Chorea Sancti Viti in Lexicon medicum anno 1696.
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Biomedical subjects
Publications and source records attributed to Ivan Rektor.
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Cortical excitability and cortico-cortical inhibition were examined in twenty-one patients suffering from idiopathic rotational cervical dystonia. Polymyography of cervical muscles, somatosensory evoked potential recordings, and paired transcranial magnetic stimulation were used to assess the dystonic disorder. The results were compared with those obtained in a group of sixteen healthy age-matched volunteers. Statistically significant differences between the patient group and the control group were found when the amplitude values of the mean P22/N30 component measured at F [3, 4] and C[3, 4]' electrode positions were compared. The mean amplitude of P22/N30 in both of these electrode positions contralaterally to the direction of head deviation was significantly higher in the patient group (p <or= 0.05). The mean side-to-side P22/N30 amplitude ratio was calculated in both groups in the F[3, 4] and C[3, 4]' electrode positions: there was a significant difference between the two groups. The mean ratio (calculated contralaterally/ipsilaterally in the patient group and left/right side in the control group) was significantly higher in the patient group (p <or= 0.05). There were statistically significant differences between the two groups when the mean values of MEP amplitudes following paired stimuli at short and medium interstimulus intervals (ISI)) were compared. The percentage of amplitude reduction registered at short ISI was significantly lower in the patient group when both 3 ms ISI and 5 ms ISI were considered, and when the hemisphere contralateral to the direction of head deviation was stimulated. There was also a difference (with the short ISI) when the hemisphere ipsilateral to the direction of head deviation was stimulated, but this difference was not significant (p < 0.5). Almost all of the amplitude changes following the paired stimulus at the longer ISI, i. e. 10, 15, and 20 ms were significantly different when the patient group was compared with control group: when the ipsilateral hemisphere was stimulated, the amplitude of conditioned responses was significantly higher following all three paired stimuli (with 10, 15, and 20 ms ISI) at the p <or= 0.05 significance level; when the contralateral hemisphere was stimulated, they were significantly higher following the 10 and 20 ms ISI paired stimuli (significance level p <or= 0.05). The interhemispheric difference in the patient group was significant only for the paired stimuli using 3 and 5 ms (short) ISI and 15 and 20 ms (medium) ISI. There was a significantly decreased inhibition at 3 and 5 ms ISI when the hemisphere contralateral to the direction of head deviation was stimulated, as compared with the hemisphere ipsilateral (p <or= 0.05). Similarly, there was a significantly increased facilitation at 15 and 20 ms when the hemisphere contralateral to the direction of head deviation was stimulated, as compared with the hemisphere ipsilateral (p <or= 0.05). The results indicate that a disorder of both cortical excitability and intracortical inhibition exists in patients with cervical dystonia, and that this disorder is lateralized, i. e. it is located within the hemisphere contralateral to the direction of head deviation.
The P3 wave of event-related potentials was recorded with intracranial electrodes in 24 epileptic patients during the pre-surgical evaluation of epilepsy surgery. Three different cognitive auditory paradigms were used: (1) odd-ball paradigm with no output required (PGI) where patients had simply to recognize target tones, (2) odd-ball with motor response (PGII), where patients had to press a button in response to target tones, and (3) odd-ball with both counting task and motor response (PGIII), where patients had to recognize target tones, press a button in response to them, and count their number. The occurrence of P3 potential, its latency and amplitude, and the dependence of P3 latency on the task complexity were calculated. Identifiable P3 potentials in all the three paradigms were recorded from locations in mesial cortex (18 locations mesial temporal, eight locations mesial frontal, two locations mesial parietal) and lateral sites (eight sites lateral temporal, five lateral frontal, and two lateral parietal). P3 latency values ranged from 257 to 320 ms in all explored cortical areas when PGI was used; they significantly increased or decreased during PGII and PGIII, depending on the task and structure explored. In the mesial temporal cortex, the changes of P3 latency between paradigms were minimal. In the mesial parietal cortex, there was significant P3 delay in both PGII and PGIII relative to PGI. In the mesial frontal cortex, there was a significant latency decrease in PGII, and practically identical mean latency in PGI and PGIII. In all lateral cortices (temporal, frontal and parietal), there was always a P3 latency increase in PGII and PGIII relative to PGI, the most significant results being observed in the parietal and frontal lateral areas. The results support the multi-generator theory of P3. Prolongation of the mean P3 latency in lateral frontal and parietal cortices when the paradigm involved the execution of a motor task might reflect specific gating in this area during active movements, while the absence of modification in the temporal lobe may reflect minimal involvement of this region in motor planning or processing. The prolongation of mean P3 latency in practically all lateral structures in PGIII suggests that most cortical areas were involved in the cognitive functions needed for this test. The finding of reduction and subsequent prolongation of P3 latency in the mesial frontal cortex might reflect the unique specialization of this area and its specific involvement in motor processing.
Electrooculography (EOG) recordings in 21 L-DOPA-naive patients suffering from Parkinson's disease (PD) were made before and after apomorphine subcutaneous administration (ASA). The effect of apomorphine on smooth pursuit eye movements (SPEM) was studied. Age-matched healthy subjects, who underwent SPEM recordings without the ASA procedure, were examined in order to compare baseline SPEM. EOG recordings were used to compare the patient group and the control group, and to compare the SPEM before and after ASA within the patient group. Significant differences in SPEM were found between both groups, as well as in the SPEM before and after ASA. The theory that SPEM is disturbed in early PD patients was confirmed. The dopaminergic control of horizontal SPEM is supposed.
OBJECTIVE: The somatosensory evoked potentials of the median nerve (SEP) were registered intracerebrally in 12 subjects to elucidate the origin of N30 component and its behavior in the motor 'gating' tasks. METHODS: The recordings were done from the electrodes which were inserted within the cortex of frontal lobe in the pre-surgical phase of epilepsy surgery. The registrations focused on the precentral N30 SEP component and its behaviour under the 'gating' paradigms. Two different 'gating' paradigms, motor and mental, were used and the SEP then were recorded in 3 conditions: (1) normal (N) paradigm, during which the subjects were instructed not to perform any movement by the stimulated hand, or to mentally simulate the movement; (2) active movement (AM) paradigm, during which the subjects were instructed to perform the active movement as the internal motor sequence test by the fingers of the hand of the stimulated limb; (3) mental movement simulation (MMS), during which the subjects were instructed to only mentally simulate the movements performed in the previous paradigm, and this 'virtual' movement also involved the hand of the stimulated limb. The recordings were done at least twice in each paradigm and averaged runs of 2000 artefact-free sweeps were used for the analysis. RESULTS: The results demonstrated that the precentral N30 component of SEP is generated only in the pre-motor area, either dorsolaterally or mesially, which consists of Brodmann's areas 6 and 8, and their borders. Only the N30 potentials recorded there in 7 subjects had a shape and character of 'near-field' potential. The behaviour of the N30 component when recorded in the AM and MMS paradigms was different depending on the fact of whether they were recorded dorsolaterally or mesially. When there was a clear 'near-field' N30 potential recorded mesially, there was a certain gating present during the AM paradigm, i.e. during the performance of movement. However, the gating caused by the mental movement simulation in the MMS paradigm was substantially more expressed, and the N30 wave practically disappeared in some cases. On the contrary, the gating of the N30 wave, recorded in the frontal dorsolateral premotor cortex (DLPC), was almost complete when the AM (active movement) paradigm was employed, and it was only partial when the MMS paradigm (mental movement simulation) was employed. CONCLUSIONS: The results of N30 registrations in our group of patients strongly support the theory of separate generator (or generators) of the N30 wave within the premotor cortex. They also brought forward evidence that the dorsolateral premotor cortex (Brodmann's areas 6 and 8) serves as the substrate of the 'motor execution' process, and the mesial frontal cortex (Brodmann's area 6) serves as the substrate of the 'motor planning' process. Further research should focus on the mutual registration of neurophysiological phenomena and imaging phenomena to obtain new data, which will be able to more precisely elucidate the workings of the premotor cortex during the whole process of motor performance.
OBJECTIVE: To assess the contribution of different anatomical brain sites to the genesis of P3 phenomena with respect to button pressing versus mental counting tasks. METHODS: Eight intractable epileptic patients undergoing depth electrode recordings prior to their surgery participated in the study. A total of 546 cerebral sites were recorded. A standard somatosensory oddball paradigm was used. The experiment was carried out in two sessions, differing in the requested responses to targets. The averaged responses in both tasks were compared. RESULTS: After targets, two kinds of P3-like potentials were observed within different cortical sites. Task-non-specific P3 potentials were seen for both types of responses to targets. The mean amplitude of these task-non-specific P3 potentials was significantly higher in the button pressing task. The intracerebral generators of this somatosensory P3 did not differ from the known generators of auditory and visual P3s. Task-specific P3-like potentials were found much less frequently. Button pressing unequivocally generated additional P3-like potentials in the premotor cortical sites. Mental counting repeatedly evoked additional P3-like waveforms in the left-side middle and inferior temporal gyri. CONCLUSIONS: In addition to multiple intracerebral P3 generators that reflect target detection processing, other task-specific P3-like potential generators can be found in the human brain. Their activity may affect the topography and precise parameters of scalp P3 potential.
OBJECTIVE: This study concerned sensory processing (post-stimulus late evoked potential components) in different parts of the human brain as related to a motor task (hand movement) in a cognitive paradigm (Contingent Negative Variation). The focus of the study was on the time and space distribution of middle and late post-stimulus evoked potential (EP) components, and on the processing of sensory information in the subcortical-cortical networks. METHODS: Stereoelectroencephalography (SEEG) recordings of the contingent negative variation (CNV) in an audio-visual paradigm with a motor task were taken from 30 patients (27 patients with drug-resistant epilepsy; 3 patients with chronic thalamic pain). The intracerebral recordings were taken from 337 cortical sites (primary sensorimotor area (SM1); supplementary motor area (SMA); the cingulate gyrus; the orbitofrontal, premotor and dorsolateral prefrontal cortices; the temporal cortex, including the amygdalohippocampal complex; the parietooccipital lobes; and the insula) and from subcortical structures (the basal ganglia and the posterior thalamus). The concurrent scalp recordings were obtained from 3 patients in the thalamic group. In 4 patients in the epilepsy group, scalp recordings were taken separately from the SEEG procedure. The middle and long latency evoked potentials following an auditory warning (S1) and a visual imperative (S2) stimuli were analyzed. The occurrences of EPs were studied in two time windows (200-300 ms; and over 300 ms) following S1 and S2. RESULTS: Following S1, a high frequency of EP with latencies over 200 ms was observed in the primary sensorimotor area, the supplementary motor area, the premotor cortex, the orbitofrontal cortex, the cingulate gyrus, some parts of the temporal lobe, the basal ganglia, the insula, and the posterior thalamus. Following S2, a high frequency of EP in both of the time windows over 200 ms was observed in the SM1, the SMA, the premotor and dorsolateral prefrontal cortex, the orbitofrontal cortex, the cingulate gyrus, the basal ganglia, the posterior thalamus, and in some parts of the temporal cortex. The concurrent scalp recordings in the thalamic group of patients twice revealed potentials peaking approximately at 215 ms following S1. Following S2, EP occurred with latencies of 215 and 310 ms, respectively. Following S1, separate scalp recordings in 4 patients in the epilepsy group displayed EP 3 times in the 'over 300 ms' time window. Following S2, EP were presented once in the '200-300 ms' time window and 3 times in the 'over 300 ms' time window. CONCLUSIONS: The SM1, the SMA, multiple sites of the frontal lobe, some parts of the temporal lobe, the cingulate gyrus, the basal ganglia, the insula, and the posterior thalamus all participate in a cortico-subcortical network that is important for the parallel cognitive processing of sensory information in a movement related task.
Hemispheric language dominance, as determined by intracarotid short-acting barbiturate injections (Wada testing), was retrospectively evaluated in 44 right-handed patients with medically intractable left (n=26) or right (n=18) temporal lobe epilepsy (TLE). Atypical hemispheric language dominance (right or bilateral) was revealed in 13.6% of all patients investigated. A significantly higher rate of deviance from complete left hemisphere dominance was observed in left TLE (23.1%) than in right TLE (0%). Patient age at the time of seizure onset was proven a critical variable affecting atypical speech development in left TLE. The mean patient age at the time of seizure onset in left TLE patients with atypical language representation was 5.61 years, but was 13.13 years in patients with left hemisphere language dominance. Our results strongly support the influential impact of epileptiform activity spreading from the left temporal lobe structures on the reorganization of language functions in patients with early brain injury.
Three patients with advanced Parkinson's disease, all of whom developed excessive daytime sleepiness and 'sleep attacks' after the administration of entacapone, are described. This is another demonstration that inappropriate daytime sleep episodes are not exclusive to dopamine agonists.
Over the last decade, several authors have described an early negative (Ne) and a later positive (Pe) potential in scalp event-related potentials (ERPs) of incorrect choice reactions. The aim of the present study was to investigate the intracerebral origin and distribution of these potentials. Seven intractable epileptic patients participated in the study. A total of 231 sites in the frontal, temporal, and parietal lobes were investigated by means of depth electrodes. A standard visual oddball paradigm was performed, and electroencephalogram (EEG) epochs with correct and incorrect motor reactions were averaged independently. Prominent, mostly biphasic, ERP complexes resembling scalp Ne/Pe potentials were consistently observed in several cortical locations after incorrect trials. The most consistent findings were obtained from mesiotemporal structures; in addition to P3-like activity found after correct responses, an Ne/Pe complex was generally detected after incorrect trials. The Pe had a longer latency than the P3. Other generators of Ne/Pe-like potentials were located in different regions of the frontal lobe. The latency of the Ne was shortest in parietal, longer in temporal, and longest in frontal regions. Our findings firstly show that multiple cortical structures generate Ne and Pe. In addition to the rostral anterior cingulate cortex, the mesiotemporal and some prefrontal cortical sites seem to represent integral components of the brain's error-checking system. Secondly, the coupling of Ne and Pe to a complex suggests a common origin of Ne and Pe. Thirdly, the latency differences of the Ne across lobes suggest that the Ne is primarily elicited in posterior and temporal, and only later in frontal regions.
Twelve patients with levodopa-induced dyskinesias were treated with continuous subcutaneous apomorphine. A markedly significant reduction in peak dose dyskinesias occurred over a two-year follow-up.
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OBJECTIVE: The source of scalp-recorded Bereitschaftspotential (BP) remains a subject of ongoing discussion. This paper presents arguments in favour of the hypothesis that explains scalp-recorded BP as the result of the activity of both cortical and subcortical BP generators. METHODS: Intracranial recordings of BP were performed, mostly with depth electrodes in epilepsy surgery candidates. In some patients undergoing intracranial exploration, an electrode may have had contacts in the subcortical structures. RESULTS: BP is generated in several cortical and subcortical structures that are known to be directly or indirectly linked with motor control. Cortical sources of BP were displayed contralaterally to the movement in the primary motor cortex and somatosensory cortex, and bilaterally in the supplementary motor area (SMA), in the preSMA, and in the cingulate. A few other generators may be revealed in structures that have not yet been sufficiently explored. Subcortical generators of BP were found in the putamen, pallidum, caudate, and in the thalamus. In earlier recordings, BP was described rostrally to the thalamic region and in the brainstem, i.e. in the pes peripedunculi, nucleus peripeduncularis, pulvinar, and medial geniculate. CONCLUSIONS: Our observations do not explain the generation of scalp-recorded BP by the contribution of either cortical or subcortical sources alone. Intracranial cortical recordings contradict a wide distribution of scalp-recorded BP. Widely synchronised cerebral electromagnetic activity can be recorded on the scalp. We presume that in the case of BP, the weak deep dipoles might reach the scalp, as they are produced by a relatively huge mass of subcortical neuronal tissue. We strongly suspect that scalp-recorded BP represents a summation of potentials that are generated simultaneously in several cortical as well as in several subcortical structures.
PURPOSE: To investigate the effects of acute vagal nerve stimulation (VNS) on interictal epileptiform discharges (IEDs). METHODS: Fifteen epilepsy patients, all of whom had been treated with VNS for > or =6 months, entered the study. In each subject, the absolute number of IEDs was counted at the baseline period (BP), the stimulation period (SP), six interstimulation periods (IPs), and the prestimulation period (PP), by using an original paradigm. The number of IEDs at the BP and the PP was compared with the number of IEDs at the SP and IPs. The results were correlated with other variables (the duration of VNS, the value of the output current, the duration of epilepsy, the type of epilepsy, the effect of VNS, and the effect of extrastimulation). RESULTS: We observed a significantly higher reduction in the number of IEDs in the SP and all the IPs as compared with the BP. We noticed a significantly higher reduction in the number of IEDs in the SP and in the first IP as compared with the PP. The reduction of IEDs was greater in patients who responded to VNS (>50% reduction of all seizures) and in patients who responded positively to magnetic extrastimulation. There were no other significant results in the reduction of IEDs when comparing other variables. CONCLUSIONS: Short-term VNS reduces IEDs significantly. The reduction is most prominent during the SP (i.e., when the pulse generator is active). The value of reduction of IEDs is higher in patients who respond to VNS and in patients with positive experiences with magnetic extrastimulation. These results can be useful in predicting the effect of VNS.
PURPOSE: The interictal and ictal EEG activity in the basal ganglia in patients with temporal lobe epilepsy were studied during invasive EEG monitoring. METHODS: Eight epilepsy surgery candidates, each with a proven mesiotemporal seizure-onset zone, participated in the study. We used two invasive EEG methods to determine the seizure-onset zone. In both methods, diagonal electrodes were targeted into the amygdalohippocampal complex via a frontal approach and were passed through the basal ganglia with several leads. We analyzed 16 partial epileptic seizures, four of which became secondarily generalized. RESULTS: No epileptic interictal or ictal discharges were noticed in the basal ganglia. The interictal activity in the basal ganglia was a mixture of low-voltage beta activity and medium-voltage alpha-theta activity. When the ictal paroxysmal activity remained localized to the seizure-onset zone, the activity of the basal ganglia did not change. The spread of epileptic activity to other cortical structures was associated with the basal ganglia EEG slowing to a theta-delta range of 3-7 Hz. This slowing was dependent on the spread of ictal discharge within the ipsilateral temporal lobe (related to the investigated basal ganglia structures); alternatively, the slowing occurred in association with the regional spread of ictal activity from the mesiotemporal region to the temporal neocortex contralaterally to the investigated basal ganglia. Secondary generalization was associated with a further slowing of basal ganglia activity. CONCLUSIONS: The basal ganglia do not generate specific epileptic EEG activity. Despite the absence of spikes, the basal ganglia participate in changing or reflect changes in the distribution of the ictal epileptic activity.
OBJECTIVE: Rotigotine (Neupro) is formulated as a transdermal delivery system designed to provide a selective, non-ergot D3/D2/D1 agonist to the systemic blood flow over a 24-hour period. In clinical trials, patches were applied once daily and uptitrated to the individual effective dose in increments of 2 mg/24 h every week. The aim of this analysis was to determine the safety of a more rapid titration of rotigotine by assessing the tolerability of escalating transdermal doses of rotigotine given in 2 different titration schemes. METHODS: We analyzed the safety of rotigotine in 2 groups of patients with advanced stage Parkinson Disease. The starting dose of 4 mg/24 h was increased every week by 2 mg/24 h in the slow-titration group and 4 mg/24 h in the fast-titration group. The primary focus of this subanalysis was the separate tolerability of rotigotine in each randomized treatment arm, during the dose-escalation period. However, the 2 titration schemes were also compared with each other. RESULTS: The dose of first reported nausea and/or vomiting was 8 mg/24 h for the fast-titration group and 4 mg/ 24 h for the slow-titration group. There were no remarkable differences concerning the side-effect profile between the 2 different titration schemes. CONCLUSIONS: The fast-titration regimen had a similar adverse event profile to slower titration, and allowed rotigotine to be introduced quickly. This subanalysis suggests that rotigotine may be uptitrated more rapidly.