Somatosensory evoked potential

Somatosensory evoked potential

1. Somatosensory evoked potentials BY AHMED ABD EL HADY

2. Definition “E.Ps. are the measurement of the electrical potentials produced in response to stimulating the nervous system (evoked) by sensory , electrical , magnetic or cognitive stimulation ” Evoked potentials are used to detect conduction disturbances in the central nervous system. Evoked responses used for determining: 1- prognosis for severely brain-damaged patients 2-assessment of demyelinating diseases .  

3. Classification Classification of evoked potentials Sensory EP Motor EP Event related EP Visual EP Auditory EP Somatosensory EP

4. Motor evoked potentials Motor evoked potentials ( MEP ) are used to test conductivity in corticospinal pathways by stimulating the cortex from the outside of the head by transcranial magnetic stimulator or electrical pulses. This is a sort of « reversed evoked potential », because the evoked potentials are recorded from muscles.

5. Event-related potentials Event-related potentials (ERP) are evoked when a subject performs a task which involves responding rapidly and correctly to a stimulus. The change in the electrical activity of the brain is measured simultaneously for about one second. The P300 is the most common event-related potential.( ERP ) are used to judge attention and more complex cognitive processes .

6. Sensory Evoked potentials EEG is recorded during repetitive natural stimulation ( eg . tap on skin or flash of light) Sensory EP is a change in EEG resulting from stimulation of a sensory pathway: Visual pathway → VEP Auditory pathway → ABR post.column →SSEP

7. The somatosensory-evoked potential (SEP) is the response to electrical stimulation of peripheral nerves. Stimulation of almost any nerve is possible, although the most commonly studied nerves are: • Median • Ulnar • Peroneal • Tibia Brief electric pulses are delivered to the peripheral nerve with the cathode proximal to the anode. The stimulus cannot selectively activate sensory nerves, so a small muscle twitch is seen. There are no effects of the retrograde motor volley in the motor nerves on central projections of the sensory fibers.

8. Intensity of the stimulus is adjusted to activate low-threshold myelinated nerve fibers, which in the motor fibers elicits a small twitch of the innervated muscles. The compound action potential is conducted through the dorsal roots and into the dorsal columns. The impulses ascend in the dorsal columns to the gracile and cuneate nuclei where the primary afferent fibers synapse on the second-order neurons. These axons ascend through the brainstem to the thalamus. Thalamocortical projections are extensive, as are secondary intracortical associative projections. The recording is made from various levels of the nervous system, including: • Afferent nerve volley • Spinal cord • Brain

9. SEPs are particularly useful for evaluation of function of the spinal cord. Lesions of the cord may be invisible to routine imaging, including magnetic resonance imaging and myelography , yet may have devastating effects on cord function. Transverse myelitis, multiple sclerosis (MS), and cord infarction are only three of the potential causes that can be missed on structural studies. Although almost any nerve can be studied, median and tibial will be discussed here.

10. Precautions 1- stimulation aiming at sensory not motor 2- prevention of EMG artifact by making the pt. to relax 3- reduce stimulation rate to prevent EMG artifact 4- Prevent ECG artifact 5- reduction of skin-electrode contact impedence

11. Median SSEP Stimulating electrodes are placed over the median nerve at the wrist with the cathode proximal to the anode. Stimuli are square-wave pulses given at rates of 4–7/sec. Recording electrodes are placed at the following locations: • Erb’s point on each side (EP) • Over the second or fifth cervical spine process (C2S or C5S) • Scalp over the contralateral cortex ( CPc ) and ipsilateral cortex ( CPi ) • Noncephalic electrode (Ref)

12. Erb’s point is 2–3 cm above the clavicle, just lateral to the attachment of the sternocleidomastoid muscle. Stimulation at Erb’s point produces abduction of the arm and flexion of the elbow. The second and fifth spinous processes are identified by counting up from the seventh, notable by its prominence at the base of the neck. CPc and CPi are scalp electrodes halfway between C3 and P3 or C4 and P4, where CPc is contralateral to the stimulus and CPi is ipsilateral to the stimulus. These electrodes are over the motor-sensory cortex. EPi is Erb’s point ipsilateral to the stimulus. The recommended montage is: • Channel 1: CPc-CPi • Channel 2: CPi-Ref • Channel 3: C5S-Ref • Channel 4: Epi-Ref

13. Waveform Identification and Interpretation

14. • N9 = from the Epi channel (The potential recorded from Erb’s point ) Origin (Afferent volley in plexus ) • P14 = from the neck channel (The neck potentials include N13 and P14, with the latter used for clinical interpretation) Origin ( N13------- Dorsal horn neurons P14 --------- Caudal medial lemniscus) • N20 = from scalp channels (Scalp potentials include N18 and N20, but the latter is used for clinical interpretation) origin ( N18--------- Brainstem and thalamus? N20---------- Thalamocortical radiations )

15. Somatosensory-evoked potential normal data N9–P14 interval represents the time for conduction between the brachial plexus and cervical spine. P14–N20 interval represents the conduction between the cervical spine and the brain. This is called the brain conduction time (BCT).

16. Interpretation of abnormalities is as follows: • Delayed N9 with normal N9–P14 and P14–N20 intervals : Lesion in the somatosensory nerves at or distal to the brachial plexus. • Increased N9–P14 interval with normal P14–N20 interval: Lesion between Erb’s point and the lower medulla. • Increased P14–N20 with normal N9–P14 interval : Lesion between the lower medulla and the cerebral cortex.

17. Methodology Sites Upper limb: Recording : Erb’s point (N9), Cervical spine 7(N11), Cervical spine 2(N13), contralateral scalp overlying area of 1ry sensory cortex (N20). Always use the – ve electrode as recording Ground : Px to stimulation site Reference : Forehead Fz

18. Tibial SSEP The proximal stimulating electrode (cathode) is placed at the ankle between the medial malleolus and the Achilles tendon. The anode is placed 3 cm distal to the cathode. A ground is placed proximal to the stimulus electrodes, usually on the calf. Stimulus intensity is set so that each stimulus produces a small amount of plantar flexion of the toes. Recording electrodes are placed as follows: • CPi = Ipsilateral cortex between C3 and P3 or C4 and P4 • CPz = Midline between Cz and Pz • FPz = Fpz position of the 10–20 electrode system • C5S = Over the C5 spinous process • T12S = Over the T12 spinous process • Ref = Noncephalic reference

19. The montage used for routine tibial SEP is as follows: • Channel 1: CPi-Fpz • Channel 2: Cpz-Fpz • Channel 3: Fpz-C5S • Channel 4: T12S-Ref

20. Waveform Identification and Interpretation

21. LP: The lumbar potential (LP) is thought to arise from the afferent nerve volley in the dorsal roots and dorsal root entry zone. Origin ( Dorsal roots and entry zone ) N21 is best recorded at the L4 spinal level, suggesting that this potential arises from the cauda equina N34: precedes P37, but is not used for clinical interpretation. N34 is the main negative wave in the FPz-C5S derivation and is preceded by a small positive wave that is not used for interpretation (P31). Origin ( Brainstem and thalamus? ) P37: P37 is a positive potential at about 37 ms that is seen from the scalp channels. Origin (primary sensory cortex )

22. Somatosensory-evoked potential normal data The LP–P37 interval is the time from the cauda equina to the brain. This is called the central conduction time (CCT).

23. Interpretation of abnormalities is as follows: Interpretation of tibial SEPs parallels interpretation of median SEPs. Prolonged LP with normal LP–P37 interval : Peripheral or distal lesion. Peripheral neuropathy is most likely, but the slowing could be in the cauda equina . Normal LP with prolonged LP–P37 interval : Abnormal conduction between the cauda equina and the brain. Median SEP is required to localize the abnormality to the spinal cord. Normal median SEP indicates a lesion below the mid-cervical cord. Prolonged median SEP indicates a lesion above the mid-cervical cord. A second lesion below the cervical cord cannot be ruled out, however, since the P37 latency is already prolonged by the higher lesion.

24. Prolonged LP and prolonged LP—P37 interval : This suggests two lesions affecting the peripheral nerve and central conduction. A single lesion of the cauda equina is possible.

25. Clinical Correlations Transverse Myelitis Transverse myelitis produces slowing of SEPs that depends on the site of the lesion. Lesion in the lower cervical or thoracic cord increases central conduction time without having an effect on brain conduction time. With recovery, the SEPs abnormalities are improved, but may not return to normal.

26. Multiple Sclerosis SEP is abnormal in most patients with MS, and can be supporting evidence for a silent lesion or confirmatory for a myelopathy. The most common finding in MS is an increase in CCT of the tibial SEP with normal peripheral conduction (LP). This is because the tibial SEP is assessing conduction along the longest myelinated nerve tract of any of the evoked potentials. BCT of median nerve SEP is less commonly increased than tibial nerve SEP CCT. A combined increase in BCT and CCT can be due to tandem lesions, but also can be due to a single lesion in the cervical cord.

27. Peripheral Neuropathy Peripheral neuropathy slows peripheral conduction (N9 and LP) with normal BCT and CCT. The N9–P14 interval may be prolonged with lesions affecting the proximal portions of the nerves, such as Guillain – Barré syndrome (GBS). GBS may also occasionally prolong CCT, presumably by affecting the afferent nerve roots of the cauda equina .

28. Vitamin B12 Deficiency Subacute combined degeneration from vitamin B12 deficiency delays or abolishes the cervical and scalp SEPs. With treatment, the abnormalities improve, although not completely to normal. This parallels the clinical course, where there is improvement but also some persistent deficit.

29. Spinal Cord Injury Cord transection abolishes potentials above the lesion, but most lesions are incomplete, so the defect in the SEP is variable. Lesions affecting position sense are most likely to alter the SEP. SEP is not perfectly sensitive so many patients may have undetectable scalp potentials despite preservation of some cord function

30. Brain Death Brain death is usually evaluated by EEG or blood flow studies, so the SEP is not typically used as a confirmatory test. In brain death, the scalp potentials are absent, usually with preservation of cervical potentials.

31. Stroke SEPs are not commonly used for evaluation of stroke, but if performed, will show attenuation, delay, and often absence of scalp potentials with stimulation of the limbs of the affected side. Lesions of the motor-sensory cortical regions are much more likely to produce abnormal SEPs than lesions elsewhere in the brain. In general, the severity of the stroke deficit correlates with the degree of abnormality of the SEP, but wide variation is common. SEP may be absent with subtle deficit and SEP may be preserved with major deficit.

32. Other uses Monitoring during temporary clipping in aneurysm surgery has shown that a very prompt loss of cortical SSEP response (less than 1 minute after clipping) is associated with development of permanent neurologic deficit. SSEP in spinal surgeries has become standard care of monitoring. Monitoring during carotid endarterectomy . Intraoperative SSEP changes are used as an indication for shunt placement and to predict postoperative morbidity.