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NEUROPSIHOPATOLOGIE
MANUALUL DSM
DSM – Ce i se reproseaza
1. nu este transparent,
2. nu are validitate,
3. a redus numărul de simptome necesar pentru a diagnostic o boală
4. a creat noi tulburări fără o investigație serioasă asupra lor.
• In 2013, the American Psychiatric Association published the 5th edition of its
Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Often referred to
as the "bible" of psychiatry, the manual only classifies mental disorders and does
not explain them or guide their treatment.
• While science should be the basis of any diagnostic system, to date, there is no
knowledge on whether most conditions listed in the manual are true diseases.
• In spite of all the progress that has been made in neuroscience over the last few
decades, the psychiatric community is no closer to understanding the etiology and
pathogenesis of mental disorders than it was fifty years ago ("DSM-5: Changes
and Controversies“ Eric G. Waldon, 2014)
NEUROPSIHOLOGIE CLINICA
• DSM poate fi considerat (spunea directorul NIMH), “în cel mai bun
caz, un dicționar, creând un set de etichete și definindu-le pe fiecare”.
• Una dintre ideile mai noi este că atât ADHD cât și anumite tulburări
de personalitate pot fi doar expresii diferite ale unei aceleiaşi
probleme care stă la baza acestor simptome
• Pentru tulburare depresiva unipolara, cinci (sau mai multe) dintre următoarele
9 simptome au fost prezente în aceeași perioada de 2 săptămâni și
reprezintă o schimbare de la modul de funcționare anterior
• Cel puțin unul dintre simptome este fie (1) dispoziție depresivă sau (2)
pierderea interesului sau a placerii
NEUROPSIHOLOGIE CLINICA
Major depression is a debilitating psychiatric illness that is typically associated with low mood
and anhedonia. Depression has a heritable component that has remained difficult to elucidate
with current sample sizes due to the polygenic nature of the disorder. To maximize sample size,
we meta-analyzed data on 807,553 individuals (246,363 cases and 561,190 controls) from the
three largest genome-wide association studies of depression. We identified 102 independent
variants, 269 genes, and 15 genesets associated with depression, including both genes and gene
pathways associated with synaptic structure and neurotransmission. An enrichment analysis
provided further evidence of the importance of prefrontal brain regions. In an independent
replication sample of 1,306,354 individuals (414,055 cases and 892,299 controls), 87 of the 102
associated variants were significant after multiple testing correction. These findings advance our
understanding of the complex genetic architecture of depression and provide several future
avenues for understanding etiology and developing new treatment approaches.
STUDIILE DE LABORATOR CONTRAZIC NOSOLOGIA PSIHIATRICA
NEUROPSIHOLOGIE CLINICA
NEUROPSIHOLOGIE CLINICA
Identification of risk loci with shared effects on five major psychiatric disorders: a
genome-wide analysis
Cross-Disorder Group of the Psychiatric Genomics Consortium
Findings from family and twin studies suggest that genetic contributions to
psychiatric disorders do not in all cases map to present diagnostic categories. We
aimed to identify specific variants underlying genetic effects shared between the
five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder,
attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder,
and schizophrenia. . Polygenic risk scores showed cross-disorder associations,
notably between adult-onset disorders. Pathway analysis supported a role for
calcium channel signalling genes for all five disorders. Finally, SNPs with evidence of
cross-disorder association were enriched for brain eQTL markers.
Our findings show that specific SNPs are associated with a range of psychiatric
disorders of childhood onset or adult onset. In particular, variation in calcium-
channel activity genes seems to have pleiotropic effects on psychopathology. These
results provide evidence relevant to the goal of moving beyond descriptive
NEUROPSIHOLOGIE CLINICA
Antidepressants are widely prescribed, but their efficacy relative to placebo is modest,
in part because the clinical diagnosis of major depression encompasses biologically
heterogeneous conditions. Here, we sought to identify a neurobiological signature of
response to antidepressant treatment as compared to placebo. We designed a latent-
space machine-learning algorithm tailored for resting-state electroencephalography
(EEG) and applied it to data from the largest imaging-coupled, placebo-controlled
antidepressant study (n = 309). Symptom improvement was robustly predicted in a
manner both specific for the antidepressant sertraline (versus placebo) and
generalizable across different study sites and EEG equipment. This sertraline-
predictive EEG signature generalized to two depression samples, wherein it reflected
general antidepressant medication responsivity and related differentially to a repetitive
transcranial magnetic stimulation treatment outcome. Furthermore, we found that the
sertraline resting-state EEG signature indexed prefrontal neural responsivity, as
measured by concurrent transcranial magnetic stimulation and EEG. Our findings
advance the neurobiological understanding of antidepressant treatment through an
EEG-tailored computational model and provide a clinical avenue for personalized
treatment of depression.
NEUROPSIHOLOGIE CLINICA
MACHINE LEARNING/BIG DATA DIAGNOSTIC AND PREDICTION
"In the future, we're not going to be saying, 'This patient has schizophrenia,' We're going to be
saying, 'This patient has this subtype' or 'this abnormal pattern,' rather than having a wide
umbrella under which everyone is categorised."
NEUROPSIHOLOGIE CLINICA
CONCLUZII
SI TOTUSI….
Molecular Psychiatry 19 November 2021
NEUROPSIHOLOGIE CLINICA
Putting the “mental” back in “mental disorders”: a
perspective from research on fear and anxiety