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Controversies on the clinical and therapeutic approach and on the nosological classification of catatonia.

INTRODUCTION

Two fundamental approaches to catatonia have influenced profoundly the current practice. The first refers to catatonia as indicative of schizophrenia, while the other consists of a symptom-centred view positing that catatonic symptoms are motor symptoms pinpointed in numerous psychiatric pathologies, including neuroleptic malignant syndrome. The second approach encourages giving up the exclusive use of antipsychotics as medication for catatonia (1, 2).

Early and correct diagnosis of catatonia has a vital importance. A significant proportion of patients with catatonic syndrome also exhibit a subsidiary psychiatric condition, reason for which therapeutic intervention is often postponed. Unless treated early on and effectively, catatonia becomes life-threatening and it may entail complications such as thromboembolism, aspiration pneumonia, urinary infections, dehydration, or dyselectrolytemia. The catatonia diagnosis per se is associated with high mortality risk (including suicide) (3). DSM-5 includes catatonia as a separate title within the larger chapter called "Schizophrenia Spectrum and Other Psychotic Disorders". Hence, premises were created for categorising catatonia separately, as distinct diagnosis entity (4, 5).

NOSOLOGICAL CLASSIFICATION OF CATATONIA

Catatonia was first coined in the 19th century as a syndrome characterized by motor, affective, and behavioural symptom. Throughout the 20th century, catatonia has been viewed as a rare motor manifestation of schizophrenia; its emergence outside the discordant spectrum was almost completely ignored. After introducing narcoleptics in the therapy of psychiatric pathology, the incidence of catatonic schizophrenia dropped; this success was credited to the new pharmacological agents. At the same time, the neuroleptic malignant syndrome was coined; it featured numerous similarities with the catatonic syndrome, and a series of recent research studies suggest a potential common origin of the two nosological entities. In this context, numerous controversies have sparkled concerning the differential diagnosis of the two syndromes (2, 5).

Psychiatric diagnoses are set, in most cases, based on the existence of certain syndromes. The catatonic syndrome still represents one of the most controversial diagnoses in psychiatry; the overwhelming majority of scientists in the field identify it with a subtype of schizophrenia. Catatonia is present in 10 % of patients with acute psychiatric pathology (just a few of whom are persons diagnosed with schizophrenia; most of them are patients with affective disorders). The second category responds very well to benzodiazepine therapy. Patients with schizophrenia have partial or weak response to benzodiazepine therapy, which suggests that the catatonic syndrome within this group has a different cause. At the same time, most individuals displaying catatonic syndrome associate psychotic elements of variable intensities and forms (6, 7, 8).

In Jasper's view, catatonia is a motor phenomenon, while psychological phenomena such as hysteria or melancholic depression do not represent primary motor phenomena, but actions and ways of expression that should be understood through psychopathological mechanisms. This is the context in which catatonia was limited to the schizophrenia spectrum, but which also drew attention on the possibility of developing predominantly motor phenomena in other psychiatric disorders, too, without encompassing them within catatonia. Modern, contemporary psychiatry has rejected Jasper's view, but it has failed to redefine catatonia in the adjusted terms of psychopathology; this has represented a fundamental setback for the research perspectives in the field. Studies suggest that, besides the contrasting definition of the two classical forms of the catatonic syndrome (hyperkinetic and characterized by psychomotor inhibition), other clinical manifestations may be included within the catatonic syndrome, depending on the type of patient and on the number of specific symptoms displayed (1, 2, 9).

Catatonia is a clinical syndrome characterized by motor inhibition, manifested by hyperkinesias or negativism, echopathy (echolalia, echopraxia, echomimia). The catatonia diagnosis in the context of a general medical condition must be based on proof that the catatonic symptomatology is due to the physio-pathological effect of the general medical condition in question. It is fundamental to rule out a primary psychiatric pathology (e.g., schizophrenia, depression with psychotic symptoms) as better explanation for catatonic symptomatology and to determine that catatonic symptoms are not part of delirium (8, 10). According to DSM-5, catatonia is a rare medical condition, most often encountered among patients with affective or psychotic psychiatric disorders. The DSM-5 diagnosis criteria for the catatonic syndrome due to general medical conditions include the presence of catatonia-specific alterations, the evidence of physio-pathological grounds for the emergence of these symptoms, by ruling out primary psychiatric pathology and delirium. DSM-5 includes the presence of catatonic symptoms consecutive to the administration of antipsychotics within neuroleptic malignant syndrome or medication-induced parkinsonism (by the gravity of symptoms). Concerning catatonia induced by non-neuroleptic substances, the proper diagnostic is medication-induced kinetic disorder (not otherwise specified). According to DSM-5 criteria, the clinical presentation is dominated by the presence of at least three of the following symptoms: stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerism, stereotypy, agitation not influenced by external stimuli, grimacing, echolalia, and echopraxia (4, 6).

Catatonia is a syndrome dominated by the motor symptomatology that accompanies numerous and diverse general and neurological general conditions. The persistent inadvertence in assimilating most cases of catatonia as forms of schizophrenia has undesirable consequences related to therapeutic success, thus determining high morbidity and mortality (11, 12).

THE CONTROVERSIAL CONNECTION BETWEEN CATATONIA AND NEUROLEPTIC MALIGNANT SYNDROME

Catatonia and neuroleptic malignant syndrome represent two life-threatening medical conditions; therapeutic success is related indissolubly to early and correct diagnosis. Predictably, the opinions related to the connection between the two syndromes are conflicting (the most common one is their classification within the same spectrum). Nonetheless, numerous other hypotheses have been issued on the nature of the connection between catatonia and neuroleptic malignant syndrome (12). The first posits that neuroleptic malignant syndrome is an iatrogenic form of catatonia (medication-induced catatonia). The second, more specific hypothesis, posits that neuroleptic malignant syndrome is an iatrogenic form of malignant catatonia. On the other hand, a third hypothesis states that the two syndromes are actually one and the same nosological entity. The fourth hypothesis includes precisely catatonia among the risk factors for neuroleptic malignant syndrome, while the fifth hypothesis concerns the heterogeneity of the neuroleptic malignant syndrome (including both the catatonic and the non-catatonic response to antipsychotic medication). Another perspective--with fewer supporters, but with ampler historical and research evidence throughout time--is the one of the clear distinction between the two medical conditions. Considering the current state-of-the-art in the field, there is not enough evidence to support or to contradict the existing hypotheses (13, 14). Medication-induced catatonia--manifested as an extrapyramidal-catatonic syndrome--was only sporadically reported by scientific literature. Thus far, specialists have failed to fully explain its connection with neuroleptic malignant syndrome and with extrapyramidal phenomena consecutive to the administration of antipsychotics (10, 15).

DIAGNOSIS CHALLENGE

For pinpointing the catatonic syndrome, specific scales may be used, such as Rogers Catatonia Scale, Bush-Francis Catatonia Rating Scale (BFCRS) (the most commonly used), Northoff Catatonia Rating Scale, and Braunig Catatonia Rating Scale. Their downside is that they fail to assess the duration and origin of catatonic symptoms (16, 17). Unfortunately, there are no specific laboratory explorations for setting the diagnosis of catatonic syndrome. However, the aforementioned scales orient the diagnosis, thus providing valuable information on the underlying conditions of catatonic symptomatology. Considering the possibility of dealing with anti-NMDAR encephalitis, it is recommended to detect anti-NMDAR IgG antibodies in the cerebrospinal fluid or in the serum. Considering that serum iron is lower in neuroleptic malignant syndrome compared to catatonic syndrome, it was confirmed that low values of serum iron are indicative of a risk factor for neuroleptic malignant syndrome consecutive to the administration of antipsychotics in patients with catatonic syndrome (8, 18).

DIAGNOSTIC TEST

Benzodiazepines are the dominant pharmacological agents used in the medication therapy of catatonia, but they are also very useful as diagnostic test. Hence, positive Lorazepam Challenge Test validates the diagnosis of catatonia. After the patient is examined for signs of catatonia, Lorazepam is administered intravenously; if there has been no change, subsequent doses are given, and the patient is again reassessed. A positive response is a reduction of at least 50 % of the symptomatology. Analogous to the Lorazepam test (given intramuscularly or per os, but with slower results), a Zolpidem Challenge Test can also be conducted (given per os, theoretically with results similar to benzodiazepines) (7, 19).

THE THERAPEUTIC APPROACH TO CATATONIA

Currently, there is serious conceptual ambiguity of the catatonia term. Nonetheless, compelling scientific evidence shows the efficacy of benzodiazepine compounds for treating this clinical syndrome (8).

On practical level, a cautious approach is recommendable: a priori, the catatonia diagnosis can be considered for a patient displaying stiffness, mutism, negativism, or (on the contrary), for a hyperkinetic and agitated patient. If catatonia is suspected, it is fundamental to monitor closely vital signs, ionogram, full blood count, and creatine phosphokinase. At the same time, it is very important to rule out (by doing an electroencephalogram) the presence of epilepsy, which can mimic catatonic symptoms (7, 19).

Benzodiazepines are the first choice for the catatonic syndrome, regardless of the underlying condition. They are positive allosteric modulators of the GABA(A) receptors that correct GABAergic functional deficit of the orbitofrontal cortex. Benzodiazepines have a favourable safety profile, an easy administration, and they record a 70-80 % rate of symptomatology remission. On the other hand, it has been proven that catatonic symptoms with chronic evolution are not equally responsive to the treatment with benzodiazepine compounds. Certain studies have even concluded that benzodiazepines are ineffective for catatonic symptoms pertaining to schizophrenia (5, 7, 18).

The efficiency of benzodiazepines depends on the administered dose (usually between 8 and 24 mg Lorazepam a day). Most authors posit that treatment should begin with 1-2 mg of Lorazepam every 4-12 hours, and then by readjusting the doses for obtaining the remission of catatonic symptoms without sedating patients more than necessary. If the dose is correct, therapeutic response is recorded within 3-7 days. However, situations have also been reported when the response was gradual and slow. Although Lorazepam is considered the first choice for treating catatonia, smaller studies have also reported the successful use of Diazepam, Oxazepam, and Clonazepam for this symptomatology. A consensus is yet to be reached concerning the duration of benzodiazepine treatment (7, 8). Usually, the treatment ceases after the full remission of symptoms and after making sure the cause was eliminated. A few cases have been reported where catatonic symptomatology relapsed after ending benzodiazepine use, which forced the clinician to prescribe it a la longue. Electro-convulsive therapy is recommended to patients who fail to respond to benzodiazepine or in cases when a rapid response is necessary in the context of life-threatening conditions such as malignant (lethal) catatonia with idiopathic fever, tachycardia, and significant oscillations of blood pressure. If the underlying condition is depression with psychotic elements, the electro-convulsive therapy may become the first therapeutic choice (18, 19).

If catatonic symptomatology does not cease after benzodiazepine or electro-convulsive therapy, it is recommended to use atypical antipsychotics, but to maintain benzodiazepines in the therapeutic regimen. While benzodiazepines are safe on a short term basis, one must consider the risk of hypoventilation in patients with obesity or sleep apnoea, the risk of syncope in elderly patients or in those with various vertiginous or ataxic phenomena, and even the risk of mood swings in case of hyperkinetic catatonia. The failure to detect early the catatonic syndrome is a consequence of limited and inaccurate information included scientific manuals, which provide an unclear picture of this nosological entity. The immediate identification of catatonia with schizophrenia has undesirable consequences, consecutive to the immediate administration of antipsychotic medication. This pharmacological approach provides low immediate results and it increases the risk of turning the catatonic syndrome into its malignant form (8, 18, 19).

Nonetheless, the supporters of Kraepelin's theory (that identifies catatonia with schizophrenia) state that antipsychotics should be administered in case of catatonic symptoms. However, they fail to consider the possibility of developing neuroleptic malignant syndrome and they simply accept the delayed resolution of symptoms. In the context of this approach, it is best to avoid the benzodiazepines that delay even more the therapeutic success (2, 5).

There are compelling clinical trials pleading for the efficiency of benzodiazepines in acute catatonic syndrome, mostly in stupor manifestations. Considering its pharmacological properties, Lorazepam is recommended on large scale as first choice medication for treating catatonia. Nonetheless, its effects (like those of other benzodiazepines used) seem limited concerning the catatonic symptoms in schizophrenia compared to those included in affective disorders (5, 20). A series of recent research indicated that only 20-30 % of the patients with schizophrenia--who display catatonic symptoms--respond to medication comprising benzodiazepine. The modest response to the administration of benzodiazepines for catatonia in the context of a schizophrenia spectrum disorder suggests that different underlying physio-pathological mechanisms may exist for acute catatonia compared to chronic catatonia. A series of retrospective studies indicate that acute catatonic syndrome responds favourably to electro-convulsive therapy. Though catatonia associated to schizophrenia is less prone to respond favourably to this type of therapeutic intervention than catatonic syndrome associated to affective disorders or to other medical conditions, electroconvulsive therapy has delivered higher results than benzodiazepine in this group of patients (3, 7, 19).

Though it is apparent that catatonic syndrome is not associated only to one type of schizophrenia (it can be displayed within numerous other general or neurological medical pathologies), it cannot be omitted that catatonic elements represent a potential dimension of psychotic disorders. This position has a strong impact on the therapeutic approach and on the direction of neurobiological research (18).

Catatonia appears in three forms in DSM 5: "Catatonia associated with another mental disorder (catatonia specifier)", "Catatonic disorder due to another medical condition", and "Unspecified catatonia". The list of signs and symptoms is identical for the first two categories, while the third illustrates an unclear category. When a clinician fails to identify an underlying psychiatric or medical condition, the solution is to diagnose catatonia as a nosological entity per se (though DSM-5 does not feature it as such) (4, 6, 8).

The common modern practice leans toward considering it a separate clinical entity, but not an independent clinical diagnosis yet. The current issue is the lack of defining catatonia from a psychopathological perspective. The definitions provided are nonspecific and full of ambiguity (2, 5).

Catatonia may also be featured within obsessive compulsive disorder, posttraumatic stress disorder, and ethanol withdrawal. Concerning teenagers and young adults with autism, the catatonic syndrome is encountered in approximately 12-17 % of the cases; at the same time, it may also be present in other development disorders or in Tic disorder. The assessment principles of the catatonic syndrome in children are similar to the ones used for adults. In 25 % of the cases, catatonia is related to general or neurological medical conditions. Recent research indicates the presence of catatonic syndrome in certain forms of encephalitis (with Anti-N-methyl-D-aspartate receptor) (1, 3). Other severe complications of catatonia include muscle contractures, nutritional deficiencies, sloughs, dramatic weight loss, and thiamine deficiency (3).

Some of the patients who display catatonic syndrome must benefit from advanced medical care, which includes IVs with fluids and feeding through nasogastric intubation, for preventing life-threatening complications. In some cases, anticoagulant therapy is also recommended for lowering the risk of venous thromboembolism in bed-ridden patients (in the context of psychomotor inhibition within catatonia) (1, 3, 20).

All types of medication given to patients with catatonic syndrome must take into account their risk of inducing catatonic symptoms. There is a certain degree of ambiguity on the role on antipsychotics for treating catatonia. Both first-generation and atypical antipsychotics have high risks of contributing to the persistence and aggravation of catatonic symptomatology, as well as of determining the onset of neuroleptic malignant syndrome. Risks are greater if the antipsychotic has an ampler D2 blockade, thus higher potential of determining extrapyramidal effects (10, 18). Nonetheless, studies have reported that atypical antipsychotics--agonist at GABA and antagonist at 5HT2--stimulate the release of dopamine in the prefrontal cortex, thus mitigating catatonic symptomatology. It is worth underscoring that the overwhelming majority of these studies were conducted on patient samples with catatonic syndrome within schizophrenia spectrum. After initiating treatment with benzodiazepine or electroconvulsive therapy and observing the remission of catatonic symptomatology, the clinician must still consider (depending on the cause) the prescription of atypical antipsychotics, for eliminating potential residual psychotic elements (especially in patients with schizophrenia) or for prophylactic purposes (in other psychotic or affective disorders). In this context, the most recommendable antipsychotics are those with minimal D2 blockade (quetiapine or olanzapine) or a partial agonist at D2 receptors (aripiprazol) (8, 9, 20).

CONCLUSIONS

Considering the confusions surrounding the concept of catatonia, the current diagnostic systems, and the specific assessment scales, there are significant differences in terms of the number of symptoms considered and their definition. Furthermore, there is still no study on the subjective experience of catatonic patients and its correlation with the clinical forms of catatonia. Similarly, there are no systematic studies on the biological markers of catatonia, though testable hypotheses on the physiopathology of catatonia have been made available. Catatonia is still an open matter, which provides the occasion for conducting numerous research studies on both the diagnostic algorithm and the therapeutic approach.

Ilinca UNTU--M.D., Ph.D. Student, "Socola" Institute of Psychiatry, Iasi, Romania

Dania Andreea RADU--M.D., Ph.D. Student, "Socola" Institute of Psychiatry, Iasi, Romania

Vasile CHIRIJA--Prof., M.D., Ph.D., "Socola" Institute of Psychiatry, Iasi, Romania

Roxana CHIRIJA--Prof., M.D., Ph.D., "Socola" Institute of Psychiatry, Iasi, Romania

ACKNOWLEDGMENTS AND DISCLOSURE

The authors declare that they have no potential conflicts of interest to disclose.

REFERENCES

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Correspondence:

Vasile CHIRITA "Socola" Institute of Psychiatry No. 36 str. Bucium, Iasi, Romania

E-mail: vasile.chirita@yahoo.com

Submission: July, 9th, 2015

Admittance: August, 20th, 2015
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Author:Untu, Ilinca; Radu, Dania Andreea; Chirita, Vasile; Chirita, Roxana
Publication:Bulletin of Integrative Psychiatry
Article Type:Report
Date:Sep 1, 2015
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