PubMed HealthSearch

Biomedical subjects

C W Hess

Publications and source records attributed to C W Hess.

At least 19 recordsLinked to original sources

Hypersomnia following paramedian thalamic stroke: a report of 12 patients.

Paramedian thalamic stroke (PTS) is a cause of organic hypersomnia, which in the absence of systematic sleep-wake studies has been attributed to disruption of ascending activating impulses and considered a "dearoused" state. However, an increasing mount of data suggests a role of the thalamus in sleep regulation and raises the possibility that a sleep disturbance contributes to hypersomnia in PTS. We evaluated 12 patients with magnetic resonance imaging-proven isolated PTS and hypersomnia with 10 to >20 hours of sleep behavior per day. Nocturnal polysomnographic findings paralleled the severity of hypersomnia. All subjects had increased stage 1 NREM sleep, reduced stage 2 NREM sleep, and reduced numbers of sleep spindles. In patients with severe hypersomnia, slow-wave (stages 3-4) NREM sleep was often reduced, but there were no major REM sleep alterations. Daytime sleep behavior was associated mostly with stage 1 sleep by electroencephalogram; there was no correlation between hypersomnia and results of nap tests. We conclude that hypersomnia following PTS is accompanied by deficient arousal during the day and insufficient spindling and slow-wave sleep production at night. These observations support the hypothesis of a dual role of the paramedian thalamus as "final common pathway' for both maintenance of wakefulness and promotion of NREM sleep.

Adolescent

[Sleep disorders in childhood].

Sleep disorders in childhood are frequent and usually harmless. They rarely point to a serious disease. Difficulty in falling asleep and nightly awakenings are age-dependent and transitory. While the largely harmless somnambulism and pavor nocturnus occur in the deep sleep of the first third of the night, the anxiety dreams of REM sleep appear preferentially in the second half of the night. Other disorders such as nocturnal enuresis and talking in sleep may occur during the whole night. It is very important to inform the parents because this helps to counter fears and false expectations. Consistent sleep hygiene needs to be developed with avoidance of irregular sleep rhythm and an unrestful sleep environment. Sometimes it is necessary to learn new behaviour patterns with the child. Only exceptionally is drug therapy indicated. However, nocturnal breathing disorders and nocturnal epilepsy do have a pathological significance and need specific therapy. In order to clarify the reasons for sleep disorders, it is necessary to keep a sleep diary, to undertake specific examinations (e.g. psychological, pneumological, neurological, urological, otorhinolaryngological and possibly using diagnostic equipment such as video-polysomnography).

Cataplexy

Sensitivity and specificity of needle electromyography: a prospective study comparing automated interference pattern analysis with single motor unit potential analysis.

In this prospective study, automated interference pattern analysis (IPA, "Willison analysis", modified by Stålberg et al. 1983) was compared to the quantitative evaluation of mean motor unit potential duration (QMUP) in 239 muscles from consecutive, unselected patients. The sensitivity and specificity of both methods were calculated with respect to the clinically derived final neurological diagnosis, with histology available for 120 examinations. Whereas specificities were not different for the methods, the sensitivity for detection of abnormal vs. normal was 49% for QMUP and 74% for IPA (P < 0.001). The sensitivity for detection of myopathy or neuropathy was 46% or 38% for QMUP and 75% (P < 0.001) or 53% (P < 0.05) for IPA. Thus, in all instances, IPA had superior sensitivity with unchanged specificity as compared to QMUP. The results of a rapid and purely qualitative visual MUP assessment were statistically not different from QMUP. Although widely used, neither of these methods has been evaluated for its reliability in unselected patients with various grades of disease. Our results indicate that in a routine setting, the best diagnostic strategy might be the automated IPA, which can be quickly obtained in several muscles, followed by muscle biopsy in unclear cases.

Adolescent

Electrophysiological characteristics of lesions in facial palsies of different etiologies. A study using electrical and magnetic stimulation techniques.

Using magnetic stimulation techniques in addition to conventional electrical stimulation, the entire facial motor pathway can be assessed electrophysiologically. To study the diagnostic yield of these examinations, 174 patients with facial palsies of a variety of etiologies were examined (85 Bell's palsies, 24 Guillain-Barré syndrome (GBS), 19 Lyme borreliosis, 17 zoster oticus, 12 meningeal affections, 10 brain-stem disorders and 7 HIV-related facial palsies). The facial nerve was stimulated electrically at the stylomastoid fossa and magnetically within its canalicular portion. Additionally, the face-associated contralateral motor cortex was stimulated magnetically. Recordings were from the nasalis or mentalis muscle, or both, using surface electrodes. Bell's palsy patients showed typically a unilateral local hypoexcitability of the facial nerve to canalicular stimulation. In GBS, bilateral latency prolongations were frequent, as expected for a myelinic disorder. In contrast, in zoster, predominant axonotmesis was unilateral, and in HIV infection sometimes bilateral. The method was very sensitive to detect subclinical dysfunctions in meningo-radiculitis and malignant meningeal diseases, either prior to the onset of palsy, or on the contralateral (clinically unaffected) side. It also distinguished reliably between central and peripheral facial motor pathway lesions. In our experience, these inexpensive and non-invasive electrophysiological techniques contribute substantially to the differential diagnosis of facial palsies.

Adult

Motion imagery in Parkinson's disease.

Patients with Parkinson's disease fail to fully profit from advance information about a target's movement in tracking tasks, possibly indicating deficient anticipation of the target's movement. Time estimation has been claimed to be deficient in Parkinson's disease. On the background of these studies, we tested the hypothesis that motion imagery is impaired in Parkinson's disease. Eleven non-demented patients with Parkinson's disease and nine age-matched controls participated in experiments testing their ability to anticipate trajectories of moving points (prediction whether two moving points would crash or not) and to estimate the time needed for completion of an invisible target's movement (a point moving around a circle). In addition, mirror drawing, a task involving motor learning and adjustment of movement to incongruent visual feedback, was tested. The Parkinson's disease patients, who failed to improve on mirror drawing, were not impaired on the imagery tasks: they estimated movement time and predicted trajectories with equal precision as the controls. Motion imagery thus appears to be intact in Parkinson's disease. However, Parkinson's disease patients did not accelerate their predictions of trajectories with practice as fast as the controls, a deficit which may be interpreted in terms of the fronto-striatal dysfunction repeatedly demonstrated in Parkinson's disease.

Aged

Diagnostic value of paraclinical tests in multiple sclerosis: relative sensitivities and specificities for reclassification according to the Poser committee criteria.

The yield of paraclinical tests was evaluated in a prospective study of 189 consecutive patients referred for suspected multiple sclerosis (142 patients with multiple sclerosis, 47 non-multiple sclerosis patients on discharge). Patients were first classified according to the Poser criteria by the clinical findings. Subsequently, the results of paraclinical tests (cranial MRI, visually evoked potentials (VEPs), somatosensory evoked potentials by tibial nerve stimulation (SSEPs), motor evoked potentials (MEPs), and analysis of CSF for oligoclonal banding and IgG-index (CSF)) were taken into account. The percentage of reclassified patients (reclassification sensitivity, RS) was always lower than the percentage of abnormal results (diagnostic sensitivity, DS), and the divergence of RS v DS differed between the tests (60% v 84% in MRI, 31% v 77% in CSF, 29% v 37% in VEPs, 20% v 68% in MEPs, and 12% v 46% in SSEPs respectively). False reclassifications of non-multiple sclerosis patients to multiple sclerosis would have occurred with all tests (MRI: six of 47 patients, (reclassification specificity 88%); CSF: one (98%); VEPs: two (96%); MEPs: two (96%); SSEPs: four (91%); P < 0.05). Although MRI had superior diagnostic capacity, 57 of the 142 patients with multiple sclerosis were not reclassified by the MRI result, 12 of whom were reclassified by CSF and 18 by one of the evoked potential (EP) studies. Of the 98 patients not reclassified by CSF, 53 were reclassified by MRI and 39 by EPs. The results suggest that for the evaluation of paraclinical tests in suspected multiple sclerosis, comparison of diagnostic sensitivities is inappropriate. In general, a cranial MRI contributes most to the diagnosis; however, due to its comparatively low specificity and its considerable number of negative results, EP or CSF studies are often useful to establish the diagnosis of multiple sclerosis.

Adolescent

[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