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PubMed2000

Interpretation of computed tomography does not correlate with laboratory or pathologic findings in surgically confirmed acute appendicitis.

BACKGROUND: Computed tomography (CT) is used increasingly to diagnose acute appendicitis, despite variable technique and interpretation. We hypothesized that CT interpretation would not reflect actual clinical-pathologic findings in all demographic patient groups. METHODS: A prospective university hospital database of 625 consecutive patients (1995-1999), all of whom were operated on for appendicitis (261, or 41.8%, within 24 hours of discretionary CT), was reviewed. CT and pathology data were obtained from final, written reports. CT criteria included free fluid or air, appendiceal visualization, mesenteric fat stranding, and blurred pericecal fat. Appendix pathology included acute, gangrenous, and perforated organs. Statistics were performed with the Fisher exact test (coordinate data) and univariate analysis of variance (continuous data); multivariate analysis of variance for independent effects on dependent variable (positive CT or pathology; P <.05). RESULTS: The mean age was 35 +/- 1 years with 46.6% being female patients. CT was done more often in women and after 1997 (both P <.05). The sensitivity and specificity of CT were 96.1% and 16.1%, respectively. The positive predictive value (PPV) and accuracy rate (A) were 90%, and 88%, respectively. After CT, the incidence of finding a normal appendix was lower (19.3% vs 12.3%, P <.05), especially if the white blood cell count (WBC) was normal (< or = 11K/microL, 6.1% vs 23.2%, P <.001). If the WBC was < or = 11K/microL with positive CT, PPV/A was 73. 7%/71.3%, whereas with WBC > 11K/microL and positive CT, PPV/A was 99.4%/93.3%. Multivariate analysis of variance showed that none of the individual variables used by the radiologist to determine a positive CT scan correlated with outcome determined by surgical pathology. A healthy appendix was predicted by a CT interpreted as negative and younger age (both P <.05), and especially by lower WBC (P <.0001), but not by gender or surgeon. CONCLUSIONS: Although the negative appendectomy rate was decreased by CT, there was no correlation between CT findings and pathologically proved disease. Other factors such as more precise patient selection by clinical criteria may also be improving outcome. A positive CT scan in a patient with a normal WBC should be interpreted with caution.

Acute Disease↗
PubMed2001

Serum and cerebrospinal fluid pathology in patients with sudden sensorineural hearing loss.

The serum and cerebrospinal fluid (CSF) pathology of patients with sudden sensorineural hearing loss (SHL), both seropositive and seronegative to Borrelia burgdorferi (Bb), was prospectively studied. Nineteen consecutive patients were included and trends between the degree of hearing recovery and serum/CSF pathology and given therapy were examined. The pilot study showed a high prevalence (68%) of pathology in serum and CSF in patients with SHL. In 54% of the patients, elevated levels of CSF proteins and/or pathological CSF cell counts were present without positive antibodies to Bb. Positive levels of antibodies against Bb or pathological proteins in CSF were associated with better hearing recovery (means of 47.2 and 51.7%, respectively). The audiometric configuration "high frequency sloping" hearing impairment was associated with the lowest degree of hearing recovery. Patients with SHL and positive serology to Bb who received antibiotic treatment (oral tetracycline), with or without steroids, had the best hearing recovery in this study (61.7 and 48.4%, respectively). In conclusion, we found a high prevalence of serum and CSF pathology in a consecutive group of patients with SHL. Early appropriate antibiotic treatment may prevent the development of major late complications of Lyme disease/borreliosis. We also find it justified to perform more general serological analyses, including CSF analysis, in patients with SHL. A more liberal approach to testing and development of test protocols for SHL patients will increase our knowledge in this field.

Adult↗
PubMedDate not supplied

Tobacco use and pathological gambling.

BACKGROUND: Evidence supports phenomenological, clinical, epidemiological and biological links between problem/pathological gambling and tobacco use. An improved understanding of the relationship would be helpful in treating individuals with co-occurring pathological gambling and nicotine dependence. METHODS: This study investigates the tobacco use behaviors of 225 adults (mean age +/- SD = 47.3 +/- 11.0 years; number of women = 120 [53.3%]) who were recruited for pharmacological treatment of pathological gambling. All subjects met criteria for pathological gambling based upon the Structured Clinical Interview for Pathological Gambling (SCI-PG), a DSM-IV-based diagnostic interview, and were assessed at baseline with multiple reliable and valid measures of gambling severity. RESULTS: 159 (70.7%) subjects were either current (n = 110; 48.9%) or prior daily smokers (n = 49; 21.8%). Compared with the group of never smokers, the group of current and prior daily smokers was more likely to be older (F = 3.55; df = 2, 222; p = 0.030), be female (chi square = 10.85; df = 2; p = 0.004), and have stronger urges to gamble (F = 128.15; df = 2,222; p < 0.001). CONCLUSIONS: Daily tobacco use in treatment-seeking pathological gamblers is common and associated with more severe urges to gamble. Treatments targeting urges in individuals with pathological gambling and current or prior daily tobacco use should be examined.

Adolescent↗
PubMed1996

Nutritional characteristics, eating pathology, and hormonal status in young women.

Ovulatory dysfunction is common in patients with eating disorders. However, many women engage in pathologic dieting behaviors without meeting the current diagnostic criteria for anorexia or bulimia nervosa. Clinical eating disorders are only the most extreme form of pathologic eating attitudes and behaviors that are present in many young women. Specific food choices and nutrient intakes may be associated with altered gonadal hormone status of these dieters. This cross-sectional study was conducted to describe the nutritional characteristics of college-aged women defined by their eating attitudes and behaviors with a previously described questionnaire. We evaluated dietary intake, body composition, and selected biochemical indicators in 76 undergraduate women. Serum concentrations of estradiol, progesterone, lipids, and carotenoids were measured on days 6, 21, and 28 of one menstrual cycle. Dietary assessment was based on food records at two 3-d intervals during the cycle. Ovulatory status was definitively determined on the basis of biochemical data for 46 of the women. Increased degree of pathologic dieting was associated with a significantly lower intake of dietary fat (P < 0.02), despite similar mean body mass index and body composition across the eating pathology groups. Serum concentration of alpha-carotene was significantly greater (P < 0.005) in association with a greater degree of eating pathology. With ovulation as a between-group factor, serum lutein concentration and dietary intake of energy and fat differed significantly between groups (P < 0.003). Nutritional characteristics associated with pathologic dieting behavior may also be associated with menstrual irregularities in young women.

Adolescent↗
PubMed1997

Central nervous system pathology in patients with the Guillain-Barré syndrome.

Thirteen autopsy cases of patients with clinical criteria of the Guillain-Barré syndrome were investigated for pathological changes and cellular composition of inflammatory infiltrates in the CNS and PNS. The survival times from the onset of neurological symptoms until death ranged from 1 day to 12 months. In the CNS, degeneration of spinal posterior tracts was seen in three cases. Mononuclear infiltrates consisted of evenly proportioned lymphocytes and macrophages in cases with survival of 1 and 2 days, whereas macrophages predominated in cases with survival of 5 days and longer. Infiltrates presented as nodular clusters around blood vessels and neurons, or were scattered diffusely. They were found within the spinal cord in eight out of 13 cases, within the medulla oblongata in eight out of 12 cases, within the pons in five out of nine cases, and in one out of four midbrains. Activation of microglia, either focal or diffuse, was found in various degrees in 11 out of 13 cases, involving the spinal cord (six out of 13 cases), the medulla oblongata (10 out of 12 cases), the pons (five out of nine cases) or as subependymal rims along the walls of the ventricular system and the central canal of the spinal cord (seven out of 13 cases). In the PNS, myelin loss (12 out of 13 cases), axonal degeneration (six out of 13 cases) and mononuclear cell infiltrates (13 out of 13 cases) were seen in segmental and cranial nerves, spinal ganglia and spinal roots in varying distribution and severity. Mononuclear cell infiltrates were composed of macrophages and T lymphocytes, with even distribution in cases with short survival (1 and 2 days), and predominance of macrophages in cases with protracted clinical course. T lymphocytes were equally composed of OPD4+ and CD8+ cells without obvious differences between cases of short and long duration, or between PNS and CNS infiltrates in 11 out of 12 cases, whilst two cases had a dominant OPD4+ subset. We conclude that CNS pathology is frequent in patients with Guillain-Barré syndrome. It involves axons with secondary myelin impairment, microglial activation and inflammatory infiltration. In this series, primary demyelination is not found in the CNS. Changes such as degeneration of spinal posterior tracts are secondary to pathology in the PNS. Inflammatory cell reactions in the CNS are similar to those in the PNS and to CNS pathology in experimental allergic neuritis. This inflammation might reflect CNS immune activation in the absence of the relevant antigen, in addition to cellular reactions accompanying secondary CNS changes. The presence of distinct pathology in the CNS is in contrast with other recent studies on the pathology of Guillain-Barré syndrome which, unlike this study, may have been influenced by recently introduced treatments.

Adult↗
PubMed2005

The slow Wallerian degeneration gene, WldS, inhibits axonal spheroid pathology in gracile axonal dystrophy mice.

Axonal dystrophy is the hallmark of axon pathology in many neurodegenerative disorders of the CNS, including Alzheimer's disease, Parkinson's disease and stroke. Axons can also form larger swellings, or spheroids, as in multiple sclerosis and traumatic brain injury. Some spheroids are terminal endbulbs of axon stumps, but swellings may also occur on unbroken axons and their role in axon loss remains uncertain. Similarly, it is not known whether spheroids and axonal dystrophy in so many different CNS disorders arise by a common mechanism. These surprising gaps in current knowledge result largely from the lack of experimental methods to manipulate axon pathology. The slow Wallerian degeneration gene, Wld(S), delays Wallerian degeneration after injury, and also delays 'dying-back' in peripheral nervous system disorders, revealing a mechanistic link between two forms of axon degeneration traditionally considered distinct. We now report that Wld(S) also inhibits axonal spheroid pathology in gracile axonal dystrophy (gad) mice. Both gracile nucleus (P < 0.001) and cervical gracile fascicle (P = 0.001) contained significantly fewer spheroids in gad/Wld(S) mice, and secondary signs of axon pathology such as myelin loss were also reduced. Motor nerve terminals at neuromuscular junctions continued to degenerate in gad/Wld(S) mice, consistent with previous observations that Wld(S) has a weaker effect on synapses than on axons, and probably contributing to the fact that Wld(S) did not alleviate gad symptoms. Wld(S) acts downstream of the initial pathogenic events to block gad pathology, suggesting that its effect on axonal swelling need not be specific to this disease. We conclude that axon degeneration mechanisms are more closely related than previously thought and that a link exists in gad between spheroid pathology and Wallerian degeneration that could hold for other disorders.

Animals↗
PubMed1994

Lifetime prevalence estimates of pathological gambling in New Zealand.

BACKGROUND: Legalized gambling has proliferated recently in many countries and is a public health issue because of the association between gambling participation and the prevalence of pathological gambling. Relatively little is known about the epidemiology of this disorder or the characteristics of pathological gamblers living in the community. This paper summarizes the major findings of a national prevalence survey of pathological gambling conducted in New Zealand; the first national survey to have been conducted to date, and compares them with the results of studies undertaken in the US and Canada. METHODS: A national adult sample of 4053 people was interviewed by telephone to determine involvement in gambling activities. The interview included the South Oaks Gambling Screen (SOGS) for pathological gambling. RESULTS: Of the sample, 2.7% (+/- 0.5%) scored as probable pathological gamblers and a further 4.2% (+/- 0.6%) scored as problem gamblers. These prevalence rates are higher than those reported in previous studies using the SOGS. Ethnicity, age, gender, employment status, having a parent who had gambling problems and regular participation in continuous forms of gambling were major risk factors. CONCLUSIONS: In New Zealand pathological gambling appears to have a lifetime prevalence approximately half that of drug abuse/dependence. The findings suggest that prevalence has increased in recent years and provide a baseline for further study. The risk factors identified give a focus for future research into aetiology, prevention and treatment.

Adolescent↗
PubMed2024

Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.

Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is detectable at autopsy in more than one-third of people beyond age 85 years and is robustly associated with dementia independent of other pathologies. Although LATE-NC has a large impact on public health, there remain uncertainties about the underlying biologic mechanisms. Here, we review the literature from human studies that may shed light on pathogenetic mechanisms. It is increasingly clear that certain combinations of pathologic changes tend to coexist in aging brains. Although "pure" LATE-NC is not rare, LATE-NC often coexists in the same brains with Alzheimer disease neuropathologic change, brain arteriolosclerosis, hippocampal sclerosis of aging, and/or age-related tau astrogliopathy (ARTAG). The patterns of pathologic comorbidities provide circumstantial evidence of mechanistic interactions ("synergies") between the pathologies, and also suggest common upstream influences. As to primary mediators of vulnerability to neuropathologic changes, genetics may play key roles. Genes associated with LATE-NC include TMEM106B, GRN, APOE, SORL1, ABCC9, and others. Although the anatomic distribution of TDP-43 pathology defines the condition, important cofactors for LATE-NC may include Tau pathology, endolysosomal pathways, and blood-brain barrier dysfunction. A review of the human phenomenology offers insights into disease-driving mechanisms, and may provide clues for diagnostic and therapeutic targets.

Humans↗
PubMed1986

Episodic and residual thought pathology in chronic schizophrenics: effect of neuroleptics.

We sought to determine the effect of neuroleptic treatment on thought disorder in chronic schizophrenics, using the Thought Disorder Index (TDI). We were able to demonstrate that high levels of thought disorder are found in chronic schizophrenic and schizoaffective patients, while in both bipolar patients and normal controls thought pathology is minimal. Moreover, the TDI appears to be particularly well suited to the characterization of thought disorder in chronic schizophrenics. For total scores on the TDI, we were unable to demonstrate a significant reduction in thought pathology, although it was evident that thought disorder as reflected in the Conceptual Disorganization and Unusual Thought Content subscales of the Brief Psychiatric Rating Scale is significantly reduced by neuroleptics. In analyses of subscores of the TDI reflecting four levels of severity, we were able to show that more severe forms of thought pathology are normalized by neuroleptics, while less severe pathology is largely unaffected. Our results suggest that neuroleptic treatment reduces thought pathology associated with acute episodes, but that somewhat milder, though still disabling, residual thought pathology persists after clinical remission has been attained.

Adult↗
PubMed2003

Multiple measures of carcinoma extent versus perineural invasion in prostate needle biopsy tissue in prediction of pathologic stage in a screening population.

The capacity of perineural invasion by carcinoma in prostate needle biopsy tissue to independently predict pathologic stage in radical prostatectomy tissues remains uncertain. We sought to determine, in a prostate specific antigen-based screening population, the ability of needle biopsy histologic grade, tumor extent, and perineural invasion to independently predict pathologic stage and margin status in the whole prostate gland. Perineural invasion, Gleason grade, percentage Gleason pattern 4/5 carcinoma, and multiple measures of needle biopsy tumor extent, including number of positive cores, percentage of positive cores, total percentage of carcinoma, greatest percentage of carcinoma in a single core, and total carcinoma length in millimeters, were captured for 215 men from a prostate specific antigen-based screening program diagnosed with prostate cancer in a median of six procured needle biopsy cores. Pathologic stage and surgical margin status were evaluated in corresponding completely embedded radical prostatectomy specimens. A logistic regression model was used to relate the endpoints of extraprostatic extension by carcinoma and/or positive margins to needle biopsy tissue findings. In univariate analyses, total percentage of carcinoma (p = 0.003), greatest percentage of carcinoma in a single core (p = 0.004), total tumor length in millimeters (p = 0.009), and fraction of positive cores (p = 0.02) were all significantly associated with extraprostatic (pT3) carcinoma, whereas all five measures of carcinoma extent in needle biopsy tissue were related to positive margins. Correlation coefficient determinations showed that all five measures of needle biopsy carcinoma extent were highly interrelated. In multivariate analyses, total percentage of carcinoma was significantly related to pathologic T stage (p = 0.003) and positive margins (p = 0.0002). In a multivariate model with the radical prostatectomy whole gland endpoint of either pT3 disease or positive margins, fraction of positive cores (p = 0.00001) was the only variable with significant predictive value. Perineural invasion by carcinoma in needle biopsy tissue was detected in 11% of cases. Neither presence nor absence of perineural carcinoma nor number nor percentage of positive nerves related to pathologic stage in univariate or multivariate analyses. Amount of carcinoma in prostate needle biopsy tissue, using multiple measurements but not perineural invasion, is a significant histologic attribute predictive of pathologic stage and margin status for men with prostate specific antigen screening detected prostatic carcinoma. Reporting of several measures of carcinoma extent in needle biopsy tissue is recommended.

Adult↗
PubMed2003

Pathologic review of negative sentinel lymph nodes in melanoma patients with regional recurrence: a clinicopathologic study of 1152 patients undergoing sentinel lymph node biopsy.

A sentinel lymph node (SLN) that is melanoma negative by pathologic examination implies absence of melanoma metastasis to that regional lymph node field. However, a small proportion of patients develop regional node field recurrence after a negative SLN biopsy. In this study, we reviewed the histopathology of negative SLNs from such patients to determine whether occult melanoma cells were present in the SLNs, to characterize the pathologic features of false-negative SLNs, and to provide recommendations for the histopathologic examination of these specimens. Between March 1992 and June 2001, of 1152 patients who had undergone SLN biopsy for primary melanomas at the Sydney Melanoma Unit, 976 were diagnosed with negative SLNs by initial pathologic examination (using 2 hematoxylin and eosin stained sections, and 2 immunostained sections for S-100 protein and HMB45), and follow-up was available in 957. Of these, 26 (2.7%) developed regional lymph node recurrence during a median follow-up period of 35.7 months. For 22 of them, the original slides and tissue blocks were available for reexamination. The original slides of each block were reviewed. Multiple further sections were cut from each block and stained with hematoxylin and eosin, for S-100, HMB45, and Melan A. Deposits of occult melanoma cells were detected in 7 of the 22 cases (31.8%). In 5 of the 7 cases, deposits of melanoma cells were present only in the recut sections. There were no significant differences in clinical and pathologic variables for those patients in whom occult melanoma cells were found by pathologic reexamination of their SLNs, compared with those in whom no melanoma cells were detected. The detection of melanoma cell deposits in only 7 of 22 false-negative SLNs suggests that mechanisms other than failure of histopathologic examination may contribute to the failure of the SLN biopsy technique in some patients. The failure rate for melanoma detection in SLNs by our routine pathologic examination, using the current protocol at our institution, was <1% (7 of 957 patients). Routinely performing more intensive histopathologic examination of SLNs is difficult to justify from a cost benefit perspective; we therefore recommend examining two hematoxylin and eosin stained sections and two immunostained sections (for S-100 and HMB45) routinely on SLNs from melanoma patients.

Adult↗
PubMed2006

Crypt dysplasia with surface maturation: a clinical, pathologic, and molecular study of a Barrett's esophagus cohort.

Little is known regarding the significance of esophageal biopsies that show dysplasia-like atypia limited to the bases of the crypts, without involvement of the surface epithelium in Barrett's esophagus (BE). The aim of this study was to evaluate the clinical, pathologic, immunohistochemical, and molecular characteristics of basal crypt dysplasia-like atypia (BCDA) with surface maturation in surveillance endoscopic mucosal biopsies to gain insight into its biologic significance. The Seattle Barrett's Esophagus Project is a prospective cohort study in which patients and their biopsies have been evaluated prospectively for clinical, pathologic, and molecular markers. As part of continued surveillance of the cohort, 206 consecutive BE patients were evaluated prospectively for BCDA between July 1, 2001 and August 13, 2003; 15 patients had BCDA (prevalence rate = 7.3%). These 15 patients were evaluated for clinical, pathologic, and immunohistochemical (p53 and MIB-1) features during the study period (2001-2003) as well as associations with clinical, pathologic, and molecular markers [17p(TP53) loss of heterozygosity (LOH), 9p(p16) LOH, tetraploidy, and aneuploidy] that were detected previously in the same patients in the cohort study (1983-2001). All BE patients with BCDA (male-to female ratio, 12:3; mean age, 72 years; mean length of BE, 7.0 cm; mean duration of BE, 95.1 months), except 2 (87%), had dysplasia or adenocarcinoma detected in biopsies either prior to or concurrent to the one that contained BCDA. In contrast, only 112 of 191 (59%) controls had neoplasia during the same time period (59%, P = 0.05). The difference between BCDA and controls was particularly significant with regard to the association with high-grade dysplasia (P = 0.004). Compared with adjacent nonatypical and nondysplastic (metaplastic) BE, areas of BCDA showed a significantly elevated prevalence rate of p53 positivity (60% vs. 13%, P<0.02) and a significantly elevated total crypt and basal crypt MIB-1 proliferation rate (P<0.001). Indeed, the MIB-1 proliferation rate in the basal portion of the crypts in BCDA was similar to that detected in conventional low- or high-grade dysplasia. Patients with BCDA showed a significantly increased rate of 17p(TP53) LOH (P = 0.016), aneuploidy (P = 0.004), and a trend in increased 9p(p16) LOH (P = 0.08), compared with control patients without BCDA. The clinical, pathologic, immunohistochemical, and molecular abnormalities were similar in BCDA cases that were considered low-grade versus those considered high-grade by histologic evaluation, except that high-grade cases tended to be older (79 years vs. 68 years, P = 0.06). BCDA with surface maturation, in mucosal biopsies from patients with BE, is an uncommon but significant pathologic change that shows a variety of proliferative and molecular abnormalities and has a high association with conventional dysplasia and/or adenocarcinoma. Based on these findings, BCDA warrants further investigation as a possible subtype of true dysplasia despite the morphologic appearance of surface maturation.

Adenocarcinoma↗
PubMedDate not supplied

Primary tumors and mediastinal lymph nodes after neoadjuvant concurrent chemoradiotherapy of lung cancer: serial CT findings with pathologic correlation.

PURPOSE: The purpose of this work was to describe the changes of primary tumor and mediastinal lymph nodes on CT after neoadjuvant concurrent chemoradiotherapy and to correlate the CT findings with pathology. METHOD: Twenty-one consecutive patients [N2 disease (n = 19) or resectable T4 and N2 disease (n = 2)] with non-small cell lung cancer underwent neoadjuvant concurrent chemoradiotherapy. Changes of primary tumor and mediastinal nodes before and after the therapy were assessed using CT. The CT findings were correlated with pathologic findings. RESULTS: With neoadjuvant therapy, decrease in T stage was achieved in 9 of 21 (43%) patients on CT. On pathology, the remaining tumor consisted mostly of fibrosis and necrosis with little proportion of viable tumor cells (mean volume 17%, range 0-55%). Decrease in nodal stage was achieved in 14 of 21 (67%) patients on pathologic examination. Seven patients had cancer cells in mediastinal lymph nodes: in 6 of 9 (67%) patients with adenocarcinoma and 1 of 12 (8%) patients with squamous cell carcinoma (p = 0.016). CONCLUSION: With neoadjuvant concurrent chemoradiotherapy, the remaining tumor consists mostly of fibrosis or necrosis. Decreased nodal stage on pathology is achieved especially in patients with N2 disease of squamous cell carcinoma. The CT findings of the tumor and mediastinal nodes are not helpful in predicting the pathology after the therapy.

Adenocarcinoma↗
PubMed1983

Effects of subliminal stimulation of oneness fantasies on manifest pathology in male vs. female schizophrenics.

This study examined the effects of subliminally activated fantasies of oneness with each parent on the manifest pathology of schizophrenic men and women. Subjects were seen individually for three subliminal stimulation sessions on different days. In each session, measures of pathological thinking and pathological behavior were obtained for a "baseline" assessment before subliminal stimulation, and a "critical" assessment after subliminal stimulation. All subjects received, in counterbalanced order, the two subliminal oneness stimuli ("mommy and I are one" and "daddy and I are one" plus congruent pictures) and a neutral-control message ("people are walking" plus a congruent picture). At the end of the last session, each subject was given a family interview and a family picture test (a card from the CAT depicting three bears at a tug of war). The aim of these procedures was to allow for an exploration of the relationship between the schizophrenic's perception of his or her early experience with each parent and his or her response to each oneness stimulus. Results for symbiotic stimulation showed, as hypothesized: a) the "mommy" stimulus reduced pathological behavior in males but not in females; b) the "daddy" stimulus reduced pathological thinking in females but not in males. Results of the family interview and picture test indicated that the more the male subjects experienced active involvement with one parent, the more they reduced pathology after the oneness stimulus involving that parent, and the less they did so after the stimulus involving the other parent. These results were discussed and suggestions for future research were offered.

Fantasy↗
PubMed1999

Pathologic evaluation of the human suprachiasmatic nucleus in severe dementia.

Sleep disruption and other circadian rhythm disturbances are frequently seen in dementia patients. In this study, we examined the suprachiasmatic nucleus (SCN), the putative site of the hypothalamic circadian pacemaker, to determine the nature and degree of pathologic changes caused by severe dementia. Neuropathologic examination indicated that among 30 patients with a clinical history of severe dementia, 22 had Braak and Braak stage V-VI Alzheimer disease, 3 had combined Alzheimer and Parkinson disease, 3 had Pick disease and 2 had severe hippocampal sclerosis. Comparisons were made with a control group composed of 13 age-matched patients with no clinical or pathological evidence of dementia or other CNS disorders. To determine the pathologic involvement within the SCN, human hypothalami were stained with: Nissl, Bielchowsky silver, thioflavin S and specific antibodies directed against vasopressin (VP), neurotensin (NT), neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), beta-amyloid (B/A4) and glial fibrillary acidic protein (GFAP). Pathologic damage was primarily limited to neuronal loss and neurofibrillary tangle formation. Only rare diffuse plaques were noted. The pathologic changes within the SCN were less severe than in the other brain regions. Morphometric analysis was accomplished using a stereological approach to sample the average total number of positively stained neurons and astrocytes in 10 different 0.1mm2 microscopic fields in the dorsal subdivision of the SCN. Patients with Alzheimer disease exhibited a significant decrease in vasopressin (9.75 vs 16.7, p < 0.001) and neurotensin (6.82 vs 9.63, p < 0.002) neurons, as well as a corresponding increase in the GFAP-stained astrocyte/Nissl-stained neuron ratio (0.54 vs 0.10, p < 0.009). These studies provide evidence that both vasopressin and neurotensin neurons are lost in Alzheimer disease, and that the astrocyte/neuron ratio is a reliable indicator of disease-related pathology within the SCN. Taken collectively, our data support the hypothesis that damage to the SCN may be an underlying anatomical substrate for the clinically observed changes in circadian rhythmicity that have been observed in Alzheimer patients.

Case-Control Studies↗
PubMed1999

Progressive supranuclear palsy with dementia: cortical pathology.

Patients with progressive supranuclear palsy (PSP) often develop dementia, and cortical pathology has been documented in PSP. However, there are no reports correlating dementia in PSP with cortical pathology. We hypothesized that cases of PSP presenting with cognitive impairment would have more severe cortical tau pathology than those without. We compared 7 cases of PSP presenting with cognitive deficits (group 1) with 4 cases of PSP that did not (group 2). The subcortical tau pathology was almost identical in both groups. The cortical tau pathology was strikingly different in group 1, in which it was on average moderate, compared with group 2, in which it was minimal. The accumulation of cortical neuronoglial tau in PSP cases with dementia suggests that neurofibrillary pathology is central to the cause of dementia in PSP.

Aged↗
PubMed2006

Visual association pathology in preclinical Alzheimer disease.

The transition from normal aging to mild cognitive impairment to Alzheimer disease (AD) is often indistinct. Imaging studies suggest early changes in posterior brain regions, including posterior temporoparietal and occipital cortex, but pathologic studies show initial changes in the medial temporal lobe with progressive neocortical involvement as cognition deteriorates. We evaluated the regional distribution of AD pathology in 41 elderly brain donors from the Framingham Heart Study who were cognitively intact, mildly impaired, or demented on the basis of probable AD. We found that 52% of the cognitively intact subjects, and all subjects with mild cognitive impairment or dementia, had dense neurofibrillary tangles (NFTs), neuropil threads, and tau-immunoreactive neurites surrounding neuritic plaques (NPs) in visual association cortex Brodmann area 19. All cognitively intact subjects with area 19 NFTs also had dense core NP and beta amyloid (Abeta) angiopathy in area 19. Area 19 pathology was occasionally present in the absence of substantial pathology in the hippocampus or entorhinal cortex and was not correlated with medial temporal lobe pathology. Dense AD pathology in area 19 is present in some cognitively intact subjects with preclinical AD. The unique metabolic, connectional, and vascular features of this region may confer enhanced vulnerability to neurodegeneration.

Aged↗
PubMed1996

A comparison of MRI and bone SPET in the diagnosis of knee pathology.

Bone single photon emission tomography (SPET) of the knees has been shown to be of diagnostic value for the investigation of knee pain. This study compared bone SPET with magnetic resonance imaging (MRI) for the diagnosis of knee disorders. Thirty-six patients were studied with modalities, performed an average of 4 months apart (range 0-10 months). There was agreement on the presence or absence and nature of pathology in 24 (67%) patients. In a further three patients, there was an abnormal SPET with equivocal change for the same pathology on MRI. Equivocal change on both modalities for the same pathology were found in one patient. Three patients had abnormalities on MRI with normal SPET, with the remaining patients having equivocal or non-specific changes on one modality only. In the majority of patients, there was agreement on the presence or absence of pathology and the nature of pathology with both modalities. Significant pathology detected on MRI was also identified by bone SPET. This initial study suggests that further work should be undertaken to evaluate the role of bone SPET as a screening test for the evaluation of knee disorders and its role in relation to MRI is justified.

Adolescent↗