Limitations Of The Paced Auditory Serial Addition Test As A Measure Of Working Memory In Multiple Sclerosis
Fisk JD, Archibald CJ
J Int NeuroPsychol Soc 2001 Mar;7(3):363-72
Dalhousie University, Halifax, Nova Scotia, Canada
PMID#11311037; UI# 21204977
The Paced Auditory Serial Addition Test (PASAT) is a commonly used procedure that combines elements of both a working memory task and a test of information processing speed.
Patients with Multiple Sclerosis (MS) have consistently been found to be impaired on this test and it has been recommended as a core outcome measure in clinical trials.
The standard score for this task is the number of correct responses at each stimulus presentation rate.
But a concern has been raised that subjects may ignore some test items in order to chunk the information into manageable portions and avoid performing several Cognitive tasks simultaneously.
To account for this strategy, one can examine the proportion of correct responses that are consecutive (termed dyads), since such responses require that the task be performed according to the instructions.
We compared a group of 35 mildly to moderately disabled MS patients and matched healthy controls on the PASAT.
The MS patients made significantly fewer correct responses at the 2 slowest presentation rates (2.4, 2.0 s/digit) while their scores at faster rates (1.6, 1.2 s/digit) did not discriminate them from controls as well.
Nevertheless, the MS patients' percentage of dyads was significantly lower than that of the control sample across all stimulus presentation rates.
While our study supports the use of the PASAT as a test that distinguishes MS patients from healthy individuals, our results also illustrate problems that lie in the interpretation of this difference in performance.
It appears that a chunking strategy may be common in the PASAT, particularly as task demands increase, and that this may mask actual performance differences.
If so, the total correct response score alone is limited as a measure of working memory and information processing speed.
More detailed analyzes of PASAT performance, coupled with other measures of information processing, may help clarify the underlying Cognitive deficits of MS patients.
Visual Object Recognition In Multiple Sclerosis
Laatu S, Revonsuo A, Hamalainen P, Ojanen V, Ruutiainen J
J Neurol Sci 2001 Apr 1;185(2):77-88
Univ of Turku, Centre for Cognitive NeuroScience, Turku, Finland
PMID#11311287; UI# 21211551
Deficits in tasks measuring Visual processing have been earlier reported in studies of MS. Yet, the nature and severity of Visual-processing deficits in MS remains unclear.
We used a new method in order to measure the different stages of Visual processing in object recognition: shape recognition, familiarity recognition, semantic categorization, and identification with naming.
Six two-choice reaction-time tasks were presented to 30 MS patients and 15 healthy controls. The patients were divided into cognitively preserved and Cognitively deteriorated study groups according to their Cognitive status.
The purpose was to find out whether deficits at specific stages of Visual processing can be found in Cognitively deteriorated MS patients.
Cognitively deteriorated MS patients did not perform as well as Cognitively preserved MS patients or healthy controls.
They were slower already at the early stage of Visual processing where discrimination of whole objects from scrambled ones was required. They also had higher error rates in tasks requiring object familiarity detection and object identification with naming.
Thus, Cognitively deteriorated MS patients had difficulties in visual shape recognition and semantic-lexical processing.
However, variation of performances was large within both of the patient groups indicating that even patients without a generalized Cognitive decline may have deficits in some stages of the visual processing.
We suggest that because of the heterogeneity of the patients, every single case needs to be examined separately in order to identify the possible deficits in Visual processing.
Human HerpesVirus 6: Diagnosis Of Active Infection
Carrigan DR, Knox KK
Am Clin Lab 2000 Aug;19(7):12
Wisconsin Viral Research Group, Ltd., 10437 Innovation Dr., Ste. 319, Milwaukee, WI 53226, USA
PMID#11317413; UI# 21215691
HHV-6 is an opportunistic Viral pathogen that has been demonstrated as the cause of often life-threatening illness in pediatric patients and transplant recipients.
A substantial body of scientific evidence links HHV-6 to the etiology of such chronic diseases as Multiple Sclerosis. For these reasons, it is important that patients in these groups be screened for possible infection with HHV-6.
Serological studies for IgG and/or IgM can be misleading, as are PCR analyzes, which cannot distinguish between latent and actively replicating virus. Currently, the only reliable method for diagnosing an active infection with HHV-6 is Viral isolation.
Long-Term ReMyelination After Optic Neuritis: A 2-Year Visual Evoked Potential And Psychophysical Serial Study
Brusa A, Jones SJ, Plant GT
Brain 2001 Mar;124(Pt 3):468-479
The National Hospital for Neurology and NeuroSurgery, Dept of Clinical NeuroPhysiology, Queen Square, London WC1N 3BG, UK
PMID# 11222447; UI# 21124580
Thirty-one patients were followed-up, at 3-month intervals for the first year and at 6-month intervals for the second year, after an episode of Optic Neuritis. The object was to confirm previous evidence for a progressive shortening of Visual Evoked Potential (VEP) latencies.
And to determine whether this is associated with any change in the clinical Ocular examination, visual fields or contrast sensitivity.
VEP latencies were found to decrease significantly during both the first and (less strikingly) the second year, the most marked changes occurring between 3 and 6 months.
Contrast sensitivity improved during the first 9 months, but subsequently tended (non-significantly) to deteriorate.
A similarly transient improvement in central visual field sensitivity was seen in a subgroup of patients with clinically overt Multiple Sclerosis.
In the data from the acutely unaffected fellow eyes, no significant changes in VEP parameters or functional indices were observed.
The findings extend those of a previous study which showed significant shortening of VEP latencies between 6 months and 3 years without significant functional improvement.
Over this period, a significant prolongation of VEP latencies occurred in the asymptomatic fellow eye, accompanied by contrast sensitivity deterioration.
Taken in conjunction, the two studies suggest that recovery processes involving ReMyelination or, possibly, ion channel reorganization proceed for at least 2 years.
The concurrent effects of insidious DeMyelination and/or Axonal degeneration (also occurring in the fellow Optic Nerve) are initially masked by the recovery process, but gradually become more evident.
The functional benefits of the long-term recovery process are relatively minor and are usually reversed within a few years.
Nevertheless, it is suggested that long-term ReMyelination may perform an important role in protecting DeMyelinated Axons from degeneration.
Understanding the factors which promote long-term ReMyelination may have significant implications for therapy in Multiple Sclerosis.