlin)

  Proximal Arm + Distal Leg /Scapuloperoneal ◦  Scapular winging ◦  FSHD, Emery-Dreifuss, LGMD: Laminopathies, Calpain, sarcoglycans

  Distal Arm + Proximal Leg ◦  IBM

  Ptosis with or without ophthalmoplegia ◦  WITH: OPMD, oculopharyngodistal myopathy, Mitochondrial, NMJ (MG, Lambert-Eaton, Botulism) ◦  WITHOUT: DMs, Congenital Myopathies, Desminopathy

  Prominent Neck extensor weakness/ Dropped head ◦  Inflammatory (PM< DM, IBM) FSHD, DM, Congenital (nemaline) myopathy, HyperPTH, Carnitine

deficiency, isolated neck extensor myopathy, HypoT, HypoK

  Bulbar weakness: OPMD ◦  Think of motor neuron diseases or NMJ

  Episodic weakness ◦  Metabolic myopathies, drugs/toxins, infections, trauma, DM/PM (rare), channelopathies,

Thyrotoxicosis

(NOTE: one disease may have several phenotypes; only a few examples are listed)

Hereditary   Muscular

Dystrophies*   Myotonias   Channelopathies   Congenital Myopathies   Metabolic

Myopathies   Mitochondrial

myopathies

Acquired   Inflammatory

myopathies   Endocrine   Associated with other

systemic illness   Drug-induced and

Toxic myopathies

  Dystrophinopathies ◦  Duchenne MD ◦  Becker MD

  Limb-Girdle MD: LGMD ◦  Many “__opathies” named based on the deficient or

defective protein   Facioscapulohumeral MD   Oculopharyngeal MD   Distal MDs   Emery-Dreifuss MD   Congenital MDs   (MD= muscular dystrophy)

  Symptoms depend on which muscles are involved > etiology   Weak = loss of muscle power   Patients may confuse this with ◦  Numb, SOB or generalized fatigue ◦  Always ask: for what specific movements or activities are you weak? Or

When do you notice weakness (i.e what are you doing)? ◦  Is there anything you can’t do now that you could do X months ago?

  Differentiate weakness from from ◦  depression/ malingering (vague description) ◦  Tendon or joint contractures ◦  Weakness secondary to pain (may have pain with passive movement)

  Course is KEY!   When did the weakness start?   Ask about infancy, childhood, adolescence, etc using both broad and specific

questions: EXAMPLES?

  Ocular: ◦  Ptosis & Diplopia

  Facial ◦  What do you ask to assess facial weakness? ◦  Drinking with a straw, whistling, blowing up balloons,

drooling; Facial expression reported by others; Photos for change over time ◦  Sleep with Eyes Open~ think FSHD

  Chewing: ask about fatigue, discomfort   Swallowing: choking, aspiration, nasal regurgitation   Speech: ◦  What type of speech is heard with myopathies? ◦  Slurred, nasal, hoarse

  What questions can you ask to assess:   Proximal upper extremity? ◦  painting the ceiling, shampooing or combing the hair, shaving,

lifting objects off high shelves   Distal upper extremity? ◦  Difficulty with buttons, zipper then opening jars, turning faucet/

door knob/ car ignition, using keys, holding silverware, writing, opening car door

  Proximal lower extremity? ◦  Rising from floor or low chair, Getting out of the bath, up from

toilet, Stairs (down=quads; up=hip extn) ◦  Gait: waddling

  Distal lower extremity? ◦  Difficulty to stand on your toes, Tripping, footdrop /slapping (ask

partner), can’t stand still /poor balance

  Neck: ◦  Ask about braking or accelerating in a car, difficulty

lifting head off the pillow, need to use hands to lift head off chest

  Diaphragm ◦  How do you ask about diaphragm weakness? ◦  SOB esp lying flat ◦  Hypoventilation, CO2 retentions: AM headaches, vivid

nightmares, daytime somnolence   Axial ◦  Can you do a sit up? ◦  Do you have trouble standing up straight? (Bent spine

Syndrome)

  Define Cramps ◦  Painful; occur when a muscle contracts in a shortened

position; muscle becomes hard, well-defined; relieved by stretching ◦  Benign or abnormal ◦  Motor units firing at high frequency

  Define Muscle Contracture ◦  Ex: metabolic myopathy ◦  Electrical silence

 Cranial Nerves ◦  Smooth, unlined face if weakness longstanding (in

an older person) ◦  Temporalis/ Masseter wasting: scalloped

appearance ◦  Jaw power ◦  lips: tented upper lip or straight line ◦  Don’t forget to check for dysarthria & phonation ◦  High arched palate: wk since childhood

  Frontal balding is seen in which myopathy? ◦ What “special” cranial nerve test could you do?

  Posture ◦  Pectoral atrophy –upward sloping pectoral fold in FSHD

  Muscle bulk ◦  Atrophy? Asses at rest & activated ◦  Hypertrophy?

  Dystrophies, myotonic disorders

◦  Abnormal muscle movements? ◦  Rippling (Caveolin3)

  Winged scapula: What Muscles? How to test? ◦  Trapezius hump in FSHD

  Palpate muscles ◦  Fibrotic: rubbery or hard; Tender: inflammatory, rhabdo, viral myositis

  Percuss: myotonia, rippling, myoedema   Look for Bony deformities (scoliosis) & Contractures (Elbows for

Emery-Dreifuss)

  Can use 4+, 4, 4- for mild, moderate, & severe weakness

  Grade 3+ “used when the muscle can move the joint against gravity and can exert a tiny amount of resistance but then collapses under the pressure of the examiner’s hand.”

 Grade 3- ex: knee that can extend only to 30-40 degrees of horizontal

  neck flexion/ extension   shoulder abduction, internal rotation, external rotation   elbow flexion/ extension   wrist flexion and extension   finger abduction and adduction   thumb abduction and flexion   hip flexion and extension   knee flexion and extension   ankle dorsiflexion and plantar flexion; inversions & eversion   dorsiflexion of the great toe   Toe flexion   Sit up   Diaphragm (if indicated): counting seated and supine

  Walking ◦  What type of gait do you expect with limb girdle

weakness? ◦  Knee hyperextension is a sign of what? ◦  Steppage gait is a sign of what? ◦  Arm swing

  Arising from Floor   Sit up from lying supine   Stepping on stool   Squat from low chair   Provocative/ Special tests are necessary when the

patient complains of weakness and you do not find it on confrontational testing!

WHAT’S THE DIFFERENTIAL DIAGNOSIS??

  Myopathies ◦  Polymyositis, IBM, ?DM, Fascioscapulohumeral dystrophy,

Myotonic Dystrophies (myotonic dystrophy with hypothyroidism, proximal myotpnic dystrophy) ◦  mitochondrial myopathy, acid maltase deficiency, carnitine deficiency ◦  hypokalemic periodic paralysis, congenital myopathy, nemaline

myopathy ◦  Endocrine: Cushing’s syndrome, Hyopthyroid myopathy,

hyperparathyroidism ◦  restricted non-inflammatory myopathy, focal myopathy -radiation

damage   Motor neuron ◦  ALS, spinal muscular atrophy, postpolio

  NMJ: MG   CIDP

 DTRs: lost in proportion to weakness   Sensory exam: normal except myofibrillar

myopathies (associated neuropathy), mitochondrial

 Coordination: normal unless very weak  No fasiculations  After the Physical Exam… ◦ Return to the history if you have not

confirmed your hypothesis

 58 yr woman with a 6 wk history of muscle aching and weakness

 Difficulty climbing stairs and rising from chairs; difficulty raising her arms above her head

 Redness of face, neck & hands

  Cranial nerves: normal

  Neck flexion 4-, Extension 5-   Shoulder abduction 4-   Elbow flexion 4-, extension 4-   Wrist flexion 4+, extension 4+   Hip flexion 3-, extension 3-, abduction 3-   Knee flexion 4-, extension 4+   Ankle dorsiflexion 4+, plantarflexion 5

  Normal DTRs   Normal Sensory exam

Gottron rash

Heliotrope rash +/- edema

V sign, +/- Shawl sign

May also see Mechanic’s Hands

  Three main types: Dermatomyositis (DM), Polymyositis (PM), Inclusion Body Myositis (IBM)

  Overall incidence of inflammatory myopathies is 1 in 100 000 per year (but estimates vary)

  DM is most common overall but   IBM is most common after age 50 yrs   PM is rarely (if ever) seen in children   PM & DM: slowly progressive limb-girdle

weakness, including neck extensors   DM: activity-induced muscle pain   IBM: finger flexor & quadriceps weakness

  Characteristic skin findings: (see prior slide)   Dysphagia   Multisystem disease can occur ◦  Pulmonary involvement (Interstitial lung disease) 10-20%, t-

histidyl transfer RNA Abs (Jo-1) ◦  Also GI, Cardiac, Joints ◦  Malignancy: 6- 45%, usually over 40 yrs; ovaries, GI tract, Lung,

Breast, Non-Hodgkin lymphomas ◦  Overlap with systemic sclerosis or other mixed connective

tissue diseases   Variants ◦  No weakness: dermatomyositis sine myositis or amyopathic

dermatomyositis ◦  Transient or unrecognized rash: dermatomyositis sine dermatitis ◦  In Children: subcutaneous calcification, “Misery”: irritable,

uncomfortable child, red face, proximal weakness, tiptoe gait due to flexion contractures

 uncommon  Diagnosis of exclusion  This is NOT DM without the rash! ◦ Mediated by CD8+ T cells which attack

muscle fibers ◦  (DM: humorally mediated microangiopathy)

 Occurs alone or in association with other autoimmune disorders

 Controversial association with malignancy

 CK normal  ANA positive 1:120  No anti-Jo1 antibodies  Muscle biopsy: diagnostic for DM   Treated with prednisone and methotrexate  Mammogram reveals suspicious lesion,

biopsy shows cancer  After surgery & chemotherapy she is able to

wean off the prednisone

  Usually >50 yrs   Slowly progressive   Dysphagia ◦  Later, in up to 2/3rds

  Spares EOM   CK: normal – 10X   EMG: myopathic motor unit potentials, fibrillations, positive

sharp waves, long & high amplitude motor units   DDx: ◦  Familial forms ◦  Hereditary: Inclusion Body Myopathy

  (IBM1): Desmin, AD   IBM2: GNE & non-GNE forms (LAMA2), AR   IBM3: myosin heavy chain IIa, AD   IBMPFD: IBM with Paget’s disease and frontotemporal

dementia; Valosin-containing protein

  IBM: Lancet Neurol 2007; 6: 620–31  PM, DM: Lancet 2003; 362: 971–82  AAN Continuum Jun 2006

  17 yr male  At age 3: hyperactive, clumsy, speech delay  At Age 4: weakness of face & shoulder girdle,

scapular winging, increased lumbar lordosis, waddling gait

 Age 12: difficulty standing up from chair, bilateral foot drop

 Currently sleeps with eyes open   FHx: ◦  none

 CK mildly raised 683 U/L (N <150U/L)  EMG normal  Muscle biopsy: myopathy (may see

inflammation!)  Bilateral hearing loss

  AD   Prevalence 50 per million   Variable penetrance; estimated that 30% of affected family members

are unaware   Onset 3- 44 yrs (usually)   FacioScapuloHumeral pattern of weakness, may be symmetric   Trapezius lump   Horizontal anterior axillary folds   Popeye arms   Abdominal muscle weakness   Hypertrophic EDB   Cardiac involvement in 4-60%   Respiratory involvement rare   Variants: ◦  Severe, rapid progressive infantile form (sporadic) ◦  Hearing loss, Coat’s disease (retinal telangiectasias) ◦  developmental delay, seizures

  DX: deletion of Chr4q35, D4Z4 repeats

  AD, incomplete penetrance   Onset usually 5th or 6th decade   Progressive ptosis, dysphagia, proximal limb weakness   Tongue: weak & atrophic   First described in a French Canadian family (1915) but

found world-wide   Prevalence 1:100 000 (1:1000 Quebec)   Complications include aspiration pneumonia &

malnutrition   Dx: PABN1 (poly(A) binding protein), GCG

trinucleotide repeats (usually 8-13; normal =6), Chr14

 Not just a myopathy: Multisystem RNA-mediated diseases!!

  2 types: ◦  Type 1 or DM1: classical form, Steinert’s disease;

congenital form is reported ◦  Type 2 or DM1: new form; PROMM (Proximal

myotonic myopathy); No congenital form  Define Myotonia?

  Delayed relaxation after muscle contraction; patients often describe this as stiffness

  EMG: spontaneous waxing and waning discharge of the muscle fiber; rate 20-150 Hz; reving engine sound

  AD, DMPK (myotonin protein kinase),Chr 19 ◦  CTG repeat expansion in 3’ UTR ◦  Mild: 50-80; Symptomatic: 80-2000

  +anticipation   Myotonia   facial & limb weakness & wasting, frontal balding, bulbar weakness   Cataracts (Christmas Tree),   Tachyarrhythmias, cardiomyopathy, conduction defects   Endocrine (hyperinsulin, adrenal atrophy, hypoT4, testicular

artophy)   altered GI motility   hypersomnia, low intelligence, hearing loss   Respiratory weakness: especially after surgery & with narcotics

 maternal inheritance only, DM1 mothers  Hypotonia at birth   Facial diplegia   Feeding and respiratory difficulties   Skeletal deformities, such as clubfoot  Mental retardation  Absent clinical myotonia in infants and

neonates  Ventriculomegaly due to brain atrophy

  PROM: proximal myotonic myopathy   AD, Zinc finger protein 9,Chr 3 ◦  CCTG repeat expansion in intron ◦  Symptomatic: 75 to >10 000 repeats

  Predominantly proximal weakness   Cataracts (slit-lamp exam)   Myalgias, Painful muscle cramps   Fluctuating weakness & stiffness   Calf pseudohypertrophy   Multisystem: ◦  Deafness, DM or insulin resistance, Hypothyroidism,

Cardiac conduction defects, GI symptoms

  Muscular dystrophies with predominantly proximal distribution of weakness (at least early in the disease)

  Recently defined group by the European Neuromuscular Group in 1995

  Constantly expanding number of genes (see Neuromuscular Disorders, January issue for yearly update)

  Important to note that one gene may have several phenotypes!

  Type 1: AD   Type 2: AR   Usually childhood or adult onset & slowly progressive   Some have cardiac involvement

Extremely oversimplified table!

  Most prevalent LGMD (?)   Onset: any but usually 2nd – 3rd decade   Weakness: Limb girdle, L/E >E/U, Scapular winging ◦  Predominant involvement of glutei & hip adductors/ posterior

compartment of the thigh, Hip abductor sparing ◦  Biceps > triceps

  Gait: Tip-toe walking, waddling gait   Contractures, calf hypertrophy   No cardiac involvement or facial weakness   CK normal to 50X   Dx: Calpain reduced on Western Blot (from muscle biopsy tissue) ◦  Caution: secondary reduction in dysferlin, dystrophin, FSHD, Titin, FKRP

& calpain levels may be normal (missense mutations)   Genetics: Many mutations (24 exons, 50kb)   Clinical Variants: ◦  Eosinophilic myositis, Pseudometabolic pstn, Calf hypertrophy,

Ventilatory insufficiency, Asymptomatic/ pre-symptomatic, Intra-familial variability

  2 phenotypes for the same gene: ◦  LGMD2B (limb-girdle weakness) ◦  Miyoshi myopathy (distal myopathy, esp gastrocs)

  Onset: late teens, early twenties (usually), slowly progressive

  Weakness: Lower extremities >upper   CK may be very elevated   Variants: ◦  Distal myopathy with anterior compartment

involvement; proximo-distal variant; subacute painful calf swelling; inflammation on muscle biopsy; etc.

  Usually No scapular winging, cardiac or respiratory involvement

  X-linked recessive   Duchenne Muscular Dystrophy (DMD): ◦  most common form of muscular dystrophy ◦  Incidence 1:3300 live male births ◦  Age of wheelchair confinement: by 13 yrs

  Becker Muscular Dystrophy (BMD): ◦  Similar phenotype to Duchenne but MILDER clinical course ◦  Incidence 1 in 18 000 to 31 000 male births ◦  Age of wheelchair confinement 16 yrs or later

  Other Dystrophinopathies: ◦  Manifesting DMD/BMD female carriers ◦  X-linked dilated cardiomyopathy ◦  Isolated quadriceps myopathy ◦  Muscle cramps with myoglobinuria

  May be evidence of myopathy at birth but usually not discovered until 2-5 yrs of age

  Difficulty running, jumping, stairs   Waddling gait, lumbar lordosis, calf

enlargement, may have leg pain   Cardiomyopathy   Cognitive impairment   Intestinal hypomotility   Scoliosis, decline in pulmonary function

usually develops after wheelchair confinement

  Mean age of death = 20 yrs +/- 3.9 yrs

 Onset later: 5-15 yrs or even later  Milder phenotype  Less cardiac & cognitive involvement  Much less GI symptoms  Neck flexor power relatively preserved  Death between 30-60 yrs from

respiratory or cardiac causes

  FSHD: AAN Continuum, Jul 2006  OPMD: Biochimica et Biophysica Acta

1772 (2007) 173–185  DM1+2: Muscle Nerve 32: 1–18, 2005  LGMDs: Neurology India. July-September,

2008; 56(3)  Duchenne & Becker Muscular

Dystrophies: AAN Continuum, Jul 2006

 55 yr Female with gradually progressive difficulty walking

 Onset: 37 yrs; difficulty getting onto a bus, needed to use her arms

 Difficulty arising from chairs, stairs  Trouble lifting heavy objects  No family history

 Mild weakness for eye closure  3/5 muscle weakness for proximal

muscles in arms and legs  Waddling gait   sensory exam normal  DTRs: 1+ Ankle jerks, otherwise 2+  CK 800  EMG: small amplitude, brief, polyphasic

myopathic potentials; myotonic discharges

 Biopsy shows nonrimmed vacuoles with increased deposition of PAS-positive material

 Acid maltase deficiency ◦  Pompe’s Disease, Glycogen storage disease type

II, a Lysosomal storage disease  Due to deficiency of the lysosomal enzyme

acid alpha-glucosidase ◦  Responsible for intralysosomal degradation of

glycogen  Gene: GAA, Chromosome 17, AR  Affects cardiac, skeletal & smooth muscle   Pompe’s –infantile onset: 1 in 33-138 000  Adult onset: 1in 40 000

  Infantile ◦  Onset in first year of life, Rapid progression, Cardiomegaly,

hypotonia, death due to cardiorespiratory failure, often death <1 yr

  Adult form: ◦  Weakness: Limb-girdle distribution (pelvic>shoulder)

  Mild forms are reported (myalgia without weakness) ◦  Respiratory involvement (but no cardiac, although this is

controversial) ◦  Pain and Fatigue may be highly prevalent (experienced by 46% &

75% of patients in some studies, respectively) ◦  Cognition, Sensory and cerebellar functions are normal ◦  CK: 1-15X normal ◦  EMG: abnormalities may be isolated to paraspinals ◦  ABSENT clinical myotonia (present on EMG) ◦  Muscle biopsy may be normal ◦  Consider Dot Blot test (here)

  Aka Type V glycogenosis   Onset: childhood   Exercise intolerance, cramps, myalgia, fatigue, poor endurance,

muscle swelling   Later: fixed weakness   Triggered by brief intense exercise or long low-intensity   Second wind phenomenon: ◦  Specific feature of McArdle’s ◦  Patients become symptomatic (ex: cramps) after beginning a physical

activity ◦  If the patients rest briefly then resume exercise they can continue

without symptoms   Episodes of myoglobinuria +/- renal failure   CK: usually elevated   Forearm exercise test: flat venous lactate curve   EMG: normal or myopathic with fibrillations or myotonic discharges ◦  Can see decrement on repetitive stimulation

  Muscle biopsy: loss of myophosphorylase activity is diagnostic

  Mitochondrial disease is caused by nuclear or mitochondrial DNA mutations

  Mitochondrial defects cause multisystem disease   Myopathies are often seen with mitochondrial disease

  Myopathy with exercise intolerance   With respiratory failure or cardiomyopathy   EOM abnormalities (CPEO), ptosis

  When to suspect mitochondrial disease? ◦  Hearing, short stature, lactic acidosis, cardiomyopathy or

conduction defects, diabetes mellitus, hypoparathyroidism, pigmentary retinopathy, cataracts, renal dysfunction, multiple lipomas, etc ◦  Seizures, sensorineural hearing loss, ataxia, cognitive, dystonia,

peripheral neuropathy, optic neuropathy, GI dysmotility ◦  Maternal inheritance

  Dx? ◦  Muscle biopsy: COX negative fibers; Ragged red fibers ◦  Genetics

 29 yr Female ◦ Had an EMG for numbness and tingling of the

first 3 digits of her right hand, Myotonic potentials were seen on EMG

 Had muscle stiffness all her life  Cramps with physical activity but did not

bother her  Rarely difficulty releasing the handle on

her briefcase   Sister and father with similar symptoms

 Normal muscle bulk and motor power   Sensation and reflexes are normal  How do you test for myotonia?  Mild eye opening myotonia, diminishes

with repeated attempts ◦ Warm up!

 Percussion myotonia is present  No handgrip myotonia

 EMG: CTS right, myotonia in all muscles  Genetic tests for DM1 & 2 negative  Dx?  Likely myotonia congenita

Ann Rev Neurosci 2006. 29:387-415

Drugs/ Toxins may induce several types of myopathies:

  Necrotizing ◦  Statins

  Inflammatory ◦  D-penicillamine

  Type I fiber atrophy ◦  Steroids

  Mitochondrial ◦  AZT

  Other types…(emetin can cause a myofibrillar myopathy)

J Neurol Neurosurg Psychiatry 2009;80:832–838.

  Statins: HMG CoA reductase inhibitors   Appear to cause mitochondrial dysfunction, possibly

due to depletion of ubiquinone (electron transport)   Order of myotoxicity:

  Ceriva > simva > lovo > prava > atorva > fluva

  Several clinical syndromes ◦  hyperCK in asymptomatic patients ~5% ◦  Myalgia with or without hyperCK ~9-25% ◦  Weakness with elevated CK ~least common

  Did the statin cause the myopathy? Coincidence? Unmask pre-existing condition?

◦  Rhabdomyolysis   High CK, myalgia, weakness, myoglobinuria +/- renal failure   Incidence: <1 per 100 000, but higher if statin in combined with

amiodarone, gemfibrozil, ciclosporin

  Some metabolic: see Carnitine disorders (esp CPT2)

 Distal myopathies  Congenital myopathies and muscular

dystrophies: ◦ Will cover these briefly during next week’s

muscle pathology session   Endocrine myopathies   ICU myopathy   Steroid myopathy

Hereditary   Muscular

Dystrophies*   Myotonias   Channelopathies   Congenital Myopathies   Metabolic

Myopathies   Mitochondrial

myopathies

Acquired   Inflammatory

myopathies   Endocrine   Associated with other

systemic illness   Drug-induced and

Toxic myopathies

 The key to the diagnosis is a good history & a careful physical exam ◦ Use the pattern of weakness to help

determine further investigations and diagnosis  There are a lot of myopathies ◦ Not everything is an inflammatory myopathy!

 Next Week: ◦ Muscle pathology ◦ More about the diagnosis of muscle disease ◦ More pediatrics (only a little!)

 Questions or comments (about this presentation or anything else):

 erin.oferrall@mail.mcgill.ca