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Biomedical subjects

W Trojaborg

Publications and source records attributed to W Trojaborg.

At least 73 records · Page 4Linked to original sources
PubMed1990

Symptomatic polyneuropathy in human immunodeficiency virus antibody seropositive men with and without immune deficiency: a comparative electrophysiological study.

Symptomatic polyneuropathy in human immunodeficiency virus (HIV) infection was studied in ten men with acquired immunodeficiency syndrome (AIDS) and in ten men without the immune deficiency. In both groups of patients electrophysiological signs of polyneuropathy of the axonal type were present in the sural, median and peroneal nerves. The AIDS patients had a greater reduction of the mean (SD) sural nerve action potential, 3.1 (2.7) microV, than in patients without AIDS, 10.2 (6.1) microV (p less than 0.01) and greater slowing of peroneal nerve conduction velocity, 42.6 (1.4) m/s in AIDS patients versus 52.6 (3.3) m/s in patients without AIDS (p less than 0.0001). These findings indicate that in most HIV infected patients the severity but not the type of neuropathy depends on whether an immune deficient state has developed. Seven patients with symptomatic polyneuropathy were treated with azidothymidine (AZT) for an average of 10 months and compared with a group of five untreated patients with similar symptoms. No effect of AZT treatment on sural or median nerve amplitude or conduction velocity or on the vibratory or temperature thresholds was observed.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Motor neuron disease and amyotrophic lateral sclerosis: relation of high CSF protein content to paraproteinemia and clinical syndromes.

From 1984 to 1988, 11 of 120 patients (9%) with motor neuron disease (MND) had paraproteins detected by serum immunofixation electrophoresis (IFE), compared with 4 (3%) by cellulose acetate gels: 1 patient had progressive spinal muscular atrophy, 5 patients had amyotrophic lateral sclerosis (ALS), and 5 patients had ALS with probable upper motor neuron signs. Four of 5 patients (80%) with cerebrospinal fluid (CSF) protein content above 75 mg/dl had paraproteins, as did 6 of 30 with values above 50 mg/dl. Four of 14 patients with cerebrospinal oligoclonal bands (OCB) also had paraproteins. Two patients with ALS, CSF protein content above 75 mg/dl, and paraproteinemia had lymphoma. We conclude the following about patients with MND: high CSF protein content (especially above 75 mg/dl) or CSF OCB makes paraproteinemia more likely; some of these patients may have lymphoma; there is an inordinately high occurrence of paraproteinemia in MND; and IFE on agarose is more sensitive than electrophoresis on cellulose acetate in detecting paraproteins. Syndromes of paraproteinemia and high CSF protein are not restricted to the lower motor neuron but qualify as "ALS" with coexisting upper motor neuron signs.

Adult↗
PubMed1989

Progressive neurological dysfunction during latent HIV infection.

OBJECTIVE--To determine whether the delayed conduction through the spinal cord and peripheral nerves seen in patients with AIDS is related to infection with HIV or to the presence of an immunodeficient state. DESIGN--Two year prospective follow up study of electrophysiological measurements in subjects positive for HIV antibody but without AIDS. SETTING--HIV screening clinic and clinical departments in a university hospital in Copenhagen, Denmark. SUBJECTS--Twelve homosexual men positive for HIV antibody who had not developed AIDS. RESULTS--Eight latencies were measured: from the ankle to T12, the wrist to C7, T12 to the cerebral cortex, C7 to the cerebral cortex, the ankle to the gluteal crease (tibial nerve), the gluteal crease to T12, the wrist to Erb's point (median nerve), and Erb's point to C7. Spinal latencies increased in all subjects at C7 by a mean of 4.2% (SE 0.9%) and in all except one at T12 by a mean of 5.5% (1.0%). The conduction time from the gluteal crease to T12 was increased by a mean of 32.0% (5.0%) whereas that in the median and tibial nerves by only 5.6% (1.0%) and 2.2% (2.2%) respectively. CONCLUSIONS--A mild and slowly progressive peripheral neuropathy of the axonal type and a more severe progressive myelopathy or myeloradiculopathy occur concomitantly with early HIV infection, possibly as the result of a direct neurotropic action of HIV.

Denmark↗
PubMed1989

[Plasmapheresis in the treatment of peripheral HIV neuropathy].

Peripheral neuropathy following HIV infection is frequently seen among HIV-positive-, ARC- and AIDS patients who often complain of debilitating paresthesias. Indirect immunofluorescence technique showed antibodies directed either to myelin and/or axons and to endothelial cells of the blood vessels within the nerve tissue. Sural nerve biopsies from five patients showed demyelination, axonal degeneration and perivascular cellular infiltration. Two of the patients had nuclear inclusions and high anti-CMV titer. Plasma exchange was undertaken on five HIV infected patients which resulted in complete disappearance of symptoms in three, incomplete remission in one and no effect in one patient. The finding of autoantibodies against different nerve tissue components, cellular infiltration, positive effect of the plasma exchange and relapse suggests that autoimmunity may play a pathogenetic role in some of the HIV infected patients with peripheral neuropathy.

AIDS-Related Complex↗
PubMed1989

Elevated pain threshold in patients with effort-induced angina pectoris and asymptomatic myocardial ischemia during exercise test.

The purpose of the present study was to analyze the prevalence of asymptomatic (silent) myocardial ischemia during exercise testing among patients with effort-induced angina pectoris, and further, to compare the pain threshold of patients with symptomatic and asymptomatic myocardial ischemia. A group of 26 patients comprised the study. In half of the patients myocardial ischemia during the exercise testing was silent and in one half it was symptomatic. Asymptomatic myocardial ischemia was defined as an asymptomatic ST-segment depression greater than or equal to 0.1 mV, lasting longer than 60 s during an exercise test. In patients with asymptomatic ischemia the pain thresholds both on toe and finger were significantly higher than in patients with symptomatic ischemia: mean values were 10.1 versus 4.9 mA on the toes, p less than 0.025, and 8.4 versus 2.5 mA on the fingers, p less than 0.01. We conclude that asymptomatic myocardial ischemia during exercise test is seen often in patients with angina pectoris and that this may be due to an increased pain threshold.

Aged↗
PubMed1989

Determinants of visual evoked potentials in preterm infants.

The latency and amplitude of N1, the first negative peak of single flash visual evoked cortical potentials (VEP) were evaluated in 86 preterm infants (25-34 weeks of gestation), investigated during the first day of life. All infants were regarded stable at the time of investigation and none had experienced severe asphyxia. Both the VEP latency and amplitude were inversely related to gestational age. When latency was corrected for age it was longer in boys than in girls. Age corrected VEP amplitude was inversely related to head circumference, umbilical cord pH and EEG activity. There was no difference between VEP parameters in asymmetrically growth retardated infants compared to those with normal growth. Administration of dexamethasone to the mother before delivery, mode of delivery, presence of hyaline membrane disease, mode of assisted ventilation or imminent development of periintraventricular haemorrhage did not affect the VEP.

Evoked Potentials, Visual↗
PubMed1989

Somatosensory evoked potentials in the evaluation of patients with stocking/glove paresthesias.

We studied 10 patients referred for suspicion of peripheral neuropathy. They all complained of paresthesias with a stocking distribution. As EMG, motor and sensory nerve conduction studies failed to confirm the clinical diagnosis, we studied somatosensory evoked potentials (SEP) following median and tibial nerve stimulation. The SEP findings were compared with controls and 10 spastic paraplegias. The evoked potential study revealed prolonged latencies of cortical potentials after tibial nerve stimulation in all the patients with paresthesias and were considered evidence of myelopathy.

Adult↗
PubMed1989

Sleep disturbances in torture survivors.

One of the main complaints in torture survivors is sleep disturbance with nightmares, too little sleep and daytime fatigue. Seven subjects, who had been exposed to torture from 6 months to seven years previously, were examined by polysomnography. All had abnormal sleep patterns compared with normal age- and sex-matched controls. The subjects woke frequently from REM sleep, had reduced REM sleep duration, absent Stage 4 sleep, short total sleep time and low sleep efficiency. This study revealed that previously healthy young persons subjected to extreme stress may develop an abnormal sleep pattern.

Adult↗
PubMed1989

Long-term neurotoxicity in patients treated with cisplatin, vinblastine, and bleomycin for metastatic germ cell cancer.

Thirty patients treated for germ cell cancer with six cycles of cisplatin, vinblastine, and bleomycin participated in a follow-up examination of neurotoxicity 49 to 106 months after treatment. Of these, 22 patients (73%) had sensory loss; half of them complained of paresthesias. The vibration perception threshold was increased in 24 patients (80%). Auditory stimulation revealed a normal latency of the first component of the brain stem-evoked potentials Pl but an increased interpeak interval between this and Pv; reflecting a central conduction defect. Motor conduction velocity (CV) along the peroneal nerve was normal. The average sural nerve CV was decreased (P less than .01) and the sensory action potential amplitude was reduced (P less than .01). Warm perception threshold was increased in 10 patients (33%). Cortical-evoked potentials after tibial nerve stimulation had increased latencies in 29 patients (97%). The peripheral CV along the tibial nerve was slowed (P less than .01) in 19 patients, and the central conduction time from Th12 to cortex was prolonged in 15 patients (P less than .01). The changes in conduction along peripheral and central pathways after tibial nerve stimulation are compatible with a toxic effect on the sensory root ganglia causing a "dying back" axonal degeneration of central and peripheral nerve fibers.

Adult↗
PubMed1989

Electrophysiologic study of experimental demyelination induced by serum of patients with IgM M proteins and neuropathy.

We induced progressive conduction block in feline sciatic nerve by endoneurial injection of serum from 2 patients with demyelinating neuropathy and an anti-myelin-associated glycoprotein (MAG) IgM M protein. The block was longlasting (up to 4 days) and affected about half the motor nerve fibers. Control serum from patients with an IgM M protein that did not react with MAG produced a transient block (less than 48 hours) that affected an average of 25% of motor fibers. Nerves with sustained block showed widespread demyelination of many nerve fibers, exceeding controls. The findings support the view that chronic demyelinating neuropathy in these patients is caused by the anti-MAG M protein.

Animals↗
PubMed1989

Congenital myasthenic syndrome in the dog breed Gammel Dansk Hønsehund: clinical, electrophysiological, pharmacological and immunological comparison with acquired myasthenia gravis.

The effect of anticholinesterase drugs on the clinical and electrophysiological features in a canine congenital myasthenic syndrome is compared with findings in acquired myasthenia gravis in dogs. Anticholinesterase treatment had no effect on muscle weakness or electrophysiological parameters in the congenital myasthenic syndrome in contrast to its effect on clinical signs and electrophysiological parameters in acquired myasthenia gravis. The lack of effect of anticholinesterase in congenital myasthenia suggests a presynaptic defect as the aetiological factor. No antibodies to acetylcholine receptors were found in the Danish dog breed Gammel Dansk Hønsehund with the myasthenic syndrome. This classifies the disease in the group of canine and human congenital myasthenic diseases.

Animals↗
PubMed1988

Clinical and electrophysiological studies of human immunodeficiency virus-seropositive men without AIDS.

Motor weakness and ataxia of lower limbs and abnormalities of somatosensory evoked potentials occur in many patients with the acquired immunodeficiency syndrome (AIDS). We studied 15 human immunodeficiency virus-seropositive subjects without AIDS and found no clinical neurological abnormalities. The mean latency of the brainstem auditory evoked potential (peak V) was increased, suggesting a central defect. Despite normal peripheral nerve conduction along the tibial nerve, the mean latency of the spinal cord potential of the twelfth thoracic vertebra was increased compared with normal, possibly indicating an incipient conduction defect at or near the spinal root ganglion or lumbar spinal cord.

Acquired Immunodeficiency Syndrome↗
PubMed1988

IgM monoclonal gammopathy and neuropathy in two siblings.

A sister and a brother with a progressive mixed axonal and demyelinating polyneuropathy were found to have a monoclonal IgM gammopathy of kappa and lambda type, respectively. Sural nerve and cutaneous nerve specimens obtained by biopsy showed deposits of IgM on myelin sheets. Sera from both patients contained antibodies directed to bovine peripheral nerve myelin as determined by ELISA technique and to normal human peripheral nerve myelin as demonstrated by indirect immunofluorescence histochemistry. These siblings may have a genetic predisposition to the formation of autoantibodies with peripheral nerve myelin as the target for the immune attack.

Aged↗
PubMed1988

Autoimmunity related to IgM monoclonal gammopathy of undetermined significance. Peripheral neuropathy and connective tissue sensibilization caused by IgM M-proteins.

In eight of 10 consecutive cases of IgM monoclonal gammopathy of undetermined significance (MGUS), the M-protein had specificity towards various tissues as estimated by direct and indirect immunofluorescence studies of skin and/or sural nerve biopsies. Five of the cases had neuropathy. In three of them, including two siblings with a demyelinating peripheral neuropathy, the IgM was bound to the myelin-associated glycoprotein (MAG) of peripheral nerves. One had axonal neuropathy with IgM activity against the peri- and endoneurium, while another case with post-infectious neuritis had IgM activity against structures in the endoneurium but no IgM autoimmunity in the direct fluorescence test. The latter improved clinically in parallel with a decrease in the M-protein indicating a pathogenetic role of the autoantibody. In three other cases, the IgM was bound to connective tissue structures, two of them also had plasma antibodies against the peri- and endoneurium in the indirect fluorescence test. Finally, two cases showed no reaction of the M-protein against any tissue structures. Since an autoimmune pathogenesis is suspected, the HLA types of seven patients are reported.

Aged↗
PubMed1987

Diagnosis of thoracic outlet syndrome. Value of sensory and motor conduction studies and quantitative electromyography.

Ten patients with wasting of hand muscles and sensory symptoms mainly in the ulnar nerve area were diagnosed as having a thoracic outlet syndrome and were operated on for it. Sensory action potentials (SAPs) from digit 5 were reduced in amplitude in eight patients and those from digit 3 in three patients, and the SAP amplitude ratio between digits 3 and 1 was decreased in five patients. Sensory and motor conduction velocity was normal in all. Quantitative electromyographic studies of ulnar and median innervated small hand muscles revealed changes compatible with chronic partial denervation in most patients. The combined findings of chronic partial denervation of the small hand muscles, decreased SAP amplitude from digit 5 and sometimes also from digit 3, and normal motor and sensory conduction velocity are compatible with a compression of the C-8 and T-1 roots or the lower trunk of the brachial plexus.

Adolescent↗
PubMed1987

Benign congenital muscular dystrophy with autosomal dominant heredity: problems of classification.

A family with autosomal dominant congenital muscular dystrophy affecting members of both sexes in three generations is described; a father and his two sons were studied. The onset of symptoms was in early childhood and progression, if any, was slow. The proximal limb muscles, the sternocleidomastoid and anterior tibial muscles were affected. One patient had torticollis and all had heel-cord shortening. An electrophysiological examination showed myopathy. There was no cardiomyopathy. Creatine kinase (CK) was elevated, and a histological study revealed a necrotizing myopathy with pronounced regeneration and formation of aberrant myofibrils (ringbinden) and fibrosis.

Adolescent↗