Visual evoked potentials (VEPs) record electrical signals from the scalp in response to visual stimuli. VEPs are useful for objectively assessing visual function, especially of the retina and optic nerve. The VEP involves presenting a visual stimulus such as a flashing light or alternating checkerboard pattern. Electrodes placed on the scalp record the P100 waveform generated in the striate and peristriate cortex in response to the stimulus. Analysis of the P100 latency, amplitude, and interocular latency difference can help detect and localize abnormalities in the retina, optic nerve, optic tract, and visual cortex.
1) VEPs are electrophysiological signals extracted from the EEG activity in the visual cortex in response to visual stimulation. They provide an objective measure of visual pathway integrity from the eye to the occipital cortex.
2) VEP waveform and components mature during early childhood, peaking around ages 5-8 years, then stabilize until aging effects begin around age 55. The "P1" component can be seen in infants by 5 weeks of age.
3) Pattern-reversal stimulation with checkerboards is most commonly used clinically. It elicits a reproducible P100 component around 100ms. Hemifield stimulation can localize lesions to the pre- or retrochiasmatic regions.
This document discusses visual evoked potentials (VEP), which assess the integrity of the visual pathways from the optic nerve to the occipital cortex. VEP can be evoked by flashes of light or patterned stimuli, with pattern VEP being most commonly used clinically. Pattern VEP involves presenting a checkerboard pattern and measuring the response to pattern onset/offset or reversal. Clinical applications of VEP include evaluating optic neuritis, multiple sclerosis, anterior ischemic optic neuropathy, and compressive lesions, as well as distinguishing organic from functional visual loss.
This document discusses visual evoked potentials (VEPs), a type of evoked potential used to objectively assess visual pathway function. It describes the different types of VEPs including transient, steady-state, pattern, and flash VEPs. Pattern VEPs using checkerboard pattern reversal are most widely used. The document outlines best practices for VEP testing including stimulus parameters, electrode placement, waveforms, interpretation of results, and clinical applications for conditions like optic neuritis and ischemic optic neuropathy. Abnormalities include prolonged latencies and reduced amplitudes. VEPs can help localize lesions anterior or posterior to the optic chiasm.
1. Visual Evoked Potentials (VEPs) provide an objective assessment of visual function, especially of the retina and optic nerve.
2. VEPs measure the electrical response of the visual cortex to visual stimuli, such as flashing lights or patterns.
3. The major components of the VEP response are the N75, P100, and N145 waves. Abnormalities in the latency and amplitude of these waves can help localize lesions along the visual pathway.
VEP provides an objective measure of visual pathway function from the retina to the visual cortex. It involves recording electrical signals from the occipital cortex in response to visual stimuli such as flashes or patterns. Abnormalities in the visual pathways or cortex can affect VEP responses by changing latencies and amplitudes. Different stimuli types evaluate different aspects of vision. Pattern reversal VEP is commonly used to assess acuity. Multifocal VEP can detect localized abnormalities. VEP is useful for diagnosing and monitoring various conditions affecting the visual system.
The document discusses visual evoked potentials (VEPs), which involve recording electrical signals from the visual cortex in response to visual stimulation. It notes that VEPs have smaller amplitudes than EEGs but can objectively assess macular function and the functional state of the visual system. It describes how steady state VEPs use rapid stimulation to produce sinusoidal waveforms while transient VEPs use discrete deflections with low rates of stimulation. It also discusses the use of flash VEPs, pattern VEPs, and other techniques and provides details on stimulation methods, components of VEP testing equipment, factors that influence VEPs, and abnormal findings that may be observed in various conditions.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
Visual evoked potentials (VEPs) measure electrical activity in the visual pathway in response to visual stimulation. VEPs use stimuli like flashing lights or alternating checkerboard patterns. Recordings are made from electrodes placed on the head. Abnormalities in VEP latency, amplitude, or waveform can indicate conditions like optic nerve damage or multiple sclerosis but do not diagnose a specific disease. VEPs are useful for evaluating visual pathway function from the retina to visual cortex but abnormalities must be interpreted within the patient's overall clinical picture.
1) VEPs are electrophysiological signals extracted from the EEG activity in the visual cortex in response to visual stimulation. They provide an objective measure of visual pathway integrity from the eye to the occipital cortex.
2) VEP waveform and components mature during early childhood, peaking around ages 5-8 years, then stabilize until aging effects begin around age 55. The "P1" component can be seen in infants by 5 weeks of age.
3) Pattern-reversal stimulation with checkerboards is most commonly used clinically. It elicits a reproducible P100 component around 100ms. Hemifield stimulation can localize lesions to the pre- or retrochiasmatic regions.
This document discusses visual evoked potentials (VEP), which assess the integrity of the visual pathways from the optic nerve to the occipital cortex. VEP can be evoked by flashes of light or patterned stimuli, with pattern VEP being most commonly used clinically. Pattern VEP involves presenting a checkerboard pattern and measuring the response to pattern onset/offset or reversal. Clinical applications of VEP include evaluating optic neuritis, multiple sclerosis, anterior ischemic optic neuropathy, and compressive lesions, as well as distinguishing organic from functional visual loss.
This document discusses visual evoked potentials (VEPs), a type of evoked potential used to objectively assess visual pathway function. It describes the different types of VEPs including transient, steady-state, pattern, and flash VEPs. Pattern VEPs using checkerboard pattern reversal are most widely used. The document outlines best practices for VEP testing including stimulus parameters, electrode placement, waveforms, interpretation of results, and clinical applications for conditions like optic neuritis and ischemic optic neuropathy. Abnormalities include prolonged latencies and reduced amplitudes. VEPs can help localize lesions anterior or posterior to the optic chiasm.
1. Visual Evoked Potentials (VEPs) provide an objective assessment of visual function, especially of the retina and optic nerve.
2. VEPs measure the electrical response of the visual cortex to visual stimuli, such as flashing lights or patterns.
3. The major components of the VEP response are the N75, P100, and N145 waves. Abnormalities in the latency and amplitude of these waves can help localize lesions along the visual pathway.
VEP provides an objective measure of visual pathway function from the retina to the visual cortex. It involves recording electrical signals from the occipital cortex in response to visual stimuli such as flashes or patterns. Abnormalities in the visual pathways or cortex can affect VEP responses by changing latencies and amplitudes. Different stimuli types evaluate different aspects of vision. Pattern reversal VEP is commonly used to assess acuity. Multifocal VEP can detect localized abnormalities. VEP is useful for diagnosing and monitoring various conditions affecting the visual system.
The document discusses visual evoked potentials (VEPs), which involve recording electrical signals from the visual cortex in response to visual stimulation. It notes that VEPs have smaller amplitudes than EEGs but can objectively assess macular function and the functional state of the visual system. It describes how steady state VEPs use rapid stimulation to produce sinusoidal waveforms while transient VEPs use discrete deflections with low rates of stimulation. It also discusses the use of flash VEPs, pattern VEPs, and other techniques and provides details on stimulation methods, components of VEP testing equipment, factors that influence VEPs, and abnormal findings that may be observed in various conditions.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
Visual evoked potentials (VEPs) measure electrical activity in the visual pathway in response to visual stimulation. VEPs use stimuli like flashing lights or alternating checkerboard patterns. Recordings are made from electrodes placed on the head. Abnormalities in VEP latency, amplitude, or waveform can indicate conditions like optic nerve damage or multiple sclerosis but do not diagnose a specific disease. VEPs are useful for evaluating visual pathway function from the retina to visual cortex but abnormalities must be interpreted within the patient's overall clinical picture.
This document provides information about visual evoked potentials (VEP) and brainstem auditory evoked potentials (BAEP). It describes how VEPs are used to assess the integrity of the visual pathway and are recorded from the scalp in response to visual stimuli. It details the anatomy of the visual pathway and different types of VEPs. It also outlines how to perform VEP testing, interpret the results, and factors that can influence VEPs. For BAEPs, it describes the auditory pathway and waves in the BAEP response. It provides details on performing BAEP testing, interpreting the results, and applications in evaluating neurological conditions.
Saccadic eye movements are fast, conjugate movements that move both eyes quickly in the same direction to bring an object of interest onto the fovea. They have a peak velocity of 30-700 degrees per second and duration of 30-100 milliseconds. The latency between a target appearing and saccade onset is normally 150-250 milliseconds, but can be shorter for "express saccades". Saccades are controlled by burst neurons that generate a pulse to move the eyes rapidly, followed by tonic activity from step neurons to hold the eyes in place against elastic forces. Lesions in different brain regions involved in generating and modulating saccades can cause abnormalities such as slowed saccades, gaze-holding failure,
This document provides guidelines for performing and interpreting somatosensory evoked potentials (SSEPs), which assess sensory nerve conduction in the upper and lower extremities. It describes stimulation and recording procedures, including electrode placement and montages. For upper extremity SSEPs following median nerve stimulation, it identifies the key components N9, N13, P14, N18, and N20 and provides criteria for abnormal findings such as absent waves or prolonged interpeak latencies. For lower extremity SSEPs following posterior tibial nerve stimulation, it identifies the components LP, P31, N34, and P37 and also provides criteria for abnormal findings.
The document discusses the blink reflex, which evaluates the trigeminal and facial cranial nerves. Stimulation of the trigeminal nerve leads to contraction of the orbicularis oculi muscle mediated by the facial nerve. This produces two responses - an early R1 response localized to the stimulated side, and a later R2 response seen bilaterally. Analysis of blink reflex latencies can identify lesions along the afferent trigeminal or efferent facial nerve pathways or in the brainstem. The blink reflex is useful for evaluating various neurological conditions that may affect these cranial nerves or central pathways.
The blink reflex is a disynaptic or multisynaptic reflex that involves the trigeminal and facial nerves. It has two responses - an early ipsilateral R1 response and a late bilateral R2 response. The blink reflex test stimulates the supraorbital nerve branch to evaluate conduction along the trigeminal and facial nerve pathways. Abnormalities in the R1 and R2 responses can localize lesions in different parts of the brainstem or peripheral nerves. The test involves recording electromyography of the orbicularis oculi muscle in response to supraorbital nerve stimulation.
The document summarizes visual evoked potentials (VEPs), including:
- VEPs measure electrophysiological signals from the visual cortex in response to visual stimuli.
- International standards exist for stimulus parameters, recording procedures, and normal values.
- Pattern-reversal VEPs eliciting the P100 wave are most commonly used clinically. Factors like check size, contrast and age affect P100 latency and amplitude.
- Abnormalities suggest defects along the visual pathway from eye to cortex. Multi-channel recordings localize defects pre- or post-chiasm.
This presentation looks at EEG signal generation, pyramidal cells, recording of EEG, source localisation, polarity, analysis of dipole, derivations, montages,
Introduction, history and neurophysiologic basis of vepkalpanabhandari19
1. VEPs measure the electrical activity in the visual cortex generated by light stimulation of the retina. They provide an objective measure of the functional integrity of the visual pathways.
2. VEPs were initially observed in the 1930s but were refined through the development of signal averaging techniques from the 1950s onward.
3. Standard VEP stimulation includes flash, pattern onset/offset, and pattern reversal, with the latter being the preferred clinical technique. Check size, luminance, and reversal rate are standardized.
The document summarizes the process of presurgical evaluation for epilepsy patients. It discusses how modern imaging techniques like video EEG monitoring, high-resolution MRI, fMRI, PET and SPECT are used to localize the epileptogenic zone noninvasively in most patients. When noninvasive methods are insufficient, invasive EEG monitoring using subdural or depth electrodes may be used. The goal is to precisely identify the brain area responsible for seizure generation to allow its surgical resection, while avoiding damage to critical functions. A classical example where surgery is often curative is mesial temporal lobe epilepsy.
This document discusses VEP (visually evoked potential) testing for evaluating the visual pathway from the eye to the brain. It describes how VEP works by measuring the electrical signal from the retina to the visual cortex in response to visual stimuli. Key points covered include the components of the VEP waveforms, how different stimuli test different visual pathways, and examples of how VEP can help evaluate conditions like glaucoma, optic neuritis, and amblyopia. The document also notes how advances in technology have made VEP more widely available in clinical practice.
Brainstem Auditory Evoked Potentials (BAEP) involves recording electrophysiological responses from the ear in response to auditory stimulation to assess the functioning of the auditory pathway. BAEP testing involves placing electrodes on the scalp to record waveforms representing activity in the auditory nerve and brainstem in response to click sounds. BAEP is useful for screening and monitoring conditions affecting the auditory pathway such as tumors near the cerebellopontine angle, multiple sclerosis, and coma. It can also be used for newborn hearing screening and evaluating stroke and tuberculous meningitis patients.
Presurgical Evaluation Of Intractable EpilepsyNeurologyKota
The document discusses the presurgical evaluation of patients with intractable epilepsy. It describes how the goal is to localize the epileptogenic zone and assess risk to functions. Various tests are used to define zones like the ictal onset zone and irritative zone. Imaging like MRI, PET, SPECT and other tests help localize the epileptogenic lesion and functional deficits. Comprehensive presurgical evaluation including neuropsychological testing is needed to determine surgical candidacy and plan appropriate treatment.
VEP and BAEP testing provide information about the integrity of the visual and auditory pathways.
VEP uses patterned visual stimulation to assess the visual pathway from the retina to the visual cortex. Unpatterned stimulation can also be used when a patient cannot cooperate. Technical factors like luminance, contrast and check size can affect VEP results. Abnormal VEPs may indicate lesions along the visual pathway.
BAEP assesses the auditory brainstem pathways by recording electrical responses to click or tone stimuli. Waves I-V represent activity in successive portions of the brainstem. Technical factors like stimulus intensity, rate and polarity affect BAEP results. Abnormal latencies or absent waves can localize lesions in
The presentation includes physiological mechanism of different functional classes of eye movements such as horizontal & vertical eye movements, saccades, persuits, vestibuloocular reflex, Bell's phenomenon and it also includes different disorders that causes abnormal supranuclear eye movements e.g. skew deviation, Perinaud syndrome, INO.
This document discusses electrodiagnostic criteria for Guillain-Barré syndrome (GBS) subtypes acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). It reviews the evolution of criteria sets over time, including those proposed by Asbury, Albers, Cornblath, Ho, Hadden, and others. Key findings include that early electrodiagnosis can be difficult, with reversible conduction failure in AMAN sometimes mimicking AIDP. Serial nerve conduction studies are important for distinguishing subtypes and determining prognosis, as features may change over time. The document also discusses pathological mechanisms and involvement of sensory fibers.
This document provides a summary of a presentation on electrodiagnosis and somatosensory evoked potentials (SEPs). It discusses the historical aspects, anatomical basis, nomenclature, instrumentation, waveforms, techniques, and clinical usage of SEPs. Specific topics covered include electrode placement, stimulus parameters, montages for upper and lower limb SEPs, waveform characteristics, factors affecting SEPs such as age, medication, and temperature.
This document discusses various types of EEG artifacts including physiological artifacts generated by the body and extraphysiological artifacts from external equipment or environment. It describes common artifacts like cardiac, electrode, eye blink, muscle activity and their characteristic appearances on EEG. The key is to ensure good preparation, electrode placement and monitoring for artifacts during EEG recording to obtain clean data for accurate interpretation.
This document describes several benign EEG variants that can have an epileptiform appearance but are not epileptogenic. It discusses characteristics of alpha variants, mu rhythm, lambda waves, rhythmic mid-temporal theta discharges, wicket spikes, subclinical rhythmic electroencephalographic discharges of adults, phantom spike-wave discharges, and small sharp spikes. These benign variants can occur during drowsiness and light sleep and are seen in specific electrode sites, with features like attenuation with eye opening or movement in the case of mu rhythm. Accurate identification requires training to distinguish them from true epileptiform discharges.
The document summarizes testing of the autonomic nervous system, including the sympathetic and parasympathetic divisions. It describes several tests used to evaluate autonomic function clinically, including heart rate variability tests like deep breathing and Valsalva maneuver, as well as sympathetic skin response testing. Preparation of patients and protocols for each test are provided. The tests can help diagnose autonomic dysfunction and define its severity and distribution.
The document summarizes the stages of sleep as assessed by polysomnography. It describes the key EEG patterns, eye movements, and muscle activity that characterize each stage:
Stage 1 is characterized by low voltage mixed frequency EEG activity, vertex sharp waves, and slow eye movements. Stage 2 involves sleep spindles and K complexes in the EEG along with occasional slow eye movements. Stage 3 contains 20-50% slow wave activity in the EEG. REM sleep involves rapid eye movements and EEG desynchronization resembling wakefulness, along with muscle atonia. The stages cycle throughout the night in a progression from light to deep sleep and back to light sleep.
This document provides an overview of auditory and visual evoked potentials. It discusses brainstem auditory evoked potentials (BAEPs) and visual evoked potentials (VEPs). For VEPs, it describes the visual pathway and how VEPs are recorded and analyzed. Common VEP waveforms like P100 are discussed along with factors that influence VEPs. For BAEPs, it outlines the auditory pathway and describes the waves recorded, including waves I-V. It discusses how BAEPs are measured and clinical applications for both VEPs and BAEPs in evaluating diseases that impact the visual and auditory pathways.
1. Evoked potentials are electrical potentials recorded from the brain following presentation of a stimulus. There are several types including visual, auditory, and somatosensory evoked potentials.
2. Visual evoked potentials assess the visual pathway by recording electrical activity in the brain in response to visual stimuli. Patterns or flashes of light are used to stimulate the retina.
3. Auditory evoked potentials evaluate the auditory pathway by recording brain activity following auditory clicks or tones. This can help detect lesions in the auditory nerve or brainstem.
This document provides information about visual evoked potentials (VEP) and brainstem auditory evoked potentials (BAEP). It describes how VEPs are used to assess the integrity of the visual pathway and are recorded from the scalp in response to visual stimuli. It details the anatomy of the visual pathway and different types of VEPs. It also outlines how to perform VEP testing, interpret the results, and factors that can influence VEPs. For BAEPs, it describes the auditory pathway and waves in the BAEP response. It provides details on performing BAEP testing, interpreting the results, and applications in evaluating neurological conditions.
Saccadic eye movements are fast, conjugate movements that move both eyes quickly in the same direction to bring an object of interest onto the fovea. They have a peak velocity of 30-700 degrees per second and duration of 30-100 milliseconds. The latency between a target appearing and saccade onset is normally 150-250 milliseconds, but can be shorter for "express saccades". Saccades are controlled by burst neurons that generate a pulse to move the eyes rapidly, followed by tonic activity from step neurons to hold the eyes in place against elastic forces. Lesions in different brain regions involved in generating and modulating saccades can cause abnormalities such as slowed saccades, gaze-holding failure,
This document provides guidelines for performing and interpreting somatosensory evoked potentials (SSEPs), which assess sensory nerve conduction in the upper and lower extremities. It describes stimulation and recording procedures, including electrode placement and montages. For upper extremity SSEPs following median nerve stimulation, it identifies the key components N9, N13, P14, N18, and N20 and provides criteria for abnormal findings such as absent waves or prolonged interpeak latencies. For lower extremity SSEPs following posterior tibial nerve stimulation, it identifies the components LP, P31, N34, and P37 and also provides criteria for abnormal findings.
The document discusses the blink reflex, which evaluates the trigeminal and facial cranial nerves. Stimulation of the trigeminal nerve leads to contraction of the orbicularis oculi muscle mediated by the facial nerve. This produces two responses - an early R1 response localized to the stimulated side, and a later R2 response seen bilaterally. Analysis of blink reflex latencies can identify lesions along the afferent trigeminal or efferent facial nerve pathways or in the brainstem. The blink reflex is useful for evaluating various neurological conditions that may affect these cranial nerves or central pathways.
The blink reflex is a disynaptic or multisynaptic reflex that involves the trigeminal and facial nerves. It has two responses - an early ipsilateral R1 response and a late bilateral R2 response. The blink reflex test stimulates the supraorbital nerve branch to evaluate conduction along the trigeminal and facial nerve pathways. Abnormalities in the R1 and R2 responses can localize lesions in different parts of the brainstem or peripheral nerves. The test involves recording electromyography of the orbicularis oculi muscle in response to supraorbital nerve stimulation.
The document summarizes visual evoked potentials (VEPs), including:
- VEPs measure electrophysiological signals from the visual cortex in response to visual stimuli.
- International standards exist for stimulus parameters, recording procedures, and normal values.
- Pattern-reversal VEPs eliciting the P100 wave are most commonly used clinically. Factors like check size, contrast and age affect P100 latency and amplitude.
- Abnormalities suggest defects along the visual pathway from eye to cortex. Multi-channel recordings localize defects pre- or post-chiasm.
This presentation looks at EEG signal generation, pyramidal cells, recording of EEG, source localisation, polarity, analysis of dipole, derivations, montages,
Introduction, history and neurophysiologic basis of vepkalpanabhandari19
1. VEPs measure the electrical activity in the visual cortex generated by light stimulation of the retina. They provide an objective measure of the functional integrity of the visual pathways.
2. VEPs were initially observed in the 1930s but were refined through the development of signal averaging techniques from the 1950s onward.
3. Standard VEP stimulation includes flash, pattern onset/offset, and pattern reversal, with the latter being the preferred clinical technique. Check size, luminance, and reversal rate are standardized.
The document summarizes the process of presurgical evaluation for epilepsy patients. It discusses how modern imaging techniques like video EEG monitoring, high-resolution MRI, fMRI, PET and SPECT are used to localize the epileptogenic zone noninvasively in most patients. When noninvasive methods are insufficient, invasive EEG monitoring using subdural or depth electrodes may be used. The goal is to precisely identify the brain area responsible for seizure generation to allow its surgical resection, while avoiding damage to critical functions. A classical example where surgery is often curative is mesial temporal lobe epilepsy.
This document discusses VEP (visually evoked potential) testing for evaluating the visual pathway from the eye to the brain. It describes how VEP works by measuring the electrical signal from the retina to the visual cortex in response to visual stimuli. Key points covered include the components of the VEP waveforms, how different stimuli test different visual pathways, and examples of how VEP can help evaluate conditions like glaucoma, optic neuritis, and amblyopia. The document also notes how advances in technology have made VEP more widely available in clinical practice.
Brainstem Auditory Evoked Potentials (BAEP) involves recording electrophysiological responses from the ear in response to auditory stimulation to assess the functioning of the auditory pathway. BAEP testing involves placing electrodes on the scalp to record waveforms representing activity in the auditory nerve and brainstem in response to click sounds. BAEP is useful for screening and monitoring conditions affecting the auditory pathway such as tumors near the cerebellopontine angle, multiple sclerosis, and coma. It can also be used for newborn hearing screening and evaluating stroke and tuberculous meningitis patients.
Presurgical Evaluation Of Intractable EpilepsyNeurologyKota
The document discusses the presurgical evaluation of patients with intractable epilepsy. It describes how the goal is to localize the epileptogenic zone and assess risk to functions. Various tests are used to define zones like the ictal onset zone and irritative zone. Imaging like MRI, PET, SPECT and other tests help localize the epileptogenic lesion and functional deficits. Comprehensive presurgical evaluation including neuropsychological testing is needed to determine surgical candidacy and plan appropriate treatment.
VEP and BAEP testing provide information about the integrity of the visual and auditory pathways.
VEP uses patterned visual stimulation to assess the visual pathway from the retina to the visual cortex. Unpatterned stimulation can also be used when a patient cannot cooperate. Technical factors like luminance, contrast and check size can affect VEP results. Abnormal VEPs may indicate lesions along the visual pathway.
BAEP assesses the auditory brainstem pathways by recording electrical responses to click or tone stimuli. Waves I-V represent activity in successive portions of the brainstem. Technical factors like stimulus intensity, rate and polarity affect BAEP results. Abnormal latencies or absent waves can localize lesions in
The presentation includes physiological mechanism of different functional classes of eye movements such as horizontal & vertical eye movements, saccades, persuits, vestibuloocular reflex, Bell's phenomenon and it also includes different disorders that causes abnormal supranuclear eye movements e.g. skew deviation, Perinaud syndrome, INO.
This document discusses electrodiagnostic criteria for Guillain-Barré syndrome (GBS) subtypes acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). It reviews the evolution of criteria sets over time, including those proposed by Asbury, Albers, Cornblath, Ho, Hadden, and others. Key findings include that early electrodiagnosis can be difficult, with reversible conduction failure in AMAN sometimes mimicking AIDP. Serial nerve conduction studies are important for distinguishing subtypes and determining prognosis, as features may change over time. The document also discusses pathological mechanisms and involvement of sensory fibers.
This document provides a summary of a presentation on electrodiagnosis and somatosensory evoked potentials (SEPs). It discusses the historical aspects, anatomical basis, nomenclature, instrumentation, waveforms, techniques, and clinical usage of SEPs. Specific topics covered include electrode placement, stimulus parameters, montages for upper and lower limb SEPs, waveform characteristics, factors affecting SEPs such as age, medication, and temperature.
This document discusses various types of EEG artifacts including physiological artifacts generated by the body and extraphysiological artifacts from external equipment or environment. It describes common artifacts like cardiac, electrode, eye blink, muscle activity and their characteristic appearances on EEG. The key is to ensure good preparation, electrode placement and monitoring for artifacts during EEG recording to obtain clean data for accurate interpretation.
This document describes several benign EEG variants that can have an epileptiform appearance but are not epileptogenic. It discusses characteristics of alpha variants, mu rhythm, lambda waves, rhythmic mid-temporal theta discharges, wicket spikes, subclinical rhythmic electroencephalographic discharges of adults, phantom spike-wave discharges, and small sharp spikes. These benign variants can occur during drowsiness and light sleep and are seen in specific electrode sites, with features like attenuation with eye opening or movement in the case of mu rhythm. Accurate identification requires training to distinguish them from true epileptiform discharges.
The document summarizes testing of the autonomic nervous system, including the sympathetic and parasympathetic divisions. It describes several tests used to evaluate autonomic function clinically, including heart rate variability tests like deep breathing and Valsalva maneuver, as well as sympathetic skin response testing. Preparation of patients and protocols for each test are provided. The tests can help diagnose autonomic dysfunction and define its severity and distribution.
The document summarizes the stages of sleep as assessed by polysomnography. It describes the key EEG patterns, eye movements, and muscle activity that characterize each stage:
Stage 1 is characterized by low voltage mixed frequency EEG activity, vertex sharp waves, and slow eye movements. Stage 2 involves sleep spindles and K complexes in the EEG along with occasional slow eye movements. Stage 3 contains 20-50% slow wave activity in the EEG. REM sleep involves rapid eye movements and EEG desynchronization resembling wakefulness, along with muscle atonia. The stages cycle throughout the night in a progression from light to deep sleep and back to light sleep.
This document provides an overview of auditory and visual evoked potentials. It discusses brainstem auditory evoked potentials (BAEPs) and visual evoked potentials (VEPs). For VEPs, it describes the visual pathway and how VEPs are recorded and analyzed. Common VEP waveforms like P100 are discussed along with factors that influence VEPs. For BAEPs, it outlines the auditory pathway and describes the waves recorded, including waves I-V. It discusses how BAEPs are measured and clinical applications for both VEPs and BAEPs in evaluating diseases that impact the visual and auditory pathways.
1. Evoked potentials are electrical potentials recorded from the brain following presentation of a stimulus. There are several types including visual, auditory, and somatosensory evoked potentials.
2. Visual evoked potentials assess the visual pathway by recording electrical activity in the brain in response to visual stimuli. Patterns or flashes of light are used to stimulate the retina.
3. Auditory evoked potentials evaluate the auditory pathway by recording brain activity following auditory clicks or tones. This can help detect lesions in the auditory nerve or brainstem.
Dorso-Lateral Geniculate Nucleus and Parallel ProcessingGauriSShrestha
The document summarizes the parallel visual pathways from the retina to the cortex. It discusses:
1) 90% of retinal ganglion cell axons project to the dorsal lateral geniculate nucleus (dLGN) in the thalamus, which relays signals to the primary visual cortex.
2) The remaining 10% project to other midbrain structures like the superior colliculus for visual reflexes and the pulvinar for attention.
3) The dLGN is laminated and retinotopically organized. It contains magnocellular and parvocellular layers that provide parallel processing of visual information to the cortex.
The retina contains photoreceptor cells that convert light into neural signals. These signals are processed in the retina and transmitted to the lateral geniculate nucleus and primary visual cortex via two main pathways - the parvocellular and magnocellular pathways. The parvocellular pathway is involved in processing color and spatial detail, while the magnocellular pathway processes motion. In the primary visual cortex, neurons respond selectively to visual features like orientation, direction of motion, and binocular disparity. Higher visual areas become specialized for functions like color perception in V4 and motion processing in V5.
MACULAR FUNCTION TEST PRESENTATION VERY IMPVidhiMadrecha
The macular function test is very important test... To understand the maula dis function and amount of disfunction. It is very useful for Central and colour vision.
This document provides information on pupillary anatomy, physiology, and examination. It discusses the normal anatomy and functions of the pupil. It describes how to perform a systematic pupillary examination, including testing the light reflex and near reflex. It covers common and uncommon disorders that can be diagnosed based on pupillary examination findings, such as Horner's syndrome and Adie's tonic pupil. The document emphasizes that the pupillary examination can provide useful clues about underlying ocular and neurological conditions.
The VEP test assesses the visual pathway from the retina to the occipital cortex by recording electrical potentials generated in the cortex in response to visual stimulation. Abnormalities in the VEP waveform such as a delayed P100 peak can indicate disorders of the anterior visual pathway like optic nerve damage from conditions including MS, optic neuritis, or tumors. The VEP is useful for testing optic nerve function but less so for lesions behind the optic chiasm where MRI is more informative.
This document discusses the pupillary pathways and various abnormal pupillary reactions that can provide diagnostic clues. It describes the innervation and pathways for both the parasympathetic pupillary constrictor and sympathetic pupillary dilator. Various reflexes like the light reflex, accommodation reflex, and near reflex pathways are outlined. Abnormal pupillary reactions like RAPD, Marcus Gunn pupil, Argyll Robertson pupil, Horner's syndrome, Adie's tonic pupil, and pupils in third nerve palsy and diabetes are also described.
1. The pupil is a circular opening located in the center of the iris that regulates the amount of light entering the eye.
2. Pupil size and reaction are controlled by two sets of muscles - the sphincter pupillae constricts the pupil in response to light, and the dilator pupillae dilates the pupil under sympathetic stimulation.
3. Abnormalities in pupil size, shape, reaction to light and near response can indicate underlying pathologies affecting the complex neurological pathways and muscles that control the pupil. Assessment of pupillary reflexes is important for localizing lesions in the afferent visual pathways or efferent autonomic pathways.
The retina contains light-sensitive photoreceptor cells that absorb light and convert it into neural signals. Rods function better in low light and mediate peripheral and night vision, while cones require brighter light and help with color vision and central vision. Photoreceptors transmit signals through a series of inner retinal neurons to the optic nerve. The retina has different cell distributions and functions in different areas, with the high-acuity fovea containing only cones. Electroretinography tests evaluate the retina's response to light stimuli and help diagnose retinal diseases and conditions.
This document provides information on neuro-ophthalmology and the anatomy and pathways related to vision. Some key points:
- The eyes are intimately related to the brain and can provide clues to central nervous system disorders. Cranial nerves III, IV, VI control extraocular muscles, while V and VII are also involved in ocular function.
- The optic nerve has three portions - orbital, intraosseous, and intracranial. It is surrounded by three meningeal sheaths and carries both visual and pupillary fibers from the retina to the brain.
- The visual pathway involves the optic nerve, optic chiasm, optic tract, lateral geniculate body, optic radiation, and
This document provides information on neuro-ophthalmology and the anatomy and pathways related to vision. It discusses:
- The relationship between the eyes and brain and how eye disorders can provide clues to central nervous system conditions.
- The anatomy of the optic nerve, its portions and sheaths, as well as lesions that can occur along the visual pathway from the eyes to the brain.
- Pupillary pathways involved in the light reflex and near reflex.
- Various optic neuropathies, papilledema, optic nerve disorders like optic neuritis and anterior ischemic optic neuropathy.
- Conditions that can affect cranial nerves like multiple sclerosis, internuclear ophthalmoplegia and orbital synd
Traumatic optic neuropathy occurs when the optic nerve is injured from blunt force trauma anywhere along its path. While high-dose steroids and optic canal decompression surgery have been used as treatments, the evidence for their efficacy is limited. For non-transected injuries, observation is typically recommended, as primary damage to the optic nerve fibers is often permanent. Effective treatment options are extremely limited, and patients should be informed of the uncertainties regarding any proposed interventions.
EEG measures the electrical activity of the brain through electrodes placed on the scalp. It can detect different wave patterns associated with different brain states. Evoked potentials involve stimulating a sensory pathway and measuring the electrical response along the pathway. This allows localization of lesions. Somatosensory evoked potentials involve stimulating a peripheral nerve like the median nerve and measuring the response along the pathway to detect spinal cord or brain injuries. Auditory evoked potentials involve measuring the brainstem response to a click stimulus to detect acoustic neuromas or other posterior fossa lesions. Both evoked potentials and EMG monitoring are used during surgery to detect injuries.
High-intensity LEDs are embedded in the flash stimulation pad
The small disc shape and silicone properties of the pad make it both flexible and lightweight
Illuminance can be set up to 20,000 lux, and different light emission times and cycles can be chosen.
A common system for placing electrodes is the “10-20 International System” which is based on measurements of head size (Jasper, 1958).
The mid-occipital electrode location (OZ) is on the midline.
The distance above the inion calculated as 10 % of the distance between the inion and nasion, which is 3-4 cm in most adults
Lateral occipital electrodes are a similar distance off the midline.
To have reliable VEPs, Intraoperatively, the following factors are important
Maintaining normal intraoperative physiological/hemodynamic parameters
Use of TIVA instead of inhalational anesthesia
Better stimulus delivery methods
Recording intraoperative ERG to ensure good retinal stimulation and
Employing optimal recording parameters
This document discusses epilepsy and anaesthesia. It provides definitions of seizures and epilepsy. It then discusses various factors that influence neuronal excitability like intrinsic factors related to ion channels and extrinsic factors like ion concentrations and synaptic remodeling. It explains the mechanisms of seizure initiation and propagation. It discusses the effects of various anaesthetic agents like inhalational agents, opioids, IV agents and local anaesthetics on seizures. It provides guidelines on perioperative management of anti-epileptic drugs. It also discusses status epilepticus, its treatment and refractory status epilepticus. The document concludes by covering various aspects of presurgical evaluation of epilepsy patients like neuroimaging, EEG, video-EEG, neuropsychological testing and WADA test
Evoked potentials are low amplitude electrical potentials recorded from the brain or peripheral nerves in response to sensory stimuli. They are used to evaluate the function of sensory and motor pathways. There are several types including sensory evoked potentials from visual, auditory and somatosensory stimulation as well as motor evoked potentials. Recording techniques involve signal averaging to detect the low amplitude signals. Evoked potentials provide objective measures for diagnosing various neurological disorders.
The document provides an overview of the pupillary pathway, including its anatomy, physiology, and clinical aspects. It describes:
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- Clinical tests to evaluate the pupillary light reflex, including for anisocoria, RAPD, and other defects.
- Causes and features of different types of pupillary defects affecting the afferent pathway (e.g. optic nerve lesions) or efferent pathway (e.g. Horner's syndrome, Adie's tonic pupil).
1. Vestibular schwannoma, also known as acoustic neuroma, is a benign tumor that arises from the vestibular nerve in the cerebellopontine angle region.
2. It is the most common tumor in this region, constituting 80% of cerebellopontine angle tumors.
3. Symptoms often include progressive hearing loss, tinnitus, and difficulty understanding speech. Cranial nerves 5, 7, 9 and 10 can also be involved.
low birth weight presentation. Low birth weight (LBW) infant is defined as the one whose birth weight is less than 2500g irrespective of their gestational age. Premature birth and low birth weight(LBW) is still a serious problem in newborn. Causing high morbidity and mortality rate worldwide. The nursing care provide to low birth weight babies is crucial in promoting their overall health and development. Through careful assessment, diagnosis,, planning, and evaluation plays a vital role in ensuring these vulnerable infants receive the specialize care they need. In India every third of the infant weight less than 2500g.
Birth period, socioeconomical status, nutritional and intrauterine environment are the factors influencing low birth weight
DECLARATION OF HELSINKI - History and principlesanaghabharat01
This SlideShare presentation provides a comprehensive overview of the Declaration of Helsinki, a foundational document outlining ethical guidelines for conducting medical research involving human subjects.
Lecture 6 -- Memory 2015.pptlearning occurs when a stimulus (unconditioned st...AyushGadhvi1
learning occurs when a stimulus (unconditioned stimulus) eliciting a response (unconditioned response) • is paired with another stimulus (conditioned stimulus)
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
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These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
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Osvaldo Bernardo Muchanga
Gastrointestinal Infections
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Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
Among gastric problems, we have GASTRITIS AND GASTRIC ULCERS as the main public health problems. Gastritis and gastric ulcers normally result from inflammation and corrosion of the walls of the stomach (gastric mucosa) and are generally associated (caused) by the bacterium Helicobacter pylor, which, according to the literature, this bacterium settles on these walls (of the stomach) and starts to release urease that ends up altering the normal pH of the stomach (acid), which leads to inflammation and corrosion of the mucous membranes and consequent gastritis or ulcers, respectively.
In addition to bacterial infections, gastritis and gastric ulcers are associated with several factors, with emphasis on prolonged fasting, chemical substances including drugs, alcohol, foods with strong seasonings including chilli, which ends up causing inflammation of the stomach walls and/or corrosion. of the same, resulting in the appearance of wounds and consequent gastritis or ulcers, respectively.
Among patients with gastritis and/or ulcers, one of the dilemmas is associated with the foods to consume in order to minimize the sensation of pain and discomfort.
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdfrightmanforbloodline
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
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The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
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5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
2. • Evoked Potentials (EP) - electrical signals generated by
the nervous system in response to sensory stimuli.
• VEP - Electrical potential differences recorded from the
Scalp in response to visual stimuli.
3. • Only means available for Objective assessment of visual
function, especially of Retina (ERG) and Optic Nerve (VEP).
• Requires less active participation of the patient - than the
subjective evaluations of perimetry and visual acuity testing.
• Discriminating disease of retina vs optic nerve
• Distinguishing types of injuries of ON, glaucoma,
inflammatory, metabolic
• Useful in monitoring conditions like MS
4. CLINICAL POINT
Ganglion cell layer
Nerve fiber layer
Inner plexiform layer
Inner nuclear layer
Outer plexiform layer
Outer nuclear layer
Photoreceptor layer
Pigment epithelium
Cells
Inner limiting membrane
Axons at surface of retina pass
optic nerve, chiasm, and tract
geniculate body
Ganglion cell
Müller cell (supporting glial ce
Amacrine cell
Bipolar cell
Horizontal cell
Rod
Cone
Pigment cells of choroid
Section through retina
Retinal Layers
14.25 THE RETINA: RETINAL LAYERS
The retina is a tissue-paper-thin piece of CNS tissue that con-
tains the photoreceptors; it is attached to the vascular tunic at
the ora serrata. The layers of the retina in the interior of the
eyeball are oriented from outer to inner. The pigment epithe-
lium is at the outer margin, followed by the outer nuclear layer
(photoreceptors), the inner nuclear layer (bipolar neurons,
amacrine and horizontal cells), and the ganglion cell layer. The
outer and inner plexiform layers are the zones of synaptic
connectivity. The ganglion cell axons form an inner nerve
metric midpoint. The fovea consists purel
vision (photopic); these cone projection
involve very little convergence. In the fove
one-to-one-to-one relationship among
neurons, and ganglion cells. The periphe
ceptors are mainly rods, for night vision
huge convergence of rods onto bipolar neu
converge onto single ganglion cells. T
achieved in the fovea, the region for color
Outer to Inner
X type Retinal GC / Parvocellular Y Type Retinal GC/ Magnocellular
Small axonal diameter Large axonal diameter
Cone Vision Rod Vision
Concentrated in central visual field Wide receptive field, peripheral retina
Low sensitivity in motion High Sensitivity in motion
Central 1 degree of retina -
Cones (peak density)
From the centre of retina
6-8 degrees - Rods (peak
density)
5. • Because signals from the temporal
field of each eye cross at the optic
chiasma
• Patterns appearing in only one
hemifield go entirely to the opposite
occipital lobe.
• With Large field stimulus (full field
stimulation), patterns from both the
hemifields, produce vectors which
ADD up to produce VEP Maximum at
occipital midline
6. Left eye Right eye
Chiasm
Chiasm
Prechiasmatic
Postchiasmatic
Optic tract
Optic
nerve
(Optic nerve)
Optic tract
Crossed
(nasal)
fibers
Uncrossed
(temporal)
fibers
Key
Optic radiations
Occipital cortex
Superior
nasal fibers
Superior
Temporal
Nasal
Retinal
fibers
Nasal
Inferior
Temporal
Inferior
nasal fibers
Inferior nasal fibers
decussate in anterior
chiasm and then
project into optic tract
as anterior fibers
Superior view
Optic pathway
(superior view)
with
E.Hatton
2:1
7. Limbic cingulate cortex
Thalamus
Pituitary gland
bes and functional areas
Pons
mental motor cortex
Medulla oblongata
Frontal
Limbic
Primary motor cortex
Parietal
Occipital
Precentral sulcus
Paracentral lobule
Somatosensory association cortex
Corpus callosum
Visual association cortex
Calcarine fissure
Primary visual cortex
Cerebellum
UB
LB
8. A. Lobes and functional areas
Pons
Medulla oblongata
Cereb
8
9
6 4
7
7
23
19
18
17
17
18
31
24
32
32
10
12 25
33
3
1 2
RAIN:
unique architec-
6
6
6
4
3,1,2
3,1,2
3,1,2
22
22
22
41
42
40
40
40
39
39
37
37
37
37
21
20
20
21
5
5
7
7 7
19
19
19
19
19
18
18
18
17
4
4
1909. His numbering of cortical areas is still used as a short-
hand for describing the functional regions of the cortex, par-
ticularly those related to sensory functions. Some overlap
17 - Primary Visual Cortex V1
18 - Secondary Visual Cortex V2
19 - Association Visual Cortex V3, V4, V5
UB
LB
Foveal projection more than peripheral retina - Foveal Magnification
GENERATOR OF VEP - STRIATE AND PERI STRIATE CORTEX
9. VISUALLY EVOKED POTENTIALS BY DONNELL J. CREEL,
https://webvision.med.utah.edu/book/electrophysiology/visually-evoked-potentials/
10. Retina
Alternating
checkerboard
pattern displayed
Optic
nerve
Optic
chiasm
Optic
tract
Lateral geniculate nucleus
Cochlear
Series of
Inferior colliculus
Latency
Amplitude
Latency
Amplitude
Lateral lemniscus
Medial geniculate body
Acoustic area of
temporal lobe cortex
Primary
visual
cortex
P1
N1
I
VI
VII
II III
IV
V
VI
VII
N2
I. Visual Evoked Potential
II. Brainstem Auditory Evoked Potential
Retino - Geniculo - Calcarine pathway
X type Retinal GC Y Type Retinal GC
Small Large
Cone Vision Rod Vision
Concentrated in central visual field Wide receptive field, peripheral retina
Low sensitivity in motion High Sensitivity in motion
PATTERN SHIFT VEP FLASH VEP
RETINO- GENICULO - CALCARINE
PATHWAY
EXTRA GENICULATE PATHWAY
11. X type Retinal GC Y Type Retinal GC
Small Large
Cone Vision Rod Vision
Concentrated in central visual field Wide receptive field, peripheral retina
Low sensitivity in motion High Sensitivity in motion
PATTERN SHIFT VEP (Patterned
Visual Stimuli)
FLASH VEP (Non patterned)
RETINO- GENICULO - CALCARINE PATHWAY EXTRA GENICULATE PATHWAY
Less - Inter & Intra - individual variability More variability
Detects Minor abnormality, More Sensitive &
Accurate
Cannot detect Minor abnormality, Less
Sensitive & Accurate
For those who can’t fixate, Steady State VEP
12.
13. Pre-Test Evaluation
• Explain the procedure, co-operation.
• Avoid Hair Spray or Oil after last hair wash
• Usual glasses, to be Worn during the test
• Ophthalmological Exam results to be reviewed. - Visual
acuity, pupillary diameter, visual field
• Avoid any miotic/ mydriatic drug 12hrs before the test
14. Procedure
• Standard disc EEG electrodes used.
• Skin should be prepared by abrading and degreasing.
• Two Channel vs Four Channel VEP (Electrode Placement)
15. Electrode Placement
2 channel VEP
Channel 1 - Oz - Fz
Channel 2 - Oz - linked ear
4 channel VEP
Channel 1 - Oz - Fz
Channel 2 - Pz - Fz
Channel 3 - L5 - Fz
Channel 4 - R5 - Fz
Impedance < 5 kilo ohms
Oz - actually located at the middle point of Variation Range of Calcarine fissure
12 cm above the nasion
Reference Electrode
Recording Electrode
5 cm above the Inion
16. International 10 - 20 System
• Oz - 3-4cm above inion (10% of
distance between inion and
nation, which is about 3-4 cm in
normal adults)
• Fz - 11cm above nasion
• O1, O2 - 2.5 cm lateral to Oz
• A1 A2 ear
• Cz - ground
Queens Montage
• MO (Mid Occipital) - 5cm above
inion, in midline
• MF (mid frontal) - 12cm above
nasion, in midline
• LO, RO (left right occiptial) - 5cm
left and right of MO
• A1/A2 - ear
• Ground - Vertex
Source - Guidelines on Visual Evoked Potentials,
American Clinical Neurophysiology Society, 2008
17. Transient Pattern
Reversal VEP
• Peak response occurs approximately
50-250 ms after stimulus. By convention
in neurophysiology - Upward - Negative,
Downwards - Positive.
• First negative - N75 (suggested to be
input from Dorsal LGN to the striate
cortex) Lack of consistency in latency, and
are sometimes present / absent
• Second positive - P100 (suggested to be
excitatory outflow of 17 to 18,19/
secondary inhibitory response at 17)
• Third Negative - N145
• Inter ocular latency difference - significant
- 6-10 ms, as they are less variable,
hence more important than the absolute
latency measurements (more variable)
Source - Aminoff’s Electrodiagnosis in Clinical Neurology 6th ed.
18. FIG. 2. PVEP to full-field stimulation shows the rostral—caudal extent of the occipital
components N75, P100, and N 145. These may be maximal above or below the
midoccipital site in normal individuals with a minimal amplitude response as the
midoccipital lead. The frontal N100 component may be recorded widely over the anterior
ad . C c , 30 ; a , .97/ ; ; 256 . Source - Guidelines on Visual Evoked Potentials,
American Clinical Neurophysiology Society, 2008
19. P100 is the most positive peak
• Prolonged P100 - demyelination (in most typical abnormality, all peaks prolonged)
20. • Two primary features - time elapsed since stimulus (latency), magnitude of
deflection from baseline (amplitude)
• Amplitude of P100 is highly variable, therefore it is difficult to establish normal values. Some
labs measure N70 to P100, P100 to N145,
• Depends on state of arousal, and other patient and condition specific factors. Therefore
before labelling abnormal, caution should be exercised
• Constant monitoring is required. Patient should maintain visual fixation, throughout the study.
(vs Malingering pt)
Source - Aminoff’s Electrodiagnosis in Clinical Neurology 6th ed. ,
Clinical Neurophysiology by UK Misra & J Kalita, 3rd ed
21. • Average of 100 - 200 stimuli - one response. With low
amplitudes upto 400 stimuli.
• The values can be compared to the standard normative
data. Peak latencies are more consistent, than amplitudes.
• At least 2 responses to be recorded. The P100 latency
measured in these should be within 2.5 ms difference,
(>6-10ms abnormality), in between - technical
difference.
• Peak to peak amplitude of N75 - P100
22. Kothari R, Bokariya P, Singh S, Singh R. A Comprehensive Review on Methodologies Employed for Visual Evoked
Potentials. Scientifica (Cairo). 2016;2016:9852194. doi:10.1155/2016/9852194
Time period analysed after each stimulus 1/5th to 1/2 a second
Luminance - intensity of light from visible spectrum per unit area traveling in
a given direction, P100 latency increases with decrease of luminance
VEPs are generally recorded under ambient photopic
conditions in a standard, normally illuminated room.
Contrast - luminance difference between two adjacent elements in the visual
scene, Low contrast responses have smaller amplitudes, broader peaks,
prolonged latency
32. • Routine Traditional VEP, done in Pattern Shift,
checkerboard pattern is FULL FIELD STIMULATION.
• That means, the Stimulus varies consistently ACROSS A
LARGE PORTION OF THE VISUAL FIELD.
33. Abberant
waveform
• A VEP waveform is considered
aberrant if it can be recorded
Reproducibly but a P100 peak can
not be identified.
• Many of aberrant responses,
contain too many peaks, rather than
too few.
• W shaped P100 - bifid P100 - when
frontal N100 and occipital P100 are
asynchronous. This is seen only in
frontal or central reference. i.e. Oz-
Fpz / Oz - Pz
• Can be seen normally in Oz - A1
leads. (occipital leads)
• Can be abolished by asking the
patient to look at the upper edge of
the pattern, rather than central.
Normal
Normal
Supernumerary
P175 etc. -
Transient
oscillations of
occipital cortex
34. Walsh P, Kane N, Butler S The clinical role of evoked potentials Journal of Neurology, Neurosurgery & Psychiatry 2005;76:ii16-ii22.
35. Multifocal Transient VEP
• In contrast to full field
stimulation, Multifocal technique
divides the Visual Field into a
fixed number of sectors, each of
which follows its own sequence
of stimulus changes.
• Hence, each sector can have on
of the two states, inverted
checkerboards.
• Smaller check sizes in the centre
for stimulating the macular
vision, larger check sizes in
periphery, to stimulate the
peripheral retinal vision.
• The multifocal VEP demonstrates
equivalent, or superior test
repeatability when compared to
standard automated perimetry.
Source - Aminoff’s Electrodiagnosis in Clinical Neurology 6th ed.
36. Source - Aminoff’s Electrodiagnosis in Clinical Neurology 6th ed.
• The waveforms are usually the same as standard
VEP, but phase reversal takes place at the mid
horizontal meridian, caused by the calcarine fissure
40. a. Full field VEP recording
from Oz - Fpz, 53 yr old
woman, leading to
temporal dispersion
which is difficult to
interpret
b. Multifocal VEP confirms
abnormality by
demonstrating central
amplitude decrement in
left eye (blue)
Source - Aminoff’s
Electrodiagnosis in Clinical
Neurology 6th ed.
41. P100 on standard pattern reversal VEP -
178, 179 normal brain mri
Normal P100 latency on multifocal VEP
Source - Aminoff’s Electrodiagnosis in Clinical Neurology 6th ed.
42. Stimulation Patterns
• Pattern Shift VEP - Checker Board pattern.
• The size of the stimulus, at the retina will depend on its size on the monitor, and
the distance of the subject from the screen.
• The total stimulus size will determine the area of the visual field subject to
stimulation, and check size will impact the neuronal cell population which is
generating the response.
• Hence, larger check sizes, will stimulate more of peripherally located RGCs
• Smaller check sizes, will stimulate more of centrally located RGCs
• But smaller check sizes - have risk of error due to refractive errors. Larger check
sizes, will not produce adequate central field stimulation. (pattern shift VEP)
• IFCN recommends, check size that subtend 24 - 32 minutes of visual arc.
43. W = 380 mm / 8 large squares = 47 mm
B = 57.3 X 47 mm divided by 90 mm
= 30 minutes of visual arc
subtended by both the vertical and horizontal dimensions. The visual angle subtended by
an indi id al elemen f he a e n a he bjec e e i e e ed in ei he min e
degrees of arc. The tangent of the visual angle is equal to the check width divided by the
distance from the eye to the screen.
The angle can therefore be calculated as:
B = arctan W/D
This can be approximated for small angles by the formula:
B= A* W/D
where W is the width of the unit in millimeters, D is the distance from the screen to the
eye in millimeters, and B is the visual angle in minutes of arc when A = 3438 and in
degrees of arc when A = 57.3.
Size of stimulus field. The size of the total stimulus field is specified by the visual angle
i b end a he bjec e e, mea ed a de c ibed ab e f individual pattern units.
Location and designation of stimulus field types. A fixation point must be provided for
the subject that is distinct from the reversing pattern itself. The location of the fixation
in i h ega d he im l field de e mine he egi n f he bjec i al field
to be stimulated. A pattern that extends equally to both sides of the fixation point is
referred to as a full-field stimulus. A pattern restricted to a small region of central vision,
such as 2-4 , with central fixation is designated a central-field stimulus. A pattern
presented to one side of the fixation point in one-half of the visual field, such as right half
or left half, is designated a half-field or hemi-field stimulus. A pattern presented to a
small sector of the visual field is designated a partial-field stimulus, with the location
described relative to the fixation point. Half-field stimuli presented in an alternating
fashion with reversal of left and right half fields sequentially, with a central fixation spot,
are designated alternating half field stimuli.
Whenever half-field or partial-field stimuli are used, the fixation point should be
displaced to the nonstimulated visual field by a small amount, such as 1 check width of
10. This helps prevent stimulation of both retinal hemifields or regions outside the
44. Checkerboard Pattern
with Red Fixation Point
Vertical Grating Pattern Shift Vep
Used when checkerboard pattern
misses trivial defects.
Used. Most Commonly
Simplicity Reliability
Because the primary visual system is arranged to emphasise detection of edges and movement,
shifting patterns with multiple edges and contrasts are the most appropriate way to assess visual
function, rather than bright flashes of unpatterned light.
45. • Stimulus Field Types - Fixation point is provided for the
subject that is distinct from the reversing pattern itself.
1. Full field stimulation
2. Central field stimulation
3. Partial field stimulation (not yet useful in clinical
practice)
4. Alternating half field stimulation (not yet useful in
clinical practice)
Anterior to chiasma
Posterior to chiasma
46. Full Field Stimulation
Left eye Right eye
Chiasm
Chiasm
Prechiasmatic
Postchiasmatic
Optic tract
Optic
nerve
(Optic nerve)
Optic tract
Crossed
(nasal)
fibers
Uncrossed
(temporal)
fibers
Key
Optic radiations
Occipital cortex
Superior
nasal fibers
Superior
Temporal
Nasal
Retinal
fibers
Nasal
Inferior
Temporal
Inferior
nasal fibers
Inferior nasal fibers
decussate in anterior
chiasm and then
project into optic tract
as anterior fibers
Superior view
Optic pathway
(superior view)
with
E.Hatton
• Most sensitive in detecting visual system Anterior
to Optic Chiasma
• Majority of P100 responses arise in neural
elements of the eye subserving the central 8-10
degrees of the visual field.
• Lesions that produce half or partial visual field
deficits but that spare much of central vision will
usually not produce significant changes in P100
response latency or amplitude. Such partial lesions
in prechiasmal, postchiasmal, or chiasmal
locations may produce changes in response
topography, but are best tested for using partial
visual field stimulation
Performed Mono-ocularly
Visual Fixation should be centre of the screen (red
dot)
47. Flash VEP
• More variable than pattern
VEPs across subjects, but
are usually quite similar
between eyes of an
individual subject.
• Multiple positive and
negative peaks.
• Source - extra geniculate
pathway
• Great variability, limits their
utility, as it is difficult to
differentiate between
normal and abnormal
• Hence, American Clinical
Neurophysiology society
has advised that ONLY
COMPLETE ABSENCE OF
A FLASH RESPONSE CAN
BE CONSIDERED
DEFINITELY ABNORMAL.
48. •They are useful for patients who are unable or unwilling to
cooperate for pattern VEPs, and when optical factors
such as media opacities prevent the valid use of pattern
stimuli, INFANTS
•Provide rudimentary information, only that the visual
information is reaching the brain.
•Can be done with both eyes closed
•Can be done with opacity of the media
•Not affected by refractive errors
•Preservation of response of FVEP suggests that visual
pathways are at least partially intact, absence indicates
no useful visual function.
•Asymmetry of FVEP may occur at site of structural
lesions.
49. • The VEP to flash stimulation consists of a series of negative and
positive waves. The earliest detectable component has a peak time
of approximately 30 ms poststimulus and components are
recordable with peak latencies of up to 300 ms. Peaks are
designated as negative and positive in a numerical sequence.
• This nomenclature is recommended to differentiate the flash VEP
from the pattern-reversal VEP. The most robust components of the
flash VEP are the N2 and P2 peaks. Measurements of P2 amplitude
should be made from the positive P2 peak at around 120 ms to the
preceding N2 negative peak at around 90 ms.
• Flash rate - 1 HZ
Note that with a
e is recorded Fig. 4 A normal flash VEP
123
50. Note that with a
e is recorded Fig. 4 A normal flash VEP
123
124
124
130
130
90
90
51. cs often make it difficult to compare specific response components betwe
ubjects.
ash VEP to LED goggle stimulation. Response waveforms may be quite
tency and amplitude abnormalities must be interpreted with caution (see
52.
53.
54. Stimulation of half of the field gives rise to stimulation of
contralateral occipital cortex
P100 to be expected to be prolonged on the opposite to side of
hemi field stimulation
Walsh P, Kane N, Butler S The clinical role of evoked
potentials Journal of Neurology, Neurosurgery &
Psychiatry 2005;76:ii16-ii22.
55. Pattern Onset/Offset VEP
Blocks of black and white appear and disappear, followed by plain gray background.
Without decrease in luminance
• greater inter-subject variability than pattern-reversal VEPs.
• Effective for detection or confirmation of malingering
• evaluation of patients with nystagmus
• as the technique is less sensitive to confounding factors such as poor fixation, eye
movements or deliberate defocus.
• Standard VEPs to pattern onset/offset stimulation typically consists of three main
peaks in adults; C1 (positive, approximately 75 ms), C2 (negative, approximately 125
ms), and C3 (positive, approximately 150 ms). Amplitudes are measured from the
preceding peak.
mately 150 ms) (see Fig. 3). Amplitudes are mea-
sured from the preceding peak.
comparison of amplitud
the sensitivity of the V
Fig. 3 A normal pattern onset/offset VEP. Note that with a
300 ms sweep only the pattern onset response is recorded Fig. 4 A normal flash VEP
56. • Stimulation rate - 4-8 Hz
• The responses overlap each other, and
appear as sinusoidal wave form, which
persist during the period of stimulation.
• Also known as Repetitive Evoked
Potentials.
• Repetitive evoked potentials whose
constituent discrete frequency
components remain constant in
amplitude and phase over an infinitely
long time period.
• Children
Source - Clinical Neurophysiology by UK
Misra & J Kalita, 3rd ed
Steady State VEP’s
57. Factors affecting VEP
• Not affected by direction of change of checks in
checkerboard pattern. Horizontal or Vertical
• Size of checks - Smaller check size - largest peak
amplitude, smallest peak latency.
• A person with good visual acuity - produces shortest
latency and largest amp. With Small check size, person
with poor visual acuity - with Large check size.
58. Patient Factors
• Sex - P100 latencies, shorter for women than men
• Age - multifocal VEP latency, increases with age, particularly in men, (@ 2.5
ms/ decade after 5th decade)
• Pupil size - pupil dilatation, will reduce P100 latency, mainly in Full Field
Pattern stimulation and vice versa, not in Full field flash VEP. Standard -
recording with pupils normal. (dilatation - more light, constriction - less light)
Average pupillary constriction of 1.75mm increases average latency by 4.6ms.
• Eye Dominance - Dominant eye - shorter latency, higher amplitude
• Eye Movement - reduced P100 amplitude, Latency not affected. eg.
nystagmus patients
• Body Temp - only in demyelinating lesions, like MS.
• Some studies have shown, P100 latency to decrease when concentrating
more
60. Usefulness
• Disease of anterior optic pathway may produce prolonged
P100 latencies without detectable alteration in Visual
Acuity, Colour Vision, Pupillary Reactivity, Fundoscopy, or
Perimetry.
• If Visual Acuity is decreased, and PVEP is normal, it is
very unlikely that optic nerve or chiasma is the lesion.
61. Diseases
1. Multiple Sclerosis
• Screening for Asymptomatic Lesions in MS is the most
common use. (eg. dissemination in space)
• It has been calculated that a plaque of 1 cm in size , can
lead to P100 delay of about 25 ms.
• Classical pattern - Assymetrical prolongation of P100
latency, with relative preservation of amplitudes.
• No relationship between VEP and Visual Clinical
complaints was found.
62. 2. NMO
• Unrecordable P100 waveform, and reduced amplitude of
P100 have reported to be characteristic unlike prolonged
P100 latency and normal P100 amplitude in MS.
63. 3. Optic Neuritis
• If in Uni Ocular ON, VEP is prolonged only on the affected
side, not on opposite side, lesser chances of it to be MS.
• Optic neuropathy is found in peripheral neuropathies like -
CMT, giant axonal neuropathy, neuropathy associated
with macroglobulinemia
65. Other
Demyelinating diseases like
• Adreno-Leuko dystrophy
• Meta-chromatic Leuko dystrophy
• Hereditary spastic paraparesis
Vitamin B12 deficiency - asymmetric, bilateral prolongation of
P100 latency.
Vitamin E deficiency in patients with Abetalipoproteinemia
66. Optic Neuropathy in HIV patients.
Alcohol, Tobacco
CO poisoning, reduced amplitude and prolonged latency
Ethambutol, Desferoxamine, Quinine
Vigabatrin, Valproate
Amiodarone
67. • Not been found to be useful in Cortical Lesions.
• Abnormal in Optic Nerve Glioma, NF1
68. Compressive lesions affecting VEP
• Papilledema - later stages, when it becomes severe
enough to compress the optic nerve
• Raised ICT, hydrocephalus, pseudotumor cerebri
• Extrinsic compression of the Anterior Chiasmal pathway
results in Loss of amplitude, destruction of wave form,
prolonged P100 latency. (latency prolongation less as
compared to demyelinating disorders).
69. • Most imp. Differential for optic neuritis is retinal disorder -
central serous retinopathy.
• Many patients have been labelled as MS in the past
falsely, due to prolonged VEP, having CSR
• CSR resolves spontaneously.
• PVEP delays can be seen with a variety of other acute
and chronic retinal disorders. Hence, complete
ophthalmological examination is mandatory.
70.
71.
72. Electro Retinogram
• ERG can be recorded from corneal
surface by a contact lens embedded with
a corneal ring electrode, and a
conjunctival reference from periorbital
skin , by small electrodes attached at the
lateral canthi.
• Stimulus - Strobe light, (ganz field -
whole field)
• Cones - shorter refractory period -
therefore a high frequency stimulus can
be used to assess. (30hz)
• Rods - (20hz)
• Typically recorded with patient’s pupils
Dilated after mydriatics
• ERG responses classified negative when
dips below baseline, positive when goes
above.
A - stimulation of photoreceptors (rods and cones) 15ms
B - activation of retinal interneurons from inner nuclear
layer 30-35ms
C wave - retinal pigment epithelium
D wave - OFF bipolar cells
73. • Pattern Reversal ERG can be recorded with alternating
checkerboard stimulus.
• PERG - characterised by negative wave around 50ms N50 and
positive deflection at around 95ms P95
• P95 is thought to reflect the b wave - activation of RGC.
• It was found that in individuals with abnormal VEP, P95 was
prolonged, but P50 was almost always preserved. But in those
with normal VEP, both could be prolonged.
• Hence also distinguishes abnormality between Photoreceptors and
RGCs.