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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 3  |  Issue : 2  |  Page : 110-115

Electroencephalogram abnormalities in borderline personality disorder


1 Department of Psychiatry, Government Mohan Kumaramangalam Medical College Hospital, Salem, Tamil Nadu, India
2 Department of Neurology, Government Mohan Kumaramangalam Medical College Hospital, Salem, Tamil Nadu, India

Date of Submission12-Feb-2019
Date of Decision18-Mar-2019
Date of Acceptance17-May-2019
Date of Web Publication18-Dec-2019

Correspondence Address:
Prof. S Sivakumar
Department of Neurology, Government Mohan Kumaramangalam Medical College Hospital, Salem, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aip.aip_6_19

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  Abstract 


Background: Borderline personality disorder (BPD) shows aberrant behavior, which is associated with difficulties in emotions and processing. Seizure-like activity has been invoked as underlying factors in BPD. However, the occurrence and significance of electroencephalogram (EEG) abnormalities in BPD received little attention. The aim of this study was to assess the EEG abnormalities in BPD and to compare with healthy controls. Methods: Sixty consecutive BPD patients attending the psychiatry unit and 60 healthy controls were selected for the study. All were subjected for EEG assessment and appropriate statistical analysis was done. Results: There was no significance in sociodemographic profile between cases and controls. Thirty-one percent of cases had EEG abnormalities and only 3.3% of the controls had EEG abnormalities. 19 of the 60 patients had EEG abnormalities of which 2 (10.5%) had mild , 6 (31.5%) moderate, and 11 (57.8%) had severe category of BPD. Predominantly, sharp waves and spike waves were seen in severe type and nonspecific waves (slowing) in mild and moderate types. Conclusion: EEG abnormalities were significantly higher in BPD than healthy population. However, the electrophysiological investigation of BPD is limited, and no longitudinal studies have been attempted so far. Longitudinal studies are particularly useful to reveal the electrophysiological aberrations in BPD.

Keywords: Borderline personality disorder, electroencephalogram, focal slowing, sharp waves


How to cite this article:
Shankar S, Selvaraj C, Sivakumar S. Electroencephalogram abnormalities in borderline personality disorder. Ann Indian Psychiatry 2019;3:110-5

How to cite this URL:
Shankar S, Selvaraj C, Sivakumar S. Electroencephalogram abnormalities in borderline personality disorder. Ann Indian Psychiatry [serial online] 2019 [cited 2020 Jul 13];3:110-5. Available from: http://www.anip.co.in/text.asp?2019/3/2/110/262247




  Introduction Top


Borderline personality disorder (BPD) is a well-recognized syndrome. It is characterized by brief episodes of affective manifestations, emotional lability, unstable interpersonal relationship, impulsive, unpredictable behavior, and self-mutilation. Considerable evidence also points that impulsivity is one of the earliest components, out of which subsequent dysfunction emerges.[1]

The estimated prevalence of BPD is approximated 1.6%. Approximately 60%–70% of BPD have attempted suicide with 8%–10% successfully completed suicide.[2],[3] BPD constitutes a large burden on the resources of mental health services.

BPD is an independent disorder with at least two possible biological subtypes: an affective subtype and a psychotic subtype. Coccaro and Kavoussi suggested that the identification of such subtypes can be useful in guiding treatment choices.[4]

Although BPD is the most frequently diagnosed personality disorder, the pathophysiological process involved in the syndrome remains unclear. Neurotransmitter abnormalities were described by many authors. Positron-emission tomography has shown the existence of brain abnormalities.[5] Epilepsy-like phenomenon has also been invoked since some of the clinical features of BPD resemble the characteristic observed in epileptic patients.[6]

Over the past few decades, electrophysiology has contributed substantially to the understanding of normal brain functions as well as brain function deviations in psychopathological conditions. Electrophysiological technology is noninvasive and relatively inexpensive, helping in probing the pathophysiology of BPD. Electroencephalogram (EEG) studies have been carried out based on the hypothesis that abnormal brain electrical activity or focal brain dysfunction, or both, particularly in the temporal lobes, plays a significant role in the pathogenesis of BPD characterized by impulsiveness and affective instability. A number of case reports have been described in patients who were diagnosed with BPD, who were subsequently found to have complex partial seizures documented by epileptic discharges over one or both temporal regions. As early as the mid-1980s, the presence of significant EEG abnormalities, definitive and less definitive, in BPD patients are well documented. Furthermore, minor EEG abnormalities that are not suggestive of epilepsy but may be contributing to episodic behavior disorder (e.g., 14- and 6-per-second positive spikes) are seen in more than one-fourth of BPD patients, as well as in some other personality disorders. In this latter respect, the presence of these controversial waveforms may be associated with elevations of specific behaviors (e.g., impulsivity) found within the overall BPD symptom cluster profile.

Pickar and Tanahashi have found significant abnormalities in EEG scalp records of BPD patients and also reported that EEG abnormalities in BPD are not due to abnormal cortical foci but rather a nonspecific EEG localizable brain dysfunction.[7]

In a meta-analysis by Shelley et al., the respective prevalence rate of EEG abnormalities was estimated to be between 5.8% and 4.6%; however, most of the studies are hampered by methodological problems; the samples size was rather small or EEG assessment was not done in a blind way.[8] Although the hypothesis of a relationship with epilepsy is difficult to support, there is an excess of EEG abnormal activity, which can indicate brain dysfunction in patients with BPD.[9] EEG abnormalities in BPD can be an evidence of brain dysfunction of people suffering from this debilitating disorder. Borderline individuals showed a much higher incidence of symptoms commonly seen in complex partial seizures or episodic dyscontrol and higher incidence of EEG abnormalities particularly posterior sharp waves. Developing a thorough understanding of the neurobiology of BPD is essential for the development of effective preventive, therapeutic, and rehabilitative approaches to BPD.[8]

Limberg et al. showed that a better understanding of electrophysiological abnormalities in BPD will also facilitate the examination of the relationship between abnormalities related to child abuse and those identified in other adult patients.[10] The aim of this study was to explore EEG abnormalities in patients with BPD and to compare it with healthy controls so as to help in understanding the neurobiology of BPD and it's therapeutic implications.


  Methods Top


60 consecutive patients attending the psychiatry outpatient unit fulfilling the Diagnostic and Statistical Manual of Mental Disorders Fifth Edition (DSM-5)[11] criteria for BPD were enrolled as cases with 60 age-matched healthy controls after ethical clearance from the institutional ethical board and written informed consent. Only those who were willing to participate and had normal physical and neurological examination/computed tomography CT brain were included in the study. Those with epilepsy, head injury, history of encephalitis, comorbid psychiatric illness or substance dependence or on psychotropic drugs were excluded from the study. BPD cases with presenting complaints such as impulsivity, aggressiveness, self-injurious behavior, and suicidal attempts were selected for the study, whereas BPD cases with past or present history of any psychiatric illness were excluded from the study as psychiatric illness could alter EEG waves.

Tools

Semi-structured pro forma

Semi-structured pro forma was used for recording the sociodemographic and clinical details as per the interview techniques proposed by Gunderson et al.[12] Participants were evaluated using the DSM-5 criteria for BPD of which five criteria are required to make a diagnosis of BPD.[11] We categorized BPD into three groups for comparison purpose. Those who fulfilled 5–6 criteria in DSM-5 were classified as mild, 6–7 criteria as moderate, and those who fulfilled all the 9 criteria as severe. Those who had 4 or <4 were considered as not having BPD.

Electroencephalogram recording

Digital EEG was recorded with Recorders and Medicare Systems 32-bit EEG machine. An EEG wave is the representation of the differences in electrical potential between an electrode placed on the scalp and a reference electrode placed elsewhere on the head. Total duration of 40 min using the International 10–20 Electrode Placement System with standard activation procedures was done. Computer analysis was not attempted. The EEG was interpreted by neurologists specialized in EEG and epilepsy, who was blind about the study. When abnormalities were found, they were classified in terms of location, wave pattern, and frequency. Only definite abnormalities were classified as abnormal, abnormalities for age were judged with reference to current established normative criteria published in EEG literature.

If abnormality was strongly suspected, but the resting EEG normal, activation procedures were used in EEG to increase the probability of recording abnormal patterns. Strenuous hyperventilation and photic stimulation (stimulation of the visual cortex using light) were the most common activation procedures employed.

Sociodemographic scale

Social status was assessed using modified Kuppuswamy Sociodemographic Scale 2018 by Saleem, which consists of five classes includes upper, upper middle, lower middle, upper lower, and lower. The five classes were categorized based on occupation of the head of the family, education of the head of the family, and total monthly income of the family.[13]

Statistical design

The statistical design was formulated using the data collected, as above for each of the scales and sociodemographic variables, the central values and dispersion were calculated. In comparison of data for categorical variables, Chi-square test was used. SPSS 20.0 version (SPSS 20, IBM, Armonk, NY, United States of America) was used for the statistical analysis.


  Results Top


Majority of the cases and controls were under <25 years of age, with a female preponderance, were unmarried, employed with 12th grade education and belonged to middle and upper classes. No statistical significant differences were seen.

[Table 1] shows the comparison of sociodemographic profile between cases and controls, which shows no difference.
Table 1: Sociodemographic variables

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[Table 2] EEG abnormalities were seen in 19 cases and 2 controls with epileptiform discharges seen in 13 cases and both the controls.
Table 2: EEG abnormalities between cases and controls

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[Table 3] As per the DSM 5 criteria, EEG abnormalities were more in cases having more than 6 criteria for BPD diagnosis as compared to those satisfying only 5 criteria. In patients having all 9 criteria 57% of the cases showed EEG abnormalities.
Table 3: EEG abnormalities and BPD criteria

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[Table 4] shows the pattern of EEG abnormalities. Epileptiform discharges of spike and sharp waves were more common with severe category and nonepileptiform activity (focal slowing) was seen with moderate and mild categories.
Table 4: Pattern of EEG abnormalities in BPD cases

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  Discussion Top


Sociodemographic characteristics

We did not find any statistical significant differences among the variables in both the groups which is in keeping with the study by Zimmerman.[14]

Dahl and Akhtar et al. showed higher number of male cases though we had a female preponderance. A 2-year prospective study of self-injury found 2:1 ratio of women-to-men when the primary sources of patients were hospitals and physicians.[15],[16]

Rachel et al. showed slightly higher rates of BPD in females, people in lower income brackets, people younger than 30 years, and individuals who were separated or divorced [17] which was partly in keeping with our results.

Borderline personality disorder criteria

Many studies categorized BPD into types based on the symptoms such as impulsive, problems in interpersonal relationships, and affective instability rather than DSM criteria scores.[7],[8]

Electroencephalogram

Standard EEG studies were carried out under the hypothesis that abnormal brain electrical activity and/or focal brain dysfunction, particularly in the temporal lobes, plays a significant role in the pathogenesis of BPD characterized by impulsiveness and affective instability.

EEG abnormalities in BPD seen were of two types:

Nonepileptiform abnormal pattern

Nonepileptiform abnormal pattern consisted of slow waves. Slow waves were further divided into focal slowing and diffuse slowing. In our study, 6 persons with BPD showed focal slowing restricted to only specific region that was either frontal or temporal right side. The most prominent focal slowing was delta activity which ranged from 0.5 Hz to 3.5 HZ. It often consisted of an increase in slow frequency rhythms and/or a loss of normal higher frequency rhythms. [Figure 1] shows focal slow waves in the left anterior frontal region.
Figure 1: Focal slow wave in the left anterior frontal region

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No persons in control group showed any focal or diffuse abnormalities. Persons with BPD showed no diffuse abnormalities. No cases or control showed asymmetry either in amplitude or frequency.

Similar to our study, right-sided involvement was described by Flasbeck et al. Frontal EEG asymmetry is associated with alexithymia in patients with BPD. This finding is in accordance with neurophysiological models of alexithymia that implicate the right hemisphere impairment in emotion processing and could suggest that frontal EEG asymmetry is a potential biomarker of relevant psychopathology in these patients.[18]

Frontotemporal distribution was also described by Snyder and Pitts. They showed patients with BPD have a significantly higher rate of both definitive and less definitive EEG abnormalities compared with a group with dysthymic disorder. In this report, older BPD patients had more severe EEG abnormalities. Abnormalities (mainly slowing) were most frequently bilateral and of frontal, temporal, or frontotemporal distribution.[19]

De la Fuente et al. reported a 40% incidence of diffuse EEG slowing in a group of unmedicated BPD patients. None of their patients received neuroleptic drugs for at least 2 months, and all other medications were withdrawn for 10 days or 15 days for tricyclic antidepressants and monoamine oxidase inhibitors. However, in our study, no persons had diffuse slowing.[20]

The finding of a high prevalence of slow wave abnormalities in BPD patients is in support of an earlier report by Tanahashi. He found a significantly higher incidence of slowing of background activity among the BPD groups (84.4% of BPD patients vs. controls).[7]

Studies also have reported between 40% and 80% incidence of generalized slowing of the intrinsic background activity in BPD patients, with the lower incidence figures being derived from studies that exclude participants with comorbid axis I disorders, current drug abuse, or known neurological problems.

Epileptiform abnormal pattern

Epileptiform activity mainly consists of spike and sharp waves. Spike wave is a transient, which is clearly distinguished from the background activity with pointed peak, with a duration from 20 to 70 ms, whereas sharp wave is a transient which is clearly distinguished from the background activity, with pointed peak with a duration from 70 to 200 ms.

14 cases and 2 controls showed focal epileptiform activity.

BPD patients also showed a much higher incidence of paroxysmal EEG activity, particularly posterior sharp waves. [Figure 2] shows generalized sharp wave transients. Archer et al. found that 6.3% of a group of 16 adolescents with BPD had bilateral spike-and-wave discharges, whereas none of the 10 participants in a comparison group with other personality disorders had similar discharges.[21]
Figure 2: Generalized sharp wave transients in a case of borderline personality disorder

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Tanahashi also reported spike-and-wave complexes (of the 6 s variety) in 31% of the BPD patients.[7]

Cowdry et al. reported in their study that 5 of 17 cases and 3 of 16 controls showed nonspecific abnormalities and 4 out of 17 and 1 out of 16 subjects showed specific abnormalities which included focal slowing or spike-and-wave pattern. Positive spikes appeared in patients with high scores for high-impulse action, whereas spike-and-wave pattern was observed in patients with high scores of abnormalities in interpersonal relationships. EEG abnormalities in BPD illustrate not only the presence of abnormal cortical foci but also a nonspecific EEG localizable brain dysfunction.[22]

DSM V and EEG

We found that those who satisfied all the 9 DSM V criteria for BPD had a greater prevalence of EEG abnormalities (11 patients) as compared to 6 and 2 patients each who satisfied 7/8 criteria and 5/6 criteria respectively. This shows that persons who fulfilled more criteria had focal epileptiform discharges than other groups, which was statistically significant [Figure 3].
Figure 3: The pattern of electroencephalogram abnormalities in cases and controls

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Ogiso et al. provided evidence of different EEG correlates of BPD symptom profiles. Using subscales of the diagnostic interview for BPD, they found the presence of positive spikes to correlate with impulsivity and the presence of spike-and-wave phantoms to be correlated with high scores on interpersonal relationship dysfunction. The phantom spike-and-wave discharges were also correlated with the presence of neurovegetative symptoms (e.g., headaches and body aches). More recently, positive spikes were found to be a correlate of attention deficit disorder.[23] Ogiso et al. emphasized the observation that no one pattern characterized the entire sample, and that in some patients, the EEG was perfectly normal.[23] Similarly, Drake et al. found that BPD patients who presented with psychogenic seizures had normal EEGs.[24]

Cowdry and Gardner found a high prevalence of EEG abnormalities based on BPD symptoms.[25]

A number of EEG studies linked BPD to complex partial seizures. Andrulonis et al. found that 27% of BPD had evidence of EEG abnormalities. Several episodic or paroxysmal symptoms are common in BPD and temporal lobe epilepsy.[26],[27] Carbamazepine has shown to be effective in decreasing paroxysmal symptoms.[28]

These findings of EEG abnormalities in BPD provide support for the Jacksonian biopsychosocial model of BPD. The Jacksonian model asserts that many of the symptomatic features of BPD including dysregulated effect, identity disturbance, somatization, and dissociation are caused by disrupted connections in the prefrontal cortex.

In summary, two types of EEG abnormalities found in some BPD patients. The first is the presence of epileptiform discharges. This type of abnormality is likely to indicate a decreased threshold for seizure activity or cortical excitability and may be predictive of responsiveness to anticonvulsant therapy. The second type of standard EEG abnormality is the presence of diffuse EEG slowing.

The presence of a static (nonprogressive waves) and nonmetabolic diffuse EEG slowing could indicate that the patients are in a more difficult group, who are less likely to respond to pharmacotherapy.

Limitations

We did not use any emotional challenges during EEG recording as it is known that the emotional tasks or stressors may impact EEG abnormalities. The current emotional status of the patients was not assessed. Studies with a larger sample size would be more conclusive.


  Conclusion Top


We found EEG abnormalities in BPD patients especially in those satisfying all criteria for diagnosis. Electrophysiological investigations of BPD have the potential to contribute to our understanding of the different pathophysiological processes that may be aberrant in BPD patients. Developing a thorough understanding of the neurobiology of BPD is essential for the development of effective preventive, therapeutic, and rehabilitative approaches to BPD. Longitudinal studies with a comprehensive examination of the electrophysiological profiles of this patient group and correlation with symptom clusters would probably yield useful information about subtypes and treatment avenues for these patients.

Ethical statement

This study was approved by Institutional Ethics Committee with reference number GMKMCH/2623/IEC/01/2016-64 obtained on 30th December 2016.

Declaration of Patient Consent

Patient consent statement was taken from each patient as per institutional ethics committee approval along with consent taken for participation in the study and publication of the scientific results / clinical information /image without revealing their identity, name or initials. The patient is aware that though confidentiality would be maintained anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Berlin HA, Rolls ET, Iversen SD. Borderline personality disorder, impulsivity, and the orbitofrontal cortex. Am J Psychiatry 2005;162:2360-73.  Back to cited text no. 1
    
2.
Grant BF, Chou SP, Goldstein RB, Huang B, Stinson FS, Saha TD, et al. Prevalence, correlates, disability, and comorbidity of DSM-IV borderline personality disorder: Results from the wave 2 national epidemiologic survey on alcohol and related conditions. J Clin Psychiatry 2008;69:533-45.  Back to cited text no. 2
    
3.
Trull TJ, Jahng S, Tomko RL, Wood PK, Sher KJ. Revised NESARC personality disorder diagnoses: Gender, prevalence, and comorbidity with substance dependence disorders. J Pers Disord 2010;24:412-26.  Back to cited text no. 3
    
4.
Coccaro EF, Kavoussi RJ. Biological and pharmacological aspects of borderline personality disorder. Hosp Community Psychiatry 1991;42:1029-33.  Back to cited text no. 4
    
5.
De La Fuente JM, Goldman S, Stanus E, Vizuete C, Morlán I, Bobes J, et al. Brain glucose metabolism in borderline personality disorder. J Psychiatr Res 1997;31:531-41.  Back to cited text no. 5
    
6.
Harris CL, Dinn WM, Marcinkiewicz JA. Partial seizure-like symptoms in borderline personality disorder. Epilepsy Behav 2002;3:433-8.  Back to cited text no. 6
    
7.
Tanahashi Y. Electroencephalographic studies of borderline personality disorder. Juntendoigaku 1988;34:207-19.  Back to cited text no. 7
    
8.
Shelley BP, Trimble MR, Boutros NN. Electroencephalographic cerebral dysrhythmic abnormalities in the trinity of nonepileptic general population, neuropsychiatric, and neurobehavioral disorders. J Neuropsychiatry Clin Neurosci 2008;20:7-22.  Back to cited text no. 8
    
9.
Boutros NN. Diffuse electroencephalogram slowing in psychiatric patients: A preliminary report. J Psychiatry Neurosci 1996;21:259-63.  Back to cited text no. 9
    
10.
Limberg A, Barnow S, Freyberger HJ, Hamm AO. Emotional vulnerability in borderline personality disorder is cue specific and modulated by traumatization. Biol Psychiatry 2011;69:574-82.  Back to cited text no. 10
    
11.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Health Disorders: DSM-5. 5th ed. Washington, DC: American Psychiatric Association; 2013.  Back to cited text no. 11
    
12.
Gunderson JG, Kolb JE, Austin V. The diagnostic interview for borderline patients. Am J Psychiatry 1981;138:896-903.  Back to cited text no. 12
    
13.
Saleem SM. Modified Kuppuswamy scale updated for year 2018. Indian J Res 2018;7:217-18.  Back to cited text no. 13
    
14.
Zimmerman M. Improving the recognition of borderline personality disorder in a bipolar world. J Pers Disord 2016;30:320-35.  Back to cited text no. 14
    
15.
Dahl AA. Borderline disorders – The validity of the diagnostic concept. Psychiatr Dev 1985;3:109-52.  Back to cited text no. 15
    
16.
Akhtar S, Byrne JP, Doghramji K. The demographic profile of borderline personality disorder. J Clin Psychiatry 1986;47:196-8.  Back to cited text no. 16
    
17.
Tomko RL, Trull TJ, Wood PK, Sher KJ. Characteristics of borderline personality disorder in a community sample: Comorbidity, treatment utilization, and general functioning. J Pers Disord 2014;28:734-50.  Back to cited text no. 17
    
18.
Flasbeck V, Popkirov S, Brüne M. Frontal EEG asymmetry in borderline personality disorder is associated with alexithymia. Borderline Personal Disord Emot Dysregul 2017;4:20.  Back to cited text no. 18
    
19.
Snyder S, Pitts WM Jr. Electroencephalography of DSM-III borderline personality disorder. Acta Psychiatr Scand 1984;69:129-34.  Back to cited text no. 19
    
20.
De la Fuente JM, Tugendhaft P, Mavroudakis N. Electroencephalographic abnormalities in borderline personality disorder. Psychiatry Res 1998;77:131-8.  Back to cited text no. 20
    
21.
Archer RP, Struve FA, Ball JD, Gordon RA. EEG in borderline personality disorder. Biol Psychiatry 1988;24:731-2.  Back to cited text no. 21
    
22.
Cowdry RW, Pickar D, Davies R. Symptoms and EEG findings in the borderline syndrome. Int J Psychiatry Med 1985;15:201-11.  Back to cited text no. 22
    
23.
Ogiso Y, Moriya N, Ikuta N, Maher-Nishizono A, Takase M, Miyake Y, et al. Relationship between clinical symptoms and EEG findings in borderline personality disorder. Jpn J Psychiatry Neurol 1993;47:37-46.  Back to cited text no. 23
    
24.
Drake ME Jr., Pakalnis A, Phillips BB. Neuropsychological and psychiatric correlates of intractable pseudoseizures. Seizure 1992;1:11-3.  Back to cited text no. 24
    
25.
Cowdry RW, Gardner DL. Pharmacotherapy of borderline personality disorder. Alprazolam, carbamazepine, trifluoperazine, and tranylcypromine. Arch Gen Psychiatry 1988;45:111-9.  Back to cited text no. 25
    
26.
Andrulonis PA, Glueck BC, Stroebel CF, Vogel NG, Shapiro AL, Aldridge DM, et al. Organic brain dysfunction and the borderline syndrome. Psychiatr Clin North Am 1981;4:47-66.  Back to cited text no. 26
    
27.
Andrulonis PA, Vogel NG. Comparison of borderline personality subcategories to schizophrenic and affective disorders. Br J Psychiatry 1984;144:358-63.  Back to cited text no. 27
    
28.
Coccaro EF. Clinical outcome of psychopharmacologic treatment of borderline and schizotypal personality disordered subjects. J Clin Psychiatry 1998;59 Suppl 1:30-5.  Back to cited text no. 28
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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