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Biomedical subjects

Tom Brismar

Publications and source records attributed to Tom Brismar.

8 recordsLinked to original sources
PubMed2007

C-Peptide replacement therapy and sensory nerve function in type 1 diabetic neuropathy.

OBJECTIVE: C-peptide replacement in animals results in amelioration of diabetes-induced functional and structural abnormalities in peripheral nerves. The present study was undertaken to examine whether C-peptide administration to patients with type 1 diabetes and peripheral neuropathy improves sensory nerve function. RESEARCH DESIGN AND METHODS: This was an exploratory, double-blinded, randomized, and placebo-controlled study with three study groups that was carried out at five centers in Sweden. C-peptide was given as a replacement dose (1.5 mg/day, divided into four subcutaneous doses) or a dose three times higher (4.5 mg/day) during 6 months. Neurological examination and neurophysiological measurements were performed before and after 6 months of treatment with C-peptide or placebo. RESULTS: The age of the 139 patients who completed the protocol was 44.2 +/- 0.6 (mean +/- SE) years and their duration of diabetes was 30.6 +/- 0.8 years. Clinical neurological impairment (NIA) (score >7 points) of the lower extremities was present in 86% of the patients at baseline. Sensory nerve conduction velocity (SCV) was 2.6 +/- 0.08 SD below body height-corrected normal values at baseline and improved similarly within the two C-peptide groups (P < 0.007). The number of patients responding with a SCV peak potential improvement >1.0 m/s was greater in C-peptide-treated patients than in those receiving placebo (P < 0.03). In the least severely affected patients (SCV < 2.5 SD below normal at baseline, n = 70) SCV improved by 1.0 m/s (P < 0.014 vs. placebo). NIA score and vibration perception both improved within the C-peptide-treated groups (P < 0.011 and P < 0.002). A1C levels (7.6 +/- 0.1% at baseline) decreased slightly but similarly in C-peptide-and placebo-treated patients during the study. CONCLUSIONS: C-peptide treatment for 6 months improves sensory nerve function in early-stage type 1 diabetic neuropathy.

Adult↗
PubMed2004

Time course and variability of power in different frequency bands of EEG during resting conditions.

The aim of the present study was to evaluate the variability of EEG power spectrum data, considering the time course of the EEG spectrum in resting conditions, and the relationship between the spectral parameters and the length of the analyzed segments. Recordings were performed in 57 normal subjects, with a protocol consisting of regular cycles with open eyes (5 s) followed by closed eyes (55 s) repeated during 10 min. Towards the end of the recording there was a decrease in the alpha and beta power and an increase in the delta and theta power. The coefficient of variation (CV) for the power of 4 s epochs was in the range 0.49-0.67 (delta), 0.53-0.58 (theta), 0.58-0.76 (alpha), 0.37-0.49 (beta) and 0.09-0.12 for the alpha peak frequency. CV decreased with the increase of the sample size, being inversely proportional to the square root of the sample size. Increasing the recording length from 40 to 400 s increased CV by 36% (alpha), 41% (beta), 29% (delta) and 35% (theta), while the standard error of the mean decreased by 55-60%. It is concluded that the power estimates of the EEG activity are heavily dependent on the length of the analyzed segments, and the way they are selected. This observation is particularly relevant for clinical and drug studies where short recordings are often used, thus significantly biasing the estimation of the EEG parameters. The present data provide an estimate on the minimal length of EEG required for a given level of variability.

Adult↗
PubMed2004

Long-range temporal correlations in alpha and beta oscillations: effect of arousal level and test-retest reliability.

OBJECTIVE: The aim of the present study was to evaluate test-retest reliability and condition sensitivity of long-range temporal correlations in the amplitude dynamics of electroencephalographic alpha and beta oscillations. METHODS: Twelve normal subjects were measured two times with a test-retest interval of several days. Open- and closed-eyes conditions were used, representing different levels of arousal. The amplitude of the alpha and beta oscillations was extracted with bandpass filtering and the Hilbert transform. The long-range temporal correlations were quantified with detrended fluctuation analysis. RESULTS: The amplitude dynamics of the alpha and beta oscillations demonstrated power-law long-range temporal correlations lasting for tens of seconds. These correlations were degraded in the open- compared to the closed-eyes condition. Test-retest statistics demonstrated that the long-range temporal correlations had significant reliability, which was greatest in the closed-eyes condition. CONCLUSIONS: The presence of long-range temporal correlations indicates that the amplitude of neuronal oscillations at a given time is dependent on the amplitude at times as remote in the past as tens of seconds. The reliability of long-range temporal correlations suggests that the mechanisms generating the amplitude fluctuations are not perturbed over several days. The systematic changes in the scaling exponents at different levels of arousal indicate that these changes occur on many time scales (5-80 s) as a result of modifications in the intrinsic dynamics of the neuronal oscillations. SIGNIFICANCE: This study demonstrates that the dynamics of spontaneous neuronal oscillations possess long-range temporal correlations with properties suitable for functional and clinical studies.

Adult↗
PubMed2003

Amelioration of sensory nerve dysfunction by C-Peptide in patients with type 1 diabetes.

Studies have demonstrated that proinsulin C-peptide stimulates the activities of Na(+),K(+)-ATPase and endothelial nitric oxide synthase, both of which are enzyme systems of importance for nerve function and known to be deficient in type 1 diabetes. The aim of this randomized double-blind placebo-controlled study was to investigate whether C-peptide replacement improves nerve function in patients with type 1 diabetes. Forty-nine patients without symptoms of peripheral neuropathy were randomized to either 3 months of treatment with C-peptide (600 nmol/24 h, four doses s.c.) or placebo. Forty-six patients (15 women and 31 men, aged 29 years, diabetes duration 10 years, and HbA(1c) 7.0%) completed the study. Neurological and neurophysiological measurements were performed before and after 6 and 12 weeks of treatment. At baseline the patients showed reduced nerve conduction velocities in the sural nerve (sensory nerve conduction velocity [SCV]: 50.9 +/- 0.70 vs. 54.2 +/- 1.2 m/s, P < 0.05) and peroneal nerve (motor nerve conduction velocity: 45.7 +/- 0.55 vs. 53.5 +/- 1.1 m/s, P < 0.001) compared with age-, height-, and sex-matched control subjects. In the C-peptide treated group there was a significant improvement in SCV amounting to 2.7 +/- 0.85 m/s (P < 0.05 compared with placebo) after 3 months of treatment, representing 80% correction of the initial reduction in SCV. The change in SCV was accompanied by an improvement in vibration perception in the patients receiving C-peptide (P < 0.05 compared with placebo), whereas no significant change was detectable in cold or heat perception. In conclusion, C-peptide administered for 3 months as replacement therapy to patients with early signs of diabetic neuropathy ameliorates nerve dysfunction.

Adult↗
PubMed2003

Loss of sensory discrimination after median nerve injury and activation in the primary somatosensory cortex on functional magnetic resonance imaging.

OBJECT: The aim of this study was to assess the effects of median nerve injury and regeneration on neuronal activation in the somatosensory cortex by means of functional magnetic resonance (fMR) imaging and somatosensory evoked potentials (SSEPs). METHODS: Ten injured male patients (mean age 26 years) were examined 15 to 58 months after a total transection of the median nerve at the wrist that was repaired with epineural sutures. Two-point discrimination was lost in Digit II-III and sensory nerve conduction displayed decreased velocity (-29%) and amplitude (-84%) in the median nerve at the wrist. The fMR images were obtained during tactile stimulation (gentle strokes) performed separately on the volar surface of either Digit II-III or Digit IV-V (eight patients: two were excluded because of movement artifacts). The SSEPs were obtained using electrical stimulation proximal to the median nerve lesion. CONCLUSIONS: Patients with loss of sensory discrimination after median nerve damage and regeneration had larger areas of activation in fMR imaging near the contralateral central sulcus during tactile stimulation of the injured compared with the noninjured hand. The increase relative to the unaffected hand was 43% (p < 0.02) for Digit II-III stimulation and 46% (p < 0.02) for Digit IV-V stimulation. The SSEP data showed normal latency and amplitude. The enlarged area of cortical activation may be the result of reorganization, and it may indicate that larger cortical areas are involved in the discriminatory task after a derangement of the peripheral input.

Adolescent↗
PubMed2002

Loss of temporal lobe beta power in young adults with type 1 diabetes mellitus.

Cognitive defects have been reported in type 1 diabetes mellitus with possible correlation to recurrent episodes of hypoglycemia. The purpose of the present study was to identify signs of brain dysfunction with quantitative EEG in adults with insulin-dependent (type 1) diabetes. Patients (n = 49) with type 1 diabetes and controls (n = 51) were recruited. All patients had good glycemic control, no diabetic polyneuropathy and a minor history of severe hypoglycaemia. EEG was recorded for 15 min following a standardized protocol, power spectra were obtained from 236-584 s of artefact-free EEG from each subject and EEG was repeated in diabetic patients after 3 and 9 months. The most pronounced finding was a loss of fast oscillations (alpha, beta and gamma activity) in both posterior temporal regions, with p< 0.001 for beta and p< 0.05 or 0.01 for alpha and gamma activity in the diabetes patients. A decrease in beta activity was also present bilaterally in the anterior temporal and occipital regions (p< 0.05 or 0.01). The alpha peak frequency was lower in patients than in controls, with reductions bilaterally in the temporo-central regions (p< 0.01). These changes were not found to correlate to a previous history of hypoglycaemia. The alpha and beta power showed a high test-retest reliability at both 3 and 9 months (0.88-0.92). The focal decrease in temporal lobe fast activity suggests that these brain regions are preferentially affected by type 1 diabetes. This abnormality may be related to the mechanism underlying the cognitive dysfunction described in diabetes.

Adult↗
PubMedDate not supplied

Impaired glucose tolerance and insulinopenia in the GK-rat causes peripheral neuropathy.

BACKGROUND: Recent studies indicate that impaired glucose tolerance (IGT) in man is a causative factor in idiopathic sensory neuropathy, and that insulinopenia may contribute substantially to the severity of diabetic peripheral neuropathy. The effect of sustained IGT and progressive insulinopenia in the absence of overt hyperglycemia on peripheral nerve abnormalities was examined in the Goto-Kakizaki (GK)-rat. METHODS: Two and eighteen-month-old GK rats with decreased glucose tolerance and overt insulinopenia, respectively, were examined with respect to nerve function, structure, morphometry and molecular integrity, and were compared to age-matched control rats. RESULTS: Both 2-(p < 0.001) and 18-month-old (p < 0.001) GK rats showed reduced body weight. Blood glucose levels following glucose tolerance tests were elevated in both the 2-month and the 18-month-old GK rats. Fasting plasma insulin levels in the 2-month GK rats were increased threefold (p < 0.05) but decreased by 71% (p < 0.001) in the 18-month GK rats. The two-month GK rats showed a normal nerve conduction velocity, whereas in the 18-month GK rats it was reduced to 76% (p < 0.001) of control values. No morphometric abnormalities were found in the 2-month GK rats, whereas the 18-month GK rats showed loss of small myelinated fibers (p < 0.001), atrophy and loss of unmyelinated axons (p < 0.05) and an increased (p < 0.01) frequency of regenerating fibers. In the older GK rats, both mRNA and protein expression of nerve growth factor (NGF) in the sciatic nerve were significantly reduced (p < 0.001 and p < 0.05), and NGFR TrkA (high affinity NGF receptor) and NGFRp75 (low affinity NGF-receptor) protein expression was reduced in dorsal root ganglia (DRG) (both p < 0.05). These changes were accompanied by significantly reduced protein expressions of substance P (SP) and calcitonin gene-related protein (CGRP) in DRG's (both p < 0.001) as well as a 40% (p < 0.001) decrease in SP and a 62% (p < 0.001) decrease in CGRP-positive DRG neurons. In the sciatic nerve, SP and CGRP protein expression was decreased by 71% (p < 0.01) and 79% (p < 0.01), respectively. CONCLUSION: IGT combined with hyperinsulinemia for 2 months have no detectable effect on peripheral nerve function or structure. In contrast, IGT and subsequent insulinopenia result in a functional and structural neuropathy associated with impaired NGF support and neuropeptide synthesis. We suggest that these abnormalities are mainly due to insulinopenia rather than hyperglycemia.

Animals↗