The prognostic value of evoked responses from primary somatosensory and auditory cortex in comatose patients.

OBJECTIVE: To evaluate somatosensory and auditory primary cortices using somatosensory evoked potentials (SEPs) and middle latency auditory evoked potentials (MLAEPs) in the prognosis of return to consciousness in comatose patients. METHODS: SEPs and MLAEPs were recorded in 131 severe comatose patients. Latencies and amplitudes were measured. Coma had been caused by transient cardiac arrest (n=49), traumatic brain injury (n=22), stroke (n=45), complications of neurosurgery (n=12) and encephalitis (n=3). One month after the onset of coma patients were classified as awake, still comatose or dead. Three months after (M3), they were classified into one of the 5 categories of the Glasgow outcome scale (GOS). RESULTS: At M3, 41.2% were dead, 47.3% were conscious (GOS 3-5) and 11.5% had not recovered consciousness. None of the patients in whom somatosensory N20 and auditory Pa were absent did return to consciousness and in the post-anoxic group, reduced cortical amplitude too was always associated with bad outcome. Conversely, N20 and Pa were present, respectively, in 33/69 and 34/69 patients who did not recover. CONCLUSIONS: The prognostic value of SEPs and MLAEPs in comatose patients depends on the cause of coma. Measurement of response amplitudes is informative. Abolition of cortical SEPs and/or cortical MLAEPs precludes post-anoxic comatose patients from returning to consciousness (100% specificity). In any case, the presence of short latency cortical somatosensory or auditory components is not a guarantee for return to consciousness. Late components should then be recorded.

Vestibular-evoked myogenic potentials: a method to assess vestibulo-spinal conduction in multiple sclerosis patients.

Vestibular-evoked myogenic potentials (VEMPs), elicited by acoustic stimulation, have been proposed in the assessment of the vestibulo-cervical reflex pathways. The procedure has been previously validated in several otovestibular disorders. The aim of this study was to investigate patients affected by multiple sclerosis (MS) in the attempt to clarify the underlying physiopathogenetic mechanisms and the clinical utility of VEMPs in detecting vestibulospinal involvement in this disease. VEMPs were obtained according to the technique described by Colebatch and Halmagyi [Neurology 42 (1992) 1635]. We averaged the surface tonic electromyogram from right and left sternocleidomastoid muscle, after bilateral click stimulation (click duration 0.1 ms, repetition rate 3 Hz, intensity 140 dBSPL, 256 stimuli, repeated at least twice). In all cases, we obtained the biphasic, initially positive, p13-n23 wave pattern. P13 peak latency was bilaterally or unilaterally delayed in 8 out of 15 patients (mean delay: 2.2 ms; p < 0.01 on right and <0.05 on left side) and peak-to-peak amplitude significantly reduced (mean amplitude loss: 130 microV; p < 0.01 on right and <0.05 on left side). Their overall diagnostic yield resulted in 60%. In conclusion, the present findings prove that VEMPs are delayed in p13 component and altered in amplitude in MS patients. We hypothesise that these changes might be the result of a conduction impairment in vestibulo-spinal fibres, producing a morphologic alteration of the myogenic responses.

Asymmetric scalp distribution of pattern visual evoked potentials during interictal phases in migraine.

The N70 and P100 components of transient pattern visual evoked potentials (P-VEPs) were measured in migraine patients, with and without aura, and in normal subjects in order to evaluate their latency, amplitude and occipital scalp distribution. The aim was to find any typical electrophysiological abnormalities in migraine. P-VEP N70 and P100 were analyzed in 59 patients without any known visual field defect. Mean latency and amplitude values were within normal ranges for either N70 and P100 all over the occipital scalp; the only significant abnormality we found was related to the absolute right-left amplitude ratio either for N70 and P100 waves, providing an asymmetry in P-VEP scalp distribution; this finding was detected in 78.9% of patients with aura and 72.5% without aura. Our results show that in migraine patients, both P-VEP waves N70 and P100, have an asymmetric topographic distribution, even during interictal phases, that can be explained by a cortical disturbance in agreement with the neural hypothesis of headache.

Effects of grating spatial orientation on visual evoked potentials and contrast sensitivity in multiple sclerosis.

Previous studies suggest a delay of pattern visual evoked potentials (PVEPs) in multiple sclerosis (MS) depending on grating orientation. We examined a group of 14 patients with definite MS recording PVEPs to vertical and horizontal grating and analysing latency and amplitude of P60, N70 and P100 waves. We evaluated contrast sensitivity (CS) to dark and bright bars of several spatial frequencies (SF). The aim was to evaluate the diagnostic value of evoked responses and CS in revealing involvement of cortical structures. PVEPs to 1 degrees cycle/degree (c/d) vertical bars were abnormal in 25% for P60, in 32% for N70 and in 36%, for P100; in 25%, 36% and 42% respectively at 4 c/d; as regards horizontal bars at 1 c/d we found alterations of P60, N70 and P100 in 11%, 19% and 27% respectively; at 4 c/d in 19%, 27%) and 35%. CS resulted more abnormal for vertical grating, with a maximum impairment for 3.7 c/d SF. We may conclude that the use of vertical grating in clinical routine is more reliable both for PVEPs and CS testing; in addition CS can be abnormal even with normal PVEPs: this could mean an early impairment of CS and provide useful indications about a subclinical involvement of visual cortex.

Changes in long-latency reflexes onset latencies across full-wave rectified and non-rectified recordings.

Electrically elicited long-latency reflexes (LLRs) were obtained from thenar muscles by either fully rectified or non-rectified raw recordings in 10 healthy volunteers. The LLR II onset latencies were significantly (P < 0.0001) delayed on rectified (mean +/- SD: 49.8+/-2.9 ms) compared to raw (45.3+/-2.3 ms) recordings, with a mean difference of 4.4 ms. These data show that, according to the recording technique employed, the LLR II onset latencies can change considerably. The possible implications on cortical relay time (CRT) calculation and the understanding of the intracortical connections physiology are discussed.

Impaired ascendant central pathways conduction in impotent diabetic subjects.

OBJECTIVES: Diabetic impotence is generally due to peripheral neuropathy, but a central pathway impairment has also been suggested. We evaluated somatosensory transmission in a group of impotent diabetic men to assess the role of central nervous system (CNS) involvement. MATERIALS AND METHODS: Somatosensory evoked potentials (SEPs) of pudendal (pdn) and posterior tibial (ptn) nerves were recorded in 74 patients. Type and duration of diabetes, severity of sexual dysfunction, medium term metabolic control, occurrence of microangiopathic chronic complications and autonomic neuropathy were evaluated. RESULTS: Our data show an impairment of central conduction times in pdn (25.7%) and ptn (39.2%) greater than peripheral nervous impairment (pdn 12.2%, ptn 8.1%), in impotent diabetic patients without any further major complication. Central nervous conduction delay resulted to be correlated with poor glycemic control. Significant evident autonomic dysfunction was found only in a minority of cases. CONCLUSION: Our data might suggest that altered conduction along CNS and somatic peripheral neuropathy might develop independently. We confirm the hypothesis of a "central diabetic neuropathy" and suggest that central sensory pathways involvement, not related to peripheral impairment, could play a role in the pathogenesis of erectile dysfunction in diabetic patients.

Nasopharyngeal electrode recording of somatosensory evoked potentials as an indicator in brain death.

Median nerve somatosensory evoked potentials were recorded in 28 comatose patients, eight of whom were progressing from coma to eventual brain death and in 11 brain dead patients using electrodes over the scalp, neck and nasopharynx (nasopharyngeal electrode). This recording technique was used to assess the different derivation of brainstem P14 wave activity. It showed that in the midfrontal scalp to the nasopharynx derivation a clear P14 was present in all comatose patients. This component disappeared during the passage from coma to brain death. In a separate group, simultaneous direct recordings in the vicinity of the dorsal column nuclei and with a nasopharyngeal electrode were made in five patients undergoing neurosurgical procedures at the craniocervical junction with the same somatosensory evoked potential monitor. We found that the P14 recorded with the nasopharyngeal electrode in the neurosurgical patients corresponded in latency and morphology with the P14 recorded directly on the surface of the craniocervical junction and more specifically in the vicinity of the nucleus cuneatus. The nasopharyngeal electrode provides non-invasive access to the ventral brainstem at the medullo-pontine level and the disappearance of the P14 shows a clear sign of involvement of the craniocervical junction in brain dead patients. Our study showed that with a simple montage the nasopharyngeal electrode is an effective non-invasive monitor for brainstem activity and can be used as an early diagnostic indicator of brainstem death.