Iraqi Board Neurology study materials
Iraqi Board Neurology study resources

Iraqi Board Neurology: Clinical Neuroimaging and Electrodiagnostics (EEG, EMG/NCS)

Iraqi Board Neurology · Work through your exam, one topic at a time.

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Clinical Neuroimaging and Electrodiagnostics (EEG, EMG/NCS)

This domain tests whether you can read a study rather than order it. Expect a description of a scan or a nerve conduction table and a request for the underlying process.

Imaging first principles

  • Acute blood is hyperdense on CT (roughly 40 to 80 Hounsfield units); infarct becomes hypodense only after 12 to 24 hours.
  • Early ischaemic signs: loss of grey-white differentiation, insular ribbon sign, hyperdense middle cerebral artery.
  • Diffusion-weighted imaging is positive within minutes; a low ADC map confirms true restricted diffusion, which also occurs in abscess, prion disease and highly cellular tumours.
  • Gadolinium enhancement implies blood-brain barrier breakdown.

EEG

  • The 10-20 system is standard; the normal posterior dominant alpha rhythm is 8 to 13 Hz and attenuates with eye opening.
  • Hyperventilation provokes absence seizures with 3 Hz spike-wave discharges; photic stimulation provokes a photoparoxysmal response.
  • Temporal periodic discharges suggest herpes simplex encephalitis; hypsarrhythmia suggests West syndrome; burst suppression suggests severe encephalopathy.

Nerve conduction and EMG

  • Demyelinating: conduction velocity below 70 percent of the lower limit, distal latency above 130 percent, conduction block with proximal-to-distal amplitude ratio under 0.5.
  • Axonal: reduced sensory or motor amplitudes with preserved velocity.
  • EMG: fibrillation potentials and positive sharp waves mean active denervation; large polyphasic motor units mean reinnervation; short small polyphasic units mean myopathy.
  • Repetitive stimulation: a decrement over 10 percent supports myasthenia gravis; an increment over 100 percent supports Lambert-Eaton myasthenic syndrome.

Worked example

A man has three weeks of ascending weakness. Studies show normal sensory amplitudes, reduced compound muscle action potential amplitudes, conduction velocity of 28 m/s in two nerves, prolonged distal latencies and conduction block. That is a demyelinating pattern; with the time course it fits Guillain-Barre syndrome rather than axonal neuropathy or myopathy.

Traps

Interpreting amplitude loss caused by submaximal stimulation; forgetting that cold limbs slow conduction by about 2 m/s per degree; treating a normal EEG as excluding epilepsy.