We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save this undefined to your undefined account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you used this feature, you will be asked to authorise Cambridge Core to connect with your undefined account.
Find out more about saving content to .
To save this article to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Quality of life (QoL) is a growing issue in medicine, particularly in the
evaluation of rehabilitative care. The concept of QoL is included in and expands
the definition of health given by the WHO (World Health Organization) and
comprises complete physical, mental, and social well-being. It expresses the
degree of satisfaction in various areas as a result of the opportunities that
arise during one's lifetime despite the restrictions and impediments that life
itself puts forth. The last decade has exponentially increased the number of
studies on QoL, although they are still limited.
Methods
We performed a literature review on the QoL scales used in patients with
neurological disorders.
Results
Recent studies have shown the importance of QoL assessment because standard
treatments do not assess the treatment impact felt by the patient. In fact, by
understanding the impact of treatment on survival and QoL, one can make a clearer
interpretation of the health of the patient.
Conclusion
This review has adopted an innovative holistic methodological approach, which
allowed a global evaluation of the comfort reported by the patients. The scales
applied in this study allowed to choose the most suitable therapeutic strategies
and programme individual therapeutic treatment.
The main aim of the present study was to replicate a previous finding in major depressive disorder (MDD) of association between reduced hippocampal volume and the long variant of the di- and triallelic serotonin transporter polymorphism in SLC6A4 on chromosome 17q11.2. Secondarily, we also hypothesised that 5-HTTLPR may be a risk factor for MDD.
Methods
Quantitative magnetic resonance imaging (MRI) of the hippocampus was studied in 23 inpatients suffering from MDD and in 33 healthy controls. Normalised volumetric MRI data of hippocampus were assessed with adjustment for total brain volume and tensor-based morphometry was used to elucidate structural brain differences. A triallelic genetic marker resulting from two SLC6A4 promoter region polymorphisms, 5-HTTLPR and rs25531, was analysed for association with MDD and quantitative traits.
Results
Healthy controls had a smaller relative hippocampal volume (relative to brain size) but a larger total brain volume compared with patients with MDD. For patients compared with healthy controls, atrophy was found in the right temporal lobe and pons medulla. Allele and genotype frequencies were strikingly different from the previous study that we aimed to replicate, and no significant associations with the serotonin transporter polymorphism were found.
Conclusions
The present quantitative and morphometric MRI study was not able to replicate the previous finding of association between reduced hippocampal volume in depressed patients and the serotonin transporter polymorphism.
Glycine regulates glutamatergic neurotransmission, and several papers have reported the relationship between glycine and schizophrenia. The dysbindin-1 (DTNBP1: dystrobrevin-binding protein 1) gene is related to glutamatergic neurotransmission and has been found to be a strong candidate gene for schizophrenia. In this study, we clarified the relationship between dysbindin, glutamate, and glycine with in vivo microdialysis methods.
Methods
We measured extracellular glycine and glutamate levels in the striatum of sandy (sdy) mice using in vivo microdialysis methods. Sdy mice express no dysbindin protein owing to a deletion in the dysbindin-1 gene. In addition, we measured changes in those amino acids after methamphetamine (METH) administration.
Results
The basal levels of extracellular glycine and glutamate in the striatum of sdy mice were elevated. These extracellular glutamate levels decreased gradually after METH administration and were not subsequently different from those of wild-type mice.
Conclusions
These results suggest that dysbindin might modulate glycine and glutamate release in vivo.
There has been increasing evidence that the γ-aminobutyric acid (GABA)ergic system is involved in the neurobiology of anxiety. The present study aimed to investigate the role of GABAergic systems in the modulation of anxiety in the medial prefrontal cortex (mPFC) of rats using the elevated plus maze test.
Methods
Rats were anaesthetised with a mixture of ketamine and xylazine, and then special cannulae were inserted stereotaxically into the mPFC. After 5–7 days of recovery, the effects of intra-mPFC administration of GABAergic agents were studied.
Results
Bilateral injection of the GABAA receptor agonist muscimol (0.25, 0.5 and 1 μg/rat) produces an anxiolytic-like effect, shown by significant increases in the percentage of open-arm time (%OAT) and percentage of open-arm entries (%OAE). Intra-mPFC administration of the GABAA receptor antagonist bicuculline (0.25, 0.5 and 1 μg/rat) produces significant anxiogenic-like behaviour. However, intra-mPFC injection of the GABAB receptor agonist baclofen (0.05, 0.1 and 0.2 μg/rat) and the GABAB receptor antagonist CGP35348 (5, 10 and 15 μg/rat) did not alter %OAT and %OAE significantly.
Conclusion
The results of the present study demonstrate that the GABAergic system of the mPFC modulates anxiety-related behaviours of rats through GABAA receptors.
Comorbid personality pathologies may affect the outcome of patients with major depression (MD). The dopamine transporter gene DAT1 (SLC6A3) has been suggested to play a role in both depression and specific personality traits. The aim of this study was to assess five polymorphisms of the DAT1 gene (rs2550948, rs2975226, rs6347, rs27072, and 3′-VNTR) to determine whether this gene influences personality traits in patients with MD or its subgroups.
Methods
The DAT1 polymorphisms were analysed in 463 unrelated Han Chinese MD patients. The personality traits, novelty seeking (NS), and harm avoidance (HA), were examined using the Tridimensional Personality Questionnaire. The patients were also divided into four clinical subgroups on the basis of differences in their sex (male or female) and age at disease onset (early or late).
Results
There was no association between the DAT1 gene and either NS or HA in the total MD sample or in the sex-based subgroups. However, early-onset MD patients with the G/G genotype of rs2550948 and the T/T genotype of rs2975226 had lower NS scores than did patients with the other genotypes (pcorrected = 0.05 for rs2550948 and pcorrected = 0.005 for rs2975226).
Conclusion
Our study suggests that DAT1 promoter variants possibly influence specific personality traits in the early-onset subgroup of depressed patients in the Han Chinese population. Further prospective cohort studies are required to verify our preliminary finding and to confirm the effects of personality susceptibility on long-term disease outcomes.
Methylphenidate (MPD) is a drug prescribed for the treatment of attention deficit/hyperactivity disorder and its therapeutic effect is attributed to the inhibition of dopamine.
Methods
Young male Wistar rats were administered MPD (1, 2, 5, or 10 mg/kg) once a day or an intraperitoneal injection of saline for 28 days (chronic treatment) or for 1 day (acute treatment). Two hours after the last administration the animals were decapitated and their striatum was dissected.
Results
In this work, we show that continued treatment with MPD is capable of modifying the levels of phosphorylation of proteins JNK1/2 (c-Jun amino-terminal kinases 1 and 2) and ERK1/2 (extracellular signal-regulated kinases 1 and 2). Whereas the level of phosphorylation of protein ERK increased significantly, that of proteins JNK1/2 diminished.
Conclusion
The alteration in the level of activation of mitogen-activated protein kinases can be a molecular mechanism through which MPD exerts its therapeutic effect.
Intracranial epidermoid cysts are congenital cysts. They comprise 0.2–1.8% of primary intracranial tumours and are four to nine times as common as dermoid cysts.
Case report
We here in present the case of a 32-year-old man who reported sudden onset of symptoms of a depressive symptomatology and particularly severe headache, accompanied by fatigue, depressed mood most of the day, marked diminished interest or pleasure in all or almost all activities, insomnia and diminished ability to think or concentrate. Brain magnetic resolution imaging examination revealed a pineal epidermoid cystic lesion, visualised in the posterior part of the third ventricle, with a maximum diameter of ∼2.8 cm and obstructing the aqueduct of Sylvius, causing obstructive hydrocephalus.
Discussion
Pineal cysts may enlarge over time, because of either increased cyst fluid or intracystic haemorrhage, and become symptomatic. Brain radiological investigations in patients with depressive symptomatology may be substantial.
Marfan syndrome (MFS) is an autosomal dominant disorder of fibrillin-1 gene mutations, with the involvement of cardiovascular, skeletal, and ocular systems. In addition to physical abnormalities, MFS patients are also found to be susceptible to schizophrenia and other psychiatric conditions.
Objectives
Awareness of the association between MFS and psychiatric conditions would improve the clinical management of MFS patients to reduce the risk or even to prevent the development of psychiatric complications in MFS patients.
Methods
Here, we describe a male MFS patient who manifested incoherent speech and impaired cognitive and social function at the age of 40 years.
Results and conclusion
His mental dysfunction could be attributed to his bilateral cerebral infarction, which is a neurovascular complication associated with MFS.
The differentiation between a ‘non-organic’ depressive episode and an organic depressive disorder on the basis of clinical grounds might be challenging.
Methods
We report a case with an initially typical severe depressive episode without any focal neurological deficits.
Results
Only medical history from a third party raised doubts about this provisional diagnosis. Brain magnetic resonance imaging revealed a highly malignant diffuse large intracerebral B-cell lymphoma in the right frontal lobe changing the diagnosis into an organic depressive disorder. The patient recovered after neurosurgical resection, chemotherapy and autologous stem cell transplantation.
Conclusion
This report helps to reduce possible errors in the differential diagnosis of depressive disorders by underlining the importance of a comprehensive medical history including anamnesis from a third party and neuroimaging, especially in first or atypical manifestation of depressive disorders.