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Biomedical subjects

P D Thompson

Publications and source records attributed to P D Thompson.

At least 37 records · Page 2Linked to original sources
PubMed2001

Task-dependent control of human masseter muscles from ipsilateral and contralateral motor cortex.

Corticotrigeminal projections to human masseter motoneuron pools were investigated with focal transcranial magnetic stimulation (TMS). Responses in left and right masseter muscles were quantified from the surface electromyogram (EMG) during different biting tasks. During bilateral biting, TMS elicited motor evoked potentials (MEPs) in both masseter muscles. On average, the MEP area in the masseter contralateral to the stimulus was 39% larger than in the ipsilateral muscle, despite comparable pre-stimulus EMG in both muscles. MEPs elicited while subjects attempted unilateral activation of one masseter muscle were compared with those obtained in the same muscle during a bilateral bite at an equivalent EMG level. MEPs in the masseter contralateral to the stimulated hemisphere were significantly smaller during unilateral compared with bilateral biting. There was no significant difference in the size of ipsilateral MEPs during ipsilateral and bilateral biting. We conclude that the corticotrigeminal projections to masseter are bilateral, with a stronger contralateral projection. The command for unilateral biting is associated with a reduced excitability of corticotrigeminal neurons in the contralateral, but not the ipsilateral motor cortex. We suggest that this may be accomplished by reduced activity of a population of corticotrigeminal neurons which branch to innervate both masseter motoneuron pools.

Adult↗
PubMed2001

The clinical and MRI correlate of ischaemia in the ventromedial midbrain: Claude's syndrome.

The eponymous syndrome of Claude is caused by a lesion of the red nucleus and adjacent third nerve nucleus, resulting in the combination of an ipsilateral oculomotor palsy and contralateral ataxia. The MRI correlate of this syndrome has only occasionally been described. We present three cases with MRI findings which confirm the association of this clinical syndrome with infarction of the ventromedial midbrain. The coexistence of hypertension and small vessel ischaemia in two cases suggests this type of infarct may arise as a result of small vessel disease.

Aged↗
PubMed2001

Exercise in the treatment of lipid disorders.

As a result of scientific evaluation, we know that exercise has a positive impact on the lipid and lipoprotein profile, and we have a greater understanding for the necessary amount of exercise needed to cause these changes. In the case of hyperlipidemic disorders, we know the primary means for intervention is pharmacological, and that diet, weight loss, and exercise are viewed as adjunctive therapies. Because much is known about the exercise training-induced plasma lipid and lipoprotein modifications as well as the lipoprotein enzyme changes, future research should continue to focus on the molecular basis for these changes. For example by knowing a person's apo E genotype, we gain better comprehension as to why some individuals respond to exercise, while others do not. Another area for further investigation is the assessment of drug and exercise interaction. Presently, little is known regarding the use of lipid-lowering drugs and the impact of exercise. Finally, these investigations could provide new insights for better understanding the exercise CAD protective effects. The future challenge is to better understand the impact that regular exercise participation has in optimizing the lipid and lipoprotein profile with individuals with special lipid disorders.

Coronary Artery Disease↗
PubMed2001

Arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) is a cardiomyopathy characterized pathologically by fibrofatty replacement primarily of the RV and clinically by life-threatening ventricular arrhythmias in apparently healthy young people. The prevalence of the disease has been estimated at 1 in 5,000 individuals, although this estimate will likely increase as awareness of the condition increases among physicians. Arrhythmogenic RV cardiomyopathy is recognized as a cause of sudden death during athletic activity because of its association with ventricular arrhythmias that are provoked by exercise-induced catecholamine discharge. Diagnosis may be difficult because many of the electrocardiographic abnormalities mimic patterns seen in normal children, and the disease often involves only patchy areas of the RV. For this reason, international diagnostic criteria for ARVC were proposed by an expert consensus panel in 1996. Treatment is directed to preventing life-threatening cardiac arrhythmias with medications and the use of implantable defibrillators. This article will present in detail the etiology, clinical presentation, diagnosis and management of this condition.

Anti-Arrhythmia Agents↗
PubMed2001

The stiff-man syndrome and related disorders.

The stiff-man syndrome (SMS) is characterised by rigidity and spasm of predominantly axial and proximal limb muscles. The cause of the condition is unknown but the finding of antibodies to glutamic acid decarboxylase (GAD) in approximately 60% of patients has suggested an autoimmune basis. Pathological findings are limited to a small number of cases which are reviewed in this paper. In some, evidence of an inflammatory aetiology has been found, and there appears to be overlap with progressive encephalomyelitis with rigidity (PER) which may present with a similar clinical picture. The spontaneous muscle activity in SMS and PER is of central origin, related to release of polysynaptic spinal and brainstem reflexes. The SMS is readily distinguished from the continuous muscle activity, spasm and cramps of Isaac's syndrome and neuromyotonia which originate in the peripheral nervous system. Fasciculations, myokymia, myotonia and complex repetitive discharges are characteristic of these peripheral neuromuscular disorders.

Encephalomyelitis↗
PubMed2001

Changes in corticomotor representations induced by prolonged peripheral nerve stimulation in humans.

OBJECTIVE: Manipulation of afferent input can induce reorganization within the sensorimotor cortex which may have important functional consequences. Here we investigate whether prolonged peripheral nerve stimulation can induce reorganization within the human motor cortex. METHODS: Using transcranial magnetic stimulation, we mapped the scalp representation of the corticospinal projection to hand muscles in 8 normal subjects before and after 2h of simultaneous repetitive electrical stimulation of the ulnar and radial nerves at the wrist. Control mapping experiments were conducted in 6 subjects. RESULTS: Following nerve stimulation, larger motor-evoked potentials were evoked from more scalp sites. The induced changes were most apparent in first dorsal interosseous, but were also seen in other hand muscles. The increases in area of the representational maps were accompanied by changes in the location of the optimal site for evoking responses in first dorsal interosseous, and changes in the centres of gravity of the maps. CONCLUSIONS: Prolonged afferent stimulation induces an increase in excitability of the corticospinal projection. This is accompanied by a significant shift in the centre of gravity of the stimulated muscles which we propose is evidence of a non-uniform expansion in their cortical representation.

Adult↗
PubMed2001

Focal myelin swellings and tomacula in anti-MAG IgM paraproteinaemic neuropathy: novel teased nerve fiber studies.

Focal myelin swellings and tomacula in teased nerve fibers from a case of IgM anti-myelin-associated glycoprotein (MAG) paraproteinaemic neuropathy were examined using a novel technique. Five different morphologic abnormalities were identified--myelin sheath outfolding, myelin sheath infolding, enlargement of the adaxonal space, myelin degeneration, multiple increased concentric loops--and a combination of these structural abnormalities often occur in association with myelin degeneration. Similar structural changes were found in externally normal segments of teased fibers without evidence of myelin swelling or tomacula from the same case. These structural abnormalities are consistent with a disturbance of the normal adhesion functions of MAG in the maintenance of axon-myelin relationships.

Aged↗
PubMed2001

Pathophysiology of bradykinesia in Parkinson's disease.

Bradykinesia means slowness of movement and is one of the cardinal manifestations of Parkinson's disease. Weakness, tremor and rigidity may contribute to but do not fully explain bradykinesia. We argue that bradykinesia results from a failure of basal ganglia output to reinforce the cortical mechanisms that prepare and execute the commands to move. The cortical deficit is most apparent in midline motor areas. This leads to particular difficulty with self-paced movements, prolonged reaction times and abnormal pre-movement EEG activity. Movements are often performed with normally timed EMG bursts but the amount of EMG activity is underscaled relative to the desired movement parameters. There are also abnormalities in sensory scaling and sensorimotor integration. The brain appears to be able to compensate to some degree for the basal ganglia deficit. There is overactivity in the lateral premotor areas during task performance and movements can be speeded by giving sensory cues. Attention to movement is also beneficial. However, we propose that the engagement of compensatory processes may also lead to reduced performance in other tasks. For example, patients' problems in performing more than one task at the same time could result from lack of sufficient resources both to compensate for their basal ganglia deficit and to run two tasks simultaneously. Surgical therapies are unlikely to work solely by normalizing basal ganglia output to that seen in healthy individuals. It seems more plausible that surgery removes an interfering signal that allows more efficient compensation by other structures.

Animals↗
PubMed2001

The acute versus the chronic response to exercise.

PURPOSE: There is strong and consistent evidence that a single exercise session can acutely reduce triglycerides and increase high-density lipoprotein (HDL) cholesterol (HDL-C), reduce blood pressure, and improve insulin sensitivity and glucose homeostasis. Such observations suggest that at least some of the effects on atherosclerotic cardiovascular disease (ASCVD) risk factors attributed to exercise training may be the result of recent exercise. RESULTS: These acute and chronic exercise effects cannot be considered in isolation. Exercise training increases the capacity for exercise, thereby permitting more vigorous and/or more prolonged individual exercise sessions and a more significant acute effect. The intensity, duration, and energy expenditure required to produce these acute exercise effects are not clearly defined. The acute effect of exercise on triglycerides and HDL-C appears to increase with overall energy expenditure possibly because the effect maybe mediated by reductions in intramuscular triglycerides. Prolonged exercise appears necessary for an acute effect of exercise on low-density lipoprotein (LDL) cholesterol (LDL-C) levels. The acute effect of exercise on blood pressure is a low threshold phenomenon and has been observed after energy expenditures requiring only 40% maximal capacity. The acute effect of exercise on glucose metabolism appears to require exercise near 70% maximal, but this issue has not been carefully examined. CONCLUSIONS: Exercise has definite acute effects on blood lipids, blood pressure, and glucose homeostasis. Exercise also has acute effects on other factors related to atherosclerosis such as immunological function, vascular reactivity, and hemostasis. Considerable additional research is required to define the threshold of exercise required to produce these putatively beneficial effects.

Adult↗
PubMed2001

Intermodal comparison of energy expenditure at exercise intensities corresponding to the perceptual preference range.

PURPOSE: This study compared the rate of energy expenditure among six popular exercise machines at intensities corresponding to ratings of perceived exertion (RPE) for fairly light (RPE-11), somewhat hard (RPE-13), and hard (RPE-15) in 9 healthy men and 10 healthy women. METHODS: A maximal exercise test on each exercise machine was used to anchor the Borg 15-point category scale. Subjects performed three submaximal exercise tests at selected RPEs on a treadmill, stair-stepper, cycle ergometer, rowing ergometer, cross-country ski simulator, and rider. The submaximal tests on each exercise device were performed in random order and were 6 min in duration with 15-min rest between trials. Oxygen uptake, heart rate, and blood lactate concentration were measured during the final 2 min of each exercise intensity. RESULTS: Energy expenditure at each RPE was highest on the treadmill and ski simulator in men, and on the treadmill, ski simulator, and rowing ergometer in women. Energy expenditure in men and women at all RPEs was lowest on the rider and cycle ergometer. Energy expenditure at a given RPE was greater in men than women on all exercise machines, but men and women used a similar percentage of their machine specific peak oxygen uptake at each RPE on all machines. Heart rate was generally similar among the machines and between both men and women at each RPE. CONCLUSIONS: Our results indicated that there are large differences in energy expenditure between exercise machines and between men and women at intensities perceived to be fairly light, somewhat hard, and hard. Consequently, subjects can expend more calories at the same RPE during treadmill and ski simulator exercise, for example, than during exercise with other devices. This may have important implications for the health benefits of different exercises and in promoting long term exercise adherence.

Adult↗
PubMed2001

Distinct retinoid X receptor activation function-2 residues mediate transactivation in homodimeric and vitamin D receptor heterodimeric contexts.

The vitamin D receptor (VDR) stimulates transcription as a 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3))-activated heterodimer with retinoid X receptor (RXR). RXR also forms homodimers to mediate 9-cis retinoic acid (9-cis RA)-induced gene expression. Both receptors possess a C-terminal hormone-dependent activation function-2 (AF-2), a highly conserved region that binds coactivators to transduce the transcriptional signal. By replacing single amino acids within the AF-2 of human RXR alpha (hRXR alpha) or mouse RXR beta (mRXR beta), the contribution of these residues to transactivation by the RXR-VDR heterodimer and the RXR-RXR homodimer was evaluated. In 9-cis RA-responsive homodimers, the second and fourth positions of the AF-2 (leucine and glutamate respectively) are essential. However, in the context of an RXR-VDR heterodimer activated by 1,25(OH)(2)D(3), alteration of these two RXR residues has little effect. Instead, AF-2 residues located towards the C-terminus, such as the penultimate position (L455 in hRXR alpha or L441 in mRXR beta), are crucial for RXR-VDR heterodimers. Indeed, L455A mutant RXR exerts a dominant negative effect on RXR-VDR transcriptional responsiveness to 1,25(OH)(2)D(3). Further experiments with a mutant hRXR alpha (F313A) which elicits 9-cis RA-independent transactivation as a homodimer demonstrate that, when heterodimerized with VDR, this RXR mutant is incapable of activating the RXR-VDR heterocomplex in the absence of the VDR ligand. Taken together, these results indicate that RXR is a subordinate, yet essential transcriptional partner in RXR-VDR-mediated activation of gene expression. Furthermore, a functional switch in RXR AF-2 signaling occurs between RXR residues in the homodimeric versus the heterodimeric states, likely reflecting different interactions between subregions of the AF-2 and coactivator(s).

Alitretinoin↗
PubMed2000

Cortical myoclonus and cerebellar pathology.

OBJECTIVE: To study the electrophysiologic and pathologic findings in three patients with cortical myoclonus. In two patients the myoclonic ataxic syndrome was associated with proven celiac disease. BACKGROUND: The pathologic findings in conditions associated with cortical myoclonus commonly involve the cerebellar system, but there has only been one report of cerebellar pathology in a patient in whom cortical myoclonus was physiologically characterized antemortem. METHODS: Cortical somatosensory evoked potentials (SEPs) were recorded and EEG activity was averaged preceding myoclonic electromyographic activity. In one patient cortico-cortical inhibition was tested using two paired ipsilateral magnetic stimuli over the motor strip. Neuropathologic examination was carried out, including linear Purkinje cell densities/millimeter calculations for different regions of the cerebellum. RESULTS: The electrophysiology showed evidence of dysfunction of the sensorimotor cortex with enlarged SEPs and a time-locked cortical potential preceding the action myoclonus. In addition, motor cortical inhibition was abnormal in one case. Pathology showed unremarkable primary sensory, motor, and premotor cerebral cortices, except for unilateral gliosis of the motor cortex in one case. The cerebellum showed patchy atrophy and ongoing degeneration. A striking feature was the greater severity of Purkinje cell loss and Bergmann gliosis in the outer aspects than in the depths of the folia. CONCLUSIONS: Pathologic abnormalities are paradoxically mainly located in the cerebellum in some patients with cortical myoclonus, despite clear electrophysiologic evidence of cortical dysfunction. This observation suggests that enhanced excitability of the sensorimotor cortex may arise as a distant effect of cerebellar pathology.

Adult↗
PubMed2000

Increased blink rate in advanced Parkinson's disease: a form of 'off'-period dystonia?

Blink rates were measured in 25 patients with fluctuating Parkinson's disease in the "off' and "on" periods. In 17 patients, the "off"-period blink rate was low and increased after administration of levodopa. In the remaining eight patients, the "off"-period blink rate was high and returned to normal levels after levodopa. It is suggested that increased blink rate in the latter group represents a new form of "off"-period dystonia.

Adult↗
PubMed2000

A randomized controlled trial of smoking cessation counseling after myocardial infarction.

BACKGROUND: Smoking cessation after myocardial infarction (MI) has been associated with a 50% reduction in mortality but in-hospital smoking cessation interventions are rarely part of routine clinical practice. METHODS: One hundred cigarette smokers consecutively admitted during 1996 with MI were assigned to minimal care or to a hospital-based smoking cessation program. Intervention consisted of bedside cessation counseling followed by seven telephone calls over the 6 months following discharge. Primary outcomes were abstinence rates measured at 6 months and 1 year post-discharge. RESULTS: At follow-up, 43 and 34% of participants in minimal care and 67 and 55% of participants in intervention were abstinent at 6 and 12 months. respectively (P<0.05). Abstinence rates were calculated assuming that participants lost to attrition were smokers at follow-up. Intervention and self-efficacy were independent predictors of smoking status at follow-up. Low self-efficacy combined with no intervention resulted in a 93% relapse rate by 1 year (P<0.01). CONCLUSIONS: A hospital-based smoking cessation program consisting of inpatient counseling and telephone follow-up substantially increases smoking abstinence 1 year after discharge in patients post-MI. Patients with low self-efficacy are almost certain to relapse without intervention. Such smoking cessation programs should be part of the management of patients with MI.

Adult↗