Male–female differences in left-handedness in Sardinia,Italy

Males were consistently found to be more likely than females to report left-hand preference in single-hand tasks, but the literature reports negative results too. Using data from a large sample in Sardinia, we aimed at testing the links of left-handedness with sex, age, residence, and seasonality of birth. A total of 4239 participants (males = 1589; females = 2650) were recruited in public places such as high schools, university classes, or gyms in one of the major islands of Italy. Hand preference was established with the question: Which hand do you normally use to write legibly? The monthly distribution of births was studied with the Rayleigh test. In the sample, 270 female participants reported left-hand preference in writing (10.2%) versus 161 male participants (10.1%). Left-hand preference in writing was negatively related to age, with increasing left-hand preference in the younger generations. Left-hand preference in writing was not more common in urban than in suburban or rural settings. The month of birth was found to have a seasonal effect on the left-handed (p=.031) but not on the right-handed (p=.80) participants, and this seasonal effect was more evident in males (p=.04) than in females (p =.26). In our sample males were not more likely to report left-hand preference in writing than females. On the other hand, left-hand preference does vary by age and, in all likelihood, this is an effect of the reduced cultural pressure to write with the right hand in the younger generations.     

Involvement of the α<Subscript>1D</Subscript>-adrenergic Receptor in Methamphetamine-Induced Hyperthermia and Neurotoxicity in Rats

Methamphetamine (METH) is a psychostimulant that damages nigrostriatal dopaminergic terminals, primarily by enhancing dopamine and glutamate release. α₁-adrenergic receptor (AR) subtype involved in METH-induced neurotoxicity in rats was investigated using selective α₁-AR antagonists. METH neurotoxicity was evaluated by (1) measuring body temperature; (2) determining tyrosine hydroxylase (TH) immunoreactivity levels; (3) examining levels of dopamine and its metabolites; and (4) assessing glial fibrillary acidic protein (GFAP) and microglial immunoreactivity in the striatum. METH caused a decrease in dopamine and TH levels and induced hyperthermia which is an exacerbating factor of METH neurotoxicity. Concurrently, METH increased GFAP expression and the number of activated microglia. Pretreatment with prazosin, a nonselective α₁-AR antagonist, completely abolished METH-induced decrease in both dopamine and TH and caused a partial reduction in hyperthermia. Prazosin also prevented METH-induced increase in both GFAP expression and the number of activated microglia. In vivo microdialysis analysis revealed that prazosin, however, does not alter the METH-induced dopamine release in the striatum. The neuroprotective effects of prazosin could be mimicked by a selective α_1D antagonist, BMY 7378, but not by selective α_1A or α_1B antagonists. These results suggest that the α_1D-AR is involved in METH-induced hyperthermia and neurotoxicity in rats.     

Dural haemorrhage in non‐traumatic infant deaths: does it explain the bleeding in ‘shaken baby syndrome’?

A histological review of dura mater taken from a post-mortem series of 50 paediatric cases aged up to 5 months revealed fresh bleeding in the dura in 36/50, the bleeding ranging from small perivascular haemorrhages to extensive haemorrhage which had ruptured onto the surface of the dura. Severe hypoxia had been documented clinically in 27 of the 36 cases (75%). In a similar review of three infants presenting with classical 'shaken baby syndrome', intradural haemorrhage was also found, in addition to subdural bleeding, and we believe that our findings may have relevance to the pathogenesis of some infantile subdural haemorrhage. Recent work has shown that, in a proportion of infants with fatal head injury, there is little traumatic brain damage and that the significant finding is craniocervical injury, which causes respiratory abnormalities, severe global hypoxia and brain swelling, with raised intracranial pressure. We propose that, in such infants, a combination of severe hypoxia, brain swelling and raised central venous pressure causes blood to leak from intracranial veins into the subdural space, and that the cause of the subdural bleeding in some cases of infant head injury is therefore not traumatic rupture of bridging veins, but a phenomenon of immaturity. Hypoxia with brain swelling would also account for retinal haemorrhages, and so provide a unified hypothesis for the clinical and neuropathological findings in cases of infant head injury, without impact or considerable force being necessary.     

<Superscript>18</Superscript>F-FP-CIT PET imaging and SPM analysis of dopamine transporters in Parkinson’s disease in various Hoehn &; Yahr stages

To investigate the usefulness of 18F-FP-CIT PET for assessing the severity of Parkinson’s disease (PD) at various clinical stages, 41 patients with PD were divided into early (Hoehn&Yahr I-II, n = 23) and advanced (Hoehn&Yahr III-IV, n = 18) subgroups. 18F-FP-CIT PET was performed in these patients and 12 normal subjects. 18F-FP-CIT uptake in striatal subregions and its correlation with UPDRS were first evaluated by ROI analysis, and between-group differences were also analyzed by Statistical Parametric Mapping (SPM). Our results showed that striatal 18F-FP-CIT binding were significantly reduced to 70.9% (caudate), 46.8% (anterior putamen) and 24.0% (posterior putamen) in early PD compared with that of the control, and to 52.0%, 34.5% and 16.5% correspondingly in advanced PD, respectively. There was significant negative correlation between total motor UPDRS score of all parkinsonian patients and 18F-FP-CIT uptake in caudate nucleus (r = −0.53, p < 0.001), anterior putamen (r = −0.53, p < 0.001) and posterior putamen (r = −0.61, p < 0.001). SPM comparison of 18F-FP-CIT uptake between early or advanced PD and the control group showed significant decline in striatum, predominantly localized on the contralateral side and in the dorsal-posterior putamen. These results indicate that 18F-FP-CIT PET can serve as a suitable biomarker to represent the severity of PD in early and advanced stages. Received in revised form: 11 June 2006     

<Emphasis Type="Italic">N</Emphasis><Superscript>ε</Superscript>-Carboxymethyllysine in diabetic and non-diabetic polyneuropathies

Increased oxidative stress and advanced glycosylation are important factors in the development of diabetic neuropathy. In non-diabetic neuropathies their influence has not been investigated in detail so far. We studied the localisation of N(epsilon)-carboxymethyllysine (CML) - a biomarker for oxidative stress - by immunohistochemistry in sural nerve biopsies of 31 patients with different polyneuropathies [diabetic polyneuropathy (n=5), alcohol-associated polyneuropathy (n=4), vitamin B12-deficient polyneuropathy (n=6), chronic inflammatory demyelinating polyneuropathy (CIDP) (n=6), vasculitic neuropathy (n=6), Charcot-Marie-Tooth disease type I (CMT I) (n=4)] and 4 normal controls. CML was detected in the perineurium of patients with diabetic, alcohol-associated, vitamin B12-deficient and vasculitic polyneuropathies. Epineurial, perineurial and endoneurial vessels were CML positive in diabetic, vitamin B12-deficient and vasculitic polyneuropathies. CML was also found in mononuclear inflammatory cells in vasculitic neuropathy. In CIDP and normal controls there was only marginal perineurial CML deposition in 2/6 and 1/4 cases. In CMT I no CML was detected. Immunohistochemical results were confirmed by immunoblot. Our data suggest a role of oxidative stress in the pathogenesis not only of diabetic but also of alcohol-associated, vitamin B12-deficient and vasculitic polyneuropathies. It may be a minor pathogenetic factor in CIDP and may not be involved in CMT I. Underlying causes for increased oxidative stress may be an elevated production of reactive oxygen species and an impairment of antioxidative defences. Therefore, an antioxidative treatment should be considered in alcohol-associated, vitamin B12-deficient and vasculitic polyneuropathy.     

Immunoglobulin<Emphasis Type="Italic"> KM</Emphasis> genes in Guillain-Barré syndrome

Guillain-Barré syndrome is associated with antecedent Campylobacter jejuni infection. Only a minority of the infected individuals, however, develops the disease, implying a role for genetic factors in conferring susceptibility. To determine the role of immunoglobulin KM genes (genetic markers of the constant region of κ chains) in the etiology of this syndrome, we genotyped 83 patients and 196 healthy controls from Norway for KM1 and KM3 alleles by polymerase chain reaction-restriction fragment length polymorphism. The frequency of KM3 homozygotes was significantly increased in patients compared with controls (86.7% vs. 74%, P=0.01, odds ratio=2.3). Conversely, the frequency of KM1/KM3 heterozygotes was significantly decreased in patients compared with controls (13.3% vs. 26%, P=0.01, odds ratio=0.4). These results suggest that KM genes may be relevant to the etiology of Guillain-Barré syndrome. Electronic Publication     

Amyloid-Positronenemissionstomographie mit [<Superscript>18</Superscript> F]-Florbetaben in der Demenzdiagnostik

Background

To this day the definite diagnosis of Alzheimer’s disease still relies on post-mortem histopathological detection of neurofibrillary tangles and beta-amyloid deposits. Amyloid positron emission tomography (PET) is a new diagnostic tool that enables the in vivo quantification of pathological beta-amyloid deposits. The aim of the current study was to evaluate to what extent ¹⁸F-florbetaben-PET (FBB-PET) influences the diagnosis of patients with dementia.

Material and methods

Imaging with FBB-PET was performed on 33 patients from our outpatient department for cognitive neurology. Beforehand all patients underwent a comprehensive clinical, neuropsychiatric and laboratory examination as well as imaging by means of magnetic resonance imaging (MRI) and fluorodeoxyglucose-PET. The working diagnoses before and after FBB-PET imaging were compared.

Results

17 out of 33 patients were scored as FBB-PET positive. In four cases the initial diagnosis had to be changed to Alzheimer’s disease (three cases) and cerebral amyloid angiopathy (one case) due to the positive FBB-PET scan. 16 patients showed a negative FBB-PET scan. In three patients the initial diagnosis of Alzheimer’s disease could be ruled out due to the negative FBB-PET scan. Overall, in 7 out of 33 examined patients the initial diagnosis had to be changed because of the findings of the FBB-PET scan. In 24 patients the initial diagnosis was confirmed by the results of the FBB-PET scan.

Conclusion

Amyloid-PET is currently no standard procedure in the diagnosis of dementia; however, it can be a helpful additional diagnostic tool when used according to the “Appropriate Use Criteria” and the S3 guidelines on dementia in cases of unclear clinical presentation, atypically early age of onset as well as in patients with persistent or progressive unexplained mild cognitive impairment. By facilitating early diagnosis amyloid-PET imaging allows patient selection for therapeutic drug trials.

     

Where does obsessive–compulsive disorder belong in DSM‐V?

A reclassification of obsessive-compulsive disorder (OCD) into a new diagnostic category spectrum of "obsessive-compulsive spectrum disorders" (OCSDs) has recently been proposed, with considerable debate, for the forthcoming Diagnostic and Statistical Manual-Fifth Edition (DSM-V). This paper provides a critical analysis of the available empirical data regarding this conceptual and nosological shift. Specifically, we review research on shared commonalities and differences between OCD and the putative OCSDs in relation to their clinical presentation, phenotype, neurobiology, and treatment response. We conclude that a reclassification of OCD into a separate OCSD spectrum is premature and not supported by the currently available data.     

Role of Aromatic Side Chains in Amyloid β-Protein Aggregation

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Outcome measures in neuromuscular disease: is the world still flat?

Valid, responsive, and meaningful outcome measures for the measurement of the impairment, activity limitations, and quality of life in patients with neuromuscular disease are crucial to identify the natural history of disease and benefits of therapy in clinical practice and trials. Although understanding of many aspects of neuromuscular diseases has advanced dramatically, the development of outcome measures has received less attention. The scales developed from Rasch theory by the PeriNomS Group represent the biggest significant shift in thought in neuromuscular outcome measures for decades. There remain problems with many of them, and further developments are required. However, incorporating them into our outcome sets for daily use and in clinical trials will lead to the more efficient capture of meaningful change and will result in better assessment of individuals and groups of patients in both clinical trials and neurological practice.     

What constitutes a ‘Good’ recovery outcome in post‐acute Guillain–Barré syndrome? Results of a Nationwide Survey of post‐acute GBS sufferers in the United Kingdom

Background: Eighty percent of people with Guillain–Barré Syndrome (GBS) are said to achieve ‘good’ outcome. ‘Good’ outcome has been defined as either of the top two scores (0 = Healthy, 1 = minor symptoms or signs, able to run) on a 7‐point ordinal scale called the F‐score. This assessment of ‘good’ outcome appears to be an arbitrary benchmark. This study is the first assessment of the differences in outcome between post‐acute GBS sufferers reporting these scores. It attempts to compare the physical and emotional differences between respondents reporting ‘0’ and ‘1’ on the F‐Score. Methods: A postal survey was administered to respondents through the UK Guillain–Barré Syndrome Support Group’s national database and included items relating to general patient data, general mobility, F‐Score, Hospital Anxiety and Depression Scale, SF 36 and Fatigue Severity Scale. Results: One thousand five hundred and thirty‐five members were surveyed, and of 884/1535 (58%) questionnaires were returned. Results indicate significant differences between those scoring ‘0’ on the F‐Score and those scoring ‘1’ in the post‐acute phase in terms of anxiety, depression, physical functioning, fatigue and wheelchair use on discharge. Conclusions: Significantly poorer outcomes for those scoring ‘1’ on the F‐Score suggest that only those scoring ‘0’ should constitute a ‘good’ outcome in GBS.     

Changes in the mRNA Levels of α<Subscript>2A</Subscript> and α<Subscript>2C</Subscript> Adrenergic Receptors in Rat Models of Parkinson’s Disease and <Emphasis Type="SmallCaps">l</Emphasis>-DOPA-Induced Dyskinesia

The changes in the mRNA levels of α_2A and α_2C adrenoceptors were investigated in unilateral 6-OHDA-lesioned rat model of Parkinson’s disease and l-DOPA-induced dyskinesia using in situ hybridization. In the untreated 6-OHDA-lesioned rats, α_2A expression was elevated in the locus coeruleus (160 ± 8% and 142 ± 8% in lesioned and unlesioned sides compared to the comparable side in sham-operated rats). Following long-term (21 days, twice daily) treatment with l-DOPA (25 mg/kg l-DOPA methyl ester plus benserazide 6.25 mg/kg) in 6-OHDA-lesioned rats, levels of α_2A adrenoceptor mRNA in the locus coeruleus were decreased, compared to the 6-OHDA-lesioned rats, returning to the levels of α_2A mRNA in the sham-operated rats. α_2A adrenoceptor expression was not changed in other brain regions in any treatment group. There was no change in α_2C expression in the rostral or caudal striatum in which the highest density of α_2C mRNA is present. In conclusion, the data presented in this study demonstrate an increase in α_2A adrenoceptor mRNA in the locus coeruleus in the 6-OHDA-lesioned rat model of Parkinson’s disease. In addition, the data show that repeated treatment with l-DOPA in 6-OHDA-lesioned rats, which induces dyskinesia, restores α_2A mRNA levels. These changes of α_2A mRNA expression, observed in the locus coeruleus, might be of importance to basal ganglia transmission and motor function.     

Does early treatment improve outcomes in N‐methyl‐d‐aspartate receptor encephalitis?

N‐methyl‐d ‐aspartate (NMDA) receptor encephalitis is a treatable cause of autoimmune encephalitis in both children and adults. It is still unclear if the natural history of the condition in children is altered by early treatment with immunosuppressive therapy. We looked at the outcomes of five children (two males, three females; mean age 6y 9mo, range 4–8y) who were treated empirically for autoimmune encephalitis within a brief period of presentation. Features that led clinicians to suspect autoimmune encephalitis included prominent neuropsychiatric features, movement disorder, seizures, and dysautonomic features. Immunosuppressive therapy was carried out in all cases. In this series of children, in whom the median time from symptom onset to treatment was 5 days and median length of time for follow‐up was 24 months, four out of the five (80%) recovered to their baseline. Early initiation of immunosuppressive therapy may result in improved clinical outcomes.     

Preprothyrotropin-releasing hormone<Subscript>178–199</Subscript> affects tyrosine hydroxylase biosynthesis in hypothalamic neurons

ProThyrotropin-releasing hormone (proTRH) is a prohormone widely distributed in many areas of the brain. After biosynthesis, proTRH is subjected to post-translational processing to generate TRH and seven non-TRH peptides. Among these non-TRH sequences, we found previously that preproTRH_178–199 could regulate the secretion of prolactin in suckled rats by their pups. Dopamine (DA), the main regulator of prolactin secretion, is produced in dopaminergic tyrosine hydroxylase (TH)-positive neurons in the hypothalamic arcuate nucleus (ARC). In this study we investigated whether prolactin release during the estrous sexual cycle is regulated by prepro TRH_178–199 through its effecton DA neurons of the ARC. We observed that biotinylated prepro TRH_178–199 bound to neurons in the ARC; this was higher during proestrus than during diestrus. Binding of preproTRH_178–199 to DA neurons was seen only during proestrus in the ARC. Using primary neuronal hypothalamic cultures we found that preproTRH_178–199peptide decreased TH levels in a dose-responsive manner, whereas intra-ARC administration of preproTRH_178–199 induced a 20-fold increase in plasma prolactin levels. Together, these results suggest a potential role for preproTRH_178–199 in regulating dopaminergic neurons involved in the inhibition of pituitary prolactin release.     

Can we trust depression screening instruments in healthy ‘old‐old’ adults?

OBJECTIVE: Despite a growing understanding of late-life depression, few studies focus on the old-old, those 75 years and over. We wished to characterize depressive symptoms and determine the accuracy of two common screening instruments for major and minor depression in a population of old-old retirees. METHODS: Participants lived independently in one of two Continuing Care Retirement Communities and volunteered for an in-home interview about cancer screening attitudes. As part of this baseline interview, they were screened with the Geriatric Depression Scale (GDS) and the Center for Epidemiologic Studies-Depression (CES-D) scale. Those agreeing to a second interview received an evaluation using the Structured Clinical Interview for DSM-IV (SCID-IV), performed by a geriatric psychiatrist within two weeks of the initial interview. RESULTS: In an educated and cognitively intact group of retirees averaging 80 years of age, the GDS and CES-D performed poorly using standard cutpoints in detecting both major (sensitivity 60% for both) and minor (sensitivity 33% and 50%, respectively) depression. One in five participants had significant depression as confirmed by SCID-IV evaluation. Twelve percent had major depression and 7% had minor depression. Most participants had their first episode of either after age 60. CONCLUSIONS: Contrary to most studies evaluating the GDS and CES-D for accuracy in detecting late-life depression, these instruments at standard cutpoints performed poorly in this group of healthy older adults. The healthy old-old may require novel screening interventions to detect clinically significant depression.