Degree Of Cerebral Atrophy Research Articles

Estimation of Human Cerebral Atrophy Based on Systemic Metabolic Status Using Machine Learning.

BackgroundBased on the assumption that systemic metabolic disorders affect cognitive function, we have developed a deep neural network (DNN) model that can estimate cognitive function based on basic blood test data that do not contain dementia-specific biomarkers. In this study, we used the same DNN model to assess whether basic blood data can be used to estimate cerebral atrophy.MethodsWe used data from 1,310 subjects (58.32 ± 12.91years old) enrolled in the Brain Doc Bank. The average Mini Mental State Examination score was 28.6 ± 1.9. The degree of cerebral atrophy was determined using the MRI-based index (GM-BHQ). First, we evaluated the correlations between the subjects' age, blood data, and GM-BHQ. Next, we developed DNN models to assess the GM-BHQ: one used subjects' age and blood data, while the other used only blood data for input items.ResultsThere was a negative correlation between age and GM-BHQ scores (r = -0.71). The subjects' age was positively correlated with blood urea nitrogen (BUN) (r = 0.40), alkaline phosphatase (ALP) (r = 0.22), glucose (GLU) (r = 0.22), and negative correlations with red blood cell counts (RBC) (r = −0.29) and platelet counts (PLT) (r = −0.26). GM-BHQ correlated with BUN (r = −0.30), GLU (r = −0.26), PLT (r = 0.26), and ALP (r = 0.22). The GM-BHQ estimated by the DNN model with subject age exhibited a positive correlation with the ground truth GM-BHQ (r = 0.70). Furthermore, even if the DNN model without subject age was used, the estimated GM-BHQ showed a significant positive correlation with ground truth GM-BHQ (r = 0.58). Age was the most important variable for estimating GM-BHQ.DiscussionAging had the greatest effect on cerebral atrophy. Aging also affects various organs, such as the kidney, and causes changes in systemic metabolic status, which may contribute to cerebral atrophy and cognitive impairment. The DNN model may serve as a new screening test for dementia using basic blood tests for health examinations. Finally, the blood data reflect systemic metabolic disorders in each subject—this method may thus contribute to personalized care.

The Value of Corpus Callosum Measurement in the Diagnosis of Cerebral Atrophy.

The study aimed to investigate the relationship between the corpus callosum area (CCa) and the degree of cerebral atrophy in patients with cerebral atrophy. 119 patients with brain atrophy were grouped according to the degree of brain atrophy. Median sagittal CCa and intracranial area (ICa) were measured, and the ratio of corpus callosum to the intracranial area (CCa-ICa ratio) was calculated. The data were analyzed using ANOVA. CCa significantly reduced in patients with cerebral atrophy, and the degree of cerebral atrophy was found to be positively correlated with the degree of reduction in the CCa. The reduction in the CCa and the CCa-ICa ratio in the median sagittal can be used as a reference indicator for the diagnosis and grading of brain atrophy in clinical practice.

Pay attention to the basal ganglia: a volumetric study in early dementia with Lewy bodies

BackgroundCortical and subcortical cognitive impairments are usually found in dementia with Lewy bodies (DLB). Roughly, they comprise visuo-constructive/executive function and attention/processing speed impairments, whereas memory would remain relatively spared. In this study, we focused on the neuro-anatomical substrates of attention and processing speed, which is still poorly understood. For the purpose of the study, we examined the correlations between behavioral scores measuring the speed of processing and the degree of cerebral atrophy in patients with prodromal to moderate DLB.MethodsNinety-three prodromal to moderate DLB patients (mean MMSE = 25.5) were selected to participate in the study as well as 28 healthy elderly subjects (mean MMSE = 28.9), matched in terms of age and educational level. The Trail Making Test A (TMTA) and the Digit Symbol Substitution Test (DSST) were used to assess attention and processing speed. Behavioral performances were compared between patients and healthy control subjects. Three-dimensional MRI images were acquired for all participants, and correlational analyses were performed in the patient group using voxel-based morphometry (VBM).ResultsThe behavioral results on both the TMTA (p = .026) and the DSST (p < .001) showed significantly impaired performances in patients in comparison with control subjects. In addition, correlational analyses using VBM revealed for the TMTA negative correlations in the caudate nucleus (left cluster peak significant at .05 FWE corrected), the putamen, the left thalamus, and the subthalamic nuclei (p < .05 FDR corrected). Some positive correlations associated with the DSST were found in the right inferior frontal gyrus, the left thalamus, and the left cerebellum (p < .001 uncorrected).ConclusionsThe behavioral results are in line with the literature on the DLB cognitive profile and confirm the existence of attention and processing speed impairment. Interestingly, VBM analysis revealed the involvement of the basal ganglia, in particular, the left caudate nucleus, which is part of the attention cerebral network, suggesting an important role of this structure for attentional processing speed. This also suggests the clinical implication of damage in this region relatively early in the course of the disease.

Silencing of long noncoding RNA MEG3 enhances cerebral protection of dexmedetomidine against hypoxic-ischemic brain damage in neonatal mice by binding to miR-129-5p.

Hypoxic-ischemic brain damage (HIBD) is a leading cause of neonatal acute mortality and chronic nervous system injury. Recently, it has been found that long noncoding RNAs (lncRNAs) play a significant role in the neurodevelopment and etiopathogenesis of HIBD. Here, the researchers aimed to determine the role of lncRNA maternally expressed gene (MEG3) in the therapeutic effect of dexmedetomidine (DEX) in neonatal mice with HIBD through the regulation of microRNA-129-5p (miR-129-5p). HIBD models were established in C57/BL6 neonatal mice. Subsequently, the target relationship between MEG3 and miR-129-5p was predicted and verified. The neonatal mice were injected with DEX, ad-shMEG3, and mimics and inhibitors of miR-129-5p to identify roles of MEG3 and miR-129-5p in therapeutic effects of DEX on neuronal apoptosis and injury, cerebral atrophy, and learning and memory ability of neonatal mice with HIBD. MEG3 directly targeted and inhibited the expression of miR-129-5p. Silencing of MEG3 or upregulation of miR-129-5p effectively promoted the therapeutic effect of DEX on neonatal mice with HIBD. Silencing of MEG3 or upregulation of miR-129-5p reduced the neuronal apoptosis rate and degree of cerebral atrophy, and also enhanced the learning and memory ability of HIBD neonatal mice. Collectively, the key findings obtained from the present study support the notion that MEG3 silencing enhances the therapeutic effect of DEX on neonatal mice with HIBD by binding to miR-129-5p.

The neuropsychological profiles and semantic-critical regions of right semantic dementia.

IntroductionPrevious literature has revealed that the anterior temporal lobe (ATL) is the semantic hub of left-sided or mixed semantic dementia (SD), whilst the semantic hub of right-sided SD has not been examined.MethodsSeventeen patients with right-sided SD, 18 patients with left-sided SD and 20 normal controls (NC) underwent neuropsychological assessments and magnetic resonance imaging scans. We investigated the relationship between the degree of cerebral atrophy in the whole brain and the severity of semantic deficits in left and right-sided SD samples, respectively.ResultsWe found the semantic deficits of right-sided SD patients were related to bilateral fusiform gyri and left temporal pole, whilst the left fusiform gyrus correlated with the semantic performance of left-sided SD patients. Moreover, all the findings couldn't be accounted for by total gray matter volume (GMV) or general cognitive degradation of patients.DiscussionThese results provide novel evidence for the current semantic theory, that the important regions for semantic processing include both anterior and posterior temporal lobes.

The Left Fusiform Gyrus is a Critical Region Contributing to the Core Behavioral Profile of Semantic Dementia.

Given that extensive cerebral regions are co-atrophic in semantic dementia (SD), it is not yet known which critical regions (SD-semantic-critical regions) are really responsible for the semantic deficits of SD. To identify the SD-semantic-critical regions, we explored the relationship between the degree of cerebral atrophy in the whole brain and the severity of semantic deficits in 19 individuals with SD. We found that the gray matter volumes (GMVs) of two regions [left fusiform gyrus (lFFG) and left parahippocampal gyrus (lPHG)] significantly correlated with the semantic scores of patients with SD. Importantly, the effects of the lFFG remained significant after controlling for the GMVs of the lPHG. Moreover, the effects of the region could not be accounted for by the total GMV, general cognitive ability, laterality of brain atrophy, or control task performance. We further observed that each atrophic portion of the lFFG along the anterior–posterior axis might dedicate to the loss of semantic functions in SD. These results reveal that the lFFG could be a critical region contributing to the semantic deficits of SD.

Case report – his and hers neurology

A 81-year-old retired postal worker who lived with his wife presented with collapse into a chair and a witnessed unresponsive episode. His family also described a reduction in mobility over a ten-year period, with long-standing urinary symptoms, more help needed to dress his lower half and worsening memory. His past medical history included a coronary bypass graft 20 years previously, osteoarthritis, hypertension and poor mobility deemed secondary to severe intermittent claudication. On physical examination, he had peripheral pitting oedema and distal weakness. He had absent reflexes but intact sensation to all modalities. His gait showed markedly decreased stride length and a weakness on dorsiflexion of both feet. Laboratory serum tests were normal except for chronic renal impairment (eGFR 34). A myeloma screen was negative. Admission ECG, CXR and 24 hour ECG tape were also normal. A CTand MRIscan of the brain showed enlarged ventricles in keeping with a degree of cerebral atrophy. MRI of the spine showed multi-level disc bulging with foramenal stenosis but no root compression. CSF sampling showed moderately raised protein only. A diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) was made on a clinical basis and this was confirmed on nerve conduction studies. Intravenous immunoglobulin was given and a six-metre walk test showed an improvement from

Disruption of cerebral networks and cognitive impairment in Alzheimer disease

To examine the relation between measures of whole-brain white matter connectivity and cognitive performance in patients with early Alzheimer disease (AD) using a network-based approach and to assess whether network parameters provide information that is complementary to conventional MRI markers of AD. Fifty patients (mean age 78.8 ± 7.1 years) with early AD were recruited via a memory clinic. In addition, 15 age-, sex-, and education-matched control participants were used as a reference group. All participants underwent a 3-T MRI scan and cognitive assessment. Diffusion tensor imaging-based tractography was used to reconstruct the brain network of each individual, followed by graph theoretical analyses. Overall network efficiency was assessed by measures of local (clustering coefficient, local efficiency) and global (path length, global efficiency) connectivity. Age-, sex-, and education-adjusted cognitive scores were related to network measures and to conventional MRI parameters (i.e., degree of cerebral atrophy and small-vessel disease). The structural brain network of patients showed reduced local efficiency compared to controls. Within the patient group, worse performance in memory and executive functioning was related to decreased local efficiency (r = 0.434; p = 0.002), increased path length (r = -0.538; p < 0.001), and decreased global efficiency (r = 0.431; p = 0.005). Measures of network efficiency explained up to 27% of the variance in cognitive functioning on top of conventional MRI markers (p < 0.01). This study shows that network-based analysis of brain white matter connections provides a novel way to reveal the structural basis of cognitive dysfunction in AD.

Intracranial Air Correlates with Preoperative Cerebral Atrophy and Stereotactic Error during Bilateral STN DBS Surgery for Parkinson’s Disease

Objective: We examine the effect of intracranial air on stereotactic accuracy during bilateral deep brain stimulation (DBS) surgery for Parkinson’s disease (PD). We also assess factors that may predict an increased risk of intracranial air during these surgeries. Methods: 32 patients with PD underwent bilateral DBS surgery. The technique used for implantation of the leads has been standardized in over 800 subthalamic nucleus (STN) implantations. For lead implantation, the goal of the neurophysiological technique is identification of the STN and its borders with 3 microelectrode recording (MER) tracks. We examined the number of tracks and the degree of deviation from the planned target on each side. Total intracranial air (TIA) was then compared in these groups. We also examined the relationship between the TIA and length of surgery, ventricular volume and the degree of atrophy. Results: Side 2 in this series required more MER tracks. The TIA was larger in patients with more than 3 MER tracks on side 2 of surgery. There was more deviation from the target on side 2. In addition, the TIA in patients with >1 mm of vector deviation on side 2 was more than in those without. The TIA correlated with the number of tracks on side 2 as well as with the degree of the second euclidean deviation on side 2. There was a correlation of degree of atrophy with TIA. Conclusion: In bilateral STN DBS for PD, intracranial air may contribute to error in stereotactic accuracy especially on the second side. In addition, there is a correlation between the accumulated volume of intracranial air and the degree of cerebral atrophy.

Measuring Cerebral Atrophy and White Matter Hyperintensity Burden to Predict the Rate of Cognitive Decline in Alzheimer Disease

To determine if baseline measurements of cerebral atrophy and severity of white matter hyperintensity (WMH) predict the rate of future cognitive decline in patients with Alzheimer disease (AD). Data were drawn from the Predictors Study, a longitudinal study that enrolls patients with mild AD and reassesses them every 6 months with use of the Columbia modified Mini-Mental State (mMMS) examination (score range, 0-57). Magnetic resonance images were analyzed to determine the severity of WMH, using the Scheltens scale, and the degree of atrophy, using the bicaudate ratio. Generalized estimating equations were used to determine whether severity of baseline magnetic resonance image measurements and their interaction predicted the rate of mMMS score decline at subsequent visits. Three university-based AD centers in the United States. At baseline, 84 patients with AD from the Predictors Study received structural magnetic resonance imaging and were selected for analysis. They had a mean of 6 follow-up evaluations. Main Outcome Measure The mMMS score. Generalized estimating equation models demonstrated that the degree of baseline atrophy (beta = -0.316; P = .04), the severity of WMH (beta = -0.173; P = .03), and their interaction (beta = -6.061; P = .02) predicted the rate of decline in mMMS scores. Both degree of cerebral atrophy and severity of WMH are associated with the rapidity of cognitive decline in AD. Atrophy and WMH may have a synergistic effect on future decline in AD, such that patients with a high degree of both have a particularly precipitous cognitive course. These findings lend further support to the hypothesis that cerebrovascular pathological abnormalities contribute to the clinical syndrome of AD.

Clinical proteomics in neurodegenerative disorders

Neurodegenerative disorders are characterized by neuronal impairment that eventually leads to neuronal death. In spite of the brain's known capacity for regeneration, lost neurons are difficult to replace. Therefore, drugs aimed at inhibiting neurodegenerative processes are likely to be most effective if the treatment is initiated as early as possible. However, clinical manifestations in early disease stages are often numerous, subtle and difficult to diagnose. This is where biomarkers that specifically reflect onset of pathology, directly or indirectly, may have a profound impact on diagnosis making in the future. A triplet of biomarkers for Alzheimer's disease (AD), total and hyperphosphorylated tau and the 42 amino acid isoform of beta-amyloid, has already been established for early detection of AD before the onset of dementia. However, more biomarkers are needed both for AD and for other neurodegenerative disorders, such as Parkinson's disease, frontotemporal dementia and amyotrophic lateral sclerosis. This review provides an update on recent advances in clinical neuroproteomics, a biomarker discovery field that has expanded immensely during the last decade, and gives an overview of the most commonly used techniques and the major clinically relevant findings these techniques have lead to.

C1q-Deficiency Is Neuroprotective Against Hypoxic-Ischemic Brain Injury in Neonatal Mice

This study was undertaken to determine whether the initial component of the classical complement (C) activation pathway contributes to hypoxic-ischemic brain injury in neonatal mice. Hypoxia-ischemia (HI) was produced in C1q(-/-) and wild-type (WT) neonatal mice. At 24 hours after HI, neonatal mouse reflex performance and cerebral infarct volume were assessed. Long-term outcomes were measured by water-maze performance and degree of cerebral atrophy at 7 to 8 weeks after HI. Activation of circulating neutrophils, and C1q, C3, and neutrophil deposition in brains were examined. C1q(-/-) mice were significantly protected against HI (mean+/-SE infarct volume in C1q(-/-) mice=17.3+/-5.5% versus 53.6+/-6.8% in WT mice; P<0.0001) and exhibited significantly less neurofunctional deficit compared with WT mice. Immunostaining revealed significantly greater deposition of C3 (and C1q) as well as granulocytes in the infarcted brains in WT mice compared with C1q(-/-) animals. Activation of circulating leukocytes was significantly decreased in C1q(-/-) mice compared with WT mice, which correlated strongly (r=0.7) with cerebral infarct volumes. Cerebral deposition of C1q and C3 after hypoxic-ischemic insult is associated with significantly greater neurologic damage in WT mice compared with C1q(-/-) mice, providing strong evidence that the classical C pathway contributes to the hypoxic-ischemic brain injury. Significantly decreased activation of circulating neutrophils associated with diminished local accumulation and attenuation of brain injury in C1q(-/-) mice suggests a potential cellular mechanism by which C1q mediates neurodegeneration in HI.

Anaesthesia in elderly patients with neurodegenerative disorders: special considerations.

Neurodegenerative diseases are increasingly common in elderly patients, who present a particular anaesthetic challenge. The majority of people over the age of 70 years have some degree of cerebral atrophy. The pathogenesis of neurodegenerative diseases is due to alterations in the transport, degradation and aggregation of proteins. Alterations in physiology that occur with advancing age affect both the pharmacokinetics and pharmacodynamics of drugs used in the elderly. Changes in pharmacokinetics result in either increased or reduced drug concentrations depending on the variable contributions of absorption, metabolism and elimination. The distribution of a drug depends on its protein binding, cardiac output and blood volume, which are all altered in the elderly. Metabolism and excretion of drugs are also affected due to changes in hepatic and renal mass and blood flow in the elderly. A number of drugs are used in neurodegenerative disorders including antidepressants, benzodiazepines, antipsychotics, acetylcholinesterase inhibitors and levodopa. Polypharmacy is a common problem, which can lead to adverse drug interactions and an exacerbation of dementia. Levodopa, bromocriptine and tricyclic antidepressants are known to cause orthostatic hypotension in patients with neurodegenerative disease. Elderly patients are liable to excessive sedation from benzodiazepines in both the pre- and postoperative period; therefore these drugs should be prescribed in low doses. For induction of general anaesthesia propofol is a suitable agent in patients with neurodegenerative disease due to its rapid metabolism, but may not be suitable in patients with Parkinson's disease as it can induce spontaneous involuntary movements. Volatile inhalational agents should be administered carefully in the elderly, as they are more sensitive to the depressant cerebral and cardiovascular effects. Levodopa should be avoided in conjunction with halothane, which sensitises the heart to catecholamines. Co-administration of monoamine oxidase inhibitors and opioids should be avoided as it can cause agitation, muscular rigidity, sweating and hyperpyrexia. If an anticholinergic agent is required, then glycopyrronium bromide is the drug of choice in this group of patients, as it does not cross the blood brain barrier. Patients should continue to take their usual medications in hospital and do not let the change in routine alter the times at which treatments are administered. This is particularly relevant to the timing of levodopa in Parkinson's disease, as missed treatment can be detrimental. Regional anaesthesia may, however, have significant advantages in patients with Parkinson's disease, who can continue to take oral levodopa preoperatively, during surgery, if required, and early in the postoperative period. Anti-emetic drugs such as phenothiazines, butyrophenones and metoclopramide should be used carefully in the postoperative period in these patients as their antidopaminergic effects may induce or exacerbate parkinsonian effects.

Atrofia cerebral en pacientes con esclerosis múltiple tratados con bolos periódicos de metilprednisolona

In the last years advances in the treatment of the remittant and secondary progressive forms of the multiple sclerosis (MS) have taken place. In the primary progressive forms (PP) the side effects of potentially useful drugs prevent their use; in some studies an improvement of the evolution with the intravenous administration of periodic pulses of methylprednisolone (MP) has been observed. To evaluate if periodic pulses of intravenous MP injected every 4-6 weeks increase the degree of cerebral atrophy of the patients with PP MS. We studied 11 patients with PP MS treated during 33 months with periodic pulses of intravenous MP. The degree of cerebral atrophy was evaluated in axial cuts of 10 mm of studies of magnetic resonance with the indices of Evans, bicaudate, bifrontal, frontal spears and bithalamic. The statistical evaluation of the results was made applying the test of Wilcoxon-Mann-Whitney. There are not statistically significant differences in the degree of cerebral atrophy with any of the used indices. Periodic pulses of intravenous MP do not accelerate the cerebral atrophy in patients with progressive forms of multiple sclerosis.

White matter lesions, quantitative magnetic resonance imaging, and dementia.

The authors performed quantitative and qualitative image analysis on a sample of the elderly population of Cache County, Utah, relating neuroimaging findings to Mini-Mental Status Examination (MMSE) scores and the presence of the apolipoprotein E epsilon4 allele. Neuroimaging measures included white, gray, and hippocampal volumes; a ventricle-to-brain ratio (VBR); and qualitative ratings of white matter lesions (WMLs) in the periventricular (PV) and centrum semiovale (CS) regions. Subjects included 85 persons with possible and probable Alzheimer disease (AD), 21 with vascular dementia (VaD), 30 with cognitive symptoms classified as mild/ambiguous (M/A), a heterogenous group of 39 non-AD or VaD subjects but diagnosed with some form of neuropsychiatric disorder ("Mixed Neuropsychiatric" group), and 20 normal control subjects aged 65 years or older. Controlling for age, sex, and length of disease, the authors found that AD and VaD subjects differed significantly from control subjects on WMLs, but only the VaD subjects significantly differed from M/A subjects. The two dementia groups also displayed, as expected, significant cerebral atrophy. The WMLs generally increased with age and severity of dementia. PV WMLs were significantly but only modestly associated with white matter volume loss and greater impairment on the MMSE. Modest correlations were also present between the quantitative measures of cerebral structure and MMSE performance. However, when degree of cerebral atrophy was controlled by using the VBR measure, WML effects on MMSE performance became nonsignificant, with the only significant relationship remaining being that between hippocampal volume and MMSE performance. There were no significant qualitative or quantitative findings related to presence of the epsilon4 allele and MMSE performance. The role of WMLs in aging and dementia is discussed.

Simple two-step swallowing provocation test for elderly patients with aspiration pneumonia

Although many pulmonologists and geriatricians recognise that silent aspiration and swallowing disorder are very important for the pathogenesis of aspiration pneumonia and nosocomial pneumonia in elderly patients, 1 Kikuchi R Watabe N Konno T et al. High incidence of silent aspiration in elderly patients with community-acquired pneumonia. Am J Respir Crit Care Med. 1994; 150: 251-253 Crossref PubMed Scopus (279) Google Scholar , 2 Teramoto S Matsuse T Ouchi Y Foreign body aspiration into the lower airways may not be unusual in older adults. Chest. 1998; 113: 1733-1734 Crossref PubMed Scopus (18) Google Scholar a videofluoroscopic examination, which is the most reliable method to detect aspiration and swallowing disorder, can not be done for all elderly patients. 3 Daniels SK Brailey K Priestly DH et al. Aspiration in patients with acute stroke. Arch Phys Med Rehabil. 1998; 79: 14-19 Summary Full Text PDF PubMed Scopus (318) Google Scholar A simple method for screening swallowing disorder may help to avoid having to refer all elderly patients to special dysphagia centres for videofluoroscopic study. However, it has been suggested that bedside clinical evaluation alone underestimates the frequency of aspiration in patients with swallowing disorder. 4 Splaingard ML Hutchins B Sulton LD Chaughuri G Aspiration in rehabilitation patients: videofluoroscopy vs bedside clinical assessment. Arch Phys Med REhabil. 1988; 69: 637-640 PubMed Google Scholar Here we show that a simple two-step swallowing provocation test was particularly useful in detecting swallowing disorder in elderly patients with aspiration pneumonia. 24 patients with aspiration pneumonia, mean age 73 (SD 4) years, had experienced an episode of observed aspiration with chest radiography evidence of an inflammatory response in a dependent pulmonary segment, with an increased white blood cell count (>10 000/mm 3 Daniels SK Brailey K Priestly DH et al. Aspiration in patients with acute stroke. Arch Phys Med Rehabil. 1998; 79: 14-19 Summary Full Text PDF PubMed Scopus (318) Google Scholar ). 24 controls, mean age 71 (3) years, had cerebral ischaemic diseases. A various degree of cerebral atrophy and lacunar infarction were found in both groups by cerebral computed tomography and magnetic resonance imaging. A simple two-step swallowing-provocation test (STS-SPT) was done on all patients. STS-SPT was estimated by the swallowing response and latent time for swallowing following bolus injection of 0·4 mL or 2·0 mL of distilled water at the suprapharynx through a small nasal catheter (internal diameter 0·5 mm) in a supine position. 5 Teramoto S, Sudo E, Matsuse T, et al. Impaired swallowing reflex in patients with obstructive sleep apnea syndrome. Chest (in press). Google Scholar The appropriate placement of catheter tip at suprapharynx was identified by visual inspection. 5 Teramoto S, Sudo E, Matsuse T, et al. Impaired swallowing reflex in patients with obstructive sleep apnea syndrome. Chest (in press). Google Scholar

Chronic subdural haematoma: a possible relationship with tamoxifen

Five patients operated on between 6 months and 7 years earlier for breast cancer were surgically treated for chronic subdural haematoma. This unusual association may be explained on the basis of known factors such as coagulative impairment subsequent to chemotherapy, a degree of cerebral atrophy or mild trauma. On the other hand, since four of the patients were taking antioestrogen therapy to control the disease, it is speculated that the oestrogenic properties of tamoxifen may have contributed to subdural bleeding.

Cerebrospinal fluid proteins in patients with leucoaraiosis: Possible abnormalities in blood-brain barrier function

Some CSF protein abnormalities have been proposed as a possible marker for vascular dementia. We studied the CSF protein levels and albumin ratio in 21 patients (mean age 64.04 ± 7.5) with progressive bilateral motor impairment, and a CT picture of leucoaraiosis. Seven of these patients also presented with dementia. Twenty-seven Alzheimer's disease patients (mean age 59.59 ± 5.30) without leucoaraiosis were taken as controls. We also evaluated the correlations of the albumin ratio values with the diagnosis of dementia, the severity of cognitive impairment, the degree of cerebral atrophy and presence of infarcts on CT, and the abnormalities in CSF circulation, found on isotopic cisternography, in the leucoaraiosis group. After controlling for age and sex, the patients with leucoaraiosis showed greater CSF albumin levels (0.27 mg/l ± 0.11 vs. 0.21 mg/l ± 0.06; covariance analysis P = 0.066), CSF IgG values ( 4.68 mg 100 ml ± 1.45 vs. 2.85 mg 100 ml ± 1.03 ; covariance analysis P < 0.001), and a higher albumin ratio (0.0078 ± 0.0027 vs. 0.0058 ± 0.0019; covariance analysis P = 0.013) than those with Alzheimer's disease. The variations of these parameters were not apparently related to the presence of dementia in the leucoaraiosis group. A significantly higher albumin ratio was observed in patients with a slowed CSF circulation compared to those with normal CSF circulation (0.0086 ± 0.0028 vs. 0.0059 ± 0.0019; covariance analysis P = 0.05). We conclude that, independently from the presence of dementia, patients with leucoaraiosis have CSF abnormalities consistent with functional blood-brain barrier alterations.

Leuko-Araiosis, Cerebral Atrophy, and Cerebral Perfusion in Normal Aging

To elucidate the role of leuko-araiosis observed on computed tomographic imaging among normal populations, 37 neurologically and cognitively normal volunteers ages 18 to 88 years were studied. Local cerebral blood flow was measured using stable xenon-enhanced computed tomography. Severity of leuko-araiosis and cerebral atrophy were graded on computed tomographic images. Leuko-araiosis was observed in 21.6% of normal volunteers, in 52.2% of patients with multi-infarct dementia (n = 23), and in 61.5% of patients with dementia of the Alzheimer type (n = 13). When multiple regression analysis was applied among normal volunteers, the degree of cerebral atrophy, advancing age, and local cerebral blood flow reductions of subcortical white matter correlated and contributed in that order of precedence to the presence and severity of leuko-araiosis. Combination of the unusual vascular anatomy of periventricular white matter together with cerebral hypoperfusion appears to be related to the occurrence of leuko-araiosis observed among neurologically and cognitively normal subjects. Further investigations should determine whether leuko-araiosis among this population is a risk factor for later cognitive impairments.

Efficient Treatment of Neurogenic Bladder Disorders in Multiple Sclerosis with Initial Intermittent Catheterization and Ultrasound-Controlled Training

Out of 350 multiple sclerosis (MS) patients, 197 had residual urine (RU), on average 113 ml on admission. Treatment with initial intermittent catheterisation and bladder training normalized the neurogenic bladder disorders (NBD) in most patients; the RU was 28 ml on average at discharge. Continence improved with the reduction of RU. Even in those 37 patients with a RU of over 200 ml on admission, this management reduced the average RU to 83 ml on discharge. Patients with a RU of over 50 ml had bacteriuria 3 times more often than patients with a lower RU. In patients admitted with a long-term catheter, the catheter was removed; these patients had an average RU of 166 ml on admission, 23 ml on discharge. There was a highly significant correlation between high RU and the degree of cerebral atrophy. Patients with more than 50 ml RU at discharge were those with severe cerebral atrophy, tetraplegia and dementia. The different patterns of NBD were merely different states of the same NBD under different training conditions. Since NBD occurs about a 1,000 times more often than bowel incontinence with the same lesions in MS, it is not the cerebrospinal lesions per se, but the peripheral vicious circle they trigger, which leads to detrusor hyperactivity and dyssynergy. The peripheral pathogenetic mechanism is urinary retention leading to bladder overextension. Urodynamic investigations beyond the measurement of RU (by ultrasound) are not necessary for the treatment of NBD in most MS patients. The noninvasive and inexpensive therapy described here is effective.