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Awareness of illness is a form of self-knowledge concerning information about the pathological state, its functional consequence, and the way it affects the patient and his interaction with the environment. Unawareness of illness has raised much interest for its consequences on compliance with treatment, prognosis, and the patient's quality of life. This review highlights the great complexity of this phenomenon both at phenomenological and etiopathogenic levels in stroke, traumatic brain injury, psychosis, dementias, and mood disorders. In particular, the clinical expression is characterized by failure to acknowledge being ill, misattribution of symptoms, and noncompliance with treatment. Unawareness of illness may also be linked with characteristics that are peculiar to each individual disturbance, such as symptom duration and cognitive impairment. Despite a long-lasting interest in the clinical characteristics of unawareness, only recently has the focus of research investigated pathogenic mechanisms, with sometimes controversial results. The vast majority of studies have pointed out a remarkable involvement of the right hemisphere. Specifically, functional and structural changes of the dorso-lateral prefrontal cortex and some other frontal areas have often been found to be associated with awareness deficit, as well as parieto-temporal areas and the thalamus, although to a lesser extent. These data indicate the present difficulty of localizing a specific cerebral area involved in unawareness and suggest the existence of possible brain circuits responsible for awareness. In conclusion, phenomenological manifestations of poor awareness are well outlined in their complexity, whereas neuroanatomic and neuropsychological findings are still too vague and sparse and need further, greater efforts to be clarified. [ABSTRACT FROM AUTHOR]

Chronic cocaine and heroin users display a variety of central nervous system (CNS) dysfunctions including impaired attention, teaming, memory, reaction time, cognitive flexibility, impulse control and selective processing. These findings suggest that these drugs may alter normal brain functions and possibly cause neurotoxicity. Neurotrophins are a class of proteins that serve as survival factors for CNS neurons. In particular, nerve growth factor (NGF) prays an important role in the survivor and function of cholinergic neurons white brain-derived neurotrophic factor (BDNF) is involved in synaptic plasticity and in the maintenance of midbrain dopaminergic and cholinergic neurons. In the present study, we measured by enzyme-linked immunosorbent assay (ELISA) the NGF and BDNF levels in serum of three groups of subjects: heroin-dependent patients, cocaine-dependent patients and healthy volunteers. Our goat was to identify possible change in serum neurotrophins in heroin and cocaine users. BDNF was decreased in heroin users whereas NGF was decreased in both heroin and cocaine users. These findings indicate that NGF and BDNF may play a rote in the neurotoxicity and addiction induced by these drugs. In view of the neurotrophin hypothesis of schizophrenia the data also suggest that reduced fever of neurotrophins may increase the risk of developing psychosis in drug users. [ABSTRACT FROM AUTHOR]

A number of studies have demonstrated that affective disorders in epilepsy represent a common psychiatric comorbidity; however, most of the classic neuropsychiatric literature focuses on depression, which is actually prominent, but little is known about bipolar depression, and very little about mania, in epilepsy. Biochemical, structural, and functional abnormalities in primary bipolar disorder could also occur secondary to seizure disorders. The kindling paradigm, invoked as a model for understanding seizure disorders, has also been applied to the episodic nature of bipolar disorder. In bipolar patients, changes in second-messenger systems, such as G-proteins, phosphatidylinositol, protein kinase C, myristoylated alanine-rich C kinase substrate, or calcium activity have been described, along with changes in c-fos expression. Common mechanisms at the level of ion channels might include the antikindling and the calcium-antagonistic and potassium outward current-modulating properties of antiepileptic drugs. All these lines of research appear to be converging on a richer understanding of neurobiologica[ underpinnings between bipolar disorder and epilepsy. Mania, which is the other side of the coin in affective disorders, may represent a privileged window into the neurobiology of mood regulation and the neurobiology of epilepsy itself. Future research on intracellular mechanisms might become decisive for a better understanding of the similarities between these two disorders. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article concerning the use of oxcarbazepine (OXC) in the treatment of bipolar disorder (BD) headed by W. Pratoomsri in the previous issue.