Brain Atrophy Changes Research Articles

Some neuropsychiatric and MRI manifestations in patients with multiple sclerosis

Background Neuropsychiatric abnormalities are common in multiple sclerosis (MS) patients. Cognitive dysfunction affects ∼40% of MS patients. Advances in neuroimaging are increasing our understanding of the pathogenesis of these disorders. Aim This study aimed to assess the possible neurological and psychiatric complications and cognitive impairment in MS patients and to correlate the psychiatric symptoms with clinical types, severity, and MRI findings in MS patients. Participants and methods This is a cross-sectional descriptive study that was carried out on 25 patients diagnosed with definite MS according to McDonald’s criteria. All patients were subjected to a semi-structured interview that included demographic data and full neurological and psychiatric examination, Expanded Disability Status Scale (EDSS) evaluation, Mini-Mental State Examination (MMSE), and MRI brain with assessment of the lesions number, site, and brain atrophy. Results This study included 25 adults, 19 women and six men. They ranged in age from 22 to 55 years, mean age 33±9 years. The mean disease duration was 6.4±3 years. Sixty-four percent of the patients were married. Sixty-four percent of the patients had the relapsing remitting type of MS. Fatigue was the most prevalent symptom (96%), followed by sphincter troubles, (80%) visual symptoms (76%), dizziness (64%), sexual dysfunction (60%), and pain (56%). EDSS showed that 44% of the patients had moderate disability, 32% of the patients needed intermittent or constant unilateral assistance, and 24% of the patients needed constant bilateral support. On applying the Structural Clinical Interview for DSM-IV Axis I (SCID-I), it was found that depression (60%), dysthymia (60%), and generalized anxiety disorder (68%) were the most prevalent psychiatric presentations. For the MMSE, 24% of the patients showed an MMSE score between 17 and 25 and 4% the patients showed scores less than 17. Assessment of MRI brain showed that atrophic brain changes were present in 72% of the patients. All the patients studied had supratentorial plaques and 44% had frontal plaques. Infratentorial lesions were present in 72% of MS patients. Conclusion and recommendations Attention should be focused on the other important presentations of the disease such as psychiatric disorders and cognitive impairments, and a comprehensive biopsychosocial neuropsychiatric approach should be adopted, which is essential for optimal care of patients with MS.

Matrix metalloproteinase levels in early HIV infection and relation to in vivo brain status

Matrix metalloproteinases (MMPs) have been implicated in human immunodeficiency virus (HIV)-associated neurological injury; however, this relationship has not been studied early in infection. Plasma levels of MMP-1, MMP-2, MMP-7, MMP-9, and MMP-10 measured using Luminex technology (Austin, TX, USA) were compared in 52 HIV and 21 seronegative participants of the Chicago Early HIV Infection study. MMP levels were also examined in HIV subgroups defined by antibody reactivity, viremia, and antiretroviral status, as well as in available cerebrospinal fluid (CSF) samples (n = 9). MMPs were evaluated for patterns of relationship to cognitive function and to quantitative magnetic resonance measurements of the brain derived in vivo. Plasma MMP-2 levels were significantly reduced in early HIV infection and correlated with altered white matter integrity and atrophic brain changes. MMP-9 levels were higher in the treated subgroup than in the naïve HIV subgroup. Only MMP-2 and MMP-9 were detected in the CSF; CSF MMP-2 correlated with white matter integrity and with volumetric changes in basal ganglia. Relationships with cognitive function were also identified. MMP-2 levels in plasma and in CSF correspond to early changes in brain structure and function. These findings establish a link between MMPs and neurological status previously unidentified in early HIV infection.

Cortical Thickness in Frontotemporal Dementia, Mild Cognitive Impairment, and Alzheimer's Disease

Cortical thickness analysis has been proposed as a potential diagnostic measure in memory disorders. In this retrospective study, we compared the cortical thickness values of 24 patients with frontotemporal dementia (FTD) to those of 25 healthy controls, 45 symptomatic subjects with stable mild cognitive impairment (S-MCI), 15 subjects with progressive mild cognitive impairment (P-MCI), and 36 patients with Alzheimer's disease (AD). The patterns of regions of thinning in FTD when compared to controls and also S-MCI patients showed similar trends; thinning of the bilateral frontal poles and bilateral medial temporal lobe structures, especially the anterior part of the gingulum, the uncus, and parahippocampal gyri. Cortical thinning in FTD was also found on the boundary regions of parietal and occipital lobes. In the P-MCI group compared to FTD, the trend of thinning in small distinct areas of the parietal and occipital lobes was observed. The FTD and AD groups did not differ statistically, but we found trends toward thinning in FTD of the left cingulate gyrus, and the left occipitotemporal gyri, and in AD of the inferior parietal, occipitoparietal, and the pericalcarine regions, more in the right hemisphere. In FTD, increased slowness in the executive test (Trail-Making A) correlated with the thinner cortex, whereas the language tests showed the lower scores, the thinner cortex in the left hemisphere. Cortical thickness might be a tool for detecting subtle changes in brain atrophy in screening of dementia prior to the development of diffuse or lobar atrophies.

Certain new aspects of etiology and pathogenesis of Alzheimer’s disease

The research focuses on the possibility of early detection of AD-specific vascular and atrophic brain changes in families which have a tendency to inherit the disease. The research includedthree families with AD inheritance. All patientsunderwent: cognitive function assessment(MMSE),determination of dementia severity(CDR) and AD stages (TDR), computed tomography (CT), magnetic resonance imaging (MRI), scintigraphy of the brain (SG), rheoencephalography (REG), and cerebral multigated angiography (MUGA). All patients with different AD stages, as well as their descendants, have specific atrophic changes in the temporal lobes of the brain. The degree of these changes increases as AD becomes more severe and ranges from 4% - 8% (TDR-0) to 33% - 62% (TDR-3) of the total mass of a healthy person’s temporal lobes. Simultaneously, thepatients examined have changes of microcirculation manifested by reduction of the capillarybed in the temporal and frontalparietal regions,the development of multiple arteriovenousshunts in the same areas, early venous dumping, anomalous expansion of venoustrunks that receive blood from the arterialvenous shunts, venous stasis on the frontoparietal boundary. Similar changes are found among AD patients’ descendants aged 8 - 11, the only difference being in the degree of temporal lobes atrophy which is 4.7%. This proves that microcirculatory disorders are primary and atrophic changes of the temporal lobes are secondary in AD development. The data obtained indicate that the examination of AD patients’ relatives should begin well before the possible manifestations of the disease, even in childhood. It will allow to reveal the possibility of inheritance and the signs of the disease at the earliest possible stage and to begin its treatment in time.

Aβ(42) induced MRI changes in aged rabbit brain resembles AD brain

Alzheimer’s disease is the most common form of dementia and is structurally characterized by brain atrophy and loss of brain volume. Aβ is one of the widely accepted causative factors of AD. Aβ deposition is positively correlated with brain atrophy in AD. In the present study, structural brain imaging techniques such as Magnetic Resonance Imaging (MRI) were used to measure neuroanatomical alterations in Alzheimer’s disease brain. MRI is a non-invasive method to study brain structure. The objective of the present study was to elucidate the role of Aβ on brain structure in the aged rabbit brain. Among 20 aged rabbits, one batch (n=10) rabbits was injected chronically with Aβ(1–42) and another batch (n=10) with saline. The MRI was conducted before Aβ(1–42)/saline injection and after 45days of Aβ(1–42)/saline injection. All the aged rabbits underwent MRI analysis and were euthanized after 45days. The MRI results showed a significant reduction in thickness of frontal lobe, hippocampus, midbrain, temporal lobe and increases in the lateral ventricle volume. We also conducted an MRI study on AD (n=10) and normal (n=10) cases and analyzed for the thicknesses of frontal lobe, hippocampus, midbrain, temporal lobe and lateral ventricle lobe. We found significant reductions in thickness of the frontal lobe and the hippocampus. However, no significant reduction in the thickness of midbrain, temporal lobe or increase in the lateral ventricle volume was observed compared to normal. Correlations in brain atrophy changes between rabbit brain and human AD brain were found for frontal lobe and hippocampal regions. In contrast, other regions such as midbrain, temporal lobe, and lateral ventricles were not correlated with rabbit brain atrophy changes in the corresponding regions. The relevance of these changes in AD is discussed.

Progression of brain atrophy and cognitive decline in diabetes mellitus

To investigate progression of MRI-assessed manifestations of cerebral degeneration related to cognitive changes in a population of elderly patients with diabetes mellitus (DM) compared to age-matched control subjects. From a randomized controlled trial (PROSPER study), a study sample of 89 patients with DM and 438 control subjects without DM aged 70-82 years were included for brain MRI scanning and cognitive function testing at baseline and reexamination after 3 years. Changes in brain atrophy, white matter hyperintensities (WMHs), number of infarctions, and cognitive function test results were determined in patients with DM and subjects without DM. Linear regression analysis was performed with correction for age, gender, hypertension, pravastatin treatment, educational level, and baseline test results. In patients with DM, baseline MRI parameters were correlated with change in cognitive function test result using linear regression analysis with covariates age and gender. Patients with DM showed increased progression of brain atrophy (p < 0.01) after follow-up compared to control subjects. No difference in progression of WMH volume or infarctions was found. Patients with DM showed increased decline in cognitive performance on Stroop Test (p = 0.04) and Picture Learning Test (p = 0.03). Furthermore, in patients with DM, change in Picture Learning Test was associated with baseline brain atrophy (p < 0.02). Our data show that elderly patients with DM without dementia have accelerated progression of brain atrophy with significant consequences in cognition compared to subjects without DM. Our findings add further evidence to the hypothesis that diabetes exerts deleterious effects on neuronal integrity.

Diffuse damage in pediatric traumatic brain injury: A comparison of automated versus operator-controlled quantification methods

This investigation had two main objectives: 1) to assess the comparability of volumes determined by operator-controlled image quantification with automated image analysis in evaluating atrophic brain changes related to traumatic brain injury (TBI) in children, and 2) to assess the extent of diffuse structural changes throughout the brain as determined by reduced volume of a brain structure or region of interest (ROI). Operator-controlled methods used ANALYZE® software for segmentation and tracing routines of pre-defined brain structures and ROIs. For automated image analyses, the open-access FreeSurfer program was used. Sixteen children with moderate-to-severe TBI were compared to individually matched, typically developing control children and the volumes of 18 brain structures and/or ROIs were compared between the two methods. Both methods detected atrophic changes but differed in the magnitude of the atrophic effect with the best agreement in subcortical structures. The volumes of all brain structures/ROIs were smaller in the TBI group regardless of method used; overall effect size differences were minimal for caudate and putamen but moderate to large for all other measures. This is reflective of the diffuse nature of TBI and its widespread impact on structural brain integrity, indicating that both FreeSurfer and operator-controlled methods can reliably assess cross-sectional volumetric changes in pediatric TBI.

Distinct Brain Volume Changes Correlating with Clinical Stage, Disease Progression Rate, Mutation Size, and Age at Onset Prediction as Early Biomarkers of Brain Atrophy in Huntington's Disease

Searching brain and peripheral biomarkers is a requisite to cure Huntington's disease (HD). To search for markers indicating the rate of brain neurodegenerative changes in the various disease stages, we quantified changes in brain atrophy in subjects with HD. We analyzed the cross-sectional and longitudinal rate of brain atrophy, quantitatively measured by fully-automated multiparametric magnetic resonance imaging, as fractional gray matter (GM, determining brain cortex volume), white matter (WM, measuring the volume of axonal fibers), and corresponding cerebral spinal fluid (CSF, a measure of global brain atrophy), in 94 gene-positive subjects with presymptomatic to advanced HD, and age-matched healthy controls. Each of the three brain compartments we studied (WM, GM, and CSF) had a diverse role and their time courses differed in the development of HD. GM volume decreased early in life. Its decrease was associated with decreased serum brain-derived-neurotrophic-factor and started even many years before onset symptoms, then decreased slowly in a nonlinear manner during the various symptomatic HD stages. WM volume loss also began in the presymptomatic stage of HD a few years before manifest symptoms appear, rapidly decreasing near to the zone-of-onset. Finally, the CSF volume increase began many years before age at onset. Its volume measured in presymptomatic subjects contributed to improve the CAG-based model of age at onset prediction. The progressive CSF increase depended on CAG mutation size and continued linearly until the last stages of HD, perhaps representing the best marker of progression rate and severity in HD (R(2)= 0.25, P < 0.0001).

Is Intracranial Atherosclerosis an Independent Risk Factor for Cerebral Atrophy? A Retrospective Evaluation

BackgroundOur purpose was to study the association between the intracranial atherosclerosis as measured by cavernous carotid artery calcification (ICAC) observed on head CT and atrophic changes of supra-tentorial brain demonstrated by MRI.MethodsInstitutional review board approval was obtained for this retrospective study incorporating 65 consecutive patients presenting acutely who had both head CT and MRI. Arterial calcifications of the intracranial cavernous carotids (ICAC) were assigned a number (1 to 4) in the bone window images from CT scans. These 4 groups were then combined into high (grades 3 and 4) and low calcium (grades 1 and 2) subgroups. Brain MRI was independently evaluated to identify cortical and central atrophy. Demographics and cardiovascular risk factors were evaluated in subjects with high and low ICAC. Relationship between CT demonstrated ICAC and brain atrophy patterns were evaluated both without and with adjustment for cerebral ischemic scores and cardiovascular risk factors.ResultsForty-six of the 65 (71%) patients had high ICAC on head CT. Subjects with high ICAC were older, and had higher prevalence of hypertension, diabetes, coronary artery disease (CAD), atrial fibrillation and history of previous stroke (CVA) compared to those with low ICAC. Age demonstrated strong correlation with both supratentorial atrophy patterns. There was no correlation between ICAC and cortical atrophy. There was correlation however between central atrophy and ICAC. This persisted even after adjustment for age.ConclusionAge is the most important determinant of atrophic cerebral changes. However, high ICAC demonstrated age independent association with central atrophy.

Severe degenerative change of multiple organs mediated by chronic active Epstein–Barr virus infection with infected T-cell expansion

We here report the case of a young Japanese woman diagnosed with chronic active Epstein-Barr virus (EBV) infection. Intensive therapy with the CHOP regimen was partially able to control virus expansion, but various central nervous system symptoms appeared and gradually progressed. EBV-encoded RNA, detected using in situ hybridization, disclosed the presence of EBV in liver and bone marrow tissue, and real-time PCR revealed the presence of EBV in the cerebrospinal fluid (CSF) and serum. CD3+CD4+CD8-CD56- T-cell expansion in the peripheral blood (PB) and CSF was also observed. Atrophic brain changes were progressive, and the patient died of central nervous system disturbance and pulmonary hemorrhage a year after diagnosis. Autopsy revealed that EBV-infected T lymphocytes with a phenotype similar to those seen in PB and CSF had infiltrated multiple organs: the lymph nodes, bone marrow, endocardium, pericardium, myocardium, spleen, liver, and spinal cord. There have been few previous reports of severe degenerative changes in the myocardium, liver, and spinal cord in patients with EBV infection. Although EBV occasionally infiltrates the central nervous system and brain, atrophic changes mediated by EBV are rare. The autopsy results of this case suggest the possibility of EBV-mediated, severe degenerative changes in multiple organs.

Glial and neuronal damage markers in patients with anorexia nervosa

Anorexia nervosa (AN) commonly arises during adolescence leading to interruptions of somatic and psychological development as well as to atrophic brain changes. It remains unclear whether these brain changes are related to the loss of neurons, glia, neuropil or merely due to fluid shifts. We determined leptin levels and two brain-derived damage markers: glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) of 43 acute AN patients and 50 healthy control woman (HCW). Peripheral GFAP and NSE concentrations of AN patients were not elevated and not different from HCW. Subjects with particularly low leptin concentration, indicating severe malnutrition, did not show abnormal values either. During weight recovery the marker proteins remained unchanged. Our preliminary results are in line with neuroimaging studies supporting the reversibility of brain changes in AN and do not substantiate hypotheses relying on the extensive damage of brain cells as an explanation for cerebral atrophy in AN.

Short-term brain atrophy changes in relapsing–remitting multiple sclerosis

The objective of this study was to establish whether the time interval of 3 months is sufficient to detect whole-brain atrophy changes in patients with relapsing–remitting (RR) multiple sclerosis (MS). Another aim was to assess the value of monthly gadolinium (Gd)-enhanced magnetic resonance imaging (MRI) and of different Gd-enhancement patterns as predictors of brain atrophy.Thirty patients with RRMS (mean disease duration 4.9 years, mean age 34.4 years and mean Expanded Disability Status Scale [EDSS] 1.4) were assessed at baseline and monthly for a period of 3 months with clinical and MRI examinations. Calculations of baseline and monthly absolute and percent changes of MRI measures have been obtained using two semiautomated (Buffalo and Trieste) and one automated (SPM99) segmentation method. Changes of brain parenchymal fraction (BPF) were investigated according to Gd-enhancement patterns. Mean absolute and percent changes of BPF did not significantly differ at any time point in the study for any of the three methods. There was slight but not significant decrease of BPF from baseline to month 3: −0.0004 (0.05%), p=0.093 for Trieste; −0.0006 (0.07%), p=0.078 for Buffalo; and −0.0006 (0.08%), p=0.081 for SPM99 method. In ring-enhancement positive patients, there was a significant difference between baseline and month 3 changes of BPF, EDSS, and number of relapses. Over the study period, we did not demonstrate differences between changes of BPF according to the presence of Gd enhancement. Longitudinally, multiple regression analysis demonstrated that the only clinical or MRI parameter that predicted BPF decrease was the mean absolute change of ring-enhancing lesion load (R=0.62, p=0.003). The noteworthy findings of this study are (1) the observation that a significant brain atrophy progression cannot be detected over a 3-month period in RRMS; (2) the demonstration that the ring-enhancement pattern may contribute to more severe brain tissue loss in the short term; and (3) the lack of relationship between the presence and duration of Gd-enhancement activity and brain volume changes in the short term.

Determinants of Benton Facial Recognition Test performance in normal adults.

Clinical investigations have found that lesions of the right cerebral hemisphere can disrupt face perception. Much less is known about the determinants of facial discrimination in healthy adults, although age-related differences in many cognitive abilities have been shown to correlate with simple processing speed and variation in regional brain volumes. In this study, 174 healthy adults between the ages of 20 and 92 were asked to match pictures of unfamiliar faces. After their performance was regressed on age, sex, education, and perceptual comparison speed, adding terms for frontal lobe volume, nonfrontal volume, and ventricle-to-brain ratio (VBR) derived from magnetic resonance imaging improved the model and accounted for 35% of the variance in facial discrimination. VBR and processing speed alone accounted for nearly 34% of the variance. These findings suggest that both normal atrophic brain changes and decreases in processing speed contribute to individual differences in facial discrimination.

Pharmacotherapy of Early-Onset Depression: Update and New Directions

Although an increased recognition of depressive disorders in youth represents a positive conceptual change over the past decades, there still is a very limited amount of research on useful treatment interventions. The paucity of data is particularly keen for the use of psychotropic drugs. For example, by applying the criteria suggested by the International Psychopharmacology Algorithm Project, there barely are enough first-grade ("Level A," meaning at least two RCTs) data supporting the short-term efficacy of antidepressants (the SSRIs) in the treatment of juvenile depression. And yet, limited data have not translated into limited use in routine clinical practice. In fact, the use of antidepressant medications has increased exponentially over the last decade, a change that is especially conspicuous for individuals less than 18 years of age. The perceived safety of the SSRIs and other novel antidepressants is partly at the root of their increased popularity. Data regarding their safety are likewise quite limited, however, and essentially are nonexistent for longer-term use. Based on the reviewed data, a medication algorithm for the treatment of early-onset depression can be suggested (Fig. 1). The algorithm underscores the need for adequate evaluation and diagnostic assessment, with particular attention to comorbid conditions (such as a bipolar diathesis) that may dictate alternative treatment strategies. In general, psychotherapy is the initial approach to juvenile MDD, with medication use reserved for more severe cases or those not responding to psychotherapy alone. Given that only two types of psychotherapy and two SSRIs have adequate controlled short-term efficacy data, all but the initial steps must be undertaken guided by clinical judgment and an individualized risk-benefit analysis. An algorithm such as this one, based on the very limited efficacy and safety data available, may be viewed as setting priorities for a comprehensive research agenda, more than dictating rigid treatment guidelines. In closing, it can be suggested that future research on the pharmacotherapy of early-onset depressive disorder pay particular attention to the following three aspects: 1. Too many drugs, too few data: Rapid advances in drug development have led to a plethora of available antidepressant agents. It is clear that there are many more agents available than can be adequately studied at present. Because many such agents are mechanistically similar, if not identical, it may be wise to focus research efforts on truly novel agents, particularly those (such as the CRH receptor antagonists, or those affecting neurosteroidogenesis) whose action is based on preclinical and clinical pathophysiologic disease paradigms. 2. Longitudinal follow-up and maintenance studies: Essentially all reviewed treatment studies have been short-term trials. There is a marked paucity of longer-term follow-up data, or of naturalistic and "real-world" effectiveness studies. For example, one of the few studies addressing maintenance pharmacotherapy for early-onset depression has demonstrated surprisingly high recurrence rates, even for those subjects actively on maintenance medication. 3. Long-term safety: Clinicians and parents alike often face difficult decisions regarding the long-term exposure of antidepressant drugs on the developing brain. Although no definitive long-term safety data are likely to become available anytime soon, real risks, such as suicide, and potential sequelae of long-term exposure to the underlying illness itself need all to be part of any decision-making process. Preclinical studies have shown that brain-derived neurotrophic factor (BDNF) levels can be upregulated by antidepressants, and low BDNF factors have been associated with atrophic brain changes in recurrent forms of adult MDD. Although these observations require specific application to juvenile forms of the disorder, they raise the exciting prospect that the natural course of the illne

Anti-ageing effect of aged garlic extract in the inbred brain atrophy mouse model.

1. The effects of chronically administered aged garlic extract (AGE) on the age-related changes in a novel strain of senescence accelerated mouse (SAM) characterized by age-related brain atrophy (SAMP10) were investigated. 2. A solid diet containing 2% (w/w) AGE was given to SAM from 2 months of age. 3. The grading score of senescence in SAMP10 at 10 months of age was significantly higher than that of SAMR1, a reference strain for SAMP10. 4. Administration of AGE prevented the increase in the grading score of SAMP10 and SAMR1. 5. In behavioural evaluation, AGE improved learning and memory deficits of SAMP10 in both the passive and conditioned avoidance tests as well as the spatial memory test. 6. Treatment with AGE in SAMP10 prevented the decrease in brain weight and the atrophic changes in frontal brain at 12 months of age. 7. These results raise the possibility that AGE prevents physiological ageing and may be beneficial for age-related cognitive disorders in humans.

Brain morphology and intelligence

Although the correlations are modest (∼ r = 0.35), brain size as determined by magnetic resonance imaging has been positively related to measures of psychometric intelligence. Three studies dealing with brain size‐IQ relationships are presented in patients who have suffered traumatic brain injury (TBI). Study 1 was an examination of whether the brain size‐IQ relationship was proportionally maintained in response to TBI‐induced atrophie changes in the brain. Study 2 was an examination of whether smaller brain size at the time of injury was a risk factor for more significant decline in IQ after injury. Study 3 was an examination of whether focal lesion volume plays a role in postinjury brain size‐IQ relations. Results indicated that trauma‐induced atrophic brain changes are related neither to postinjury IQ nor focal lesion volume. However, patients with TBI with smaller brain size at the time of injury did have significantly lower postinjury IQ scores when compared to a matched group that had larger premorb...

Cortical atrophy in young adults with a history of hyperactivity in childhood

A computed tomographic (CT) brain scan study was conducted in 24 young males treated and followed up for hyperactivity since childhood. Compared to 27 matched controls, adults with a history of hyperactivity had a significantly greater frequency of cerebral atrophy. No differences in cerebellar atrophy frequency or in lateral cerebral ventricle-to-brain ratio (VBR) were found. The possible associations of hyperactivity or perhaps stimulant drug treatment to atrophic brain changes are discussed.

Neuropsychological characteristics and atrophic brain changes in senile and presenile dementia

Groups of presenile ( n = 41) and senile ( n = 97) dementia patients were compared on neuropsychological measures and volumetric estimates of atrophy and ventricular enlargement as depicted on computerized axial tomography. Despite their significantly greater age, the senile patients were not markedly significant different on neuropsychological measures when the effect of education was covaried. Likewise, there were no significant differences between the two groups in terms of cortical atrophy despite that variable's known relationship with age. Ventricular size was not significantly different between groups when age effects were statistically controlled. It is concluded that the pathologic effects of presenile dementia are roughly equivalent to the total of the effects of both the disease and aging processes in senile dementia. Therefore, the disease appears to be more dramatic when it occurs in younger patients. It may be that younger patients are less healthy than older patients presenting with the disease and, consequently, are less able to withstand its effects. The present sample is compared with those of other studies reporting a markedly more pathologic presentation associated with presenile relative to senile dementia.

Neuropsychological characteristics and atrophic brain changes in senile and presenile dementia

Groups of presenile ( n = 41) and senile ( n = 97) dementia patients were compared on neuropsychological measures and volumetric estimates of atrophy and ventricular enlargement as depicted on computerized axial tomography. Despite their significantly greater age, the senile patients were not markedly significant different on neuropsychological measures when the effect of education was covaried. Likewise, there were no significant differences between the two groups in terms of cortical atrophy despite that variable's known relationship with age. Ventricular size was not significantly different between groups when age effects were statistically controlled. It is concluded that the pathologic effects of presenile dementia are roughly equivalent to the total of the effects of both the disease and aging processes in senile dementia. Therefore, the disease appears to be more dramatic when it occurs in younger patients. It may be that younger patients are less healthy than older patients presenting with the disease and, consequently, are less able to withstand its effects. The present sample is compared with those of other studies reporting a markedly more pathologic presentation associated with presenile relative to senile dementia.

Analysis of Atrophic Changes of Brain by Computed Tomography

Inaba, Y.; Komatsu, K.; Ohata, M.; Yoshida, R.; Tanaka, K.; Matsunaga, M. Author Information