What is Catatonic Syndrome?
Catatonic syndrome (catatonia) (ancient Greek – to stretch, strain) – psychopathological syndrome (group of syndromes), the main clinical manifestation of which is movement disorders. For the first time catatonia is described by Calbaum (1874) as an independent mental illness, subsequently Kraepelin is attributed to schizophrenia.
Lucid catatonia, accompanied by productive psychopathological disorders in the form of delusions, hallucinations, mental automatisms, is observed, apparently, only in schizophrenia. “Empty” catatonia and catatonia, accompanied by stupefaction, are found in brain tumors, primarily in tumors of the basal parts of it, in traumatic psychosis, mainly in the late period of traumatic brain injury, in acute epileptic psychosis, in infectious and toxic psychoses, in progressive paralysis.
Catatonic syndrome occurs in children and adults. The latter – mostly up to 50 years. In later life, catatonic disorders are rare. In children, catatonic disorders are manifested by motor stereotypes (often rhythmic) – “manege” run, repetitive movements of the limbs, body or grimace, walking on tiptoe, etc.
Often there are echolalia, mutism and verbigeration, stereotyped impulsive movements and actions. Catatonic disorders in children can take the form of regressive behavior – a child of 5-6 years old sniffs and licks the objects around him. Catatonic syndrome reaches its highest intensity (primarily in schizophrenia) at the onset of the disease at the age of 16-17-30 years. Especially this intensity concerns stuporous disorders. After 40 years, newly emerged pronounced catatonic disorders are rare. For women aged 40–55 years, for the first time, emerging catatonic disorders very much resemble hysterical — expressive speech and facial expressions, theatrical behavior, hysterical comrade, etc.
Causes of Catatonic Syndrome
The exact cause of the catatonia is unknown, but many hypotheses have been proposed.
According to Northoff (2002), “modulation from top to bottom” in the basal ganglia, due to the deficiency in the cortex gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter of the brain, can explain the motor symptoms of catatonia. This explanation may be based on the pronounced therapeutic effect of benzodiazepines, which cause an increase in GABA activity. Similarly, it is believed that increased activity of glutamate, the main excitatory neurotransmitter, also underlies neurochemical disorders (Northoff et al, 1997).
Osman and Khurasani (1994) believe that catatonia is caused by a sudden and massive dopamine blockade. This may explain why antipsychotic drugs that block dopamine do not generally benefit from catatonia. Indeed, in acute dopamine deficiency, these drugs actually lead to a worsening of the condition.
Catatonia is said to be caused by the resumption of increased activity of the cholinergic and serotonergic systems after clozapine is canceled (Yeh et al, 2004).
In chronic catatonia with pronounced impairment of speech, positron emission tomography (PET) revealed bilateral metabolic disturbances in the thalamus and frontal lobes (Lauer et al, 2001).
According to a very interesting hypothesis proposed by Moskowitz (2004), catatonia can be understood as an evolutionary reaction of fear in herbivores when meeting with carnivores, whose predator instincts are triggered by movement. Such a response, still preserved, is now expressed in many severe mental or somatic diseases, in which a catatonic stupor may be a typical response due to the “end state” in response to a sense of imminent death.
Symptoms of Catatonic Syndrome
Catatonic arousal and catatonic stupor are distinguished in the structure of catatonic syndrome.
There are two forms of catatonic excitement:
- Pathetic catatonic arousal is characterized by gradual development, moderate motor and speech arousal. In a speech a lot of pathos, echolalia can be noted. The mood is heightened, but it has not the character of hyperthymia, but exaltation, periodical laughter is periodically observed With increasing symptoms, features of hebephrenia appear – hebephrenal-catatonic arousal. Impulsive actions are possible. Disorders of consciousness does not occur.
- Impulsive catatonic excitement develops sharply, the actions are swift, often violent and destructive, and are socially dangerous. Speech consists of separate phrases or words, characterized by echolalia, ecopraxia, perseveration. With the utmost severity of this type of catatonic excitation, the movement is chaotic, they can become choreiform in nature, patients are prone to self-harm, are silent.
Catatonic stupor is characterized by motor inhibition, silence, muscle hypertension. Patients may be in a constrained state for several weeks or even months. All kinds of activity, including instinctive, are violated. There are three types of catatonic stupor:
- A stupor with wax flexibility (cataleptic stupor) is characterized by freezing the patient for a long time in his adopted or given position, even very uncomfortable. Without responding to loud speech, they can respond to quiet whisper speech, spontaneously release in the conditions of night silence, becoming available to the contact.
- The negativistic stupor is characterized, along with motor inhibition, by the patient’s constant opposition to any attempts to change his posture.
- A stupor with stupor is characterized by the greatest severity of motor inhibition and muscle hypertension. Patients take and retain embryoposis for a long time; a symptom of an airbag may be observed.
Mutual transitions of one type of stupor to another, pathetic excitement into an impulsive one are possible, although this is rarely observed. Mutual transitions of catatonic excitation into a stupor and vice versa are possible: pathetic excitement can be replaced by cataleptic stupor, impulsive – by negativistic or stupor with stupor, just as a stupor can suddenly be interrupted by an appropriate type of excitation.
When cataleptic stupor can be observed hallucinations, delusional disorders, sometimes signs of impairment of consciousness on the type of oneiroid – so-called. oneiric catatonia, on leaving which most of the productive symptoms are amnesized. Negativistic stupor and stupor with stupor presented so-called. lucid (clear, pure) catatonia, in which there are no productive symptoms, no stupefaction, patients are oriented, aware of and remember the surrounding.
Catatonic syndromes are observed in schizophrenia, infectious, organic and other psychoses. According to two studies, catatonic symptoms are observed in 12-17% of young people with autism.
The catatonic syndrome is characterized by stereotypies (repetitions of the same kind) of movements and postures; verbiger (monotonous repetition of words and phrases); echosymptoms – repetition of the movements of another person (echoraxia, or echokinesia), or of his words and phrases (echolalia, or echodia); negativism (with passive negativity, the patient does not fulfill the requests addressed to him, with the active – makes other actions instead of the proposed actions, with paradoxical negativity produces actions directly opposite to those that he is asked to perform); catalepsy – a disorder of motor function, which consists in the fact that certain parts of the patient’s body (head, arms, legs) can maintain their position; in addition, the patient himself may solidify for a long time in some, even uncomfortable position.
In some cases, the clinical picture is exhausted by the listed symptoms (“empty” catatonia), but often affective, hallucinatory, and delusional disorders are also observed in the catatonic syndrome. Consciousness in some patients remains undisturbed (lucid catatonia), in others the symptoms of catatonic syndrome appear against the background of stupefaction, more often oneiroid (oneiric catatonia). After the acute condition of the patient, there is amnesia of real events, but he can tell (fragmentary or in sufficient detail) about the disorders observed at that time.
Movement impairment in the form of a stupor with catatonic syndrome (catatonic stupor) is expressed in increased muscle tone. The patient moves little and slowly (subacteous state) or lies, sits or stands motionless for hours and days (stupor state). Often, somatic and vegetative disorders are accompanied by a catatonic stupor: cyanosis and swelling of the extremities, drooling, excessive sweating, seborrhea, low blood pressure. Against the background of a stupor, other catatonic symptoms appear in various combinations and different intensities. In the most severe cases, the patient lies in the fetal position, all of his muscles are extremely tense, his lips are stretched forward (stupor with muscular stupor).
Movement disturbance in the form of excitation with catatonic syndrome (catatonic excitation) is expressed in the form of unmotivated (impulsive) and inadequate actions; in the movements and verbal expressions of the patient echo symptoms, active negativism, stereotypes are noted. Suddenly, arousal may be replaced for a short time by a catatonic stupor and mutism (lack of verbal communication); often it is accompanied by severe affective disorders (anger, rage, or indifference and indifference). Sometimes with exalted arousal, patients clown around, grimace, grimace, make unexpected, ridiculous antics (hebephrenic syndrome).
Catatonic syndrome is more common in catatonic schizophrenia; however, it is usually combined with hallucinations, delusions and mental automatisms. Sometimes “empty” catatonia is observed with organic brain damage (for example, with tumors), traumatic, infectious and intoxication psychosis, etc.
Diagnosis of Catatonic Syndrome
Differential diagnosis of catatonia
Although catatonia is traditionally associated with schizophrenia, it is more common in affective disorders (Pommepuy & Januel, 2002). For example, Abrams and Taylor (1976) noted that in a sample of 55 people with catatonia, only four had schizophrenia, and more than two-thirds had affective disorders, especially mania. Similar results were reported by Barnes and colleagues (1986): in their sample of 25 people, only one had schizophrenia, and nine had affective disorders.
Older age may be a significant risk factor for catatonia in depression (Starkstein et al, 1996). Catatonia can also develop in postpartum mental disorders (Lai & Huang, 2004).
Temporal epilepsy is the recognized cause of catatonia (Kirubakaran et al, 1987).
The potential risk of developing catatonia is associated with a sudden discontinuation of clozapine, which is eliminated when you resume taking this drug (Yeh et al, 2004).
Immobility observed in severe dementia may be a catatonic state that occurs in other serious organic disorders and may be treatable with lorazepam (Alisky, 2004).
There have been publications on specific clinical cases in which it was indicated that patients with thrombotic thrombocytopenic purpura may have a higher risk of developing catatonia (Yacoub et al, 2004).
Cocaine-induced catatonia (Gingrich et al, 1998) and ecstasy (Masi et al, 2002) have been reported. Medicines prescribed by doctors, such as ciprofloxacin (Akhtar & Ahmad, 1993), can also cause catatonia.
Disorders of metabolism, such as hyponatremia, can cause catatonia (Lee & Schwartz, 1997); patients with rare metabolic disorders, such as Wilson’s disease and Tay-Sachs disease (Rosebush et al, 1995), can also develop this condition.
Traumatic brain injury and somatic illness at the onset of psychosis are more common among patients who later develop catatonia than among patients without it (Wilcox & Nasrallah, 1986). Severe infectious diseases suffered in childhood, including rheumatic attack, are associated with an increased risk of developing catatonia in the period of adulthood (Wilcox, 1986).
Hysteria is also traditionally referred to as the cause of catatonia.
No significant minority has a reason (Barnes et al, 1986). Benegal and colleagues (1993), who reported high prevalence of idiopathic catatonia, found that it is more common among women.
Catatonia in ICD – 10 and DSM – IV
It is gradually becoming more and more obvious that catatonia is more often the result of affective disorders than schizophrenia. However, historically, catatonia is more associated with schizophrenia. After Kalbaum’s first description of catatonia, Kraepelin included it as a type of dementia praecox (early dementia, formerly called schizophrenia), and when Bleuler introduced the concept of schizophrenia, he identified catatonia as one of the subtypes of schizophrenia. This prejudice, which gives schizophrenia too much space in discussions about catatonia, continues to be reflected in ICD – 10 (World Health Organization, 1992) and DSM – IV (American Psychiatric Association, 1994).
The diagnosis of catatonic schizophrenia in ICD – 10 (category F20.2) requires that the patient clearly shows at least one of the following catatonia characteristics for two weeks: stupor, agitation, congestion in various postures, negativity, rigidity, wax flexibility and “command automatism” (automatic subordination).
If a patient with severe depression is in a stupor, then a diagnosis of a “severe depressive episode with psychotic symptoms” (F32.3) is made, even if there are no delusions and hallucinations.
Similarly, a diagnosis of “mania with psychotic symptoms” (F30.2) will be made to a patient with manic stupor.
Thus, with depression or mania, only a stupor, the most extreme manifestation of catatonia, seems to be of diagnostic value, whereas a much wider range of relevant symptoms is required for the diagnosis of schizophrenia.
Catatonia due to somatic diseases is diagnosed as “organic catatonic disorder” (F06.1).
DSM – IV
In DSM – IV, a diagnosis of “schizophrenia, catatonic type” (code 295.20) is made if at least two of the following symptoms dominate in the clinical picture: motor immobility, excessive motor activity, extreme negativism, bizarre voluntary movements, and also echolalia / echopraxia.
If an organic cause is identified, then a “catatonic disorder due to a somatic condition” is diagnosed (code 293.89).
As in ICD – 10, DSM – IV does not have a separate diagnostic category for catatonia, due to depression or mania, but catatonia may be an additional specific feature in affective disorders.
Treatment of Catatonic Syndrome
The treatment is carried out in a psychiatric hospital; It is aimed at the underlying disease.
Benzodiazepines are the drugs of choice for catatonia. Patients who do not respond or do not respond sufficiently to benzodiazepines require electroconvulsive therapy (ECT).
In a prospective open-label study (Ungvari et al, 1994a), 18 patients with catatonia were treated with either oral lorazepam or intramuscular diazepam: 16 showed significant clinical improvement within 48 hours, and two had complete remission after just one dose. However, nine patients subsequently required ECT to achieve further improvement. Rosebush and colleagues (1990) reported a more pronounced and rapid therapeutic response to lorazepam – in 12 of the 15 patients with catatonia, the symptoms completely disappeared within two hours. Low doses of benzodiazepines are effective both in catatonic stupor and in catatonic excitation (Ungvari et al, 1994b). Organic catatonia also responds well to benzodiazepine treatment (Rosebush et al, 1990, 1995).
Like benzodiazepines, ECT is effective against catatonia due to either functional mental disorders (including schizophrenia) or organic causes (Rohland et al, 1993); it is effective even in hysterical catatonia (Dabholkar, 1988). Benegal et al. (1993) reported a good therapeutic response to ECT in a sample of 65 patients with catatonia, including 30 individuals with idiopathic catatonia, 19 with schizophrenia, and 16 with depression. The duration of the disease was shorter in the group of patients with idiopathic catatonia. In addition, the number of ECT sessions required for improvement did not depend on the main diagnosis.
Emergency application of ECT is the treatment of choice for malignant catatonia (Pommepuy & Januel, 2002). The ECT guidelines for the Royal College of Psychiatrists (Scott, 2005) clarify that ECT can be performed for catatonia if treatment with lorazepam has been ineffective.
Antipsychotic drugs are usually not recommended during the catatonic treatment, even if it is caused by a psychotic illness, such as schizophrenia, since the risk of provoking a malignant neuroleptic syndrome increases significantly. However, they can be effective in therapeutically resistant catatonia: Hesslinger and colleagues (2001) reported a patient with a catatonia resistant to benzodiazepine treatment, who had a striking and lasting improvement after using risperidone. In a literature review, Van Den Eede and colleagues (2005) concluded that atypical antipsychotics may be useful in the treatment of non-malignant catatonia.
Kritzinger and Jordaan (2001) suggest that carbamazepine is effective in both acute and supportive treatment of catatonia: in a sample of nine patients, four were completely amenable to treatment with carbamazepine, one was partial, and the remaining four had no significant improvement.
The combination of lithium and antipsychotic medication may be a treatment option for a therapeutically resistant catatonic stupor (Climo, 1985).
Mastain and colleagues (1995) reported that zolpidem was effective in a patient with benzodiazepine and ECT-resistant catatonia.
According to the descriptions of specific cases, amantadine (Northoff et al, 1999) and memantine are effective in catatonia (Thomas et al, 2005). They are antagonists of the N-methyl-d-aspartate receptor (NMDA). Glutamate acts on the NMDA receptor, and if this receptor is blocked, the neurochemical equilibrium shifts towards GABA. Thus, both pro-GABA and anti-glutamate drugs appear to be useful in catatonia.
Catatonia, of course, almost always requires inpatient treatment. The patient needs intensive nursing care and regular monitoring of the main indicators of the vital functions of the body. The somatic condition of the patient, especially with prolonged catatonia, may justify intravenous fluid administration and parenteral nutrition. If a malignant neuroleptic syndrome is diagnosed, then it is preferable to continue treatment in the somatic unit. Treatment methods for neuroleptic malignant syndrome, in addition to benzodiazepines and ECT, include muscle relaxants (for example, dantrolene sodium) and dopamine agonists (for example, bromkriptin).