Experimental Models and Types of Higher Nervous Activity
Fundamental concepts regarding the pathophysiology of neuroses were established in the laboratory of academician I.P. Pavlov through animal experiments. The basic principle of creating a neurosis is setting an insoluble (unmanageable) task. This is achieved by overstraining the process of excitation or inhibition, as well as disrupting their mobility.
The classic modeling method is the "collision" (shshibka). This is a clash in the cerebral cortex between excitation and inhibition processes based on opposing instincts. For example, applying a strong noxious stimulus (electric shock) at the moment of feeding or mating.
The probability of nervous process breakdown depends on the type of higher nervous activity (HNA):
- Weak type (Melancholic): both processes are depleted; passive-defensive reactions dominate.
- Strong unbalanced type (Choleric): weakness of inhibition leads to an excitatory type of neurosis with active-search reactions.
- Strong balanced inert type (Phlegmatic): pathological mobility of nervous processes forms.
- Strong balanced mobile type (Sanguine): the most resilient; breakdown is possible only under rigid "collision" and ultra-strong stimuli.
Etiology and Pathogenesis
The primary cause of development is psychological trauma. However, a situation becomes pathogenic only in the presence of specific personality traits: hyper-actualization of the problem and assigning it excessive biological or social significance. The pathogenesis is based on a neurotizing conflict—an attitude where a rational solution becomes unachievable.
The formation of a neurosis includes ideational processing—a prolonged process of analyzing the situation and fear of being unable to adapt to it. A crucial feature of this pathology is that this stage of thinking does not yield a positive result.
At the microstructural level, a prolonged insoluble conflict leads to physical damage to the CNS:
- Membranes of dendritic spine apparatuses are disrupted.
- The number of ribosomes in cortical neurons decreases.
- Degeneration of individual hippocampal cells occurs.
- Local microcirculation disorders arise.
Stages of Development and Autonomic Manifestations
The development of a neurosis follows a clear ontogenetic sequence. The body's reactions are engaged in stages:
- Autonomic (primary response).
- Sensomotor.
- Affective.
- Ideational.
Autonomic disorders (vegetative neurosis, neurocirculatory dystonia) are the earliest component. They arise due to centrogenic regulation disorders. Patients complain of cardialgia, arrhythmias, dyspnea, blood pressure fluctuations, and dyspepsia.
The pathophysiological essence of these reactions lies in their inadequacy: there is a discoordination of the body's integrated response (dissociation between locomotor and autonomic components) and a loss of adaptive significance. Symptoms frequently develop against a background of asthenia—weakness, irritability, and insomnia.
Clinical Forms
In modern classification (ICD-10), neuroses are categorized under heading F4 (neurotic, stress-related, and somatoform disorders). Traditionally, three main forms are distinguished:
- Obsessive-compulsive neurosis (obsessive-compulsive disorder). The cause is a conflict between a desire and the impossibility of its fulfillment. A pathological focus of excitation forms in the cortex. The trigger can be fear or a situation where a person doubts their actions (e.g., whether they forgot to turn off the iron).
- Hysteria. A defense reaction to an insoluble situation. Characterized by a "mosaic" of variable symptoms: from dissociative amnesia and suicidal blackmail to hysterical seizures, transient blindness, and mutism (refusal to speak, which does not distress the patient). Vegeto-somatic manifestations are psychogenic in nature.
- Neurasthenia. Chronic fatigue syndrome, frequently encountered in students and high school pupils under excessive workloads.