Ovidiu C. Banea, Halldór Skúlasson, Ingvar H. Ólafsson, Aron D. Jónasson and Eysteinn Ívarsson
52 y.o. with meningocele.
MEP with direct cortical stimulation (560 V to the left and 890 V to the right) with train of five from C1-C2 and C3-C4 to:
- Right EDC, APB, TA, AH
- Left APB, TA, AH
SSEP were performed from lower tibialis nerve and recorded to FpZ-Cz´ and from median nerves to Fpz-C3´ and Fpz-C4´. Both were controlled at popliteal fossa level (TN) and spinal C7 (TN and MN).
D wave was obtained rotral and caudal to the defect with D-wave electrodes after stimulation at 1Hz continuously (199V)
TOF was used from rioght median nerve to right APB. was 100-99% during the entire surgery.
EEG was analized from C4´-Fpz and Fpz-C3´channels.
At the beginning of the surgery MEP was obtained in the upper limbs and left lower limb muscles. Right AH muscle was very difficult to elicit with 890 V, while TA in the right side was not obtained. At the end of the surgery the MEP were similar with those obtained at the beginning.
SSEP showed normal latencies during all the procedure. At the middle of the surgery, SSEP from right TN decreased 10-20% in amplitude. Rapidly we confirmed the decreased TA when asked the anaesthesiologist. After 5 minutes the SSEP recovered baseline values.
D-Wave was unchanged during all the spine manipulations and the defect corrective procedures.
The IONM was successful and all modalities showed normal evolution. We do not expect sensory or motor new neurological deficits.
On 11th of August 2018 VAFO project started officially with the first healthy subject data acquirement in the Icelandic Center for Neurophysiology, Department of Biomedical Engineering, Reykjavik University.
Valerio Gargiulo, Fabio Barollo, Eysteinn Ívarsson and Martin Freiler
Dr Sigurjón Stefánsson gave us important insights on methodology of P50 and P300.
Continuous averaging is still a desired EEG system option to avoid artifacts during recordings.
A team of young researchers leaded by biomedical engineer Dr Paolo Gargiulo, from Reykjavík University, Department of Biomedical Engineering performed successfully the first data acquiring for a healthy subject recording P300, P50 and dense array 256-channel EEG.
P300 was first used in Iceland by Sigurjón B. Stefánsson and Anna L. Möller since the nineties.
Scientific data was published in 1995 and 2001 and 2005.
In July 2017 P300 returned to Iceland in Clinical Neurophysiology Unit of Landspitali (here).
P50 was acquired first time in patient with tinnitus on 20th of February 2018 in a paired-stimulus
or conditioning-testing paradigm, (S1, conditioning click; S2, testing click; 500 ms inter-click interval; 10,000 ms inter-pair interval). This was a trial of 30 paired stimulus with sensory gating with stimulus in the left and observed from Cz-A2 (right cortex) and with absent wave and response from the left Cz-A1 channel when stimulus was applied for the right ear.
Today the team formed by:
Viktor Díar Jónasson, Clinical Psychology master student at the Department of Psychology, Reykjavik University
Fabio Barrolo, PhD student at Reykjavik University Iceland / Aston University, Birmingham, UK, Biomedical Engineering
Valerio Gargiulo, Research assistant at the Icelandic Center for Neurophysiology, legal advisor and EEG technologist at Department of Biomedical Engineering, Reykjavík University
Eysteinn Ívarsson, Psychologist and technologist at Clinical Neurophysiology Unit, National University Hospital of Iceland
Ovidiu Banea, PhD student at Reykjavík University, Department of Biomedical Engineering and Clinical Neurophysiologist MD at National University Hospital of Iceland
performed both P300 and P50 acquisition with dense array 256 channel EEG system at the Icelandic Center for Neurophysiology, Department of Biomedical Engineering, Reykjavík University
Two days ago a BBC news announce that the computer generated word "Laurel" produced an internet debate if this is heard as "laurel" or "yanny".
The sound specialists run to explain how the humans are losing the higher frequencies listening ability with the age and this why we might listen the world with lower frequencies as is would be "laurel".
I was listening the playback and for two days since the Head of Neurology Department and one colleague told me the story and the new internet debate news, I always had listen the "yanny" word.
30 minutes ago I started to listen "laurel" word.
Yes, I know the word was created by computer and is an artificial voice the human cannot reproduce. The sounds are fake and the frequency differences are very difficult to assess by a computer voice generator. I remember the applications when you press a word text and suddenly you could listen it. This happened more than 6-7 years ago. There was no tonality, no stops or pause between words, no comma. You had to do everything.
But what happened to me? Why did I hear "laurel".
I did something before changes occurred. And I said to me, yes.
The gabaergic neurons from my cortex are weaker (the inhibitory mechanisms of my cortex were diminished by the substance intake) and the sub-cortical areas and temporal lobe auditory cortex or let us say the auditory biological neural network is now a little bit more "awake" and can hear the lower frequency. Or the higher frequencies are perceived with more glutamatergic (excitatory neurons) mechanisms? Is this known? Ono et al 2017 found that responses to pure tones of both inhibitory and excitatory classes of neurons were similar in their thresholds, response latencies, rate-level functions, and frequency tuning, but GABAergic neurons may have higher spontaneous firing rates.
The auditory phantom perception biological neural network (BNN)
involved in the subjective tinnitus perception
The debate is easy: We are in front of unknown auditory perception mechanisms of a fake *artificial* sound. It seems that all is in our brain and that the gabaergic inhibitory mechanisms are involved. As much as you approach the freedom of the deeper brain structures (by forming gaps in the cortex "analytical" system) you will listen differently the word.
Results: All modalities could be performed with exception of blink
reflex which was not elicited.
Incidents: At the end of the surgery we observed decrement of right
facialis (Orbicular oris muscle), CoMEP
decrement of more than 80% which did not recover throughout the rest of the
surgery. Surgeons explained that "there was a bleeding around the
nerve". They started cooling,irrigate and "treat" the lesion.Mapping showed also partial decrement, but
recovered after 20 minutes when stimulation was performed proximally.
Our protocol for corticobulbar
MEP was double train: 1st train formed by 5 stimuli with 50 ms duration (ISI
2ms), 2nd train (single pulse 50 ms)ITI
(inter-train interval) 40 ms.
LIMIT: The assessment was possible for the right Orbicularis oris muscle and slightly for
the right Orbicularis oculi muscle.
No responses were obtained from the left muscles (we didn´t increase the
stimulus intensity to look for the better Threshold-level ) and we consider the
absence of other muscle MEP ipsilaterally (e.g. mentalis) as a serious limit of
Right Orbicularis oris
Corticogeniculate MEP decrement
Mapping with 0,3 mA baseline
Mapping with 0,86 mA (after the decrement was seen in CoMEP)
modalities with exception ofCoMEP
showed similar findings at the end as at the beginning of the surgery. R1
(Trigeminofacial reflex) was not possible to elicit during this surgery.
was useful to drive the surgery moments before debulking and after the surgical
removal of the tumor.We expect partial
facial nerve dysfunction (temporary deficit) in the right side.
after surgery, the patient showed 60% function of facial nerve preserved, Grade
III (of VI) on House-Brackmann. Other VIII, IX and XII monitored cranial nerves
didn´t show deficit 24 h after the surgery.
as a measure of corticogeniculate motor tracts with different and variable
assessment protocols should be considered as mandatory when trigeminofacial
reflex (R1) cannot be monitored and the interpretation of the amplitude loss
should be verified with anesthesist, neurosurgeons and with T-L technique
(Calancie B, 2017).
Neuromonitoring of CPA mass by Alba León Jorba & Ovidiu C. Banea (Oct 2014 IMGB)
Questions for TMS research scientific community in Denmark
From November 22nd to November 24th 2017, Danish Research Center for Magnetic Resonance (DRCMR) will host a new TMS workshopwith special focus on multimodal combinations of TMS with other neuroimaging techniques (EEG-TMS, fMRI-TMS).
DRCMR is located in Hvidovre Hospital, a university hospital located at 9 km from Copenhagen which is administered by the Capital Region of Denmark.
Neurophysiology Plus will be represented at this meeting but also during the 20th to 22nd period for a better understanding of the center facilities, protocols used and technical equipment.
We look mostly to have a valuable and critical analysis input from the team leaded by Prof Dr Hartwig Roman Siebner on the Icelandic proposed study.
In this proposed clinical applied research project members of Neurophysiology Unit and Neurosurgery department from Reykjavik University and National University Hospital of Iceland are trying to analyze if TMS-EEG modality can be used or not to assess functional cortical tissue and brain effective connectivity in patients with brain tumors.
In Iceland, another simple technique, TMS motor evoked potentials (TMS-EMG) started to be used for preoperative mapping in 2016. We set and marked the position for the intraoperative direct stimulation (IONM) as in the nineties when this technique was described.
On the beginning of November 2017 neurosurgery department was interested on this procedure of preoperative mapping with neuronavigation. Again we used the available devices and we were able to map motor hotspots of the upper limb and speech area in a healthy subject. On 28th of November the team will investigate and perform motor and speech mapping in two patients with brain tumors located in eloquent areas of the brain. It will be for the first time that neuronavigated mapping is applied and used for the Icelandic brain tumor patients.
And the question remains: Is there a reason to believe that TEPs (TMS-EEG evoked potentials) can be used to assess better the "non-eloquent" brain cortical tissue and give a better map of the non-affected brain areas in order to avoid new post-intervention neurological deficit in patients with brain tumors ?