Biomedical subjects

Johannes Jakobsen

Publications and source records attributed to Johannes Jakobsen.

9 recordsLinked to original sources

PubMed2006

Muscle weakness: a progressive late complication in diabetic distal symmetric polyneuropathy.

The aim of the study was to determine the progression of muscle weakness in long-term diabetes and its relation to the neuropathic condition. Thirty patients were recruited from a cohort of 92 diabetic patients who participated in a study on muscular function 6-8 years earlier. Nine subjects were nonneuropathic, 9 had asymptomatic neuropathy, and 12 had symptomatic neuropathy. Thirty matched control subjects who participated in the initial studies were also included. At follow-up, isokinetic dynamometry at the ankle, electrophysiological studies, vibratory perception thresholds, and clinical examination (neuropathy symptom score and neurological disability score [NDS]) were repeated. The annual decline of strength at the ankle was 0.7 +/- 1.7% in control subjects, 0.9 +/- 1.9% in nonneuropathic patients, 0.7 +/- 3.1% in asymptomatic neuropathic patients, and 3.2 +/- 2.3% in symptomatic neuropathic patients. In the symptomatic patients, the decline of muscle strength at the ankle was significant when compared with matched control subjects (P = 0.002) and with the other diabetic groups (P = 0.023). Also, the annual decline of muscle strength at the ankle was related to the combined score of all measures of neuropathy (r = -0.42, P = 0.03) and to the NDS (r = -0.52, P = 0.01). In patients with symptomatic diabetic neuropathy, weakness of ankle plantar and dorsal flexors is progressive and related to the severity of neuropathy.

Adult↗

PubMed2005

Residual neuropathy in long-term population-based follow-up of Guillain-Barré syndrome.

OBJECTIVE: To estimate the occurrence of residual neuropathy and its self-reported health consequences in a population-based group of patients with Guillain-Barré syndrome (GBS) and to characterize quantitatively the concomitant motor, sensory, and autonomic impairments. METHODS: Forty patients (mean age 46 years) with a confirmed diagnosis of GBS were studied a mean of 7 years (range 1 to 13 years) after the acute attack together with 40 healthy control subjects. The Dyck minimal criteria of neuropathy, the Neuropathy Symptom Score, the Neuropathy Disability Score, the Short Form-36 (SF-36) generic health questionnaire, isokinetic dynamometry at ankle and wrist, quantitative sensory testing of thresholds for vibration, cold, and pain, autonomic function tests, nerve conduction studies, and a summed Neuropathy Rank Sum Score (NRSS) were applied. RESULTS: Nineteen patients (48%) had residual neuropathy, which was independent of follow-up time. The patients with GBS reported lower health status than control subjects on the SF-36 Physical Component Summary Scale (PCS; p = 0.01), and the PCS scores correlated with the NRSS (r = -0.41, p = 0.009). In patients with GBS, muscle strength at ankle dorsal flexion was reduced by 13.9% (p = 0.001), sensory thresholds for vibration were increased in the foot (p < 0.05), and sensory thresholds for cold were increased in the hand and foot (p < 0.05), whereas autonomic functions and pain thresholds were unaffected. CONCLUSIONS: Residual neuropathy affecting large- and medium-sized myelinated fibers endures long after the acute attack of Guillain-Barré syndrome in approximately half of all patients, leads to motor and sensory dysfunction, and shows a trend toward impairing self-reported physical health status.

Adult↗

PubMed2005

Electrophysiological signs of permanent axonal loss in a follow-up study of patients with Guillain-Barré syndrome.

The neurophysiological mechanisms for persisting impairment of motor function after Guillain-Barre syndrome (GBS) were assessed in 37 unselected patients 1-13 years after diagnosis. For evaluation of reinnervation and axonal loss, macroelectromyography (macro-EMG) including measurement of fiber density (FD) was performed. Data from neuropathy symptom score, neuropathy disability score, nerve conduction studies, and quantitative sensory examination were ranked and summed to a neuropathy rank sum score (NRSS). The isokinetic muscle strength at the ankle was measured. Signs of axonal loss with increase of either macro motor unit potential (macro-MUP) amplitude or FD occurred in 76% of patients. The macro-MUP amplitude correlated with muscle strength and with NRSS. Patients with evidence of residual neuropathy had increased macro-MUP amplitude and FD as well as decreased muscle strength compared to patients without evidence of residual neuropathy. We conclude that axonal loss takes place in a substantial number of GBS patients and is associated with permanent muscle weakness caused by insufficient reinnervation. Possible patterns of pathology are discussed in relation to the macro-EMG findings.

Adult↗

PubMed2005

Magnesium supplementation and muscle function in patients with alcoholic liver disease: a randomized, placebo-controlled trial.

OBJECTIVE: The study was undertaken in order to evaluate the effect of magnesium (Mg) supplementation on muscle contents of Mg, muscle strength, muscle mass and sodium, potassium pumps (Na,K-pumps) in patients with alcoholic liver disease. Retrospectively, patients were also stratified according to spironolactone treatment. MATERIAL AND METHODS: The study comprised a placebo-controlled, randomized trial in which 59 consecutive patients with alcoholic liver disease were treated with Mg intravenously and orally (12.5 mmol daily) or placebo for 6 weeks. Muscle content of Mg, maximum isokinetic muscle strength, skeletal muscle mass and muscle content of Na,K-pumps were measured before and after Mg supplementation. RESULTS: Muscle Mg did not increase during the trial (paired t-test), but Mg supplementation and the duration of pre-study spironolactone treatment were independent predictors of muscle Mg (multiple regression). Muscle strength increased by 14% during the trial (p<0.001) and muscle mass increased by 11% (p=0.05), but with no difference between placebo and Mg treatment. Spironolactone treatment was associated with a 33% increase in the content of Na,K-pumps (p<0.001). CONCLUSIONS: Six weeks of Mg supplementation did not increase muscle Mg, although Mg supplementation and spironolactone treatment were independent predictors of muscle Mg. The intervention had no effect on muscle strength and mass, but both increased during the study, probably owing to the general care and attendance to the patients.

Administration, Oral↗

PubMed2004

Selective loss of calcitonin gene-related Peptide-expressing primary sensory neurons of the a-cell phenotype in early experimental diabetes.

To evaluate the possible role of neuropeptide immunoreactive primary sensory neurons on the development of nociceptive dysfunction in diabetes, the absolute numbers of immunoreactive substance P and calcitonin gene-related peptide (CGRP) dorsal root ganglion (DRG) cell bodies were estimated in diabetic and nondiabetic BALB/C (p75(+/+)) and p75 receptor knockout (p75(-/-)) mice with unilateral sciatic nerve crush. The total numbers of immunoreactive substance P A-cells, substance P B-cells, CGRP A-cells, and CGRP B-cells in L5DRG were estimated using semithick consecutive sections and the optical fractionator. After 4 weeks of streptozotocin-induced diabetes, the number of immunoreactive CGRP A-cells was reduced from 692 +/- 122 to 489 +/- 125 (P = 0.004) in p75(+/+) mice on the noncrushed side. In p75(-/-) mice, there was no such effect of diabetes on the immunoreactive CGRP A-cell number. In p75(+/+) and p75(-/-) mice, there was no effect of diabetes on the immunoreactive CGRP B-cell number, nor was there any effect of diabetes on the immunoreactive substance P B-cell number. Sciatic nerve crush was associated with a substantial loss of L5DRG B-cells in diabetic and nondiabetic p75(+/+) mice and with substantial loss of immunoreactive substance P cells in diabetic p75(+/+) mice. In diabetic and nondiabetic p75(-/-) mice, there was no crush effect on neuropeptide expression. It is concluded that experimental diabetes in the mouse is associated with loss of immunoreactive CGRP primary sensory neurons of the A-cell phenotype, that this loss could play a role for the touch-evoked nociception in the model, and that the neuronal immunoreactive CGRP abnormality possibly is mediated by activation of the p75 neurotrophin receptor.

Animals↗

PubMed2004

Muscle strength in type 2 diabetes.

Motor function in type 2 diabetes is largely unknown. In 36 type 2 diabetic patients and in 36 control subjects matched for sex, age, weight, height, and physical activity, strength of flexors and extensors at elbow, wrist, knee, and ankle was assessed at isokinetic dynamometry. The degree of neuropathy was determined by clinical scores, nerve conduction studies, and quantitative sensory testing. Eventually, all results were summed to obtain a neuropathy rank-sum score (NRSS). The degree of nephropathy and retinal condition were also evaluated. Diabetic patients had a 17 and 14% reduction of strength of ankle flexors (P < 0.02) and ankle extensors (P < 0.03), respectively. At the knee, strength of extensors and flexors was reduced by 7% (NS) and 14% (P < 0.05), respectively. At the elbow and wrist, muscle strength was preserved. The NRSS was related to the strength at the ankle (r = -0.45, P < 0.01) and knee (r = -0.42, P < 0.02). Following multiple regression analysis, the NRSS but not the degree of nephropathy or retinopathy was related to strength at the ankle and knee. In conclusion, type 2 diabetic patients may have muscle weakness at the ankle and knee related to presence and severity of peripheral neuropathy.

Aged↗

PubMed2004

Atrophy of foot muscles: a measure of diabetic neuropathy.

OBJECTIVE: Diabetic neuropathy is a length-dependent process that leads to reduced muscle strength and atrophy of leg muscles in some patients. We hypothesized that intrinsic foot muscles are atrophied in diabetic neuropathy and that the degree of atrophy is a measure of motor dysfunction closely related to the neuropathic process. RESEARCH DESIGN AND METHODS: Consecutive cross-sectional magnetic resonance images of the nondominant foot were obtained for stereological determination of the total volume of the intrinsic foot muscles (VFM) in 23 long-term diabetic patients with (n = 15) and without (n = 8) chronic neuropathy and in 23 matched healthy nondiabetic control subjects. Based on clinical examination, nerve conduction studies, and quantitative sensory examination, a neuropathy rank-sum score was calculated for each patient. RESULTS: Total VFM was 86 +/- 52, 165 +/- 34, and 168 +/- 42 cm3 in neuropathic patients, nonneuropathic patients, and healthy control subjects, respectively (P < 0.001). There was a close inverse relationship between the neuropathy rank-sum score and the VFM (r = -0.75, P < 1 x 10(-5)). CONCLUSIONS: Total volume of the foot muscles is halved in patients with diabetic neuropathy. Atrophy of foot muscles is closely related to the severity of neuropathy and reflects motor dysfunction.

Adult↗

PubMed2003

No further loss of dorsal root ganglion cells after axotomy in p75 neurotrophin receptor knockout mice.

The role of the p75 neurotrophin receptor for neuronal survival after nerve crush was studied in L5 dorsal root ganglia (DRG) of knockout mice and controls with assumption-free stereological methods. Numbers of neuronal A- and B-cells were obtained using the optical fractionator and optical disector techniques. At birth, the total number of DRG neurons was 10,000 +/- 2,600 in control mice compared with 5,100 +/- 1,300 in p75 knockout mice. During postnatal development, 1,400 neuronal B-cell bodies were lost in p75 knockouts (2P < 0.05) and 1,100 in controls (NS), whereas the A-cell population remained stable. After a sciatic nerve crush, the total neuron loss in controls was 15.4% +/- 3.5% (2P < 0.05) and 22.7% +/- 5.1% (2P < 0.05) at days 14 and 42, respectively. In contrast, there was no loss in total number of neurons after crush in p75 knockout mice. Neuronal A-cell number was unchanged after the crush in p75 knockouts as well as in controls at both times. At 14 days, the population of B-cells was reduced by 24.8% +/- 3.6% in controls and by 6.1% +/- 3.5% in p75 knockouts, this difference being significant (2P < 0.001). At 42 days, the B-cell loss was 29.6% +/- 5.5% in controls and 4.2% +/- 6.4% in p75 knockouts (2P < 0.001). In conclusion, the lack of the p75 receptor results in neuronal DRG cells that are resistant to nerve injury, pointing to a role for the receptor in apoptosis.

Animals↗

PubMed2002

MRI volume measurements of hypointense objects. A phantom study using stereological methods.

Volume estimates made from thick slabs overestimate the volume of a positive contrast particle in a translucent matrix and underestimate its volume if the particle has negative contrast and the matrix is opaque. For T2-weighted MRI high signal objects the bias can be corrected according to simple geometric models. For negative contrast or hypointense objects the magnitude of the bias is unknown and no corrections have yet been put forward. We wanted to determine the bias of MRI measurements of hypointense objects of known diameter surrounded by a positive contrast solution. One, 3 and 5 mm slices with three different contrast concentrations were obtained according to a stereological MRI protocol. Results were compared with the true object size to estimate the bias. A simple correction for the bias could not be developed due to interslice cross-talk. Cross-talk makes an object appear in more MRI slices than corresponding to its physical size and larger than the true diameter. For phantom measurements an empirical correction could be developed, but for measurements of non-ideal objects such as brain structures the validity of the correction would be unpredictable. Besides avoiding or reducing cross-talk, the best way to deal with this bias is to measure the object's maximal contrast from edge to edge, a solution which is not perfect.

Magnetic Resonance Imaging↗