Psychiatry Psychiatry and psychopharmacotherapy named after. P.B. Gannushkina No. 05 2022

Catatonia is a psychopathological syndrome with a predominance of psychomotor and autonomic disorders in the motor sphere, characterized by a clinical picture of agitation or stupor, which is unmotivated.

In the International Classification of Diseases (ICD-10), the disorder is considered within the framework of catatonic schizophrenia. This interpretation makes it difficult to diagnose the disorder.

Catatonic states of excitement and stupor can quickly replace each other. They arise autochthonously and are functional in nature. Catatonia may not be accompanied by stupefaction (lucid), or may be accompanied by oneiric stupefaction.

Catatonic stupor is characterized by increased muscle tone and immobility. Stupor can develop quickly or gradually. With gradual development, slowness, angular movements, prolonged freezing in one place (substupor), etc. initially appear. Over time, the severity of stupor increases.

Variants of motor stupor:

• Depressive;
• Catatonic;
• Hallucinatory;
• Apathetic;
• dissociative (“hysterical”);
• affective-shock.

Types of motor excitation:

• Manic;
• Anxious;
• Hallucinatory;
• Delusional;
• Affective-shock;
• Dissociative (“hysterical”);
• Against the background of confusion: delirium, twilight confusion.

Catatonic excitation develops suddenly, often rapidly moving from a state of stupor.

Catatonia is also characterized by other clinical manifestations:

Mutism is an unmotivated refusal to speak during normal functioning of the speech apparatus. Passive and active negativism is an unmotivated refusal to perform actions (for example, changing a position) or performing opposite actions. Motor and speech stereotypies - pretentiousness of movements and facial expressions. Echopraxia and echolalia are unmotivated repetition of the actions and phrases of others.

Causes

Specific reasons for the development of catatonia have not been established. The disorder may be initiated due to:

• Concomitant mental disorders (depression, bipolar disorder, schizophrenia, schizotypal disorder, acute psychosis);

• Substance and alcohol use;

• Neurological diseases (epilepsy, multiple sclerosis, Parkinson's disease, brain tumors, dementia);
• Metabolic and endocrine disorders (Cushing's syndrome, hyperthyroidism, Sheehan's syndrome);
• Autoimmune diseases (systemic lupus erythematosus, antiphospholipid syndrome), etc.

Genetic predisposition to certain mental disorders plays a great role. Some infectious diseases can also cause the development of catatonic stupor.

Catatonic disorders in the clinical picture of acute psychotic states

AV Kuznetsov IP Pavlov First St.
Petersburg State Medical University Summary

Catatonia is a psychopathological syndrome characterized by a variety of motor disorders, including stupor, exaltation and multiple symptoms.
Initially, the same cases were qualified as a subtype of schizophrenia, but later the point of view of researchers on this problem was changed towards expanding the diagnosis of catatonic manifestations among patients suffering from affective pathology, neurological and infectious diseases. Finally, the idea of ​​catatonia as a nonspecific syndrome was formed. For syndrokinesis and syndromotaxis of catatonia patterns studying, 150 patients were examined who had acute endogenous psychoses with catatonic symptoms. Several groups were identified, characterized by a different spectrum of acute catatonic symptoms (main, additional and optional) during psychotic attacks. Differences between the groups were revealed depending on the spectrum of residual catatonic disorders. The results of this study allow us to assess the role of the underlying disease in the pathogenesis of catatonia. Keywords
: catatonia, schizophrenia, affective disorders, acute psychosis
For citation
: AV Kuznetsov. Catatonic disorders in the clinical picture of acute psychotic states. Psychiatry and psychopharmacotherapy. 2020; 5:27–31.

Pathogenesis

There is no consensus on the pathogenesis of catatonia. Studies have shown that disruption of communication between cortical structures, the thalamus and the basal ganglia play an important role in the occurrence of catatonic symptoms, therefore, in addition to clinical assessment, when studying catatonia, it is worth taking into account the results of neuroimaging and neuropsychological examinations. The hypothesis is based on a lack of gamma-aminobutyric acid (GABA) in the basal ganglia. Normally, GABA reduces the intensity of emotional reactions, such as anger, fear or anxiety.

In modern literature, there are often cases of catatonia caused by abrupt withdrawal of drugs used to treat catatonic states and accompanying mental disorders. This therapy uses mechanisms to increase GABA activity in the basal ganglia, which has a positive therapeutic effect. With abrupt withdrawal of drugs, an increase in motor symptoms often occurs (the phenomenon of “rebound catatonia”).

It is possible that catatonia develops as a result of severe anxiety, in response to stress. Therefore, scientists suggest that catatonic states are directly related to affective and other mental disorders that are accompanied by symptoms of severe anxiety.

Catatonia and the immune system

Definition of catatonia and its clinical picture

Catatonia is a psychomotor disorder accompanied by negativism, mutism, stupor, characteristic posture, echo phenomena, ambivalence and stereotypies. There are catonic stupor and catatonic excitation.

Activation of the innate immune system is associated with mutism and psychomotor retardation, which partly constitute the neurovegetative features of catatonia. Evidence for acute phase activation in catatonia is sparse and contradictory, and it is unclear whether this feature is secondary to stupor. Understanding the pathogenesis of catatonia is critical given the high rate of complications including pressure ulcers, infections, and venous thromboembolism

Forms of catatonia

Various forms of catatonia (delayed catatonia, malignant catatonia and neuroleptic malignant syndrome) are highly comorbid.

Causes of catatonia

A variety of viral, bacterial, and parasitic infections are associated with catatonia, but it is primarily associated with infections of the central nervous system. The most common cause of autoimmune catatonia is N-methyl-D-aspartate receptor (NMDAR) encephalitis, which may account for the full spectrum of catatonic properties. A systematic review found that 20% of catatonia has a common cause, of which CNS inflammation (including both infectious and immune causes) accounts for 29%. In catatonia, laboratory evidence of infection (such as isolation of the organism in the serum or viral DNA in the cerebrospinal fluid) has been reported in 69% of cases. A strict temporal relationship between infection and catatonia was found in 66% of cases. A previous mental disorder was reported in 13% and a previous physical disorder in 21% of cases.

Two cases of catatonia in pernicious anemia have been reported, both of which responded to vitamin B12 supplementation. Vitamin B12 deficiency can also cause catatonia. In thyroid disease, catatonia has been reported in patients with thyroid autoantibodies with hyperthyroidism, hypothyroidism, and a euthyroid state. However, catatonia also occurs in hypothyroidism due to thyroidectomy; therefore, it remains unclear whether thyroid status or the presence of autoantibodies is a causally significant factor. In systematic lupus erythematosus, 51 cases of catatonia have been reported, usually with high titers of antinuclear antibodies and double-stranded DNA; however, further comparisons are difficult because testing groups differed across studies. One group of researchers reported 84 cases of childhood catatonia, of which they suspected 7 to be of autoimmune origin, including two patients with signs of inflammation who responded to immunosuppression but in whom no known disease could be diagnosed

PANDAS

PANDAS and the broader concept of pediatric acute neuropsychiatric syndrome (PANS) are characterized by the sudden onset of obsessive behavior or motor tics. This behavior may be associated with molecular mimicry, in which the antigens of the infectious agent are similar and provoke an immune response of the host to the CNS's own antigens. Antistreptococcal antibodies are often positive, although results from immunotherapy have been mixed. One case was reported of a boy who, in addition to obsession, developed symptoms of catatonia after being infected with group A streptococcus; he responded well to lorazepam and plasmapheresis.

Autoimmune encephalopathies

Autoimmune encephalopathies, as examples of autoimmune diseases directed at CNS targets, deserve special consideration. T cell-mediated disorders, such as acute demyelinating encephalomyelitis, can sometimes present with catatonia. However, catatonia is more often a feature of autoimmune encephalitis associated with antineuronal antibodies. These antibodies can cause the antigen to be internalized, inhibiting its function. Catatonia was reported in two patients with anti-GABA-A receptor antibodies, which is not surprising given the central role of benzodiazepines in the treatment of catatonia. Catatonia may be more common than these reports suggest because rigorous psychiatric phenotyping has not been performed in this population. In one of the catatonic patients, anti-GABA-A receptor antibodies were present in the serum at initial presentation but not in the context of relapse, highlighting that testing serum in only one case may increase the risk of missing a clinically significant syndrome

Immune system in psychoneurological disorders

Immune dysregulation is gaining increasing interest in the pathogenesis underlying neuropsychiatric disorders such as narcolepsy, some types of dementia, depression and psychosis, with similar findings from biochemical, neuroimaging, genetic and autopsy studies. There is room here for both the innate immune system, which is concerned with a rapid, non-directed response to signals associated with pathogens or injury, and the adaptive immune system, which realizes its activity over a longer period of time and involves the selection and maturation of antigen-specific T cell and B cell mediated responses.

Infection as a cause of catatonia

How infection can lead to catatonia is unclear from the literature. Possibilities include a direct neurotoxic effect, a psychological response to infection, or mediation of the acute phase response. In most cases, we are talking about known neurotropic viruses, which indicates a direct neurotoxic effect. Some bacterial agents, such as Borrelia burgdorferi and Treponema pallidum, are also known to infect the central nervous system.

NMDA encephalitis

The immunological response may also be important, given that in some neurological disorders, such as meningoencephalitis, the damage is caused primarily by an immune response.

Autoimmunity appears to cause catatonia not so much due to systemic inflammation as due to the downstream effects of specific exposure to extracellular antigens. The specific association with NMDAR encephalitis supports the hypothesis of glutamatergic hypofunction in catatonia. In several cases, the authors have suggested an overt immune response to explain catatonia, such as in childhood autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) or in N-methyl-D-aspartate receptor (NMDAR) encephalitis, thought to be caused by yellow fever vaccination infection. herpes simplex virus or Epstein-Barr virus infection.

Depression and inflammation

Although cases of overt catatonia in the context of infections are dramatic, a more common neuropsychiatric manifestation of infection is a broader phenotype of illness behavior resembling depression. This presentation includes decreased motor activity, oral intake, and social interaction (as a reminder to my Blog reader, these are all seen in catatonia). Psychomotor activity is also slowed during mild experimentally induced infection. This may be due to impaired spatial memory and abnormal activity in parts of the brain involved in interoception. Therefore, the brain's response to inflammation, if severe, can lead to a complex movement disorder such as catatonia.

In response to an acute stressor, immune cell trafficking occurs with the movement of white blood cells to and within the target organ. However, during chronic stress, increased monocyte production and microglial activation lead to neuroinflammation and are associated with depressive behavior. Depression is often associated with elevated levels of proinflammatory cytokines, granulocytes and monocytes. Regarding the subtypes of depression, atypical depression (characterized by mood reactivity, hyperphagia, hypersomnia, and “lead heaviness”) is most often associated with elevated markers of inflammation. Conversely, lethargy is more often observed in melancholic depression, which is less associated with a peripheral proinflammatory state. Seasonal affective disorder has also been associated with a proinflammatory state, but to date there has been little research on the motor phenotype of this disorder.

Neuroleptic malignant syndrome and inflammation

Neuroleptic malignant syndrome is a severe neuropsychiatric disorder caused by the use of antipsychotic drugs and characterized by muscle rigidity, autonomic dysfunction and altered consciousness. Patients taking antipsychotic drugs with preexisting catatonia have an increased risk of developing neuroleptic malignant syndrome compared with patients without catatonia (3.6% vs. 0.07–1.8%). Given that there are no clinical features that can reliably distinguish neuroleptic malignant syndrome from malignant catatonia, some authors consider neuroleptic malignant syndrome to be a specific form of antipsychotic-induced malignant catatonia. Residual catatonia often persists after complete resolution of neuroleptic malignant syndrome.

Some authors have suggested that inflammation is important in the pathogenesis of neuroleptic malignant syndrome, and acute phase reactions such as leukocytosis, thrombocytosis , and low serum iron levels are often observed. Low serum iron is a promising biomarker here. It has been suggested that in neuroleptic malignant syndrome, proinflammatory cytokines may reduce levels of the neuroprotective kynurenic acid by impairing the activity of dopaminergic neurons in the midbrain, causing extreme sensitivity to further antipsychotic-induced reductions in dopaminergic signaling. However, the inflammatory profile in the blood may be a consequence of rhabdomyolysis rather than a primary pathology. Serotonin syndrome, a rare side effect of antidepressants, has also been described as a form of drug-induced catatonia, but to our knowledge no studies have been published linking this syndrome to the immune system

Acute phase reaction

The acute phase response is the primary priority of the innate immune system. The response is initiated by activation of monocytes and macrophages by a stimulus such as muscle tear, infection, physical trauma, or psychological stress. In response to these stimuli, cells release proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha (TNF-α), which in turn act on receptors throughout the body to promote fever , anorexia, muscle catabolism and activation of the hypothalamic-pituitary-adrenal axis. It is important to note that these cytokines also alter protein synthesis in the liver, causing increased production of acute phase proteins such as C-reactive protein (CRP), procalcitonin, ferritin, and fibrinogen. Several features of malignant catatonia bear marked similarities to the acute phase reaction, including fever, motor hypoactivity, and autonomic disturbances. The concentration of high-sensitivity CRP was measured in one study and was found in patients in a catatonic state, but the absolute concentration of CRP was not very high (1·23 mg/dL).

Creatine kinase is not an acute-phase marker, but since it is a marker of muscle breakdown, enzyme levels are sometimes elevated as a consequence of the acute-phase response. The evidence for increased CK levels in catatonia is mixed and may be considered a result of muscle rigidity and excessive immobilization rather than an indication of primary muscle pathology. In one study, elevated creatine kinase predicted a good response to lorazepam treatment

One study found that levels of the acute phase marker and fibrin degradation product D-dimer were increased in all catatonic patients tested, with a mean value 3 times higher than in non-catatonic psychiatric patients. This finding is consistent with the increased risk of venous thromboembolism in catatonia.

Low serum iron to be present in catatonia given the similarities with neuroleptic malignant syndrome. Low serum iron is an established feature of the acute phase response and occurs due to increased production of ferritin and hepcidin by the liver. Two uncontrolled studies showed that 25% to 44% of catatonic episodes were accompanied by serum iron concentrations below the normal range. The authors of one of the negative studies, which used patients not taking medication, suggested that in other reports, iron levels may have been reduced due to the effect of antipsychotic drugs. In several studies, low serum iron levels in catatonia have been associated with subsequent development of neuroleptic malignant syndrome. This association may exist because iron is a cofactor in dopamine synthesis, so the combination of low iron, which reduces dopamine production, and antipsychotic drugs, which block dopamine receptors, may lead to the abnormal hypodopaminergic signaling characteristic of neuroleptic malignant syndrome.

Neuroglial disorders in catatonia

Abnormalities of the brain's white matter, which is made up of glial cells, have been linked to schizophrenia, depression and autism. 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP) is an oligodendrocyte-specific myelin protein. In a mouse model, heterozygotes for the CNP loss-of-function genotype exhibited axonal degeneration and low-grade inflammation, along with a depressive and catatonic phenotype. Moreover, this behavior was alleviated by the removal of microglia, suggesting that microglia-mediated neuroinflammation underlies the phenotype. When this polymorphism was examined in people with schizophrenia, a striking association with catatonic-depressive behavior was found, and this finding was replicated in an independent cohort. Mutations in the mouse genes encoding two other myelin proteins (myelin basic protein [MBP] and myelin proteolipid protein [PLP]) also result in a catatonic phenotype. How glial dysfunction—due to relevant polymorphisms or other factors—may contribute to the psychomotor features of catatonia clearly represents an important topic for future research.

Psychological stress and infection

Psychological stress and infection cause the release of proinflammatory cytokines, leading to a state of motor hypoactivity. In a normal psychomotor response, this event may be adaptive, allowing energy to be conserved to eliminate a pathogen or avoid a stressor and resolve when the stressor ends. However, in depression, a prolonged pro-inflammatory state can be maladaptive and cause further dysfunction. Immobilization itself can also lead to activation of the innate immune system

Treatment

Response rates to benzodiazepines and electroconvulsive therapy (ECT) are high, regardless of the cause of catatonia. In some cases, catatonia resolves with antimicrobial therapy.

Consequences of treatment

The mainstay of current treatment for catatonia is benzodiazepines and ECT, neither of which is considered an immunomodulatory therapy. Benzodiazepines are positive allosteric modulators of the γ-aminobutyric acid (GABA)-A receptor. Although research into the function of GABA in the immune system is in its infancy, research evidence suggests that GABA signaling plays a role in suppressing immune responses. Lymphocytes express GABA-A receptors, and activation of these receptors reduces the production of proinflammatory cytokines. However, one study looking at catatonia found that higher monocyte predicted failure to respond to benzodiazepines. Data on distinguishing between different benzodiazepines are limited, but some benzodiazepines, such as diazepam and lorazepam (both established treatments for catatonia), but not clonazepam, also bind to translocator protein (TSPO), a mitochondrial protein associated with phagocyte activity, immune cell migration, and cytokine . In rats, diazepam reduces TSPO in the brain and reduces the number of inflammatory cells in the central nervous system, conferring a protective function against experimental autoimmune encephalomyelitis.

There are few reports of other GABA-A receptor modulators, but there are epidemiological studies that suggest that zolpidem use is associated with higher rates of infections (including pyelonephritis, which is unlikely to be associated with respiratory depression), suggesting that the drug may also have an immunosuppressant role.

ECT

Regarding ECT, it appears that a single session activates the immune system, increasing concentrations of the cytokines IL-1β, IL-6, IL-10, and TNF-α. However, a course of several sessions appears to reduce immune system activity, at least in animal studies

Minocycline

Minocycline is an antimicrobial drug that also has anti-inflammatory properties. The drug has been shown to prevent stress-induced changes in microglia in rodents. and has been proposed as an adjunctive treatment for schizophrenia. Some evidence suggests that minocycline may reduce negative symptoms in schizophrenia, some of which (eg, paucity of speech, affective blunting, and abulia) overlap with catatonia. However, a 2022 double-blind randomized trial specifically looking at the drug's effect on negative symptoms found no benefit. There are no studies that we are aware of examining minocycline specifically for the treatment of catatonia, but there are reports of two patients with schizophrenia and severe catatonic features who responded well to minocycline in the absence of infection.

Conclusion

Activation of the innate immune system may lead to the neurovegetative features of catatonia, but data on the acute phase response in catatonia are preliminary and sometimes conflicting. Moreover, it is unknown whether peripheral inflammation occurs in catatonia secondary to immobility and muscle breakdown. Studies of the relationship of catatonia to the adaptive immune system reveal a strong and specific association with NMDAR encephalitis, which can cause a full spectrum of catatonic properties. This finding suggests that adaptive immunity may cause catatonia through action on certain extracellular antigens rather than activation of the immune system per se. Additionally, this illustrates the importance of glutamatergic function in catatonia. The more autoimmune diseases are characterized, the more cases of catatonia can be explained in this way.

Symptoms

There are many clinical signs of catatonic syndrome. Symptoms are often related to the motor area. With catatonic stupor, the patient becomes numb or completely immobile. Muscle tone is increased, especially in the head and shoulder girdle. The chewing muscles are toned, the lips are pulled forward (proboscis symptom), the person lies on his back, holding his head above the pillow (the “air cushion” symptom). Less severe conditions occur in the form of catalepsy. Muscle tone may alternate with complete relaxation, and epileptiform seizures are sometimes observed. The state of catatonic excitement is characterized by incoherent speech, absurd rhyming, and echolalia.

In severe cases, the attack of stupor with catalepsy is prolonged, mutism, lack of reaction of the pupils to intense painful stimuli (Bumke's symptom), and persistent insomnia are noted.

Stupor may be accompanied by oneiric stupefaction, delusions and hallucinations. Motor disturbances manifest themselves in combination with a feeling of stiffness of the body and the inability to move, with stupor, or a feeling of muscle looseness with motor excitement.

In catatonic states, the following symptoms may occur:

• catatonic stupor or substupor - complete or partial immobility, often in a sitting or standing position;
• catalepsy - a person remains in one position for a long time;
• waxy flexibility - long-term preservation of the position that another person gives the patient;
• negativism—resistance when another person tries to change the patient’s position;
• mutism – prolonged silence;
• stereotypy - repeated monotonous movements;
• catatonic agitation - increased disordered motor activity;
• echolalia/echopraxia - copying the words and movements of another person;
• pretentiousness of facial expressions and movements.

In addition to the main symptoms, manifestations of disruption of the autonomic nervous system may occur. With catatonia, there may be an increase in body temperature to subfebrile, a feeling of thirst, increased blood pressure, and tachycardia. Often patients refuse water and food.

The detailed picture of catatonic stupor and agitation does not differ in clinical manifestations in adolescents and adults. Oneiric catatonia often occurs against the background of the manic phase in schizoaffective psychosis; it is much less common in depression and attacks of fur-like schizophrenia, especially in adolescents. Hebephrenic syndrome is characteristic of adolescence and the malignant course of schizophrenia. As a rule, catatonic symptoms appear against the background of this syndrome.

Fibril catatonia develops with symptoms of oneiric, neurological and somatic disorders. A febrile attack is characterized by manic-delusional, hallucinatory and depressive syndromes. With more pronounced psychosis, fantastic delirium appears. The patient is in a state of agitation or stupor.

Body temperature rises sharply to febrile and higher. There is no relationship with somatic and infectious diseases. Blood pressure rises, tachycardia and increased sweating are present. The person is in an excited state and feels very thirsty. Excitement gives way to stupor or sub-stupor. General health worsens. The feeling of thirst and hunger disappears, the skin becomes dry, and swelling appears. If assistance is not provided in a timely manner, congestion in the lungs, bedsores and other complications may develop.

Most often, attacks of febrile catatonia are observed in people 41-50 years old. They are characterized by a severe course and a high risk of death.

With primary manifestations of catatonia, you should immediately consult a doctor. With timely diagnosis and effective treatment, the condition can be normalized without further development of complications.

Story

As an independent mental disorder, the catatonic form of schizophrenia was first described by the German psychologist Karl Ludwig Kahlbaum in the sixties of the 19th century. He announced this syndrome at a congress of psychiatrists in Innsbruck, noting that he has special symptoms that, in addition to the emotional sphere, also affect the motor sphere.

Kahlbaum's disease, as it is often called in memory of its discoverer, can appear in people under 50 years of age at any period of life, even in the youngest. In children it can be determined by monotonous movements of the body, in children 5–6 years old - by sniffing and licking surrounding objects. But usually catatonia strikes people aged 16–30 years. The first signs appear earlier in males.

It should be noted that earlier, until the fifties of the twentieth century, such a serious disease occurred quite often, especially among young people, but since then this trend has declined. Currently, only 1–3 patients with schizophrenia are diagnosed with it.

Classification

Catatonic states are classified based on the severity of clinical manifestations and the nature of the course of the disorder. Currently, there are two types of catatonia: benign and malignant. Malignant catatonia is the most severe form of the disorder and poses a threat to the patient’s life (“lethal” or “febrile” catatonia).

Febrile catatonia is an acute mental disorder accompanied by a deterioration in general physical condition: increased body temperature, somatovegetative disturbances, homeostasis disorders, deterioration in the functional ability of body systems. The condition develops without connection with somatic diseases. With such a course of the disorder, there is a possible risk of developing cerebral edema and multiple organ failure

Catatonia that occurs at the onset of the disease is considered primary (often observed in schizophrenia). If catatonic manifestations develop against the background of a prolonged course of the disease, catatonia is secondary.

Often in psychiatry, a classification of catatonia is used, based on the pattern of the underlying disorder and the predominance of catatonia syndrome over other symptoms. According to these signs, minor and extensive catatonia are distinguished.

Mild (small) catatonia

. is a reduced version of the catatonic syndrome, in which some simple manifestations are present. Negativism is not clearly expressed, substuporous states, short-term stops of movements and speech, episodic echolalia, isolated grimaces and unexpected actions are noted. The patient enters into dialogue only under duress, is reluctant to answer questions, his speech is mannered, and he avoids visual and tactile contact with the interlocutor. This condition is most often observed in developing schizophrenia.

According to the degree of severity, catatonic excitation is:

• ecstatic - patients are mobile, talk a lot;
• hebephrenic - ridiculous, inappropriate jokes, unmotivated and unreasonable gaiety predominate;
• impulsive - unexpected actions, often destructive and aggressive;
• silent - motor agitation with aggression and destructive actions.

Silent (mute) catatonic agitation

. The person makes meaningless, chaotic movements and resists other people’s attempts to help. During this period of arousal, there is a risk of harm to yourself and others.

Impulsive catatonic agitation

. Development is fast. A person copies the movements and phrases of nearby people. Speech is limited to a chaotic set of phrases. There is a tendency towards cruelty and destructive actions, and a high risk of self-injury.

Ecstatic

. Symptoms increase gradually. At the beginning, there is little motor and speech activity. The nature of the speech is mannered, echolalia (copying other people's words) is possible, and laughter often occurs for no apparent reason.

Degrees of severity of catatonic stupor:

Cataleptic

(with waxy flexibility). Muscle tone is increased, a person can maintain an uncomfortable position for a long time. Manifested by symptoms: catalepsy, waxy flexibility (maintains a position devoted to another person), “air cushion” (characteristic position on the back with the head raised above the pillow).

With negativism

. More pronounced muscle tension. There is sharp opposition to passive movements and attempts by other people to change the patient’s posture. Mutism is often observed.

Rigid

. Muscle tone is very pronounced. Due to the predominance of flexor muscle tone, the person is in the fetal position (knees brought to the stomach, hands pressed to the chest). Trying passive movements increases muscle tension. Muscle tone decreases during deep sleep.

Catatonic states are divided into two types - oneiric and lucid, depending on the presence of clouding of consciousness. With oneiric clouding of consciousness, ecstatic, impulsive, hebephrenic excitement, stupor with waxy flexibility and substuporous states develop. With lucid catatonia, stupor with negativism often develops.

Oneiric catatonia

combines a state of stupor and a dream-like state with vivid scene-like hallucinations, which the patient can talk about after emerging from the stupor. During stupor, the patient is most often disoriented and unable to perceive surrounding events; perception occurs in a distorted form with dream-like fantasies.

Lucid catatonia

represents a stupor without clouding of consciousness. The perception of what is happening around is not distorted. The patient is normally oriented in time and space, remembers the events that occurred while in a stuporous state. Sometimes partial amnesia occurs regarding one's own movements and behavior. The patient may not remember his own impulsive actions, prolonged immobility, etc.

Taking into account diagnostic approaches, catatonia is classified according to provoking factors:

Catatonia developed against the background of concomitant mental disorders. Most often, catatonic schizophrenia is considered (if motor disorders are the main clinical symptoms of the disorder), affective disorders with catatonic symptoms, and others.

Catatonia due to somatic illness. Catatonic syndrome may indicate neurological, infectious and other diseases with metabolic disorders.

Unspecified catatonia. Catatonic states without correlation with other mental and somatic disorders.

Complications

The development of complications is often associated with late diagnosis and incorrect approach to treating the disorder.

When treating people with severe forms of catatonia, difficulties may arise in the daily care of patients, as a result of which complications may develop:

• aspiration pneumonia - occurs due to the difficulty of eating in patients with mutism and the risk of aspiration;
• risk of deep vein thrombosis and pulmonary embolism due to immobility in people with catatonia;
• metabolic disorders associated with dehydration and exhaustion of the body - patients with catatonia may not eat or drink for a long time;
• disorders of the gastrointestinal tract (constipation, intestinal obstruction, etc.)
• urinary retention or incontinence;
• neuromuscular complications (flexion contracture, nerve palsy)
• formation of bedsores.

Also, in a state of catatonic excitement, the patient poses a danger to himself and others. The sudden onset of an attack of stupor can lead to an accident, overtaking a person driving a car, while crossing the road, at work, etc.

Complications of severe forms of catatonia are difficult to treat due to the difficulties in contact between the patient and the doctor.

Diagnostics

When diagnosing catatonic states, it is important to correctly assess the patient’s clinical condition. When collecting anamnesis and examination, it often turns out that the person used psychoactive substances, which most likely contributed to the development of catatonic syndrome. It is worth considering the likelihood of developing symptoms of catatonia during treatment with psychotropic drugs for concomitant diseases.

Psychometric scales are used to diagnose the disorder. The most commonly used is the Bush-Francis Catatonic Disorder Scale. It allows you to determine the presence and severity of catatonic symptoms over a certain period of time. Other rating scales are also used.

Electroencephalography (EEG), CT, MRI and neuropsychological examinations allow us to suggest the localization of disorders in the brain and diagnose the functional state of higher mental functions.

Differential diagnosis is carried out with other mental and somatic disorders accompanied by motor disorders. The most clinically similar to the catatonic syndrome is Parkinson's disease, but the disease is accompanied by a number of specific symptoms that make it possible to differentiate it from catatonia (tremor, apraxia of walking).

Catatonia is differentiated from schizophrenic catatonia, acute psychoses with motor agitation, conversion disorders and other conditions with severe motor retardation or agitation, and neurological symptoms.

Catatonic state: general description

The syndrome was first described at the end of the 19th century by the German psychiatrist K. Kahlbaum, and for a long time it was considered as a separate disease, and doctors noted that even despite intensive treatment, there is a high probability of an unfavorable, progressive course. At the beginning of the 20th century, catatonic disorders were described exclusively as one of the typical symptoms of schizophrenia, and only in the early 2000s was the connection of such a disorder not only with other mental, but also with somatic diseases established and proven.

What is “catatonia” in simple words? The pathology is accompanied by severe movement disorders from complete immobility to acute agitation. At the same time, patients do not react at all to speech addressed to them and aggressively perceive attempts to calm them down.

The pathogenetic mechanisms of the occurrence of catatonic symptoms are not completely known today. There are several hypotheses for its development:

• disturbances in the production and metabolism of neurotransmitters, mainly γ-aminobutyric acid, and to a lesser extent, dopamine;
• organic lesions of individual foci of the brain, in particular, the orbitofrontal cortex, basal ganglia;
• neuroendocrine changes caused by pheochromocytoma, thyrotoxicoma, hypoparathyroidism (however, endocrinopathies are only one of the provoking factors in the development of affective catatonic syndrome);
• an autoimmune inflammatory process affecting the central nervous system.

Forecast

Mild forms of catatonia usually do not have a strong impact on the patient’s further social adaptation and respond well to treatment. Treatment is carried out in a psychiatric hospital. In case of severe somatic diseases, hospitalization is carried out in a specialized department (neurological, oncological). A poor prognosis is associated with catatonia of a malignant course, due to the risk of death, and the presence of catatonia in children, adolescents and the elderly with schizophrenia. Such people require constant psychiatric treatment. Relapses of catatonic states most often occur with the idiopathic version of the disorder or in the presence of concomitant affective disorders. If a person has renal failure, Parkinson's disease, or alcohol addiction, the dysfunction of the brain is chronic, which can also lead to relapses.

In most cases, the prognosis of catatonic syndrome depends on the course of the underlying disease and timely treatment.

Materials and methods

150 patients aged from 19 to 80 years (average value - 42.83±14.65 years) suffering from schizophrenia, bipolar affective and schizoaffective disorders were examined. Each diagnostic group consisted of 50 people. The study included patients admitted to a psychiatric hospital as an emergency hospitalization. Selection was carried out using the screening block of the verified Bush Fransis Catatonia Rating Scale (BFCRS). The criterion for inclusion in the study was the presence of 4 or more points when assessed by the BFCRS screening block. Exclusion criteria were severe comorbid organic, drug-related pathologies. All patients were assessed using the full version of the BFCRS to assess their symptom profile. Repeated assessment of the BFCRS was also carried out at the stage of relief of the psychotic state. Residual catatonic symptoms, their compliance with screening criteria, as well as persistent residual psychopathological symptoms were recorded. The distribution of quantitative data was checked for normality using the Shapiro-Wilk test. To describe quantitative data with a normal distribution, the following were used: arithmetic mean (M) and standard deviation (SD), presented as M(SD). Absolute values ​​and percentages were used to describe qualitative data. Nonparametric statistics methods were used to assess differences between data that were not normally distributed. In the case of comparison of mean values ​​of quantitative data in independent samples, the Mann-Whitney test and the Kruskal-Wallis test were used. Comparisons of qualitative data in the case of independent groups were performed using Pearson's chi-square as well as Fisher's exact test. In the course of data systematization, cluster analysis methods were used. Differences were considered statistically significant at p<0.05.

Treatment in Re-Alt

When treating catatonia that has developed against the background of another mental or physical disorder, therapy is aimed mainly at the underlying disease. Therefore, it is very important for the effectiveness of treatment to conduct a thorough diagnosis. At the Re-Alt mental health center, specialists conduct a detailed analysis of each clinical case and assess the patient’s mental and somatic status in order to individually select treatment tactics.

The most effective method of treating catatonia is the use of drugs from the group of benzodiazepine tranquilizers. Pharmacotherapy helps reduce muscle tone and eliminate other manifestations of catatonia. Treatment uses drugs with sedative, anticonvulsant effects, and muscle relaxants.

If drug treatment is ineffective, electroconvulsive therapy may be prescribed.

Febrile catatonia is a medical emergency. Treatment is carried out inpatiently. Measures are prescribed to maintain and normalize the functioning of all body systems. Antibacterial therapy is prescribed to prevent complications. After stabilization of the condition, electroconvulsive therapy is performed