Shock therapies in Spain (1939–1952) after the Civil War: Santa Isabel National Mental Asylum in Leganés

The first third of the twentieth century changed the therapeutical landscape with the emergence of new treatments for the mentally ill in asylums. However, the historiography of their use in Spanish psychiatric establishments has been scarcely studied. The popularization of barbiturate sleep therapies, insulin shock, cardiazol therapy, electroshock and leucotomy spread from the beginning of the century. However, the Spanish Civil War and Spain’s isolation during Franco’s autarky (1939–52) made their implementation difficult. Through historiographic research using medical records as documentary sources, this work analyses the socio-demographic conditions of the asylum population during the first decade of Franco’s dictatorship. The treatments used in Leganés Mental Asylum are described and are compared with those used in other Spanish psychiatric institutions.

EFFECT OF INSULIN SHOCK ON OXIDATIVE MODIFICATION OF PROTEINS IN THE NERVOUS TISSUE OF THE BRAIN OF LABORATORY RATS

The rationale for the study of the formation of products of oxidative modification of proteins (OMP) in the nervous tissue in an experimental study of the effects of insulin shock was the literature data indicating that, oxidative destruction of proteins is one of the early indicators of tissue damage. The OMP considered as a factor in the pathogenesis of nervous tissue in many diseases. In some studies, there is information about the effect of experimental GP on oxidative processes in blood serum, red blood cells, adrenal glands and some other tissues, but the effect of this pathology on the processes of free radical oxygenation in the nervous tissue not studied. The purpose of this article was to evaluate changes in the level of OMP in the nervous tissue of laboratory rats under the influence of insulin shock. The experiment was performed on 32 sexually mature mongrel male rats weighing 380–400 g (age 6 months), divided into 4 groups of 8 individuals: control (intact) group, group 1-laboratory animals exposed to a single insulin shock (1 time per day, 1 day); group 2 – laboratory rats exposed to a double insulin shock (1 time per day, 2 days); group 3 – laboratory rats exposed to triple exposure to insulin shock (1 time per day, 3 days). Rats of the experimental groups insulin (3.5 Units) subcutaneously were injected. The presence of hypoglycemic coma determined by the appearance of convulsions. Animals that are intact at this time remained in their cells. Experimental animals slaughtered by decapitation on a guillotine. The material for research was a homogenate of nervous tissue obtained by the method Of Kutlubaev M. A. and co-authors. The study of the level of OMB in nervous tissue was performed using the Dubinina E. E. method, based on the reaction of oxidized amino acid residues of protein with 2,4-dinitrophenylhydrazine (2,4 – DNFG) with the formation of anhydrous 2,4 – DNFG. Measurements of supernatant extinction at wavelengths (λ) of 356, 370, 430 and 530 nm performed using a 5400-UV spectrophotometer (Ekros-Analytica, Russia). Statistical processing of the experiment results performed using the student’s parametric t-test, since the experimental data obeyed the law of normal distribution. It was found, that insulin shock and experimental hyperinsulinemia (HI) contributed to a decrease in free radical protein oxidation in rat nervous tissue homogenate, reducing the total level of OMP carbonyl products in all the study groups exposed to insulin shock: in the 1st group – by 37.6 % (n=8; p≤0.01), in the 2nd group – by 40.4 % (n=8; p≤0.01), in the 3rd group – by 40.8 % (n=8; p≤0.01). Experimental HI causes significant changes in the level of OMP products in the nervous tissue of laboratory animals, which expressed in a decrease in aldehyde and ketone derivatives of both the main and neutral characters in comparison with the indicators of the intact group. In all three groups with experimental HI, compared with the intact group, there was a significant decrease in primary and secondary carbonyl products of OMP, which indicates that free radical oxidation processes associated with both fragmentation of protein molecules and their aggregation suppressed under conditions of insulin shock. At one- and three-time exposure to HI, primary markers of oxidative stress, formed mainly due to fragmentation of protein molecules, prevailed among the carbonyl products of OMP in the nervous tissue. The content of primary and secondary carbonyl products was almost equal when the HI applied twice, which indicates that the processes of fragmentation and aggregation of protein molecules were almost the same under these conditions. In all three experimental groups, compared with the intact group, there was a significant decrease in carbonyl products of both neutral and basic nature due to a decrease in free radical damage to neutral and basic amino acids of protein molecules. In all the study groups, including the intact group, the level of OMPo was significantly lower than the level of OMPn. The most pronounced differences between the level of carbonyl products of OMP and OMPo were observed with three-fold HI, and the least pronounced-with a single one. With increasing duration of insulin shock, the spectrum of carbonyl products of OMP shifted towards increasing the content of the main products, as the role of the main amino acids as targets for damage to protein molecules by free radicals increased.

From hypomania to mania after correcting severe hypoglicemia: A case report to recall insulin shock therapy

IntroductionIn the early 20th century, shock therapies developed worldwide as the most effective means to treat severe mental illness. In 1927, Manfred Sakel introduced the newly discovered insulin as a means to treat opioid-addicted patients, by relieving withdrawal symptoms. After noticing that some psychotic patients notably recovered from their psychotic symptoms after accidental insulin comas, he extended this technique to schizophrenic patients, arguing that up to 70% of his patients improved with this therapy. Insulin shock therapy soon spread all-over the world and became one of the most important treatments for severe mental illness. Regardless of the high-rate complications, insulin shock therapy only declined after the introduction of anti-psychotic drugs.ObjectiveDescription of a clinical case.MethodsNon-systematic review of literature and case report.ResultsA 70-year-old female with type-1 bipolar disorder and type-2 diabetes was referred to a psychiatry emergency department (ED) for 2-week behavioral disorder, featuring restlessness, agitation, insomnia, verbiage and persecutory delusions. In the ED, she presented calm, cooperating, with a subtle humor elation and slight disinhibition. The speech was somewhat confusing, but with normal debit. Delusional thought or hallucinations were not evident. Severe hypoglycemia was first detected by capillary glucose measurement and confirmed by a blood test. After the blood glucose was corrected she became gradually more restless, talkative, disinhibited, with clear humor elation, compatible with a manic state.ConclusionWe discuss if this case might be explained by the severe hypoglycemia and its correction, linking it to insulin shock therapy, reviewing this procedure's history, controversies and current developments.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Functional state of rat brain mitochondria at hypoglycemia convulsive syndrome and different ways of its arresting

Respiratory and phosphorylation functions of rat brain mitochondria was studied under conditions insulin shock and after its treatment with glucose or glutamate (in combination with inhalation of hypercapnic gas mixture - air enriched with 7% СО2). Certain differences in the effects of the applied agents were found. Phosphorylation ability of mitochondria did not reach the normal level even one day after both ways of convulsive state treatment. Some respiratory parameters suggest that unfavorable changes in the respiratory chain functioning mainly occur at the respiratory chain complex I.