Tulburarea bipolara (TB), incluzand clasificari mai specifice, cum ar fi tulburarile bipolare I si bipolare II, este o afectiune caracterizata prin episoade de manie, hipomanie si/sau depresie [1]. Se crede ca afecteaza mai mult de 1% din populatia lumii si este considerata o cauza proeminenta a dizabilitatii la tineri [2]. Desi ramane neclar daca TB urmeaza un curs de dezvoltare in principal progresiv (adica neurodegenerativ), ceea ce este evident este ca probabilitatea deteriorarii functionale creste pe durata vietii unui individ [3, 4, 5]. Studiile neurocognitive sustin cel putin o contributie partiala neuroprogresiva la TB, cu disfunctia cognitiva considerata o trasatura bine documentata a starilor simptomatice si eutimice ale afectiunii [6, 7]. In contextul unei functionari intelectuale relativ conservate, disfunctiile executive si deficientele in memoria de lucru/atentie, viteza de procesare si invatarea verbala si memoria sunt cele mai frecvent enumerate deficiente la indivizii eutimici ce sufera de TB [6, 7, 8, 9].

In timp ce relatia dintre tulburarea cognitiva si TB este bine stabilita, etiologia si posibili moderatori ai acestei disfunctii sunt mai putin clare. Acest lucru este in continuare complicat de rata ridicata de comorbiditati la aceasta populatie, care poate avea si un impact negativ asupra cunoasterii, cum ar fi utilizarea substantei, respectarea slaba a tratamentului si sanatatea cardiovasculara compromisa [1, 10]. De exemplu, in timp ce unele meta-analize raporteaza asociatiile dintre tulburarile cognitive si variabilele de gravitate TB (de exemplu, durata bolii, numarul de episoade maniacale, numarul de spitalizari), altele nu gasesc astfel de asociatii [6, 10, 11]. Mai exact, in ceea ce priveste medicamentele antipsihotice, unii autori au raportat efecte negative asupra cognitiilor [6, 12], in timp ce autorii in favoarea unui model neuroprogresiv al TB considera ca medicamentele (de exemplu, litiu, acid valproic si antipsihotice atipice) pot fi de fapt neuroprotectoare in prezenirea cauzelor biochimice ale leziunilor neuronale [3].

Atat studiile neuroimagistice structurale cat si cele functionale au sporit intelegerea generala a neurofiziologiei TB, cu modificari ale dispozitiei considerate a fi rezultatul anomaliilor structurale si functionale in cadrul circuitelor striatal-talamo-prefrontal [13]. Studiile neuroimagistice structurale ofera o perspectiva specifica asupra surselor potentiale de disfunctie neurocognitiva, deoarece anumite anomalii structurale si reduceri ale volumului materiei cenusii (de exemplu, regiunile prefrontale, anterior cingulate și subgenuale) par sa devina mai evidente in timp [3, 4, 5, 13].

Directiile viitoare de cercetare privind relatia dintre disfunctia cognitiva si TB includ standardizarea procedurilor de testare neuropsihologica (de exemplu, Societatea Internationala pentru Tulburari Bipolare-Baterie pentru Evaluarea Neurocognitiei, ISBD-BANC [14]), variabilele TB (de exemplu, definirea/criteriile eutimiei) si praguri de afectare cognitiva pentru a reduce eterogenitatea in cadrul studiilor [6]. In plus, studiile de control randomizate pot furniza informatii suplimentare privind efectele tratamentului medicamentos si alte variabile cauzale asupra cognitiei [6, 15]. In mod specific, ramane neclar daca tratamentul timpuriu si lung cu medicamente, cum ar fi litiul, observat ca reduce moartea celulelor si creste volumul materiei cenusii, imbunatateste, de asemenea, functionarea cognitiva in timp [3, 4]. In cele din urma, cercetarea privind cognitia la adultii in varsta cu TB si studiile prospective care investigheaza modele de insuficienta cognitiva si declin pe toată durata vietii sunt limitate. O mai buna intelegere a disfunctiei cognitive la adultii in varsta, precum si a caracteristicilor neuroprogressive ale TB, va fi de ajutor in setarile clinice pentru diferentierea sursei de insuficienta cognitiva la persoanele mai in varsta diagnosticate cu tulburare bipolara.


Surse:

  1. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5®). American Psychiatric Pub.
  2. Grande, I., Berk, M., Birmaher, B., & Vieta, E. (2016). Bipolar disorder. The Lancet, 387(10027), 1561-1572. Link: https://www.ncbi.nlm.nih.gov/pubmed/26388529
  3. Berk, M. (2009). Neuroprogression: pathways to progressive brain changes in bipolar disorder. International Journal of Neuropsychopharmacology, 12(4), 441-445. Link: https://www.ncbi.nlm.nih.gov/pubmed/18922203
  4. Lim, C. S., Baldessarini, R. J., Vieta, E., Yucel, M., Bora, E., & Sim, K. (2013). Longitudinal neuroimaging and neuropsychological changes in bipolar disorder patients: review of the evidence. Neuroscience & Biobehavioral Reviews, 37(3), 418-435. Link: https://www.ncbi.nlm.nih.gov/pubmed/23318228
  5. Savitz, J. B., Price, J. L., & Drevets, W. C. (2014). Neuropathological and neuromorphometric abnormalities in bipolar disorder: view from the medial prefrontal cortical network. Neuroscience & Biobehavioral Reviews, 42, 132-147. Link: https://www.ncbi.nlm.nih.gov/pubmed/24603026
  6. Bourne, C., Aydemir, Ö., Balanzá‐Martínez, V., Bora, E., Brissos, S., Cavanagh, J. T. O., … & Ferrier, I. N. (2013). Neuropsychological testing of cognitive impairment in euthymic bipolar disorder: an individual patient data meta-analysis. Acta Psychiatrica Scandinavica, 128(3), 149-162. Link: http://onlinelibrary.wiley.com/doi/10.1111/acps.12133/full
  7. Quraishi, S., & Frangou, S. (2002). Neuropsychology of bipolar disorder: a review. Journal of affective disorders, 72(3), 209-226. Link: https://www.ncbi.nlm.nih.gov/pubmed/12450638
  8. Robinson, L. J., Thompson, J. M., Gallagher, P., Goswami, U., Young, A. H., Ferrier, I. N., & Moore, P. B. (2006). A meta-analysis of cognitive deficits in euthymic patients with bipolar disorder. Journal of affective disorders, 93(1), 105-115. Link: https://www.ncbi.nlm.nih.gov/pubmed/16677713
  9. Torres, I. J., Boudreau, V. G., & Yatham, L. N. (2007). Neuropsychological functioning in euthymic bipolar disorder: a meta‐ Acta Psychiatrica Scandinavica, 116(s434), 17-26. Link: https://www.ncbi.nlm.nih.gov/pubmed/17688459
  10. Cullen, B., Ward, J., Graham, N. A., Deary, I. J., Pell, J. P., Smith, D. J., & Evans, J. J. (2016). Prevalence and correlates of cognitive impairment in euthymic adults with bipolar disorder: A systematic review. Journal of Affective Disorders, 205, 165-181. Link: http://www.jad-journal.com/article/S0165-0327(16)30753-4/fulltext
  11. Robinson, L. J., & Nicol Ferrier, I. (2006). Evolution of cognitive impairment in bipolar disorder: a systematic review of cross‐sectional evidence. Bipolar disorders, 8(2), 103-116. Link: http://onlinelibrary.wiley.com/doi/10.1111/j.1399-5618.2006.00277.x/abstract
  12. Torrent, C., Martinez-Arán, A., Daban, C., Amann, B., Balanzá-Martínez, V., del Mar Bonnín, C., … & Vieta, E. (2011). Effects of atypical antipsychotics on neurocognition in euthymic bipolar patients. Comprehensive psychiatry, 52(6), 613-622. Link: https://www.ncbi.nlm.nih.gov/pubmed/21295774
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