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Three groups of torture victims were studied with the aim of establishing a concept of psychotherapy for such victims. Analysis of the first group, consisting of 200 case-reports made by Amnesty International medical groups, resulted in a general outline of the psychological methods of torture and their main impact on the victims. A second group of 24 torture victims was examined by the authors, and a quantitative assessment of long-term neuropsychological complaints and a qualitative insight into these symptoms achieved. In-depth interviews with victims in the third group which, consisted of the victims from the second group and six others, together with the results from the other two groups, formed the basis of a concept of psychotherapy for torture victims. [ABSTRACT FROM AUTHOR]

The concentrations of IgG subclass antibodies (Ab) to acetylcholine receptor (AchR) were quantified in 36 patients with myasthenia gravis (MG) treated with pyridostigmine only, and in eight patients who underwent thymectomy, using an IgG subclass-specific immunoprecipitation assay, IgGI, IgG2, IgG3, and IgG4 subclass Ab to AchR were present in 100%, 33%, 64% and 39% of the pyridostigmine-treated patients, respectively. The concentration of IgGI Ab increased significantly with disease severity as graded by the Osserman-Genkins classification (rs = 0.37, P < 0 05), IgG 1 and IgG3 subclass protein concentrations were significantly higher (P &lt 0.0003) in the 36 pyridostigmine-treated MG patients than in 44 age- and sex-matched healthy subjects, Thymectomy induced an appreciable reduction in anti-AchR IgGI concentration in two patients, whereas six patients showed no changes in Ab to AchR, The results support the hypothesis that binding of anti-AchR IgGI and IgG3 on AchR in the neuromuscular junction followed by complement-mediated cell lysis or phagocytosis, may play a role in the pathogenesis of MG. [ABSTRACT FROM AUTHOR]

Autoimmune encephalitis with antibodies against neuronal surface antigens is diagnosed with increasing frequency in recent years. If treated early and aggressively, these conditions often respond favourably to immunotherapy. We describe the clinical features, diagnosis and treatment of the two most common types of autoimmune encephalitis with antibodies against the N-methyl-D-aspartate receptor or the leucine-rich glioma-inactivated 1 protein. Together, these two conditions comprise 80% of the autoimmune encephalitis cases diagnosed in Denmark. Autoimmune encephalitides with rare antibodies are also summarized.

Autoimmune synaptic encephalitis (ASE) is a recently recognized disease entity. The early and correct diagnosis of ASE is of importance, since the prognosis depends on the early onset of treatment. We present two Danish case reports of ASE: a 15-year-old boy presenting with a severe course of N-methyl-D-aspartate-encephalitis including persistent cognitive deficits, and a 59-year-old woman with coeliac disease presenting with leucine-rich glioma inactivated 1-encephalitis including dyskinesia, epilepsy, psychiatric features and vocal tics.

The term autoimmune synaptic encephalitis (ASE) comprises encephalitides associated with autoantibodies against structures of the neuronal synapse. We review four types of ASE (anti-N-methyl-D-aspartate receptor encephalitis, anti-α-amine-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor encephalitis, anti-gamma-aminobutyric acid receptor 1 encephalitis and anti-leucine-rich glioma-inactivated 1 encephalitis) including their epidemiology, clinical characteristics and treatment.

We studied 65 patients with myasthenia gravis (MG). Clinical, neurophysiological, immunological, and histological findings suggested the coexistence of a presumed autoimmune myopathy. The clinical features were persistent pyridostigmine-resistant weakness and atrophy of striated muscles. The myopathy was found more often in patients with late-onset MG than in those with early-onset (37% vs 13%). Patients with myopathy were also prone to have other immune disorders (47% vs 13%). Elevated titres of antibodies against titin were detected more often in patients with electromyography (EMG) evidence of myopathy than in the sera of those without, and only in late-onset MG cases., (Copyright Lippincott Williams & Wilkins)

The annual incidence rate of myasthenia gravis (MG) was estimated as 4.6 per million population, and the rate was found to be constant in calendar-time. Age- & sex-specific incidence rates disclosed a bimodal appearance for both sexes. According to the epidemiological data, the age limit between early onset and late onset of MG should be set at 50 years. The point prevalence rate has increased in time from 41 per million population in 1950 to 77 in 1988, and model calculation predicts an increased rate of 83 in year 2000. This reflects an improvement in the prognosis of MG. Standardized mortality rate for MG was estimated as 1.87. The total patient population was weighted 6 to 4 with predominance of females. A decrement of the muscle action potential (AP) and of the muscle twitch (TW) was found in 72% and 49% of the cases respectively, the diagnostic yield being proportional to the severity of MG. Post-tetanic facilitation of AP and TW was found in 25% and 20% of the cases respectively. The analogue estimates for post-tetanic exhaustion were 44% and 25% respectively. An abnormal staircase phenomenon was present in 37% of MG patients. Neurophysiological evidence of myopathy, which was not correlated to the degree of neuromuscular transmission failure, was found in 19% of the patients, more often in cases with late onset than in those with early onset (31% compared with 11%). The occurrence of myopathy was associated with pathological muscular biopsy (78%), and with anti-striated muscle antibodies (53%) suggesting that a myopathy of possibly autoimmune origin may coexist with MG. The overall diagnostic sensitivity of anti-AChR antibodies RIA was found to be 88%, the positivity being proportionate to the clinical severity of MG (ocular MG: early onset 71%, late onset 88%; severe generalized MG: early onset 89%, late onset 98%). The finding of anti-AChR antibodies is highly specific for MG (>99.9%). The distribution of antibodies titres was approximately lognormal. The concentration of the antibodies correlated with the clinical severity of the disease, female or male gender, and the pathology of the thymus gland. The improved outlook for MG during the last 4 decades may be ascribed to the combined results of all the new modalities of treatment. Experimental results towards selective plasma exchange are expounded. As opposed to MG patients with hyperplasia or involution of the thymus gland, thymoma cases exhibited exacerbation of the clinical course and also of the anti-AChR antibody titres after thymectomy. Possible steps to circumvent the therapeutical impasse in thymoma cases are discussed, such as combined immunosuppressive therapy along with surgery or conservative treatment for as long as possible.

Blood-brain barrier (BBB) passage of the flow tracer ethylenediylbis-L-cystein diethylester (bicisate, ECD) was measured repeatedly in five patients by means of the intravenous (i.v.) double-indicator technique using 24Na+ as an intravascular cotracer. After i.v. injection, the arterial concentration curve of 99mTc-bicisate was delayed and dispersed compared with that of the intravascular cotracer, presumably due to lung retention of the flow tracer. The corrected cerebral venous output curves were fitted using a three-compartment model with four parameters. At resting cerebral blood flow (CBF) values, the unidirectional brain extraction was 0.57 +/- 0.05, the permeability-surface area product for passage from blood to brain (PS1) was 0.48 +/- 0.07 ml/g/min, and the distribution volume for bicisate was 0.74 +/- 0.20 (mean +/- SD). In a single patient, BBB transport after i.v. injection of bicisate was compared with that of a similar flow tracer, d,l-hexamethylpropyleneamine oxime (HM-PAO), and similar values were found for the two tracers. In 19 rats, the brain extraction of bicisate was measured by means of the intracarotid double-indicator technique. The brain extraction was measured at resting, decreased, and increased CBF values. Low CBF values were obtained by hyperventilation and high values by hypercapnia. The degree of backflux of tracer from brain to blood was evaluated by means of the three-compartment model and was found to be negligible in these experiments. The brain extraction was 0.70 +/- 0.1 and PS1 was 0.94 +/- 0.27 ml/g/min. During hypercapnia, CBF increased from 0.77 to 1.09 ml/g/min, leading to a significant decrease in brain extraction, from 0.70 to 0.56.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrical and mechanical responses to single shocks, slow and fast nerve stimulation (RNS), quantitated EMG, anti-acetylcholine receptor (AChR) and anti-striated muscle (SM) antibodies (ab) were determined in 145 patients with myasthenia gravis (MG). Anti-AChR ab were found in 93% of the myasthenic sera. Decrement of muscle and mechanical responses occurred in 72% and 49%, respectively, the diagnostic yield being positively related to severity of MG. Anti-AChR ab were found in 81% of patients without RNS abnormalities. Decrement at RNS occurred in 33% of the cases without anti-AChR ab compared with 78% of those with elevated titres. Regional curare test (RCT) was diagnostic in 75% of cases with normal RNS. As the combined diagnostic yield of RNS and anti-AChR ab was 96%, RCT and single fibre EMG are rarely indicated. Post-tetanic facilitation and exhaustion, and an abnormal staircase phenomenon occurred in 25%, 44% and 37%, respectively. None of these parameters correlated with severity, type or onset of MG. EMG evidence of myopathy, positively correlated with the presence of anti-SM ab, occurred in 19% of patients examined, 3 times more frequent in those with late onset of MG than in those with early onset; thus myopathy of possible autoimmune origin may coexist with MG. An adequate electrophysiological diagnostic strategy for MG patients is proposed.

Protein A-Sepharose and tryptophan polyvinyl alcohol affinity gels have been evaluated as possible agents for the selective, extracorporeal removal of anti-acetylcholine receptor (AChR) antibodies from the sera of patients with myasthenia gravis. Protein A-Sepharose was shown to be very effective. Specific anti-AChR IgG antibodies of subclasses 1 and 2 were reduced to the same extent (i.e. from 50 to 60% decrease) as the total IgG, although the latter was present at concentrations more than a 1000-fold greater. Anti-AChR antibody of subclass IgG3 was less effectively adsorbed. A full-scale in vitro experiment using one plasma volume and an automatic continuous monitor demonstrated the removal of 43% of the circulating anti-AChR antibodies and the IgG within 70 min, which is comparable to the amount removed by the present, unselective, membrane plasma exchange technique. In contrast, tryptophan polyvinyl alcohol was not effective in immunoadsorption under these circumstances.

Nine patients with chronic pain in the wrist secondary to lunatomalacia and non-union of the scaphoid bone were treated by denervation of the wrist joint. This operation was first presented by Wilhelm in 1966. We have been using a modified technique. The purpose of the operation is to achieve relief of pain by selective neurotomy without impairment of hand function and with preservation of wrist mobility. Eight patients were considerably improved; one was not helped at all. No appreciable progression of the pathological changes have occurred radiographically during the period of follow-up. We find our results encouraging and the method worth trying.

Monoclonal anti-human IgG subclass antibodies have been used in an immunoprecipitation assay for the determination of anti-acetylcholine receptor IgG subclasses in plasma from patients with myasthenia gravis. Solubilized acetylcholine receptors labelled with 125I-alpha-bungarotoxin were incubated with patient plasma. Monoclonal mouse antibodies to human IgG subclasses 1-4 were added to the incubation and finally precipitated with anti-mouse IgG antibody. A maximal IgG subclass precipitation of 62-76% was determined with 125I-labelled myeloma IgG subclasses 1-4 added to normal human plasma. The anti-IgG subclass antibodies were added in excess which ensured that the precipitation of IgG2, IgG3 or IgG4 were unchanged, and that of IgG1 was only reduced by 17%, when the plasma IgG concentration was increased by a factor of two. The anti-IgG subclass antibodies were highly specific for their complementary subclasses. Determination of the IgG subclass of the anti-acetylcholine receptor antibodies from 8 patients with myasthenia gravis showed that IgG1 and IgG3 antibodies are predominant. This may support the hypothesis that complement mediated lysis of the neuromuscular end-plate plays a pathogenetic role in myasthenia gravis.

The concentrations of IgG subclass antibodies (Ab) to acetylcholine receptor (AchR) were quantified in 36 patients with myasthenia gravis (MG) treated with pyridostigmine only, and in eight patients who underwent thymectomy, using an IgG subclass-specific immunoprecipitation assay. IgG1, IgG2, IgG3, and IgG4 subclass Ab to AchR were present in 100%, 33%, 64% and 39% of the pyridostigmine-treated patients, respectively. The concentration of IgG1 Ab increased significantly with disease severity as graded by the Osserman-Genkins classification (rs = 0.37, P less than 0.05). IgG1 and IgG3 subclass protein concentrations were significantly higher (P less than 0.0003) in the 36 pyridostigmine-treated MG patients than in 44 age- and sex-matched healthy subjects. Thymectomy induced an appreciable reduction in anti-AchR IgG1 concentration in two patients, whereas six patients showed no changes in Ab to AchR. The results support the hypothesis that binding of anti-AchR IgG1 and IgG3 on AchR in the neuromuscular junction followed by complement-mediated cell lysis or phagocytosis, may play a role in the pathogenesis of MG.