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Biomedical subjects

S Mossman

Publications and source records attributed to S Mossman.

At least 19 recordsLinked to original sources
PubMed1998

Implicit learning in Parkinson's disease: evidence from a verbal version of the serial reaction time task.

Evidence suggests that patients suffering from Parkinson's Disease (PD) demonstrate less sequence learning in the serial reaction time (SRT) task devised by Nissen and Bullemer (1987). One of the problems with this task is that it is motor intensive and, given the motor difficulties which characterize Parkinson's disease (e.g., tremor, impaired facility of movement, rigidity, and loss of postural reflexes), allows the possibility that patients with PD are capable of sequence learning but are simply unable to demonstrate this through a decrease in reaction time over trials. The present study examined the performance of patients with PD and healthy controls, matched for verbal fluency, on a verbal version of the SRT task where the standard button-pressing response was replaced by a spoken response. Thirteen nondementing patients with PD and 11 healthy controls were administered the SRT task. The PD group demonstrated less sequence learning than the controls and this was independent of age and severity of illness. The results add support to those studies which have found impaired sequence learning using the standard form of the SRT task.

Adult↗
PubMed1997

Partial ocular tilt reaction due to unilateral cerebellar lesion.

We report on two patients each with tonic, contraversive partial ocular tilt reactions due to unilateral cerebellar lesions: one patient had had a caudal cerebellar hemorrhage, the other a posterior inferior cerebellar artery territory infarct. Both patients had tonic contraversive conjugate ocular torsion; one had skew deviation; neither had a head tilt. One patient had no specific neurologic deficit apart from the conjugate ocular torsion, which was first suspected because of a deviation of the subjective visual horizontal. These observations imply that the ocular tilt reaction (OTR), a brainstem otolith-ocular reflex of probable utricular origin, is under the inhibitory control of the ipsilateral caudal cerebellum, possibly the nodulus, and that a patient with a cerebellar infarct can present with imbalance as the only neurologic symptom and with conjugate ocular torsion as the only specific neurologic sign.

Aged↗
PubMed1991

The neck-eye reflex in patients with reduced vestibular and optokinetic function.

It is accepted that the neck-eye loop (cervico-ocular reflex, COR) is enhanced following loss of vestibular function and that this helps to restore gaze stability during head movements. In this paper we address the question of which structures and/or mechanisms may participate in such plastic enhancement by investigating the COR in 2 patients with absent vestibular function and reduced smooth pursuit-optokinetic eye movements (SP-OKN). The patients had multisystem atrophy involving the vestibular system and the cerebellum. The COR (elicited by angular motion of the trunk relative to the fixed head and angular motion of the head relative to the fixed trunk) was not enhanced in these 2 patients when compared with normal subjects, in contrast to previous findings in a group of patients with absent vestibular function alone. Measurements of slow phase eye movement velocity during SP-OKN stimuli and during combined COR-OKN stimulation (head oscillation relative to the stationary trunk in the light) showed identical values in these two conditions, which indicates that the neck-eye loop did not contribute to gaze stability during head movements. The absence of plastic enhancement of the COR in these patients may be secondary to interruption of SP-OKN pathways at various possible sites and/or to involvement of the vestibulocerebellum, which is known to mediate adaptive plasticity in the vestibulo-ocular reflex.

Darkness↗
PubMed1990

Alphaherpesvirus saimiri infection in rabbits. 1. Light and electron microscopy study of cutaneous spinal nerves.

A light and electron microscopic study was undertaken to determine pathological changes in cutaneous spinal nerves of rabbits following intradermal inoculation with alphaherpesvirus saimiri (alpha HVS) isolate KM 322. Infected rabbits were killed at 3, 10, 17, 45 days and 2 years after infection. No abnormalities were seen at 3 days postinoculation. In the nerves of the rabbits killed at 10, 17 and 45 days after infection, axonal (Wallerian-type) degeneration was the main pathological feature. Regeneration, manifested by axonal sprouting, was observed in the nerves of the rabbits killed at 45 days post-inoculation. Neural fibrosis and paucity of unmyelinated axons was the final outcome. The severity of the neural damage not only varied according to the progression of the disease but between nerves taken from the same rabbit. This was probably associated with variation in the numbers of virus particles that had reached the dorsal root ganglion of the dermatome served by a particular nerve. Since alpha HVS (isolate KM 322) provides a model system for the study of virus latency in dorsal root ganglia, and consequently for the study of varicellazoster infection in man, these findings give further insight into the pathology of herpetic neuropathy.

Animals↗
PubMed1990

Alphaherpesvirus saimiri infection in rabbits. 2. Morphometric studies of cutaneous spinal nerves.

To provide a better insight into the ultrastructural pathology of herpetic neuropathy, quantitative studies were made on cutaneous spinal nerves of normal rabbits and rabbits intradermally infected with alphaherpesvirus saimiri (alpha HVS) isolate KM 322. Marked reductions in the numbers and densities of myelinated and unmyelinated axons were found in the nerves of the rabbits killed 17 and 45 days after the infection. Abnormalities in the size distribution of unmyelinated axons were seen at 45 days post-inoculation where axonal sprouting caused a noticeable shift in the fiber population. Two years after virus inoculation reduction in unmyelinated axons and abnormalities in the fiber size distributions characterized by smaller diameters of both myelinated and unmyelinated axons were detected. In these nerves conspicuous fibrosis caused a significant increase in the endoneurial area. At this stage of the infection regenerative changes involving myelinated fibers were found. Since attempts to detect spontaneous reactivation of alpha HVS infection in rabbits have been unsuccessful, the finding of regeneration 2 years after exposure seems in agreement with the view that regenerated myelinated fibers never attain their original size. In the present study although both types of fibers were damaged, morphometric data suggest that unmyelinated axons were more severely affected. Whether this seemingly selective involvement was due to spreading of the virus between axons sharing the same Schwann cell subunit remains to be proved.

Animals↗
PubMed1989

Unilateral reversal of smooth pursuit and optokinetic nystagmus.

A patient is presented who has had three six-month episodes of oscillopsia over the last eight years. During the episodes, abnormal smooth pursuit and optokinetic nystagmus were noted, but there were no other abnormalities. Oculography during the most recent episode demonstrated that when tracking from right to left, the patient's smooth pursuit was reversed. There are several features of the case which suggest that the aetiology may be a form of congenital nystagmus. A possible alternative mechanism whereby such an abnormality might arise as an acquired lesion is discussed.

Adult↗
PubMed1988

Passive transfer of myasthenia gravis by immunoglobulins: lack of correlation between AChR with antibody bound, acetylcholine receptor loss and transmission defect.

The effects of serum Ig from 7 myasthenia gravis patients on neuromuscular transmission was investigated by passive transfer to mice. A protocol of 60 mg/day for 3 days produced mouse serum levels of anti-mouse AChR that were similar to those in the MG patients, and resulted in corresponding levels (2-76%) of mouse muscle AChR with antibody bound in situ. However, AChR loss was only greater than 20% with one MG preparation. Nevertheless, there was a marked neuromuscular defect in mice injected with 3 preparations which did not necessarily correlate with the degree of AChR loss or the amount of AChRs with antibody bound in situ. We conclude that in some MG patients part of the defect in neuromuscular transmission may result from antibodies binding to other components of the neuromuscular junction.

Adolescent↗
PubMed1986

Myasthenia gravis without acetylcholine-receptor antibody: a distinct disease entity.

Immunoglobulin preparations from eight patients with clinical features of myasthenia gravis, in whom no serum antibody against acetylcholine receptor (AChR) could be detected, were injected intraperitoneally into mice. Neuromuscular transmission was significantly impaired compared with mice receiving control human immunoglobulin. No antibody bound to the mouse AChR was detected, but there was a small loss (9.4%) of AChR in the mouse diaphragms. Mice injected with myasthenic AChR-antibody-positive immunoglobulin and mice growing hybridoma cells secreting monoclonal AChR antibody showed similar impairment of neuromuscular transmission, but 75% and 94%, respectively, of their muscle AChR had antibody bound and AChR losses were 47% and 60%. The results suggest that a pathogenetic immunoglobulin antibody interferes with neuromuscular transmission in these AChR-antibody-negative patients by binding to non-AChR determinants at the neuromuscular junction. This form of myasthenia is immunologically and physiologically distinct from the AChR-antibody-positive form.

Adolescent↗
PubMed1980

Interaction between diflunisal and warfarin.

The effect of diflunisal on steady-state warfarin dynamics and kinetics was studied in five healthy men taking daily subtherapeutic doses of warfarin. Diflunisal 500 mg twice daily for 2 wk increased the percentage unbound warfarin from 1.02% to 1.24% and lowered total warfarin from 741 to 533 ng/ml, but did not alter the anticoagulant response (prothrombin complex activity, PCA). When diflunisal was discontinued but warfarin continued, there was a loss of anticoagulant effect and a difference in the rates at which percentage unbound warfarin and total warfarin concentration returned to prediflunisal levels. There was a correlation between plasma diflunisal and percentage unbound warfarin. Diflunisal reduced both the maximum plasma protein-binding capacity for warfarin and the apparent association constant.

Absorption↗
PubMed1979

Cimetidine: interaction with oral anticoagulants in man.

In 6 patients anticoagulated with warfarin, nicoumalone, or phenindione the addition of cimetidine prolonged the prothrombin-time (PT) by a mean of 12.6 s (range 5--23 s). In 7 volunteers taking daily subtherapeutic doses of warfarin the addition of cimetidine increased the PT from 19.4 to 22.9 s and the plasma-warfarin concentration from 0.96 to 1.76 microgram/ml. Cimetidine reduced the single-dose clearance of warfarin and antipyrine. The basis of the interaction between cimetidine and oral anticoagulants is probably inhibition of drug metabolism. Care should be exercised in concomitant therapy.

Acenocoumarol↗