Burnout syndrome, described since the 1970s by Herbert Freudenberger, has shown a worsening in recent years, culminating in the last year with the unexpected evolution to excitus in some doctors, which results in encephalopathic involvement of the central nervous system. , probably by affecting mainly the reticular system of the brainstem mostly involved in maintaining the tone of the cerebral cortex.
In severe formulas, the damage is lethargic. Comatose changes in the central nervous system appear to have an organic substrate. They cannot be explained only by overwork and stress.
Interestingly, in Asian countries such as Japan, China, where there are labor-intensive regimes, not as many cases have been reported as in America and Europe.
The same type of psychogenic asthenia is described in Chronic Fatigue Syndrome (S.O.C.). This syndrome, also called “asthenic neurosis”, has in common asthenia, decreased alertness and depression. The difference is that S.O.C is more common in women and is sometimes accompanied by secondary symptoms of toxic-infectious type (fever, chills, myalgias, astalgia) and has a good prognosis, without vital damage.
There may be two variants of the same syndrome with different etiologies or different genetic susceptibility, having a common pathogenic mechanism. The reticulated ascending activator and inhibitory descending reticulated system appear to be mainly involved, presenting a multitude of synapses.
It is possible that mental asthenia is generated by antibodies that block nerve influx at various levels, similar to the blockage of neuromotor plaque in myasthenia gravis.
The damage is not of the classic type (bacterial, viral, parasitic, fungal, metabolic or toxic primitive or secondary) but can be an immune type.
The lack of obvious extrapyramidal neurological signs can be explained by diffuse damage and chronic evolution, as in myasthenia gravis (the neuron probably gains resistance, because the damage is not direct, but indirect, through blocking antibodies).
In myasthenia gravis, a mechanism of antibody blockade in the neuro-muscular plate is described, without inflammatory lesions or with minimal lesions.
In both myasthenia gravis and myastheniform syndrome, the neurological examination may not show clinical signs, the diagnosis being made by myasthenic test, respectively myastheniform test and immunological determinations.
The theory of blockade by agglutination (type V mechanism – according to some authors, IIb -) of hypersensitivity reactions is also found in the disease “Basedow Graves” (TSH receptor stimulating antibodies). In insulin-resistant diabetes is inhibition of insulin binding to the insulin receptor.
Neutralizing antibodies of the intrinsic factor also appear in Biermer’s anemia and in parabiermeric anemias antibodies can appear through cross-reactions, in bothriocephalus. Antibodies can be obtained by cross-reactivity with microbial or chemical antigens.
Choline is one of the main mediators used by many parasites: is it possible that, through cross-reactivity, it causes the synthesis of peripheral antiacetylcholine antibodies, in myasthenia gravis, in the CNS damage – cerebral acetylcholine?
In Alzheimer’s disease, where the theory of sleeping parasites is widely circulated, the same mechanism with cerebral antiacetylcholine antibodies may be involved because this disease also associates mental asthenia, sometimes accompanied by depression.
Another large group of psychic asthenias is the group of drug-induced asthenics. Interferon has, as its main adverse reaction, marked asthenia, reversible upon discontinuation of treatment. Some authors have described interferons as having CNS neurotransmitter properties, so asthenia may be induced by direct action on the central nervous system or by an immune mechanism (many chronic autoimmune manifestations and antiinterferon antibodies occur in chronic hepatitis treated with interferon).
Interferon-induced asthenia is sometimes very marked but subsides fairly quickly when treatment is stopped and no cases of exitus have been reported, so it appears to be more induced by a direct mechanism.
In Burnout syndrome, asthenia persists for several months to several years after removal from the professional environment, so an immune mechanism seems to be involved. The causative agent can be one of the chemicals in the work environment, common in all environments (“job syndrome”), and memory lymphocytes in immunological memory can persist for several years after the antigen is removed.
In myasthenia gravis, in the final stages, the exitus occurs through an immune blocking reaction in the respiratory muscles, without inflammatory, metabolic or toxic lesions.
If the same immune-blocking mechanism works in the reticular system of the brainstem in Burnout syndrome, plasmopheresis tests may be effective.
Burnout syndrome, unlike chronic fatigue syndrome, occurs more frequently in men. It has asthenia symptoms, decreased physical and mental tone, decreased mental performance and professional effectiveness.
Chronic fatigue syndrome has been renamed “myalgic encephalitis” or “chronic immune dysfunction syndrome” and has been studied by the research team at the National Cancer Institute (USA, 1985) and a team of German researchers on the involvement of herpes type I viruses. or II or HHV – 6 virus, the agent roseola infantum in children. Later, the studies were completed with magnetic resonance imaging.
Other possible agents involved are: Ebstein-Bars virus (inconsistently present anti-Ebstein-Bars antibodies), candida albicans (possibly etiologically parasitic).
In Romania, in Bucharest, two cases that met the diagnostic criteria were treated: Gay Holmes – Atllanta, 1988 – (excluding other causes of asthenia), cases improved with Albendazole treatment.
One of the cases was with positive canis anti-toxic antibodies, the other with undetectable canis anti-toxic antibodies, with positive treatment under sample treatment with Albendazole and Diethylcarbamazine.
In addition to the infectious etiology, the possible chemical etiology was also discussed in the chronic fatigue syndrome. The disease was first described in the “industrial world”, being framed by some researchers in the “multiple chemical sensitivity syndrome” by the action of various chemicals (formaldehyde, heavy metals – lead, magnesium, cadmium -, preservatives, dyes, food flavors, dioxin – information published in “Medical Agenda, 1993-1994, Bucharest).
In chronic fatigue syndrome, infectious etiology seems more likely and in burnout syndrome, chemical etiology in people with genetic susceptibility.
Researchers at Griffith University have identified biomarkers of sceening and evolution: the singular polymorphism of nucleotides.
The increased frequency of Burnout syndrome in the medical field, where there have been deaths in doctors, points to the most used agent in all professional environments in America and Europe: solutions for washing surfaces (floors) or products resulting from their action on floors.
Resistance to surgeons who, paradoxically, do intense work and also to nurses, is in support of the immunological theory: it seems that they have resistance through intense and prolonged contact with the hands.
Upon removal from the environment, the symptoms persist for a longer time (variable, up to several months or several years) through the persistence of immunological memory, thus supporting the idea that the mechanism is not directly toxic but probably immunological.
Among the hypersensitivity reactions, it most likely appears to be type V (II b) which has myasthenia gravis as a prototype. Other types of hypersensitivity are clinically and paraclinically excluded:
– allergic type I, mediated by specific IgE;
– type IIa, mediated by antibodies and complement;
– type III, mediated by circulating immune complexes – prototype serum disease;
– type IV granulomatous (granulomatous reactions to silicon dioxide, talc), frequently encountered in occupational diseases, tested by the lymphoblastic transformation test.
Type V (II b) with antibodies that alter signaling at surface cellular receptors, similar to myasthenia gravis, remains under discussion. Antibodies can be cross-reacted with infectious or chemical antigens. Some severe exacerbations may require plasmapheresis.
Among the Ig classes, the most frequently involved in this type of reactions are IgG and IgN. The IgG4 subclass does not bind to Fc receptors for macrophage or complement, so it does not have much opromizer capabilities. His half-life is 23 days and he participates a lot in placental transfer and passive skin anaphylaxis.
It is also included in allergic desensitization treatments with a protective role against IgE antibodies. Sometimes, the single-chain form (with a single L chain and a single H chain) is found, which participates in the blocking reactions.
Regarding the geographical distribution of the syndrome, the studies showed a high frequency of exhaustion in Spain and Portugal, a high frequency of depression and low asthenia in Germany and a low frequency of exhaustion in England.
According to some American studies, neurology occupies high places and oncology after others. Here, patients have a particularly slow gait, perhaps distorting the floor solutions by prolonged friction.
Patients who died in these wards are among the doctors who used the emergency room for more than two days; they may have experienced a surplus in antigenic loading, including at night, in sleep (possible inhaler?).
This would explain why clinical wards have a higher incidence versus research wards and medical student communities. It is also possible to count the age criterion or the genetic criterion (Japan).
It seems that, by distorting the flooring solutions, iodinated or similar products are generated because asthenia is accentuated by the consumption of foods that seem rich in iodine (black bread, nuts). High resistance in surgery would be an additional argument as surgeons use iodized compounds a lot. It seems that the Asian breed also shows a genetic resistance to these products. The British also seem to have a higher resistance, while the Americans have a lower resistance.
Mihaela Ghimpu
Clinical immunology specialist
and allergology