Laminar organization of the extraocular muscles of the rabbit.

Studies of bilateral hemispheric somatosensory evoked potentials (SEP) were carried out on 17 comatose patients following closed-head injury. Control evoked potentials were obtained from 74 normal volunteers. A prognosis of potential recovery or nonrecovery from coma was made in all 17 patients based on the SEP analyses. All subjects underwent bilateral median and peroneal nerve stimulation and responses were averaged from scalp electrodes placed over the somatotopic sensory cortex for the wrist and leg. The prognostic outcome of all 17 patients was accurately predicted following SEP analysis. Results show that 4 of 17 patients with prognoses of “positive recovery” had eight defined SEP peaks present within a time base analysis of 300 ms. Twelve patients with prognoses of “negative recovery” had five or less SEP peaks present within a time base of 500 ms. The majority of the “negative recovery” patients showed only SEP primary waveform components consisting of two peaks. The data suggest a potentially useful method using SEP analysis to prognosticate the possible recovery from clinical coma.     

Diagnosis of thoracic outlet syndrome Relative value of electrophysiological studies

The diagnostic utility of various electrophysiological techniques was evaluated in patients with thoracic outlet compression syndrome (TOCS). Our results suggest that in true neurogenic TOCS, there is no standard electrophysiological picture, but that this evolves with the severity of the syndrome. The first changes observed are electromyographic, followed by changes in F-wave and SEPs, followed finally by changes in nerve conduction parameters. EMG study was certainly more informative, showing neurogenic damage not only in limbs with neurological signs but also in about 1/4 of limbs with only subjective symptoms. The study of F-wave and SEPs does not seem to be particularly helpful, however, in view of the peculiar changes found in these patients, SEPs may be a useful complement to EMG. Nerve conduction studies were of little utility since changes in these parameters are only found in patients with long-standing anomalies and severe atrophy.     

Somatosensory evoked potentials induced by stimulating a variable number of nerve fibers in rat

Somatosensory evoked potentials (SEPs) were recorded from rat spinal cord (sSEPs) and cerebral cortex (cSEPs). Stimulus sites included either one or both sural nerve branches having different fiber populations (group A), or distal to a lesion of controlled size of the sural nerve made 1 week earlier (group B). In the two groups of animals, amplitudes of SEPs correlated with the quantity of large myelinated nerve fibers. Peak latencies of sSEPs in group A related to the ratio of sizes of transmitting fibers. sSEPs and cSEPs in both groups A and B could be recorded in a reproducible fashion by stimulating sural nerve branches or lesioned nerve trunks containing only 100 or less nerve fibers greater than 4 m?m in size. Thus, presence of sSEPs or cSEPs after stimulation distal to a lesion site does not insure that many nerve fibers have continuity with the central nervous system (CNS). © 1993 John Wiley & Sons, Inc.     

Magnetic stimulation of muscle evokes cerebral potentials

Somatosensory evoked potentials (SEPs) were recorded from the scalp in man to magnetic stimulation of various skeletal muscles. The potentials consisted of several components, the earliest of which decreased in latency as the stimulated site moved rostrally, ranging from 46 msec for stimulation of the gastrocnemius, to 14 msec for stimulation of the deltoid. Experiments were performed to distinguish the mechanisms by which magnetic stimulation of the muscle was effective in evoking these cerebral potentials. For the gastrocnemius, the intensity of the magnetic stimulus needed for evoking cerebral potentials was less than that required for activating mixed or sensory nerves in proximity to the muscle belly (eg, posterior tibial nerve in the popliteal fossa, sural nerve at the ankle). Vibration of the muscle or passive lengthening of the muscle, procedures which activate muscle spindles, were accompanied by a significant attenuation of the potentials evoked by magnetic stimulation of the muscle. Anesthesia of the skin underlying the stimulating coil had no effect on the latency or amplitude of the early components of the magnetically evoked potentials, whereas electrically evoked potentials from skin electrodes were abolished. Thus, the cerebral potentials accompanying magnetic stimulation of the muscle appear to be due to activation of muscle afferents. We suggest that magnetic stimulation of muscle can provide a relatively simple method for quantifying the function of muscle afferents originating from a wide variety of skeletal musculature.     

Invertebrate immune diversity

The arms race between hosts and pathogens (and other non-self) drives the molecular diversification of immune response genes in the host. Over long periods of evolutionary time, many different defense strategies have been employed by a wide variety of invertebrates. We review here penaeidins and crustins in crustaceans, the allorecognition system encoded by fuhc, fester and Uncle fester in a colonial tunicate, Dscam and PGRPs in arthropods, FREPs in snails, VCBPs in protochordates, and the Sp185/333 system in the purple sea urchin. Comparisons among immune systems, including those reviewed here have not identified an immune specific regulatory “genetic toolkit”, however, repeatedly identified sequences (or “building materials” on which the tools act) are present in a broad range of immune systems. These include a Toll/TLR system, a primitive complement system, an LPS binding protein, and a RAG core/Transib element. Repeatedly identified domains and motifs that function in immune proteins include NACHT, LRR, Ig, death, TIR, lectin domains, and a thioester motif. In addition, there are repeatedly identified mechanisms (or “construction methods”) that generate sequence diversity in genes with immune function. These include genomic instability, duplications and/or deletions of sequences and the generation of clusters of similar genes or exons that appear as families, gene recombination, gene conversion, retrotransposition, alternative splicing, multiple alleles for single copy genes, and RNA editing. These commonly employed “materials and methods” for building and maintaining an effective immune system that might have been part of that ancestral system appear now as a fragmented and likely incomplete set, likely due to the rapid evolutionary change (or loss) of host genes that are under pressure to keep pace with pathogen diversity.     

What causes hemiataxia after lacunar ischaemic stroke? A cliniconeurophysiological study

Both cerebellar dysfunction and proprioceptive deficits have been described as the cause of the ataxia in patients with ataxic hemiparesis. In order to determine the cause of the ataxia, we investigated the sensory modalities and performed median nerve somatosensory evoked potentials (SEPs) in 19 patients with hemiataxia following lacunar ischaemic stroke. All patients had computer tomography (CT) and/or magnetic resonance imaging (MRI) of the brain. SEP results were reviewed for correlation with clinical features and infarct location and size. In all patients, eye closure did not worsen the ataxia. There was no difference between the mean latency of the SEP components from the affected and non-affected hemisphere of the brain in all patients. Only two of the 19 patients had abnormal SEPs. There was no correlation between SEP findings, clinical features and location or size of the infarcts. The discovery of normal SEPs in most cases and the clinical aspects of the ataxia suggest that hemiataxia following lacunar ischaemic stroke is usually of the cerebellar type and that disturbed proprioception is unlikely as the cause in most patients. Cerebellar-like ataxia is most likely caused by disruption of the cerebellar pathways at the level of the internal capsule or corona radiata, i.e. either the ascending dentatorubrothalamocortical or the descending corticopontocerebellar pathways.     

The role of somatosensory evoked potentials in spinal dysraphism – do they have a prognostic significance?

Somatosensory evoked potentials (SEP) are not routinely used in spinal dysraphism. In this study 38 patients (29 children and 9 adults) with spinal dysraphism were prospectively studied with the objective of evaluating whether SEPs were a prognostic tool that could be used to predict clinical improvement after repair of a spinal dysraphic lesion. For all patients, preoperative SEP and postoperative SEP (within 1 week of operation) were recorded. Fifteen of these patients also had follow-up postoperative SEP recordings taken within 3 months of operation. A clinical examination was performed at the time of each SEP. Thirty patients had tethered cord, 12 had diastematomyelia and 15 had intra- and/or extradural tumours, which included lipomas and dermoid and epidermoid tumours. Twenty-one children and all adults had abnormal preoperative SEPs. Sixteen children and 4 adults had improved SEPs postoperatively. All these children and 2 of the 4 adults also experienced clinical improvement. Improvement in SEPs preceded clinical improvement in 12/20 patients. We observe that SEPs have a good prognostic value. Received: 14 December 1997     

Somatosensory evoked potentials during the ideation and execution of individual finger movements

Scalp somatosensory evoked potentials (SEPs) were recorded in 10 volunteers after median nerve stimulation, in four experimental conditions of hand movements performance/ideation, and compared with the baseline condition of full relaxation. The experimental conditions were (a) self-improvised hand-finger sequential movements; (b) the same movements according to a read sequence of numbers; (c) mental ideation of finger movements; and (d) passive displacement of fingers in complete relaxation. Latencies and amplitudes of the parietal (N20, P25, N33, and P45) and frontal peaks (P20–22, N30, and P40) were analyzed. Latencies did not vary in any of the paradigms. Among the parietal complexes, only the P25-N33 amplitude was significantly reduced in (a), (b), (c), and (d) and the N20-P25 was reduced in (a) and (d); among frontal waves, N30 and P40 were significantly reduced (20–75%) in (a) and (b). Coronal electrodes showed amplitude decrements maximal at the frontal-rolandic positions contralateral to the stimulated side. © 1996 John Wiley & Sons, Inc.     

Effects of methyl prednisolone,dimethyl sulphoxide and naloxone in experimental spinal cord injuries in rats

The effects of methyl prednisolone (MPD), dimethyl sulphoxide (DMSO), and naloxone were examined in 38 albino rats after making an impact spinal cord injury on the midthoracic segments with a modified Allen’s weight dropping trauma method. Somatosensorial evoked potentials (SEPs) were recorded before and 12 h and 14 d after the injury from epidurally inserted electrodes on the parietal cortex with sciatic nerve stimulations. Lower extremity, motor functions of the animals were also examined. It may be concluded that in this study model, DMSO has a moderate effect which can be demonstrated clinically and through SEPs. Naloxone has no effect on the clinical outcome but causes reasonable improvement electro-physiologically.     

"Numb, clumsy hands" and tactile agnosia secondary to high cervical spondylotic myelopathy: a clinical and electrophysiological correlation

Four patients presented with a distinctive syndrome of "numb, clumsy hand" and tactile agnosia. Myelography and computed tomographic myelography (CTM) of the cervical spine documented major spondylotic compressive lesions mainly between the C3 and C5 levels. The cortical responses of dermatomal somatosensory evoked potentials (DSEPs) revealed progressively prolonged peak latencies and progressively decreased amplitudes of early components from C6 to C8 dermatomal stimulation. In comparison, the C5 and L2 DSEPs were affected to a lesser extent. This finding suggests that high cervical cord compression may produce dysfunction of the dorsal column caudal to the direct compressive sites. In other words, the funiculus cuneatus of C6-8 cord is most affected in high cervical myelopathy. Moreover, the funiculus cuneatus is within the border zone susceptible to an overall reduction in blood flow. We conclude therefore, that ischemia secondary to cord compression is the pathophysiology resulting in this unique syndrome of "numb, clumsy hands" and tactile agnosia.