Biomedical subjects

Josef Zentner

Publications and source records attributed to Josef Zentner.

At least 19 recordsLinked to original sources

PubMed2007

A new clinico-pathological classification system for mesial temporal sclerosis.

We propose a histopathological classification system for hippocampal cell loss in patients suffering from mesial temporal lobe epilepsies (MTLE). One hundred and seventy-eight surgically resected specimens were microscopically examined with respect to neuronal cell loss in hippocampal subfields CA1-CA4 and dentate gyrus. Five distinct patterns were recognized within a consecutive cohort of anatomically well-preserved surgical specimens. The first group comprised hippocampi with neuronal cell densities not significantly different from age matched autopsy controls [no mesial temporal sclerosis (no MTS); n = 34, 19%]. A classical pattern with severe cell loss in CA1 and moderate neuronal loss in all other subfields excluding CA2 was observed in 33 cases (19%), whereas the vast majority of cases showed extensive neuronal cell loss in all hippocampal subfields (n = 94, 53%). Due to considerable similarities of neuronal cell loss patterns and clinical histories, we designated these two groups as MTS type 1a and 1b, respectively. We further distinguished two atypical variants characterized either by severe neuronal loss restricted to sector CA1 (MTS type 2; n = 10, 6%) or to the hilar region (MTS type 3, n = 7, 4%). Correlation with clinical data pointed to an early age of initial precipitating injury (IPI < 3 years) as important predictor of hippocampal pathology, i.e. MTS type 1a and 1b. In MTS type 2, IPIs were documented at a later age (mean 6 years), whereas in MTS type 3 and normal appearing hippocampus (no MTS) the first event appeared beyond the age of 13 and 16 years, respectively. In addition, postsurgical outcome was significantly worse in atypical MTS, especially MTS type 3 with only 28% of patients having seizure relief after 1-year follow-up period, compared to successful seizure control in MTS types 1a and 1b (72 and 73%). Our classification system appears suitable for stratifying the clinically heterogeneous group of MTLE patients also with respect to postsurgical outcome studies.

Adult↗

PubMed2006

Comparison of manual tracing versus a semiautomatic radial measurement method in temporal lobe MRI volumetry for pharmacoresistant epilepsy.

INTRODUCTION: The aim of this study was to test a modified radial semiautomated volumetry technique (radial divider technique, RDT) versus the manual volumetry technique (MVT) for proportionality of temporal subvolumes in 30 patients with drug-resistant temporal lobe epilepsy. METHODS: Included in the study were 30 patients (15 female, 15 male; mean age 39.6 years) with pharmacoresistant epilepsy (mean duration 26.6 years). MRI studies were performed preoperatively on a 1.5-T scanner. All image processing steps and volume measurements were performed using ANALYZE software. The volumes of six subregions were measured bilaterally; these included the superior temporal gyrus (STG), middle + inferior temporal gyrus (MITG), fusiform gyrus (FG), parahippocampal gyrus (PHG), amygdala (AM), and hippocampus (HP). Linear regression was used to investigate the relationship between the comparable subvolumes obtained with MVT and RDT. RESULTS: Very high correlations (R (2) >0.95) between RDT and MVT were observed for the STG + MITG and the STG + MITG + FG, but low correlations for the PHG subvolumes and the combined PHG + HP + AM subvolumes. These observations were independent of the side of the pathology and of hemisphere. CONCLUSION: The two measurement techniques provided highly reliable proportional results. This series in a homogeneous group of TLE patients suggests that the much quicker RDT is suitable for determining the volume of temporolateral and laterobasal temporal lobe compartments, of both the affected and the non-affected side and the right and left hemisphere.

Adolescent↗

PubMed2006

Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients.

Granule cell dispersion (GCD) in the dentate gyrus is a frequent feature of Ammon's horn sclerosis (AHS) which is often associated with temporal lobe epilepsy (TLE). It has been hypothesized that GCD may be caused by an abnormal migration of newly born granule cells. To test this hypothesis, we used markers of proliferation and neurogenesis and immunocytochemical methods as well as quantitative Western blot and real-time RT-PCR analyses in surgically resected hippocampi from TLE patients and controls. Below the age of 1 year, Ki-67-immunopositive nuclei were detected in the subgranular zone of the dentate gyrus, but not in the dentate of TLE patients independent of age. The expression of the proliferation marker minichromosome maintenance protein 2 (mcm2) and of doublecortin (DCX) decreased significantly with age in controls and in TLE patients, but the expression of both proteins was independent of the degree of AHS and GCD. Quantitative real-time RT-PCR confirmed these findings at the level of gene expression. In contrast, immunocytochemistry for glial fibrillary acidic protein (GFAP) and vimentin as well as Golgi staining revealed a radially aligned glial network in the region of GCD. GFAP-positive fiber length significantly increased with the severity of GCD. These results indicate that epileptic activity does not stimulate neurogenesis in the human dentate gyrus and that GCD probably does not result from a malpositioning of newly generated granule cells, but rather from an abnormal migration of mature granule cells along a radial glial scaffold.

Adolescent↗

PubMed2006

Functional neuroimaging of emotional learning and autonomic reactions.

This article provides a selective overview of the functional neuroimaging literature with an emphasis on emotional activation processes. Emotions are fast and flexible response systems that provide basic tendencies for adaptive action. From the range of involved component functions, we first discuss selected automatic mechanisms that control basic adaptational changes. Second, we illustrate how neuroimaging work has contributed to the mapping of the network components associated with basic emotion families (fear, anger, disgust, happiness), and secondary dimensional concepts that organise the meaning space for subjective experience and verbal labels (emotional valence, activity/intensity, approach/withdrawal, etc.). Third, results and methodological difficulties are discussed in view of own neuroimaging experiments that investigated the component functions involved in emotional learning. The amygdala, prefrontal cortex, and striatum form a network of reciprocal connections that show topographically distinct patterns of activity as a correlate of up and down regulation processes during an emotional episode. Emotional modulations of other brain systems have attracted recent research interests. Emotional neuroimaging calls for more representative designs that highlight the modulatory influences of regulation strategies and socio-cultural factors responsible for inhibitory control and extinction. We conclude by emphasising the relevance of the temporal process dynamics of emotional activations that may provide improved prediction of individual differences in emotionality.

Animals↗

PubMed2006

Presynaptic opioid receptors on noradrenergic and serotonergic neurons in the human as compared to the rat neocortex.

1. Electrically evoked release of [3H]-noradrenaline ([3H]-NA) or [3H]-5-hydroxytryptamine ([3H]-5-HT) in slices of human and the rat neocortex was used to characterize presynaptic opioid receptors. 2. Release of [3H]-NA in rat neocortical slices was reduced only by the mu-receptor agonist DAMGO (pIC50: 7.27, CI95: [7.22, 7.32]; Imax: 77.6+/-1.6%; antagonized by naloxone: pA2: 8.88, CI95: [8.78, 8.98]). 3. Release of [3H]-NA in human neocortical slices was unaffected by DAMGO, but inhibited by the delta-receptor agonist DPDPE (Imax: 25.7+/-2.2%) and the kappa-receptor agonist U-50,488H (19.7+/-2.7% inhibition at 1 microM). Both effects were antagonized by naltrindole (1 microM). 4. Release of [3H]-5-HT in rat neocortical slices, was inhibited by DAMGO (10 microM) and U-50,488H (1 and 10 microM) only in the presence of the 5-HT receptor antagonist methiotepin (1 microM). 5. Release of [3H]-5-HT in human neocortical slices was unaffected by DPDPE, but U-50,488H (Imax: 40.8+/-8.3%; antagonized by 0.1 microM norbinaltorphimine) and DAMGO (16.4+/-3.9% inhibition at 1 microM; antagonized by 0.1 microM naloxone) acted inhibitory. 6. Release of [3H]-5-HT in human neocortical slices was reduced by nociceptin/orphanin (0.1 and 1 microM). These effects were antagonized by the ORL1 antagonist J-113397 (1-[(3R,4R)-1-cyclo-octylmethyl-3-hydroxymethyl-4-piperidyl]-3-ethyl-1,3-dihydro-2H-benzimidazol-2-one; 0.1 microM). 7. This study provides evidence for significant species differences in opioid receptor-mediated modulation of NA and 5-HT-release in human vs rat neocortex. In rats, mu-opioid receptors modulate NA release, but 5-HT release is only weakly affected by mu- and kappa-opioids. In contrast, NA release in human neocortex is modulated via delta-opioid receptors, but 5-HT release mainly via kappa-opioid receptors. In addition also the ORL1 receptor seems to be involved in 5-HT release modulation.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed2006

K(+)-evoked [(3)H]-norepinephrine release in human brain slices from epileptic and non-epileptic patients is differentially modulated by gabapentin and pinacidil.

The modulation of K(+)-evoked [(3)H]-norepinephrine ([(3)H]-NE) release by gabapentin (GBP) and pinacidil (PIN), a known K(ATP) agonist, was examined in human brain slices. We compared the pharmacological effects on NE-release in human epileptic neocortex and epileptic hippocampus to non-epileptic neocortex. GBP (100 microM) decreased [(3)H]-NE release by 22% in non-epileptic neocortical slices, whereas this inhibition was absent in slices from epileptic hippocampus and epileptic neocortex. PIN (10 microM) also reduced [(3)H]-NE release by 30% in non-epileptic neocortical slices and only by 5% in epileptic hippocampal slices. The blockade of voltage-gated calcium channels by omega-conotoxins MVIIA and MVIIC (0.1 microM) reduced [(3)H]-NE release in epileptic and non-epileptic neocortical slices to the same extend. The data show a marked reduction in K(+)-evoked [(3)H]-NE release by GBP and PIN in epileptic hippocampus and neocortex, suggesting an alteration of K(ATP) channel function, whereas the effects of the calcium channel modulators omega-conotoxins MVIIA and MVIIC are similar in both epileptic and non-epileptic neocortex.

Adrenergic alpha-Agonists↗

PubMed2006

The effects of stimulation pattern and sevoflurane concentration on intraoperative motor-evoked potentials.

The usefulness of intraoperative monitoring of motor-evoked potentials (MEPs) during inhaled anesthesia is limited by the suppressive effects of volatile anesthetics on MEP signals. We investigated the effects of different stimulation patterns and end-tidal concentrations of sevoflurane on intraoperative transcranial electrical MEPs. In 12 patients undergoing craniotomy, stimulation patterns (300-500 V, 100-1000 Hz, 1-5 stimuli) and multiples (0.5, 0.75, and 1.0) of minimum alveolar concentration (MAC) of sevoflurane were varied randomly while remifentanil was administered at a constant rate of 0.2 microg x kg(-1) x min(-1). MEPs were recorded from thenar and hypothenar muscles and analyzed without knowledge of the respective MAC. Three-way analysis of variance revealed significant main effects for increasing stimulation intensity, frequency, and number of stimuli on MEP amplitude (P < 0.05). Maximum MEP amplitudes and recording success rates were observed during 4 stimuli delivered at 1000 Hz and 300 V. A significant main effect of sevoflurane concentration (0.5 versus 0.75 and 1 MAC multiple) on MEP amplitude was observed at the thenar recording site only (P < 0.05). In conclusion, MEP characteristics varied significantly with changes in stimulation pattern and less so with changes in sevoflurane concentration. The results suggest that high frequency repetitive stimulation allows intraoperative use of MEP monitoring during up to 1 MAC multiple of sevoflurane and constant infusion of remifentanil up to 0.2 microg x kg(-1) x min(-1).

Adult↗

PubMed2005

Binding affinity and agonist activity of putative endogenous cannabinoids at the human neocortical CB1 receptor.

We investigated the affinity of putative endocannabinoids (2-arachidonylglycerol, 2-AG; noladin ether, virodhamine) for the human neocortical CB1 receptor. Functional activity of these compounds (including anandamide, AEA) was determined by examining basal and forskolin-stimulated cAMP formation. Assays were performed with synaptosomes, prepared from fresh human neocortical tissue. Receptor affinity was assessed from competition binding experiments with the CB1/2 agonist [3H]-CP55.940 in absence or presence of a protease inhibitor to assess enzymatic stability. Noladin ether and virodhamine inhibited [3H]-CP55.940 binding (Ki: 98, 1740 nM, respectively). Protease inhibition decreased the Ki value of virodhamine (Ki: 912 nM), but left that of noladin ether unchanged. 2-AG almost lacked affinity (Ki lymphoblasic )10 microM). Basal cAMP formation was unaffected by AEA and noladin ether, but strongly enhanced by 2-AG and virodhamine. Forskolin-stimulated cAMP formation was inhibited by AEA and noladin ether (IC50: 69, 427 nM, respectively) to the same extent as by CP55.940 (Imax each approximately 30%). Inhibitions by AEA or noladin ether were blocked by the CB1 receptor antagonist AM251. Virodhamine increased forskolin-stimulated cAMP formation, also in presence of AM251, by approximately 20%. 2-AG had no effect; in presence of AM251, however, 10 microM 2-AG stimulated cAMP formation by approximately 15%. Our results suggest, that AEA and noladin ether are full CB1 receptor agonists in human neocortex, whereas virodhamine may act as a CB1 receptor antagonist/inverse agonist. Particularly the (patho)physiological role of 2-AG should be further investigated, since its CB1 receptor affinity and agonist activity especially in humans might be lower than generally assumed.

Adolescent↗

PubMed2005

Unchanged glutamine synthetase activity and increased NMDA receptor density in epileptic human neocortex: implications for the pathophysiology of epilepsy.

We investigated whether alterations in glutamate metabolising glutamine synthetase activity occur in human epileptic neocortex, as shown previously for human epileptic hippocampus [Eid, T., Thomas, M.J., Spencer, D.D., Rundén-Pran, E., Lai, J.C.K., Malthankar, G.V., Kim, J.H., Danbolt, N.C., Ottersen, O.P., de Lanerolle, N.C., 2004. Loss of glutamine synthetase in the human epileptic hippocampus: possible mechanism for raised extracellular glutamate in mesial temporal lobe epilepsy. Lancet 363, 28-37]. Glutamine synthetase activity was equivalent in both non-epileptic and epileptic human neocortex. Epileptic tissue, however, was characterised by a 37% increase in the density of synaptosomal NMDA receptor sites compared to non-epileptic tissue, as revealed by a radioligand binding assay (B max(non-epileptic) 1.45 pmol/mg protein and B max(epileptic) 1.99 pmol/mg protein, P < 0.05). Our findings shed some doubts on a role of glutamine synthetase in the pathophysiology of epilepsy in the neocortex. However, the detection of a significantly reduced enzymatic activity in the epileptic amygdala supports the assumption that the enzyme defect is localized to the epileptic mesial temporal lobe of corresponding patients.

Adolescent↗

PubMed2005

The brain tumor board: lessons to be learned from an interdisciplinary conference.

BACKGROUND: The aim of this study is to analyze the work of the interdisciplinary Brain Tumor Board (BTB) which was established at Freiburg University Hospital in 1998. PATIENTS AND METHODS: From January 1998 to December 2003, a total of 1,516 patients were discussed in 259 meetings of the BTB. The protocols of the BTB were analyzed retrospectively. RESULTS: In 79% of the patients, the diagnosis was based on histological findings or a typical radiological appearance of a lesion, or both. This group was composed of 4 subgroups: 28% benign skull base tumors (19% meningiomas, 4% pituitary adenomas, 3% acoustic schwannomas, 2% others), 24% primary brain tumors of glial origin (8% glioblastomas, 12% gliomas other than glioblastomas, 5% oligoastrocytomas or oligodendrogliomas), 19% brain metastases, and 8% other brain or skull base tumors. In 13% of the cases, the exact diagnosis was still unknown when the patient was presented. 8% of the presentations were motivated by nontumorous interdisciplinary problems (e.g. arterio-venous malformations). The recommendations given by the BTB included: 23% further diagnostic procedures (11% non-invasive examinations, 12% stereotactic biopsies), 57% active antitumoral therapy (22% resection, 17% fractionated radiotherapy, 13% radiosurgery, 5% chemotherapy, <1% embolization), 20% no treatment (14% watchful waiting, 6% supportive care). 91% of the BTB recommendations were realized within 3 months. CONCLUSION: Interdisciplinary care seems to be particularly necessary in patients with benign skull base tumors, gliomas and brain metastases. Decisions made in a small interdisciplinary group of experts have a high potential of subsequently being realized.

Academic Medical Centers↗

PubMed2005

The modifying effects of stimulation pattern and propofol plasma concentration on motor-evoked potentials.

The quality of intraoperative motor-evoked potentials (MEPs) largely depends on the stimulation pattern and anesthetic technique. Further improvement in intraoperative MEP recording requires exact knowledge of the modifying effects of each of these factors. Accordingly, we designed this study to characterize the modifying effect of different stimulation patterns during different propofol target plasma concentrations (PTPCs) on intraoperatively recorded transcranial electrical MEPs. In 12 patients undergoing craniotomy, stimulation patterns (300-500 V; 100-1000 Hz; 1-5 stimuli) were varied randomly at different PTPCs (2, 4, and 6 microg/mL). Remifentanil was administered unchanged at 0.2 microg . kg(-1) . min(-1). MEPs were recorded from the thenar and hypothenar muscles. Analysis of MEPs was blinded to the PTPC. Three-way analysis of variance revealed significant main effects of increasing stimulation intensity, frequency, and number of stimuli on MEP amplitude (P < 0.05). Maximum MEP amplitudes and recording success rates were observed with three or more stimuli delivered at 1000 Hz and > or =150 V. A significant main effect of PTPC (2 vs 4 and 6 microg/mL) on MEP amplitude was observed at the thenar recording site only (P < 0.05). An amplitude ratio calculated from corresponding MEPs evoked by double and quadruple stimulation proved to be insensitive to changes in PTPC. In conclusion, MEP characteristics varied significantly in response to changes in stimulation pattern and less to changes in PTPC.

Adult↗

PubMed2005

Rapid and fully automated visualization of subdural electrodes in the presurgical evaluation of epilepsy patients.

For rapid visualization of subdural electrodes with respect to cortical and subcortical structures, we describe a novel and fully automated method based on coregistration, normalization, optional cerebellum masking, and volume rendering of 3D MR imaging data taken before and after implantation. The key step employs the skull-stripped preimplantation image as a mask to also remove the skull in the postimplantation image. The extracted brain is presented in 3D with the electrodes directly visible by their susceptibility artifacts. Compared with alternative methods, ours is based on freely available software and does not require manual intervention.

Adolescent↗

PubMed2004

Focal cortical dysplasias: surgical outcome in 67 patients in relation to histological subtypes and dual pathology.

The purpose of this study was to assess whether the histological subtype of focal cortical dysplasia and dual pathology affect surgical outcome in patients with medically intractable epilepsy due to focal cortical dysplasia (FCD). We retrospectively analysed the outcome of 67 patients from 2 to 66 years of age at follow-up periods of 6 to 48 months after epilepsy surgery. Histological subtypes were classified according to Palmini and included a few cases with mild histological abnormalities corresponding to the definition of mild malformations of cortical development. The seizure outcome was classified according to Engel and evaluated at the last follow-up visit as well as at follow-up periods of 12 and 24 months after surgery. The outcome in patients with FCD and additional hippocampal pathology (dual pathology) was analysed separately. Distribution of histological subtypes differed in temporal and extratemporal localization, with a significantly higher extratemporal prevalence of FCD type 2. There was a tendency towards better postsurgical outcome related to the last follow-up visit in patients with more subtle abnormalities classified as mild malformations of cortical development (mMCD) (63% Engel Ia), FCD type 1a (67% Engel Ia) and FCD type 1b (55% Engel Ia) compared with patients with FCD type 2a (43% Engel Ia) and FCD type 2b (Taylor type) (50% Engel Ia). Considering the outcome at follow-up periods over 12 and 24 months, complete seizure-freedom was achieved significantly more often in patients with FCD type 1 and mMCD than with FCD type 2, and seizure reduction by less than 75% (Engel IV) occurred in more patients with FCD type 2a compared with the other subgroups. This tendency was seen in the whole patient group and in the extratemporal subgroup. Patients with dual pathology almost always had temporal lobe epilepsy; the outcome in this patient group was generally favourable (66% complete seizure-freedom at the last follow-up visit). The outcome remained almost constant with longer periods of follow-up. We conclude that patients with FCD type 1 and mMCD had a better outcome compared with those with more severe forms of cortical dysplasia. A higher incidence of FCD type 1 in temporal localization did not allow the effects of histological subtype and localization to be separated. A subanalysis of extratemporal FCDs, however, revealed a similar tendency for a better outcome with FCD type 1, suggesting that the histological subtype itself seems to be at least a relevant cofactor influencing postsurgical outcome.

Adolescent↗

PubMed2004

Characterization of nicotinic receptors inducing noradrenaline release and absence of nicotinic autoreceptors in human neocortex.

UNLABELLED: Presynaptic facilitatory nicotinic receptors (nAChRs) on noradrenergic axon terminals were studied in slices of human or rat neocortex and of rat hippocampus preincubated with [3H]noradrenaline ([3H]NA). During superfusion of the slices, stimulation by nicotinic agonists for 2 min only slightly increased [3H]NA outflow in the rat neocortex, but caused a tetrodotoxin-sensitive. Ca(2+)-dependent release of [3H]NA in rat hippocampus and human neocortex. In both tissues a similar rank order of potency of nicotinic agonists was found: epibatidine >> DMPP > nicotine approximately cytisine > or = acetylcholine; choline was ineffective. In human neocortex, the effects of nicotine (100 microM) were reduced by mecamylamine, methyllycaconitine, di-hydro-beta-erythroidine (10 microM, each) and the alpha3beta2/alpha6betax-selective alpha-conotoxin MII (100/200 nM). The alpha3beta4 selective alpha-conotoxin AuIB (1 microM), and the alpha7 selective alpha-conotoxin ImI (200 nM) as well as alpha-bungarotoxin (125 nM) were ineffective. Glutamate receptor antagonists (300 microM AP-5, 100 microM DNQX) acted inhibitory, suggesting the participation of nAChRs on glutamatergic neurons. On the other hand, nAChR agonists were unable to evoke exocytotic release of [3H]acetylcholine from human and rat neocortical slices preincubated with [3H]choline. IN CONCLUSION: (1) alpha3beta2 and/or alpha6 containing nAChRs are at least partially responsible for presynaptic cholinergic facilitation of noradrenergic transmission in human neocortex; (2) nicotinic autoreceptors were not detectable in rat and human neocortex.

Acetylcholine↗

PubMed2004

EEG and MEG source analysis of single and averaged interictal spikes reveals intrinsic epileptogenicity in focal cortical dysplasia.

PURPOSE: Simultaneous interictal EEG and magnetoencephalography (MEG) recordings were used for noninvasive analysis of epileptogenicity in focal cortical dysplasia (FCD). The results of two different approach methods (multiple source analysis of averaged spikes and single dipole peak localization of single spikes) were compared with pre- and postoperative anatomic magnetic resonance imaging (MRI). PATIENTS: We studied nine children and adolescents (age, 3.5-15.9 years) with localization-related epilepsy and FCD diagnosis based on MRI. Five patients underwent epilepsy surgery, two of them after long-term recording with subdural grid electrodes, and one after intraoperative electrocorticography. METHODS: The 122-channel whole-head MEGs and 33-channel EEGs were recorded simultaneously for 25 to 40 min. Interictal spikes were identified visually and used as templates to search for similar spatiotemporal spike patterns throughout the recording. With the BESA program, similar spikes (r > 0.85) were detected, averaged, high-pass filtered (5 Hz) to enhance spike onset, and subjected to multiple spatiotemporal source analysis with a multishell spherical head model. Peak activity from single spikes was modeled by single dipoles for the same subset of spikes. Source localization was visualized by superposition on T1-weighted MRI and compared with the lesion identified in T1- and T2-weighted MRI. In the five cases undergoing epilepsy surgery, the results were correlated with invasive recordings, postoperative MRI, and outcome. RESULTS: In all cases, the analysis of averaged spikes showed a localization of onset- and peak-related sources within the visible lesion for both EEG and MEG. Of the single spikes, 128 (45%; total 284) were localizable at the peak in MEG, and 170 (60%) in EEG. Of these, 91% localized within the lesion with MEG, and 93.5% with EEG. In three of five patients operated on, the resected area included the onset zones of averaged EEG and MEG spike activity. These patients had excellent postoperative outcome, whereas the others did not become seizure free. CONCLUSIONS: Consistent MEG and EEG spike localization in the lesional zone confirmed the hypothesis of intrinsic epileptogenicity in FCD.

Cerebral Cortex↗

PubMed2004

Complex visual hallucinations (Charles Bonnet syndrome) in visual field defects following cerebral surgery. Report of four cases.

The development of visual hallucinations after loss of vision is known as the Charles Bonnet syndrome. This phenomenon was first described in 1760 by Charles Bonnet and others during their observations of elderly patients with degeneration of the retina or cornea. To date a clear association between visual hallucinations and neurosurgical procedures has not been reported. Because of their clear demarcation, however, surgical lesions in the cerebrum offer a unique opportunity to determine the pathoanatomical aspects of visual hallucinations. During a 3-year period, 41 consecutive patients who acquired visual field defects after neurosurgery were examined for the occurrence of visual hallucination. Postoperatively, four of these patients experienced visual hallucinations. In two of them an upper quadrantanopia developed after the patients had undergone selective amygdalohippocampectomy. In the other two patients a complete hemianopia developed, in one case after resection of a parietal astrocytoma and in the other after resection of an occipital glioblastoma multiforme. The visual hallucinations were transient and gradually disappeared between 4 days and 6 months postoperatively. The patients were aware of the fact that their hallucinations were fictitious and displayed no psychosis. Electroencephalographic recordings were obtained in only two patients and epileptic discharges were found. Deafferentiation of cortical association areas may lead to the spontaneous generation of complex visual phenomena. In the present series this phenomenon occurred in approximately 10% of patients with postoperative visual field defects. In all four cases the central optic radiation was damaged between the lateral geniculate nucleus and the primary visual cortex. The complex nature of the visual hallucination indicates that they were generated in visual association areas.

Adult↗

PubMed2003

Monitoring of cerebral perfusion pressure during intracranial hypertension: a sufficient parameter of adequate cerebral perfusion and oxygenation?

OBJECTIVE: A cerebral perfusion pressure (CPP) oriented treatment is a widely accepted standard for patients with intracranial hypertension. In an animal model of controlled intracranial hypertension we investigated whether CPP is a reliable parameter of sufficient cerebral perfusion and oxygenation. Using near-infrared reflexion spectroscopy the effect of decreasing CPP due to increasing intracranial pressure (ICP) on cerebral tissue oxygenation was studied. METHODS: Ten rabbits were subjected to artificially elevated ICP using the cisterna-magna infusion technique. Regional cerebral O(2) saturation of hemoglobin (tiSO(2)), regional tissue concentration of hemoglobin (tiHb), and CPP were recorded continuously. CPP was investigated with respect to tiSO(2). Electrocortical activity was simultaneously recorded by two-channel EEG to determine the onset of ischemia. RESULTS: Reduced CPP due to increased ICP led to a continuous decrease in tiSO(2.) There was progressive suppression of EEG frequency and amplitude with decreasing CPP in all animals. Onset of EEG-silence due to elevated ICP was observed in a wide range of CPP-values between 9 and 42 mmHg. At the same time tiSO(2) varied merely between 0 and 5%. CONCLUSIONS: Regarding the EEG effects due to increased ICP (EEG silence), CPP values showed a wide interindividual variability, in contrast to tiSO(2). In our animal model the sole calculation of CPP did not reflect adequate cerebral perfusion.

Animals↗

PubMed2003

S(+)-ketamine attenuates myogenic motor-evoked potentials at or distal to the spinal alpha-motoneuron.

UNLABELLED: We investigated the effect of S(+)-ketamine on spinal cord evoked potentials (ESCPs) and myogenic motor-evoked potentials after electrical stimulation of the motor cortex in a rabbit model. This study was designed to characterize the relationship between ESCP characteristics and corresponding changes in compound muscle action potentials (CMAPs) derived from fore and hind limbs. Direct (D) and indirect (I) corticospinal volleys (ESCP) from the upper and lower thoracic spinal cord, recorded by two bipolar epidural electrodes, were assessed during IV administration of 0.02, 0.05, 0.1, and 0.2 mg. kg(-1) x min(-1) of S(+)-ketamine, each before and after neuromuscular blockade (0.4 mg/kg of cisatracurium), in 16 New Zealand White rabbits after single-pulse bipolar electrical stimulation of the motor cortex at 50 (threshold), 60, and 70 V. CMAP amplitudes at fore and hind limbs were significantly suppressed (P < 0.01) during infusion at 0.1 and 0.2 mL x kg(-1) x min(-1), whereas neither corresponding D- nor I-waves were altered. Similar findings were obtained during variation of stimulus amplitude (50-70 V). Multivariate regression analysis of CMAP amplitudes and various ESCP characteristics demonstrated no apparent interparametric association. These findings indicate that S(+)-ketamine modulates CMAP independent from corticospinal D- and I-wave-mediated facilitation at or distal to the spinal alpha-motoneuron. IMPLICATIONS: S(+)-Ketamine combines several anesthetic properties suitable for total IV neuroanesthesia, including minimal effects on neurophysiological monitoring. Recording of neural and myogenic responses after electrical stimulation of the motor cortex indicates that S(+)-ketamine modulates myogenic motor-evoked potentials by a peripheral mechanism at or distal to the spinal alpha-motoneuron.

Action Potentials↗