Can we grade social cognition defects in schizophrenia?

05 10 2016

Social cognition defect is  a core feature of schizophrenia.This include defects in emotion processing, social perception, theory of mind  (mental state attribution) and attributional style/biases. These defects are seen in prodromes, first episode,   while the disease is in remission and in first degree relatives . These are more associated with negative symptoms .Only few studies have looked at the relationship between social cognition defects and functioning. Understanding the social cognition status might help to tailor interventions to suit individual needs.This may improve functional outcomes.

Rocca and colleagues from Italy report the results of a cluster analysis  of 809 individuals with schizophrenia living in the community across Italy. A matched control group was also studied. Symptom severity ( using PANSS), negative symptoms ( using Brief Neg symptoms scale), social cognition ( Emotional intelligence Test, Facial emotion identification test, awareness of social interference test) and functional status ( Specific Level of functioning scale & Validation of real life outcomes) were measured.

Cluster analysis revealed three clusters :  unimpaired, impaired, and very impaired social cognition.Proportions were :unimpaired (42%), impaired (50.4%) and very impaired (7.5%). Functioning decreased parallel to decrease in social cognition. Theory of mind tests  ( to know how the individual understands others mental state) were important for cluster definition.

The awareness of social interference test ( checking sarcasm and lying) was good enough to help grade the three clusters. Patients who were able to detect sarcasm were more likely to be in the unimpaired group. Unimpaired group had higher grasp of sarcasm. Those in impaired group were better able to detect lies than very impaired.

Why does this happen? comprehension of lies/deceit is acquired before sarcasm/ irony. sarcasm involves more complex inferential chains. so if the individual can detect sarcasm , probably he/she has unimpaired social cognition. If they cannot detect deceit/lie, they may have very impaired social cognition.

How do we take this in to practice? The social interference test use video based vignettes. Clinicians need their  own culturally relevant vignettes ( may be movie clips might help ) to test this.

Authors agree that the natural stability of these clusters were not tested in this study- this being a cross sectional study. However, this is the first study using best available tools to measure the relevant constructs.


Once we classify the defects in social cognition what do we do? Would various social skills training help? Would training in virtual settings benefit ? Would improving these measures thorough interventions translate to real benefits in outcomes?… We don’t know…yet.

Summary of article : Social cognition in people with schizophrenia: a cluster-analytic approach.Rocca P, Galderisi S, Rossi A, Bertolino A, Rucci P, Gibertoni D, Montemagni C, Sigaudo M, Mucci A, Bucci P, Acciavatti T, Aguglia E, Amore M, Bellomo A, De Ronchi D, Dell’Osso L, Di Fabio F, Girardi P, Goracci A, Marchesi C, Monteleone P, Niolu C, Pinna F, Roncone R, Sacchetti E, Santonastaso P, Zeppegno P, Maj M; Italian Network for Research on Psychoses.

Psychol Med. 2016 Oct;46(13):2717-29. doi: 10.1017/S0033291716001100.PMID:27649341

Social deprivation leads to psychosis?

05 08 2016

 Does incidence  schizophrenia vary between countries? Faris and  Dunham (1939) showed that disorganised neighbourhoods in Chicago had higher rates of schizophrenia sparking all sorts of explanations for this. WHO study in 1980’s found that incidence of  narrowly defined schizophrenia did not differ across countries, but  broadly defined illness did differ significantly across countries. In 2004, MCgrath et al summarised all relevant data from 161 studies and showed that there is a five fold difference across countries. It is also thought that there are possible significant regional differences  with in countries as well.

What would explain such geographical differences? It is possible that factors like social deprivation, population density, urbanicity, social capital and social fragmentation may have some roles to play. There are theoretical meanings and explanatory models attached to these factors.

Is social deprivation associated with higher incidence of psychosis ? Brian O’Donoghue, Eric Roche and Abbie Lane  looked at association between the level of social deprivation at the neighbourhood level and the incidence of psychotic disorders in this systematic review.They included 28 studies in the analysis.

Three types of places ( place of birth , place when high risk status was positive , place   when schizophrenia emerged)  and their association with illness status was explored  in these studies.Most studied ( 21 studies)  deprivation of the place where illness emerged.


Most studies (17/23)  show that there is an association between incidence of illness and the level of social deprivation at the time of presentation.

Social deprivation at place of birth is less studied keeping the ‘drift theory’ alive.  The largest study on this question ( place of birth ) did not support an association. However, a well designed Israel study ( Werner , 2007) showed that  individuals who later on develop schizophrenia were more likely to be born in deprived areas.

Social causation can occur ( if at all it is happening), through multiple, direct/ indirect channels ( weaker social cohesion, poorer support systems). Established risk factors ( family history ,cannabis use, traumatic experiences )  can be more prevalent in such areas. They may also have more residential mobility in childhood which is now shown to be another possible risk factor.We do not know how much  gene- environment interaction  may be explaining these observed associations. The  EU-GEI study  ( European Genetic Interaction Study), which is now established,  is likely to offer some insights .

How would we know more about environmental effects ?  This review suggest that more studies on UHR/ psychotic symptoms in general population are needed to  identify vulnerability periods and associated environmental risk factors.

Understanding these relationships have some practical , immediate relevance when we allocate resources , for example for early intervention services . Psychiatric Mapping Translated into Innovation for Care (PsyMaptic) is an example of a resource that predict the incidence in a geographical area to inform resource allocation. However, in countries where basic mental health data is lacking, these are distant dreams.

Summary of the article.

Neighbourhood level social deprivation and the risk of psychotic disorders: a systematic review.

O’Donoghue B, Roche E, Lane A.

Soc Psychiatry Psychiatr Epidemiol. 2016 Jul;51(7):941-50. doi: 10.1007/s00127-016-1233-4. Epub 2016 May 13. Review.


Youth with psychotic experiences have brain tissue loss

05 01 2016

Psychotic disorders like schizophrenia have long been established to have accompanying changes in brain structure and function. Hippocampal volume loss is the most significant and consistent of such changes. Medial temporal lobe seems to be the area where most changes occur. Volume reductions seen in unaffected relatives make us support the idea of heritable phenotypes.

Youth who are classified as high risk,  who later convert to psychosis ,also have  (North American Prodrome Longitudinal Study consortium , 2015 ) accelerated gray matter loss in frontal cortex compared with non- converters and healthy comparators. what about those who experience some psychotic spectrum experiences?

Do non-help seeking youth who experience psychotic spectrum symptoms have structural changes in brain? Transition to psychosis in this group will be lower than the high risk groups. Large imaging studies haven’t addressed this question so far.Philadelphia Neu- rodevelopmental Cohort (PNC) is trying to answer this question. Theodore D. Satterthwaite and team from University of Pennsylvania Perelman School of Medicine report the findings of their study.

The cohort comprises 1429 individuals ( mean age around 15) . PS symptoms were present in 408 participants. This was assessed using the GOASSESS interview ( combination of questions from K SADS, PRIME, Scale of prodromal symptoms).Analysis is based on the final sample of 391 youth with Psychotic spectrum  features (PS group) and 400 Typically Developing youth (TD group) 8 to 22 years old.


Youth with Psychotic spectrum  symptoms had reduced intra cranial volume as compared with typically developing youth. They showed marked reduction in gray matter volume. Difference was more in older participants. Volume loss was more marked in medial temporal lobe.Greater severity of PS symptoms was associated with volume reduction in bilateral medial temporal lobe.

It is important to note that this is  a community based study and participants were non help seeking. Still, the changes  mirrors that seen in both adults with clinically diagnosed psychotic disorders and youth at clinical risk. One could say that regions affected are part of the default mode network. (large functional network critical for internally directed attention, theory of mind, social cognition, and memory).


Adolescents with psychotic spectrum experiences have identifiable brain structural changes. These are similar to those observed in established psychotic disorders.imaging phenotypes are important in evaluating risk of conversion to psychosis. This may ,in future, help in early identification and intervention.

summary of the article :

Structural Brain Abnormalities in Youth With Psychosis Spectrum Symptoms. Satterthwaite TD, Wolf DH, Calkins ME, Vandekar SN, Erus G, Ruparel K, Roalf DR, Linn KA, Elliott MA, Moore TM, Hakonarson H, Shinohara RT, Davatzikos C, Gur RC, Gur RE.JAMA Psychiatry. 2016 May 1;73(5):515-24.


Do autism risk increase with parental age difference?


Population based studies have shown that older paternal age is linked to Autistic Spectrum Disorders (ASD).Risk is thought to increase with maternal age also.  Are these  ( ie paternal and maternal age) independent risk factors ? Is age difference between parents also important ?

Sandin et al address this important question using combined population based cohorts from various countries set up as International Collaboration for Autism Registry Epidemiology (ICARE). Children were followed from birth to reported diagnosis of ASD. The cohort  comprised of 5766794 births across Denmark, Sweden , Norway, Israel and Western Australia.0.54% of these children received a diagnosis of  ASD and 0.18% had  AD.


Independent effects: Increasing paternal age was associated with more ASD. Relative to fathers aged 20–29 years, fathers 50 years or older had a statistically significantly increased risk for offspring with ASD (RR=1.66 95% CI:1.49–1.85).  Maternal age showed a U shaped relationship. Relative to mothers aged 20–29 years, mothers younger than 20 years had a statistically significantly increased risk for offspring with ASD (RR=1.18 95% CI:1.08–1.29. After 30 years, increasing maternal age  increased risk of ASD.

Data also show evidence to combined effect as well. Risk was highest when both parents were older. Increasing age difference between parents also increased the risk. Lowest risk was shown by couples that generated the majority of births, specifically, 29–39-year-old fathers and 25–35-year-old mothers. Relative risk increased in all directions from this region as the parental age difference increased.

Limitations: We do not have information on confounding factors ( Socio economic status , parental psychiatric history, obstetric complications etc). For example:  Individuals who are shy and aloof  ( may be traits of ASD) ,can be be over represented in older parents)

Conclusions: Increasing paternal age as well as maternal age increase the risk of ASD.Increasing difference in parental age is also a risk factor.

Summary of the article:

Autism risk associated with parental age and with increasing difference in age between the parents.Sandin S, Schendel D, Magnusson P, Hultman C, Surén P, Susser E, Grønborg T, Gissler M, Gunnes N, Gross R, Henning M, Bresnahan M, Sourander A, Hornig M, Carter K, Francis R, Parner E, Leonard H, Rosanoff M, Stoltenberg C, Reichenberg A.Mol Psychiatry. 2016 May;21(5):693-700.


How much do Schizophrenia cost to the society?


Schizophrenia is one of the most disabling disorders. The cost of this illness to individuals and society is enormous. But do we really know how much it costs to the society ?

Cost estimates are calculated by multiplying cost per patient with the prevalence of the illness. Prevalence estimates vary widely. A systematic review calculated  (Saha et al 2005) life time prevalence  as 0.4% and the period prevalence (1–12 months) as 0.33%. cost calculation also involves employment rate of individuals with schizophrenia. This also varies widely. In western societies 12%- 39%  of those with schizophrenia are reported as employed. There are various uncertainties around this data as well.

Evensen et al from Oslo report a unique study that sheds light on the costs of schizophrenia.  This is a  population based study from Norway.  It used a top-down design, where data from national registers for the period January 1 to December 31, 2012 were used to  (aggregate figures of actual  resource consumtption) calculate costs. Direct (treatment and community care) and indirect (ie, social security payments and lost productivity) costs were  also taken in to account.Costs related to premature mortality, volunteer and family care, and the criminal justice system were not included.

They  used  a very comprehensive approach to get all information ( IP care, Op care, GP care, medication use, home care, social benefits ) making this one of the best addressing this issue.


The average 12 month prevalence of schizophrenia was 0.17% for the entire Norwegian population.This would be 0.22% for those aged above 18. Employment rate in general ppulation in teh age group 30-50 is  around 80% compared with around 10% in those with schizophrenia. The employment rate (full time and part time) among those of working age was 10.24%–10.5% of the men and 9.8% of the women.

Total national cost associated with schizophrenia is USD  890 million/ year.The average cost per individual with schizophrenia was USD 106,014.00 . One third of total societal cost is due to hospitalisation. 18 % of all hospital days are due to schizophrenia, and 14% of all OP visits are due to schizophrenia . Lost productivity cost accounted for 29% of the total cost.

Studies from UK and Sweden have showed lesser proportion of expenses attributed to IP care ( 8-16%). Norway has more number of beds than others ( 83 beds/ 100,000) compared to around 50 in UK) and this may be a factor.

This is a unique study which adds to the argument that poor  mental health is a big economic drain on communities world wide.

Comments: In  many countries  individuals are left to their own resources leading to impoverishment , debt and early death.  In countries like Norway, where society take responsibility for mental health services, greater effort and resources are allocated to improve population mental health, provide most effective service and to research best options. Mental health is a serious matter for such welfare societies.

Summary of the article

 Prevalence, Employment Rate, and Cost of Schizophrenia in a High-Income Welfare Society: A Population-Based Study Using Comprehensive Health and Welfare Registers.

Evensen S, Wisløff T, Lystad JU, Bull H, Ueland T, Falkum E. Schizophr Bull. 2016 Mar;42(2):476-83.


Can brain electric stimulation improve stroke recovery?


Stroke is the leading cause of disability. Recovery  is aided by active movement training and new learning. Improving neural plasticity is expected to bring additional benefits. Transcranial direct current stimulation (tDCS) to the motor cortex is known to enhance excitability and facilitate motor learning in healthy individuals.

Two recent systematic reviews (Bastani, Jaberzadeh 2012,  Butler et al 2013) provided initial evidence for the use of ipsilesional anodal tDCS in chronic stroke.

Would combining motor training with anodal tDCS improve rehabilitation outcome?

Claire Allman and colleagues at Oxford report the results of a randomized, sham controlled , parallel  group study  in 24 patients at least 6 months after a first unilateral stroke not directly involving the primary motor cortex. 1191 patients were assessed for eligibility. 26 were randomized to receive either anodal tDCS or sham treatment. 24 completed the intervention.

Intervention:  During the intervention period, participants conducted daily, supervised one hour sessions of motor training program (GRASP) over 9 days. For the first 20 min of each session, tDCS electrodes were positioned on the participant’s scalp to deliver either brain stimulation via tDCS or sham treatment. Clinical assesments and MRI were done at multiple points.


At 3 months, upper limb ability in patients receiving repeated sessions of anodal tDCS to the ipsilesional motor cor- tex  was significantly better compared to the sham-treated group when tDCS was paired with motor training.  Clinical improvements were associated with increased activation of ipsilesional motor cortical areas.Structural MRI revealed intervention-related increases in gray matter volume in cortical areas, including ipsilesional motor and premotor cortex after anodal tDCS but not sham treatment.

How is tCDS working ? Is it true recovery/ ie original pathways for movement being restored? or is it compensation only ? If it is improving learning through local disinhibition, is  this task specific or can this be generalised to non trained items? There are many unanswered questions.

Larger studies are needed to  identify patient  characteristics that would help clinicians to  spot who would benefit from this intervention.


tCDS is showing promising benefits in stroke rehabilitation.

Summary of the article

Ipsilesional anodal tDCS enhances the functional benefits of rehabilitation in patients after stroke. Claire Allman, Ugwechi Amadi Anderson M. Winkler, Leigh Wilkins,Nicola Filippini Udo Kischka,Charlotte J. Stagg,Heidi 16 March 2016 Vol 8 Issue 330 330re1.


Is parental depression associated with poor school grades of children at age 16 ?

15. 03. 2016

Depression has wider effects. Children with depressed parents are more likely to have poor language development. Children  of mothers with postnatal depression have lower IQ scores at age 11 years. Poor school performance is also reported among such children. Such associations could well be due to confounfing factors. Parental health, life style, education, income- all these can be related to both depression and children’s poor performance. If there is an independent association, this is significant as poor scholastic performance is associated with poor future health.


Hanyang Shen and colleagues at Drexel University School of Public Health, USA analysed data from one million children to answer this question. This was a nation wide Swedish  cohort of children born from 1984 to 1994. National school register provided the data on school grades. Data on parental depression was obtained from national patient register.

Parental depression diagnoses occurring before the start of the child’s final compulsory year were only included. Data was collected on a comprehensive list of covariates ( parental income, education, alcohol use,parental age at birth, maternal smoking ,family size etc).


3.0% of mothers and 2.1% of fathers had depression before the final year of child com- pulsory education. There is a significant association between parental depression and poor academic performance. Maternal depression and paternal depression are associated with −0.80 (95% CI, −0.83 to −0.77) and −0.73 (95% CI, −0.77 to −0.69) lower deciles of school grades.Once covariates were taken in to account, these associations  decreased to −0.45 (95% CI, −0.48 to −0.42) and −0.40 (95% CI, −0.43 to −0.37) lower deciles.



Service registers may show an under estimate of true occurrence of depression. However,  a subsample , with better ascertainment, also showed similar results. Information on child mental health was not available. Data on whether children were living with  both parents  for the duration of the study were not available.


Maternal depression and paternal depression are  (both) independently associated with lower academic performance of children at 16 years.This is significant even after adjusting for possible covariates. Depression at any time has negative effect. Analysis suggested that parental depression at any  period was independently associated with worse school performance. Subsample ( where more info was collected) showed that maternal depression has larger effect.


Parental depression need to be considered as a serious family mental health  problem. Early identification, and treatment is likely to minimise negative effects on children. Children of parents with depression require extra attention to reduce the ill effects of such depression. Depression has intergenerational effects. Interventions could reduce such effects.

Summary of the article

Associations of Parental Depression With Child School Performance at Age 16 Years in Sweden.Shen H, Magnusson C, Rai D, Lundberg M, Lê-Scherban F, Dalman C, Lee BK.JAMA Psychiatry. 2016 Mar 1;73(3):239-46.

Neuro inflammation and psychosis: new evidence


Patho-etiology of psychosis is not well understood. Neuro inflammation is one possibility. Studies have suggested that microglia, the immune cells of  the CNS, are involved. Pro inflammatory cytokines ( peripheral markers) are elevated in psychosis. Grey matter volume reductions are seen parallel to such elevations.These changes are seen in both schizophrenia and in ultra high risk groups.

Can we measure the microglial activity in the brain ? PET imaging using radioligands specific for a protein  (18kD translocator-protein (TSPO)) which is expressed on microglia is one possibility. This method of enquiry has shown increased microglial activity in individuals with schizophrenia. Severe symptoms of schizophrenia is often proceeded by a prodromal phase of attenuated symptoms. One third of individuals who meet high risk criteria develop psychosis within 2 yr follow up period. Would Ultra High Risk individuals also show  elevated microglial activity ?

Peter Bloomfield and team from Imperial College London studied this in 58 subjects. This included 14 ultrahigh risk patients & 14 controls, 14 schizophrenia patients & their  14 controls.Ultra-high-risk individuals were assessed with the Comprehensive Assessment of the At-Risk Mental States. All subjects underwent MRI and PET study.


There were no demographic differences between different groups. The binding ratio of the ligand [11C]PBR2 was elevated in Ultra high risk group and schizophrenia group.The elevation in ultra high risk group was specific to the subclinical psychotic symptoms. These high risk individuals were not on any medications and were new to services, we could assume that the observed changes are not due to medications or  previous illness. During the study, one participant developed  psychosis and this patient had the highest binding of ligand.

This study show that elevated microglial activity predates diagnosable , frank psychosis.

Limitations: Researchers used a relative quantification method ( ie binding expressed as ratio of binding in cortical grey matter to whole brain) and it is not clear whether high binding ratio is due to higher TSPO expression in cortical grey matter or lower expression elsewhere. We do not now know the predictive power of such high binding . i.e. does high binding mean more transition to florid psychosis? The association of high bidding ratio with high prodromal symptom severity observed in this study point to the higher chance of tradition with high binding.

It is unclear whether the   18kD translocator-protein (TSPO)  activity expressed by microglia is a protective mechanism triggered by disease process or it is a primary neuro inflammatory process linked to risk factors for psychosis and the development of subclinical symptoms.

The observation that anti inflammatory medications may reduce negative symptoms (for example: Minocycline reduce symptoms early in illness) and that some antipsychotics possess some degree of anti-inflammatory activity add to to the idea that  neuro inflammatory process is involved in psychosis.


Neuro inflammation is emerging as a consistent finding in psychosis. It needs to be seen how microglial activity changes over the time when individual’s mental state /diagnosis changes.

Summary of the article

Microglial Activity in People at Ultra High Risk of Psychosis and in Schizophrenia: An [(11)C]PBR28 PET Brain Imaging Study. Bloomfield PS, Selvaraj S, Veronese M, Rizzo G, Bertoldo A, Owen DR, Bloomfield MA, Bonoldi I, Kalk N, Turkheimer F, McGuire P, de Paola V, Howes OD.Am J Psychiatry. 2016 Jan 1;173(1):44-52.

Can anxiety damage your heart?


Mind and Heart work in an interconnected way, perhaps more than between any other organs . Allgulander reviews the relationship between anxiety and cardiac heath in this article

Anxiety is a risk  factor for cardiac morbidity. A large scale study ( with 52 095 participants in 19 countries) reported in 2013 that after adjusting for comorbidity,  diagnoses of depression,panic disorder, specific phobia, posttraumaticstress disorder, and alcohol use disorders were associated with heart disease onset [odds ratios(ORs) 1.3–1.6]. (Scott et al 2013 ).  Associations with anxiety were greater in magnitude than those with depression.

A swedish military conscript study showed that anxiety state at age 18- 20 increased the risk of MI at follow up ( average 37 years) by more than 2 fold (Janzsky ,2008). A Taiawanse study found that nearly 5% of those with panic disorder were to develop MI in the next year ( compared to control rate of nearly 3%).

Prospective studies have shown that individuals with cardiac disorders do worse when they also suffer from anxiety.

What about acute physiological changes related to anxiety?

Takotsubo cardiomyopathy ( ‘broken heart’ syndrome) was first reported in Japan. Takotsubo is a trap used to catch octopus and  has a narrow neck and a round bottom. Left ventricle temporarily become weak and its shape changes. Majority of people with this ‘heart attack’ have experienced emotional stress. The condition is temporary and reversible. Left ventricle will return to normal shape in days/weeks. Pre existing  anxiety and depression are reported more often among sufferers.

White coat hypertension is tother condition to be considered here. Reports suggest that this may not be benign, i.e. it is associated with other pathological changes.It may have a social anxiety component , but there are no studies to delineate different contributors.

Exposure to both acute and chronic mental stress is associated with an increased incidence of adverse cardiac events. Imminent missile attacks, natural disasters, football match days, start of working week especially after holidays – all are shown to  increase cardiac events. Mental stress induced myocardial schema (MSMI) is an important current area of research.Mental stress triggers transient myocardial ischaemia in 30–70% of patients withpre-existing CAD. A 2014 metaanalysis (Wei et al 2014) showed that MSIMI was associated with a twofold increased risk of a combined end point of cardiac events or total mortality.


Anxiety is a risk factor for cardiac morbidity. Anxiety adversely affects cardiac patients. Recognition and treatment of anxiety is important in improving the outcomes in cardiac disorders.

Summary of the article :

Anxiety as a risk factor in cardiovascular disease. Allgulander C.

Curr Opin Psychiatry. 2016 Jan;29(1):13-17.

Can anxiety damage human brain? Current Opinion Psy.Jan.2016


Occasional and temporary anxiety is a normal part of life.It helps to direct our attentional resources to pertinent information in the environment and mobilise appropriate behaviour in response.Persistent or excessive anxiety is pathological. Would such anxiety cause any deleterious effects on brain? Linda Mah and colleagues ( Canada) review the present evidence to answer this question.

Amygdala is key in threat detection.Prefrontal cortex play crucial role in threat appraisal. Hippocampus helps to build the contextual sense of the event. Balanced activities in these systems result in emotional regulation.

In anxiety disorders, detection threshold is low, amygdala become hyperactive and  PFC control over amygdala is poor.Hippocampus fails to discriminate between threat and safety cues (impaired discriminative conditioning) and this lead to  overgeneralisation of fear stimulus.

It is well known that anxiety is a risk factor for disorders like depression.Significant psychosocial stress in middle age is shown to increase the risk for developing Alzheimer’s disease 20 years later.Presence of anxiety among those with Mild cognitive impairment can also increase the risk of conversion to dementia.

Anxiety increase glucocorticoids and this lead to hippocampal atrophy and diminished neurogenesis. This may explain the cognitive dysfunctions associated with anxiety. Persistent anxiety can cause loss of dendrites and spines in Pre frontal cortex.

Stress-induced damage to the hippocampus and PFC is not completely irreversible. Antidepressants ( desipramine, SSRI) and Lithium as well as CBT  can restore some of the above brain changes.There is a range of evidence ( mostly animal studies) to support this idea.


Pathological anxiety can cause  damages  (structural and functional) to brain. Interventions can mitigate these changes. It is not known whether anxiety interventions can reduce the risk of developing neuropsychiatric conditions (dementia/depression).

Summary of the article

Can anxiety damage the brain? Mah L, Szabuniewicz C, Fiocco AJ. Curr Opin Psychiatry. 2016 Jan;29(1):56-63.PMID: 26651008