Neuro-investigations
EEG
Evoked Potentials
ENS & EMG
EEG lecture ILOs
 Enumerate indications of EEG
 Describe different types of EEG
 Enumerate the different MRI sequences ...
Indication of EEG
 Some diseases as herpes simplex encephalitis ??
 Sleep disorders
 Altered level of consciousness & b...
Facts
 It must be stressed that the diagnosis
of epilepsy is a clinical one. EEG is
normal in 10-40% of patients with
epi...
Facts
 EDs are recorded on the first EEG in 30%
to 50% of patients with epilepsy and in 60%
to 90% by the third EEG. Addi...
Types of EEG
The International 10-20 system of
electrode placement
FPZ
FZ
CZ
PZ
OZ
T1
T3
T5
FP1
F7
F3 C3
P3
TP3
O1
EEG Interpretation
 Duration of the wave (Frequency of the waves):
1) Delta range of frequency: 0.5-3.5 Hz
2) Theta range...
Normal EEG
 1) Alpha rhythm: normal rhythm in adult during
wakefulness especially seen posteriorly with eyes
closed
2) B...
Abnormal EEG
 A) Theta or delta slowing: either focal or generalized
B) Persistent frequency asymmetries of greater than...
E.g.
Magnetoenchephalography
 Recording of the magnetic field of electrocerebral
activity
Evoked Potentials lecture ILOs
 Enumerate indications of EEG
 Describe different types of EEG
 Enumerate the different ...
Visual Evoked Potentials
Brainstem auditory evoked potentials
(BSAEPs)
 cochlea:
 acoustic nerve:
 cochlear nerve:
 superior olivary nucleus in...
Somatosensory evoked potential (SEP)
the cervical cord
lower brain stem
Upper brain stem
cortex
Motor evoked potential (MEP)
EMG lecture ILOs
 Enumerate indications of EEG
 Describe different types of EEG
 Enumerate the different MRI sequences ...
Normal Electromyography
 At rest:
 On contraction:
 Recruitment and Interference Patterns:A B
Abnormal Resting EMG
Abnormal MUAP
N
M
Abnormal Recruitment &
Interferences Patterns
EMG sequence of events in nerve injury
 Immediately after nerve injury:
 Incomplete injury:
 Late recruitment
 picket-...
ENG lecture ILOs
 Enumerate indications of EEG
 Describe different types of EEG
 Enumerate the different MRI sequences ...
Electro Neurography “ENG” or
Nerve Conduction Study “NCS”
1) The distal latency
 2) Response amplitude:
Demyelination
Ax...
F-wave
Supramaximal stimulus at a short duration
H reflexes
submaximal stimulus at a long duration
Neurophysiological investigations
Neurophysiological investigations
Neurophysiological investigations
Neurophysiological investigations
Neurophysiological investigations
Neurophysiological investigations
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  • EDs are recorded on the first EEG in 30% to 50% of patients with epilepsy and in 60% to 90% by the third EEG. Additional EEGs do not increase the yield further. Thus, 10% to 40% of patients with epilepsy will not have interictal discharges, even with repeated EEGs. (EEG in master lectures)
    EEG is abnormal in 2–4% of the population who do not have epilepsy. (EEG in master lecture)
  • A standard EEG takes about 30 minutes to perform. Patients are usually awake, lying down with eyes closed.
    Provocation EEG: In addition to passive recording, provocation techniques are also routinely employed, usually hyperventilation and photic stimulation, which can sometimes induce epileptiform changes on EEG. Sleep deprived EEG involves the patient remaining awake overnight, and then having EEG done first thing the following morning. Sleep can bring out epileptiform abnormalities on EEG, which may not be apparent on routine EEG.
    Various electrodes used for invasive recordings A) Depth electrode implanted with the orthogonal approach to record from the medial and lateral portions of the temporal lobe. B) Subdural strip electrode inserted to cover the cortical area. C) Sphenoidal electrodes are often used to record from the mesial or anterior aspects of the temporal lobe in the region of the foramen ovale.
    Digital EEG is simple recording and interpreting of routine EEG using computer based technology. Its advantages are easy storage, copying, montage reformating, adjustable filter and allows for more complex analysis with special computer programs as spikes search frequency calculation and comparison between the two sides.
    EEG (or electroencephalogram) is a recording of brainwave activity. QEEG (Quantitative EEG), popularly known as brain mapping, refers to a comprehensive analysis of brainwave frequency bandwidths that make up the raw EEG. QEEG is recorded the same way as EEG, but the data acquired in the recording are used to create topographic color-coded maps that show electrical activity of the cerebral cortex. It provides complex analysis of such brainwave characteristics as symmetry, phase, coherence, amplitude, power and dominant frequency. The QEEG findings are then compared to a normative database. This database consists of brain map recordings of several hundred healthy individuals. Comparisons are displayed as Z scores, which represent standard deviations from the norm. QEEG results are presented as Z scores. Z scores represent Standard Deviations (SD) from the norm and span from -3 to +3. Thus a Z score of +2 means that the result is 2 Standard Deviations higher than the norm (+2SD) and exceeds 98% of the age-matched people in the normative sample. A Z score of 0 represents the norm and is color-coded green. Red and blue colors on the maps show brainwave activity that is 3 SDs above or below the norm.
  • The placement of recording electrodes is generally based on the international 10-20 system, in which the placement of electrodes is determined by measurements from four standard positions on the head: the nasion, inion, and right and left preauricular points. When this system is used, most electrodes are about 5 to 7 cm from the adjacent electrodes, in an adult.

    Midline electrodes (midline placements by z).: Five electrodes: Fpz, Fz. Cz. Pz and Oz
    Hemispheric electrodes: Odd number on left
    Left hemisphere Right hemisphere
    T1 (for temporal tip not standard) T2 (for temporal tip not standard)
    Temporal electrodes (6): T3 T4
    T5 T6

    FP1 (frontal pole) FP2
    Frontal electrodes: F3 (upper frontal) F4
    F 7 (lower frontal) F8

    Central electrodes: C3 (central sulcus) C4
    Parietal electrodes: P3 P4
    Tempro-parital electrodes (not standard):
    TP3 TP4
    Occipital electrodes: O1 O2

    The potential fluctuations at each electrode are recorded, either in bipolar mode (i. e., differences in potential between adjacent electrodes) or in unipolar mode (i. e., differences in potential between each electrode and a reference electrode).
  • Evaluation of the EEG for clinical purposes involves definition of
    1) Description of the EEG waves:
    a) Frequency, (For descriptive purposes, EEG activity is usually characterized on the basis of frequency)
    b) Amplitude,
    c) Distribution of the electrical activity that is present,
    d) Its response to external stimulation such as eye opening.
    e) The degree of synchrony and symmetry over the two sides of the head is noted.
    The presence of any focal activity is determined and its nature characterized.
    A) Frequency: There are four ranges of frequency
    1) Delta range of frequency: 0.5-3.5 Hz
    2) Theta range of frequency: 4-7.5 Hz
    3) Alpha range of frequency: 8-12.5 Hz
    4) Beta range of frequency: 13 Hz or more
    B) Amplitude: There are three ranges of amplitudes
    1) Low amplitude: less than 20 µV
    2) Medium amplitude: 25-95 µV
    3) High amplitude: more than 100 µV
    C) Rhythmicity: It is rhythmic when it is relatively with constant frequency and arrhythmic if there are mixed frequencies. The different normal rhythms are the following
  • Alpha rhythm:
    1) This rhythm is found most typically over the posterior portions of the head during wakefulness, but it may also be present in the central or temporal regions.
    2) It is seen best when the patient is resting with the eyes closed. The alpha rhythm is attenuated or abolished by visual attention and affected transiently by other sensory stimuli and by other mental alerting activities (e.g., mental arithmetic) or by anxiety.
    3) Alpha activity is well formed and prominent in many normal subjects but is relatively inconspicuous or absent in about 10 percent of instances.
    4) Character of the wave:
    Frequency: Have a frequency of between 8 and 13 Hz, but in most adults it is between 9 and 11 Hz. It is not strictly monorhythmic but varies over a range of about 1 Hz even under stable conditions. a persistent difference in alpha frequency of more than 1 to 2 Hz between the two hemispheres is generally regarded as abnormal. The side with the slower rhythm is more likely to be the abnormal one, but it is usually difficult to be certain unless other abnormalities are also found.
    Shape: It is usually sinusoidal in configuration and sometimes has a spiky appearance; a spindle configuration denotes a beating phenomenon that results from the presence of two (or more) dominant frequencies.
    Amplitude: may wax and wane spontaneously in amplitude. alpha rhythm may normally be up to 50 percent greater in amplitude over the right hemisphere, possibly because this is the nondominant hemisphere or because of variation in skull thickness. A more marked asymmetry of its amplitude may have lateralizing significance but is difficult to interpret unless other EEG abnormalities are present, because either depression or enhancement may occur on the side of a hemispheric lesion.
    Beta rhythm:
    1) This rhythm is found most typically over the frontal portions of the head during drowsiness, light sleep, and rapid eye movement (REM) sleep .
    2) Beta ehythm not affected much by eye closure.
    3) Character of the wave:
    Frequency: Any rhythmic activity that has a frequency greater than 13 Hz is referred to as beta activity. Frequency increase with drowsiness and REM sleep.
    Shape:
    Amplitude: It usually has an amplitude of less than about 30 µV. the amplitude of beta activity may be increased either ipsilateral or contralateral to a lesion involving one cerebral hemisphere; and that an amplitude asymmetry is common in normal subjects, with beta activity being up to 30 percent lower on one side than the other.
    Theta rhythms:
    Activity with a frequency between 4 and 7 Hz is referred to as theta activity
    Theta and slower activity is usually very conspicuous in children but becomes less prominent as they mature.
    Some theta activity is often found in young adults, particularly over the temporal regions and during hyperventilation, but in older subjects theta activity with amplitude greater than about 30 µV is seen less commonly except during drowsiness. Focal or lateralized theta activity may be indicative of localized cerebral pathology.
    Delta rhythms:
    Activity that is slower than 4 Hz is designated delta activity.
    Activity of this sort is the predominant one in infants and is a normal finding during the deep stages of sleep in older subjects. When present in the EEG of awake adults, delta activity is an abnormal finding.
    Delta activity, responsive to eye opening, is commonly seen posteriorly (intermixed with alpha activity) in children and sometimes in young adults; it is then designated posteriorslow waves ofyouth. The spontaneous occurrence interictally of posterior, rhythmic slow waves is well described in patients with absence seizures.
  • General changes. Slowing of the background rhythm in the awake patient is abnormal, as is acceleration of background activity (e. g., in the form of a beta rhythm). The latter is often due to medication use.
    Focal findings. Slowing of background activity (e. g., in the form of theta or delta waves) limited to a circumscribed area of the brain reflects focal cortical disfunction. Findings of this type are often due to structural lesions of the brain (e. g., tumors).
    Sharp waves: waves with duration 70-200 ms
    Spikes discharge: waves with duration 20-70 ms
    Spikes with a prolonged following wave [the “spike and wave” pattern]:
  • Figure 15.5 Right hemispheral PLEDs in a 65-year-old patient with herpes simplex encephalitis. (From  Pedley TA, Emerson RG. Clinical neurophysiology. In: Bradley WG, Daroff RB, Fenichel GM, et al.,  eds. Neurology in Clinical Practice. 2nd ed. Boston: Butterworth-Heinemann; 1996:460, with  permission.)
  • It is a special application of EEG in which the EEG is recorded simultaneously with a number of other electrophysiological parameters. It is used to assess sleep and sleep disturbances. The EEG changes that normally occur during sleep are related to the progression of the individual through various sleep stages, including deep or REM sleep (REM = “rapid eye movement”). The recorded parameters include eye movements (by electro-oculography), respiratory excursion, airflow in the nostrils, muscle activity (by surface EMG), cardiac activity (by ECG), and the partial pressure of oxygen (by transcutaneous pulse oximetry). These are displayed together with the EEG in a polygraph recording (polysomnogram).
  • Less than one pico tesla (10-12 Tesla)
  • General principles. Evoked potentials are used to assess the integrity of individual functional systems (visual, auditory, somatosensory, or motor).
    Visual evoked potentials (VEP). The patient fixates on a video screen displaying a checkerboard pattern in which the white and black fields are regularly and periodically inverted, while electrical potentials are recorded through a needle electrode in the scalp at the occiput. Evoked potentials are obtained by summation; the largest fluctuation is a positive wave that appears 100 milliseconds after the stimulus. Delay of this wave is found early in the course of optic neuritis and persists thereafter.
    Fig. 4.19 Visual evoked potentials (VEP). A 38-year-old woman with multiple sclerosis and right optic neuritis. The cortical response on the right side is significantly delayed compared to the normal left side.
  • The normal AEP contains up to seven different waves, each of which is generated by a different structure along the chain of impulse transmission. The most constant waves are wave I, III, V and other waves II, IV, VI, and VII may be normally absent.
    Normality or abnormality is determined by the presence or absence of wave I, II, or V and by the interpeak latencies between them as compared with statistical norms.
    These waves represent
    CM in picture for cochlea
    Wave I is nerve potential in acoustic nerve. It may have more than one peak.
    Wave II is nerve potential in cochlear nerve
    Wave III for superior olivary nucleus in lower pons. It may have more than one peak.
    Wave IV for lateral lemniscus in mid or upper pons. This wave may be fused with wave V
    Wave V upper pons or inferior colliculi in lower mid brain.
    Clinical applications of BSAEPs include:
    1) Differentiate cochlear hearing loss (as there will be no changes in waves latency) from retrocochlear hearing loss (the sensitivity of BSAEPs in diagnosis acoustic neuroma is up to 96%)
    2) Assessment of hearing in non cooperative patient as mentally retarded or infant.
    3) Intraoperative monitoring in vestibular neuretomy or in removal of acoustic neuroma with hearing preservation. Intraoperative monitoring of BSAEPs indicate neural tissue compromise if distal latency prolonged by ≥ 10% or decrease amplitude by ≥ 50%
    4) In diagnosis of brain stem death: BAEP is resistant to drugs as anesthetic agents and generalized seizure so it will be present even in presence of flat EEG. If all criteria of brain death are applied but the BAEP is still intact so mostly drug overdose is underlying the coma.
  • When a repetitive electrical stimulus is applied to the skin, impulses are generated at the terminal sensory branch of a peripheral nerve and conducted centrally via the peripheral nerve, nerve root, posterior columns/ spinothalamic tract, medial lemniscus, and thalamocortical connections.
    The commonest abnormalities are the asymmetry between both sides in latencies, amplitudes or both.
    The components of median-nerve SSEP testing that are important to clinical interpretation include
    1) Erb point potential: It records as the afferent volley traverses the brachial plexus.
    2) N13: The central gray matter of the cervical cord.
    3) P14: The lower brain stem, most likely in the caudal medial lemniscus
    3) N18: attributed to postsynaptic potentials generated in the rostral brain stem; and
    4) N20: corresponding to activation of the primary cortical somatosensory
    The posterior tibial SSEP is analogous to the median SSEP and includes components generated in
    1) the gray matter of the lumbar spinal cord,
    2) brain stem, and
    3) primary somatosensory cortex.
    SSEPs are commonly used to monitor the integrity of the spinal cord during neurosurgical, orthopedic, and vascular procedures where there is risk of injury; SSEPs may detect adverse changes before they become irreversible.
    Although SSEPs primarily reflect the function of the dorsal columns, they are generally sensitive to spinal cord damage produced by compression, mechanical distraction, or ischemia.
  • Motor evoked potentials (MEPs) comparable to SSEPs are able to assess the whole motor pathways from the cortical level down to the distal muscle and therefore are affected in lesions of the peripheral (peripheral nerve, plexus) and central (spinal, cortical) nervous system.
    Technique: In awake subjects, a rapidly alternating magnetic field produced by a ring shaped transcranial magnetic impulse generator (TMS) induces a stimulating electrical current in the motor cortex and enables non-painful excitation of cortical motoneurons to induce action potentials in the cortex and travel down the pyramidal pathway to the muscles then throughthe corticospinal tract of the spinal cord till muscles. Surface electrodes placed on an arm or leg muscle are used to record the summed motor potentials.
    Epilepsy, cardiac pacemakers, and ferromagnetic intracranial implants are contraindications for transcranial magnetic stimulation for any purpose, including MEP
  • CMAP Electrode Placement.
    A) Over the endplate region.
    B) Off the endplate region
    Recruitment pattern:
    Definition: A motor unit consists of one motor neuron and all of the muscle fibers it contracts. All muscles consist of a number of motor units and the fibers belonging to a motor unit are dispersed and intermingle amongst fibers of other units. The muscle fibers belonging to one motor unit can be spread throughout part, or most of the entire muscle, depending on the number of fibers and size of the muscle. When a motor neuron is activated, all of the muscle fibers innervated by the motor neuron are stimulated and contract. The activation of one motor neuron will result in a weak but distributed muscle contraction. As a muscle begins to contract more, the first activated motor unit begins to fire repeatedly at a specific frequency, usually at a minimum of 4 to 5 Hz. As demand for more strength increases, the firing frequency of the motor unit increases until a second motor unit is recruited. The specific firing frequency of the first recruited motor unit at the moment the second motor unit appears is the recruitment frequency.
    Recruitment pattern in neuropathic lesion (Late recruitment): Abnormally high recruitment frequencies appear as motor units are lost, forcing surviving units to fire at faster and faster rates before additional units appear, because of reduced numbers of motor units available for recruitment.
    Recruitment pattern in myopathic lesion (Early recruitment): In contrast, because most motor units are smaller and weaker, owing to loss of muscle fibers, lower recruitment frequencies are seen in myopathies (early recruitment). Consequently, motor units must be activated earlier than in normal subjects to generate the same levels of force.
    Interferences pattern:
    Definition: The interference pattern is the overlapping pattern generated by the simultaneous activation of large numbers of MUAPs during maximal contraction; the spike density and the amplitude of the summated response (envelope amplitude) are assessed. This response typically appears as a dense band of competing waveform activity at slow sweep speeds, which normally obscures the baseline tracing. Normal recruitment from low- to intermediate- to full contraction should produce a full interference pattern with a conical onset, as amplitudes increase progressively with the recruitment of larger and larger motor units to generate increasing force.
    Interferences pattern in neuropathic lesion (picket-fence pattern): despite maximal contraction incomplete or reduced interference patterns are seen in advanced denervating disorders as more and more motor units drop out, ultimately leaving a picket-fence pattern, termed discrete recruitment. Maximal voluntary effort must be elicited before interference patterns are accurately assessed because poor volitional effort also produces an incomplete pattern; weakness due to central motor neuron injury may also result in reduced recruitment.
    Interferences pattern in Myopathic lesion: In contrast, full interference patterns, despite weakness, occur with myopathic disorders. A full pattern appears almost immediately with minimal effort, owing to the large numbers of weakened motor units that are required to generate low levels of force. This pattern also has a lower envelope amplitude because the size of the constituent motor unit potentials is reduced.
  • EMG activity at rest:
    Picture reference: [chapter edt: Armin Curt, Uta Kliesch. Chapter title: Neurophysiological Investigations. Chapter number: 12 in Spinal Disorders Fundamentals of Diagnosis and Treatment book. Book edit: Norbert Boos · Max Aebi (Editors) 2008 Springer-Verlag Berlin Heidelberg]
    Insertion activity: Normal muscle is electrically silent except for insertion activity which occurs secondary to mechanical stimulation of the muscle fiber by the insertion of the needle and it stops within 2 seconds after needle insertion.
    Sharp positive spikes: Its significances are the same as spontaneous fibrillation and it may occur interchanging with it. It may be seen in chronically denervated muscle, such as in neuropathy, motor neurone disease, or in acute myopathy.
    Spontaneous Fibrillation activity: Fibrillation potentials are due to single muscle fibers contracting, and indicate active denervation (before all fibers became fibrotic), as occurs in neurogenic disorders such as neuropathy (usually take 3-5ws after acute neuropathy to develop) and in muscle disease as myositis. When it occurs it remains for months or years (but with decreasing amplitude) till either muscle re-innervation or fibrosis.

    Spontaneous activity generated by the muscle
    – fibrillation potentials (fibs)
    – positive sharp wave (PSW)
    – myotonic discharges
    – complex repetitive discharges
    - fasciculations
    Spontaneous activity generated by the nerve
    – myokymic discharges
    – cramps
    – neuromyotonic discharges
    – tremors
    – multiples (multiple motor unit potentials, i.e. doublets or triplets)
    – *fasciculations
    N.B. Fasciculations can be considered muscle or nerve generated.

  • Abnormalities in motor unit action potentials:
    Large amplitude & long duration action potentials ± polyphasic: In neuropathy, collateral reinnervation causes potentials of large amplitude and long duration.
    Small amplitude & short duration ± polyphasic: in myopathies and muscular dystrophies, where potentials are of small amplitude and short duration.
    Polyphasic potentials: are found in limited numbers in normal muscle, and care must be exercised in attaching any pathologic significance to them unless they are present in excessive numbers and have abnormal amplitude or duration.
    Satellite potentials: Motor unit action potentials are sometimes followed by smaller potentials called satellite potentials. These can appear at any point after the termination of the motor unit action potential. Such potentials sometimes occur after an interval of about 15 to 25 msec or more. These late components of motor unit action potentials have been reported in both neurogenic disorders and muscle diseases such as polymyositis and muscular dystrophy.
  • Recruitment pattern:
    Definition: A motor unit consists of one motor neuron and all of the muscle fibers it contracts. All muscles consist of a number of motor units and the fibers belonging to a motor unit are dispersed and intermingle amongst fibers of other units. The muscle fibers belonging to one motor unit can be spread throughout part, or most of the entire muscle, depending on the number of fibers and size of the muscle. When a motor neuron is activated, all of the muscle fibers innervated by the motor neuron are stimulated and contract. The activation of one motor neuron will result in a weak but distributed muscle contraction. As a muscle begins to contract more, the first activated motor unit begins to fire repeatedly at a specific frequency, usually at a minimum of 4 to 5 Hz. As demand for more strength increases, the firing frequency of the motor unit increases until a second motor unit is recruited. The specific firing frequency of the first recruited motor unit at the moment the second motor unit appears is the recruitment frequency.
    Recruitment pattern in neuropathic lesion (Late recruitment): Abnormally high recruitment frequencies appear as motor units are lost, forcing surviving units to fire at faster and faster rates before additional units appear, because of reduced numbers of motor units available for recruitment.
    Recruitment pattern in myopathic lesion (Early recruitment): In contrast, because most motor units are smaller and weaker, owing to loss of muscle fibers, lower recruitment frequencies are seen in myopathies (early recruitment). Consequently, motor units must be activated earlier than in normal subjects to generate the same levels of force.
    Interferences pattern:
    Definition: The interference pattern is the overlapping pattern generated by the simultaneous activation of large numbers of MUAPs during maximal contraction; the spike density and the amplitude of the summated response (envelope amplitude) are assessed. This response typically appears as a dense band of competing waveform activity at slow sweep speeds, which normally obscures the baseline tracing. Normal recruitment from low- to intermediate- to full contraction should produce a full interference pattern with a conical onset, as amplitudes increase progressively with the recruitment of larger and larger motor units to generate increasing force.
    Interferences pattern in neuropathic lesion (picket-fence pattern): despite maximal contraction incomplete or reduced interference patterns are seen in advanced denervating disorders as more and more motor units drop out, ultimately leaving a picket-fence pattern, termed discrete recruitment. Maximal voluntary effort must be elicited before interference patterns are accurately assessed because poor volitional effort also produces an incomplete pattern; weakness due to central motor neuron injury may also result in reduced recruitment.
    Reduced interference patterns can be assessed as soon as the very first few days after a lesion to disclose a pathological innervation (not like acute denervation potentials which occur after a mean of 21 days) but the patient needs to cooperate and perform a voluntary activation.
    Interferences pattern in Myopathic lesion: In contrast, full interference patterns, despite weakness, occur with myopathic disorders. A full pattern appears almost immediately with minimal effort, owing to the large numbers of weakened motor units that are required to generate low levels of force. This pattern also has a lower envelope amplitude because the size of the constituent motor unit potentials is reduced.

  • Immediately after nerve injury:
    Incomplete injury:
    Recruitment pattern: Late recruitment Abnormally high recruitment frequencies appear as motor units are lost, forcing surviving units to fire at faster and faster rates before additional units appear, because of reduced numbers of motor units available for recruitment.
    Interferences pattern: picket-fence pattern Immediately after the development of an acute neuropathic lesion, EMG reveals no abnormality other than a reduction in the number of motor unit action potentials under voluntary control in affected muscles. A complete interference pattern is not seen during maximal effort despite an increase in the firing rate of individual units (late recruitment).
    Complete injury: As there is no surviving unit, so that no electrical activity is recorded during attempted voluntary contraction.
    Within the first few weeks (Up to 5 weeks) from injury: The amount of insertion activity increases after several days and abnormal spontaneous activity may subsequently be found, although its appearance may be delayed for up to 5 weeks, depending on the site of the lesion. In particular, fibrillation potentials are usually detected sooner when the lesion is close to the muscle than when a more distant lesion is present.
    If nerve regeneration started: When a muscle fiber is denervated, reinnervation can be accomplished in two ways. They are either through regenerating new axons (after successful nerve repair) that reach the muscle fibers after they have traveled through the distal nerve stump or through collateral sprouting with the denervated muscle fibers seeking new nerve sprouts from adjacent axons.
    If regeneration is secondary to nerve regeneration: MUAP will be short in duration small in amplitude and polyphasic
    If regeneration is secondary to collateral sprouting: MUAP will be long in duration large in amplitude and polyphasic
    If no nerve regeneration: In patients with chronic partial denervation, insertion activity is increased and spontaneous fibrillation, positive sharp waves, and complex repetitive discharges are found. Fasciculation potentials are often conspicuous in patients with diseases such as motor neuron disease or poliomyelitis, in which the lower motor neurons in the spinal cord are affected, but they may also be found with more peripheral lesions.
  • In electrodiagnostic terminology, negative refers to an upward deflection from baseline and positive refers to a downward deflection from baseline
    In motor and sensory nerves conduction studies the following parameters are recorded:
    1) The distal latency
    2) Response amplitude:
    3) Response area:
    4) Conduction velocity:
    The nerve conduction studies most commonly performed are compound muscle action potentials (CMAPs) for motor nerves, sensory nerve action potentials (SNAPs) for sensory nerves, compound nerve action potentials (CNAPs) for mixed (sensory and motor) nerves
    Sensory nerve conduction study is more sensitive than motor nerve conduction study in detecting early or mild nerve disorders so in CT syndrome sensory median conduction is studied and not the motor median conduction.
    As a rule, nerve conduction study is done only on myelinated nerve fibers because unmyelinated fibers conduct extremely slowly, and do not contribute significantly to the CMAPs and SNAPs.
    Velocities in myelinated nerves range from 40 to 70 m/sec. Unmyelinated axons, in contrast, are much slower – in the range of 1–5 m/sec.
    A demyelinated axon is a myelinated nerve that has lost its myelin covering. This does not become an unmyelinated nerve. While an unmyelinated axon can conduct an impulse along its entire length, a demyelinated axon may not be able to conduct across a demyelinated area. This loss of conduction across a lesion is referred to as conduction block.
    The differences between SNAP and CMAP are the following:
    1) SNAP are smaller in amplitude
    2) SNAP are typically triphasic with positive phase then negative then positive (CMAP are typically “when the recording electrode is directly over the end plate” biphasic with negative phase at the start).
    3) Conduction velocity of SNAP are faster than CMAP
    4) To calculate conduction velocity of SNAP no need for two point stimulation as no conduction through MNJ.
    Differentiation between demyelination disease and axons degeneration by the following:
    In demyelination the main criteria are:
    1) prolonged distal latency
    2) Slow conduction velocity
    3) prolonged F-waves latency
    In axona degeneration the main criteria are: DA
    1) Decrease Amplitude (as the SNAP is normally of smaller amplitude than CMAP so decrease amplitude may be more appreciable in motor conducting studies but other tests as EMG should be done to rule out othe muscular causes for low amplitude of CMAP)
    2) Decrease Area
    Normal values of Median nerve sensory conduction study:
    Active electrode site: 2nd digit
    Stimulation site: Wrist
    Segment name: Wrist–mid palm
    Onset latency <3.5 ms
    Amplitude >20.0 microvolts
    Velocity >45.0 m/s (meters/sec) [Although every lab has its own standards of normal, in general a velocity of less than 44 meters/second across the carpal tunnel indicates slowing.
    Normal values of Median nerve motor conduction study
    Active electrode site: Abductor pollicis brevis
    Stimulation site: Wrist
    Segment name: Elbow-wrist
    Onset latency <4.2
    Amplitude >4.0 mellivolt
    Velocity >50.0
  • F-wave recordings are not considered to be reflexes since only the motor branches of a peripheral nerve become involved.
    This NCS evokes a small late response from a short duration supramaximal stimulation.
    The electrical stimulation of a peripheral nerve induces a bidirectional electrical volley with a direct motor response (M-response of the orthodromic volley) and an antidromic volley propagating to the alpha-motoneuron, inducing an efferent motor response which travels back on the peripheral motor nerve fibers producing muscle action potential (F-wave) after a delay of 20-50 msec according to the distance of the stimulating electrode from the spinal cord.
    Indications [chapter edt: Armin Curt, Uta Kliesch. Chapter title: Neurophysiological Investigations. Chapter number: 12 in Spinal Disorders Fundamentals of Diagnosis and Treatment book. Book edit: Norbert Boos · Max Aebi (Editors) 2008 Springer-Verlag Berlin Heidelberg]
    F-waves are sensitive to spinal cord excitability responses (expressed as a percentage of F-wave responses to 20 stimuli) can be applied to diagnose the level of spinal shock as they become abolished or reduced. They are sensitive to demyelinating motor neuropathies (e.g., diabetes mellitus) and complement NCS.
    Limitations [chapter edt: Armin Curt, Uta Kliesch. Chapter title: Neurophysiological Investigations. Chapter number: 12 in Spinal Disorders Fundamentals of Diagnosis and Treatment book. Book edit: Norbert Boos · Max Aebi (Editors) 2008 Springer-Verlag Berlin Heidelberg]
    F-waves are not sensitive enough to assess the extent of intramedullary and peripheral axonal nerve damage (no quantification of damage). The responses are not related to spasticity and are recordable only in somemotor nerves (ulnar, median, tibial nerves).
  • It is initiated with a submaximal stimulus at a long duration (0.5–1.0 milliseconds)
    It differs in that the initial nerve stimulated is a sensory nerve (Ia fibers). The signal in conducted proximally up to where the sensory nerve synapses with the motor nerve. The signal then returns down the motor axon and is recorded peripherally.
    It is obtained when the stimulus is sub maximal so no direct compound motor action potential is generated or if generated it will be of low amplitude. When super maximal stimulation is applied normal compound motor action potential will be generated and H reflex will be blocked by collision of impulses that will be generated antidromic by the super maximal stimulation and the coming orthodromic impulse of H reflex.
    The H-reflex is less affected by spinal shock (it is reestablished within 24 h after SCI) than clinical reflexes and the F-wave.
  • Neurophysiological investigations

    1. 1. Neuro-investigations
    2. 2. EEG Evoked Potentials ENS & EMG
    3. 3. EEG lecture ILOs  Enumerate indications of EEG  Describe different types of EEG  Enumerate the different MRI sequences and their main usages  Describe EEG procedure  Interpret normal EEG  Interpret common abnormalities in EEG  Define Polysomnography & Magneto- enchephalography
    4. 4. Indication of EEG  Some diseases as herpes simplex encephalitis ??  Sleep disorders  Altered level of consciousness & brain death  Epilepsy:  Identify a focal or lateralized epileptogenic source, provide a guide to prognosis follow the course of the disorder
    5. 5. Facts  It must be stressed that the diagnosis of epilepsy is a clinical one. EEG is normal in 10-40% of patients with epilepsy. EEG is abnormal in 2–4% of the population who do not have epilepsy.
    6. 6. Facts  EDs are recorded on the first EEG in 30% to 50% of patients with epilepsy and in 60% to 90% by the third EEG. Additional EEGs do not increase the yield further. Thus, 10% to 40% of patients with epilepsy will not have interictal discharges, even with repeated EEGs. Sleep deprivation, hyperventilation, and photic stimulation increase the yield of EDs in some patients.
    7. 7. Types of EEG
    8. 8. The International 10-20 system of electrode placement FPZ FZ CZ PZ OZ T1 T3 T5 FP1 F7 F3 C3 P3 TP3 O1
    9. 9. EEG Interpretation  Duration of the wave (Frequency of the waves): 1) Delta range of frequency: 0.5-3.5 Hz 2) Theta range of frequency: 4-7.5 Hz 3) Alpha range of frequency: 8-12.5 Hz 4) Beta range of frequency: 13 Hz or more  Amplitude of the wave:  Shape of the wave: Short duration = High frequency Low amplitude Long duration = Low frequency High amplitude
    10. 10. Normal EEG  1) Alpha rhythm: normal rhythm in adult during wakefulness especially seen posteriorly with eyes closed 2) Beta rhythm: normal rhythm in adult seen in frontal region and not affected by eye opening 3) Theta and delta rhythms: Seen in children and young adults especially in frontal and temporal regions.
    11. 11. Abnormal EEG  A) Theta or delta slowing: either focal or generalized B) Persistent frequency asymmetries of greater than 1 Hz between corresponding scalp regions C) Epileptiform discharge: 1) Sharp waves: duration 70-200 ms  2) Spikes discharge: duration 20-70 ms
    12. 12. E.g.
    13. 13. Magnetoenchephalography  Recording of the magnetic field of electrocerebral activity
    14. 14. Evoked Potentials lecture ILOs  Enumerate indications of EEG  Describe different types of EEG  Enumerate the different MRI sequences and their main usages  Describe EEG procedure  Interpret normal EEG  Interpret common abnormalities in EEG  Define Polysomnography & Magneto- enchephalography
    15. 15. Visual Evoked Potentials
    16. 16. Brainstem auditory evoked potentials (BSAEPs)  cochlea:  acoustic nerve:  cochlear nerve:  superior olivary nucleus in lower pons:  lateral lemniscus in mid or upper pons:  upper pons or inferior colliculi
    17. 17. Somatosensory evoked potential (SEP) the cervical cord lower brain stem Upper brain stem cortex
    18. 18. Motor evoked potential (MEP)
    19. 19. EMG lecture ILOs  Enumerate indications of EEG  Describe different types of EEG  Enumerate the different MRI sequences and their main usages  Describe EEG procedure  Interpret normal EEG  Interpret common abnormalities in EEG  Define Polysomnography & Magneto- enchephalography
    20. 20. Normal Electromyography  At rest:  On contraction:  Recruitment and Interference Patterns:A B
    21. 21. Abnormal Resting EMG
    22. 22. Abnormal MUAP N M
    23. 23. Abnormal Recruitment & Interferences Patterns
    24. 24. EMG sequence of events in nerve injury  Immediately after nerve injury:  Incomplete injury:  Late recruitment  picket-fence pattern  Complete injury:  Within the first few weeks (Up to 5 weeks):  Sharp positive spikes.  Spontaneous Fibrillation .  If nerve regeneration started:  MUAP: short, small & polyphasic  MUAP long, large & polyphasic  If no nerve regeneration: nerve regeneration collateral sprouting
    25. 25. ENG lecture ILOs  Enumerate indications of EEG  Describe different types of EEG  Enumerate the different MRI sequences and their main usages  Describe EEG procedure  Interpret normal EEG  Interpret common abnormalities in EEG  Define Polysomnography & Magneto- enchephalography
    26. 26. Electro Neurography “ENG” or Nerve Conduction Study “NCS” 1) The distal latency  2) Response amplitude: Demyelination Axona Degeneration
    27. 27. F-wave Supramaximal stimulus at a short duration
    28. 28. H reflexes submaximal stimulus at a long duration

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