ARTÍCULO ORIGINAL

DOI: https://doi.org/10.20453/rnp.v83i1.3683

Comparison of the cognitive profile in patients with alcoholism and schizophrenia

Comparación del perfil cognitivo de pacientes con alcoholismo y esquizofrenia

Maria V. Belon-Hercilla 1,a, Lucia Denegri-Solís 2,b, Marcio Soto-Añari 1,c

1 Centro de Investigación en Psicología, Departamento Académico de Psicología, Universidad Católica San Pablo, Arequipa, Perú

2 Universidad Nacional de San Agustín. Arequipa, Perú

a Licenciada en Psicología; b Doctora en Psicología; c Doctor en Neurociencia

SUMMARY

Recent studies report a high prevalence of psychotic and substance use disorders sharing common brain mechanisms that may affect cognitive performance, response to treatment, the ability to commit to it and, consequently, increase the risk of relapse. Objective: To compare cognitive performance in patients with alcoholism and schizophrenia. Material and Methods: Observational study designed to evaluated 18 patients with schizophrenia and 32 with mental disorders due to alcohol consumption. The short neuropsychological battery NEUROPSI, validated in Spanish, was the main study instrument. Results: Significant differences were found between both groups in areas of executive function and long-term memory, with the sub-group of patients with schizophrenia showing greater deterioration levels. Conclusion: The results assist in explaining and understanding the difficulties that patients with schizophrenia experience in the functions of behavior regulation and information retrieval.

KEYWORDS: Neuropsychology, schizophrenia, alcoholism, memory, executive function.

RESUMEN

Estudios recientes muestran que una alta prevalencia de trastornos psicóticos y por consumo de sustancias comparten mecanismos cerebrales comunes que pueden afectar el rendimiento cognitivo, la adhesión al tratamiento y, con ello, aumentar el riesgo de recaídas. Objetivo: Comparar el rendimiento cognitivo en pacientes con alcoholismo y con esquizofrenia. Material y Métodos: Estudio observacional que evaluó a 18 pacientes con esquizofrenia y 32 con trastorno mental debido a consumo de alcohol. Se utilizó la batería neuropsicológica breve NEUROPSI, validada en español. Resultados: Se encontraron diferencias significativas entre ambos grupos en áreas de función ejecutiva y memoria declarativa (a largo plazo), con mayores puntajes de deterioro en el grupo de pacientes con esquizofrenia. Conclusiones: Los resultados permiten comprender y explicar las dificultades observadas en pacientes con esquizofrenia en cuanto a funciones de regulación conductual y recuperación de información.

PALABRAS CLAVE: Neuropsicología, esquizofrenia, alcoholismo, memoria, función ejecutiva.

INTRODUCTION

It is well known that mood, psychotic and substance use disorders are the most prevalent mental illnesses in the southern region of Peru (1), where, in addition, mental health services are limited or inadequate for both, assessment and follow-up interventions and, particularly, those related to the neuropsychological examination of cognitive profiles. The literature related to this topic reports on the difficulties at familiar, social and professional levels, as well as compliance with treatment programs (2). In this context, the results of neuropsychological evaluations have been associated to the level of commitment to treatment, its results and relapse risks, with a greater cognitive impairment seemingly related to better levels of recovery among patients with schizophrenia and alcohol abuse or dependence (3,4, 5, 6) .

Moreover, Chambers et al., report that, in many cases, there is a close relationship between vulnerability to addiction and schizophrenia, the former preceding the latter (7), which also seems to be related to abnormal brain development (8). In addition, neural abnormalities in schizophrenia appear to match the neural substrates that regulate addictive behaviors, e.g.,mesolimbic and mesocortical circuits (7). Many studies claim that patients with schizophrenia and alcohol dependence or abuse disorder show an active neurophysiological involvement of these circuits eventually leading to cognitive impairment (9). Against this background, the most affected cognitive skills in both types of patients would be attentional control, abstract reasoning, cognitive flexibility, strategic global planning, sequential response, and working memory (3,6,10, 11, 12). All these processes are linked to the executive function (13); but, not to be forgotten, verbal memory, verbal fluency and motor speed also seem to be affected (14).

In schizophrenia, marked cognitive deficits have been described mainly in the areas of attention and visual working memory (6,4,9); within the impaired attentional system, deterioration predominates in the areas of executive attentional network (in charge of inhibitory control) (15) and sustained attention (16). These shortcomings are more noticeable when the disease has evolved for longer periods. Within the memory problems, episodic memory shows most damage (16); the memory system is, in fact, the most demanding of all processes because it requires a temporal-space context (17).

Thus, cognitive impairment in executive function is a permanent and central feature of schizophrenia, in cases of both, remission or relapse (5). Executive function has to do with an integrated set of cognitive skills involved in the generation, monitoring and control of goal-directed behaviors (18). The alterations in executive functions have historically been considered prototypical pathology of the frontal lobe, mainly through lesions affecting prefrontal dorsolateral (19), orbitofrontal (20) and cingulate (21) regions. As a whole, this would cause a “dysexecutive syndrome” affecting the regulation of cognition and behavior. Laurenson et al., (5) found that cognitive processes related to attentional and semantic components, not only cognitive inhibition, are impaired.

In the alcoholism camp, Corral-Varela & Cadaveira (2) report that not all alcoholics manifest cognitive impairments. That is, changes observed in executive functions and memory are interpreted as increased impulsivity and specific vulnerability of the frontal lobes to the toxic effects of alcohol (12, 22, 23). Besides, in substance abuse patients, there would be a further deterioration at both attentional level and in the processing of emotions, in addition to impairment in executive functions. However, Bates et al., (22) and Cabe et al., (3), indicate that the strength of the different cognitive impairments present in alcoholic patients is varied and very heterogeneous.

In a review of brain and cognitive impairment in alcohol-dependent subjects, Bernardin et al., showed a “striking” level of brain atrophy in the frontal lobes, the limbic system and the cerebellum (24). These were related to alterations in executive function, memory systems and motor coordination. The authors concluded that it is important to analyze the cognitive processes in these patients in order to better tailor the treatment and alleviate the difficulties of daily life.

In short, there are patterns of deterioration in memory and executive function, seemingly associated to deficiencies in prefrontal and temporal-medial structures in both disorders. However, the level of deterioration brought about by these pathologies vis- à-vis the brain circuits, remains uncertain, considering especially the close linking between addiction and schizophrenia during the CNS developmental process (7).

Given this reality it is necessary to have a better understanding of the cognitive profile of the two disorders, as it could help to improve the treatment, achieve its goals more effectively, and strengthen the patients’ cognitive processes. This could even be an important predictor of remission and patient’s functionality (3, 5). Such is the objective of our study: to compare the cognitive performance of both patients with schizophrenia and alcohol-dependent patients by means of a short test battery of neuropsychological evaluation (NEUROPSI). This analysis will allow us to identify the levels of cognitive involvement and use it as a foundation to a better sequence of treatment and follow-up of these patients.

MATERIAL AND METHODS

This is an observational/comparative study on patients with pre-existing clinical diagnoses. Fifty patients were tested, 18 with the clinical diagnosis of mental disorders due to alcohol (F10), and 32 diagnosed with schizophrenia (F20), at the NationalHospital ES SALUD “Carlos Seguin Escobedo” in the city of Arequipa, Perú. The probands’ ages ranged between 17 and 70 years, with an average of 50. 70% of the sample was male(n = 35), and 30%, female (n = 15). From a clinical view, there was a high variability in duration of illness and number of hospitalizations (table 1).

Table 1. Clinical and sociodemographic features of the sample.

 

Minimum

Maximum

Mean

SD

Age

17

70

45.92

11.515

Years of education

1

17

11.73

3.019

N° of Hospitalizations

0

10

1.92

2.029

Time of illness

0

576

201.00

148.176

Frecuency

Percentage

Sex

Male

35

70

Female

15

30

Diagnostic

Alcoholism (F10)

18

36

Schizophrenia (F20)

32

64

We used the Mexican version of the brief neuropsychological test battery (in Spanish) NEUROPSI, developed by Ostrosky, Ardila and Rosselli in 1994. This battery has not been used in previous psychometric studies in Peru. It assesses cognitive functions such as orientation, attention and concentration, language, memory, executive functions, reading, writing and arithmetic. It takes approximately 25 to 30 minutes to be individually performed, by probands aged 16 or more, and can be applied to illiterate and poorly educated people.

Assessment sessions, approximately 50 minutes long, were conducted in hospital settings. After the assessment and rating of the test battery, raw scores were converted to z scores to better appreciate the eventual contrasts between the two groups. Nonparametric contrast statistic tests were used.

RESULTS

The results show significant differences in executive function (U = 154, p <.05), memory (U= 162.5, p <0.05), and the overall score (U = 164, p<0.05) between the two groups (table 2).

 

Table 2. Comparison of means in NEUROPSI scores between clinical entities.

Alchoholic patients

Ezquizophrenia patients

Mean

SD

Mean

SD

Mann Whitney U

p value

Orientation

5.78

.548

5.41

.946

232.5

.155

Attention

16.56

5.008

13.84

3.819

214.0

.132

Concentration

21.72

30.835

24.31

34.880

256.5

.521

Language

21.78

1.734

20.56

2.435

211.0

.115

Reading

2.28

.826

2.19

1.030

285.0

.947

Writing

1.94

.236

1.94

.354

281.5

.699

Executive F.

14.44

2.307

11.78

3.471

154.0

.006**

Memory

20.00

5.678

15.38

6.499

162.5

.011*

General score

99.12

13.720

84.77

15.970

164.0

.032*

An analysis of covariance was subsequently conducted to analyze the effect of demographic and clinical variables of the sample. It is noted that the level of education (F = 16,327, p <.05), diagnosis (F= 9.154, p <0.05) and number of hospitalizations (F= 7.537, p <.05) have a significant effect on the total scores on the NEUROPSI (table 3).

Table 3. Analysis of covariance taking the total NEUROPSI score as dependent variable.

Origin

Type III sum of squares

gl

Quadratic mean

F

Sig.

Partial eta squared

Corrected model

4448,834a

7

635.548

6.426

.000

.577

Intersection

9217.172

1

9217.172

93.190

.000

.738

Age

231.400

1

231.400

2.340

.136

.066

Hospitalizations

745.483

1

745.483

7.537

.010

.186

Time of illness months

9.070

1

9.070

.092

.764

.003

Years of instruction

1614.909

1

1614.909

16.327

.000

.331

Diagnostic

905.382

1

905.382

9.154

.005

.217

Background

1.133

1

1.133

.011

.915

.000

Diagnostic * background

326.152

1

326.152

3.298

.078

.091

Error

3263.947

33

98907

Total

355289.000

41

Total corrected

7712.780

40

to. R Squared = 577 (R square = the set, 487)

DISCUSSION

The main finding of this study was that patients with the diagnosis of alcoholism performed cognitively better than those with schizophrenia in memory and executive function. These results were similar to those of other investigations (25, 26, 27, 28) also reporting on several factors that could mediate the degree of cognitive impairment in both groups. However, it has also been mentioned that in addition to memory and executive functions, other processes such as attention are severely affected in both groups of patients. This would be associated with the alteration level of the circuits that underly these processes (20).

It is known that the brain involvement of a patient with schizophrenia includes the prefrontal and medial temporal cortices (21), whereas in the case of alcoholics, the medial temporal involvement is greater (29). Thus, the profile of alterations observed in executive functions and memory, correspond to these areas; which may even be associated with alterations in executive memory components, including encoding and retrieval of information. In the case of alcoholic patients, the main impact would be on consolidation (30).

In the same context, Landa, et al., (27), and Barrera (25) maintain that deficiencies in both alcoholic and patients with schizophrenia, focus on working memory which, in turn, affects declarative episodic long-term memory. Yet, Landa et al., also assert that semantic memory seems to remain preserved in alcoholic patients (27), but not so in patients with schizophrenia who, rather, show severe impairment of verbal and spatial declarative memory. It is important to note that, as stated by Bustamante-Quiroz (31) and Barrera (25), these alterations are associated with chronicity and other aspects of the clinical course in schizophrenia. This would explain the impact of the number of hospitalizations in the patient’s cognitive performance. Conversely, as seen above, in patients with schizophrenia the disorder in declarative memory has been attributed to a dysfunction of the medial temporal lobe (26), while in alcoholic patients, it may be due to a deficiency in the memory circuit that includes structures vulnerable to thiamine deficit reaching, on occasions, clinical levels of Wernicke - Korsakoff encephalopathy (32).

On the other hand, the executive functions are clearly affected in both conditions. Neuropsychological explanations can be found in underactive frontal lobes, measured by functional neuroimaging techniques (33). For schizophrenia, the most significant dysfunction occurs in the dorsolateral prefrontal cortex (DLPFC), which would be associated with deficits in working memory (34). An abnormality in the functional connectivity between frontal and temporal lobe has also been pointed out, implying a hyperconnectivity between these regions although at a random and very inefficient activation level (35). In addition, dysfunctions have been observed in subcortical regions, with failures in the thalamus-cortical integration (32). These studies conclude that schizophrenia would be a pathology linked to a progressive disengagement of the brain.

We have observed that the pattern of cognitive impairment is strongly influenced by the education level of patients. This has been corroborated in other studies, conducted in contexts like ours (36). As it is known, exposure to formal schooling changes the brain circuits making them more efficient, and preparing them for increasingly complex and/or abstract tasks (37). This has frequently been observed in studies with healthy samples of varying schooling levels (36), and even in clinical samples (39). Therefore, it is necessary to measure the pattern and degree of involvement considering this factor and assessing its actual weight when facing the implementation of intervention strategies.

To conclude, these initial data show an interesting cognitive pattern that should be extended to a wider battery of neuropsychological assessments, including follow-up studies. In addition, it would be relevant to
deepen the neurophysiological foundations of these pathologies, especially to clarify the link between memory tasks and executive function, as well as to analyze patterns of disconnection between different brain structures. In this respect, assessments that evaluate the degree of participation of the different processes have been developed, considering that brain connectivity is more relevant than an individual process assessment, especially for outset strategies (40). Likewise, assessments must be expanded to all cognitive processes, attempting to deep in the connections between the two conditions in order to clarify the presence of dual pathology or comorbidity. Finally, it is relevant to develop intervention strategies that target the rehabilitation of cognitive processes, particularly in the area of executive functions, which seem to show very interesting prospects in the patients’ functional and social reintegration processes (41, 42).

REFERENCES

1. Zegarra-Valdivia J, Cazorla E, Chino B. Perfil clínico y epidemiológico de pacientes atendidos en el Centro de Salud Mental “Moisés Heresi” de Arequipa - Perú, entre los años 2011 y 2013. Rev Neuropsiquiatr. 2016; 79 (2): 98-107.

2. Corral-Varela M, Cadaveira F. Aspectos neuropsicológicos de la dependencia del alcohol: naturaleza y reversibilidad del daño cerebral. Rev Neurol. 2002; 35 (7): 682-687.

3. Cabé N, Laniepce A, Ritz L, Lannuzel C, Boudehent C, Vabret F, et al. Cognitive impairments in alcohol dependence: From screening to treatment improvements. L’Encéphale. 2016; 42: 74–81. Doi: http://dx.doi.org/10.1016/j.encep.2015.12.012

4. Kaneda Y, Keefe RSE. An abbreviated version of the assessment of brief Cognition in Schizophrenia (BACS). Eur J Psychiat. 2015; 29(2): 131-134.

5. Laurenson C, Gorwood P, Orsat M, Lhuillier JP, Le Gall D, Richard-Devantoy S. Cognitive control and schizophrenia: The greatest reliability of the Stroop task. Psychiatry Research. 2015; 227(1): 10-6. Doi: http://dx.doi.org/10.1016/j.psychres.2015.03.0040165-1781/& 2015

6. Manning V, Betteridge S, Wanigaratne S, Best D, Strang J, Gossop M. Cognitive impairment in dual diagnosis inpatients with schizophrenia and alcohol use disorder. Schizophr Res. 2009;114(1-3): 98-104. doi:10.1016/j.schres.2009.05.020

7. Chambers RA, Krystal JH, Self DW. A Neurobiological Basis for Substance Abuse Comorbidity in Schizophrenia. Biol Psychiatry. 2001;50(2): 71–83.

8. Durand M, Barlow H. Psicopatología: Un enfoque integral de la Psicología anormal. Ciudad de México: Thomson; 2007.

9. Balogh N, Égerházi A, Berecz, R. Neurocognitive changes in patients with schizophrenia during relapse and early remission. Eur J Psychiat. 2015; 29(3): 199-209.

10. Giancola P, Tarter F. Executive cognitive functioning and risk for substance abuse. American Psychological Society. 1999; 10 (3): 203-205. Doi: https://doi.org/10.1111/1467-9280.00135

11. Villegas MÁ, Alonso MM, Benavides R, Guzmán FR. Consumo de alcohol y funciones ejecutivas en adolescentes: una revisión sistemática. Aquichan. 2013; 13(2): 234-246.

12. Dos Santos M, Quarti T, Duarte de Moraez JF, Ferrão Y, Da Silva M. Desempeño neuropsicológico y características sociodemográficas en pacientes alcohólicos en tratamiento. Adicciones. 2014; 26 (3):221-229.

13. Stuss DT, Knight RT, Eds. Principles of frontal lobe function. London: Oxford University Press; 2002.

14. Jaramillo P, Ruiz J, Fuentes I. Relations between neurocognitive, emotional processing and social functioning in schizophrenia. Psychology, society and education. 2011; 3 (2): 99-112.

15. Fuentes L. Déficit de atención selectiva en la esquizofrenia. Rev Neurol. 2001; 32(4): 387-391.

16. Lieberman J, Scott T, Perkins D. Tratado de esquizofrenia. Ciudad de México: Ars Medica; 2008.

17. Maestú, F, Martín P. Memoria. In: Enríquez P. (eds.) Neurociencia cognitiva: una introducción. Madrid: Universidad Nacional de educación a distancia (UNED); 2011. p. 107-126.

18. Ríos M, De Noreña D. Funciones ejecutivas. In: Enríquez P, Eds. Neurociencia Cognitiva: una introducción. Madrid: Universidad Nacional de educación a distancia; 2011. p. 181-200

19. Goldman-Rakic P. Functional architecture of the dorsolateral prefrontal cortex in monkeys and humans. In: Stuss D, Knight R, Eds. Principles of frontal lobe function. London: University Press;2002. p. 85-95.

20. Rolls E. The functions of the orbitofrontal cortex. In: Stuss D, Knight R, Eds. Principles of frontal lobe function. London: Oxford University Press; 2002. p.354-375.

21. Mayber H. Mapping mood: an evolving emphasis in frontal limbic interactions. En: Stuss D, Knight R, Eds. principles of frontal lobe function. Londres: Oxford University Press; 2002. p. 375-391.

22. Bates ME, Buckman JF, Nguyen TT. A role for cognitive rehabilitation in increasing the effectiveness of treatment for alcohol use disorders. Neuropsychol Rev. 2013; 23(1): 27–47. doi: 10.1007/s11065-013-9228-3.

23. Verdejo-Garcia A. Cognitive training for substance use disorders: Neuroscientific mechanisms. Neuroscience and Biobehavioral Reviews. 2016;68:270-280.1 doi: http://dx.doi.org/10.1016/j.neubiorev.2016.05.018

24. Bernardin F, Maheut-Bosser A, Paille F. Cognitive impairments in alcohol-dependent subjects. Front Psychiatry. 2014; 5:78. doi: 10.3389/fpsyt.2014.00078

25. Barrera A. Los trastornos cognitivos en la esquizofrenia. Revista Chilena Neuropsiquiatría.2006; 44(3): 215-221.

26. Pardo V. Trastornos cognitivos en la esquizofrenia. I. estudios cognitivos en pacientes esquizofrénicos, puesta al día. Rev Psiquiatr Urug. 2005; 69(1):71-83.

27. Landa N, Fernández-Montalvo J, Tirapu J. Alteraciones neuropsicológicas en el alcoholismo: una revisión sobre la afectación de la memoria y las funciones ejecutivas. Adicciones. 2004,16(1): 41-52.

28. Calvo H. Alcohol y neuropsicología. Trastornos Adictivos. 2003; 5(3): 256-68.

29. Chanraud S, Leroy C, Martello C, Kostogianni N, Delain, F, Aubin H, Reynaud M, Martinot J. Episodic memory in detoxified alcoholics: Contribution of grey matter microstructure alteration. PLoS ONE, 2009; 4(8): e6786. Doi: https://doi.org/10.1371/journal.pone.0006786

30. Baddeley AD. Human memory: Theory and Practice. Hove: Psychology Press; 1997.

31. Bustamante-Quiroz R. Las funciones cognitivas en la esquizofrenia: hipótesis explicativas del déficit cognitivo y variables de interés clínico. Revista Peruana de Psiquiatría. 2010; 1(2): 68-76.

32. Kopelman M. What does a comparison of Korsakoff syndrome and the alcoholic thalamic infarction tell us about thalamic amnesia? Neuroscience & Biobehavioral Reviews. 2015; 54: 46-56. doi:https://doi.org/10.1016/j.neubiorev.2014.08.014

33. Gur R, Gur R. Functional magnetic resonance imaging in schizophrenia. Dialogues Clin Neurosci. 2010;12(3):333-343.

34. Ojeda N, Sánchez P, Elizagárate E, Yöller AB,Ezcurra J, Ramírez I, Ballesteros J. Evolución de los síntomas cognitivos en la esquizofrenia: una revisión de la literatura. Actas Esp Psiquiatr. 2007;35(4):263-270.

35. Houck J, Cetin M, Mayer A, Bustillo J, Stephen J, Aine C, et al. Magnetoencephalographic and functional MRI connectomics in schizophrenia via intra- and inter-network connectivity. Neuroimage. 2017; 15: 96-106. doi: 10.1016/j.neuroimage.2016.10.011

36. Soto-Añari M, Cáceres-Luna G. Funciones ejecutivas en adultos mayores alfabetizados y no alfabetizados. Revista Chilena de Neuropsicología. 2012; 7(3): 127-133

37. Ardila A, Bertolucci P, Braga L, Castro-Caldas A, Judd T, Kosmidis MH, et al. Illiteracy: the neuropsychology of cognition whithout Reading. Arch Clin Neuropsychol. 2010; 25(8): 689–712. doi: 10.1093/arclin/acq079

38. Soto-Añari M, Rivera R, Cáceres-Luna G, Huillca F. Fluidez verbal fonológica y semántica en adultos mayores: comparación del rendimiento a partir de variables sociodemográficas. Revista Peruana de Psicología y Trabajo Social. 2012; 1(2):34-41.

39. Caamaño-Isorna F, Corral M, Montes-Martinez A, Takkouche, B. Education and dementia: A meta- analytic study. Neuroepidemiology. 2006; 26(4): 226-232. doi: 10.1159/000093378

40. Yubero R, Gil P, Paul N, Maestú F. Influence of memory strategies on memory test performance: a study in healthy and pathological aging. Neuropsychol Dev Cogn B Aging Neuropsychol Cogn. 2011; 18(5):497-515. doi: 10.1080/13825585.2011.597840

41. Fuentes PI, Roder V, Ruiz JC. Cognitive rehabilitation programs in schizophrenia: current status and perspectives. International Journal of Psychology and Psychological Therapy. 2010, 10(2):191-204.

42. Vargas M. Posibilidades de rehabilitación neurocognitiva en la esquizofrenia. Rev Neurol. 2004; 38 (5): 473-482.

Financiamiento: Investigación financiada con recursos propios.

Declaración de conflictos de interés: Los autores declaran no tener conflictos de interés.

Corresponding author:

Marcio Soto-Anari

Department of Psychology at Universidad Católica San Pablo

Urb. Campiña Paisajista S/N Quinta Vivanco - Barrio de San Lázaro, Arequipa, Peru

Phone: 51-54-605630 anexo 316

E-mail: msoto@ucsp.edu.pe

Recibido: 23/10/2019

Aceptado: 24/03/2020