[The new graduate education ruling for neurology].
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Curriculum↗
Biomedical subjects
C W Hess
Publications and source records attributed to C W Hess.
[25 years of valproate in Switzerland].
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Epilepsy↗
[Developments in neurophysiology in the 19th century].
The rise of neurophysiology in the 19th century was kindled by Luigi Aloysius Galvani's revolutionary claim for animal electricity at the end of the preceding century. He was first challenged by Allessandro Giuseppe Antonio Anastasio Volta who showed that the muscle twitch in Galvani's experiment was the result of electric stimulation rather than of an enabled biological current. The controversy between Galvani and Volta became a predominant and stimulating issue among the scientists of the early century and found its ultimate elucidation only 40 years later by the pioneering work of Carlo Matteucci of Pisa and Emil Heinrich Du Bois-Reymond of Berlin, who both deserve the reknown as founders of modern neurophysiology. As the first influential promoter and mastermind of the experimental physiology, François Magendie of Paris primarily investigated the nervous system and inaugurated the lesion experiments to clarify specific functions of neural structures. Johannes Müller founded the German school of physiology with its eminent neurophysiological offspring: Du Bois-Reymond, Hermann Ludwig Ferdinand von Helmholtz, and Eduard Friedrich Wilhelm Pflüger. It was Helmholtz's merit to have for the first time precisely assessed the motor conduction velocity by measuring the time interval between two different stimulation sites of the sciatic nerve of the frog. In their brilliant work published in 1870 Gustav Theodor Fritsch and Eduard Hitzig demonstrated that appropriately located focal electrical stimulation of the exposed cortex of dogs induces movement of the contralateral limbs and unequivocally disproved the then prevailing dogma of holistic capacity of the hemispheres, which denied localised functions within the cortex.(ABSTRACT TRUNCATED AT 250 WORDS)
Europe↗
[The diagnostic significance of additional electrophysiological studies in suspected neurogenic thoracic outlet syndrome].
The neurogenic thoracic outlet syndrome (TOS) is a controversial clinical entity, since unambiguous diagnostic criteria are lacking and abnormal findings are absent in many patients. To evaluate electrodiagnostic methods a retrospective analysis was done comprising all 75 patients with suspected TOS who had been examined electrophysiologically in our laboratory in the last 5 years. 35 of the 75 patients were finally diagnosed as having TOS, but only 10 of them had a corresponding electrophysiological pathology. 6 had "classic" TOS with clinically obvious sensorimotor deficits, whereas in 4 the electrophysiologic findings were the only abnormalities (in 3 of 4, only minor neurographic anomalies were found). Proximal motor stimulation techniques did not improve the diagnostic yield. We conclude that electrodiagnostic methods are of little value in the diagnosis of TOS if there are no clinical abnormalities. The electrophysiological examinations did however reveal distal entrapment neuropathies in 15 of 75 patients (12 carpal tunnel syndromes). The frequent detection of such neuropathies in our patients is interesting and it justifies per se electrodiagnostic examination of the patient with suspected TOS.
Adolescent↗
[Neurology of consciousness and of consciousness disorders].
The two physiologic components of conscious behaviour, namely arousal (vigilance) and content of consciousness (presence of mind), may be affected differently, depending on the type and distribution of the underlying brain disease. Disturbance of arousal primarily affects wakefulness and awareness and leads to obtundation, stupor and coma. States of reduced arousal are caused by bilateral lesions of the so-called ascending reticular activating system (ARAS), which is situated in the upper brainstem and the paramedian diencephalon. If, on the other hand, cognitive and mnemic function are degraded, the contents of consciousness are disordered; depending on the extent of the disturbance, confusion, lethargy and, finally, a vegetative state ensues. The chronic vegetative state (coma vigil) describes a condition of total mental loss with preserved vegetative functions and arousal. Degraded cognitive and mnenic functions results from either toxic-metabolic or extensive structural disorders of the cerebral cortex, where the limbic and mesial frontal areas play a dominant role for conscious behaviour. If the function of extensive areas of both hemispheres is suddenly depressed, temporarily reduced arousal also results. In order to differentiate between toxic-metabolic and structural brain diseases, the motor reactions, the ocular and the pupillary reflexes must be examined apart from responsiveness.
Arousal↗
Electrophysiological characterization of pre- and postoperative facial nerve function in patients with acoustic neuroma using electrical and magnetic stimulation techniques.
Facial nerve function was examined in patients who underwent posterior fossa surgery for unilateral acoustic neuroma. Examinations took place prior to surgery (n = 47 patients), early after surgery (0-12 days, n = 16 of 47 patients), and late after surgery (187-1505 days, n = 29 of 47 patients). Clinical signs of facial palsy were present to a variable extent in 13 of 47 patients before, in 12 of 16 patients early, and in 18 of 29 patients later after surgery. Electrophysiologically, the facial nerve was stimulated electrically at the stylomastoid fossa and magnetically at its proximal intracanalicular segment. In addition, the face-associated motor cortex was stimulated magnetically. In patients with facial palsy, any of these stimulation methods resulted in a decreased amplitude of the response in the nasalis muscle. The decrease showed a linear relationship to the clinical grade of palsy, pre- and postoperatively. Corticomuscular latencies remained unchanged. We conclude that: (i) the electrophysiological characteristics of facial nerve lesions due to compression by acoustic neuromas or due to a complication of neuroma removal are those of a purely axonal neuropathy; (ii) the three stimulation techniques have a similar diagnostic yield, thus making the use of all three of them redundant; and (iii) the electrophysiological techniques allowed no prediction of the final facial nerve function.
Adult↗
Assessment of motor pathways to masticatory muscles: an examination technique using electrical and magnetic stimulation.
To study motor pathways to masticatory muscles, a new recording technique using surface electrodes was developed. The recording electrode was mounted on a spatula and inserted enorally into the pterygomandibular plica over the belly of m. masseter. Using this technique, mean latencies/amplitudes of the compound action potentials (CMAPs) in 18 healthy subjects were 1.2 ms/4.9 mV after electrical stimulation of the trigeminal nerve below the zygomatic arch, and 5.5 ms/1.1 mV after magnetic stimulation of the cortex. In 15 patients with unilateral lesions of the facial nerve, masticatory CMAPs had virtually symmetrical configuration, latency, and amplitude, excluding a major contribution of volume conducted activity from other cranial muscles. The technique was evaluated in patients after surgical treatment for trigeminal neuralgia. Patients with retrogasserian thermocoagulation and central demyelinating lesions were consistently identified.
Action Potentials↗
Influence of transcranial magnetic stimulation on the execution of memorised sequences of saccades in man.
Memorised sequences of saccades are cortically controlled by the supplementary motor area (SMA), as shown in animal experiments and in humans with isolated SMA lesions. We applied transcranial magnetic stimulation (TMS) in eight healthy subjects executing memorised sequences of saccades. Sequences of three targets were presented. Then, upon a go-signal, the subjects had to execute the appropriate sequences. Ten to fifteen sequences were performed in each experiment, and the number of errors were counted. The number of errors increased significantly if TMS was given 80 ms before or 60 ms after the go-signal, with the stimulation coil overlying the SMA. There was no significant increase in errors if different stimulation intervals were chosen (160 ms and 120 ms before the go-signal; 100 ms, 140 ms or 240 ms after the go-signal), if the coil was positioned inappropriately (e.g. over the occipital cortex), or if the stimulator output was too low. We conclude that TMS can interfere specifically with the function of the SMA during a critical time interval close to the go-signal.
Adult↗
Magnetic transcranial and electrical stylomastoidal stimulation of the facial motor pathways in Bell's palsy: time course and relevance of electrophysiological parameters.
Facial nerve motor neurography was performed at various times after the onset of Bell's palsy in 97 patients. Stimulation of the facial nerve was performed (1) electrically in the fossa stylomastoidea (ElStim), and (2) magnetically in the labryinthine segment of the facial canal (MagStim), evaluating different coil positions over the skull. Additionally, the face-associated motor cortex was stimulated magnetically in 47 patients (CxStim). A marked reduction of the amplitudes of the compound muscle action potentials (CMAP) evoked by MagStim on either m. nasalis or mentalis, or both, was observed which was clearly more pronounced than the amplitude reduction to ElStim. This discrepancy occurred very early during the disease, the mean amplitude (expressed in percent of the amplitude on the unaffected side) being 82% (S.D. 9.1) for ElStim and 1% (2.7) for MagStim at days 0-4. It persisted for several months, often when facial nerve function had recovered to normal, as assessed by clinical observation, ElStim, and CxStim. This amplitude decrease to MagStim, which appears to be related to a locally enhanced stimulation threshold of the facial nerve, is a very sensitive and reproducible finding in Bell's palsy. It may prove specific of the disorder, of diagnostic value, and of interest in the follow-up of patients during treatment trials.
Action Potentials↗
Motor-evoked responses to transcranial brain stimulation persist during cataplexy: a case report.
Magnetic brain stimulation was performed in a patient with the narcolepsy-cataplexy syndrome during and after a cataplectic status. Amplitudes and thresholds of responses in six muscles (diaphragm, lumbar erector spinae, trapezius, biceps, tibialis anterior and abductor digiti V) remained unchanged during cataplexy as compared to the normal state. Our data suggest that, similar to rapid eye movement (REM) sleep, an enhanced cortical excitability to magnetic brain stimulation may compensate for the postsynaptic spinal inhibition of muscle tone during cataplexy, and that there is no difference in this respect between axial and distal muscles. Our data agree well with other evidence of increased cortex activity during cataplexy and REM sleep.
Action Potentials↗
Multimodal electrophysiological studies including motor evoked potentials in patients with locked-in syndrome: report of six patients.
Clinical and electrophysiological findings in six patients with locked-in syndrome are reported. Motor evoked potentials (MEPs) after magnetic stimulation of the motor cortex were absent in four patients, none of whom recovered clinically. In two patients, MEPs could be obtained from the severely paretic limbs and almost full motor recovery followed. Somatosensory evoked potentials were altered in four of the patients, and brainstem auditory evoked potentials were altered in two of four patients examined, showing a clinically unsuspected tegmental involvement. The EEG showed a predominance of reactive alpha activity in all patients, documenting a preserved consciousness. It is concluded that a multimodal electrophysiological approach, in addition to clinical assessment, can be helpful in diagnosing locked-in syndrome, estimating the extension of the underlying brainstem dysfunction, and predicting functional outcome.
Adolescent↗
Electrophysiological assessment of central and peripheral motor routes to the lingual muscles.
Compound muscle action potentials (CMAPs) of the lingual muscles were recorded by especially devised bipolar surface electrodes placed on the tongue. Distinct responses were evoked in the tongue muscles by peripheral electrical stimulation of the hypoglossal nerve medial to the angle of the jaw and by transcranial magnetic stimulation of the motor cortex. With cortical stimulation during voluntary activation of the tongue muscles it proved easy to obtain responses with the characteristics of centrally evoked responses allowing reliable measurements of latencies and amplitudes. By contrast, responses from magnetic stimulation of the intracranial segment of the hypoglossal nerve were more difficult to obtain and the reproducibility was often not satisfactory. In a group of 20 healthy subjects the average distal motor latency of both sides from peripheral stimulation was 2.4 ms and the corresponding amplitude was 9.3 mV on the left and 8.6 mV on the right side (range 5.1-16.0 mV). Cortical stimulation gave responses with an average onset latency of 8.6 ms and 8.8 ms and an average amplitude of 1.8 mV and 2.6 mV on the left and right sides of the tongue respectively (range 0.7-5.6 mV). From this mean conduction times of 6.2 ms on the left and 6.4 ms on the right side (SD 1.0 ms) between cortex and mandibular angle and relative amplitudes from cortical stimulation as compared with the peripheral CMAP of 29% on the left and 21% on the right side (range 7%-66%) were calculated. In 16 patients it was possible to differentiate between a central (supranuclear) and a peripheral (intranuclear) site for the lesions of the motors routes to the lingual muscles and to show subclinical lesions in some cases. With a recording arrangement allowing selective unilateral recording of muscle activity from both sides of the tongue the assumed bihemispheric motor representation of the lingual muscles was confirmed.
Action Potentials↗
Beneficial effect of inhaled CO2 in a patient with non-obstructive sleep apnoea.
A 63-year-old man with severe non-obstructive sleep apnoea (apnoea index 28; apnoea duration 45-60s; O2 saturation between 72% and 98%), who did not respond to common modes of treatment, was successfully treated with CO2. A tent was perfused with compressed air (6 1/min) and increasing amounts of CO2. A concentration of 3% CO2 (180 ml/min) was sufficient to raise the PaCO2 above apnoea threshold and to suppress apnoeas completely. As a result, O2 saturation remained normal throughout the whole night and the symptoms of sleep apnoea disappeared. We hypothesize that the PCO2 ventilatory drive was intact in our patient and that hypocapnia was the major factor causing the non-obstructive sleep apnoea syndrome. Administration of CO2 with a constant flow system could be a safe and easy alternative for patients with non-obstructive sleep apnoea syndrome who present with hypocapnia and an intact respiratory feedback control system.
Administration, Inhalation↗
Facilitation of motor evoked potentials from magnetic brain stimulation in man: a comparative study of different target muscles.
The influence of tonic muscle contraction and stimulus intensity on compound muscle action potentials (CMAPs) elicited by magnetic brain stimulation was studied in the biceps brachii (34 subjects), the abductor digiti minimi (11 subjects), the anterior tibial muscle (12 subjects), and the soleus muscle (5 subjects). The muscles were examined at rest and with various degrees of background contraction of up to 60% of maximum force. Stimulus intensity was set at threshold (TSI) or 20% above threshold (1.2 TSI), and in one series additionally at 50% above threshold (1.5 TSI). The effect of voluntary background contraction on CMAP onset latency was similar in the four muscles tested: the latencies shortened by approximately 3 ms when the muscle changed from the relaxed to the contracted state of the 10% of maximum force. An additional increase in the background contraction up to 60% of maximum force induced only few, if any, additional decreases in latency. The uniformity of the latency shift in distal and proximal muscles conflicts with the idea of recruitment of larger and rapidly conducting motoneurons being the cause, since this hypothesis would imply a more pronounced latency reduction in distal than in proximal muscles. The shorter latency during voluntary contraction is more likely due to an enhanced synaptic efficacy at spinal level. Since the motoneurons are brought into an increased state of activity during contraction, they require less temporal summation to reach firing threshold and thus discharge earlier. The CMAP amplitudes of the different muscles were more distinctly affected by voluntary background contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Parasomnias].
Parasomnias are frequent. They usually represent either the exaggeration of a physiological phenomenon (e.g. sleep starts) or a non-disturbing, idiopathic and usually benign sleep disorder (e.g. sleep talking and bruxism), which need only counseling and improvement of sleep hygiene. However, occasionally parasomnias are of clinical relevance. They can cause insomnia or hypersomnia (e.g. 'myoclonus nocturnus'), psychosocial stress (e.g. sleep-related enuresis and sleep walking) and injuries to oneself and others (e.g. REM-parasomnia). Finally, they can be symptomatic of neurological and medical disorders (e.g. sleep paralysis and 'myoclonus nocturnus'). In these cases special investigations including video-polysomnography can establish a correct diagnosis and allow a specific treatment.
Bruxism↗
Motor and somatosensory evoked potentials in coma: analysis and relation to clinical status and outcome.
Central sensory and motor conduction were studied in 23 comatose and three brain-dead patients. Motor evoked potentials (MEPs) to transcranial magnetic (magMEP) and electrical (elMEP) stimulation were recorded from the hypothenar muscle, and somatosensory evoked potentials (SEPs) were recorded after median nerve stimulation. Comparison of clinical with evoked potential (EP) findings revealed: 1) a painful stimulus applied to the skin of the arm lowered excitation threshold to cortical stimulation and was a prerequisite to obtain MEPs in 14 instances; 2) only in braindead patients were all EPs abolished simultaneously and bilaterally; 3) MEPs (p less than or equal to 0.05, chi 2-Test), but not necessarily SEPs (p greater than 0.1) were preserved in the arms that showed normal motor reaction during clinical examination; 4) no correlation was found between EP findings and the Glasgow Coma Scale (GCS). The results of clinical and EP testing were examined in the light of the patient's outcome 10 months later: 1) fatal outcome was predicted by a GCS of three (38% of cases, p less than or equal to 0.05, Fisher's exact test), abolished brainstem- or papillary reflexes (38%, p less than or equal to 0.05), the combination of these clinical signs (54%, p less than or equal to 0.01), bilateral abolition of elMEPs (38%, p less than or equal to 0.05), magMEPs (38%, p less than or equal to 0.05), or SEPs (23%, p greater than 0.1), or a combination of clinical and EP data (85%, p less than or equal to 0.0005); 2) good outcome was predicted by a GCS of greater than or equal to 8 only in post-traumatic coma, and EPs did not help to predict fatal outcome of coma; 1) if this appears impossible on the basis of clinical data alone; 2) if a second indicator is needed to confirm a clinical impression; 3) SEPs may be first evaluated during the acute stage of coma treatment, because they can be recorded in the presence of anaesthetic or relaxant agents; 4) MEP may be studied if outcome prediction remains ambiguous, and if the clinical situation allows for discontinuation of these agents.
Adolescent↗
Influence of some anesthetic agents on muscle responses to transcranial magnetic cortex stimulation: a pilot study in humans.
The effects of some commonly used intravenous and inhalational anesthetic agents on the motor evoked responses to transcranial magnetic cortex stimulation were assessed in 17 subjects. Compound motor action potentials (CMAPs) of the abductor digiti minimi muscle were recorded. Baseline values (12 stimulations/subject) were established before anesthesia was induced with a single agent administered in steps up to a maximal dose (MaxDose). Cortical stimulation was performed and depth of anesthesia was assessed according to Guedel after each dose. A common feature was the marked intra- and interindividual variability of baseline values of CMAPs in those patients not premedicated, those premedicated, and the anesthetized patients. The average amplitude of CMAPs was related to the depth of anesthesia in a given subject, whereas onset latencies of CMAPs did not systematically change. CMAPs were markedly reduced or abolished after administration of potent sedative drugs such as midazolam (MaxDose, 0.4 mg/kg body weight), pentothal (MaxDose, 8 mg/kg), propofol (MaxDose, 2 mg/kg), and isoflurane (MaxDose, 1.9 and 3.7 vol %), as soon as patients reached Stage II and Stage III anesthesia. When fentanyl (MaxDose, 8 micrograms/kg) or nitrous oxide (MaxDose, 79%) was used, the subjects reached Stages I and II, but not Stage III. With these drugs, reliable recording of CMAPs was possible even with the maximal administered dose.
Action Potentials↗
Transcranial stimulation of the human frontal eye field by magnetic pulses.
Single transcranial magnetic pulsed stimuli were applied over the cortical area of the putative right frontal eye field (FEF) in 11 healthy subjects. An especially designed figure of eight shaped twin coil was used, to focus the stimulus, the strength of which was adjusted to the individual motor threshold of the left hand muscles. Eye positions and movements were recorded by an infrared reflection technique. Three different experiments were performed: 1. Stimulation during different primary gaze position did not evoke any discernible eye movement. 2. Stimulation just prior to visually elicited horizontal saccades did not cause a significant alteration of the latency, velocity, or amplitude of the saccades. 3. Only stimulation during an antisaccade task induced a significant latency prolongation, when the stimulus was applied between 50 to 90 ms after the target flashed up. This latency prolongation was found in all subjects for the antisaccades to the right, with a statistically significant average latency difference of +66 +/- 55.5 ms. In contrast, the antisaccades to the left were prolonged in the female subjects only by an average of +98 +/- 41.8 ms (p = 0.0064), whereas in the male subjects they did not alter with stimulation (average difference: -3 +/- 41.9 ms, p = 0.753). Significant latency prolongations were only obtained when the magnetic FEF stimuli were applied within a vulnerable period, which varied from subject to subject.
Adult↗