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PubMed1982

Response latency of brisk-sustained (X) and brisk-transient (Y) cells in the cat retina.

1. Several methods for evaluating light-evoked response latency and its variability in brisk-sustained (X) and brisk-transient (Y) retinal ganglion cells were tested. The most accurate procedure proved to be that described by Levick (1973), in which the time of the occurrence of the fourth impulse after stimulus onset is taken as an estimate of the latency.2. The shortest response latencies are obtained when the stimuli are the same size as the receptive field centre. At medium and high response amplitudes (> 150 impulses/sec) the response of brisk-transient (Y) cells to these optimal stimuli is 10-15 msec faster than that of adjacent brisk-sustained (X) cells.3. The response latency of brisk-sustained (X) cells for stimuli larger than the receptive field centre increases, whereas that of brisk-transient (Y) cells remains constant. Brisk-sustained (X) cells respond faster than do brisk-transient (Y) cells to stimuli smaller than the receptive field centre.4. No systematic difference exists between brisk-sustained (X) and brisk-transient (Y) cells in regard to the temporal variability of the response. The standard deviation of the latency for stimuli of optimal size decreases from 2.0-8.0 msec at medium stimulus contrast to 0.6-2.0 msec at high stimulus contrast.5. The response of OFF-centre cells to the disappearance of a light spot is always slower than that of an ON-centre cell of the same class to the onset of this stimulus. However, when OFF-centre cells are stimulated with dark spots, their response latency does not differ from that of ON-centre cells of the same class.6. No simple relationship exists between the response latency and the response amplitude. At medium and high discharge rates, most brisk-transient (Y) cells respond faster than an adjacent brisk-sustained (X) cell with equal response. At the same response amplitude, the latencies become shorter as the background illumination is raised. The same discharge rate can be obtained with stimuli of sub-optimal and supra-optimal size, but the latency for the larger stimulus is shorter than that for the smaller one. Latency, therefore, is an additional parameter characterizing the light-evoked response.

Action Potentials↗
PubMed1986

Development of auditory-evoked potentials in the cat. II. Wave latencies.

Brain stem and forebrain auditory-evoked potentials were studied parametrically during the first 90 postnatal days in unanesthetized kittens using tonal and click stimuli. This paper describes changes that occur in transmission time through the auditory pathway during development by analyses of the maturational time courses of latencies associated with waves of both auditory brain stem responses (ABR's) and late-occurring auditory-evoked potentials (AER's), recorded subdermally from the vertex. In response to click stimuli, ABR latencies were found to decay rapidly early in postnatal life and more slowly after the third postnatal week. Those trends were modeled as a two-stage sequential process, with a linear stage occurring between 7 and 18 postnatal days followed by an exponential stage during which adult latencies were achieved. AER latencies changes during development were less complicated, and followed a single-stage exponential time course. When threshold influences were taken into account--that is, when data were adjusted so that sensation level (SL) was constant across age--the latency-maturation curves associated with all ABR waves were adequately described by a single exponential, and latencies recorded from young animals were substantially shorter than latencies associated with the same aged animals when analyses were carried out with constant sound-pressure level (SPL) stimuli across age. In addition, the difference function, generated when isoasymptotic SPL and SL latency versus age functions were subtracted from one another, was also represented by an exponential curve, suggesting that at least two processes underlie the latency decay that occurs during postnatal development. Evoked responses to tonal stimuli throughout development were consistent with the basoapical developmental gradient that is observed anatomically.

Aging↗
PubMed2003

P300 (latency) event-related potential: an accurate predictor of memory impairment.

To determine if P300 latency changes precede and correlate with memory and mental status, patients (N=1506 aged 20-100 years) who received medical and psychiatric diagnoses (from 1997 to 2002), were assessed for P300 (N=1496), WMS-III (N=694), and MMSE (N=456). Patient and control groups included, a) normal WMS-III on all 4 subscales (N=36), b) normal WMS-III and MMSE (N=189) with subjective memory/mental status complaints, and c) medical patients with normal WMS-III and no memory complaints (N=205), and d) P300 control group without medical, psychiatric or memory problems for ROC. Patients with impaired/borderline memory had a prolonged P300 latency (P<0.02) compared to age matched non-impaired controls; in patients with normal WMS-III/MMSE, with subjective mild memory/mental status impairment, P300 latency was prolonged compared to controls (P=0.0004). The P300 latency increased by 0.72ms per year (P=7.9x10(-65)) and voltage decreased by 0.03dV per year (P=6.7x10(-10)), and both parameters were linearly correlated with the age of the subjects. Male subjects had an average voltage of 6.1dV and female 6.8dV (P=0.00009). Statistically, prolonged latency began at age range 41-50 (P=0.0002); reduced P300 voltage began at age range 51-60 (P=0.003). WMS-III memory decline for all measures began in females at age range 61-70 (P value at least=0.02) and for males at age range 61-80 (P=0.02). Prolonged P300 latency (P<0.0001) and memory impairment (at least <0.02) were greater for females than males. MMSE memory decline, male and female, began at age range 81-90 (P value of at least 0.00007). In our logistic regression model P300 latency was more predictive of WMS-III impairment than MMSE > 24. In patients whose WMS-III score is impaired < or = 69, or borderline < or = 79 (P at least=0.004), a P300 latency more prolonged than the norm (> or = 300 + 30 + Age) identifies these patients, whereas a MMSE > 24 failed. With the ROC curve, we confirmed that P300 latency could accurately identify borderline/impaired memory.

Adolescent↗
PubMed1991

Median nerve somatosensory evoked potentials: studies on latency variability as a function of subject height, limb length and nerve conduction velocity.

Report on the results of regression analysis studies concerning median nerve somatosensory evoked potentials (SEPs) latencies, as dependent variables, and subject height, limb length and nerve conduction velocity (NCV), as independent variables. The tests were performed on 23 normal volunteers. Absolute SEP latencies could be predicted by a linear regression model when the independent variable was arm length; when it was subject height, however, both exponential and polynomial models proved better, the latter showing the best coefficients of determination, R 2. Multiple linear regression with two independent variables (arm length and NCV) was found to be better than simple linear regression for predicting P/N13 latency. The regression line for EP-P/N13 latency on height was found to be a polynomial curve; although the regression was found to be significant by the "F" test (alpha = 1%), the model had a low R 2 value (0.41). The same applies to the P/N13-N19 interpeak latency regression curve, but the regression was significant for alpha = 5% in that case. Although interwave latencies are the most useful parameters for clinical interpretation of median SEPs, absolute latencies may occasionally be important, and should be corrected for body size. In unusually tall subjects, it might be useful to double-check EP-P/N13 interwave latency prolongation by estimating the maximum expected P/N13 latency, using a model that takes into account both limb length and NCV.

Body Constitution↗
PubMedDate not supplied

[Middle and late latency auditory evoked potentials in adults with AIDS].

BACKGROUND: Middle and late latency auditory evoked potentials. AIM: to verify the occurrence of middle and late latency auditory evoked potentials disorders in adults with Acquired Immunodeficiency Syndrome (AIDS). METHOD: Middle and late latency auditory evoked potentials of 8 individuals with AIDS, with ages ranging from 10 to 51 years, with normal hearing, or with sensoryneural hearing losses up to moderate, and normal results in the Auditory Brainstem Response, comparing the results with the responses obtained for a control group which was composed by 25 individuals, with ages ranging from 19 to 24 years, with no hearing complaints and with normal hearing and normal results in the Auditory Brainstem Response. RESULTS: The Pa wave latency and amplitude averages in the C3/A2 and C4/A1 modalities, and the average of the P300 wave were analyzed. No significant differences were observed in the Pa wave amplitude and latency averages between the groups, although a non-statistically significant increase was observed in the latency and a decrease in the amplitude of such wave for the research group in the C3/A2 modality. The latency of the P300 wave was significantly longer to the left for the research group. It was also observed a longer latency to the right, although this was not statistically significant. CONCLUSION: Adult individuals with AIDS do not present alterations in the middle latency auditory evoked potential and do present alterations in the cognitive potential, indicating a disorder in the cortical regions of the auditory pathway and a deficit in the cognitive processing of auditory information for this population. Such findings stress the importance of a careful investigation of the auditory function of individuals with AIDS, thus favoring the therapeutic planning.

Acoustic Stimulation↗
PubMed1962

On the discriminative control of concurrent responses: the relations among response frequency, latency, and topography in auditory generalization.

Human subjects were used in a study of auditory generalization following multiple-response discrimination training. The relations observed among stimulus intensity, response probability, and response latency were invariant with respect to whether the two vocal responses conditioned were topographically discrete, as in one experiment, or topographically continuous, as in another. The major findings were:1. The probabilities associated with a specific response were maximal over several stimulus values at the extreme ends of the continuum, then dropped sharply at stimuli intermediate to the initial S(D)'s as the probability of the alternative response increased.2. Overall response latency was inversely related to the relative frequency of the two responses at each stimulus value. When the two responses were most nearly equal in probability, latencies were maximal; when one response had close to unit or zero probability, latencies were minimal.3. Analysis of the latencies of the two responses, taken separately, revealed: (a) an increase in latency as the difference between the test stimulus and the initial S(D) increased; (b) a sharp discontinuity in the latency gradient and reversal in trend at intermediate stimulus intensities; and (c) at a given stimulus value, latencies associated with the stochastically dominant response were consistently shorter than those of the nondominant response.4. No changes in response topography (fundamental frequency) were correlated with the characteristic changes in probability and latency during stimulus generalization.

Discrimination Learning↗
PubMed1993

Wave V latency shifts with age and sex in normals and patients with cochlear hearing loss: development of a predictive model.

In order to study the combined effect of age, sex and cochlear hearing loss on the auditory brainstem response in an adult population, absolute wave V latency measurements were made in 117 ears of 64 patients with cochlear hearing loss and 105 ears of 58 otologically normal control subjects. Among normals, wave V latency was found to increase with age. Latencies in female subjects were significantly shorter than in male subjects. The best predictive model for wave V latency in normals was: wave V latency (ms) = 4.982 + 0.007 x age + 0.091 x sex, where age is measured in years and sex is given a value of 1 for females and 2 for males. In patients with hearing loss, wave V latency increase was determined largely by the degree of hearing loss and the effect of age was moderate. The influence of sex was minimal. Wave V latency in patients with hearing loss was predicted by the formula: wave V latency (ms) = 4.911 + 0.007 x hearing loss + 0.004 x age + 0.081 x sex. These predictive models can be utilized to accurately estimate expected wave V latency in patients with cochlear hearing loss.

Adult↗
PubMed2002

The latency of saccades, vergence, and combined eye movements in children and in adults.

PURPOSE: To examine the latency of eye movements in three-dimensional space (saccade, vergence, and combined saccade-vergence) in children and adults. METHODS: Fifteen normal children (4.5-12 years of age) and 15 normal adults (22-44 years of age) were tested. A standard paradigm was used to elicit pure lateral saccades at far and close viewing distance, pure vergence (convergence and divergence), and saccade combined with vergence movements. Horizontal eye movements from both eyes were recorded simultaneously by the oculometer, a photoelectric device. RESULTS: The mean latency in saccades, vergence, and combined eye movements was longer in children than in adults; the variability of such latency values was also larger in children. There was a progressive decrease with age in mean latency. All latencies approached or reached adult levels at approximately 10 to 12 years of age. Latency of saccades at close viewing distance was shorter than that at far in both adults and children. Convergence latency was longer than divergence latency in adults and most of the children. Latency of components of combined movements was longer than that of corresponding pure movements. Children initiated combined movements by triggering the vergence component first, whereas adults did not show a dominant pattern. The percentage of synchronous start of the two components was significantly higher in adults. CONCLUSIONS: Saccade- and vergence-triggering mechanisms are distinct and mature progressively and in parallel with age. The capacity for synchronization of the two components of combined eye movements develops more slowly and remains below adult level, even at the age of 12 years.

Adult↗
PubMed1986

Photoreceptor latency: analysis and definition.

Latency as a time difference between the stimulating light-pulse and the recorded potential response was studied with intracellular recording techniques on blowfly (Calliphora) visual receptors. Latency was shown to be a meaningful parameter in analysing the information content of the recorded receptor potential responses by comparing latency vs. amplitude functions using different intensities of stimulating light, stimulating angles of the incident light, ambient temperatures, and flies of different developmental stages. The maximum amplitude of the response is not sufficient to describe stimulus-response functions. With the help of the linear correlation analysis the most useful latency criterion among three widely used latency parameters (viz. the amplitude threshold (1 mV), the visual estimation (detectable voltage) and the maximum slope intersection with the base-line) was investigated. These were studied by correlating them with other commonly used response parameters. An arbitrarily chosen latency parameter that shows the lowest correlation coefficient is considered to contain more additional information from the photoreceptor voltage response than a latency parameter with high correlation. According to our analysis the most useful latency determination is proposed to be the time from the stimulus onset to the intersection of the maximum tangent at the base line, a criterion which also allows one to use concepts derived from systems analysis. The concept of latency is discussed and a definition proposed in the light of this and other recent findings.

Animals↗
PubMed1996

The peak latency of orbital presaccadic spike potential with horizontal eye movements.

PURPOSE: To investigate the peak latency of the orbital presaccadic spike potential (SP) with horizontal eye movement in normals. METHODS: Orbital SP was recorded in 28 normal subjects from 8 electrodes around the eyes with Pz as the reference while performing 5 degrees, 10 degrees, 20 degrees, 30 degrees and 40 degrees horizontal saccades to visual targets. SP peak latency was measured from SP onset to SP peak on averaged data aligned on SP peak. RESULTS: Significant main effects on SP peak latency are found for saccade size (P < 0.01), saccade direction (P < 0.01) and electrode site (P < 0.05). No significant main effect on SP peak latency is found for eye (P > 0.05). SP peak latency increases with increasing saccade size from 5 degrees to 40 degrees. SP peak latency is longer with saccades back to center than away from center, and with abducting saccades than with adducting saccades. SP peak latency differs at the electrode sites with an order from shorter to longer as follows: inner canthus (IC); inferior orbit (IO); outer canthus (OC); superior orbit (SO). CONCLUSIONS: The effects on the peak latency of orbital SP can be explained by the saccade dynamic property, volume conduction as well as physiologic and anatomic factors of the eyes and orbits. The peak latency of orbital SP can be used to reflect the temporal characteristics of ocular motor units controlling saccadic eye movement.

Adolescent↗
PubMed2002

Mouse models of cytomegalovirus latency: overview.

BACKGROUND: The molecular regulation of viral latency and reactivation is a central unsolved issue in the understanding of cytomegalovirus (CMV) biology. Like human CMV (hCMV), murine CMV (mCMV) can establish a latent infection in cells of the myeloid lineage. Since mCMV genome remains present in various organs after its clearance from hematopoietic cells first in bone marrow and much later in blood, there must exist one or more widely distributed cell type(s) representing the cellular site(s) of enduring mCMV latency in host tissues. Endothelial cells and histiocytes are candidates, but the question is not yet settled. Another long debated problem appears to be solved: mCMV establishes true molecular latency rather than a low-level persistence of productive infection. This conclusion is based on two recent advances. First, on a highly improved assay of infectivity, and second, on very sensitive RT PCRs for detecting viral transcripts during latency. In essence, infectious virus and productive cycle transcripts, such as transcripts of early-phase gene M55 (gB) and ie3 transcripts specifying the essential transactivator protein IE3, were found to be absent during mCMV latency in the lungs. OBJECTIVES: We will here review recent data on the variegated expression of IE-phase genes ie1 and ie2 during mCMV latency in the lungs, and on the expression patterns found in transcriptional foci during induced reactivation. We will discuss immunological implications of ie1 gene expression during latency and will speculate a bit on how CD8 T cells might trigger latency-associated ie1 gene expression in a regulatory circuit.

Animals↗
PubMed2006

A protein encoded by the bovine herpesvirus 1 latency-related gene interacts with specific cellular regulatory proteins, including CCAAT enhancer binding protein alpha.

Following acute infection, bovine herpesvirus 1 establishes latency in sensory neurons of trigeminal ganglia (TG). Reactivation from latency occurs periodically, resulting in the shedding of infectious virus. The latency-related (LR) RNA is abundantly expressed in TG of latently infected calves, and the expression of LR proteins is necessary for dexamethasone-induced reactivation from latency. Previously published studies also identified an alternatively spliced LR transcript which is abundantly expressed in TG at 7 days after infection and has the potential to encode a novel LR fusion protein. Seven days after infection is when extensive viral gene expression is extinguished in TG and latency is established, suggesting that LR gene products influence the establishment of latency. In this study, we used a bacterial two-hybrid assay to identify cellular proteins that interact with the novel LR fusion protein. The LR fusion protein interacts with two proteins that can induce apoptosis (Bid and Cdc42) and with CCAAT enhancer binding protein alpha (C/EBP-alpha). Additional studies confirmed that the LR fusion protein interacts with human or insect C/EBP-alpha. C/EBP-alpha protein expression is induced in TG neurons of infected calves and after dexamethasone-induced reactivation from latency. Wild-type C/EBP-alpha, but not a DNA binding mutant of C/EBP-alpha, enhances plaque formation in bovine cells. We hypothesize that interactions between the LR fusion protein and C/EBP-alpha promote the establishment of latency.

Animals↗
PubMed1999

Focal transcriptional activity of murine cytomegalovirus during latency in the lungs.

Interstitial pneumonia is a frequent and critical manifestation of human cytomegalovirus (CMV) disease in immunocompromised patients, in particular in recipients of bone marrow transplantation. Previous work in the murine CMV infection model has identified the lungs as a major organ site of CMV latency and recurrence. It was open to question whether the viral genome is transcriptionally silent or active during latency. Transcription could be latency associated and thus be part of the latency phenotype. Alternatively, transcriptional activity could reflect episodes of reactivation. We demonstrate here that transcription of the immediate-early (IE) transcription unit ie1-ie3 selectively generates ie1-specific transcripts during latency. Notably, while the latent viral DNA was found to be evenly distributed in the lungs, transcription was focal and randomly distributed. This finding indicates that IE transcription is not a feature inherent to murine CMV latency but rather reflects foci of primordial reactivation. However, this reactivation did not initiate productive infection, since ie3 gene mRNA specifying the essential transactivator IE3 of murine CMV early gene expression was not detectable. Accordingly, transcripts encoding gB were absent during latency. By contrast, during induced virus recurrence, IE-phase transcription switched from focal to generalized and ie3-specific transcripts were generated. These data imply that latency and recurrence are regulated not only at the IE promoter-enhancer and that there exists an additional checkpoint at the level of precursor RNA splicing. We propose that focal transcription reflects random episodes of nonproductive reactivation that get terminated before IE3 is expressed and ignites the productive cycle.

Animals↗
PubMed1999

Genetic studies exposing the splicing events involved in herpes simplex virus type 1 latency-associated transcript production during lytic and latent infection.

Herpes simplex virus type 1 (HSV-1) establishes latency in sensory neurons, a state in which the viral lytic genes are silenced and only the latency locus is transcriptionally active, producing the 2. 0- and 1.5-kb latency-associated transcripts (LATs). Previous experimental evidence indicates that the LATs are stable introns, and it has been reported that LAT formation is abolished by debilitating substitution mutations in the predicted splice sites during lytic infection but not latency (J. L. Arthur et al., J. Gen. Virol. 79:107-116, 1998). We have independently studied a set of deletion mutations to explore the roles of the proposed splice sites during lytic and latent infection. HSV-1 mutant viruses missing the invariant intron-terminal 5'-G(T/C) or 3'-AG dinucleotides were analyzed for LAT formation during lytic infection in vitro, when only the 2-kb LAT is produced, and during latency in mouse trigeminal ganglia, where both LATs are expressed. Northern blot analysis of total RNAs from different productively infected cell lines showed that the lytic (2-kb) LAT was not expressed by the various splice site deletion mutants. In vivo studies using a mouse eye model of latency similarly showed that the latent (2- and 1. 5-kb) LATs were not expressed by the mutants. PCR analysis with primers flanking the LAT sequence revealed the expected splice junction for LAT excision in RNA from sensory neurons latently infected with wild-type but not mutant virus. Using a virus mutant deleted in the splicing signals flanking the 556-bp region of LAT whose absence distinguishes the 1.5- and 2-kb LATs, we observed selective elimination of 1.5-kb LAT expression in latency, supporting previous suggestions that the internal region is removed by splicing. Taken together, these results demonstrate that the 2-kb LAT is formed during both lytic and latent infection by splicing at the predicted splice sites and that an additional splicing event is involved in the latency-restricted production of the 1.5-kb LAT. We have also mapped the 3' end of the lytic 2-kb LAT and discuss our results in the context of previous models addressing the unusual stability of the LATs.

Animals↗
PubMed2002

Characterization of a spontaneous 9.5-kilobase-deletion mutant of murine gammaherpesvirus 68 reveals tissue-specific genetic requirements for latency.

Murine gammaherpesvirus 68 (gammaHV68 [also known as MHV-68]) establishes a latent infection in mice, providing a small-animal model with which to identify host and viral factors that regulate gammaherpesvirus latency. While gammaHV68 establishes a latent infection in multiple tissues, including splenocytes and peritoneal cells, the requirements for latent infection within these tissues are poorly defined. Here we report the characterization of a spontaneous 9.5-kb-deletion mutant of gammaHV68 that lacks the M1, M2, M3, and M4 genes and eight viral tRNA-like genes. Previously, this locus has been shown to contain the latency-associated M2, M3, and viral tRNA-like genes. Through characterization of this mutant, we found that the M1, M2, M3, M4 genes and the viral tRNA-like genes are dispensable for (i) in vitro replication and (ii) the establishment and maintenance of latency in vivo and reactivation from latency following intraperitoneal infection. In contrast, following intranasal infection with this mutant, there was a defect in splenic latency at both early and late times, a phenotype not observed in peritoneal cells. These results indicate (i) that there are different genetic requirements for the establishment of latency in different latent reservoirs and (ii) that the genetic requirements for latency depend on the route of infection. While some of these phenotypes have been observed with specific mutations in the M1 and M2 genes, other phenotypes have never been observed with the available gammaHV68 mutants. These studies highlight the importance of loss-of-function mutations in defining the genetic requirements for the establishment and maintenance of herpesvirus latency.

3T3 Cells↗
PubMed2004

Critical role of CD4 T cells in an antibody-independent mechanism of vaccination against gammaherpesvirus latency.

We have previously demonstrated that it is possible to effectively vaccinate against long-term murine gammaherpesvirus 68 (gamma HV68) latency by using a reactivation-deficient virus as a vaccine (S. A. Tibbetts, J. S. McClellan, S. Gangappa, S. H. Speck, and H. W. Virgin IV, J. Virol. 77:2522-2529, 2003). Immune antibody was capable of recapitulating aspects of this vaccination. This led us to determine whether antibody is required for vaccination against latency. Using mice lacking antigen-specific antibody responses, we demonstrate here that antibody and B cells are not required for vaccination against latency. We also show that surveillance of latent infection in normal animals depends on CD4 and CD8 T cells, suggesting that T cells might be capable of preventing the establishment of latency. In the absence of an antibody response, CD4 T cells but not CD8 T cells are required for effective vaccination against latency in peritoneal cells, while either CD4 or CD8 T cells can prevent the establishment of splenic latency. Therefore, CD4 T cells play a critical role in immune surveillance of gammaherpesvirus latency and can mediate vaccination against latency in the absence of antibody responses.

Animals↗
PubMed1986

Subclinical cervico-spino-bulbar effects of lead: a study of short-latency somatosensory evoked potentials in workers exposed to lead, zinc, and copper.

Subclinical central and peripheral nervous system dysfunction among lead-exposed workers was studied by measuring short-latency somatosensory evoked potentials (SSEP) and maximal motor and sensory nerve conduction velocities (MCV and SCV) following stimulation of the median nerve at the wrist. The examinations were conducted in 20 gun-metal foundry workers exposed to lead, zinc, copper, and tin, with blood lead (BPb) concentrations of 16 to 64 micrograms/dl (mean, 42 micrograms/dl). The interpeak latency of SSEP in the cervico-spino-bulbar region [N9(Erb)-N13 latency] was significantly prolonged, and the MCV and SCV in the forearm were significantly slowed. Multiple regression analysis revealed that the yield of urinary lead following challenge with calcium disodium ethylenediamine tetraacetate (CaEDTA) and packed red blood cell volume were the major factors associated with the prolongation of SSEP latency in the cervico-spino-bulbar region. Similarly, the interpeak latency in the upper central nervous system (N13-N20 latency) was inversely related to the zinc concentration in erythrocytes; latency up to the Erb's point [N9(Erb) latency], which reflects conduction time in a long pathway of the sensory median nerve, was inversely related to urinary zinc level; the MCV and SCV in the palm were positively related to erythrocyte zinc concentration and plasma copper concentration, respectively. These findings suggest that the subclinical neurophysiological effects of lead occur not only in peripheral nerves but also in the central nervous system. It appears that zinc antagonizes the central and peripheral neurologic dysfunction caused by lead; similarly, copper antagonizes the peripheral sensory nerve dysfunction.

Adult↗
PubMed1989

Median to radial latency difference test in mild carpal tunnel syndrome.

Electrodiagnostic assessment of carpal tunnel syndrome (CTS) is hampered by the normal variability of conduction velocity, amplitude and duration of evoked responses, and hand temperature. Comparative testing of other nerves in the same hand may control for these variables and improve sensitivity for detection of mild focal entrapment. In consecutive cases referred for evaluation, antidromic sensory latencies were recorded from the thumb over 10 cm segments of the median and radial nerves, and the difference between these latencies was calculated. Median sensory antidromic conduction to digit III, ulnar sensory conduction, and median motor latency measurements were also made. Three hundred and thirty-three upper limbs were studied in 262 patients. All tests were normal in 73 arms. Mild conduction slowing was identified in 86 median nerves. The median-radial latency difference was increased in 87% of these mild cases. The median-ulnar latency difference was diagnostic in 88%. Either median-radial or median-ulnar latency differences were abnormal in all confirmed cases. The routine median motor and sensory distal latency tests had sensitivities of 29% and 52%, respectively. Radial responses were elicited in 99% of the hands studied. The median-radial latency difference in digit I is a sensitive indicator of mild CTS that can be measured quickly with a minimum of discomfort.

Adult↗