Biomedical subjects

Henning Andersen

Publications and source records attributed to Henning Andersen.

8 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

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↗

PubMed2005

Gender differences in epilepsy.

PURPOSE: The aim of this study was to look at gender differences in unselected populations of patients with epilepsy classified according to the 1989 International League Against Epilepsy (ILAE) criteria. METHODS: Data were obtained from two sources: (a) the EpiBase database at the outpatient clinic at the Department of Neurology, Aarhus University Hospital, Denmark, confined to adults with epilepsy (n=2,170), and (b) the Danish Twin Registry (n=318). RESULTS: In localization-related epilepsy, no overall gender difference was found in either the EpiBase population (n=1,511; w=750 (50%), m=761 (50%); p=0.80) or in the twin population (n=172; w=86 (50%), m=86 (50%); p=1.00). However, in the EpiBase population, localization-related symptomatic epilepsies were more frequent in men (n=939; w=426 (45%), m=513 (55%); p=0.005); and cryptogenic localization-related epilepsies were more frequent in women (n=572; w=324 (57%), m=248 (43%); p=0.002). In generalized epilepsy, more women than men were diagnosed in both populations [EpiBase: n=480, w=280 (58%), m=200 (42%); p<0.001; twin population: n=105, w=63 (60%), m=42 (40%); p=0.05]. The difference was confined to idiopathic generalized epilepsy [EpiBase: n=437, w=259 (59%), m=178 (41%); p<0.001; twin population: n=94, w=60 (64%), m=34 (36%); p=0.01]. CONCLUSIONS: More women than men were diagnosed with idiopathic generalized epilepsy in two epilepsy populations. Overall, no gender difference was found in localization-related epilepsy, but localization-related symptomatic epilepsies were more frequent in men, and cryptogenic localization-related epilepsies were more frequent in women The results suggest a gender susceptibility to the development of specific epilepsy subtypes.

Adolescent↗

PubMed2004

The regulation of rhinovirus infection in vitro by IL-8, HuIFN-alpha, and TNF-alpha.

The influence of three important cytokines (IL-8, TNF-alpha, and HuIFN-alpha) on ongoing rhinovirus infections has been examined in vitro, individually or as combinations. TNF-alpha was able to transform traces of HRV infections into full-blown infections. Furthermore, TNF-alpha was able to down-regulate the antiviral action of HuIFN-alpha completely, even at levels of just a few pg/ml. This suggests that the induction of TNF-alpha by HRV may be part of the virus's strategy to minimize the interferon response which is part of the host's immune defence system. However, troxerutin (a flavonoid) was able to neutralize the downregulatory action of TNF-alpha on the HuIFN-alpha system at low levels and re-establish the antiviral activity ascribed to IFN-alpha. IL-8 exerted a minor influence on the interferon system, and had no influence on rhinovirus infections. The in vitro findings are supported, in part, by recent in vivo findings in a common cold pilot study.

Cell Line↗

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↗

PubMedDate not supplied

Motor cortical excitability remains unaffected of short-term hyperglycemia in Type 1 diabetic patients.

BACKGROUND: In diabetic patients, hyperglycemia may precipitate seizures, and in experimental diabetes, indications for an increased neuronal excitability have been found. In this study, the excitability of the motor cortex and conduction of the central motor pathways were studied in diabetic patients in relation to the glycemic level. METHODS: Using a double-blind study protocol, transcranial magnetic stimulation (TMS) was performed in five Type 1 diabetic patients during normo- and hyperglycemia, using a hyperglycemic clamp technique. Single and paired-pulse transcranial magnetic and single root stimulations were applied before and after 3 h of a fixed glucose level of 5 and 16 mmol/l. The percentage of change from baseline at the two glycemic levels was calculated and compared. RESULTS: No difference in central motor conduction time was found comparing the change following normo- and hyperglycemia. Furthermore, no difference was observed for the changes in latency and amplitude following double stimulation with interstimulation intervals (ISIs) of 0-125 ms comparing normo- and hyperglycemia. CONCLUSIONS: The excitability of motor cortex and central motor nerve conduction in Type 1 diabetic patients are unaffected by short-term moderate hyperglycemia as compared with normoglycemia.

Adult↗