| Abstract | Anksioznost ili tjeskoba je normalna reakcija čovjeka na stresne i ugrožavajuće
događaje u njegovoj okolini, ali ukoliko intenzitetom i duljinom trajanja ne korelira s
inducibilnim podražajem te trajno narušava sposobnost čovjekova funkcioniranja, riječ je o
patološkoj anksioznosti, odnosno simptomu jednog od anksioznih poremećaja klasificiranih u
10. reviziji Međunarodne klasifikacije bolesti (MKB-X), odnosno klasifikaciji Američke
Psihijatrijske Asocijacije, DSM –IV. Etiologiju anksioznosti možemo zasebno razmatrati s
psihodinamskog, biologijskog i neuroznanstvenog aspekta. Temelje psihodinamskog,
odnosno psihoanalitičkog aspekta pojave tjeskobe postavio je Sigmund Freud postulatima o
tripartitnoj mentalnoj strukturi ličnosti te nastanku intrapersonalnih konflikata putem faza
psihoseksualnog razvoja koji u konačnici dovode do pojave anksioznosti. Njegove temelje
nadograđivali su brojni psihoanalitičari XX. stoljeća, od Adlera, Junga, Fromma te M. Klein i
Fairbairna kao začetnika teorije objektnih odnosa. Ako razmatramo biologijske aspekte
razvoja tjeskobe, nužno je poznavanje fiziologije mozga i uloge sustava neurotransmitera i
neuromodulatora. Najveći broj spoznaja temeljenih na farmakološkim ispitivanjima ukazuje
na hiperaktivnost noradrenergičke jezgre locus coeruleus i noradrenergičkih neuronskih
putova središnjeg živčanog sustava te smanjene aktivnosti serotoninergičkih i inhibicijskih
gabaergičkih neuronskih sustava kao ishodišnih uzročnih točaka u somatskoj i psihološkoj
simptomatologiji anksioznih poremećaja. Napretkom neuroznanosti točno su locirane regije,
strukture i mreže neuronskih krugova središnjeg živčanog sustava odgovorne za pohranu,
integriranje i kondicioniranje osjećaja straha i posljedičnih somatskih manifestacija vezanih
uz prijeteće podražaje, ali i ispoljavanje straha i pojavu tjeskobe vezane uz određeni, s
prijašnjim podražajem, vezanim kontekstom. Te neuroznanstvene spoznaje temeljene su na
Pavlovljevom modelu klasičnog kondicioniranja, a moderne neuroimaging tehnike locirale su
Papezov krug, limbički sustav i kompleks jezgara amygdala kao glavne strukture odgovorne
za procese učenja i kondicioniranja straha. U konačnici, locirani su i pojedini geni čija
varijabilnost u ekspresiji neurona „visceralnog mozga“ modulira upamćivanje straha i
somatskih anksioznih reakcija te predstavljaju potencijalna ciljna mjesta za nova
farmakoterapijska rješenja u liječenju anksioznih i ostalih s tjeskobom vezanih psihičkih
poremećaja. |
| Abstract (english) | Anxiety is a normal human reaction to stressful and threatening events in their
surroundings but if it doesn’t correlate with inducible stimulus in respect to intensity and
duration and if it permanently impairs person’s ability to function normally then we are
dealing with pathological anxiety, that is to say, a symptom of one of the anxiety disorders
classified in 10th revision of The International Classification of Diseases (ICD-10) or in
classification by American Psychiatric Association, DSM-IV. We may consider the etiology
of anxiety from psychodynamic, biological and neuroscientific aspect. The foundation of the
psychodynamic or psychoanalytic aspect was set by Sigmund Freud through his postulates
about tripartite mental structure of personality and ways of forming intrapersonal conflicts in
the course of person’s psychosexual development which finally lead to anxiety. His
groundwork was furthered by numerous 20th century psychoanalytics such as Adler, Jung,
Fromm, M. Klein and Fairbairn, the latter two having formed the object relations theory. If we
consider the biological aspects of anxiety development we need to be familiar with the
physiology of the brain and the role of the neurotransmitter and neuromodulator system. The
most of our findings based on pharmacological research point to the hyperactivity of the
noradrenergic core locus coeruleus and noradrenergic neuron pathways of the central nervous
system as well as reduced activity of serotonin and inhibitory gabaergic neuron systems which
are considered starting points for the causes in somatic and psychological symptomatology of
anxiety disorders. Due to the advancement of neuroscience we can pinpoint regions,
structures and networks of neuron circles of the central nervous system which are responsible
not only for storing, integrating and conditioning the feeling of fear and the consequent
somatic manifestations associated with threatening stimuli, but also for the overt expressions
of fear and the appearance of anxiety as a result of two contextually bound stimuli. These
neuroscientific insights are based on the Pavlovian (classical) conditioning. Modern
neuroimaging techniques have located Papez circuit, limbic system and the complex of
amygdala cores which is the primary structure responsible for the processes of learning and
fear conditioning. Finally, certain genes have been located, the variability of which in
expression of ‘visceral brain’ neurons modulates remembrance of fear and somatic reactions
to anxiety. These genes also represent the potential focal points for future
pharmacotherapeutic solutions for the treatment of anxiety and anxiety-connected psychic
disorders. |
