Late Auditory Evoked Potentials: A Method for Monitoring Drug Effects on the Central Nervous System

As shown in animal studies, 5HT1B/1D agonists can inhibit activity in the trigeminal nucleus caudalis, which may be advantageous for their antimigraine effect. To demonstrate a possible central nervous system (CNS) action of these compounds in man we studied their effect on the intensity dependence of the cortical auditory evoked potentials (IDAPs), thought to be inversely related to central serotonergic transmission. An amplitude/stimulus intensity function (ASF) slope was computed in healthy volunteers and migraine patients between attacks before and 2 h after oral 311C90 (zolmitriptan “Zomig”) 10 mg ( n=14), 311C90 5 mg ( n=7), sumatriptan 100 mg ( n=14), dexfenfluramine 15 mg ( n=4), lorazepam 1.25 mg ( n=4) and placebo ( n=14). 311C90 10 mg and, to a lesser degree, 5 mg significantly increased the mean ASF slope ( p=0.007 and 0.05 vs placebo). There was a significant positive correlation between plasma levels of 311C90 and ASF slope changes. Sumatriptan and lorazepam had little effect, but dexfenfluramine produced a significant ASF slope decrease. 311C90 is able to modify a CNS activity that is modulated by serotonin, i.e. the IDAP. This effect is probably the consequence of its super or lipophilicity compared to sumatriptan and of activation of prejunctional 5HT1B/1D autoreceptors, which lowers central serotonin release and thus the preactivation level of sensory cortices.

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Visual Evoked Potentials as Potential Biomarkers of Visual Function in Patients with Primary Sjögren’s Syndrome

Journal of Clinical Medicine ◽

10.3390/jcm10184196 ◽

2021 ◽

Vol 10 (18) ◽

pp. 4196

Author(s):

Edyta Dziadkowiak ◽

Agata Sebastian ◽

Malgorzata Wieczorek ◽

Anna Pokryszko-Dragan ◽

Marta Madej ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Evoked Potentials ◽

Visual Evoked Potentials ◽

Visual Pathway ◽

Primary Sjögren’S Syndrome ◽

Implicit Time ◽

Primary Sjogren’S Syndrome ◽

The Central Nervous System ◽

Visual Evoked

Visual evoked potentials (VEP) are changes in potentials that arise in the central nervous system. In the interpretation of the VEP test results, it is assumed that the elongation of the latency time is caused by the demyelination of the nerve fibers, and the axon damage is responsible for the decrease in the amplitude. The observed VEP deviations are not specific for specific diseases, but indicate disturbances in visual conductivity. VEP may play a diagnostic role in the early detection of visual involvement. The aim of the study was the functioning of visual pathway assessment on the basis of visual evoked potentials (VEP) examination, in patients with primary Sjögren’s Syndrome (pSS), without focal symptoms of central nervous system disorder. The effect of disease activity, as assessed by clinical parameters and antibody levels (anti-Ro52, SSA, and SSB), on the central nervous system was also evaluated. Thirty-two consecutive patient with pSS (31 females, 1 male) were included in the study. VEP was performed at baseline, and after 6 (T6) years. Their results were compared longitudinally between the baseline and T6, depending on the duration of the disease and treatment. The immunological activity of pSS was also analyzed. The group of patients showed a significant prolongation of the P100 implicit time (105.5 ± 5.1 vs. 100.6 ± 3.9; p = 0.000) and a significant higher the P100-N145 amplitude (12.3 ± 4.1 vs. 9.4 ± 3.0; p = 0.000). Abnormalities in electrophysiological parameters of VEP at baseline correlated with presentation of anti-Ro52 antibodies and aching joints. At baseline, the P100 implicit time was shorter for the patients with pSS than for those at T6 (105.50 ± 5.1 vs. 109.37 ± 5.67; p = 0.002). pSS patients without CNS involvement presented with dysfunction of visual pathway, as revealed by VEP abnormalities. Relationships were found between VEP parameters and with present of anti-Ro52 antibodies and aching joints. VEP may be a useful method for assessment and monitoring of subclinical visual deficit in the course of pSS.

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