N̄20 and P̄40 somatosensory evoked potentials: Thalamic lesions and subcortical origin

Abstract

– Three patients with well‐defined clinical and radiographic lesions have been studied with somatosensory evoked potentials (SSEPs). The data indicate that the primary scalp potentials from stimulation of both the arm and leg (N̄20 and P̄40) can be lost with thalamic lesions and would be consistent with these potentials being generated in either the thalamus or thalamocortical radiations.

Quantitative assessment of somatosensory-evoked potentials after cardiac arrest in rats: Prognostication of functional outcomes*

“…These observations indicate that burst suppression coma after CA involves abnormal coupling of the thalamic and cortical potentials and that arousal is dependent upon the restoration of the bidirectional thalamocortical coupling. A possible thalamic component of the auditory evoked potential that preceded the cortical response was reported in rats (17). A negative far-field potential that begins around 16 msec preceding N20 in humans is known to be preserved after thalamic lesions and is suggested to originate in the brainstem.…”

“…Thalamocortical pathways are shown to be especially vulnerable to hypoxic-ischemic insults (8) with a higher degree of neuronal cell death and injury in regions of the cortex and thalamus observed both in animals (9–12) and in humans (13–16). A loss of scalp potentials in patients with thalamic lesions has also been reported (17). Injury to the cortical and subcortical structures has been suggested as the cause of comatose states after ischemia (18).…”

Quantitative assessment of somatosensory-evoked potentials after cardiac arrest in rats: Prognostication of functional outcomes*

“…These observations indicate that burst suppression coma after CA involves abnormal coupling of the thalamic and cortical potentials and that arousal is dependent upon the restoration of the bidirectional thalamocortical coupling. A possible thalamic component of the auditory evoked potential that preceded the cortical response was reported in rats (17). A negative far-field potential that begins around 16 msec preceding N20 in humans is known to be preserved after thalamic lesions and is suggested to originate in the brainstem.…”

“…Thalamocortical pathways are shown to be especially vulnerable to hypoxic-ischemic insults (8) with a higher degree of neuronal cell death and injury in regions of the cortex and thalamus observed both in animals (9–12) and in humans (13–16). A loss of scalp potentials in patients with thalamic lesions has also been reported (17). Injury to the cortical and subcortical structures has been suggested as the cause of comatose states after ischemia (18).…”

Frequency dependence of cortical somatosensory evoked response to peripheral nerve stimulation with controlled afferent excitation

“…This can be explained by the nature of the source generator. P40 is thought to be generated by a thalamocortical source [27,29,49,82], because it remains unchanged in cortical lesions [29]. Its latency is mainly known to be affected by thalamic lesions [83] or neurological disorders that affect fiber conduction times (such as multiple sclerosis [84]), which may explain the lack of change in its latency with stimulation frequency.…”

Quantitative assessment of somatosensory-evoked potentials after cardiac arrest in rats: Prognostication of functional outcomes*

“…These observations indicate that burst suppression coma after CA involves abnormal coupling of the thalamic and cortical potentials and that arousal is dependent upon the restoration of the bidirectional thalamocortical coupling. A possible thalamic component of the auditory evoked potential that preceded the cortical response was reported in rats (17). A negative far-field potential that begins around 16 msec preceding N20 in humans is known to be preserved after thalamic lesions and is suggested to originate in the brainstem.…”

“…Thalamocortical pathways are shown to be especially vulnerable to hypoxic-ischemic insults (8) with a higher degree of neuronal cell death and injury in regions of the cortex and thalamus observed both in animals (9–12) and in humans (13–16). A loss of scalp potentials in patients with thalamic lesions has also been reported (17). Injury to the cortical and subcortical structures has been suggested as the cause of comatose states after ischemia (18).…”

Frequency dependence of cortical somatosensory evoked response to peripheral nerve stimulation with controlled afferent excitation

“…This can be explained by the nature of the source generator. P40 is thought to be generated by a thalamocortical source [27,29,49,82], because it remains unchanged in cortical lesions [29]. Its latency is mainly known to be affected by thalamic lesions [83] or neurological disorders that affect fiber conduction times (such as multiple sclerosis [84]), which may explain the lack of change in its latency with stimulation frequency.…”

Quantitative assessment of somatosensory-evoked potentials after cardiac arrest in rats: Prognostication of functional outcomes*

“…These observations indicate that burst suppression coma after CA involves abnormal coupling of the thalamic and cortical potentials and that arousal is dependent upon the restoration of the bidirectional thalamocortical coupling. A possible thalamic component of the auditory evoked potential that preceded the cortical response was reported in rats (17). A negative far-field potential that begins around 16 msec preceding N20 in humans is known to be preserved after thalamic lesions and is suggested to originate in the brainstem.…”

“…Thalamocortical pathways are shown to be especially vulnerable to hypoxic-ischemic insults (8) with a higher degree of neuronal cell death and injury in regions of the cortex and thalamus observed both in animals (9–12) and in humans (13–16). A loss of scalp potentials in patients with thalamic lesions has also been reported (17). Injury to the cortical and subcortical structures has been suggested as the cause of comatose states after ischemia (18).…”

Frequency dependence of cortical somatosensory evoked response to peripheral nerve stimulation with controlled afferent excitation

“…This can be explained by the nature of the source generator. P40 is thought to be generated by a thalamocortical source [27,29,49,82], because it remains unchanged in cortical lesions [29]. Its latency is mainly known to be affected by thalamic lesions [83] or neurological disorders that affect fiber conduction times (such as multiple sclerosis [84]), which may explain the lack of change in its latency with stimulation frequency.…”