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The importance of treatment adherence: catatonia, an emergency diagnosis in psychiatry.

INTRODUCTION

From an etymological point of view, the term "schizophrenia" comes from the association of two words, schizein, which means "to separate", and fren, meaning "mind". Eugen Bleuler coined the term "schizophrenia" in 1911, noting thought fragmentation and loss of identity unity in patients with this mental disorder. In 1852, Morel brings a condition with the same features into discussion, but calls it dementia praecox, the rationale behind this being that the onset of the disease takes place in adolescence and the disability produced to those affected is very severe in terms of functionality.

In the same period, more precisely in 1874, Karl Kahlbaum talks about catatonia, saying it is a severe neuropsychiatric disorder characterized by prominent motor features, objectified by immobility, mutism, negativism, rigidity, stereotypies, echolalia, mannerisms. Mutism and stupor are considered to be pathognomonic features (1).

Although Kraepelin admits the presence of catatonic symptoms in manic-depressive disorders, he promotes the idea of catatonia being the main symptom of dementia praecox (2). The association between catatonia and dementia praecox suggested a poor prognosis and a possible onset of a chronic deterioration. Kraepelin's statements were essential for the further development of psychiatric nosography, although his theory about catatonia being a subtype of schizophrenia had been hidden for more than a century (3).

If detected early and properly, catatonic symptoms remit and the patient returns to their previous functioning state. The most efficient treatment for this state is considered to be represented by the intravenous administration of benzodiazepines, especially lorazepam, with a remission rate of 60-70%, regardless of the cause of the onset or the intensity of the symptoms (4), but carbamazepine (5), clonazepam, olanzapine (6), dantrolene (7) and diazepam (8) are also good. Cyclooxygenase inhibitors appear to protect against the development of catatonia induced by perphenazine on laboratory mice (9).

Intravenous treatment is preferred because of good adherence and a rapid and complete absorption. As the patients' condition improves, they are switched to oral medication (10). Electroconvulsive therapy is the treatment of choice in the case of malignant catatonia, resistant to benzodiazepines (11).

In recent literature (12), it is stipulated that the different subtypes of catatonia would be based on the existence of disturbances in the "top-down" or "bottom up" modulation of the cortical-subcortical connections, which are involved in controlling psychomotor activity. "Top down" modulation refers to the control that the cortex exercises over subcortical areas, i.e. the action of the orbitofrontal cortex over basal ganglia and caudate nucleus. This has to be distinguished from the "bottom up" modulation that takes place, for instance, in the case of basal ganglia over the motor and premotor cortical areas. In catatonia, the GABAergic-mediated deficit in the orbitofrontal cortex may result in the alteration of "top down" modulation of the caudate nucleus and the basal ganglia, via the orbitofrontal loop. In hypodopaminergic states, mediated deficits in the striatum may be translated in the alteration of "bottom up" modulation of the motor/premotor cortex.

Treatable disorders must be identified as soon as possible. In particular, neuroleptic malignant syndrome (NMS), encefalitis, non-convulsivant status epilepticus and acute psychotic disorder must be immediately diagnosed. The first three conditions represent neurological emergency diagnosis and imply prompt admission and treatment in an intensive care unit. Acute psychotic disorder requires admission into a psychiatry unit for in depth evaluation and early initiation of the treatment (13).

Both, catatonia and NMS respond well to classic antipsychotic treatment, as well as to new variants. Thus, in some cases of catatonia, the motor symptoms may be directly associated with a D2 receptor blockade in the striatum, which modulates the activity of the orbitofrontal cortex via the motor loop. Given the existence of many forms of catatonia, electro-convulsive the rapy appears to be more effective in those cases in which the "top down" modulation is affected, than in those with altered "bottom up" modulation (14).

CHIEF COMPLAINT

The patient is a 38 years old man, from Galati, and arrived with his family at "Socola" Institute of Psychiatry in May 2015, complaining of psychomotor restlessness, bizarre smiling, blunt affect, olfactory and visual hallucinations ("I can smell smoke!", "I see flames and people burning...", "The Gates of Hell are under the floor of my house and they are trying to drag me there!"), mixed insomnia, suspiciousness and delusional ideation of prejudice and prosecution ("There are many people who want to hurt me and I don't understand what's their problem with me").

PATHOLOGICAL PERSONAL HISTORY

In November 2013, he was admitted to the Infectious Diseases Hospital for sepsis of unknown etiology, infectious encephalopathy and coma (Glasgow score: 5) and had a favourable outcome. There are also other diagnosis to be mentioned: NYHA II class heart failure, stage II essential hypertension with moderate adjacent risk, grade II obesity, unspecified hepatocytolisis, druginduced extrapyramidal syndrome following long-term administration of Amisulprid (at the time of admission).

FAMILY HISTORY: no relevant data.

LIVING AND WORKING CONDITIONS

He lives in a house with his parents, in rural area, he graduated in constructions and worked as an engineer for five years, he's not married and he's of orthodox Christian faith.

The patient does not show signs of addictive behaviour.

HISTORY OF THE PRESENT ILLNESS

The patient reports the presence of two psychotic episodes in his medical history, the first one occurring in 2012, with psychomotor restlessness, aggressive behaviour and delusional ideation of prejudice and persecution, for which he was admitted to "Socola" Hospital, and another similar episode occurring in March 2015, for which he was admitted to the Psychiatry Hospital of Galati and released in a partial remission state with the following treatment plan: Amisulprid, 200 mg (1-0-2), Sermion, 30 mg (0-1-0), Pramistar, 600 mg (0-1-0), Rivotril, 2 mg (0-0-1).

In May 2015, the symptoms reappear and the patient is admitted to "Socola" Hospital. In addition, a drug-induced extrapyramidal syndrome is observed (due to Amisulprid). During hospitalization, the evolution was favourable and the patient was released with the following regimen: Olanzapine, 5 mg (0-0-1), Amisulprid, 200 mg (1/2-0-1/2), Rivotril, 2 mg (0-0-1), Romparkine, 2 mg (1/2-0-1/2). In August 2015, the administration of Amisulprid was stopped, while the dose of Olanzapine was raised to 7.5 mg/day, and in October, because of the favourable outcome, the dose of Olanzapine was brought back to 5 mg/day. At the end of December, the patient is brought in the emergency room by the family, due to catatonic symptoms, being non-responsive to stimuli and presenting psychomotor inhibition, verbal negativism and refusal of alimentation. After slowly recovering, the patient is released with the following treatment plan: Abilify, 15 mg/day, Depakine Chrono, 300 mg/day and Imovane, 7,5 mg/day.

In January 2016, we initiated the treatment with Abilify Maintena, 1 ml i.m., in conjunction with Abilify, 10 mg/day p.o., Romparkine, 2 mg x 1 + 1/2/day, Seroquel XR, 200 mg x 1/2/day and Gerodorm, 40 mg x 1/day. We gradually lowered the doses of Abilify p.o. and Seroquel, the current treatment plan being the following: Abilify Maintena, 1 ml i.m./month, Romparkine, 2 mg x 1/day and Gerodorm, 40 mg x 1/day.

EXAMINATION OF THE PRESENT CLINICAL STATE

We observed an increased volume of the abdomen, due to the subcutaneous tissue, diffuse pain in the right flank and the right iliac fossa, extrapyramidal muscular rigidity (positive cogwheel sign) and akinesia with masked facies, choppy speech and slow, broad movements of the limbs.

PSYCHIATRIC INTERVIEW

Psychodiagnosis of expression:

--attitude: partially cooperating, slightly increased psychomotor activity;

--clothing: neat, adequate to the hospital, good hygiene;

--voice: medium tonality and intensity, not modulated by affectivity;

--eye contact: fixed on the examiner;

--mimic: hypomobile;

--pantomimic: gestural activity reduced in amplitude and slightly disorganized.

Awareness:

--sensation: slight hypoesthesia;

--perception: olfactory and visual hallucinations ("I can smell smoke", "I see flames", "I see shadows raising from the floor");

--attention: spontaneous hypoprosexia, slight distractibility;

--memory: fixation and evocation hypomnesia;

--thought: disturbances in thought flow, bradipsychism, sometimes incoherence, delusional ideation of prejudice, persecution and prosecution;

--imagination: no disturbances.

Affectivity and motivation:

--mood: fluctuating;

--emotions: affective flattening, detachment from family members (sister, parents);

--feelings: worthlessness;

--passions: poorly structured;

--motivation: periods of disturbances in the initiation of activities;

--instincts:--appetite--increased;

--conservation--he denies autolytic ideation;

--sexual--no modification.

Effector functions:

--volition: hypobulia;

--motor conduct: self-conduction and selfcare capacity slightly diminished;

--activity: increased lag time in verbal communication;

--behaviour: disorganised with a tendency towards social withdrawal;

--sleep: of poor quality, fragmented, druginduced.

Synthesis functions:

--conscience: temporo-spatial oriented, auto and allopsychic; partial insight;

--intellect: in accordance with educational background;

--character: appropriate attitude towards the examiner.

POSITIVE DIAGNOSIS

Paranoid schizophrenia:

--delusional ideation of prejudice, persecution and prosecution;

--olfactory and visual hallucinations;

--disorganized thinking;

--negative symptoms with blunted affect and social withdrawal.

DIFFERENTIAL DIAGNOSIS

--other forms of schizophrenia;

--schizo-affective disorder;

--persistent delusional disorder;

--polymorphic psychotic disorder;

--psychotic disorder due to general living conditions or substance-induced psychosis;

--personality disorders;

--mental retardation.

OUTCOME: favourable.

PROGNOSIS:

Positive factors:

--the presence of a social support network (sister);

--good compliance to the current treatment;

--absence of a family history of schizophrenia;

--absence of structural abnormalities of the brain.

Negative factors:

--civil status--unmarried;

--multiple relapses.

DISCUSSIONS

The lack of adherence is a major obstacle to the effectiveness of a treatment, especially in psychiatry, and it includes the following aspects: refusal of taking the treatment, underdosing, intermittent dosing, premature discontinuation, overdosing, leading to therapeutic inefficacy or significant health risks. Factors influencing noncompliance include those related to the patient, to the physician, to the disease traits, to the characteristics of the regimen and various other contextual ones. In the cases of patients diagnosed with schizophrenia, it is often difficult to obtain therapeutic adherence, family support being many times necessary.

In this particular case, voluntary underdosing and discontinuation of the treatment led to relapses and the rapid onset of catatonia. Following the initiation of a depot antipsychotic treatment and after establishing a good collaboration with the family of the patient, we obtained a good outcome, the patient currently having achieved a better social integration and having regained autonomy, self-conduction and selfcare capacity.

CONCLUSIONS

Schizophrenia is a debilitating psychiatric disorder, involving important alteration of perception, thought and affectivity, subsequently leading to social impairment, loss of autonomy, feelings of worthlessness, autolytic ideation and suicidal attempts in many cases. The traits of this condition, associated with the social stigma around it, can result in poor adherence to the current treatment options, which further leads to relapses and deterioration of the patients' health and social status. Thus, obtaining good results in volves not only an early correct diagnosis, but also creating a safe environment for the patient and achieving a good collaboration with the patients' social support network.

Correspondence: Raluca Mihaela FRINCU

Ph. D. Student, Department of Psychiatry, "Gr. T. Popa" University of Medicine and Pharmacy, No. 16 Str. Universitatii, zip code 700115, Iasi, Romania Fourth Year Resident, "Socola" Psychiatry Institute, No. 36, Sos. Bucium, zip code 700282, Iasi, Romania

Tel.: +40 742 795 086 E-mail: ralucafrincu@yahoo.com

Submission: June, 7th, 2016 Acceptance: July, 25th, 2016

ACKNOWLEDGMENTS AND DISCLOSURE

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

REFERENCES

(1.) Francis, A. Catatonia: diagnosis, classification, and treatment. Curr Psychiatry Rep 2010.

(2.) Kraepelin, E. Psychiatrie: ein Lehrbuch fur Studirende und Aertze. 6th ed. Leipzig: Barth Verlag, 1899.

(3.) Fink, M. Rediscovering catatonia: the biography of a treatable syndrome. Acta Psychiatr Scand Suppl 2013; (441): 1-47 [PMID: 23215963 DOI: 10.1111/acps.12038].

(4.) Hawkins, J. M., Archer, K. J., Strakowski, S. M., Keck, P. E. Somatic treatment of catatonia. Int J Psychiatry Med 1995.

(5.) Askenazy, F., Dor, E., Benoit, M., Dupuis, G., Serret, S., Myquel, M. et al. Catatonie chez une adolescente de 14 ans: traitement par clorazepam et carbamazepine et evolution a dix ans [Catatonia in a 14 year-old girl: Treatment with clonazepam and carbamazepine, a 10-year follow-up]. L'Encephale. 2009.

(6.) Chang, C. H., Hsiao, Y. L., Hsu, C. Y., Chen, S. T. Treatment of catatonia with olanzapine: a case report. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Nov 13. 33(8):1559-60. [Medline].

(7.) England, M. L., Ongur, D., Konopaske, G. T., Karmacharya, R. Catatonia in psychotic patients: clinical features and treatment response. J Neuropsychiatry Clin Neurosci. 2011 Spring. 23(2):223-6. [Medline].

(8.) Huang, Y. C., Lin, C. C., Hung, Y. Y., Huang, T. L. Rapid relief of catatonia in mood disorder by lorazepam and diazepam. BiomedJ. 2013 Jan-Feb. 36(1):35-9. [Medline].

(9.) Gupta, A., Dhir, A., Kumar, A., Kulkarni, S. K. Protective effect of cyclooxygenase (COX)-inhibitors against druginduced catatonia and M PTP-induced striatal lesions in rats. Pharmacol Biochem Behav. 2009 Dec. 94(2):219-26. [Medline].

(10.) Huang, Y. C., Lin, C. C., Hung, Y. Y., Huang, T. L. Rapid relief of catatonia in mood disorder by lorazepam and diazepam. Biomed J. 2013 Jan-Feb. 36(1):35-9. [Medline].

(11.) Bush, G., Fink, M., Petrides, G., Dowling, F., Francis, A. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand, 1996.

(12.) Northoff, G. What catatonia can tell us about "top-down modulation": a neuropsychiatry hypothesis. Behav Brain Sci 2002; 25: 555-577; discussion 578-604 [PMID: 12958742 DOI: 10.1017/S0140525X02000109].

(13.) Lahutte, B., Cornic, F., Bonnot, O., Consoli, A., An-Gourfinkel, I., Amoura, Z. Multidisciplinary approach of organic catatonia in children and adolescents may improve treatment decision making. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Mar 7. [Medline].

(14.) Chiou, Y. J., Lee, Y., Lin, C. C., Huang, T. L., A Case Report of Catatonia and Neuroleptic Malignant Syndrome with Multiple Treatment Modalities: Short Communication and Literature Review, Medicine (Baltimore). 2015 Oct; 94(43):e1752. doi: 10.1097/MD.

(15.) ICD 10.

Raluca M. Frincu, Livia A. Lupsa, Gabriela Stefureac, Cristinel Stefanescu
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Title Annotation:Case Reports
Author:Frincu, Raluca M.; Lupsa, Livia A.; Stefureac, Gabriela; Stefanescu, Cristinel
Publication:Bulletin of Integrative Psychiatry
Article Type:Report
Date:Sep 1, 2016
Words:2281
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