Scielo RSS <![CDATA[The European Journal of Psychiatry]]> vol. 20 num. 2 lang. es <![CDATA[SciELO Logo]]> <![CDATA[The neuropsychiatry in the age of subspecialization]]> <![CDATA[Lesion Location in Depression Post Traumatic Brain Injury Using Magnetic Resonance Spectroscopy: Preliminary Results from a Pilot Study]]> OBJECTIVE: To determine the metabolic status of the brain in post traumatic brain injury(TBI) depression using proton magnetic resonance spectroscopy (MRS). DESIGN: Case-control study including 5 TBI depressed subjects and 5 age matched non-TBI non-depressed controls. METHODS: Metabolic status was assessed using proton MRS. Ratios of N-acetylaspartate (NAA), choline (Cho) and total creatine (Cr) were calculated in frontal cortex, basal ganglia and thalamus. RESULTS: NAA/Cho or NAA/Cr ratios were significantly reduced in the TBI depressed group compared to controls in frontal cortex, basal ganglia and thalamus. CONCLUSION: Reduced levels of NAA in frontal regions, basal ganglia and thalamus in TBI depression suggest neuronal damage or dysfunction which may be a associated with the primary brain injury or with depressed mood. <![CDATA[ApolipoproteinE ε4 allelic variant, cognitive decline and psychosis in Alzheimer disease: a review of the literature and suggestions for upcoming studies]]> Apolipoprotein E (ApoE) ε4 allele represents a well known vascular risk factor for developing Alzheimer disease (AD) and differences in ApoE genotypes may explain a part of the variability in AD phenotypes. In fact, ApoE ε4 allele possession seems to be associated with a more precocious age of onset, greater episodic memory impairment, and psychotic symptoms. The first question we discuss regards the role of ApoE ε4 on cognitive progression of AD. In fact, while a general agreement exists about the role played by ApoE ε4 on the precocious onset of AD, cognitive decline has been differently associated with ApoE ε4 allele possession in AD patients in a continuum of faster decline, no effect, and slower decline. An attemptable interpretation is that the biological processes leading to the onset of AD are different from those involved in determining its clinical course. The second question regards the possible relationship between the presence of the degenerative pathological hallmarks of the disease in specific cerebral areas and different cognitive or behavioural symptoms. In fact, there is evidence that degenerative pathology in hippocampal formation and frontal cortex reflects the progression of cognitive deficits in brain aging and AD and that hypometabolism in right frontal lobe and greater frontal neuropsychological deficits occur in AD patients with psychosis in comparison to those without. The third question regards, specifically, the relationship between ApoE ε4 variant and behavioural symptoms. In fact, there is evidence supporting the link between being carriers of ApoE ε4 allele and severity of delusions, mostly at the early stage of the illness. In an interpretative challenge, we suggest that the link between being carriers of ApoE ε4 allele and suffering from delusions in AD may be explained by frontal lobe dysfunctions. Finally, we hypothesize that the most precocious onset of AD illness, described in carriers of ApoE ε4 allelic variant, may also be related to the precocious onset of psychotic symptoms, which produces caregiver and patient distress and requires immediate assessment and treatment. <![CDATA[The Role of the Mammillary Bodies in Memory: A Case of Amnesia Following Bilateral Resection]]> BACKGROUND AND OBJECTIVES: Craniopharyngioma (CP) patients typically show good neuropsychiatric outcome following tumor resection. We present the case of a 51-year old woman who sustained damage to white matter pathways during surgery resulting in a disconnection of the Papez circuit (loss of bilateral mammillary bodies, columns of the fornix and mammillothalamic tracts). METHODS AND RESULTS: Neuropsychological evaluations were completed at 10 and 30 weeks post-operatively, and indicated both retrograde and severe anterograde amnesia, as well as persistent depression. At the second evaluation, most cognitive deficits had improved, but memory and mood deficits remained. Metamemory and priming remained intact. CONCLUSIONS: This case illustrates a profound neuropsychiatric morbidity associated with a surgery that is typically considered benign and confirms the well-known dissociation between explicit recollection of newly learned information and less conscious forms of learning and memory. This rare pathology provides further information regarding the role of the mammillary bodies in memory. <![CDATA[The prevalence, clinical correlates and treatment of apathy in Alzheimer's disease]]> The aim for this article is to review the frequency, clinical correlates and treatment of apathy in Alzheimer's disease. Apathy is currently defined as diminished motivation as expressed in poor goal-oriented behaviours and cognitions. A structured clinical interview and a specific set of diagnostic criteria to diagnose apathy in dementia have been recently validated. There are several valid and reliable scales to measure the severity of apathy in adults with neuropsychiatric disorders. Apathy is present in about 20% of patients with mild dementia and in 60% of those with severe dementia. Among patients with Alzheimer's disease, apathy is significantly associated with older age, the presence of depression, and more severe cognitive and functional deficits, and also predicts a faster cognitive and functional decline. The mechanism of apathy in neuropsychiatric disorders is still unknown, but several studies suggest an important role for frontal lobe and basal ganglia dysfunction. There are no specific randomized controlled trials of psychoactive compounds to treat apathy in neuropsychiatric disorders. Evidence from case reports and small case series suggest the usefulness of psychostimulants to treat apathy in traumatic brain injury, whereas pharmacological trials for behavioural and psychological problems in dementia suggest that anticholinesterases may have some efficacy. <![CDATA[The Neuropsychiatry of Hematopoietic Stem Cell Transplantation]]> BACKGROUND AND OBJECTIVES: Regimens incorporating hematopoietic stem cell transplantation (HSCT) have become widely utilized in disease treatments, particularly for cancer. These complex treatment programs also expose patients to central nervous system (CNS) toxicities from chemotherapy, irradiation, infection, metabolic effects and immunosuppression. METHODS: Relevant recent medical literature from Medline and bibliographies in pertinent publications are reviewed with a focus on those cases and studies pertaining to neuropsychiatric effects of HSCT. RESULTS: High rates of neuropsychiatric sequelae occur on a continuum from acute to chronic. Adverse outcomes include focal CNS deficits and severe global manifestations such as seizures, encephalopathy and delirium. More graduated effects on cognition, energy and mood are frequently seen, impacting patient function. CONCLUSIONS: Additional research on neuropsychiatric outcomes and treatment interventions is needed in the HSCT setting. Risks for neuropsychiatric deficits should be part of an ongoing informed consent discussion among treating physicians, patients and families.