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I am a DREAMER...well almost...Continue Reading »
Meet Gabriela. A DREAMER... well almost... She missed the age-at entry requirement by a couple of months.
After reading her story, don't you think she more than deserves a shot too?
"I, Gabriela Monico, hereby declare as follows: My name is Gabriela Monico. I am a resident of California. I was born in San Salvador, El Salvador. I came to the United States in November 2005 on…
Done DreamingMy name is Esmy Jimenez. I was raised in a small town in Washington State known for agriculture and friendly people. I graduated from the local high school as the Senior Class President. I was in National Honor Society and enrolled in all the AP classes my school provided. I even ran on the cross country team and (attempted) to play tennis. On weekends I worked for a catering company…Continue Reading »
No Papers Necessary.Continue Reading »
My name is Pat. My first "American" family member got to these shores in 1621. His name is William Claiborne and there is a plaque dedicated to him in the church at Jamestown. However, the other half of my family is Irish. The Irish side of my family, while I am not certain, very likely arrived here without any papers since they fled here during the famine. So, in…
I am an American, but I live in the shadows...In 1998, I met my immigrant husband in Chicago while I was in AmeriCorps and going to school. By that time, he had been in the US for almost 10 years--he had earned his GED, learned English, and moved up from his original position as dishwasher to become a kitchen manager. We fell in love. In 2002, we got married in his hometown in Mexico. We were told that petitioning…Continue Reading »
I Teach Americans. So What?While sitting at a scholarship pageant, I remember how an idyllic teenage girl explained that her dream was to become a teacher. I was a cynical teen in those days and so I rolled my eyes as her sweet, but very breathy voice tinkled the words, "I believe the children are our future. Teach them well and let them lead the way." I had to chew on the sides of…Continue Reading »
My rich immigrant backgroundOn my father's side I am a 3rd generation American. My great-parents immigrated from Italy in 1903. On my mother's side, our family came from Spain, through Mexico, then settled in the Provincia de Nueva Mexico in the Kingdom of New Spain - what is now know as the State of New Mexico, during the Reconquista. We've been here since before there even was a United States of America! We…Continue Reading »
American Is Supporting Immigration Reform Now.My father immigrated to America when he was 11 years old. My maternal grandmother came to this country in her twenties. They contributed to the United States through their work, the taxes they paid and the values they taught their families. The same is true today. We need immigration reform that respects and strengthens families, encourages civic engagement and provides equal educational and career opportunities for all. America can't wait.Continue Reading »
Don't Be A SuckerHere's a video contribution to what it means to be an American.Continue Reading »
Mother in Law's storyMy mother in law was born in what is now AZ. When she was born it was not a state. She was a very conscientious person and voted in every election. When she was 65 and applied for State benefits, she was told the I D she had was not valid. It took months to straighten this out and finally, her marriage certificate stated she was born in AZ. My…Continue Reading »
MigrantsI am Irish through and through but I've never been to Ireland. I HAVE gone to the US Mexico border several times a year to volunteer with No More Deaths and Borderlinks, providing supplies, footcare and advocacy. The migrants are human beings. They laugh, tell stories and love their families. They are like us, only poor, displaced and harmed by our past and present immigration policies. We are all Americans.…Continue Reading »
Jeff Hawkins shares his definition of "American"Continue Reading »
Jeff Hawkins is the inventor of the Palm Pilot and a long-time mogul in Silicon Valley.
This is how he defines "American."
Mayor Paul Bridges shares his definition of "American"Continue Reading »
Republican Mayor Paul Bridges is one of more than a dozen plaintiffs suing Georgia and its governor, trying to stop the state's new immigration law.
They won a reprieve in July when a federal judge...
Let's Talk.
What would you do?


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You can now invite anyone to meet at your favorite Starbucks.
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30 year old man | DeSoto, TX, USA | Seeking women 21-31 within 50 miles
I have a career, my own place, my own car. I think that should get me through the basics.
I am a reliable person. I take what I say and do seriously and tend to set my own standards pretty high. Preferably, my partner would be a balance to me. She would ideally be a laid back person who knows how to juggle fun, family, friends, and her career. I always make the best effort to be completely honest and open. I'm pretty busy with work most of the time, and it takes me out of town most of the week. Therefore, my weekends are really my time to relax and make up for any fun I missed out on during the week. I am looking for someone who is comfortable going out with me. I have a huge family, so you will likely see me out with them out weekends. At times, I can be forgetful, but I am detail-oriented. When I care for someone, I care for that person openly and have no shame in showing it. I tend to teeter between being a social butterfly and a hermit. I like to be active at any rate and hit the town, watch a play, hike, run, or just have a plain cup of coffee. If you are a huge planner and like to explore then you might be the girl for me, and I am the guy for you. Oh, I am a huge sucker for smiles. I would do almost anything to see a genuine, sweet smile. :D
Coffee and conversation , Cooking , Dining out , Hobbies and crafts , Movies/Videos , Museums and art , Music and concerts , Exploring new areas , Nightclubs/Dancing , Performing arts , Playing sports , Shopping/Antiques , Travel/Sightseeing , Video games , Volunteering , Wine tasting
Golf, Martial arts, Other types of exercise, Running, Soccer, Walking / Hiking, Weights / Machines
I exercise 1-2 times per week.
I like Birds, Cats, Dogs, Exotic Pets, Fish, Horses, Other
I used to have dogs growing up, but I just can't anymore because of my schedule. Not too fond of cats, but I guess that is not really for me to worry about huh?
Middle of the Road
California is one of my favorite places. I have family there and visit when I can. Chicago is also fun. I like to travel in general.
The University of Texas at Arlington, Arlington, TX
Dubstep, trance, techno, rock, hip hop, basically anything catchy. I am not a music snob by any means. Food? EVERYTHING. There is not much I am not willing to try. I am Vietnamese which means if it moved at one point then I probably ate it.
I go to Karate training once a week right now. Wish I have time to go more. I try to be active. Hikes, runs, walking, just about anything to get me out of the house. Though I do enjoy watching movies before bed to unwind.
I do not do too much leisurely reading. Never was my thing, but I do stay up to date reading the news everyday. My interest tends to gear towards science, business, or technology.
Z{{Cta}} {{#if HasMoreInfo}} ?{{CtaSecondary}} {{/if}}
|What he is looking for
|5'6" (167cms)
|4'0" (121cms) to 5'6" (167cms)
|Body type:
|Athletic and toned
|Slender, About average, Curvy, Athletic and toned, Full-figured
|I'll tell you later
|Black, Blue, Brown, Grey, Green, Hazel
|No preference
|No Way
|No Way, Occasionally
|Social Drinker
|Never, Social Drinker, Regularly, Moderately
|Other profession
|No preference
I work for a consulting firm. I specifically work with in the healthcare and IT industry.
|I'll tell you later
|$35,001 to $50,000, $50,001 to $75,000, $75,001 to $100,000, $100,001 to $150,000, $150,001+
|Never Married
|Never Married
|Have kids:
|Wants kids:
|Not sure
|Definitely, Someday, Not sure, Probably not, No
|Asian, Latino / Hispanic, Middle Eastern, Native American, Pacific Islander, White / Caucasian
I am Vietnamese. Born in the States and raised in Dallas. I can speak Vietnamese fluently.
|I'll tell you later
|Agnostic, Atheist, Buddhist / Taoist, Christian / Catholic, Christian / LDS, Christian / Protestant, Hindu, Jewish, Spiritual but not religious, Other, Christian / Other
|English, Other
|No preference
|Graduate degree
|Some college, Associates degree, Bachelors degree, Graduate degree, PhD / Post Doctoral
I have my Masters in Healthcare Administration and my Bachelors in Biology, Chemistry Minor.

subset: commoncrawl


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Bullet Club in King of Trios
CHIKARA is doing another King of Trios event, and they have managed to pull off a bit of a coup by signing three of the most popular free agents on the independent wrestling circuit. AJ Styles, Nick Jackson and Matt Jackson will be competing in the tournament and representing the Bullet Club, their massively popular stable from New Japan. No word yet on who they will be facing first that night, but there is a very good chance they win it all.
March 3, 2015


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Admit it: Even if you're the type of girl who often defaults to missionary, you probably have a dark desire to explore your inner perv.
Well, you can. All you need is a tour guide.
Enter sexpert Emily Dubberley, a prolific sex writer and author of Friendly Fetish: A Beginner's Guide to Kink.
Dubberley has tested more than 500 sex toys, worked as a lube taster and engaged in any number of depraved activities in the name of study—think sploshing, working as a dominatrix and attending an orgy. Yes, the lady has experience. Here are her tips for discovering a fetish (or rolling with the one that began when you watched Secretary).
Finding Your Kink
As it turns out, bookworm types are well-equipped for a fetish-finding mission, which, not surprisingly, starts with research. Dubberley suggests that you first find an erotic story that gets you off. Her site, Cliterati, has free stories for every kink.
As you're reading, look for what excites you and analyze why you're turned on. If you like tales of group sex, is it the thought of sex with lots of people or being watched that gets you off? "Start by exploring stuff in fantasy and discover where your limits lie," Dubberley says.
Testing the Waters
Once you've nailed your fantasy, it's time to introduce the topic to a partner you trust. If you fancy ponyplay but are afraid of what he'll think, leave an erotic story on his bedside table and gauge his reaction. If he's disgusted, Dubberley says you can always backtrack and say, "I thought it was a bit odd, too." But if he's on board, recruit him to research the act with you.
For those interested in bondage, Dubberley recommends enrolling in a beginner's class. After all, tying knots can even be tricky for boy scouts, and there are all sorts of practical precautions used to avoid cutting off circulation and such. "You'll need to know which bits of the body not to put pressure on," Dubberley says. "These are quite good things to know from a safety standpoint."
The Dirty Details
When making fantasy a reality, there are a few key rules: Don't be drunk, high or without a safe word. Your physical and mental health are at stake—fetish acts can bring many underlying issues to the surface—and you don't want that bottle of wine to mask any danger.
Dubberley also advises talking through the entire act beforehand and going easy with equipment. (Those interested in metal handcuffs might opt for spank ties, which boast foam-covered wire that lets you wriggle free.) And don't be distraught if your fantasy doesn't translate. "You're experimenting," Dubberley says. "That does not mean you know what the result is going to be."
Then again, you might be a changed woman. "It can be fantastically liberating, and it can be a way to work through lots of issues as well," Dubberley says.
"If you've felt like you've been treated badly by men, you might find it empowering to give a bloke a spanking."
Read the rest on Lemondrop.
- Now That's Hot—NYC Firefighters Pose in Two New 2010 Calendars
- Dating Sites Use DNA to Find Your Perfect Match—Creepy or Genius
- Can Men and Women Be 'Just Friends' as Adults?


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ChoiceTeles provides a thorough analytical chronology of the emergence of intellectuals, networks, political entrepreneurs, and patrons as a new level of political competition in the legal arena, which he contends has made elections themselves less significant. . . . This is an exceptionally valuable resource for understanding recent changes, both liberal and conservative, in the legal and political spheres.
— R. Heineman


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The authors sought to compare gray matter changes in First Episode Schizophrenia (FES) compared with Fronto-Temporal Lobar Degeneration (FTLD) using meta-analytic methods applied to neuro-imaging studies.
A systematic search was conducted for published, structural voxel-based morphometric MRI studies in patients with FES or FTLD. Data were combined using anatomical likelihood estimation (ALE) to determine the extent of gray matter decreases and analysed to ascertain the degree of overlap in the spatial distribution of brain changes in both diseases.
Data were extracted from 18 FES studies (including a total of 555 patients and 621 comparison subjects) and 20 studies of FTLD or related disorders (including a total of 311 patients and 431 comparison subjects). The similarity in spatial overlap of brain changes in the two disorders was significant (p = 0.001). Gray matter deficits common to both disorders included bilateral caudate, left insula and bilateral uncus regions.
There is a significant overlap in the distribution of structural brain changes in First Episode Schizophrenia and Fronto-Temporal Lobar Degeneration. This may reflect overlapping aetiologies, or a common vulnerability of these regions to the distinct aetio-pathological processes in the two disorders.
Keywords:Schizophrenia/pathology; FTLD/pathology; Meta-analysis; Magnetic resonance imaging/methods; Humans; Brain/pathology; Brain mapping; Imaging processing; Computer-Assisted/methods
Schizophrenia is a disorder characterised by positive symptoms (hallucinations and delusions), thought disorder and negative symptoms (such as apathy). Brain imaging studies have identified structural changes both early in the presentation of the illness and more extensive changes later in the course of the illness [1]. The distribution of changes has been replicated between studies [2], and may be considered a 'structural signature' of schizophrenia within the brain. However, an adequate explanation for this spatial distribution remains elusive. Models have been proposed involving genetic factors coding neuro-protein variants resulting in abnormal development of limbic and frontal-temporal-subcortical networks [3]. However, it remains uncertain which neuro-chemical pathways are responsible and how they cause the spatial changes.
FTLD is characterised by declines in social function, interpersonal conduct, emotional blunting, speech and language abnormalities and loss of insight [4]. It is associated with degeneration of the prefrontal and anterior temporal cortices [5]. However, the topographical distribution of structural brain changes is heterogeneous amongst different patient groups, reflecting behavioral and pathological variants. Although the most common histological feature is tauopathy [6], over half of all patients, including those with a family history of the condition, have no abnormality in the tau gene or protein [7], consistent with pathological and aetiological heterogeneity.
In this study, we investigate whether there is overlap in the distribution of brain changes in First Episode Schizophrenia (FES) and Fronto-Temporal Lobar Degeneration (FTLD). There is evidence for similarities in clinical, neuropsychological and neuroimaging findings in patients with FTLD and schizophrenia [8]. In some cases, patients with FTLD have been diagnosed with a schizophrenia-like psychotic illness years before the dementia diagnosis is made [9]. Echopraxia, echolalia, aprosody of speech, utilisation behavior, 'negative' symptoms, self-neglect, and bizarre, compulsive, and stereotyped behaviors are well recognised in both disorders. Executive dysfunction with relative preservation of visual perception and spatial skills [7,10] and deficits in social cognition, theory of mind, empathy and affect recognition have been identified in both disorders [11].
Frontal, temporal and hippocampal atrophy [12,13] and regionally specific reductions in the anterior corpus callosum [14,15] and anterior hippocampus [16,17] have been described in MRI studies of both FTLD and schizophrenia. Frontal hypoperfusion on single photon emission tomography or positron emission tomography constitutes one of the imaging criteria for the diagnosis of frontotemporal dementia [18], and is also one of the most robust functional imaging findings in the schizophrenia literature in patients with chronic and first-episode illness [19]. There is also recent evidence that schizophrenia and FTLD co-occur in some families, suggesting the possibility of a common vulnerability to these disorders [20]. While the pathology of schizophrenia remains uncertain, there have been considerable advances in elucidating the complex and heterogeneous pathology of FTLD [21,22]. We have chosen to examine FES rather than chronic schizophrenia because the structural changes in FES may more accurately reflect the pathological changes of the disorder, and may minimize the confounding effects of long-term medication and other aspects of chronic illness. Different antipsychotics have individual volumetric effects on brain structure [23,24] and therefore, patients with FES were used in order to reduce heterogeneity.
The aim of this review is to determine the distribution of brain changes in FTLD and FES, by employing an established meta-analytic technique (anatomical likelihood estimation, ALE) [25] that is widely used for coordinate-based meta-analyses of neuroimaging data by converting the co-ordinates of peak gray matter changes from multiple published studies into spatial probability maps. However, the accuracy and extent of these maps is dependent on the total number of peak co-ordinates available from published studies. Therefore, this study employs a new statistical approach to investigate the degree of spatial correspondence between the two disorders, taking into account the greater availability of data co-ordinates for FTLD than FES. The comparison of brain changes between an individual MRI scan and maps for different disorders may become increasingly important for early diagnosis, as currently, diagnoses of psychiatric disorders are made on the basis of clinical manifestations and associated psychosocial disturbances. There are current initiatives to encourage the classification of mental disorders for research purposes, such as the RDoC (Research Domain Criteria) approach [26]. Several MRI-based studies have attempted to distinguish between patients and healthy subjects with high accuracy (ranging from 75 to 92%) [27]. Therefore, the statistical technique described in this paper for assessing spatial overlap may have wider clinical utility in the future.
The PRISMA (preferred reporting items for systematic reviews and meta-analyses) guidelines were followed to conduct this review [28].
Literature search
A comprehensive keyword search of EMBASE (from 1980), PsycINFO (from 1801) and Medline (from 1950), was conducted using the following search strategy. The following Boolean phrase was used: {([Magnetic Resonance Imaging] OR [MRI]) AND ([Schizophrenia] OR [schizo*] OR [FTLD] OR [Fronto-Temporal Lobar Degeneration) AND ([Voxel] OR [VBM])}. Both free-text and expanded medical subject headings were be used. The search strategy was supplemented using a cited reference search, and by inspecting the reference lists of included articles. The search was conducted in January 2011. No time span was specified for date of publication.
Criteria for inclusion/exclusion
Studies were considered for the review using the following inclusion criteria: 1) they were published in English as a peer-reviewed article (rather than a letter, abstract, or case report); 2) they compared a sample of formally diagnosed subjects with a group of unrelated healthy control subjects; 3) they utilized voxel-based analysis of gray matter in structural MRI scans to investigate differences in whole-brain; and 4) they reported the three-dimensional co-ordinates of changes in stereotactic space.
FTLD studies were considered if they consisted of subjects with Fronto-Temporal Lobar Degeneration or related diagnoses, such as Semantic Dementia. FES studies were considered if they included a group of subjects with schizophrenia or related diagnoses, specifically first episode schizoaffective disorder or psychosis. Only first-episode schizophrenia patients were included, therefore, papers must have documented that patients were experiencing symptoms related to psychosis without a prior diagnosis without administration of prior antipsychotic medication in order to be included in our meta-analysis.
Studies were excluded if: 1) there were insufficient data to extract the number of subjects in each group; 2) there were fewer than five subjects in either the patient group or the comparison group; 3) the comparison groups consisted of patients with minor non-psychiatric illnesses; 4) the patient group in the schizophrenia studies consisted of subjects with child-onset schizophrenia or chronic schizophrenia beyond the stage of first-episode psychosis; 5) the studies used region-of-interest volumetric analyses, or the deformation- or tensor-based volumetric methods for measuring regional brain volumes; and 6) the data contributed to another publication, in which case the publication with the largest group size under study was selected.
Data abstraction
Data were extracted from two independent investigators (BO and IEW) and were double-checked. Information gathered from the studies included the authors, year of publication, demographic variables (number of subjects, age at baseline and gender), illness variables (diagnosis and duration of illness), and the reported stereotactic coordinates related to the comparisons between structural MRI scans of patients and controls from every selected study. Co-ordinates that were reported in the stereotactic space of the Montreal Neurological Institute (MNI) were converted to Talairach coordinates using the Lancaster transform (icbm2tal) in the GingerALE 2.0 program [29]. Talairach co-ordinates that had been generated by the Brett transform applied to statistical parametric mapping MNI co-ordinates were transformed back to MNI space in GingerALE and then to Talairach space using the Lancaster transform.
Statistical analysis
Meta-analyses were performed using the Talairach stereotactic coordinates derived from the included studies. Meta-analyses were carried out using GingerALE 2.0 [29]. This uses the technique of Activation Likelihood Estimation (ALE) [25] and permits weighting of studies in the meta-analysis, e.g. based on sample size. This modification of ALE treats the spatial conjunction of co-ordinates from separate studies as more significant than conjunction of co-ordinates from a single study. The probability values can then be interpreted on an image-wide basis after correction for multiple testing using the False Discovery Rate, a method which controls the proportion of type 1 errors (false positives) among significant results [30].
Descriptive meta-analyses were then performed to identify the distribution of brain changes in FES and FTLD, when compared to control subjects. The overlap of these two distributions was measured.
Spatial overlap testing
We tested the overlap of the FTLD co-ordinates with the FES spatial map generated by ALE using a randomisation method based on our previous work hybridising ALE spatial techniques with GSMA (Genome Scan Meta-Analysis) statistical methods [31].
For each FTLD study, the reported loci of maximal anatomical difference were modeled as the peaks of three-dimensional Gaussian probability density functions with full-width half-maximum of 7 mm, within a brain mask of size N of linear dimension 2 mm. The voxels in this probability image were then ranked from N (highest probability) to 1 (lowest probability), giving voxels of equal probability a mean rank. This created a rank image for each study which was smoothed with a 7 mm Gaussian filter. This image was masked with the First Episode Schizophrenia spatial map generated by ALE and the total value of ranks within the mask was calculated. The total for all studies of ranks within the mask was calculated ('FES Mask Total').
A null distribution for the FES Mask Total result was derived by 1000 permutations of the same process, but using an equal number of co-ordinates for each study derived from a random uniform distribution of coordinates within the brain mask. The probability of a FES Mask Total under the null hypothesis was calculated as the proportion of permutations giving a value equal or greater than the actual value.
The data set being tested was included in the ranking of all known outcomes. The significance threshold was set at p < 0.05.
The electronic literature search of the three databases yielded 396 articles, of which 181 were retrieved in full-text format. 56 studies were identified as being potentially appropriate to be included in the meta-analysis, and the inclusion and exclusion criteria was used throughout the selection process to yield 38 articles appropriate for use in the meta-analysis. Figure 1 displays a flow diagram that shows the reasons for exclusion at each stage of the selection process.
Figure 1. Study flow and reasons for exclusion.
A total of eighteen FES studies and twenty FTLD studies were identified for inclusion in the meta-analysis (Table 1), having published MRI co-ordinates of gray matter changes in FES or FTLD patients and healthy controls [32-69]. The FES studies included a total of 555 patients and 621 comparison subjects, and the FTLD studies included a total of 311 patients and 431 comparison subjects. Among the FES patient group, the smallest size sample was 13 schizophrenia patients [44], and the largest size sample was 68 schizophrenia patients [40]. Among the FTLD patient group, the smallest size sample was 6 patients [50,62], and the largest size sample was 51 patients [60]. All included studies were published from 2000 to 2010.
Table 1. Studies included in the Meta-analyses
ALE meta-analyses
Eighteen FES studies included 185 co-ordinates of gray matter decreases. Meta-analysis of this data identified gray matter decreases in regions including bilateral head of caudate nucleus, bilateral insula, bilateral amygdala/uncus region and bilateral superior temporal region (Figure 2).
Figure 2. Regions of gray matter change in FES and FTLD subjects. Regions of gray matter decreases in FES subjects compared with controls (red), regions of gray matter decreases in FTLD subjects compared with controls (yellow), and overlapping regions of gray matter decreases controls (orange), displayed on a brain template. The left side of the image represents the left side of the brain. The Talairach level (z co-ordinate) is given above each horizontal slice.
Twenty FTLD studies provided 260 co-ordinates of gray matter decreases. Meta-analysis of this data identified gray matter decreases in regions including bilateral head of caudate nucleus, bilateral insula, bilateral amygdala/uncus region and bilateral superior temporal region (Table 2, Figure 2).
Table 2. Regions of gray matter decreases in FES and FTLD subjects compared with controls
Common changes in FES and FTLD
Gray matter decreases were present in both disorders in regions including bilateral caudate head, left insula and bilateral uncus region (Figure 3).
Figure 3. Gray matter deficits in FES subjects (red) and FTLD subjects (yellow). Congruent changes in both disorders are shown in orange. Brain changes are shown in three-dimensional views with brain sections removed (A, B), a sagittal plane (C), an axial plane (D) and a coronal plane (E). The Talairach co-ordinate for each plane is given above each image (C, D, E) (P = posterior, A = anterior, S = superior, L = left).
The spatial congruence between the disorders was estimated by percentage overlap. The FTLD map of gray matter decreases comprised 2450 voxels in a brain mask of 201069 voxels. The FES map of gray matter decreases comprised 888 voxels in a brain mask of 201069 voxels. The overlap between the FTLD and FES maps was 124 voxels. Therefore the overlap of FTLD within FES was 14% (compared to an expected overlap of 1.2% if the FTLD map was randomly distributed in the brain mask). The overlap of FES within FTLD was 5% (compared to an expected overlap of 0.4% if the FES mask was randomly distributed in the brain mask). Applying the spatial overlap testing method, the overlap of the FTLD co-ordinates with the FES spatial map generated by ALE was significant (p = 0.001).
In this study, we identified overlap in the distribution of brain changes in First Episode Schizophrenia (FES) and Fronto-Temporal Lobar Degeneration (FTLD). We found that the two disorders involved gray matter deficits in common regions (p = 0.001). These included the basal ganglia (bilateral caudate head), paralimbic (left insula) and limbic (bilateral uncus) regions, as shown in Figure 4. To our knowledge, this is the first meta-analysis that compares neuro-structural profiles between FES and FTLD. Our study presents a novel method using ALE analyses to derive a statistical test for the chance overlap of the spatial distribution of the two disorders.
Figure 4. Venn diagram to summarise the distinct and overlapping regions of gray matter deficits found in FES and FTLD.
One approach to investigating the spatial distribution of brain changes in schizophrenia involves conceptualising the disorder as affecting several neural sub-systems which are individually affected in other neuro-psychiatric disorders with genetic or syndromal links to schizophrenia. For example, there is evidence that bipolar disorder and schizophrenia share susceptibility genes, and gray matter deficits of bipolar disorder overlap with those of schizophrenia but are more limited to paralimbic regions involved in emotion regulation [70-72]. Temporal lobe epilepsy is also associated with psychotic episodes with similarities to schizophrenia and is associated with gray matter deficits in limbic regions, overlapping with those of schizophrenia [73-75]. Autistic spectrum disorders and schizophrenia share gray matter deficits in the limbo-striato-thalamic circuitry [76], possibly reflecting shared genetic [77,78] and environmental [79-82] risk factors.
Previous results of meta-analyses and structural neuro-imaging studies of FES and FTLD
These results confirm those of previous meta-analyses of the two disorders, using smaller samples of primary studies. Several previous meta-analyses using 'region-of-interest' analyses have examined gray matter deficits in schizophrenia [83,84], with consistent findings of medial temporal lobe atrophy [85-88]. Patients with FES also have smaller whole-brain volume, with greater lateral ventricular volume [89]. Frontal [90,91] and temporal [37] volumes have been reported to be smaller at first episode, and basal ganglia are also affected early in the illness [33,92]. The ALE method has also been used to investigate brain structural abnormalities in schizophrenia derived from studies using voxel-based morpometry analyses [1,93]. In a recent meta-analysis by Chan et al., patients with FES had lower gray matter volumes in frontal, temporal, striatal, and cerebellar regions compared with both control subjects and people who are at genetically high-risk of developing schizophrenia [94]. They mapped progressive changes from the high-risk stage to the first-episode stage, clarifying potential markers for disease risk (anterior cingulate and right insula volume reduction) and for disease onset (caudate volume reduction) [94].
In FTLD, a meta-analysis of voxel-based morphometry studies found predominant frontal and temporal lobe involvement, with specific patterns of atrophy in the three clinical subtypes of FTLD, namely, FTD (frontotemporal dementia), SD (semantic dementia) and PNFA (progressive non-fluent aphasia) [95]. Correspondingly, diagnostic criteria for FTLD create a 'triple dissociation' of these subtypes with a high diagnostic accuracy clinically [96]. The clinical characteristics of each subtype of FTLD correspond well with the neuroanatomical deficits found.
Functional significance of implicated regions and symptoms of FES and FTLD
The involvement of the basal ganglia (bilateral gray matter decreases in the caudate head in both disorders) agrees with Middleton and Strick's prediction that abnormalities within cortico-striatal circuits may underlie neuropsychiatric symptoms [97,98]. Anatomical studies have revealed discrete connections between the basal ganglia and the cerebral cortex, reciprocally interconnecting a large and diverse set of cortical areas [99]. Dysregulation and abnormal dopaminergic transmission in these loops may contribute to hyperkinetic movements as well as cognitive impairments [100-102]. Robbins [103] proposed that the heterogeneous range of core symptoms associated with psychosis, appearing to be associated with a range of structural and functional abnormalities, might be explained by a frontal-striatal hypothesis, where an altered balance in the flow of information between through the basal ganglia could explain the seemingly disparate symptoms and characteristics of schizophrenia and psychotic episodes in FTLD. Our results indicate that the basal ganglia loop in particular incorporating the head of the caudate nucleus, are affected by FES and FTLD, which may at least partly explain their shared symptoms.
Our findings reveal that both disorders are characterised by reduced volumes of various paralimbic and limbic structures. Neuroanatomists and cytoarchitectologists have grouped the regions shown to be affected in FES and FTLD, namely the superior temporal gyrus (temporal pole), rostral and caudal anterior cingulate, posterior cingulate, orbital frontal cortex, insula, and parahippocampal regions, into the paralimbic cortex [104,105]. There is documented evidence to support paralimbic dysfunction in various psychiatric disorders, namely psychopathy [106], bipolar disorder [72], psychotic symptoms in depressive disorder [107] and attention deficit hyperactivity disorder [108]. Our results also indicate that both disorders are characterised by reduced caudate size, lesions of which cause impairments in learning, memory [109] and behaviour through the selection of appropriate sub-goals based on an evaluation of action-outcomes [110]. This may reflect the common symptomatology between the two disorders.
Explanation for congruence
Various explanations need to be considered for the overlap in gray matter deficits between the two disorders. Firstly, the result could be due to coincidence. However, we have applied a statistical test to the spatial congruence which suggests that this is highly unlikely (the p value for the null hypothesis of a random distribution of FTLD co-ordinates within the FES spatial map was p = 0.001). Secondly, the symptoms of neuropsychiatric disorders are related to the anatomy of the brain pathology. Therefore, the selection of schizophrenia and FTLD, which share certain symptoms (as described above) may constrain the anatomical findings towards certain brain regions, in the absence of any other more meaningful connection between the neuropathology of the two disorders. The evidence that schizophrenia and FTLD co-occur in some families [6] suggests the possibility of a more fundamental connection between the two disorders. Thirdly, the neuropathology of the two disorders may be (at the neurochemical pathway level) distinct but the common network identified in this study may be 'a final common pathway' in the pathological process of both disorders, or a common reaction to such processes.
There are limitations of this meta-analysis. Firstly, by meta-analysing co-ordinates of maximum change from primary studies there is a loss of spatial information. This reduces the spatial resolution of the results. Secondly, as more primary studies are published the distribution of changes in each disorder may become more extensive as there is improved power to detect changes. Thirdly, there are alternative approaches for investigating spatial overlap of two disorders. For example, Yu et al., used a post-hoc meta-analytic estimation of the extent to which gray matter compares with controls in bipolar disorder and schizophrenia by using a modification of the ALE method [71]. Lastly, the mean age of patients with FES was 24.4 years, whereas in FTLD, the mean age was 63.6 years (Table 1). There are no validated methods to account for these differences in an ALE meta-analysis, and it is possible that some of the results may have been affected by "normal" structural brain aging processes [111]. Anatomical likelihood estimation analyses are a relatively novel and changing technique, and as time progresses, standardisation of meta-analysis techniques will help researchers evaluate results from different studies more objectively.
Future directions
In the future, localized gray matter deficits detected via the above analyses may be combined with those identified in activation studies of cognitive deficits in schizophrenia and FTLD, in order to understand the correlation between functional and structural connectivity in both disorders. For example, the structural MRI gray matter deficits could be used as nodes for a network analysis [112], as can now be done on individual scans [113], which may be utilized to investigate and compare functional connectivity changes in FES and FTLD.
In summary, we reviewed data from 18 FES studies and 20 studies of FTLD that used voxel-based morphometry to identify common structural brain abnormalities. The brain regions found to be significantly affected included gray matter deficits in the bilateral caudate, left insula and bilateral uncus regions. The overlap in distribution of the disorders does not necessarily indicate a fundamental sharing of neurochemical pathology between FES and FTLD. However, we propose that the emerging genetic, pathological and clinical typology of FTLD may provide a model for the deconstruction of subtypes of schizophrenia.
Competing interests
BO, IEW and SML disclose that they have no competing interests. EB is employed half-time by GlaxoSmithKline (GSK) and half-time by the University of Cambridge and is a stockholder in GSK.
Authors' contributions
BO and IEW devised the study and wrote the first draft of the manuscript. BO ascertained the studies and extracted the data. IEW checked and analysed the data. EB and SML participated in the design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.
The listed authors were solely involved the in designing the study, data acquisition, analysis and interpretation, as well as drafting and revising the manuscript, with no external contributions. SML has received financial support from Pfizer (formerly Wyeth) in relation to imaging studies of people with schizophrenia, but this played no role in influencing this study.
Ellison-Wright I, Glahn DC, Laird AR, Thelen SM, Bullmore E: The anatomy of first-episode and chronic schizophrenia: an anatomical likelihood estimation meta-analysis.
Am J Psychiatry 2008, 165(8):1015-23. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Keshavan MS, Tandon R, Boutros NN, Nasrallah HA: Schizophrenia, "just the facts": what we know in 2008 Part 3: neurobiology.
Schizophr Res 2008, 106(2–3):89-107. PubMed Abstract | Publisher Full Text
Goghari VM, Sponheim SR, MacDonald AW 3rd: The functional neuroanatomy of symptom dimensions in schizophrenia: a qualitative and quantitative review of a persistent question.
Neurosci Biobehav Rev 2010, 34(3):468-86. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Neary D, Snowden JS, Gustafson L, Passant U, Stuss D, Black S, Freedman M, Kertesz A, Robert PH, Albert M, Boone K, Miller BL, Cummings J, Benson DF: Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria.
Neurology 1998, 51:1546-54. PubMed Abstract | Publisher Full Text
Mohandas E, Rajmohan V: Frontotemporal dementia: An updated overview.
Indian J Psychiatry 2009, 51(Suppl 1):S65-9. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Taniguchi S, McDonagh AM, Pickering-Brown SM, Umeda Y, Iwatsubo T, Hasegawa M, Mann DM: The neuropathology of frontotemporal lobar degeneration with respect to the cytological and biochemical characteristics of tau protein.
Neuropath Appl Neurobiol 2004, 30:1-18. Publisher Full Text
Momeni P, Wickremaratchi MM, Bell J, Arnold R, Beer R, Hardy J, Revesz T, Neal JW, Morris HR: Familial early onset frontotemporal dementia caused by a novel S356T MAPT mutation, initially diagnosed as schizophrenia.
Clin Neurol Neurosurg 2010, 112(10):917-20. PubMed Abstract | Publisher Full Text
Velakoulis D, Walterfang M, Mocellin R, Pantelis C, McLean C: Frontotemporal dementia presenting as schizophrenia-like psychosis in young people: clinicopathological series and review of cases.
Br J Psychiatry 2009, 194(4):298-305. PubMed Abstract | Publisher Full Text
Pantelis C, Barnes TR, Nelson HE, Tanner S, Weatherley L, Owen AM, Robbins TW: Frontal-striatal cognitive deficits in patients with chronic schizophrenia.
Brain 1997, 120(Pt 10):1823-43. PubMed Abstract | Publisher Full Text
Shamay-Tsoory SG, Aharon-Peretz J, Levkovitz Y: The neuroanatomical basis of affective mentalizing in schizophrenia: comparison of patients with schizophrenia and patients with localized prefrontal lesions.
Schizophr Res 2007, 90(1–3):274-83. PubMed Abstract | Publisher Full Text
Lawrie SM, Abukmeil SS: Brain abnormality in schizophrenia. A systematic and quantitative review of volumetric magnetic resonance imaging studies.
Br J Psychiatry 1998, 172:110-20. PubMed Abstract | Publisher Full Text
Velakoulis D, Wood SJ, Wong MT, McGorry PD, Yung A, Phillips L, Smith D, Brewer W, Proffitt T, Desmond P, Pantelis C: Hippocampal and amygdala volumes according to psychosis stage and diagnosis: a magnetic resonance imaging study of chronic schizophrenia, first-episode psychosis, and ultra-high-risk individuals.
Arch Gen Psychiatry 2006, 63(2):139-49. PubMed Abstract | Publisher Full Text
Kaufer DI, Miller BL, Itti L, Fairbanks LA, Li J, Fishman J, Kushi J, Cummings JL: Midline cerebral morphometry distinguishes frontotemporal dementia and Alzheimer's disease.
Neurology 1997, 48(4):978-85. PubMed Abstract | Publisher Full Text
Walterfang M, Wood AG, Reutens DC, Wood SJ, Chen J, Velakoulis D, McGorry PD, Pantelis C: Morphology of the corpus callosum at different stages of schizophrenia: cross-sectional study in first episode and chronic illness.
Br J Psychiatry 2008, 192(6):429-34. PubMed Abstract | Publisher Full Text
Laakso MP, Frisoni GB, Kononen M, Mikkonen M, Beltramello A, Geroldi C, Bianchetti A, Trabucchi M, Soininen H, Aronen HJ: Hippocampus and entorhinal cortex in frontotemporal dementia and Alzheimer's disease: a morphometric MRI study.
Biol Psychiatry 2000, 47:1056-63. PubMed Abstract | Publisher Full Text
Velakoulis D, Stuart GW, Wood SJ, Smith DJ, Brewer WJ, Desmond P, Singh B, Copolov D, Pantelis C: Selective bilateral hippocampal volume loss in chronic schizophrenia.
Biol Psychiatry 2001, 50:531-9. PubMed Abstract | Publisher Full Text
McKhann GM, Albert MS, Grossman M, Miller B, Dickson D, Trojanowski JQ: Clinical and pathological diagnosis of frontotemporal dementia: report of the Work Group on Frontotemporal Dementia and Pick's Disease.
Arch Neurol 2001, 58:1803-9. PubMed Abstract | Publisher Full Text
Velakoulis D, Pantelis C: What have we learned from functional imaging studies in schizophrenia? The role of frontal, striatal and temporal areas.
Aust N Z J Psychiatry 1996, 30:195-209. PubMed Abstract | Publisher Full Text
Schoder D, Hannequin D, Martinaud O, Opolczynski G, Guyant-Maréchal L, Le Ber I, Campion D: Morbid risk for schizophrenia in first-degree relatives of people with frontotemporal dementia.
Br J Psychiatry 2010, 197:28-35. PubMed Abstract | Publisher Full Text
Pickering-Brown SM: The complex aetiology of frontotemporal lobar degeneration.
Exp Neurol 2007, 206(1):1-10. PubMed Abstract | Publisher Full Text
Aswathy PM, Jairani PS, Mathuranath PS: Genetics of frontotemporal lobar degeneration.
Ann Indian Acad Neurol 2010, 13(Suppl 2):S55-62. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Goghari VM, Lang DJ, Khorram B, Götz J, Vandorpe RA, Smith GN, Kopala LC, Barr AM, Honer WG: Anterior internal capsule volumes increase in patients with schizophrenia switched from typicalantipsychotics to olanzapine.
J Psychopharmacol 2011, 25(5):621-9. PubMed Abstract | Publisher Full Text
Molina V, Reig S, Sanz J, Palomo T, Benito C, Sánchez J, Pascau J, Desco M: Changes in cortical volume with olanzapine in chronic schizophrenia.
Pharmacopsychiatry 2007, 40(4):135-9. PubMed Abstract | Publisher Full Text
Eickhoff SB, Laird AR, Grefkes C, Wang LE, Zilles K, Fox PT: Coordinate-based activation likelihood estimation meta-analysis of neuroimaging data: A random-effects approach based on empirical estimates of spatial uncertainty.
Hum Brain Mapp 2009, 30:2907-2926. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Morris SE, Cuthbert BN: Research Domain Criteria: cognitive systems, neural circuits and dimensions of behaviour.
Dialogues Clin Neurosci 2012, 14(1):29-37. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Takayanagi Y, Takahashi T, Orikabe L, Mozue Y, Kawasaki Y, Nakamura K, Sato Y, Itokawa M, Yamasue H, Kasai K, Kurachi M, Okazaki Y, Suzuki M: Classification of first-episode schizophrenia patients and healthy subjects by automated MRI measures of regional brain volume and cortical thickness.
PLoS One 2011, 6(6):e21047. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Liberati A, Altman DG, Tetzlaff J, Mulrow C, Gøtzsche PC, Ioannidis JP, Clarke M, Devereaux PJ, Kleijnen J, Moher D: The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate healthcare interventions: explanation and elaboration.
BMJ 2009, 339:b2700. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Laird AR, Fox PM, Price CJ, Glahn DC, Uecker AM, Lancaster JL, Turkeltaub PE, Kochunov P, Fox PT: ALE meta-analysis: controlling the false discovery rate and performing statistical contrasts.
Hum Brain Mapp 2005, 25:155-164. PubMed Abstract | Publisher Full Text
Verhoeven KJF, Simonsen KL, McIntyre LM: Implementing false discovery rate control: increasing your power.
Oikos 2005, 108:643-647. Publisher Full Text
Ellison-Wright I, Ellison-Wright Z, Bullmore E: Structural brain change in Attention Deficit Hyperactivity Disorder identified by meta-analysis.
BMC Psychiatry 2008, 8:51. PubMed Abstract | BioMed Central Full Text | PubMed Central Full Text
Bergé D, Carmona S, Rovira M, Bulbena A, Salgado P, Vilarroya O: Gray matter volume deficits and correlation with insight and negative symptoms in first-psychotic-episode subjects.
Acta Psychiatr Scand 2011, 123(6):431-9. PubMed Abstract | Publisher Full Text
Chua SE, Cheung C, Cheung V, Tsang JT, Chen EY, Wong JC, Cheung JP, Yip L, Tai KS, Suckling J, McAlonan GM: Cerebral grey, white matter and CSF in never-medicated, first-episode schizophrenia.
Schizophr Res 2007, 89:12-21. PubMed Abstract | Publisher Full Text
Douaud G, Smith S, Jenkinson M, Behrens T, Johansen-Berg H, Vickers J, James S, Voets N, Watkins K, Matthews PM, James A: Anatomically related grey and white matter abnormalities in adolescent-onset schizophrenia.
Brain 2007, 130:2375-86. PubMed Abstract | Publisher Full Text
Ebdrup BH, Glenthøj B, Rasmussen H, Aggernaes B, Langkilde AR, Paulson OB, Lublin H, Skimminge A, Baaré W: Hippocampal and caudate volume reductions in antipsychotic-naive first-episode schizophrenia.
J Psychiatry Neurosci 2010, 35(2):95-104. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Jayakumar PN, Venkatasubramanian G, Gangadhar BN, Janakiramaiah N, Keshavan MS: Optimized voxel-based morphometry of gray matter volume in first-episode, antipsychotic-naive schizophrenia.
Prog Neuropsychopharmacol Biol Psychiatry 2005, 29:587-91. PubMed Abstract | Publisher Full Text
Job DE, Whalley HC, McConnell S, Glabus M, Johnstone EC, Lawrie SM: Structural gray matter differences between first-episode schizophrenics and normal controls using voxel-based morphometry.
Neuroimage 2002, 17:880-9. PubMed Abstract | Publisher Full Text
Kasparek T, Prikryl R, Mikl M, Schwarz D, Ceskova E, Krupa P: Prefrontal but not temporal grey matter changes in males with first-episode schizophrenia.
Prog Neuropsychopharmacol Biol Psychiatry 2007, 31:151-7. PubMed Abstract | Publisher Full Text
Kubicki M, Shenton ME, Salisbury DF, Hirayasu Y, Kasai K, Kikinis R, Jolesz FA, McCarley RW: Voxel-based morphometric analysis of gray matter in first episode schizophrenia.
Neuroimage 2002, 17(4):1711-9. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Lui S, Deng W, Huang X, Jiang L, Ma X, Chen H, Zhang T, Li X, Li D, Zou L, Tang H, Zhou XJ, Mechelli A, Collier DA, Sweeney JA, Li T, Gong Q: Association of cerebral deficits with clinical symptoms in antipsychotic-naive first-episode schizophrenia: an optimized voxel-based morphometry and resting state functional connectivity study.
Am J Psychiatry 2009, 166(2):196-205. PubMed Abstract | Publisher Full Text
Meda SA, Giuliani NR, Calhoun VD, Jagannathan K, Schretlen DJ, Pulver A, Cascella N, Keshavan M, Kates W, Buchanan R, Sharma T, Pearlson GD: A large scale (N = 400) investigation of gray matter differences in schizophrenia using optimized voxel-based morphometry.
Schizophr Res 2008, 101(1–3):95-105. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Molina V, Sanz J, Villa R, Pérez J, González D, Sarramea F, Ballesteros A, Galindo G, Hernández JA: Voxel-based morphometry comparison between first episodes of psychosis with and without evolution to schizophrenia.
Psychiatry Res 2010, 181(3):204-10. PubMed Abstract | Publisher Full Text
Price G, Cercignani M, Chu EM, Barnes TR, Barker GJ, Joyce EM, Ron MA: Brain pathology in first-episode psychosis: magnetization transfer imaging provides additional information to MRI measurements of volume loss.
Neuroimage 2010, 49(1):185-92. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Salgado-Pineda P, Baeza I, Perez-Gomez M, Vendrell P, Junque C, Bargallo N, Bernardo M: Sustained attention impairment correlates to gray matter decreases in first episode neuroleptic-naive schizophrenic patients.
Neuroimage 2003, 19:365-75. PubMed Abstract | Publisher Full Text
Schaufelberger MS, Duran FL, Lappin JM, Scazufca M, Amaro E Jr, Leite CC, De Castro CC, Murray RM, McGuire PK, Menezes PR, Busatto GF: Grey matter abnormalities in Brazilians with first-episode psychosis.
Br J Psychiatry Suppl 2007, 51:s117-22. PubMed Abstract
Venkatasubramanian G: Neuroanatomical correlates of psychopathology in antipsychotic-naïve schizophrenia.
Indian J Psychiatry 2010, 52(1):28-36. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Whitford TJ, Farrow TF, Gomes L, Brennan J, Harris AW, Williams LM: Grey matter deficits and symptom profile in first episode schizophrenia.
Psychiatry Res 2005, 139:229-38. PubMed Abstract | Publisher Full Text
Witthaus H, Kaufmann C, Bohner G, Ozgürdal S, Gudlowski Y, Gallinat J, Ruhrmann S, Brüne M, Heinz A, Klingebiel R, Juckel G: Gray matter abnormalities in subjects at ultra-high risk for schizophrenia and first-episode schizophrenic patients compared to healthy controls.
Psychiatry Res 2009, 173(3):163-9. PubMed Abstract | Publisher Full Text
Yoshihara Y, Sugihara G, Matsumoto H, Suckling J, Nishimura K, Toyoda T, Isoda H, Tsuchiya KJ, Takebayashi K, Suzuki K, Sakahara H, Nakamura K, Mori N, Takei N: Voxel-based structural magnetic resonance imaging (MRI) study of patients with early onset schizophrenia.
Ann Gen Psychiatry 2008, 7:25. PubMed Abstract | BioMed Central Full Text | PubMed Central Full Text
Adlam AL, Patterson K, Rogers TT, Nestor PJ, Salmond CH, Acosta-Cabronero J, Hodges JR: Semantic dementia and fluent primary progressive aphasia: two sides of the same coin?
Brain 2006, 129(Pt 11):3066-80. PubMed Abstract | Publisher Full Text
Boccardi M, Sabattoli F, Laakso MP, Testa C, Rossi R, Beltramello A, Soininen H, Frisoni GB: Frontotemporal dementia as a neural system disease.
Neurobiol Aging 2005, 26(1):37-44. PubMed Abstract | Publisher Full Text
Boxer AL, Rankin KP, Miller BL, Schuff N, Weiner M, Gorno-Tempini ML, Rosen HJ: Cinguloparietal atrophy distinguishes Alzheimer disease from semantic dementia.
Arch Neurol 2003, 60(7):949-56. PubMed Abstract | Publisher Full Text
Chang JL, Lomen-Hoerth C, Murphy J, Henry RG, Kramer JH, Miller BL, Gorno-Tempini ML: A voxel-based morphometry study of patterns of brain atrophy in ALS and ALS/FTLD.
Neurology 2005, 65(1):75-80. PubMed Abstract | Publisher Full Text
Desgranges B, Matuszewski V, Piolino P, Chételat G, Mézenge F, Landeau B, de la Sayette V, Belliard S, Eustache F: Anatomical and functional alterations in semantic dementia: a voxel-based MRI and PET study.
Neurobiol Aging 2007, 28(12):1904-13. PubMed Abstract | Publisher Full Text
Gee J, Ding L, Xie Z, Lin M, DeVita C, Grossman M: Alzheimer's disease and frontotemporal dementia exhibit distinct atrophy-behavior correlates: a computer-assisted imaging study.
Acad Radiol 2003, 10(12):1392-401. PubMed Abstract | Publisher Full Text
Gorno-Tempini ML, Dronkers NF, Rankin KP, Ogar JM, Phengrasamy L, Rosen HJ, Johnson JK, Weiner MW, Miller BL: Cognition and anatomy in three variants of primary progressive aphasia.
Ann Neurol 2004, 55(3):335-46. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Grossman M, McMillan C, Moore P, Ding L, Glosser G, Work M, Gee J: What's in a name: voxel-based morphometric analyses of MRI and naming difficulty in Alzheimer's disease, frontotemporal dementia and corticobasal degeneration.
Brain 2004, 127(Pt 3):628-49. PubMed Abstract | Publisher Full Text
Kanda T, Ishii K, Uemura T, Miyamoto N, Yoshikawa T, Kono AK, Mori E: Comparison of grey matter and metabolic reductions in frontotemporal dementia using FDG-PET and voxel-based morphometric MR studies.
Eur J Nucl Med Mol Imaging 2008, 35(12):2227-34. PubMed Abstract | Publisher Full Text
Kim EJ, Rabinovici GD, Seeley WW, Halabi C, Shu H, Weiner MW, DeArmond SJ, Trojanowski JQ, Gorno-Tempini ML, Miller BL, Rosen HJ: Patterns of MRI atrophy in tau positive and ubiquitin positive frontotemporal lobar degeneration.
J Neurol Neurosurg Psychiatry 2007, 78(12):1375-8. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Libon DJ, McMillan C, Gunawardena D, Powers C, Massimo L, Khan A, Morgan B, Farag C, Richmond L, Weinstein J, Moore P, Coslett HB, Chatterjee A, Aguirre G, Grossman M: Neurocognitive contributions to verbal fluency deficits in frontotemporal lobar degeneration.
Neurology 2009, 73(7):535-42. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Massimo L, Powers C, Moore P, Vesely L, Avants B, Gee J, Libon DJ, Grossman M: Neuroanatomy of apathy and disinhibition in frontotemporal lobar degeneration.
Dement Geriatr Cogn Disord 2009, 27(1):96-104. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Mummery CJ, Patterson K, Price CJ, Ashburner J, Frackowiak RS, Hodges JR: A voxel-based morphometry study of semantic dementia: relationship between temporal lobe atrophy and semantic memory.
Ann Neurol 2000, 47(1):36-45. PubMed Abstract | Publisher Full Text
Nestor PJ, Graham NL, Fryer TD, Williams GB, Patterson K, Hodges JR: Progressive non-fluent aphasia is associated with hypometabolism centred on the left anterior insula.
Brain 2003, 126(Pt 11):2406-18. PubMed Abstract | Publisher Full Text
Pardini M, Huey ED, Cavanagh AL, Grafman J: Olfactory function in corticobasal syndrome and frontotemporal dementia.
Arch Neurol 2009, 66(1):92-6. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Pereira JM, Williams GB, Acosta-Cabronero J, Pengas G, Spillantini MG, Xuereb JH, Hodges JR, Nestor PJ: Atrophy patterns in histologic vs clinical groupings of frontotemporal lobar degeneration.
Neurology 2009, 72(19):1653-60. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Rabinovici GD, Seeley WW, Kim EJ, Gorno-Tempini ML, Rascovsky K, Pagliaro TA, Allison SC, Halabi C, Kramer JH, Johnson JK, Weiner MW, Forman MS, Trojanowski JQ, Dearmond SJ, Miller BL, Rosen HJ: Distinct MRI atrophy patterns in autopsy-proven Alzheimer's disease and frontotemporal lobar degeneration.
Am J Alzheimers Dis Other Demen 2007, 22(6):474-88. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Rosen HJ, Gorno-Tempini ML, Goldman WP, Perry RJ, Schuff N, Weiner M, Feiwell R, Kramer JH, Miller BL: Patterns of brain atrophy in frontotemporal dementia and semantic dementia.
Neurology 2002, 58(2):198-208. PubMed Abstract | Publisher Full Text
Seeley WW, Crawford R, Rascovsky K, Kramer JH, Weiner M, Miller BL, Gorno-Tempini ML: Frontal paralimbic network atrophy in very mild behavioral variant frontotemporal dementia.
Arch Neurol 2008, 65(2):249-55. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Williams GB, Nestor PJ, Hodges JR: Neural correlates of semantic and behavioural deficits in frontotemporal dementia.
Neuroimage 2005, 24(4):1042-51. PubMed Abstract | Publisher Full Text
Bora E, Fornito A, Yücel M, Pantelis C: The effects of gender on grey matter abnormalities in major psychoses: a comparative voxelwise meta-analysis of schizophreniaand bipolar disorder.
Yu K, Cheung C, Leung M, Li Q, Chua S, McAlonan G: Are Bipolar Disorder and Schizophrenia Neuroanatomically Distinct?
An Anatomical Likelihood Meta-analysis. Front Hum Neurosci 2010, 4:189.
Ellison-Wright I, Bullmore E: Anatomy of bipolar disorder and schizophrenia: a meta-analysis.
Schizophr Res 2010, 117(1):1-12. PubMed Abstract | Publisher Full Text
Sundram F, Cannon M, Doherty CP, Barker GJ, Fitzsimons M, Delanty N, Cotter D: Neuroanatomical correlates of psychosis in temporal lobe epilepsy: voxel-based morphometry study.
Br J Psychiatry 2010, 197(6):482-92. PubMed Abstract | Publisher Full Text
Cascella NG, Schretlen DJ, Sawa A: Schizophrenia and epilepsy: is there a shared susceptibility?
Neurosci Res 2009, 63(4):227-35. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Labate A, Cerasa A, Gambardella A, Aguglia U, Quattrone A: Hippocampal and thalamic atrophy in mild temporal lobe epilepsy: a VBM study.
Neurology 2008, 71(14):1094-101. PubMed Abstract | Publisher Full Text
Cheung C, Yu K, Fung G, Leung M, Wong C, Li Q, Sham P, Chua S, McAlonan G: Autistic disorders and schizophrenia: related or remote? An anatomical likelihood estimation.
PLoS One 2010, 5(8):e12233. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Burbach JP, van der Zwaag B: Contact in the genetics of autism and schizophrenia.
Trends Neurosci 2009, 32:69-72. PubMed Abstract | Publisher Full Text
Goodman AB: A family history study of schizophrenia spectrum disorders suggests new candidate genes in schizophrenia and autism.
Psychiatr Q 1994, 65:287-297. PubMed Abstract | Publisher Full Text
McGrath J, Eyles D, Mowry B, Yolken R, Buka S: Low maternal vitamin D as a risk factor for schizophrenia: a pilot study using banked sera.
Schizophr Res 2003, 63:73-78. PubMed Abstract | Publisher Full Text
Cannell JJ: Autism and vitamin D.
Med Hypotheses 2008, 70:750-759. PubMed Abstract | Publisher Full Text
Brown AS: Prenatal infection as a risk factor for schizophrenia.
Schizophr Bull 2006, 32:200-202. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Chess S: Autism in children with congenital rubella.
J Autism Child Schizophr 1971, 1:33-47. PubMed Abstract | Publisher Full Text
Sommer I, Ramsey N, Kahn R, Aleman A, Bouma A: Handedness, language lateralisation and anatomical asymmetry in schizophrenia: meta-analysis.
Br J Psychiatry 2001, 178:344-351. PubMed Abstract | Publisher Full Text
Konick LC, Friedman L: Meta-analysis of thalamic size in schizophrenia.
Biol Psychiatry 2001, 49:28-38. PubMed Abstract | Publisher Full Text
Wright IC, Rabe-Hesketh S, Woodruff PWR, David AS, Murray RM, Bullmore ET: Meta-analysis of regional brain volumes in schizophrenia.
Am J Psychiatry 2000, 157:16-25. PubMed Abstract | Publisher Full Text
Zakzanis KK, Poulin P, Hansen KT, Jolic D: Searching the schizophrenic brain for temporal lobe deficits: a systematic review and meta-analysis.
Psychol Med 2000, 30:491-504. PubMed Abstract | Publisher Full Text
Nelson MD, Saykin AJ, Flashman LA, Riordan HJ: Hippocampal volume reduction in schizophrenia as assessed by magnetic resonance imaging: a meta-analytic study.
Arch Gen Psychiatry 1998, 55:433-440. PubMed Abstract | Publisher Full Text
Chance SA, Esiri MM, Crow TJ: Amygdala volume in schizophrenia: post-mortem study and review of magnetic resonance imaging findings.
Br J Psychiatry 2002, 180:331-338. PubMed Abstract | Publisher Full Text
Vita A, De Peri L: Hippocampal and amygdala volume reductions in first-episode schizophrenia.
Br J Psychiatry 2007, 190:271. PubMed Abstract | Publisher Full Text
Shenton ME, Dickey CC, Frumin M, McCarley RW: A review of MRI findings in schizophrenia.
Schizophr Res 2001, 49:1-52. PubMed Abstract
Ananth H, Popescu I, Critchley HD, Good CD, Frackowiak RSJ, Dolan RJ: Cortical and subcortical gray matter abnormalities in schizophrenia determined through structural magnetic resonance imaging with optimized volumetric voxel-based morphometry.
Am J Psychiatry 2002, 159:1497-1505. PubMed Abstract | Publisher Full Text
Salgado-Pineda P, Baeza I, Pérez-Gómez M, Vendrell P, Junqué C, Bargalló N, Bernardo M: Sustained attention impairment correlates to gray matter decreases in first episode neuroleptic-naive schizophrenic patients.
Neuroimage 2003, 19:365-375. PubMed Abstract | Publisher Full Text
Leung M, Cheung C, Yu K, Yip B, Sham P, Li Q, Chua S, McAlonan G: Gray matter in first-episode schizophrenia before and after antipsychotic drug treatment.
Anatomical likelihood estimation meta-analyses with sample size weighting. Schizophr Bull 2011, 37(1):199-211.
Chan RC, Di X, McAlonan GM, Gong QY: Brain anatomical abnormalities in high-risk individuals, first-episode, and chronic schizophrenia: an activation likelihood estimation meta-analysis of illness progression.
Schizophr Bull 2011, 37(1):177-88. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Schroeter ML, Raczka K, Neumann J, YvesVon Cramon D: Towards a nosology for frontotemporal lobar degenerations - a meta-analysis involving 267 subjects.
Neuroimage 2007, 36(3):497-510. PubMed Abstract | Publisher Full Text
Lund T, Groups M: Clinical and neuropathological criteria for frontotemporal dementia.
J Neurol Neurosurg Psychiatry 1994, 57:416-418. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Middleton FA, Strick PL: Basal ganglia output and cognition: evidence from anatomical, behavioral, and clinical studies.
Brain Cogn 2000, 42:183-200. PubMed Abstract | Publisher Full Text
Middleton FA, Strick PL: Basal ganglia and cerebellar loops: motor and cognitive circuits.
Brain Res Rev 2000, 31:236-250. PubMed Abstract | Publisher Full Text
Delong MR, Wichman T: Circuits and circuit disorders of the basal ganglia.
Arch Neurol 2007, 64(1):20-24. PubMed Abstract | Publisher Full Text
Gao WJ, Wang Y, Goldman-Rakic PS: Dopamine modulation of perisomatic and peridendritic inhibition in prefrontal cortex.
J Neurosci 2003, 23:1622-1630. PubMed Abstract | Publisher Full Text
Cassady SL, Adami H, Moran M, Kunkel R, Thaker GK: Spontaneous dyskinesia in subjects with schizophrenia spectrum personality.
Am J Psychiatry 1998, 155(1):70-5. PubMed Abstract | Publisher Full Text
Fish B, Marcus J, Hans SL, Auerbach JG, Purdue S: Infants at risk for schizophrenia: Sequelae of a genetic neurointegrative defect.
Arch Gen Psychiatry 1992, 49:221-235. PubMed Abstract | Publisher Full Text
Robbins TW: The case of frontostriatal dysfunction in schizophrenia.
Schizophr Bull 1990, 16(3):391-402. PubMed Abstract | Publisher Full Text
Garey LJ: Brodmann's Localisation in the Cerebral Cortex. London: Smith-Gordon; 1994. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Mesulam MM: Principles of Behavioural and Cognitive Neurology. New York: Oxford University Press; 2000.
Kiehl KA: A cognitive neuroscience perspective on psychopathy: evidence or paralimbic system dysfunction.
Psychiatry Res 2006, 142(2–3):107-28. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Skaf CR, Yamada A, Garrido GE, Buchpiguel CA, Akamine S, Castro CC, Busatto GF: Psychotic symptoms in major depressive disorder are associated with reduced regional cerebral blood flow in the subgenual anterior cingulate cortex: a voxel-based single photon emission computed tomography (SPECT) study.
J Affect Disord 2002, 68(2–3):295-305. PubMed Abstract | Publisher Full Text
Rubia K: "Cool" inferior frontostriatal dysfunction in attention-deficit/hyperactivity disorder versus "hot" ventromedial orbitofrontal-limbic dysfunction in conduct disorder: a review.
Biol Psychiatry 2011, 69(12):e69-87. PubMed Abstract | Publisher Full Text
Grahn JA, Parkinson JA, Owen AM: The role of the basal ganglia in learning and memory: neuropsychological studies.
Behav Brain Res 2009, 199(1):53-60. PubMed Abstract | Publisher Full Text
Grahn JA, Parkinson JA, Owen AM: The cognitive functions of the caudate nucleus.
Prog Neurobiol 2008, 86(3):141-55. PubMed Abstract | Publisher Full Text
Vemuri P, Wiste HJ, Weigand SD, Knopman DS, Trojanowski JQ, Shaw LM, Bernstein MA, Aisen PS, Weiner M, Petersen RC, Jack CR Jr: Alzheimer's disease neuroimaging initiative: Serial MRI and CSF biomarkers in normal aging, MCI, and AD.
Neurology 2010, 75(2):143-51. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Zalesky A, Fornito A, Bullmore ET: Network-based statistic: identifying differences in brain networks.
Neuroimage 2010, 53(4):1197-207. PubMed Abstract | Publisher Full Text
Tijms BM, Seriès P, Willshaw DJ, Lawrie SM: Similarity-based extraction of individual networks from gray matter MRI scans.
Cereb Cortex 2012, 22(7):1530-41. PubMed Abstract | Publisher Full Text
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Introducing the MBR Rapid Module Builder Framework (MBR Addon Builder) for ExpressionEngine. MBR Addon Builder is an application framework for ExpressionEngine that makes it possible to develop robust and secure ExpressionEngine add ons for a fraction of the time and cost possible using conventional methods. MBR Addon Builder includes many core components that make it possible to develop secure and powerful data driven applications for ExpressionEngine with advanced settings panels, form builders for gathering customer input, and maintenance systems that simplify installation, upgrades, and skinning
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Aging NYC stickballers keeps street game alive
NEW YORK They run with a little less speed, hit with a little less power and worry less about shattering nearby windows, but a graying crew of stickball enthusiasts is keeping the urban sport alive and honoring the legends who shaped the game.
Six players from around the country were being added Friday to the 144 people already in the Stickball Hall of Fame, selected by a committee of so-called old-timers who have followed the sport since its heyday in the 1940s and '50s.
Their grading scale is not exactly scientific. The game's lore is passed on in stories and arguments about whether the Pleasant Avenue Boys were better than the 100th Street Boys and which pitcher was harder to hit, which batter most feared at the plate.
"We don't have statistics; we have bragging rights," said Carlos Diaz, 64, a hospital administrator who held the first induction ceremony a dozen years ago and now runs the Stickball Community Gallery out of an old storefront in East Harlem.
"When we were playing, if you broke a window, you ran or the cop would come and take the stick away from you and put it down the manhole covers," Diaz said.
The game is played on city streets in New York City's neighborhoods and took off around the turn of the 20th century. It's a form of baseball with a twist: Instead of bats, hitters use broomsticks; instead of baseballs, pink rubber balls; instead of three strikes, each batter gets just one swing to hit the ball off the bounce; and instead of a baseball diamond, the field is determined by street lamps, manhole covers and parked cars.
Teams were largely reflections of the neighborhoods where they played: Italian players from Queens, black players from Harlem, Spanish players from East Harlem. Professional baseball players such as Rusty Torres and former New York Yankees manager Joe Torre played growing up in Brooklyn.
The game was more than a diversion, said Alfred Jackson, who was still shagging fly balls barehanded at age 78. He proudly identified himself as from 112th and Lexington, recalling a time when every block had a team.
"Every Sunday you'd see the kids out playing stickball in the street, and the cops chasing us," he said. "We played for money. It's how we got money to pay for whatever we needed - food, clothes, rent. And not every Sunday was a winning Sunday."
George "Lolin" Osorio, a Hall of Famer from Puerto Rico who moved to Manhattan in 1945, told of watching the older guys play when he was a kid. They would play for big money, and give the kids a quarter to run up on the roof and fetch the balls.
But the game has lost popularity with time, said Diaz. Players moved away, first to fight in wars overseas and later as the ravages of drugs and crime stripped city neighborhoods of their safety, their populations and their sense of community. A small group of followers including George Vega, who was being inducted Friday, kept the game alive by playing in the late 1970s, '80s and '90s.


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Celebrities Supporting Breast Cancer Awareness | Pictures
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See the Stars Fighting For a Breast Cancer Cure
October is Breast Cancer Awareness Month, a time when women around the globe get together to stand up for the cause. A-listers like Jennifer Aniston, Reese Witherspoon, and Miley Cyrus have taken the stage too, putting on their sneakers for charity walks or partying in pink. There are plenty of famous breast cancer survivors who have also gotten involved.
You can get involved, too, whether it's sharing tips on how to lower breast cancer risks or by informing yourself and your loved ones about foods to eat to prevent the disease. In honor of Breast Cancer Awareness Month, keep reading for pics of top celebs showing their support.
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Has this been posted? If not, you have got to start following this shit! Rihanna's 7 day tour is a circus! It's not being serialized by Gawker. Pix, tweets, candid Youtube video of streaker on plane, everything. Here's the beginning of the first article... [quote]The Rihanna plane, which earlier today was on the verge of anarchy, officially descended into total chaos somewhere between Berlin and London. Journalists are chanting, Australians are streaking, and passengers are being forced to consume strange foods. Now go click on the link. LMFAO
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