ABPN Neuromuscular Medicine cheat sheet

Upper motor neuron signs: spasticity, hyperreflexia, Babinski sign, and loss of superficial abdominal reflexes; lower motor neuron signs: fasciculations, atrophy, hypotonia, and hyporeflexia.

Nerve conduction: demyelination suggested by conduction velocity <70% of normal, distal latency >130% upper limit, or >50% conduction block; axonal loss suggested by reduced amplitude with relatively preserved velocity.

Needle EMG timing: fibrillation potentials and positive sharp waves appear 2-3 weeks after acute nerve injury; motor unit remodeling with large polyphasic potentials develops over months.

Myopathic EMG: short-duration, low-amplitude, polyphasic motor unit potentials with early recruitment; neurogenic EMG: long-duration, high-amplitude potentials with reduced recruitment.

Repetitive nerve stimulation: >10% decrement in compound muscle action potential amplitude is abnormal; maximal decrement typically occurs at 2-3 Hz in myasthenia gravis.

Sensory nerve action potential is preserved in a preganglionic lesion (e.g., radiculopathy) but lost in a postganglionic lesion (e.g., plexopathy or peripheral neuropathy).

Anterior horn cell disease produces both lower motor neuron signs and, when corticospinal tracts are involved, upper motor neuron signs without sensory loss (e.g., ALS).

Myasthenia gravis: fatigable weakness, ptosis, diplopia, bulbar symptoms; check acetylcholine receptor antibodies, MuSK antibodies, and chest imaging for thymoma.

Guillain-Barre syndrome: ascending symmetric weakness with areflexia, albuminocytologic dissociation in cerebrospinal fluid after the first week, and nadir within 4 weeks; monitor vital capacity and treat with IVIG or plasma exchange.

CIDP: progressive or relapsing weakness over >8 weeks with demyelinating nerve conduction findings; first-line treatment is IVIG, corticosteroids, or plasma exchange.

ALS: progressive upper and lower motor neuron signs with no sensory loss; riluzole and edaravone are disease-modifying options, and noninvasive ventilation improves survival.

Duchenne muscular dystrophy: X-linked dystrophin deficiency, proximal weakness, calf pseudohypertrophy, elevated creatine kinase, and cardiomyopathy; corticosteroids slow decline.

Lambert-Eaton myasthenic syndrome: proximal weakness, hyporeflexia, autonomic symptoms, and presynaptic voltage-gated calcium channel antibodies; screen for small cell lung cancer.

Inflammatory myopathies (dermatomyositis, polymyositis, immune-mediated necrotizing myopathy): proximal weakness with elevated creatine kinase; dermatomyositis shows Gottron papules and heliotrope rash.

Toxic and metabolic neuropathies: diabetes, alcohol, vitamin B12 deficiency, and chemotherapy (vincristine, cisplatin) are common causes of length-dependent distal symmetric polyneuropathy.