Biomedical subjects

Guillen Fernández

Publications and source records attributed to Guillen Fernández.

4 recordsLinked to original sources

PubMed2006

Memory formation by neuronal synchronization.

Cognitive functions not only depend on the localization of neural activity, but also on the precise temporal pattern of activity in neural assemblies. Synchronization of action potential discharges provides a link between large-scale EEG recordings and cellular plasticity mechanisms. Here, we focus on the role of neuronal synchronization in different frequency domains for the subsequent stages of memory formation. Recent EEG studies suggest that synchronized neural activity in the gamma frequency range (around 30-100 Hz) plays a functional role for the formation of declarative long-term memories in humans. On the cellular level, gamma synchronization between hippocampal and parahippocampal regions may induce LTP in the CA3 region of the hippocampus. In order to encode spatial locations or sequences of multiple items and to guarantee a defined temporal order of memory processing, synchronization in the gamma frequency range has to be accompanied by a stimulus-locked phase reset of ongoing theta oscillations. Simultaneous gamma- and theta-dependent plasticity leads to complex learning rules required for realistic declarative memory formation. Subsequently, consolidation of declarative memories may occur via replay of newly acquired patterns in so-called sharp wave-ripple complexes, predominantly during slow-wave sleep. These irregular bursts induce longer lasting forms of synaptic plasticity in output regions of the hippocampus and in the neocortex. In summary, synchronization of neural assemblies in different frequency ranges induces specific forms of cellular plasticity during subsequent stages of memory formation.

Action Potentials↗

PubMed2005

Unilateral intracarotid amobarbital procedure for language lateralization.

PURPOSE: The determination of language dominance as part of the presurgical workup of patients with pharmacoresistant epilepsies has experienced fundamental changes. With the introduction of noninvasive functional magnetic resonance imaging (fMRI), the number of patients receiving intracarotid amobarbital procedures (IAPs) for assessment of language dominance has decreased considerably. However, recent studies show that because of methodologic limitations of fMRI, IAP remains an important tool for language lateralization. The current study examines whether unilateral instead of bilateral IAP is an adequate way to apply IAP with reduced invasiveness. METHODS: We retrospectively examine the predictive value of unilateral IAP for the results of bilateral IAP based on a sample of 75 patients with various types of language dominance. Target parameters are the prediction of the language-dominant hemisphere and the identification of patients with atypical language dominance. For language assessment based on unilateral IAP, we introduce the measure hemispheric language capacity (HLC). RESULTS: Unilateral IAP performed on the side of intended surgery quantifies language capacity contralateral to the intended surgery. It detects atypical (bilateral or right) language dominance in the majority of patients. Experience with a separate series of 107 patients requiring presurgical language lateralization shows that in >80%, bilateral IAPs are redundant. CONCLUSIONS: Unilateral IAP is principally sufficient for language lateralization in the presurgical evaluation of patients with pharmacoresistant epilepsies. Necessity of bilateral IAP is restricted to few indications (e.g., callosotomy). In times of noninvasive language lateralization, we propose unilateral IAP as the method of choice for the verification of doubtful (bilateral) fMRI activation patterns.

Adolescent↗

PubMed2003

Neuronal substrates of sensory gating within the human brain.

BACKGROUND: For the human brain, habituation to irrelevant sensory input is an important function whose failure is associated with behavioral disturbances. Sensory gating can be studied by recording the brain's electrical responses to repeated clicks: the P50 potential is normally reduced to the second of two paired clicks but not in schizophrenia patients. To identify its neural correlates, we recorded electrical traces of sensory gating directly from the human hippocampus and neocortex. METHODS: Intracranial evoked potentials were recorded using hippocampal depth electrodes and subdural strip and grid electrodes in 32 epilepsy patients undergoing invasive presurgical evaluation. RESULTS: We found evidence of sensory gating only in the hippocampus, the temporo-parietal region (Brodmann's areas 22 and 2), and the prefrontal cortex (Brodmann's areas 6 and 24); however, whereas neocortical habituating responses to paired clicks were peaking around 50 msec, responses within the hippocampus proper had a latency of about 250 msec. CONCLUSIONS: Consistent with data from animal studies, our findings show that the hippocampus proper contributes to sensory gating, albeit during a time window following neocortical habituation processes. Thus, sensory gating may be a multistep process, with an early phase subserved by the temporo-parietal and prefrontal cortex and a later phase mediated by the hippocampus.

Adult↗

PubMed2002

Interictal EEG abnormalities in patients with psychogenic nonepileptic seizures.

PURPOSE: To examine interictal EEG abnormalities in patients with psychogenic nonepileptic seizures (PNESs). METHODS: (a) Retrospective study of EEG reports of 187 consecutive patients with PNES seen at the Department of Epileptology, Bonn, Germany; (b) Blinded, multirater comparison of EEGs of all PNES patients with no other clinically recognizable cause of EEG disturbance (n = 50) and healthy controls (n = 50). RESULTS: Of 187 consecutive patients with PNESs, 57 patients had PNESs and epilepsy (PNES+E), and 130 patients, PNESs alone. The diagnosis of additional epilepsy was based on ictal (video-) EEG or on the critical assessment of all clinical data by an experienced epileptologist. Retrospective review of all available EEG reports showed that 92.9% of patients in the PNES+E and 53.8% in the PNES-only group had one or more abnormal EEGs (median number of EEGs per patient, three; range, one to 42). In the PNES-only group, EEG changes were nonspecific in 42.3% of patients. Only 50 of 130 patients with PNESs alone had no other clinically recognizable cause of EEG disturbance and entered the controlled study. In this study, 18% of patients and 10% of controls had abnormal EEGs. The frequency of epileptiform EEG changes was similar to that in previous population studies in both groups (2.0%). CONCLUSIONS: PNESs often occur in patients with organic brain disease. Even in patients with PNESs alone and no clinically recognizable cause of EEG disturbance, nonspecific abnormalities are found 1.8 times as often as in healthy controls. Interictal EEG changes are common in patients with PNESs and, in isolation, should not be interpreted as evidence of epilepsy.

Adolescent↗