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1.
Several controlled trials have shown that the dopamine agonist, Trivastal (piribedil), is active in the treatment of Parkinson's disease, particularly with regard to tremor. To determine its efficacy as monotherapy in patients previously untreated with levodopa, a 3-month multicentre study was conducted with Trivastal 50 mg LP in 113 patients with idiopathic Parkinson's disease. The study population consisted of 66 men and 47 women, aged 63.1, SD 0.6 (43–79) years with a 2.1, SD 0.2 (1–15) year history of Parkinson's disease. Mean disease stage was 1.82 (1–4) by the Hoehn and Yahr classification. Tremor was the predominant clinical feature in 42 patients; the remaining 71 patients displayed the full parkinsonian syndrom. Trivastal 50 mg LP was prescribed stepwise up to doses of 150–250 (207, SD 6.4) mg/day at the end of 3 months. No concomitant antiparkinsonian medication was given. Patients were clinically assessed at 1, 2 and 3 months on the Webster scale, a specific tremor scale and the HARD depression scale. Mean results were as follows in the 90 patients completing the study. On the Webster scale, tremor fell from 1.7 to 1 (–41%,P<0.001), bradykinesia=" from=" 1.5=" to=" 0.8=">0.001),>P<0.001) and=" rigidity=" from=" 1.3=" to=" 0.9=">0.001)>P < 0.001);=" on=" the=" specific=" scale,=" rest=" tremor=" decreased=" in=" daily=" duration=" and=" amplitude=" from=" 3.9=" to=" 2.4=">P < 0.001)=" and=" from=" 2.9=" to=" 2.1=">P < 0.001),=" respectively.=" the=" 32=" patients=" in=" whom=" tremor=" was=" the=" predominant=" feature=" improved=" their=" total=" score=" on=" the=" webster=" scale=" from=" 5.8=" to=" 4.7=">P<0.05) and=" their=" tremor=" score=" from=" 1.7=" to=" 1.2=">0.05)>P < 0.05).=" the=" 58=" patients=" with=" the=" full=" parkinsonian=" syndrom=" improved=" their=" total=" webster=" score=" from=" 11.8=" to=" 6.9=">P < 0.001).=" eight=" of=" the=" ten=" items=" on=" the=" scale=" were=" significantly=" reduced,=" from=" between=" 33%=" (facial=" expression)=" to=" 53%=" (manual=" bradykinesia).=" the=" depression=" rating=" fell=" from=" 10.2=" to=" 7.3=">P < 0.001),=" the=" most=" marked=" improvement=" being=" in=" mood=" and=" inhibition.=" in=" conclusion,=" monotherapy=" with=" trivastal=" 50=" mg=" lp=" at=" a=" mean=" dose=" of=" 200=" mg/day=" is=" effective=" within=" 1=" month=" regarding=" the=" major=" features=" of=" parkinson's="> 相似文献
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3.
Srinivasan Savithiry Kusum Kumar 《Molecular and chemical neuropathology / sponsored by the International Society for Neurochemistry and the World Federation of Neurology and research groups on neurochemistry and cerebrospinal fluid》1994,21(1):1-11
To investigate the role of Ca2+-independent forms of protein kinase C (PKC) in ischemic neuronal injury, mRNA expression of PKC was studied by Northern blot analysis. Ischemia was produced in gerbils by 10-min bilateral carotid artery occlusion and was followed by recirculation for 15 min, 6 h, and 24 h. Brains of postischemic and sham-operated animals were removed, forebrains fresh frozen, and processed for Northern blot analysis. Three synthetic oligonucleotide probes based on published cDNA sequences of rat brain PKC for the isozymes δ, ε, and ζ were utilized for hybridization. Northern blot analysis showed increased hybridization signal for all three PKC isozymes examined in the 6- and 24-h postischemic groups. Of these, the twofold increases in the expression of PKC δ and ζ were statistically significant in comparison to the control. These results suggest that the mRNA levels of Ca2+-independent forms of PKC, in particular, δ and ζ, are temporally stimulated by ischemic injury in the brain and may imply an important role of the enzyme in postischemic neuronal damage. However, since the protein itself was not examined in this study, the significance of the increased expression cannot be ascertained. However, it may reflect a compensatory response to the loss of PKC reported to occur in the reperfusion phase. 相似文献
4.
Pritchard AL Harris J Pritchard CW Coates J Haque S Holder R Bentham P Lendon CL 《Journal of neurology, neurosurgery, and psychiatry》2007,78(2):123-126
Background
Patients with Alzheimer''s disease and dementia commonly suffer from behavioural and psychological symptoms of dementia (BPSD). A genetic component to BPSD development in Alzheimer''s disease has been demonstrated. Several studies have investigated whether the exon 4 ε2/ε3/ε4 haplotype of the apolipoprotein E (APOE) gene is associated with BPSD, with variable results.Objective
We investigated the exon 4 polymorphisms and extended this study to include promoter polymorphisms and the resultant haplotypes across the gene.Methods
Our large independent cohort of 388 patients with longitudinal measures of BPSD assessed by the Neuropsychiatric Inventory was used to analyse whether any of these variants were associated with the presence of BPSD.Results
We revealed several significant relationships before correction for multiple testing. The exon 4 haplotype was associated with hallucinations and anxiety, A‐491T with irritability, T‐427C with agitation/aggression and appetite disturbances, and T‐219C with depression. Haplotype analyses of all variants did not reveal any statistically significant findings.Conclusions
Our data and a review of previous studies showed a diversity of relationships, suggesting that these findings might be due to chance and so collectively do not support a role for the APOE gene in BPSD.Many patients with dementia display behavioural and psychological symptoms of dementia (BPSD). Unlike cognitive decline, BPSD do not continuously exist in a patient once they have occurred. Genetic determinants of BPSD in Alzheimer''s disease have been proposed from studies on families.1,2,3 It has been hypothesised that the genes that increase the risk for Alzheimer''s disease may also determine the presence of BPSD.4 The ε4 allele of the apolipoprotein E (APOE) gene is the only risk factor robustly associated with Alzheimer''s disease. However, previous investigations on APOE have produced inconsistent findings on BPSD, with some researchers reporting associations with a variety of different symptoms and alleles4,5,6,7,8,9,10,11,12,13,14,15,16 (summarised in the table provided online at http://jnnp.bmjjournals.com/supplemental), whereas others find no relevant relationships.17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33 We used a large independent clinical cohort of patients with Alzheimer''s disease, with longitudinal data on BPSD to further extend these studies, and additionally investigated promoter polymorphisms of APOE, which have been shown to independently incur risk of Alzheimer''s disease in some studies.34 相似文献5.
Valsasina P Agosta F Benedetti B Caputo D Perini M Salvi F Prelle A Filippi M 《Journal of neurology, neurosurgery, and psychiatry》2007,78(5):480-484
Background
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with severe cervical cord damage due to degeneration of the corticospinal tracts and loss of lower motor neurones. Diffusion tensor magnetic resonance imaging (DT MRI) allows the measurement of quantities reflecting the size (such as mean diffusivity) and orientation (such as fractional anisotropy) of water‐filled spaces in biological tissues.Methods
Mean diffusivity and fractional anisotropy histograms from the cervical cord of patients with ALS were obtained to: (1) quantify the extent of tissue damage in this critical central nervous system region; and (2) investigate the magnitude of the correlation of cervical cord DT MRI metrics with patients'' disability and tissue damage along the brain portion of the corticospinal tracts. Cervical cord and brain DT MRI scans were obtained from 28 patients with ALS and 20 age‐matched and sex‐matched controls. Cord mean diffusivity and fractional anisotropy histograms were produced and the cord cross‐sectional area was measured. Average mean diffusivity and fractional anisotropy along the brain portion of the corticospinal tracts were also measured.Results
Compared with controls, patients with ALS had significantly lower mean fractional anisotropy (p = 0.002) and cord cross‐sectional area (p<0.001). Mean diffusivity histogram‐derived metrics did not differ between the two groups. A strong correlation was found between mean cord fractional anisotropy and the ALS Functional Rating Score (r = 0.74, p<0.001). Mean cord and brain fractional anisotropy values correlated moderately (r = 0.37, p = 0.05).Conclusions
Cervical cord DT MRI in patients with ALS allows the extent of cord damage to be graded. The conventional and DT MRI changes found are compatible with the presence of neuroaxonal loss and reactive gliosis, with a heterogeneous distribution of the pathological process between the brain and the cord. The correlation found between cord fractional anisotropy and disability suggests that DT MRI may be a useful adjunctive tool to monitor the evolution of ALS.Amyotrophic lateral sclerosis (ALS) is the most common adult‐onset motor neurone disease, characterised by a progressive and simultaneous degeneration of upper and lower motor neurones.1,2 In its typical form, the disease begins either in one limb or with a combination of bulbar and corticobulbar symptoms, and continues with progressive weakness of the bulbar, limb, thoracic and abdominal musculature.1,2 By using a variety of conventional magnetic resonance imaging (MRI) sequences, several studies3,4,5,6,7,8,9,10,11,12,13,14,15 have shown changes in signal intensity along the brain portion of the corticospinal tracts, particularly in the posterior limb of the internal capsule and cerebral peduncles, varying between 25% and 80%. Reduced magnetisation transfer ratios in the internal capsule8,11 and N‐acetylaspartate levels in the motor cortex13,16,17 of patients with ALS have also been observed. However, none of these studies has reported a correlation between such magnetic resonance abnormalities and the degree of disability.8,11,13,16,17Diffusion‐tensor magnetic resonance imaging (DT MRI) enables the random diffusional motion of water molecules to be measured and thus provides quantitative indices of the structural and orientational features of the central nervous system (CNS).18 DT MRI has been used to assess quantitatively the tissue damage of the brain portion of the corticospinal tracts in ALS,12,19,20,21,22,23 and all studies have shown increased mean diffusivity (indicating a loss of structural barriers limiting the motion of water molecules) and decreased fractional anisotropy (indicating a loss of tissue organisation). However, brain DT MRI studies also resulted in heterogeneous clinicopathological correlations, as some authors found a moderate correlation between brain DT MRI metrics and the severity of disability,12,21,23 but others did not.19 In the past few years, DT MRI has also been used successfully to grade the extent of cervical cord damage associated with demyelinating conditions.24,25,26Considering that the cervical cord in ALS is one of the most affected portions of the CNS (owing to the combined presence of neuronal loss in the anterior horns of the grey matter and degeneration of the corticospinal tracts), we obtained mean diffusivity and fractional anisotropy histograms of the cervical cord from patients with ALS with the following aims: (1) to quantify the extent of tissue damage in this critical CNS region; and (2) to investigate the magnitude of the correlation of cervical cord DT MRI metrics with patients'' disability and tissue damage along the brain portion of the corticospinal tracts. 相似文献6.
Bronnick K Emre M Lane R Tekin S Aarsland D 《Journal of neurology, neurosurgery, and psychiatry》2007,78(10):1064-1068
Objective
To compare the profile of cognitive impairment in Alzheimer''s disease (AD) with dementia associated with Parkinson''s disease (PDD).Methods
Neuropsychological assessment was performed in 488 patients with PDD and 488 patients with AD using the Mini‐Mental State Examination (MMSE) and the Alzheimer''s Disease Assessment Scale‐cognitive subscale (ADAS‐cog). Logistic regression analysis was used to investigate whether the diagnosis could be accurately predicted from the cognitive profile. Additionally, the cognitive profiles were compared with a normative group using standardised effect sizes (Cohen''s d).Results
Diagnosis was predicted from the cognitive profile, with an overall accuracy of 74.7%. Poor performance of the AD patients on the orientation test in ADAS‐cog best discriminated between the groups, followed by poor performance of the PDD patients on the attentional task in MMSE. Both groups showed memory impairment, AD patients performing worse than PDD patients.Conclusion
The cognitive profile in PDD differs significantly from that in AD. Performance on tests of orientation and attention are best in differentiating the groups.Alzheimer''s disease (AD) and Parkinson''s disease (PD) are the most common neurodegenerative diseases in the elderly. AD is primarily a dementing disease whereas PD is mainly characterised by a movement disorder. However, dementia is common among patients with PD (PDD), with an average point prevalence of 31%1 and a cumulative prevalence close to 80%.2 In PD, dementia is associated with rapid motor3 and functional decline,4 and increased mortality.5Cortical Lewy body pathology correlates best with dementia in PD6,7,8,9; subcortical pathology10 and AD‐type pathology11 have also been found to be associated with PDD. In addition to differences in morphological changes, AD and PDD also differ in the regional pattern of the pathology. In AD the first and most pronounced changes are found in the entorhinal cortex and parahippocampal region,12 subsequently involving neocortical areas, including the posterior association cortices.13 In contrast, in patients with PD without dementia, brainstem nuclei and other subcortical structures are initially affected.14 In PDD, limbic areas, neocortical association cortices, and the motor cortex and primary sensory cortical areas are thought to be successively involved with disease progression.15Given the difference in the distribution and progression of pathology in AD and PDD, it is expected that their cognitive profiles would also differ.16,17 AD is characterised by memory loss emerging in the early stages of the disease,18 primarily involving learning and encoding deficits19 which are associated with medial temporal lobe pathology.20,21,22,23 As the disease progresses, deficits in language, praxis, visuospatial and executive functions gradually develop. In contrast, the cognitive deficits in the early stages of PDD are characterised by executive dysfunction, including impairment in attention24 and working memory,25,26,27 reflecting involvement of brainstem nuclei and frontal–subcortical circuits; deficits in visuoperceptual28,29,30 and visuoconstructional tasks are also frequent.31 Memory impairment is often present26,32,33,34 but whether it is primarily a consequence of frontally mediated executive deficits resulting in poor learning efficacy and retrieval, or whether involvement of limbic areas directly related to memory encoding (such as hippocampal atrophy) also contribute to memory impairment, is debated. Patients with PDD have difficulties in retrieving newly learned material, but perform better in recognition,35 indicating that executive, rather than encoding, deficits, is the underlying mechanism. Conflicting results, however, have been reported recently36,37 which could indicate that the type and mechanisms of memory deficits may vary within the PD group.32Most studies investigating the cognitive profile of PDD patients included small samples which were not community based and thus not necessarily representative of the PD population at large. As there is evidence of interindividual heterogeneity,33 such studies may not adequately reflect the cognitive profile of patients with PDD. In order to assess the profile of cognitive deficits in PDD compared with AD in larger patient populations, we analysed the baseline cognitive data from large clinical trials conducted with the cholinesterase inhibitor rivastigmine.38,39 相似文献7.
Julien CL Thompson JC Wild S Yardumian P Snowden JS Turner G Craufurd D 《Journal of neurology, neurosurgery, and psychiatry》2007,78(9):939-943
Background
Psychiatric symptoms are a common feature of Huntington''s disease (HD) and often precede the onset of motor and cognitive impairments. However, it remains unclear whether psychiatric changes in the preclinical period result from structural change, are a reaction to being at risk or simply a coincidental occurrence. Few studies have investigated the temporal course of psychiatric disorder across the preclinical period.Objectives
To compare lifetime and current prevalence of psychiatric disorder in presymptomatic gene carriers and non‐carriers and to examine the relationship of psychiatric prevalence in gene carriers to temporal proximity of clinical onset.Methods
Lifetime and current psychiatric histories of 204 at risk individuals (89 gene carriers and 115 non‐carriers) were obtained using a structured clinical interview, the Composite International Diagnostic Interview. Psychiatric disorders were classified using both standardised diagnostic criteria and a more subtle symptom based approach. Follow‐up of gene carriers (n = 51) enabled analysis of the role of temporal proximity to clinical onset.Results
Gene carriers and non‐carriers did not differ in terms of the lifetime frequency of clinical psychiatric disorders or subclinical symptoms. However, gene carriers reported a significantly higher rate of current depressive symptoms. Moreover, the rate of depression increased as a function of proximity to clinical onset.Conclusions
Affective disorder is an important feature of the prodromal stages of HD. The findings indicate that depression cannot be accounted for by natural concerns of being at risk. There is evidence of a window of several years in which preclinical symptoms are apparent.Huntington''s disease (HD) is an inherited neurodegenerative disorder, characterised by motor dysfunction, cognitive impairment and psychiatric disturbance. HD is associated with a wide range of psychiatric disturbances, including affective disorders,1,2,3 irritability,4,5,6 apathy1,3,6 and psychosis.4,7,8 Both major depression1,2,4,9 and more subtle mood disturbances10 have been reported to predate clinical onset, conventionally defined by onset of motor symptoms. However, the basis for psychiatric symptoms remains unclear. Depression has been observed to occur up to 20 years before the onset of motor symptoms,9,11 raising the possibility that psychiatric symptoms are an early indicator of HD and result from incipient neurodegenerative changes. However, the finding that psychiatric symptoms tend to cluster in certain HD families might indicate that psychiatric changes have a genetic basis and reflect a “switching on” of the HD gene early in life.2,8 High rates of psychiatric disturbance have also been observed in HD family members who do not carry the genetic mutation,9,10 raising the alternative possibility that affective changes arise in response to emotional stressors, such as being at risk, or the burden of growing up in a family with affected members. A more thorough understanding of the underlying basis of psychiatric changes in preclinical gene carriers is crucial, as future therapeutic strategies are most likely to target such individuals.Previous psychiatric studies of at risk individuals have yielded inconsistent results. Earlier studies reported high lifetime rates of psychiatric disorder in preclinical gene carriers (eg, 18% major affective disorder),2 whereas more recent studies indicate little difference between rates for gene carrier and non‐carrier groups.10,12,13,14 A number of factors may account for these discrepancies. The majority of earlier reports were limited to retrospective observation of affected individuals and therefore lacked appropriate controls.4,5 The advent of predictive testing has enabled direct comparison of at risk individuals who have the HD mutation and those who do not, thereby controlling for social and environmental factors.10,12,13,14 Whereas the majority of earlier studies lacked standardised assessment criteria,4,7 more recent studies have utilised operational diagnostic criteria, although these have in turn been criticised for failing to detect the more subtle psychiatric disturbances that can occur in HD.3,15Few studies have taken account of the temporal distance to onset of motor symptoms. It is now well established that the clinical onset of HD is typically preceded by a prodromal period of several months or years during which non‐specific mild neurological signs arise intermittently.16 The difficulty in establishing exact dates of onset for retrospective cases may have led to the inclusion in earlier studies of individuals who were already in the early stages of HD. Studies of presymptomatic individuals have typically recruited participants without motor signs, who may have been further from clinical onset.The present study is a double blind comparison of lifetime and current prevalence of psychiatric disorders in preclinical gene carriers and non‐carriers, using a combination of standardised psychiatric diagnostic criteria and a more subtle symptom based approach. Follow‐up of gene carriers has enabled analysis of the role of temporal proximity to clinical onset. 相似文献8.
Maria T. Caserta 《Molecular and chemical neuropathology / sponsored by the International Society for Neurochemistry and the World Federation of Neurology and research groups on neurochemistry and cerebrospinal fluid》1994,22(3):197-210
Neuropeptide Y (NPY)-containing neurons are depleted in the cortices of individuals with Alzheimer disease (AD), yet spared in the striatum of patients with Huntington chorea. It is unknown whether this neuronal phenotype is inherently susceptible to the neurodegenerative processes that are a hallmark of AD. To study this question, the murine trisomy 16 model of Down syndrome and Alzheimer disease was investigated. Since trisomic fetuses diein utero, studies were carried out on primary cultures of dissociated cortical neurons. These were prepared from 15-d gestational trisomy 16 fetuses and their littermate euploid controls, and examined by immunocytochemical staining for neuropeptide Y at 7 and 12 d in vitro. Trisomy 16 neurons were also grown on euploid glial carpets, whereas euploid neurons were grown on trisomic glia. The results demonstrate a significant increase in the number of NPY neurons and a stunting in the dendritic arbor of these neurons in trisomic vs euploid cortex. Both of these parameters could be normalized by direct contact with euploid glia. When euploid cortex was plated on trisomic glia, the number of NPY neurons and their morphology were altered so that they began to resemble trisomic NPY cortical neurons. These results indicate a dysregulation of NPY neuronal expression and differentiation in trisomy 16 cortex that are modifiable by interaction with euploid glia and imply an abnormal trophic (glial) environment in trisomic cortex. 相似文献
9.
Ryuichi Fukuyama Yohko Murakawa Stanley I. Rapoport 《Molecular and chemical neuropathology / sponsored by the International Society for Neurochemistry and the World Federation of Neurology and research groups on neurochemistry and cerebrospinal fluid》1994,23(2-3):93-101
To understand the possible role of amyloid precursor protein (APP) in human lymphocytes, and the regulation of APP gene expression in this cell type, we determined levels of cellular APP protein and of mRNA in human T-cell-derived Jurkat cells that were treated with lectin, phorbol ester, and calcium ionophore. We also related these levels to cell aggregation and adhesion. Cell-cell aggregation and cell-plastic adhesion were observed over a 24-h period after incubating cells for 2 h with phytohemagglutinin or phorbol myristate acetate. Cells treated with a calcium ionophore showed no aggregation or adhesion. Western blots indicated no obvious alteration in the level of cellular APP with different treatments. Northern blots showed a significant transient increase of APP mRNA after incubation with the calcium ionophore, whereas phorbol ester treatment showed a slight increase of APP mRNA. We analyzed the level of APP mRNA in human peripheral T cells which had been separated from peripheral lymphocytes. The level increased transiently by up to threefold after treatment with calcium ionophore plus phorbol esters. These data suggest that cell-cell aggregation and cell-matrix adhesion by human lymphocytes are not associated with an increased level of cellular APP protein or of mRNA. 相似文献
10.
Kizawa M Mori K Iijima M Koike H Hattori N Sobue G 《Journal of neurology, neurosurgery, and psychiatry》2006,77(8):967-969
Patients having neuropathy associated with Sjögren''s syndrome may present with pain and superficial sensory involvement in the absence of sensory ataxia. Treatment for this form of associated neuropathy has not been established. The case of a patient with painful sensory neuropathy associated with Sjögren''s syndrome, whose symptoms, particularly pain, responded well to intravenous immunoglobulin both at onset and in a relapse, is reported. Other patients with painful sensory neuropathy associated with Sjögren''s syndrome may also be candidates for intravenous Ig treatment.Ataxic sensory neuropathy associated with Sjögren''s syndrome is well recognised.1,2,3 Pathologically, the underlying lesion is a sensory ganglionopathy affecting predominantly large neurones and their axons.2,4 Intravenous immunoglobulin (Ig) treatment is reported to be effective in sensory ataxic neuropathy occurring in people with Sjögren''s syndrome.5,6,7,8 Recently, another type of neuropathy associated with Sjögren''s syndrome was reported to affect small sensory axons in patients presenting with pain and superficial sensory involvement as opposed to sensory ataxia.1,4,9,10,11 The treatment for this type of neuropathy remains uncertain. We describe a patient with painful sensory neuropathy associated with Sjögren''s syndrome, in whom intravenous Ig treatment dramatically reduced painful symptoms. 相似文献
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12.
del Mar Matarín M Pueyo R Poca MA Falcón C Mataró M Bargalló N Sahuquillo J Junqué C 《Journal of neurology, neurosurgery, and psychiatry》2007,78(7):760-763
Background
Adult normal pressure hydrocephalus (NPH) is one of the few potentially treatable causes of dementia. Some morphological and functional abnormalities attributed to hydrocephalus improve following treatment.Objectives
We focused on analysis of changes in cerebral metabolites using proton magnetic resonance spectroscopy (1H‐MRS) after NPH treatment, and its clinical and cognitive correlation.Methods
1H‐MRS, neuropsychological and clinical status examinations were performed before and 6 months after shunting in 12 adults with idiopathic NPH. We obtained N‐acetyl‐aspartate (NAA), choline (Cho), myoinositol (MI) and creatine (Cr) values.Results
After surgery, NAA/Cr was significantly increased. Moreover, NAA/Cr values were related to cognitive deterioration.Conclusion
MRS could be a marker of neuronal dysfunction in NPH.Normal pressure hydrocephalus (NPH) is a potentially treatable cause of dementia,1,2 characterised by progressive cognitive dysfunction, gait disturbance and urinary incontinence associated with ventricular enlargement and abnormalities in CSF dynamics. In these patients, some morphological and functional abnormalities attributed to hydrocephalus improve after treatment.3,4,5 Proton magnetic resonance spectroscopy (1H‐MRS) allows non‐invasive in vivo measurement of brain metabolites. Findings from MRS studies reveal that 1H‐MRS is a potentially non‐invasive technique with sufficient sensitivity to detect subtle changes in neuronal function in neurodegenerative diseases, allowing investigation of neuronal injury or dysfunction6,7 and the assessment of treatment efficacy.8,9,101H‐MRS studies in patients with hydrocephalus are scarce.6,7,11,12,13,14,15 Changes in cerebral metabolites after treatment with hydrocephalus using this technique have been analysed in only two studies, which concentrated exclusively on the results of lactate metabolites.11,12The aim of our study was to describe changes in other major metabolites, using 1H‐MRS, before and after treatment in idiopathic NPH patients, and to obtain preliminary data on their clinical and cognitive correlation, which could serve as the basis for larger studies with control subjects. 相似文献13.
M. Bellani S. Calderoni F. Muratori P. Brambilla 《Epidemiology and psychiatric sciences》2013,22(3):217
This brief review aims to examine the structural magnetic resonance imaging (sMRI) studies on corpus callosum in autism spectrum disorders (ASD) and discuss the clinical and demographic factors involved in the interpretation of results.Key words: autism spectrum disorders (ASD), corpus callosum, magnetic resonance imaging (MRI), volumesAutism spectrum disorders (ASD) are a heterogeneous group of neurodevelopmental pathologies whose diagnosis is based on the behavioural symptoms (Muratori et al. 2011) and whose intervention strategies aimed at improving socio-communicative skills as well as daily life abilities (Bellani et al. 2011). The neuroanatomical correlates of ASD are not fully elucidated. However, consistent findings based on structural magnetic resonance imaging (sMRI) data reported widespread cerebral abnormalities that include differences between ASD patients and controls in total brain volume, fronto-parieto-temporal and cerebellar regions. Moreover, a replicated altered corpus callosum (CC) size has been reported in the first sMRI analyses (for a review, see Brambilla et al. 2003). In particular, the altered CC has been considered as an anatomical substrate of processing and integration deficits peculiar to ASD, supporting the hypothesis of abnormal cortical connectivity in autism (Just et al. 2007). The CC is the largest commissural white matter (WM) tract in the human brain, and is conventionally divided into anterior CC, which comprises the rostrum, genu, rostral body, anterior mid-body and posterior CC, which includes the posterior mid-body, isthmus and splenium (Witelson, 1989). This primary WM structure connects homologous and heterotopic cortical areas of the two cerebral hemispheres and it is thought to be involved in motor and sensory integration as well as in higher cognitive function, including abstract reasoning, problem solving, ability to generalize, planning, social skills, attention, arousal, language comprehension and expression of syntax and pragmatics, emotion, memory (Paul et al. 2007). Recent investigations have employed a three-dimensional volumetric measurement of CC in ASD and frequently reported a reduction in the overall structure (Hardan et al. 2009; McAlonan et al. 2009; Duan et al. 2010; Anderson et al. 2011; Frazier et al. 2012), or in one or more components of this axonal pathway, including the anterior (Alexander et al. 2007; Keary et al. 2009; Thomas et al. 2011), the posterior sub-regions (Waiter et al. 2005) or some of the anterior and posterior regions contemporaneously (Vidal et al. 2006). The reductions in the CC volume is present over a wide age-range, since it is reported in ASD studies involving children (Vidal et al. 2006; Hardan et al. 2009; McAlonan et al. 2009; Frazier et al. 2012), adolescents (Waiter et al. 2004, 2005; Alexander et al. 2007) and adults (Keary et al. 2009; Ecker et al. 2010; Anderson et al. 2011; Thomas et al. 2011). On the other hand, the sparse literature on CC volume in low-functioning ASD (Riva et al. 2011) prevents us from drawing inferences about the influence of IQ on CC volume and calls for further investigation. Only a relatively few studies did not reveal significant CC volume differences between ASD patients and typically developing controls; in particular, this finding has been reported more often in voxel-based morphometry (Waiter et al. 2004; Bonilha et al. 2008; Ke et al. 2008; Ecker et al. 2010; Toal et al. 2010; Cheng et al. 2011; Mengotti et al. 2011; Calderoni et al. 2012) than in region of interest-based (Hong et al. 2011) analyses. Notably, to our knowledge, there have been no published studies reporting volumetric increase of CC (2012), whereas a cross-sectional approach failed to detect such relationship (Alexander et al. 2007). In addition, volume reduction in the CC has been found to correlate with core ASD features such social deficits, repetitive behaviours and sensory abnormalities (Frazier et al. 2012), as well as executive function and complex motor tasks deficits (Keary et al. 2009). Table 1.Studies investigating CC volumetry in patients with ASD compared with typically developing control subjects
Open in a separate windowAD, autistic disorder; ASD, autism spectrum disorders; ASP, Asperger''s syndrome; DD, developmental delay; DLD, developmental language disorder; CC, corpus callosum; DTI, diffusion tensor imaging; HFA, high-functioning autism; LFA, low-functioning autism; no DD, without developmental delay; n.r., not reported; PIQ, performance IQ; ROI, region of interest; TD, typically developing control subjects; VBM, voxel-based morphometry.*Follow-up study.In sum, although there is more evidence to support the notion that the CC volume, especially its anterior sectors, is decreased in ASD, there are some suggestions that no differences relative to controls occurs. Specifically, the CC volume reduction may be related to altered patterns of connectivity between brain areas, and in turn it might be responsible for some of the cardinal behavioural impairments of ASD. However, a number of crucial questions remain unanswered: volumetric alterations of the CC are specific to ASD or are a more general marker of abnormal brain development shared with other neuropsychiatric disorders? What is the relationship between alterations of the CC volume and demographic and clinical variables such as age, gender, handedness, intellective functioning, severity of symptoms, psychiatric comorbidity, psychotropic medications? What is the contribution of different CC subdivisions to overall CC volume alterations? Do the CC volume alterations persist into adulthood? What are the underlying neuropathological changes (e.g. reduction in number and/or size of axons, impaired myelination, excessive synaptic pruning) responsible for decreased CC volume? Future dedicated studies should aim to address these issues more specifically. 相似文献
Study | Subjects | Age years (SD) | Full-scale IQ | MRI methods | Significant findings in ASD relative to controls |
---|---|---|---|---|---|
Herbert et al. (2004) | 13 AD 21 DLD 29 TD | 9.0 (0.9) 8.2 (1.6) 9.1 (1.2) | PIQ > 80 PIQ > 80 n.r. | Quantitative volumetric analysis, 1.5 T | No differences in CC volume |
Waiter et al. (2004) | 16 ASD 16 TD | 15.4 (2.24) 15.5 (1.6) | 100.4 (21.7) 99.7 (18.3) | VBM, 1.5 T | No differences in CC volume |
Waiter et al. (2005) | 15 ASD 16 TD | 15.2 (2.2) 15.5 (1.6) | 100.5 (22.4) 99.7 (18.3) | VBM, 1.5 T | Reduction in CC volume, particularly in the posterior regions |
Vidal et al. (2006) | 24 HFA 26 TD | 10.0 (3.3) 11.0 (2.5) | 95.9 (11.5) 104.8 (11.7) | Three-dimensional surface models, 3 T | Reduction in the splenium and genu of CC |
Alexander et al. (2007) | 43 ASD 34 TD | 16.2 (6.7) 16.4 (6.0) | PIQ 107.5 (13.0) PIQ 112.8 (12.1) | DTI, 3.0 T | Reduction in CC volume, particularly in the anterior regions |
Bonilha et al. (2008) | 12 AD 16 TD | 12.4 (4) 13.2 (5) | n.r. n.r. | VBM, 2.0 T | No differences in CC volume |
Ke et al. (2008) | 17 HFA 15 TD | 8.9 (2.0) 9.7 (1.7) | 108.8 (19.1) 109.8 (19.2) | VBM, 1.5 T | No differences in CC volume |
Hardan et al. (2009) | 22 ASD 23 TD | 10.7 (1.4) 10.5 (1.4) | 95.1 (20.4) 116.2 (13.2) | ROI manual tracing, 1.5 T | Reduction in CC volume |
Keary et al. (2009) | 32 ASD 34 TD | 19.8 (10.2) 18.6 (9.1) | 102.9 (13.6) 104.0 (10.5) | ROI manual tracing, 1.5 T | Reduction in CC volume, particularly in the anterior regions |
McAlonan et al. (2009) | 18 HFA 18 ASP 54 TD | 11.6 (2.9) 11.2 (2.5) 10.7 (2.7) | VIQ 114.8 (19.1) VIQ 109.8 (16.2) VIQ 117.1 (18.1) | VBM, 1.5 T | Reduction in the genu of CC in HFA and ASP |
Duan et al. (2010) | 30 ASD 28 TD | Age range: 3–30 Age range: 3–30 | ≥ 40 n.r. | ROI manual tracing, 1.5 T | Reduction in CC volume and in all its sub-regions |
Ecker et al. (2010) | 22 ASD 22 TD | 27 (7) 28 (7) | 104 (15) 111 (10.0) | VBM, 3.0 T | No differences in CC volume |
Toal et al. (2010) | 26 AD 39 ASP 33 TD | 30 (8) 32 (12) 32 (9) | 84 (23) 106 (15) 105 (12) | VBM, 1.5 T | No differences in CC volume |
Anderson et al. (2011) | 53 HFA 39 TD | 22.4 (7.2) 21.1 (6.5) | PIQ 101.3 (16.5) PIQ 114.2 (13.9) | Automated volumetric segmentation, 3.0 T | Reduction in CC volume |
Cheng et al. (2011) | 25 ASD 25 TD | 13.7 (2.5) 13.5 (2.1) | 101.6 (18.9) 109.0 (9.5) | VBM, 1.5 T | No differences in CC volume |
Hong et al. (2011) | 18 HFA 16 TD | 8.7 (2.2) 9.8 (1.9) | 105.2 (21.1) 106.1 (20.1) | ROI manual tracing, 1.5 T | No differences in overall CC volume and its sub-regions |
Mengotti et al. (2011) | 20 AD 22 TD | 7.0 (2.7) 7.7 (2.0) | Evaluated, but n.r. | DTI and VBM, 1.5 T | No differences in CC volume |
Riva et al. (2011) | 21 LFASD 21 TD | 6.6 (2.5) 6.10 (2.1) | 52.5 (9.8) normal IQ | VBM, 1.5 T | No differences in CC volume |
Thomas et al. (2011) | 12 HFA 18 TD | 28.5 (9.7) 22.4 (4.1) | 106.9 (10.5) 111.6 (9.9) | DTI, 3.0 T | Reduction in the body of CC |
Calderoni et al. (2012) | 38 ASD (19 with DD, 19 no DD) 38 controls (19 with DD, 19 TD) | 4.4 (1.5) 4.4 (1.6) | 72 (20) 73 (25) | VBM, 1.5 T | No differences in CC volume |
Frazier et al. (2012) | 23 ASD 23 TD | 10.6; range: 8–12 10.5; range: 7–13 | 94.6 (20.0) 116.2 (13.2) | ROI manual tracing, 1.5 T | Reduction in CC volume |
Frazier et al. (2012)* | 18 ASD 19 TD | 13.1; range: 9–15 12.4; range: 9–16 | 94.6 (20.0) 116.2 (13.2) | ROI manual tracing, 1.5 T | Reduction in CC volume, with the exception of rostral body |
14.
Friedhelm Helling Philip O. Livingston 《Molecular and chemical neuropathology / sponsored by the International Society for Neurochemistry and the World Federation of Neurology and research groups on neurochemistry and cerebrospinal fluid》1994,21(2-3):299-309
Gangliosides are known to be suitable targets for immune attack against cancer but they are poorly immunogenic. Active immunization with ganglioside/BCG or liposome vaccines results in moderate titer IgM antibody responses of short duration. Covalent attachment of poorly immunogenic antigens to immunogenic proteins is a potent method for inducing an IgG antibody response. GD3, a dominant ganglioside on malignant melanoma, was modified by ozone cleavage of the double bond in the ceramide backbone, an aldehyde group introduced and used for coupling via reductive amination to ε-aminolysyl groups of proteins. Utilizing this method, GD3 conjugates were constructed with:
- Synthetic multiple antigenic peptide (MAP) constructs expressing 4 repeats of a malaria T-cell epitope;
- Outer membrane proteins (OMP) ofNeisseria meningitidis;
- Cationized bovine serum albumin;
- Keyhole limpet hemocyanin (KLH); and
- Polylysine.
15.
Eliyas Jeffay Angela Sekely Michel Lacerte Konstantine K. Zakzanis 《Psychiatry, Psychology and Law》2021,28(1):135
The Personality Assessment Inventory (PAI) is a reliable multidimensional psychometric inventory that is increasingly being used in the medical–legal context. To date, 18 language adaptations of the PAI exist, yet only the Spanish, Greek and German language versions have been examined psychometrically. This study evaluated the psychometric properties of the French-Canadian version of the PAI by comparing mean scale and subscale scores between the French-Canadian and English language versions, and analyzing the internal consistency and mean item inter-correlations (MICs) of each version in a sample of 50 bilingual university students. Cronbach’s alphas ranged from −.57 to .80 in the French-Canadian version and from −1.10 to .83 in the English version, with most scales being below .70, indicating inadequate internal consistency. In addition, most of the MICs were below .20, indicating a lack of item homogeneity. Caution is given to this adaptation of the PAI in the medical–legal context. Key words: bilingual, language adaptation, medical–legal, Personality Assessment Inventory, psychological assessment, psychometrics, reliabilityThe generalizability of psychological tests with specific populations is an insidious problem in clinical psychology and may have significant implications in the context of a medical–legal examination. For example, if psychologists are asked to objectively substantiate the breadth, severity and veracity of subjective symptomatology and come to a diagnostic opinion, it is essential that such opinions are based on firm scientific grounds in order to meet legal standards and be accepted by the courts. This is especially important since psychologists are asked to suggest/comment on the efficacy of treatment, determine disability benefit or comment on the permanence or seriousness of a psychological injury, all in the ultimate context of assisting the trier of fact in a medical–legal setting. The Standards of Educational and Psychological Testing state that translating a measure into another language does not ensure the construct measured remains comparable to the original test (American Educational Research Association, American Psychological Association & National Council on Measurement in Education, 2014). As such, the examination of language adaptations is an essential part of the study of cultural differences and similarities (Ellis, 1989). This does not, of course, discount the complex and distinct sub-cultural groups who speak the same language (e.g. French speakers who are Moroccan, Congolese, Belgian, etc.). Cheung (2009) explained that personality instruments developed in Western cultures are often generalized to other cultural groups with the faulty assumption that these measures are valid for all groups. When a measure is adapted for a population that differs qualitatively from the one for which it was originally developed, the reliability and validity of the test must be evaluated before it can be clinically utilized (Butcher, Derksen, Sloore, & Sirigatti, 2003; Candell & Hulin, 1986; Cheung, 2009; Geisinger, 1994; Sireci & Berberoglu, 2000) and, hence, employed in the context of a medical–legal examination. Despite these recommendations, research on the language adaptations of the Personality Assessment Inventory (PAI; Morey, 1991, 2007) has been limited.The PAI is a self-report instrument that yields a broad range of clinically relevant information, and is a widely utilized test measure of personality and psychopathology in medical–legal examinations. It was developed using a rational and quantitative method of scale development. The rational criterion emphasizes theoretically informed choices when developing items, as opposed to empirically based instruments such as the Minnesota Multiphasic Personality Inventory–2 (MMPI–2; Butcher, Dahlstrom, Graham, Tellegen, & Kaemmer, 1989). The PAI consists of 344 items that constitute four sets of non-overlapping scales: (a) four validity scales: Inconsistency, Infrequency, Negative Impression Management and Positive Impression Management; (b) 11 clinical scales: Somatic Complaints, Anxiety, Anxiety-Related Disorders, Depression, Mania, Paranoia, Schizophrenia, Borderline Features, Antisocial Features, Alcohol Problems and Drug Problems; (c) five treatment scales: Aggression, Suicidal Ideation, Stress, Nonsupport and Treatment Rejection; and (d) two interpersonal scales: Dominance and Warmth. Several advantages of the PAI include its brevity, lower reading level requirements, focus on diagnostic concepts and attention to clinical management issues. The acronyms for the scales and subscales are presented in Scale acronym Scale name Subscale acronym Subscale name Validity INC Inconsistency INF Infrequency NIM Negative Impression PIM Positive Impression Clinical SOM Somatic Complaints SOM-C Conversion SOM-S Somatization SOM-H Health Concerns ANX Anxiety ANX-C Cognitive ANX-A Affective ANX-P Physiological ARD Anxiety-Related Disorders ARD-O Obsessive-Compulsive ARD-P Phobias ARD-T Traumatic Stress DEP Depression DEP-C Cognitive DEP-A Affective DEP-P Physiological MAN Mania MAN-A Activity Level MAN-G Grandiosity MAN-I Irritability PAR Paranoia PAR-H Hypervigilance PAR-P Persecution PAR-R Resentment SCZ Schizophrenia SCZ-P Psychotic Experiences SCZ-S Social Detachment SCZ-T Thought Disorder BOR Borderline Features BOR-A Affective Instability BOR-I Identity Problems BOR-N Negative Relationships BOR-S Self-Harm ANT Antisocial Features ANT-A Antisocial Behaviors ANT-E Egocentricity ANT-S Stimulus Seeking ALC Alcohol Problems DRG Drug Problems Treatment AGG Aggression AGG-A Aggressive Attitude AGG-V Verbal Aggression AGG-P Physical Aggression SUI Suicidal Ideation STR Stress NON Nonsupport RXR Treatment Rejection Interpersonal DOM Dominance WRM Warmth