Electroencephalographic Finds - EEG According To 13 Cases of Patients Who Are Cocaine Chronic Users In Comparison To A Healthy Control Group of 10 Patients With Similar Characteristics
*Sandra López Carrillo, *Ángel Molina León, Ramón Sobrino Torrens, María Pilar Egea Cegarra, Juana María Pagán Sánchez, Carmen Rodenas Meca and Aharon Franco Giménez Psicólogo Clínico
Doctors and nurses the clinic neurophysiology service, Spain
Submission: January 23, 2017; Published: February 02, 2017
*Corresponding author: Ángel Molina León and Sandra López Carrillo, Doctors and nurses the clinic neurophysiology service, Santa Lucia Hospital, Cartagena, Murcia, Spain,Email:molinadelaasuncion@gmail.com
How to cite this article: Sandra L C, Ángel M L, Ramón S T, María P E C, Juana M P S, et al. Electroencephalographic Finds - EEG According To 13 Cases of Patients Who Are Cocaine Chronic Users In Comparison To A Healthy Control Group of 10 Patients With Similar Characteristics. Ortho & Rheum Open Access J. 2017; 4(4): 555643. DOI: 10.19080/OROAJ.2017.04.555643
Abstract
In chronic cocaine users, dysfunctional and structural findings have been found, the etiology of this dysfunction is unknown. In our group of patients MRI was completely normal and we have described a mild dysfunctional anomaly in the frontal cortex that is common denominator in this type of patients. The aim of this study is to investigate the cortical EEG activity of these patients. The question we ask is the following is cocaine which generates a dysfunctional disorder in the cortex of these patients or on the contrary on slightly dysfunctional brain the patient get into consumption of toxic.
Keywords: Cocaine; EEG; Frontal; Dysfunctional lesion; Slowing; Brain; Electroencephalogram; Cerebral areas; Drugs
Introduction
The frontal lobe is in charge of complex cognitive processes, called executive functions. These functions are mental operations which go to an end and allow a behavioral control, that is to say, they make possible that we can choose, plan and take voluntary and conscious decisions. The prefrontal cortex has the decisive role in the executive functions by integrating the information and allowing the choice of objectives and the organization of the action plans to do them. It constitutes a cerebral region which is one of the most philogenetically recent and also it is the last one to mature in the ontogenesis, the most developed in the evolutionary scale [1]. It is also involved in the social-emotional processing and control, in the cooperative work. Its responsibility in frontal functions is caused to his conexión with the amígdala (which interferes in the memory) and motivation system (limbic system) and dopamine gratification. Self-control is an important function of the frontal lobe.
Cocaine effect in the brain: within the normal process of communication, neurons release dopamine inside of the synapses, where it joins to dopamine receptors in adjacent neurons. Normally, a specialized protein called “transporter of dopamine” recycles the dopamine by returning to the transmitting neuron. When cocaine has been consumed, this one is adhered to the transporter protein of dopamine and blocks the normal process of recycling, resulting in an accumulation of dopamine in the synapses, which magnifies or exaggerates the pleasurable effects of cocaine (Figure 1).
Methods and material
We conducted a descriptive, longitudinal and retrospective study. It consists of the morphological electroencephalographic (EEG) analysis of 13 patients who are cocaine users in comparison10 healthy patients’ non cocaine users. 23 revisions EEG have been studied [2-7].
Objectives
Determine EEG alterations that chronic patients have (more than 1 year) in comparison to the patients who are not cocaine users. Identify the brain areas involved in the EEG of patients who consume cocaine. Try to prove the existence or not of structural or criptogenic lesions, or on the contrary theexistence of a minimal cortical dysfunction in patients who are addicted to cocaine.
The main objective in our study is to determine if on a normal brain cocaine induces minimal structural or/and dysfunctional changes, and if these lesions in the frontal lobe could be the cause or the consequence of the cocaine habit. See if the EEG really demonstrates the existence of dysfunctional cortical or not [7-11].
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
- Clinical case 1: normal EEG (Figure 2) See the absence of specific inter hemispheric calculable anomalies.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
CAT brain without any contrast: no evidence of acute intracranial pathology.
TAC brain without contrast: No signs of acute intracranial pathology.
Sweep: 10 milliseconds. 10 seconds per screen.
Sensitivity 7 microvolts.
Barrido: 10 milisegundos. 10 segundos por pantalla. Sensibilidad: 7 microvoltios. Sensitivity 7 microvolts.
High filter: 30 Hz. Low filter: 0.5 Hz. Sweep: 10 milliseconds. 10 seconds per screen.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
Sweep: 10 milliseconds. 10 seconds per screen. Sensitivity 7 microvolts.
We can see a focused and attenuated activity with scarce voltage. This specific morphology means epilepsy, and it is found in left front-parieto-temporal left region (F3 - F7-P3 - T3-T5 - P4) and it is slightly focused and constituted by sharp and slow waves with attenuated voltage and a specific morphology that means epilepsy [22-24]. The duration is 0.5-1 seg. This activity appears both in the ocular opening and closing which spreads partially to the adjacent areas of the right hemisphere and which is compatible with CPC against partial epileptic focus a second time widespread.
Cranial RM: without evidence of significant pathological finds.
Discrete asymmetry with temporal masts and a right higher volume, like the only find (this find is visualized in a high percentage in normal population) (Table 1).
Results (Figure 15)
In our study there is an 84% male and a 16% female, aged between 19 and 51 years old, and the average is 36 years old.
None clinical case out of all 13 contains any alteration in cerebral nuclear magnetic resonance (RMN) (Figure 16).
84.6% out of the electroencephalograms of our study reveal the existence of minimum cortical dysfunctions in frontal areas with more or less spread to adjacent cortical areas. The most affected area with a 38.5% is the front-temporal one with higher predominance of the left hemisphere. These slow activities are often registered at a 7 Hz frequency when the normal (background) tracing is 9-10 Hz. That activity lasts from 0.5 to 2 msec (Figure 17).
Conclusion and Recommendation
Frontal area is responsible for self-control, so an alteration in frontal lobe causes alteration of the executive functions, mental deterioration, personality and deshinbition behavior alterations.
Images of the brain show a decrease in dopamine receptors (D2) in a person’s brain with cocaine addiction in comparison to someone who does not consume drugs.
These minimum dysfunctional injuries support the theory, which is so often seen in the literature, that not all pathology is structural, but there is pathology with minimum dysfunctional or metabolic lesions without an associated anatomopathological substrate. That is why our study defines the importance of the EEG in the diagnosis of dysfunctional disorders like ADHD, schizophrenia, and these 13 chronic patients of cocaine with MML anodyne, as we have seen.
References
- Barkley RA (1997) Attention-deficit/hyperactivity disorder, selfregulation, and time: toward a more comprehensive theory. J Dev Behav Pediatr 18(4): 271-279.
- Fliers EA, de Hoog ML, Franke B, Faraone SV, Rommelse NN, et al. (2010) Actual motor performance and self-perceived motor competence in children with attention-deficit hyperactivity disorder compared with healthy siblings and peers. J Dev Behav Pediatr 31(1): 35-40.
- Blum K, Kozlowski (1990) influcencia del etanol y neuromoduladores. un modelo de cascada de la recompensa. Emn. Ollat H, Parvez S, Parvez H, editores; el alcohol y el comportamiento, aspectos basicos y clinicos , progreso en la investigación del alcohol.
- Steger J, Imhof K, Steinhausen H, Brandeis D (2000) Brain mapping of bilateral interactions in attention deficit hyperactivity disorder and control boys. Clin Neurophysiol 111(7): 1141-1156.
- Li F, He N, Li Y, Chen L, Huang X, et al. (2014) Intrinsic brain abnormalities in attention deficit hyperactivity disorder: a restingstate functional MR imaging study. Radiology 272: 514-523.
- Carmona S, Vilarroya O, Bielsa A, Trèmols V, Soliva JC, et al. (2005) Global and regional gray matter reductions in ADHD: a voxel-based morphometric study. Neurosci Lett 389(2): 88-93.
- Alvarez JA, Emory E (2006) Executive Function and the Frontal Lobes: A Meta-Analytic Review. Neuropsychol Rev 16(1): 17-42.
- De La Fuente A, Xia S, Branch C, Li X (2013) A review of attentiondeficit/ hyperactivity disorder from the perspective of brain networks. Front Hum Neurosci 7: 192.
- Barry RJ, Clarke AR, Johnstone SJ (2003) A review of electrophysiology in attention-deficit/hyperactivity disorder: I. Qualitative and quantitative electroencephalography. Clin Neurophysiol 114(2): 171- 183.
- Frey S, Petrides M (2000) Orbitofrontal cortex: a key prefrontal region for encording information. Proc Natl Acad Sci U S A 97(15): 8723-8727.
- Blum K, Kozlowski (1990) influcencia del etanol y neuromoduladores. un modelo de cascada de la recompensa. Emn. Ollat H, Parvez S, Parvez H, editores; el alcohol y el comportamiento, aspectos básicos y clínicos, progreso en la investigación del alcohol.
- Grafman J, Holyoak K, Boller F (1995) Structure and functions of the human prefrontal cortex. Ann N Y Acad Sci 769: 1-411.
- Alvarez Cambra R (2006) Traumatic Orthopedic Surgery Treaty. T.II. Mexico City: Editorial People and Education.
- Antoine Bechara, Hanna Damasio, Antonio R Damasio (2000) Emotion, decisión – making and the orbitofrontal cortex. Cereb Cortex 10(3): 295-307.
- G Arbonés, A Carbajal, B Gonzalvo, M González-Gross, M Joyanes (2003) Nutrición y recomendaciones dietéticas para personas mayores. Grupo de trabajo “Salud Pública” de la Sociedad Española de Nutrición (SEN). Revista Nutrición Hospitalaria 18(3): 109-117.
- Bastos A, González R, Molinero O, Salguero del Valle A (2005) Obesidad, nutrición y actividad física. Revista Internacional de Medicina y Ciencias de la Actividad Física y el Deporte 5(18): 140-143.
- Cruz AJ, otros (1999) Nutrición hospitalaria en el anciano. Revista Alimentación, nutrición y salud 6(1): 7-18.
- C0uervo M, otros (2009) Comparativa de las Ingestas Dietéticas de Referencia (IDR), de los diferentes países de la Unión Europea, de Estados Unidos (EEUU) y de la Organización Mundial de la Salud (OMS). Revista Nutrición Hospitalaria 24(4): 384-414.
- Garay J, Burdeos De Garay MF (2004) Estudio epidemiológicos internacionales sobre envejecimiento: revisión actualizada de los principales estudios. Revista Geriátrika 10(2).
- Genua M (2001) Nutrición y valoración del estado nutricional en el anciano. Matia Fundazioa 6(12): 1-21.
- Martín ML, Moreiras O, Carbajal A (2010) La actividad física como indicador de la caridad de vida en los ancianos. Revista multimedia Gerontology 10(1): 23-38.
- Meléndez A (2008) Actividades Físicas para Mayores. En: Las razones para hacer ejercicio pp. 51-70.
- Rodrigo AP (2011) Los cambios fisiológicos como factores de riesgo para la desnutrición en el anciano. En J.C. García y J.B. Rivero (Eds). Manual de atención al anciano desnutrido en el nivel primario de salud pp. 63-75.
- Ruiz-López MD, Artacho R (2010) Nutrición y envejecimiento. En: Tratado de nutrición. Nutrición humana y salud (pp. 320-343). Madrid, España; Ediciones Médica Panamerica.
- Ruiz-López MD, Artacho R, López M (2000) Recomendaciones nutricionales para los ancianos.