Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
Clinical neurophysiology rewards pattern recognition. You are given a recording or a scenario and asked which test fits, what the finding localises, and what it excludes. The recurring themes are EEG in epilepsy and encephalopathy, nerve conduction in neuropathy, repetitive stimulation in myasthenia, and evoked potentials in demyelination and prognostication.
EEG
The 10-20 system places electrodes at fixed proportional distances (Fp1/Fp2, F3/F4, C3/C4, P3/P4, O1/O2, F7/F8, T3/T4, T5/T6, Fz/Cz/Pz). The normal wakeful adult rhythm is posterior alpha at 8-13 Hz, reactive to eye opening. Hyperventilation provokes absence seizures and focal slowing; photic stimulation provokes photoparoxysmal responses. Absence seizures show 3 Hz generalised spike-and-wave with abrupt onset and offset. Hypsarrhythmia belongs to infantile spasms. Periodic lateralised epileptiform discharges in a febrile encephalopathic patient suggest HSV encephalitis. Burst suppression indicates deep anaesthesia or severe encephalopathy; electrocerebral silence supports brain death only with correct technique and exclusion of sedatives and hypothermia.
Nerve conduction and EMG
Nerve conduction separates demyelinating from axonal pathology. Demyelination slows conduction velocity (below about 70-75% of the normal mean), prolongs distal latency, and can produce conduction block (amplitude drop over 50% across a segment) with temporal dispersion. Axonal loss reduces amplitude with relatively preserved velocity. F-waves and the H-reflex are late responses testing proximal segments. Needle EMG shows fibrillations and positive sharp waves (active denervation, appearing after 2-3 weeks), fasciculations, and myotonic discharges; myopathic units are short, small and polyphasic with early recruitment, while neurogenic units are large, long and reduced in recruitment.
Evoked potentials
Visual evoked potentials: prolonged P100 latency indicates optic nerve demyelination. Brainstem auditory evoked potentials: waves I-V localise from eighth nerve to midbrain. Somatosensory evoked potentials: absent bilateral N20 cortical responses after cardiac arrest carry a poor prognosis. Motor evoked potentials assess central motor pathways.
Worked example
A patient has three weeks of ascending weakness. Nerve conduction shows slowed velocity of 34 m/s, prolonged distal latency, and conduction block across the forearm. This is demyelinating physiology - in this setting AIDP/Guillain-Barré - and predicts a raised CSF protein without pleocytosis. An amplitude-only reduction would indicate axonal injury and a worse prognosis.
Traps
A normal EEG does not exclude epilepsy. Repetitive nerve stimulation is often normal in mild myasthenia, where single-fibre jitter is more sensitive. Lambert-Eaton shows an incremental, not decremental, response. Sensory studies are preserved in ALS, which separates it from multifocal motor neuropathy.