100+ Free ABPMR Neuromuscular Medicine Practice Questions

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Question 1

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A 62-year-old presents with progressive asymmetric limb weakness, fasciculations, tongue atrophy, and brisk reflexes with Babinski signs. Needle EMG shows widespread active denervation and chronic reinnervation in bulbar, cervical, thoracic, and lumbosacral regions. Per the Awaji criteria, how is this patient classified?

Suspected ALS

Clinically probable ALS

Clinically possible ALS

Clinically definite ALS

to track

2026 Statistics

Key Facts: ABPMR Neuromuscular Medicine Exam

~200

Total MCQ Items

ABPMR Neuromuscular Medicine Subspecialty Certifying Examination

1 day

Exam Length

Single-day computer-based test at Pearson VUE

~15%

Peripheral Neuropathy Weight

Largest domain on 2026 ABPMR NMM content outline

$2,000

2026 Initial Cert Fee

ABPMR subspecialty (verify current)

1 yr

Required Fellowship

ACGME Neuromuscular Medicine fellowship

MOC

Continuing Cert

ABPMR Continuing Certification program

The ABPMR Neuromuscular Medicine exam is a 1-day computer-based test with ~200 single-best-answer MCQs. The 2026 content outline emphasizes peripheral polyneuropathies (~15%), electrodiagnostics (~12%), motor neuron disease (~12%), entrapment neuropathies (~10%), inflammatory myopathies (~10%), muscular dystrophies (~10%), neuromuscular junction disorders (~10%), congenital/metabolic/channelopathies (~9%), brachial/lumbar plexopathy (~5%), radiculopathy (~5%), and ethics/biostats (~2%). Initial certification fee is ~$2,000; 1-year ACGME fellowship required after ABPMR or ABPN primary certification.

Sample ABPMR Neuromuscular Medicine Practice Questions

Try these sample questions to test your ABPMR Neuromuscular Medicine exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 62-year-old presents with progressive asymmetric limb weakness, fasciculations, tongue atrophy, and brisk reflexes with Babinski signs. Needle EMG shows widespread active denervation and chronic reinnervation in bulbar, cervical, thoracic, and lumbosacral regions. Per the Awaji criteria, how is this patient classified?

A.Suspected ALS

B.Clinically probable ALS

C.Clinically possible ALS

D.Clinically definite ALS

Explanation: Awaji criteria require UMN and LMN signs in bulbar plus 2 spinal regions (or 3 spinal regions) for 'definite' ALS. Fasciculations on needle EMG are equivalent to fibs/PSWs as evidence of LMN dysfunction, which increases sensitivity over classic El Escorial.

2Which disease-modifying therapy for ALS is specifically indicated only in patients with confirmed SOD1 gene mutations?

A.Tofersen

B.Riluzole

C.Edaravone

D.AMX0035 (sodium phenylbutyrate-taurursodiol)

Explanation: Tofersen is an antisense oligonucleotide that reduces SOD1 mRNA and is FDA-approved only for SOD1-ALS (accelerated approval based on neurofilament light chain reduction). Riluzole, edaravone, and AMX0035 are not gene-specific.

3When is non-invasive ventilation (NIV) typically initiated in ALS based on pulmonary function testing?

A.When forced vital capacity (FVC) falls below 50% predicted or symptomatic orthopnea develops

B.Only after intubation for respiratory failure

C.At the time of diagnosis regardless of pulmonary status

D.When FVC is below 80% predicted

Explanation: NIV (bilevel PAP) is indicated when FVC <50% predicted, MIP < -60 cmH2O, nocturnal oxygen desaturation, or symptomatic respiratory insufficiency (orthopnea, morning headache). NIV improves survival and quality of life in ALS.

4A 6-month-old hypotonic infant has tongue fasciculations, absent reflexes, and paradoxical breathing. Genetic testing confirms homozygous SMN1 deletion with 2 copies of SMN2. Which therapy provides one-time IV gene replacement and is FDA-approved for SMA patients under 2 years of age?

A.Onasemnogene abeparvovec

B.Nusinersen

C.Risdiplam

D.Tofersen

Explanation: Onasemnogene abeparvovec (Zolgensma) is a one-time AAV9-delivered SMN1 gene replacement therapy FDA-approved for SMA patients <2 years. Nusinersen (ASO) and risdiplam (small molecule) modify SMN2 splicing but require ongoing dosing.

5A patient with Kennedy disease (spinobulbar muscular atrophy) presents with proximal weakness, gynecomastia, and perioral fasciculations. What is the underlying genetic mechanism?

A.CAG trinucleotide repeat expansion in the androgen receptor (AR) gene on Xq12

B.SMN1 homozygous deletion on chromosome 5q13

C.SOD1 point mutation on chromosome 21

D.PMP22 duplication on chromosome 17p

Explanation: Kennedy disease is an X-linked recessive polyglutamine disease caused by CAG repeat expansion in the androgen receptor gene. Features: adult-onset bulbar + limb weakness, perioral fasciculations, gynecomastia, infertility, elevated CK.

6What is the rationale for multidisciplinary ALS clinic care compared with general neurology follow-up?

A.Insurance mandates multidisciplinary clinics for ALS coverage

B.Only IV riluzole can be given in multidisciplinary clinics

C.Multidisciplinary clinics prolong survival and improve quality of life by coordinating respiratory, nutritional, PT/OT, speech, social work, and palliative care

D.Multidisciplinary clinics are required to perform muscle biopsy

Explanation: Randomized and cohort data show multidisciplinary ALS clinics prolong survival (by months to >1 year) and improve QoL versus general neurology care, primarily through earlier NIV, PEG, assistive technology, and palliative planning.

7Which feature favors primary lateral sclerosis (PLS) over ALS?

A.Early bulbar atrophy with tongue fasciculations

B.Widespread fibrillations and positive sharp waves on needle EMG within 2 years

C.Pure UMN signs persisting for ≥4 years without LMN involvement on EMG

D.Rapid progression with respiratory failure within 12 months

Explanation: PLS is diagnosed when pure UMN signs (spasticity, hyperreflexia, pseudobulbar affect) persist ≥4 years without LMN features on EMG. Prognosis is better than ALS. Eventual LMN involvement reclassifies the diagnosis as UMN-predominant ALS.

8In SMA, what is the prognostic significance of SMN2 copy number?

A.Higher SMN2 copy number is associated with SMA type I

B.SMN2 copy number has no effect on phenotype

C.Higher SMN2 copy number correlates with milder phenotype and later onset

D.SMN2 copy number predicts response to riluzole only

Explanation: SMN2 produces small amounts of functional SMN protein. Higher SMN2 copy number (3-4 copies) correlates with milder phenotype (types III-IV, later onset) while 1-2 copies predict severe type I. Copy number also guides therapy selection and pre-symptomatic treatment decisions.

9Riluzole, the first FDA-approved ALS therapy, works primarily by:

A.Inhibiting acetylcholinesterase

B.Scavenging free radicals

C.Blocking sodium channels in muscle

D.Modulating glutamatergic neurotransmission

Explanation: Riluzole modulates glutamate release and NMDA/AMPA signaling, reducing excitotoxicity. It extends tracheostomy-free survival by approximately 3 months. LFTs must be monitored. Edaravone (Radicava) is the free-radical scavenger.

10Which electrodiagnostic finding is most characteristic of denervation in ALS?

A.Normal needle EMG with slowed nerve conduction velocities

B.Myotonic discharges in distal hand muscles only

C.Decremental response on 3-Hz repetitive nerve stimulation

D.Fibrillations, positive sharp waves, and fasciculations with high-amplitude long-duration polyphasic motor units and reduced recruitment across multiple body regions

Explanation: ALS produces widespread active denervation (fibs, PSWs, fasciculations) plus chronic reinnervation (large, long-duration, polyphasic MUAPs with reduced recruitment). Findings must span at least 2 spinal regions plus bulbar or 3 spinal regions (Awaji).

About the ABPMR Neuromuscular Medicine Exam

The ABPMR Neuromuscular Medicine Subspecialty Certifying Examination validates expert-level knowledge in diagnosing and managing disorders of the motor neuron, peripheral nerve, neuromuscular junction, and muscle, spanning ALS and other motor neuron diseases, peripheral polyneuropathies (diabetic, CIDP, GBS, CMT, TTR amyloid), entrapment neuropathies, plexopathies, radiculopathies, inflammatory myopathies (DM/PM/IBM/IMNM), muscular dystrophies (DMD, Becker, myotonic DM1/DM2, FSHD, LGMD), congenital/metabolic myopathies and channelopathies, myasthenia gravis and LEMS, and electrodiagnostics (NCS, needle EMG, RNS, single-fiber EMG). Requires ABPMR (or ABPN) primary certification plus a 1-year ACGME-accredited Neuromuscular Medicine fellowship.

Questions

200 scored questions

Time Limit

1-day CBT

Passing Score

Criterion-referenced standard set by ABPMR

Exam Fee

~$2,000 initial certification fee (ABPMR 2026 subspecialty — verify) (American Board of Physical Medicine and Rehabilitation (ABPMR) / Pearson VUE)

ABPMR Neuromuscular Medicine Exam Content Outline

~15%

Peripheral Polyneuropathies

Diabetic (small fiber, large fiber, autonomic; duloxetine/gabapentin/pregabalin), CIDP (IVIG/PLEX/steroids, FcRn blockers — efgartigimod/rozanolixizumab/nipocalimab), GBS/AIDP (IVIG or PLEX, Miller Fisher anti-GQ1b, AMAN anti-GM1), CMT (1A PMP22 duplication, 2 axonal, CMTX1 connexin 32), HNPP, TTR amyloid (inotersen/patisiran/vutrisiran/tafamidis), vasculitic neuropathy.

~12%

Electrodiagnostics

NCS principles (temperature ≥32°C, supramaximal stim, standard distances), demyelinating vs axonal patterns, F-waves, H-reflex (S1), RNS (decrement in MG, increment in LEMS/botulism), SFEMG jitter, needle EMG spontaneous activity (fibs, PSWs, fasciculations, myotonic discharges, CRDs), MUAP morphology, recruitment.

~12%

Motor Neuron Disease

ALS (El Escorial/Awaji definite/probable/possible/suspected; UMN + LMN; riluzole, edaravone, AMX0035, tofersen for SOD1; NIV when FVC <50%; PEG; multidisciplinary care), SMA (SMN1/SMN2 copy number; nusinersen ASO, onasemnogene abeparvovec gene therapy <2 yr, risdiplam), primary lateral sclerosis, Kennedy disease (AR CAG repeat).

~10%

Entrapment Neuropathies

Median (carpal tunnel — Phalen/Tinel/Durkan, NCS grading), ulnar (cubital tunnel, Guyon), radial (posterior interosseous), peroneal (fibular head — foot drop), tibial (tarsal tunnel), suprascapular, thoracic outlet, meralgia paresthetica (LFC).

~10%

Inflammatory Myopathies

Dermatomyositis (heliotrope, Gottron, perifascicular atrophy; anti-MDA5 ILD/ulcers, anti-TIF1γ cancer/JDM, anti-Mi2, anti-NXP2), polymyositis, IBM (rimmed vacuoles, finger flexor + quadriceps, anti-cN-1A, refractory), IMNM (anti-HMGCR statin-triggered, anti-SRP).

~10%

Muscular Dystrophies

Duchenne (DMD X-linked dystrophin, Gower, pseudohypertrophy; deflazacort/prednisone; eteplirsen/casimersen/golodirsen/viltolarsen exon-skipping; delandistrogene moxeparvovec gene therapy 2023), Becker, myotonic DM1 (DMPK CTG; mexiletine), DM2 (CNBP CCTG), FSHD (D4Z4), LGMD, Emery-Dreifuss (EMD/LMNA), OPMD (PABPN1).

~10%

Neuromuscular Junction Disorders

Myasthenia gravis (AChR ~85%, MuSK, LRP4; 3-Hz RNS decrement, SFEMG jitter, ice-pack test; pyridostigmine, steroids/AZA/MMF/rituximab, efgartigimod/zilucoplan/ravulizumab, thymectomy; crisis → IVIG/PLEX), LEMS (VGCC, SCLC, incremental facilitation), botulism (antitoxin), congenital myasthenic syndromes.

~9%

Congenital, Metabolic & Channelopathies

Nemaline, central core (RYR1 — MH risk), centronuclear/myotubular (MTM1); Pompe (GAA; ERT alglucosidase alfa), McArdle (myophosphorylase, second wind), CPT-II (rhabdo with fasting); myotonia congenita (CLCN1), paramyotonia (SCN4A), hyperkalemic/hypokalemic periodic paralysis.

~5%

Brachial & Lumbar Plexopathy

Erb (upper trunk, waiter's tip), Klumpke (lower trunk, claw + Horner), Parsonage-Turner (neuralgic amyotrophy), Pancoast tumor, radiation plexopathy (myokymia on EMG, painless).

~5%

Radiculopathy

Cervical/lumbosacral patterns, dermatome/myotome/reflex mapping, needle EMG of paraspinals for root localization, H-reflex S1, F-waves, preserved SNAPs distal to DRG.

~2%

Ethics, Scholarship & Biostatistics

Genetic counseling for inherited NMD, informed consent for gene therapy, NNT, sensitivity/specificity, critical appraisal of trials.

How to Pass the ABPMR Neuromuscular Medicine Exam

What You Need to Know

Passing score: Criterion-referenced standard set by ABPMR
Exam length: 200 questions
Time limit: 1-day CBT
Exam fee: ~$2,000 initial certification fee (ABPMR 2026 subspecialty — verify)

Keys to Passing

Complete 500+ practice questions
Score 80%+ consistently before scheduling
Focus on highest-weighted sections
Use our AI tutor for tough concepts

ABPMR Neuromuscular Medicine Study Tips from Top Performers

1ALS diagnosis: Awaji criteria have largely replaced El Escorial — fasciculations on needle EMG count as evidence of LMN dysfunction (equivalent to fibs/PSWs), which increases sensitivity for earlier diagnosis. Four disease-modifying therapies: riluzole (glutamate modulator, ~3-mo survival), edaravone (free-radical scavenger), AMX0035 (sodium phenylbutyrate-taurursodiol), and tofersen (SOD1 antisense oligonucleotide — only for SOD1-positive ALS).

2CIDP red flags vs CMT: CIDP has proximal + distal weakness, elevated CSF protein (albuminocytologic dissociation), NCS showing conduction block/temporal dispersion/prolonged distal motor latency/slowed CV that is NON-uniform, and responds to IVIG/PLEX/steroids. CMT is uniformly slowed on NCS, familial, and does NOT respond to immunotherapy. New class: FcRn antagonists (efgartigimod, rozanolixizumab, nipocalimab) for seropositive refractory CIDP.

3Myasthenia gravis diagnostic pearls: AChR-Ab positive in ~85% generalized MG, ~50% ocular. MuSK-Ab seen in AChR-negative generalized MG — bulbar-predominant, tongue atrophy, poor response to AChE inhibitors, best treated with rituximab. LRP4-Ab in doubly seronegative. 3-Hz RNS shows >10% decrement; SFEMG increased jitter is most sensitive. New therapies: efgartigimod and rozanolixizumab (FcRn), zilucoplan and ravulizumab (C5 inhibitors).

4Inflammatory myopathy antibody-phenotype correlations (critical boards topic): anti-Jo1 → antisynthetase syndrome (ILD, mechanic's hands, arthritis); anti-MDA5 → DM with ILD and skin ulcers (high mortality); anti-TIF1γ → DM with cancer in adults, juvenile DM in kids; anti-Mi2 → classic DM skin; anti-NXP2 → DM with calcinosis; anti-HMGCR → statin-triggered IMNM (necrotizing); anti-SRP → severe IMNM refractory; anti-cN-1A → IBM.

5EMG/NCS localization logic: SNAPs distal to the dorsal root ganglion are PRESERVED in radiculopathy (lesion is proximal to DRG) but REDUCED in plexopathy or peripheral neuropathy (lesion involves DRG or distal fibers). This single pearl localizes radiculopathy vs plexopathy. Paraspinal needle EMG fibrillations confirm root-level pathology. H-reflex assesses S1; F-waves assess proximal motor conduction.

Frequently Asked Questions

What is the ABPMR Neuromuscular Medicine subspecialty certification?

The ABPMR Neuromuscular Medicine subspecialty certification is awarded jointly by ABPMR and ABPN to physicians who demonstrate expert-level knowledge in diagnosing and managing disorders of the motor neuron, peripheral nerve, neuromuscular junction, and muscle. Scope includes ALS and other motor neuron disease, peripheral neuropathies (diabetic, CIDP, GBS, CMT, TTR amyloid), entrapment neuropathies, plexopathy, radiculopathy, inflammatory and hereditary myopathies, congenital/metabolic myopathies and channelopathies, myasthenia gravis and LEMS, and electrodiagnostic medicine.

Who is eligible to take the ABPMR Neuromuscular Medicine exam?

Candidates must hold ABPMR (Physical Medicine and Rehabilitation) or ABPN (Neurology) primary certification in good standing and have completed 1 year of full-time training in an ACGME-accredited Neuromuscular Medicine fellowship. A valid unrestricted medical license is required. Fellowship training includes inpatient/outpatient neuromuscular clinics, electrodiagnostic medicine (EMG/NCS), muscle biopsy interpretation, and participation in multidisciplinary clinics (ALS, MDA).

What is the format of the ABPMR Neuromuscular Medicine exam?

The exam is a 1-day computer-based examination administered at Pearson VUE test centers, comprising approximately 200 single-best-answer multiple-choice questions. Question stems frequently include NCS tracings, needle EMG findings, repetitive nerve stimulation waveforms, muscle biopsy images, MRI of nerve/muscle, and antibody panels. The exam is aligned to the ABPMR Neuromuscular Medicine content outline across motor neuron disease, peripheral neuropathy, NMJ disorders, myopathy, and electrodiagnostics.

How much does the 2026 ABPMR Neuromuscular Medicine exam cost?

The 2026 ABPMR Neuromuscular Medicine initial subspecialty certification fee is approximately $2,000 (verify current fee on the ABPMR site). Cancellation and refund policies follow the ABPMR schedule with decreasing refunds as the exam date approaches. Annual ABPMR Continuing Certification (MOC) fees apply after passing. Retakes require re-registration and fee payment.

When is the 2026 exam administered?

ABPMR Neuromuscular Medicine is typically offered during a testing window in the fall. Applications generally open in late winter/early spring with a submission deadline in mid-to-late spring. Candidates schedule specific appointments with Pearson VUE after application approval. Confirm exact 2026 dates on the ABPMR subspecialty page.

How is the exam scored?

ABPMR uses criterion-referenced scoring with a passing standard set by subject-matter experts. A candidate's pass/fail result depends on performance relative to the fixed cut-score, not on other candidates. Score reports include subdomain performance to guide continued learning. Results are typically released several weeks after the testing window closes.

What are the highest-yield topics?

Highest-yield topics: ALS El Escorial/Awaji criteria and disease-modifying therapy (riluzole, edaravone, AMX0035, tofersen for SOD1); SMA genetics and therapies (nusinersen, onasemnogene, risdiplam); CIDP diagnosis and treatment including FcRn blockers; GBS subtypes and antibodies; CMT genetics; myasthenia gravis (AChR/MuSK/LRP4, RNS decrement, SFEMG, efgartigimod, thymectomy); LEMS (VGCC, SCLC, incremental facilitation); DMD exon-skipping and delandistrogene moxeparvovec; myotonic DM1/DM2; inflammatory myopathy antibody panels (MDA5, TIF1γ, HMGCR, SRP); and electrodiagnostic localization (demyelinating vs axonal, radiculopathy, entrapment).

How should I study for this exam?

Use a structured 9-15 month plan during and after fellowship. Map to the ABPMR content outline: lead with motor neuron disease and peripheral neuropathy, then NMJ and myopathy, then electrodiagnostics, then entrapment/plexus/radiculopathy. Integrate AANEM courses, Preston & Shapiro for EMG, Amato & Russell for NMD, and current MGFA/AAN/EFNS guidelines. Complete high-volume MCQs with timed sets. Take 2-3 full-length mock exams and drill EMG/NCS image libraries and muscle biopsy pathology.