• Natural catastrophe
• Neurobiology
• Neuroplasticity
• Neurotrophins
• Post-traumatic stress disorder
• Stress
• Subthreshold symptoms

Disasters such as earthquakes are events that affect wide populations causing widespread consequences including psychosocial disruption, physical threat, massive psychological stress. Mental health professionals have been increasingly called upon to assist during these acute crises.
Disasters deserve special attention among human traumas because the capacity to traumatize a great many individuals at once, being the most public of traumas, and thus offering unique opportunities to study human response to tragedy on any level. Because natural disasters are random events that expose unselected populations to trauma, they offer unique opportunities for researchers interested in studying subjects ‘triggered’ to a unique trauma, disentangling confounding issues of pre-existing risk for exposure to traumatic events.
On April 6th 2009, at 3:32 am, an earthquake (Richter Magnitude 6.3) struck L’Aquila, Italy, a town with a population of 72,000 and a ‘local health’ (i.e. Azienda Sanitaria Locale) of 105,000 inhabitants. L’Aquila earthquake caused the death of 309 people, with more than 1600 individuals injured, among which 200 were severely injured and hospitalized, and 66,000 displaced. Many buildings collapsed in the town of L’Aquila: large parts of it were completely destroyed.
In this thesis psychoneurobiology of stress caused by this traumatic event has been investigated through three studies on Brain-Derived Neurotrophic Factor (BDNF). The BDNF is a key mediator of neuronal plasticity, which stimulate a variety of cellular effects at the structural and functional levels that eventuate in the promotion of survival and differentiation of responsive neurons. Stress has been widely linked with alterations in the expression and functioning of BDNF in both animal and human clinical studies.
The aim of the first study was to investigate plasma BDNF levels in a clinical population who survived to the L'Aquila 2009 earthquake, along with the post-traumatic spectrum that considers not only full expression of Post-Traumatic Stress Disorder (PTSD) but also subthreshold manifestations such as partial PTSD. To do so a consecutive sample of 37 outpatients referring to the National Mental Health Care Service in L’Aquila for anxiety or affective symptoms after the earthquake, was compared to 15 healthy controls matched for age and gender. Eleven patients were diagnosed as not having PTSD but a different pathological condition that justified the referral and 13 patients respectively were diagnosed as showing Full or Partial PTSD. The subjects without PTSD, but with anxiety or affective disorders, and subjects with full-blown PTSD showed lower BDNF level than subjects with partial PTSD and healthy controls.
The aim of the second study was to investigate the clinical correlates of plasma BDNF levels in a clinical population showing PTSD symptomatology, along with the post-traumatic spectrum. Assessments included: Structured Clinical Interview for DSM-IV Axis-I disorders Patient Version, Trauma and Loss Spectrum-Self Report (TALS-SR) for post-traumatic spectrum symptoms and the Impact of Event Scale Revised (IES-R) for the PTSD symptomatology. Thirteen patients were diagnosed as showing Full PTSD and 13 Partial PTSD. Different relationship pattern of BDNF vs. stress symptoms has been reported in partial and full PTSD samples.
In the third study BDNF modifications in subjects that did not showed psychiatric symptoms or symptoms worsening despite having suffered relevant stress event have been investigated. We hypothesized that, in so far as no stress consequences or relapse/worsening appeared in subjects who suffered relevant stress, any BDNF variation could be due to stress exposure. To do so BDNF plasma levels have been evaluated in subjects who suffered the same stress event, i.e. a clinical and non clinical population exposed to the 2009 L’Aquila earthquake, in comparison to a population not exposed to relevant stress. Statistical difference has been observed for diagnosis factor (clinical samples vs. controls). A trend toward significance was seen for exposition factor (exposed vs. not exposed subjects); exposition by diagnosis interaction did not reach statistical significance. The exposed clinical sample showed significant higher BDNF level than the not exposed. Lack of statistical difference between exposed and not exposed subjects suggests that no BDNF modification intervened after the stressful event, but: exposed samples show the highest BDNF levels and a trend toward significance was seen; possibility of a ceiling effect, with no possibility of exceed a possible maximum level in the control sample can be considered. Clinical sample shows instead room for stress related BDNF increase. If so a BDNF increase with neuroprotective adaptive aim after stress cannot be excluded.
The findings of these studies add more insight on the mechanisms regulating BDNF levels in response to stress and further proofs on the utility of the distinction of PTSD into full and partial categories along the spectrum approach.