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Question 1Clinical Neuromuscular Disease
A 32-year-old woman develops fluctuating ptosis and diplopia that worsen through the day. She has no pupillary abnormality or limb weakness. Which clinical feature most supports myasthenia gravis?
- Fatigable weakness with normal pupillary responses Correct answer.
- Proximal weakness with autonomic symptoms
- Ascending areflexic weakness over days
- Fixed unilateral ptosis with a dilated pupil
Explanation
Myasthenia gravis produces fatigable weakness from postsynaptic acetylcholine receptor loss at the neuromuscular junction. Ocular muscles are commonly affected first, while pupillary responses remain normal because the pupil is not typically involved.
Question 2Clinical Neuromuscular Disease
A 45-year-old man has 5 days of progressive symmetric leg weakness and areflexia after a diarrheal illness. CSF shows elevated protein with normal cell count. Which is the most likely diagnosis?
- Polymyositis
- Guillain-Barré syndrome Correct answer.
- Myasthenia gravis
- Transverse myelitis
Explanation
Guillain-Barré syndrome is an acute ascending polyneuropathy with areflexia and albuminocytologic dissociation in CSF. The antecedent diarrheal illness is a classic trigger.
Question 3Clinical Neuromuscular Disease
A 60-year-old woman has acute unilateral facial weakness with inability to close the eye and loss of forehead wrinkling. There is no limb weakness. Which is the most appropriate initial management?
- Acyclovir alone
- Steroids and eye care Correct answer.
- Urgent thrombolysis for suspected stroke
- Plasmapheresis
Explanation
Bell palsy is acute lower motor neuron facial weakness; corticosteroids started early improve recovery. Eye protection is essential because lagophthalmos can lead to corneal injury.
Question 4Clinical Neuromuscular Disease
A 28-year-old man has grip myotonia, distal weakness, cataracts, and a family history of similar symptoms. Which diagnosis is most likely?
- Myotonic dystrophy type 1 Correct answer.
- Polymyositis
- Myasthenia gravis
- Hypokalemic periodic paralysis
Explanation
Myotonic dystrophy type 1 is an autosomal dominant CTG repeat disorder causing grip myotonia, distal weakness, cataracts, and cardiac conduction disease. The family history supports this multisystem diagnosis.
Question 5Clinical Neuromuscular Disease
A 58-year-old smoker reports proximal leg weakness and dry mouth. Strength briefly improves after repeated effort. Which diagnosis should be considered?
- Dermatomyositis
- Myasthenia gravis
- Amyotrophic lateral sclerosis
- Lambert-Eaton syndrome Correct answer.
Explanation
Lambert-Eaton myasthenic syndrome is a presynaptic neuromuscular junction disorder with antibodies against voltage-gated calcium channels. It causes proximal weakness, autonomic symptoms, and post-tetanic potentiation, and is often paraneoplastic.
Question 6Clinical Neuromuscular Disease
A 50-year-old woman has proximal muscle weakness, a violaceous rash around the eyes, and erythematous papules over the knuckles. Which diagnosis is most likely?
- Polymyositis
- Hypothyroidism
- Inclusion body myositis
- Dermatomyositis Correct answer.
Explanation
Heliotrope rash and Gottron papules are hallmark cutaneous signs of dermatomyositis, which causes proximal muscle weakness. Adult patients require evaluation for associated malignancy.
Question 7Clinical Neuromuscular Disease
A 62-year-old man has progressive weakness with muscle wasting and fasciculations, hyperreflexia, and no sensory loss. Which diagnosis is most likely?
- Myasthenia gravis
- Amyotrophic lateral sclerosis Correct answer.
- Chronic inflammatory demyelinating polyneuropathy
- Lumbar radiculopathy with sensory loss
Explanation
ALS is a progressive neurodegenerative disease combining upper and lower motor neuron signs in multiple regions. Sensory examination is typically normal, helping distinguish it from polyneuropathy.
Question 8Clinical Neuromuscular Disease
A 55-year-old woman has brief lancinating facial pain in the mandibular division triggered by chewing. Neurologic exam is normal. Which medication is first-line?
- Prednisone
- Amoxicillin
- Sumatriptan
- Carbamazepine Correct answer.
Explanation
Trigeminal neuralgia causes paroxysmal lancinating facial pain in a trigeminal distribution, often triggered by chewing or touch. Carbamazepine is first-line therapy.
Question 9Clinical Neuromuscular Disease
A 44-year-old man has progressive symmetric weakness and sensory loss over 3 months, areflexia, and CSF protein elevated without pleocytosis. Which feature best distinguishes CIDP from GBS?
- Progression beyond 8 weeks Correct answer.
- Presence of areflexia
- Recent Campylobacter infection
- Elevated CSF protein
Explanation
CIDP is distinguished from GBS by a chronic course, with progression or relapses beyond 8 weeks. Both conditions can cause areflexia, sensory loss, and elevated CSF protein.
Question 10Clinical Neuromuscular Disease
A 70-year-old with myasthenia gravis develops worsening bulbar weakness and respiratory distress over 2 days. Vital capacity is 15 mL/kg and falling. What is the most appropriate next step?
- Admit to ICU and prepare for intubation Correct answer.
- Start high-dose oral steroids as outpatient
- Obtain outpatient sleep study
- Discharge with oral pyridostigmine
Explanation
Myasthenic crisis causes respiratory failure from weakness of respiratory and bulbar muscles. A falling vital capacity indicates impending failure and requires ICU monitoring with preparation for intubation.
Question 11Clinical Neuromuscular Disease
A 35-year-old has descending weakness, diplopia, dysphagia, and dilated pupils after eating home-canned vegetables. Which is the most likely diagnosis?
- Myasthenia gravis
- Botulism Correct answer.
- Guillain-Barré syndrome
- Organophosphate poisoning
Explanation
Botulism causes descending flaccid weakness, bulbar dysfunction, and autonomic signs such as dilated pupils after ingestion of preformed toxin. Antitoxin should be given early.
Question 12Clinical Neuromuscular Disease
A 6-year-old child develops ascending flaccid weakness and areflexia over 2 days. A tick is found on the scalp. What is the most appropriate immediate management?
- Remove the tick Correct answer.
- Give botulinum antitoxin
- Start plasmapheresis
- Administer IVIG
Explanation
Tick paralysis is caused by a toxin in tick saliva that blocks presynaptic acetylcholine release. Removing the tick usually leads to rapid improvement, so antitoxin and immunotherapy are unnecessary.
Question 13Clinical Neuromuscular Disease
A 22-year-old man has episodic generalized weakness after high-carbohydrate meals. Reflexes are diminished during attacks; serum potassium is 2.8. Which is the most appropriate acute treatment?
- Pyridostigmine
- Potassium replacement Correct answer.
- IV glucose and insulin
- High-dose corticosteroids
Explanation
Hypokalemic periodic paralysis causes episodic weakness associated with low serum potassium after carbohydrate-rich meals. Acute treatment is potassium replacement, with avoidance of triggers and sometimes acetazolamide prophylaxis.
Question 14Clinical Neuromuscular Disease
A 30-year-old man develops severe muscle pain and dark urine after a crush injury. CK is 50,000. Which complication should be monitored most closely?
- Hypercalcemia
- Metabolic alkalosis
- Hypokalemia
- Acute kidney injury Correct answer.
Explanation
Rhabdomyolysis releases myoglobin, which can precipitate acute kidney injury. CK, renal function, electrolytes, and urine output must be monitored closely.
Question 15Clinical Neuromuscular Disease
A 40-year-old woman has right foot drop with weakness of ankle dorsiflexion and sensory loss over the dorsum of the foot after prolonged leg crossing. Which nerve is most likely affected?
- Obturator nerve in the pelvis
- Posterior tibial nerve
- Common peroneal nerve Correct answer.
- Femoral nerve at the groin
Explanation
The common peroneal nerve wraps around the fibular head, where compression causes foot drop and sensory loss over the dorsum of the foot. Ankle dorsiflexion and eversion are weakened.
Question 16Clinical Neuromuscular Disease
A 50-year-old woman has nocturnal numbness in the thumb, index, and middle fingers that improves with shaking the hand. Which is the most likely diagnosis?
- Cervical radiculopathy at C7
- Ulnar neuropathy at the elbow
- Cubital tunnel syndrome
- Carpal tunnel syndrome Correct answer.
Explanation
Carpal tunnel syndrome is median nerve compression at the wrist, causing nocturnal numbness in the thumb, index, and middle fingers. Symptoms often improve with shaking the hand.
Question 17Clinical Neuromuscular Disease
A 70-year-old man has slowly progressive weakness of the quadriceps and finger flexors, mild dysphagia, and a CK of 400. He has not responded to prednisone. Which diagnosis is most likely?
- Myasthenia gravis with fatigable weakness
- Polymyositis with proximal weakness
- Inclusion body myositis Correct answer.
- Dermatomyositis with a heliotrope rash
Explanation
Inclusion body myositis causes slowly progressive, asymmetric weakness of the quadriceps and finger flexors and is notoriously resistant to immunosuppression. Rimmed vacuoles are seen on biopsy.
Question 18Clinical Neuromuscular Disease
A farm worker presents with salivation, lacrimation, diarrhea, miosis, and muscle fasciculations after pesticide exposure. Which medication is most important after decontamination?
- Naloxone
- Succinylcholine
- Atropine Correct answer.
- Flumazenil
Explanation
Organophosphate poisoning inhibits acetylcholinesterase, producing muscarinic and nicotinic cholinergic excess. Atropine reverses life-threatening muscarinic effects, while pralidoxime reactivates the enzyme.
Question 19Clinical Neuromuscular Disease
A 65-year-old vegan has progressive numbness and unsteadiness, loss of vibration and position sense, and brisk reflexes. Which deficiency is most likely?
- Vitamin C deficiency
- Iron deficiency anemia
- Vitamin B12 Correct answer.
- Folate deficiency
Explanation
Vitamin B12 deficiency causes subacute combined degeneration of the dorsal columns and corticospinal tracts. This produces sensory ataxia with loss of vibration and position sense plus brisk reflexes.
Question 20Clinical Neuromuscular Disease
A 60-year-old man has painful asymmetric weakness and sensory loss in multiple nerve territories over weeks, with elevated ESR. Which is the most likely diagnosis?
- Mononeuritis multiplex from vasculitis Correct answer.
- Carpal tunnel syndrome
- Myasthenia gravis
- Diabetic distal symmetric polyneuropathy
Explanation
Vasculitic neuropathy produces painful asymmetric multiple mononeuropathies from ischemic nerve damage. Elevated ESR and systemic symptoms support urgent immunosuppressive evaluation.
Question 21Clinical Neuromuscular Disease
A 45-year-old man has progressive limb weakness, gynecomastia, and fasciculations. He has no sensory loss and no upper motor neuron signs. Genetic testing shows a CAG repeat expansion. Which diagnosis is most likely?
- Myotonic dystrophy type 1
- Kennedy disease Correct answer.
- Lambert-Eaton syndrome
- Amyotrophic lateral sclerosis
Explanation
Kennedy disease is X-linked spinal and bulbar muscular atrophy caused by a CAG repeat expansion in the androgen receptor gene. It causes lower motor neuron weakness, fasciculations, and gynecomastia without upper motor neuron signs.
Question 22Clinical Neuromuscular Disease
A 55-year-old ICU patient with sepsis has failure to wean, areflexia, and mild distal weakness after 2 weeks. Sensory testing is limited. Which is the most likely diagnosis?
- Myasthenia gravis
- Guillain-Barré syndrome
- Hypokalemic periodic paralysis
- Critical illness polyneuropathy Correct answer.
Explanation
Critical illness polyneuropathy occurs in sepsis and multiorgan failure, causing distal weakness, areflexia, and difficulty weaning from ventilation. Treatment focuses on the underlying illness and supportive care.
Question 23Clinical Neuromuscular Disease
A 35-year-old woman has prominent bulbar weakness, ptosis, and respiratory crises. Anti-AChR antibodies are negative. She responds poorly to pyridostigmine. Which antibody is most likely?
- Anti-aquaporin 4
- Anti-voltage-gated calcium channel
- Anti-MuSK Correct answer.
- Anti-Hu
Explanation
Anti-MuSK myasthenia gravis often presents with prominent bulbar weakness and respiratory crises, and patients frequently respond poorly to pyridostigmine. Anti-AChR antibodies are usually negative.
Question 24Clinical Neuromuscular Disease
A 30-year-old man has sudden severe shoulder pain followed by weakness and wasting of the deltoid and supraspinatus over 2 weeks. Which is the most likely diagnosis?
- Polymyositis
- Cervical spondylotic myelopathy
- Neuralgic amyotrophy Correct answer.
- Myasthenia gravis
Explanation
Neuralgic amyotrophy, or Parsonage-Turner syndrome, begins with severe shoulder pain followed by patchy weakness and atrophy in the brachial plexus distribution. Recovery is often incomplete but gradual.
Question 25Clinical Neuromuscular Disease
A 25-year-old woman has abdominal pain, confusion, and ascending weakness after taking a new medication. Urine turns dark on standing. Which diagnosis is most likely?
- Botulism
- Guillain-Barré syndrome with ascending weakness
- Acute intermittent porphyria Correct answer.
- Myasthenia gravis
Explanation
Acute intermittent porphyria causes neurovisceral attacks with abdominal pain, confusion, and ascending weakness. Urine darkens on standing because of porphobilinogen, and offending drugs must be stopped.
Question 26Clinical Neuromuscular Disease
A 38-year-old woman develops acute right facial weakness. On examination she cannot close her right eye or raise her right eyebrow, and the right corner of her mouth droops. Which feature best localizes the lesion to the peripheral facial nerve rather than a central corticobulbar lesion?
- Weakness confined to the lower face on the affected side
- Inability to wrinkle the forehead on the affected side Correct answer.
- Sparing of the platysma on the affected side
- Weakness of the lower face on the opposite side
Explanation
The upper facial muscles receive bilateral corticobulbar input, so a central lesion typically spares the forehead. A peripheral facial nerve lesion produces ipsilateral weakness of both the upper and lower face. This pattern distinguishes Bell palsy from a supranuclear stroke.
Question 27Clinical Neuromuscular Disease
A 5-year-old boy has progressive proximal weakness, uses his hands to push up from the floor when rising, and has enlarged calves. His creatine kinase is 15,000 U/L. Which diagnosis is most likely?
- Duchenne muscular dystrophy Correct answer.
- Myotonic dystrophy type 1
- Spinal muscular atrophy
- Polymyositis
Explanation
Duchenne muscular dystrophy is an X-linked disorder caused by dystrophin deficiency, producing proximal weakness, Gowers sign, calf pseudohypertrophy, and markedly elevated creatine kinase. The typical onset is in early childhood. These features are not explained by the other choices.
Question 28Clinical Neuromuscular Disease
A 32-year-old woman has fatigable ptosis and diplopia, and myasthenia gravis is suspected. Which antibody test is most commonly used and most specific to confirm the diagnosis?
- Anti-acetylcholine receptor antibody Correct answer.
- Anti-MuSK antibody
- Antinuclear antibody
- Anti-ganglioside GQ1b antibody
Explanation
Binding antibodies against the acetylcholine receptor are the most common and most specific serologic marker of generalized myasthenia gravis. Anti-MuSK antibodies occur in a minority of patients who are seronegative for acetylcholine receptor antibodies. Antinuclear and anti-GQ1b antibodies test different conditions.
Question 29Clinical Neuromuscular Disease
During general anesthesia with sevoflurane and succinylcholine, a patient develops masseter rigidity, hyperthermia, tachycardia, and metabolic acidosis. Which medication is the specific treatment?
- Flumazenil
- Pyridostigmine
- Dantrolene Correct answer.
- Neostigmine
Explanation
This presentation is malignant hyperthermia, a hypermetabolic reaction caused by uncontrolled calcium release through the ryanodine receptor. Dantrolene inhibits ryanodine receptor–mediated calcium release and is the specific antidote. Neostigmine and pyridostigmine are acetylcholinesterase inhibitors, and flumazenil reverses benzodiazepines.
Question 30Clinical Neuromuscular Disease
A 58-year-old smoker has progressive proximal weakness, dry mouth, and reduced reflexes. Lambert-Eaton myasthenic syndrome is suspected. Which electrodiagnostic finding is characteristic?
- Conduction block in multiple noncompression sites
- Decrement of more than 10% at 2- to 3-Hz repetitive stimulation
- Fibrillation potentials with normal motor unit recruitment
- Increment of the compound muscle action potential after exercise Correct answer.
Explanation
Lambert-Eaton syndrome is a presynaptic disorder caused by antibodies against voltage-gated calcium channels. Brief maximum voluntary contraction or high-frequency stimulation increases calcium influx and produces an incremental compound muscle action potential response. A decrement at low-frequency stimulation is the pattern seen in myasthenia gravis.
Question 31Clinical Neuromuscular Disease
A 20-year-old has slowly progressive distal leg weakness, high arches, absent ankle reflexes, and a parent with similar foot deformity. Nerve conduction studies show uniform demyelination. Which diagnosis is most likely?
- Chronic inflammatory demyelinating polyneuropathy with relapses
- Charcot-Marie-Tooth disease type 1 Correct answer.
- Guillain-Barré syndrome
- Distal diabetic polyneuropathy
Explanation
Charcot-Marie-Tooth disease type 1 is an inherited demyelinating neuropathy that causes distal weakness, pes cavus, areflexia, and uniform conduction slowing. The family history and chronic course are typical. Guillain-Barré syndrome is acute, and chronic inflammatory demyelinating polyneuropathy is acquired with nonuniform demyelination.
Question 32Clinical Neuromuscular Disease
A 30-year-old has grip myotonia, ptosis, facial weakness, and early cataracts, and a parent has similar symptoms. Which genetic mechanism underlies this disorder?
- CTG repeat expansion in DMPK Correct answer.
- Expansion of CAG repeats in the androgen receptor gene
- Deletion of exons in the dystrophin gene
- Point mutation in the ryanodine receptor gene
Explanation
Myotonic dystrophy type 1 is caused by a CTG trinucleotide repeat expansion in the DMPK gene. It is multisystem, with myotonia, ptosis, cataracts, cardiac conduction disease, and anticipation. The other mechanisms cause different neuromuscular disorders.
Question 33Clinical Neuromuscular Disease
A 22-year-old has asymmetric weakness of eye closure and shoulder abduction, prominent scapular winging, and no sensory loss. Which diagnosis best fits these findings?
- Lambert-Eaton syndrome with autonomic symptoms
- Myasthenia gravis with fatigable ptosis
- Facioscapulohumeral muscular dystrophy Correct answer.
- Polymyositis with elevated creatine kinase
Explanation
Facioscapulohumeral muscular dystrophy affects the facial and scapulohumeral muscles and is often asymmetric. Scapular winging is common, and sensory loss does not occur. Myasthenia gravis causes fatigable ptosis, whereas polymyositis and Lambert-Eaton syndrome produce different patterns of weakness.
Question 34Clinical Neuromuscular Disease
A 45-year-old has newly diagnosed generalized myasthenia gravis. Which test should be obtained to evaluate for a thymoma?
- Nerve conduction study
- Muscle biopsy
- Lumbar puncture
- Chest CT or MRI Correct answer.
Explanation
Thymoma occurs in a minority of patients with myasthenia gravis, and chest imaging is recommended at diagnosis to identify it. Identifying a thymoma affects surgical planning and surveillance. Lumbar puncture, nerve conduction studies, and muscle biopsy do not evaluate the thymus.
Question 35Clinical Neuromuscular Disease
A 60-year-old with type 2 diabetes has severe asymmetric thigh pain followed by quadriceps weakness and weight loss. Which diagnosis is most likely?
- Inclusion body myositis with finger flexor weakness
- Diabetic lumbosacral radiculoplexus neuropathy Correct answer.
- Lumbar spinal stenosis with neurogenic claudication
- Painful distal symmetric polyneuropathy
Explanation
Diabetic lumbosacral radiculoplexus neuropathy, also called diabetic amyotrophy, causes asymmetric proximal leg pain and weakness with weight loss. It is often self-limited and occurs in patients with diabetes. Distal symmetric polyneuropathy is symmetric and length-dependent, and inclusion body myositis has a different pattern.
Question 36Clinical Neuromuscular Disease
A 40-year-old has progressive axial rigidity, episodic painful muscle spasms triggered by startle, and anti-GAD antibodies. Which medication is first-line for symptom control?
- Propranolol
- Diazepam Correct answer.
- Levodopa-carbidopa
- Pyridostigmine
Explanation
Stiff-person syndrome reflects impaired GABAergic inhibition, causing axial rigidity and stimulus-sensitive spasms. Benzodiazepines such as diazepam enhance GABA-A activity and are first-line for symptomatic relief. Immunotherapy may be used for the underlying disorder.
Question 37Clinical Neuromuscular Disease
A 55-year-old has progressive symmetric sensorimotor polyneuropathy, papilledema, hyperpigmented skin, gynecomastia, thrombocytosis, and a monoclonal lambda protein. Which diagnosis is most likely?
- POEMS syndrome Correct answer.
- Multiple myeloma
- AL amyloidosis
- Chronic inflammatory demyelinating polyneuropathy
Explanation
POEMS syndrome combines polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes. It is associated with osteosclerotic myeloma and elevated vascular endothelial growth factor. Papilledema, thrombocytosis, and lambda light-chain restriction further support it.
Question 38Clinical Neuromuscular Disease
A 65-year-old has early autonomic symptoms, bilateral carpal tunnel syndrome, macroglossia, and a progressive sensorimotor neuropathy. A fat pad biopsy is performed. Which stain is used to confirm the suspected diagnosis?
- Periodic acid-Schiff
- Luxol fast blue
- Prussian blue
- Congo red Correct answer.
Explanation
The presentation suggests amyloid neuropathy, which often causes autonomic dysfunction, carpal tunnel syndrome, and macroglossia. Congo red staining demonstrates amyloid deposits with apple-green birefringence under polarized light. The other stains highlight iron, glycogen, or myelin.
Question 39Clinical Neuromuscular Disease
A 60-year-old smoker has subacute asymmetric numbness, sensory ataxia, pseudoathetosis, and anti-Hu antibodies. Which underlying malignancy is most strongly associated with this syndrome?
- Colonic adenocarcinoma
- Small cell lung cancer Correct answer.
- Metastatic prostate adenocarcinoma
- Invasive ductal breast carcinoma
Explanation
Anti-Hu antibodies, also called ANNA-1, are strongly associated with small cell lung cancer and paraneoplastic sensory neuronopathy. The disorder causes asymmetric sensory loss, sensory ataxia, and pseudoathetosis because of dorsal root ganglion damage. The other tumors are not classically linked to anti-Hu syndrome.
Question 40Clinical Neuromuscular Disease
A 68-year-old has bilateral shoulder and hip girdle pain with morning stiffness, an erythrocyte sedimentation rate of 80 mm/h, and a normal creatine kinase. Which diagnosis is most likely?
- Polymyositis with elevated creatine kinase
- Fibromyalgia with normal inflammatory markers
- Dermatomyositis with Gottron papules
- Polymyalgia rheumatica Correct answer.
Explanation
Polymyalgia rheumatica causes girdle pain and stiffness in older adults with a markedly elevated sedimentation rate and normal muscle enzymes. It responds promptly to low-dose corticosteroids. Inflammatory myositis typically causes objective weakness and elevated creatine kinase.
Question 41Nerve Conduction Studies
During nerve conduction studies the limb is cooled to 30 °C. Which change is expected in the tested nerve?
- Shortening of distal latency
- Slowing of conduction velocity Correct answer.
- Loss of the F-wave
- Reduction of CMAP amplitude
Explanation
Cooling slows voltage-gated sodium channel kinetics and Na+/K+-ATPase activity, so conduction velocity falls by roughly 2 m/s for each degree Celsius below about 34 °C and latencies lengthen. Amplitude and duration usually increase as temperature drops. Limbs should therefore be warmed to at least 32 °C before measurements are interpreted.
Question 42Nerve Conduction Studies
By convention, sensory conduction velocity is calculated from the latency measured to which point of the sensory nerve action potential?
- The negative peak
- The final return to baseline
- The positive peak
- The onset of the first negative deflection Correct answer.
Explanation
Onset latency reflects the fastest conducting fibers and, combined with the interelectrode distance, gives the standard sensory conduction velocity. Peak latency is more reproducible for side-to-side and nerve-to-nerve comparisons but yields a falsely fast velocity. Amplitude is conventionally measured from baseline to the negative peak.
Question 43Nerve Conduction Studies
Supramaximal stimulation in a motor nerve conduction study is confirmed when which condition is met?
- Further increases in intensity add no CMAP amplitude Correct answer.
- The stimulus artifact is taller than the CMAP
- The patient reports a strong but comfortable tingling sensation
- The CMAP duration exceeds 20 ms
Explanation
Supramaximal intensity means all motor axons in the nerve have been depolarized, which is demonstrated by raising the intensity in increments until the CMAP amplitude plateaus, then increasing by a further 20–30%. This is essential whenever amplitudes from different sites are compared. Submaximal stimulation produces spuriously low amplitudes and apparent conduction block.
Question 44Nerve Conduction Studies
Where is the ground electrode placed for a routine motor nerve conduction study?
- Over the active recording electrode
- Between the stimulating and recording electrodes Correct answer.
- On the contralateral limb
- Distal to the stimulator, over the tendon
Explanation
The ground is placed between the stimulator and the recording electrodes, usually secured with a strap and conductive paste, to provide a low-impedance common-mode reference. Good grounding reduces 60-Hz interference and shock artifact. High impedance at the ground is a common cause of a noisy tracing.
Question 45Nerve Conduction Studies
F-waves are produced by which mechanism?
- Synaptic relay through spinal interneurons
- Antidromic activation of anterior horn cells Correct answer.
- Direct depolarization of the dorsal root ganglion
- Ephaptic transmission at the neuromuscular junction
Explanation
A supramaximal stimulus travels antidromically to the anterior horn cell, which then fires orthodromically to produce the F-wave. Because this involves a backfiring pool of motor neurons, F-waves assess the proximal nerve segment and root. They occur in only a small percentage of axons and vary in latency between stimuli.
Question 46Nerve Conduction Studies
The H-reflex is most reliably recorded from which muscle?
- Biceps brachii
- Extensor digitorum brevis
- Soleus Correct answer.
- Thenar eminence
Explanation
The H-reflex is a monosynaptic Ia afferent reflex best obtained from the soleus with submaximal stimulation of the tibial nerve in the popliteal fossa. As stimulus intensity rises the M wave grows and the H-reflex disappears from collision with the antidromic motor volley. It is used chiefly to assess the S1 root.
Question 47Nerve Conduction Studies
How is the amplitude of a sensory nerve action potential conventionally measured?
- From the negative peak to the positive peak
- From the end of the shock artifact to onset
- From onset to the return to baseline
- From baseline to the negative peak Correct answer.
Explanation
Sensory amplitude is measured from the baseline to the negative peak, which is the standard reproducible value reported in most laboratories. Peak-to-peak measurement yields roughly double the value and is not interchangeable with baseline-to-peak. Consistency of method matters most for serial studies.
Question 48Nerve Conduction Studies
Which electrode placement is used for the standard sural sensory nerve conduction study?
- Active on the sole, reference on the heel
- Active over the medial malleolus, reference on the first toe
- Active over the dorsum of the foot, reference at the lateral malleolus
- Active just posterior to the lateral malleolus, reference 3–4 cm distal Correct answer.
Explanation
The sural nerve runs posterior to the lateral malleolus, so the active recording electrode is placed there with the reference several centimeters distally and stimulation about 14 cm proximally on the posterior calf. This nerve is affected early in length-dependent axonal polyneuropathies. It is also useful for the sural-sparing comparison in demyelinating disease.
Question 49Nerve Conduction Studies
Which feature on proximal stimulation best distinguishes temporal dispersion from conduction block?
- A prolonged distal latency with a preserved CMAP amplitude
- A reduced sensory amplitude with a normal motor amplitude
- An amplitude loss that is identical in every segment tested
- An increase in CMAP duration accompanying the amplitude loss Correct answer.
Explanation
In conduction block the surviving axons travel at similar velocities, so amplitude falls with little change in duration or area. In temporal dispersion, fibers conduct at different velocities and the volley spreads out, so the CMAP amplitude drops while duration and negative-peak area increase. Area loss greater than about 40% favors true block over dispersion.
Question 50Nerve Conduction Studies
For an ulnar motor study across the elbow, which stimulation protocol is standard?
- Wrist to axilla as a single long segment
- Wrist to below-elbow segment only
- Below-elbow to above-elbow segment with the elbow flexed 70–90° Correct answer.
- Above-elbow to axilla segment only
Explanation
The elbow segment is assessed by stimulating about 3 cm distal to the medial epicondyle and 7–10 cm proximal to it, with the elbow flexed 70–90°. Flexion prevents the falsely increased distance and slowing that occur when the nerve is stretched over a fully extended elbow. Segment length is measured along the nerve course and kept near 10 cm.