DSA provides images of arterial, capillary and venous phases (Figure 4.6).
Interventional neuroradiology is used to treat intracranial aneurysms and AVMs and is evolving rapidly. Magneto‐encephalography and transcranial magnetic brain stimulation are largely research tools.
Figure 4.6 DSA: (a) arterial and (b) venous phase. Left internal carotid artery injection. White arrowhead: anterior cerebral artery. White arrow: middle cerebral artery branches. Black arrow: superior sagittal sinus.
Clinical Neurophysiology
Electroencephalography
The EEG records via scalp electrodes potentials generated by millions of neurones. Precise sources of these rhythms remain uncertain. Main roles are in epilepsy, in diffuse brain diseases, in ITU and in sleep disorders. Videotelemetry – prolonged EEG recording with simultaneous film – is of value in the assessment of ‘attacks’ (Chapter 8). Sleep studies: Chapter 20.
Alpha, Theta, Delta and Beta Activity in Normal Subjects
Alpha activity seen over the occipital lobes is 8–14 Hz – some 150 μV amplitude and attenuates on eye opening.
Theta activity of 4–7 Hz is also seen, and becomes prominent during drowsiness.
Delta activity is a slower frequency, less than 4 Hz. Delta waves around 1 Hz appears during the first non‐REM sleep period.
Beta activity is a normal largely frontal rhythm faster than 14 Hz.
Epilepsy
Spikes, or spike‐and‐wave abnormalities (Figure 4.7) are hallmarks of epilepsy. However most with epilepsy have a normal EEG between seizures. Epileptic activity is either generalised or focal.
EEG Artefacts
The most common is high amplitude frontal activity from scalp muscle contraction and eye movements.
Figure 4.7 Normal EEG followed by frontal spike‐and‐wave. E: eye movement artefact.
Sharp waves describe non‐sinusoidal waveforms seen in the normal population – not diagnostic of epilepsy, but may occur in patients with seizures.
Difficulties surround EEG reports. Conclusions can only be reached within a clinical context. Useful questions:
Is there generalised epileptic activity? Is there localised epileptic activity?
Is there generalised or localised abnormal slow wave activity, and could slow waves be seen in the normal population?
Are the sharp waves reported normal?
In coma, is there any EEG responsiveness to stimulation?
Diffuse and Focal Brain Disorders
Typical EEG abnormalities appear:
Periodic lateralised epileptic discharges (PLEDS): viral encephalitis, cerebral abscess, anoxic brain damage.
Slow waves appear in many encephalopathies.
Repetitive generalised sharp waves every 0.5–1 seconds: seen in some prion cases.
High voltage slow wave complexes, every 3–10 seconds: subacute sclerosing pan‐encephalitis (SSPE).
Triphasic slow waves: metabolic disorders, typically hepatic coma.
Brainstem Death
The EEG becomes isoelectric (flat) in brainstem death and in deep coma, for example with barbiturates or hypothermia (Chapter 20).
Clinical Neurophysiology: Nerve and Muscle
See also Chapter 10.
Electromyography (EMG)
A concentric needle electrode is inserted into voluntary muscle. Amplified EMG recordings are viewed on an oscilloscope and heard through a speaker. Three main features:
Normal motor unit recruitment
Denervation and reinnervation changes
Myopathic, myotonic, myasthenic features, myokymia, cramps, hemifacial spasm or continuous motor unit activity.
Much depends upon observations of the neurophysiologist.
Normal Motor Unit Recruitment
Normal muscle at rest is silent electrically. When a single anterior horn neurone fires, all muscle fibres connected to it contract. The contraction of each muscle fibre within the motor unit is not synchronous. Interference pattern describes the appearance and sound of motor units running together during contraction.
Chronic Partial Denervation
If one anterior horn cell (A) fails, for example in motor neurone disease (MND), adjacent anterior horn cells B and C produce sprouting axons that re‐innervate muscle fibres originally supplied by A. In chronic partial denervation, the EMG reflects this: reduced numbers of polyphasic, long duration, high voltage muscle action potentials (MAPs).
Fibrillation, Fasciculation and Positive Sharp Waves
When a muscle is denervated, spontaneous contraction of individual fibres begins to occur after 7–14 days. These contractions produce tiny fibrillation potentials of amplitude <10–200 μV. Fibrillation in a limb is invisible, but visible in the tongue, typically in MND. Positive sharp waves are bi‐phasic potentials with a longer duration (<10 ms) than fibrillations and usually with amplitudes of 10–200 μV, also seen in denervation.
Fasciculation describes the visible twitching of a muscle seen in various situations. In normal people, benign fasciculation is common in calf and other muscles. In denervated muscle, fasciculation potentials are produced by spontaneous discharges of motor units, and visible – often widespread in MND.
Myopathic EMG
This is characterised by:
Individual units of low amplitude, of short duration and polyphasic
Rapid motor unit recruitment to a full interference pattern at lower