Several studies have attempted to characterize morphological brain changes due to chronic pain. Although it has repeatedly been suggested that longstanding pain induces gray matter modifications, there is still some controversy surrounding the direction of the change (increase or decrease in gray matter) and the role of psychological and psychiatric comorbidities. In this study, we propose a novel, network-oriented, meta-analytic approach to characterize morphological changes in chronic pain. We used network decomposition to investigate whether different kinds of chronic pain are associated with a common or specific set of altered networks. Representational similarity techniques, network decomposition and model-based clustering were employed: i) to verify the presence of a core set of brain areas commonly modified by chronic pain; ii) to investigate the involvement of these areas in a large-scale network perspective; iii) to study the relationship between altered networks and; iv) to find out whether chronic pain targets clusters of areas. Our results showed that chronic pain causes both core and pathology-specific gray matter alterations in large-scale networks. Common alterations were observed in the prefrontal regions, in the anterior insula, cingulate cortex, basal ganglia, thalamus, periaqueductal gray, post- and pre-central gyri and inferior parietal lobule. We observed that the salience and attentional networks were targeted in a very similar way by different chronic pain pathologies. Conversely, alterations in the sensorimotor and attention circuits were differentially targeted by chronic pain pathologies. Moreover, model-based clustering revealed that chronic pain, in line with some neurodegenerative diseases, selectively targets some large-scale brain networks. Altogether these findings indicate that chronic pain can be better conceived and studied in a network perspective.

Mental adjustment to cancer has been explored in a large body of the literature by using the Mental Adjustment to Cancer (MAC) scale. Problems in the factor structure of the scale and the need for refining the instrument have determined the development of the Mini-MAC. The aim of this study was to validate, according to a test-oriented approach, the Italian version of the Mini-MAC. Four hundred and thirty cancer patients in five centres in Northern Italy completed the Mini-MAC and the Brief Symptom Inventory (BSI). A subgroup of 153 patients filled out the instruments again within 3 months of the first assessment. The five original subscales (Fighting Spirit, Hopeless, Fatalism, Anxious Preoccupation and Cognitive Avoidance) showed acceptable levels of reliability (Cronbach alpha coefficients ranging from 0.55 to 0.80) although alphas were lower for the scales Fighting Spirit and Fatalism. Factor analysis (Varimax rotation) identified the same five factors with minor variations from the original version. Again, alpha coefficients were less robust for the factors Fighting Sprit and Fatalism. Hopeless and Anxious Preoccupation were significantly related to all the BSI psychological stress symptoms, including the Global Stress Index (GSI). Test-retest reliability showed no differences in the sub-scales scores between assessments.

Despite growing information, questions still surround various aspects of post-stroke depression (PSD). The Italian multicenter observational study Destro was designed to help clarify in a large sample the frequency and clinical impact of PSD. A total of 53 centers consecutively admitted 1064 patients with ischemic or hemorrhagic stroke, assessing them periodically in the first 9 months after the event. Patients with depression were followed for two years. Depression was diagnosed on clinical examination, verbal (Beck Depression Inventory) and non-verbal rating systems (Visual Analog Mood Scale), identifying the nosographic condition attributable to the mental state. The patient's clinical history, residual independence, and post-ictus quality of life were also taken into account. PSD was detected in 383 patients (36 %), most of whom had minor depression (80.17 %), with dysthymia, rather than major depression and adaptation disorder. About 80% developed depression within three months of the stroke. Cases with later onset tended to have less severe symptoms. Risk factors were a history of depression, severe disability, previous stroke and female sex, but not the type and site of the vascular lesion. PSD was not correlated with any increase in mortality or cerebrovascular recurrences, but these patients had lower autonomy and quality of life ratings. In conclusion, patients should be close observed in the first few weeks after a stroke in order to check for depression,which is more likely in those with clear risk factors and may spoil their quality of life.

Summary: This chapter deals with some aspects of psychiatric disturbances in people with epilepsy. Because depression and its treatment are extensively described later in this issue, they are not discussed here. The same pertains to forced normalization. Key Words: Epilepsy-Anxiety-PsychosisDepress ion-Qua1 i ty of 1 i fe-Ps e u do s ei zure s-A n t idepressants-Antipsychotics-Antiepileptic drugs.Although most people with epilepsy lead a normal emotional and cognitive life, neurobehavioral problems can be found in a large number of patients. Higher rates of psychopathology are observed in people with epilepsy relative to the general population (1,2), to other neurologic control groups (3), and to people with chronic nonneurologic disorders (1,4). In particular, increased psychopathology is more common in temporal lobe epilepsy (TLE) than in generalized epilepsy (5). Nevertheless, many issues remain highly controversial, owing in part to several methodologic problems, such as the nosographic approach, the sample examined, the type of control groups, the comparison among nonhomogeneous forms of epilepsy, and the different antiepileptic drugs (AEDs).Psychiatric disturbances can be related either to involvement of brain structures (biologic pathogenesis) or to the chronic characteristics of epilepsy (psychosocial pathogenesis). These psychiatric symptoms may develop in relationship to the seizures (in prodromal, ictal, or postictal periods) but more commonly are present in a chronic interictal condition.The wide range of clinical diversity is related to the anatomic foci, to patterns of spread, and to biologic or psychological differences among patients. Interictal behavioral changes in epilepsy remain controversial and difficult to define, mainly because pathogenesis may be attributable to several factors, such as epilepsy itself, possible brain lesions, the AEDs prescribed, and psychosocial problems (6). On the other hand, the existence of cognitive changes in epilepsy is well established, and Addrress correspondence and reprint requests to Dr. Riccardo Tom at Dipartimento di Neuroscienze, via Cherasco 11, 10126 Torino, Italy.sometimes the presence of cognitive disorders can facilitate the appearance of psychiatric disturbances (7).One of the most widely discussed problems is the incidence of psychiatric pathology in epilepsy, with a wide range of values in the literature related to the type of study. Epilepsy is characterized by a broad spectrum of severity. Ideally, patients for study trials should be selected consecutively from a general epilepsy population, but most epidemiologic studies are carried out in centers for epilepsy and include many refractory subjects who demonstrate a range of pathologic disturbances more severe than those observed in the general population of patients with epilepsy. In community studies, the prevalence of associated psychiatric disorders is low, whereas in specialty referral centers, particularly those serving indigent populations, the prevalence can rise to 25-50%: Among patient...

The objective of this study is to investigate if changes in cognitive functions can be recognised in patients undergoing chemotherapy for breast cancer. Forty women with breast cancer and without depression underwent cognitive evaluation before and after 6 months of chemotherapy; emotional evaluation was performed before and after 1, 3 and 6 months of chemotherapy. Self-reported cognitive deficit evaluation was included. Global cognitive functioning before starting chemotherapy was good. After 6 months of treatment there was a significant decline in some cognitive functions, particularly involving the attention subdomain. Objective cognitive deficit resulted independent from the emotional status. On the contrary, self-perceived mental dysfunction was unrelated to the objective cognitive decline, but it was associated with depression and anxiety. Breast cancer chemotherapy can induce domain-specific cognitive dysfunction. Patients' self-perception of mental decline is unrelated to objective cognitive deficit. Breast cancer patients negatively judge their cognitive performances if they have a negative emotional functioning.