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Biomedical subjects

M J Stevens

Publications and source records attributed to M J Stevens.

At least 73 records · Page 4Linked to original sources
PubMed1993

Osmotically-induced nerve taurine depletion and the compatible osmolyte hypothesis in experimental diabetic neuropathy in the rat.

Diabetic neuropathy results from progressive nerve fibre damage with blunted nerve regeneration and repair and may be complicated by nerve hyperexcitability resulting in pain. The naturally occurring amino acid taurine functions as an osmolyte, inhibitory neurotransmitter, and modulator of pain perception. It is also known to have neurotrophic actions. The compatible osmolyte hypothesis proposes that levels of intracellular organic osmolytes including taurine and myo-inositol, respond co-ordinately in response to changes in intracellular sorbitol or external osmolality to maintain the intracellular milieu. We hypothesize that glucose-induced sorbitol accumulation in diabetes mellitus will result in taurine depletion in peripheral nerve which may potentially impair nerve regeneration and precipitate neuronal hyperexcitability and pain. This study explored the relationships of taurine, myo-inositol and sorbitol in the rat nerve and their effects on nerve conduction velocity. Osmolyte levels and nerve conduction velocity were determined in sciatic nerve from non-diabetic and streptozotocin-induced diabetic rats, with or without dietary taurine or myo-inositol supplementation. Taurine levels decreased by 31% (p < 0.01) and myo-inositol decreased by 37% (p < 0.05) in diabetic nerve as sorbitol accumulated. Taurine supplementation of diabetic animals did not affect nerve conduction velocity but further reduced nerve myo-inositol levels. Prevention of sorbitol accumulation with the aldose reductase inhibitor sorbinil increased nerve taurine levels by 22% (p < 0.05) when compared with untreated diabetic animals. Thus, we have demonstrated an interdependence of organic osmolytes within the nerve. Abnormal accumulation of one osmolyte results in reciprocal depletion of others. Diabetic neuropathy may be an example of maladaptive osmoregulation, nerve damage and instability being aggravated by taurine depletion.

Aldehyde Reductase↗
PubMed1993

Skip metastases from testicular seminoma.

A unique case of metastatic testicular seminoma which did not initially involve the retroperitoneal lymph nodes is presented. Modern treatment, with cis-platinum based chemotherapy and involved-field irradiation, resulted in cure.

Combined Modality Therapy↗
PubMed1993

Abnormal digital pressure measurements in diabetic neuropathic foot ulceration.

The diabetic neuropathic ulcer is typically slow to heal and recurrent. Macrovascular insufficiency is usually excluded as foot pulses are present and ankle:brachial pressure ratios are not decreased. These assessments cannot however exclude more distal vascular disease. Digital pressure measurements enable a reliable assessment of the distal peripheral vascular status to be made. The aim of this study was therefore to use toe pressures to assess the contribution of distal ischaemia in the pathogenesis of the neuropathic ulcer. Sixteen diabetic patients with recurrent neuropathic foot ulceration had their toe pressures compared to 10 neuropathic patients without a history of foot ulceration, 10 diabetic control subjects, and 11 normal subjects. Four non-diabetic patients with neuropathy and foot ulceration were also assessed. All subjects had ankle:brachial pressure indices > or = 1. Toe pressure was assessed using laser Doppler flowmetry to record the return of skin blood flow. The toe:brachial pressure index (TBI) was then calculated. The diabetic patients with a history of recurrent neuropathic ulceration, had the lowest mean TBI, 0.63 +/- 0.14 (SD), compared to the non-ulcerated diabetic neuropathy patients, the diabetic control subjects, and the normal subjects. 0.84 +/- 0.11, 0.82 +/- 0.1, and 0.81 +/- 0.07, p < 0.01, respectively. Three of the four non-diabetic patients with neuropathic foot ulceration also had an abnormally low TBI. Reduced toe pressure measurements are thus found to be associated with neuropathic foot ulceration. The contribution of distal ischaemia in the pathogenesis of the diabetic neuropathic foot ulcer needs to be evaluated.

Adult↗
PubMed1993

Aldose reductase gene expression and osmotic dysregulation in cultured human retinal pigment epithelial cells.

A "compatible osmolyte hypothesis" proposes that intracellular nonionic organic osmolytes such as sorbitol, myo-inositol, taurine, betaine, and glycerophosphorylcholine respond coordinately to changes in external osmolality, thereby maintaining the intracellular ionic milieu. Osmoregulation may be the primary physiological function of aldose reductase, which catalyzes the conversion of glucose to sorbitol. Glucose-induced sorbitol accumulation in isosmotic hyperglycemic states is associated with compensatory depletion of myo-inositol and taurine. Because such depletion may predispose to chronic diabetic complications, the relationship between osmolyte shifts and aldose reductase gene expression was studied in two human retinal pigment epithelial cell lines, one exhibiting osmoregulated and the other high basal aldose reductase gene expression. High basal expression of the aldose reductase gene was associated with rapid sorbitol accumulation and myo-inositol depletion in response to hyperglycemic (20 mM) concentrations of glucose. Myo-inositol and sorbitol behaved as compensating intracellular osmolytes by accumulating markedly in response to hyperosmolality (300 mM mannitol). Thus the pattern of response of myo-inositol to hyperglycemic and hyperosmotic levels of glucose and mannitol was related to the degree of basal aldose reductase gene expression, which may therefore influence the development of diabetic complications.

Aldehyde Reductase↗
PubMed1992

The influence of assertion training on three aspects of assertiveness in alcoholics.

This study examined three outcomes of assertion training considered relevant for alcoholics: (a) assertive behavior in negative situations; (b) discomfort in negative situations that call for assertive behavior; and (c) expectations of assertive behavior in sober vs. intoxicated states. Subjects were 38 male alcoholics in an inpatient treatment program. Although some behavioral competencies were acquired after assertion training, such training did not differentially reduce discomfort in negative situations or the discrepancy between perceptions of assertiveness in sober vs. intoxicated states at posttest or at 6-week follow-up.

Adult↗
PubMed1992

Prescott Lecky: pioneer in consistency theory and cognitive therapy.

Prescott Lecky's theory of self-consistency consists of an organization of ideas that revolve around those of the self and a master motive that serves to preserve and modify the unity of ideas. Self-consistency theory anticipated several cognitive-phenomenological theories of personality and remains relevant to contemporary personality and clinical psychologists. Regrettably, Lecky left few details about the structure, processes, and development of personality. This paper first will review Lecky's career, theory, and influence. Next, the nuclear theory of the mind, attributed to Frederick Thorne, will be described. The nuclear theory refines and extends Lecky's work and will be evaluated on conceptual, empirical, and practical grounds.

Cognitive Behavioral Therapy↗
PubMed1992

Selective neuropathy and preserved vascular responses in the diabetic Charcot foot.

Charcot arthropathy is a disabling complication of diabetic neuropathy. It is however, unclear why it occurs in only a small number of neuropathic patients. We have studied 12 diabetic patients (10 insulin-dependent) with an acute Charcot arthropathy, and compared their neuropathy and vascular responsiveness with 12 diabetic patients (10 insulin-dependent) with recurrent neuropathic foot ulceration, 12 diabetic control subjects (9 insulin-dependent) and 10 normal non-diabetic subjects. The Charcot arthropathy patients demonstrated a preservation of warm perception, 6 (5.5) degrees C, but complete loss of peripheral cold perception, 10 (0) degrees C, p less than 0.001 (median (interquartile range)). This contrasted with the ulcerated neuropathy patients, who had equally severe impairement of both warm and cold sensory thresholds, 10(0.5) degrees C vs 10(1) degrees C, respectively, the diabetic control subjects who were able to detect a 2 (1.3) degrees C warm stimulus and 3 (3.5) degrees C cold stimulus and the normal subjects, whose warm threshold was 2 (1) degrees C and cold was 2 (1) degrees C. Light touch perception at the foot was preserved in the Charcot patients 4 (4) g vs 100 (50) g, p less than 0.0002, in the ulcerated neuropathy patients. Vibration perception at the great toe and cardiovascular autonomic function tests (heart rate variability, Valsalva ratio and postural systolic blood pressure fall) were abnormal in both the Charcot patients and ulcerated neuropathy group, with no differences seen between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthropathy, Neurogenic↗
PubMed1992

Complications: neuropathy, pathogenetic considerations.

The most common form of neuropathy associated with diabetes mellitus is distal symmetric sensorimotor polyneuropathy, often accompanied by autonomic neuropathy. This disorder is characterized by striking atrophy and loss of myelinated and unmyelinated fibers accompanied by Wallerian degeneration, segmental, and paranodal demyelination and blunted nerve fiber regeneration. In both humans and laboratory animals, this progressive nerve fiber damage and loss parallels the degree and/or duration of hyperglycemia. Several metabolic mechanisms have been proposed to explain the relationship between the extent and severity of hyperglycemia and the development of diabetic neuropathy. One mechanism, activation of the polyol pathway by glucose via AR, is a prominent metabolic feature of diabetic rat peripheral nerve, where it promotes sorbitol and fructose accumulation, myo-inositol depletion, and slowing of nerve conduction by alteration of neural Na(+)-K(+)-ATPase activity or perturbation of normal physiological osmoregulatory mechanisms. ARIs, which normalize nerve myo-inositol and nerve conduction slowing, are currently the focus of clinical trials. Other specific metabolic abnormalities that may play a role in the pathogenesis of diabetic neuropathy include abnormal lipid or amino acid metabolism, superoxide radical formation, protein glycation, or potential blunting of normal neurotrophic responses. Metabolic dysfunction in diabetic nerve is accompanied by vascular insufficiency and nerve hypoxia that may contribute to nerve fiber loss and damage. Although major questions about the pathogenesis of diabetic neuropathy remain unanswered and require further intense investigation, significant recent progress is pushing us into the future and likely constitutes only the first of many therapies directed against one or more elements of the complex pathogenetic process responsible for diabetic neuropathy.

Animals↗
PubMed1992

Does self-efficacy moderate intensity of pain?

75 subjects were randomly assigned to five self-efficacy conditions (High-High, High-Low, Low-High, Low-Low, and Control) in a 5 x 3 (condition x trial) design. Pressure was applied three times to an exposed finger. After baseline, subjects received false biofeedback (i.e., independent of ratings of pain) that their ability to regulate intensity of pain was either good (High-High and High-Low) or poor (Low-High and Low-Low), or there was no biofeedback (Control). After a second trial, subjects were told that their biofeedback indicated either good (High-High and Low-High) or poor (High-Low and Low-Low) regulatory ability, or they were not given biofeedback (Control). They then received a final trial. Before each trial, subjects recorded self-efficacy expectations for regulating intensity of pain. Mixed multivariate analyses of variance on ratings of intensity and self-efficacy expectations did not yield hypothesized interactions for condition x trial.

Adaptation, Psychological↗
PubMed1991

Influence of neuropathy on the microvascular response to local heating in the human diabetic foot.

1. The diabetic neuropathic foot exhibits excess arteriovenous anastomotic shunt flow due to a reduced sympathetic vasoconstrictor tone. Local axon reflexes (mediating postural vasoconstriction, for example) are preserved even in severe diabetic neuropathy. This excess shunt flow and its local neurogenic control may be important in the development of complications of the neuropathic limb. 2. The response of arteriovenous anastomoses to local heating was assessed in 13 diabetic patients with neuropathy (12 insulin-dependent), 10 diabetic control patients (seven insulin-dependent) and 10 normal control subjects. The aim was to study the local reflex control of arteriovenous flow when central sympathetic tone had been largely removed. 3. The change in skin blood flow on local heating to 44 degrees C was measured by using a laser Doppler flowmeter in standard environmental conditions with the foot at heart level. Two sites were assessed: (i) the plantar surface of the great toe (a site in which skin blood flow is dominated by arteriovenous shunt flow) and (ii) the dorsum of the foot (a site without anastomotic flow). 4. It was found that when heat was applied to the plantar surface of the great toe in the diabetic patients with neuropathy a paradoxical decrease in flow through arteriovenous anastomoses occurred, flow declining to 65% (P less than 0.05) of its resting value. This could be compared with an increase in flow over the same time period of 262% and 228% (P less than 0.01) in diabetic control patients and normal subjects, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Disabling postural hypotension complicating diabetic autonomic neuropathy.

A 35-year-old Type 1 diabetic man with severe disabling postural hypotension was studied for physiological abnormalities, precipitating factors, and effect of current treatment. A 24-h blood pressure profile indicated a diurnal variation in systolic blood pressure with the lowest values recorded between 0100 and 0600 h, during which the patient often lost consciousness on standing (mean standing systolic pressure 78 mmHg at night vs 105 mmHg in the afternoon, p less than 0.001). Food induced a profound fall in systolic pressure, both while supine and while standing erect. The systolic pressure fall during euglycaemia was 49 mmHg vs 3 mmHg during hypoglycaemia. Plasma noradrenaline and adrenaline levels were low during euglycaemia, but increased during hypoglycaemia. Therapeutic manoeuvres aimed at increasing heart rate (by atrial tachypacing) and reducing the peripheral pooling of blood (vasoconstricting drugs and gravity suit), together with the somatostatin analogue octreotide, proved ineffective. These observations demonstrate the phenomenon of post-prandial exacerbation of postural hypotension in a Type 1 diabetic patient, and indicate that despite failure of conventional methods of treatment, hypoglycaemia increased plasma catecholamines and was effective in abolishing the blood pressure fall on standing.

Adult↗
PubMed1990

The relationship of demographic variables, antepartum depression, and stress to postpartum depression.

This study examined the contributions of demographic variables, antepartum depressive symptoms, and sources of stress to level of postpartum depression. The Beck Depression Inventory (BDI) and demographic data sheet were administered to 69 women during the eighth month of pregnancy. One month after delivery, subjects completed the post-delivery questionnaire and BDI. A stratified hierarchical regression analysis revealed that marital status, antepartum depressive symptoms, and difficulty of pregnancy predicted level of postpartum depression. Somatic stressors of pregnancy may trigger depressive symptoms that persist after childbirth, particularly in unmarried mothers.

Adolescent↗
PubMed1990

Malignant psoas syndrome: recognition of an oncologic entity.

From January 1985 to January 1989 four patients with advanced cancer developed a syndrome characterized by proximal lumbosacral plexopathy and painful flexion of the ipsilateral hip with positive psoas muscle stretch test. Malignant involvement of the psoas major muscle was confirmed radiologically in all cases. Pain was intractable in 3 patients until time of death. We have termed this presentation the malignant psoas syndrome (MPS) and retrospective review of 427 oncology patients with "high risk" solid cancer culled no additional cases during the same 4-year period. We believe MPS to be a hitherto unreported complication of systemic cancer in which malignant involvement of the psoas muscle, in addition to producing severe nociceptive pain, contributes to the process of lumbosacral deafferentation. The clinical presentation, diagnosis and strategies of management of MPS are discussed.

Adolescent↗
PubMed1990

Intensity versus type of affect elicited by dissociative cognitions in moderating acute pain.

75 undergraduates were trained to use cognitions that elicited either high or low pleasure, high or low fear, or received an expectancy manipulation. Groups high in pleasure showed greater tolerance for pressure pain than other treatment groups but did not differ from expectancy; differences were not found on discomfort ratings. Results were not attributable to differential compliance with instructions, perceived effectiveness of cognitions used, or the number of cognitions used. The percentage of time during stimulation that assigned cognitions were used appeared to mediate tolerance. Expectations for improved tolerance elicited by appealing cognitions and compelling placebos may also mediate tolerance.

Adolescent↗