Structural Lesions Research Articles

Arterial Hypertension, Structural Damage of the Brain and Cognitive Test

The arterial hypertension cause brain vascular damage (white matter lesion) and the burden and progression determine their cognitive consequences. Therefore, arterial hypertension is considered the main modifiable vascular risk factor for cognitive impairment and dementia. Therefore, the aim of the current study was to evaluate the results of cognitive tests in a sample of hypertensive patients and to establish possible associations with structural brain lesions (atrophy, white matter lesions) identified by magnetic resonance imaging Were included 70 hypertensive patients from Heart-Brain study in Argentina with magnetic resonance imaging and cognitive test. Fazekas scale and the Global Cortical Atrophy were used to quantify the white matter lesions and the brain atrophy, respectively. The Mini-Mental Status Examination, Clock Drawing test and Mini-Boston Naming test were used to evaluate the cognitive status. average age 69.7 ± 10.6 years, 55.7% female). Based on the linear regression analysis, Fazekas scale and cognitive tests were inversely associated. For each grade of increase in Fazekas scale, the clock drawing test (Coef -0.56, CI 95% -1.01 -0.10, p=0.01) and the Mini-mental Status Examination (Coef -0.7, CI 95% -1.27 -0.13, p=0.01) scores decreased. The subcortical atrophy was significantly associated with the clock drawing test (OR 3.29, CI 95% 1.25-8.63; p=0.016). Conclusion: The cognitive tests, particularly the clock drawing test could be used (in the clinical routine practice) as “subrrogate” of the brain structural hypertension-mediated damage.

The value of a repeat MRI examination of the sacroiliac joints following an inconclusive initial examination.

Assess the diagnostic utility of repeat sacroiliac joint (SIJ) magnetic resonance imaging (MRI) examinations following an inconclusive initial examination performed for suspected sacroiliitis. Subjects with > 1 SIJ MRI examinations, an inconclusive first scan and at least 6 months interval between scans, were included. All scans were evaluated for the presence of structural/active SIJ lesions as well as any other pathology. Clinical data was extracted from the patients' clinical files, and any missing data was obtained by a telephone interview. Diagnosis and active/structural scores were compared between first and follow-up examinations (t test). Seventy-one subjects were included in the study, 77.4% females, mean age 41.0 ± 15 years, mean time interval between exams 30.4 ± 25.24 months. Twelve subjects performed > 2 scans. In only two subjects (2.81%), both females, MRI diagnosis changed from inconclusive to definite sacroiliitis. None of the subjects with > 2 scans had evidence of sacroiliitis in any of the following MRI examinations. Significant differences were observed between the scores of active SIJ lesion of the first and follow-up MRI (1.51/1.62, p = 0.02) but not for scores of structural lesions (1.22/1.68, p = 0.2). Repeat SIJ MRI when the first MRI is inconclusive for sacroiliitis is more valuable in ruling out than in securing diagnosis of sacroiliitis. We suggest that when MRI findings are inconclusive, decision-making should be based on clinical data.

The hemodynamic response function as a type 2 diabetes biomarker: a data-driven approach.

There is a need to better understand the neurophysiological changes associated with early brain dysfunction in Type 2 diabetes mellitus (T2DM) before vascular or structural lesions. Our aim was to use a novel unbiased data-driven approach to detect and characterize hemodynamic response function (HRF) alterations in T2DM patients, focusing on their potential as biomarkers. We meshed task-based event-related (visual speed discrimination) functional magnetic resonance imaging with DL to show, from an unbiased perspective, that T2DM patients' blood-oxygen-level dependent response is altered. Relevance analysis determined which brain regions were more important for discrimination. We combined explainability with deconvolution generalized linear model to provide a more accurate picture of the nature of the neural changes. The proposed approach to discriminate T2DM patients achieved up to 95% accuracy. Higher performance was achieved at higher stimulus (speed) contrast, showing a direct relationship with stimulus properties, and in the hemispherically dominant left visual hemifield, demonstrating biological interpretability. Differences are explained by physiological asymmetries in cortical spatial processing (right hemisphere dominance) and larger neural signal-to-noise ratios related to stimulus contrast. Relevance analysis revealed the most important regions for discrimination, such as extrastriate visual cortex, parietal cortex, and insula. These are disease/task related, providing additional evidence for pathophysiological significance. Our data-driven design allowed us to compute the unbiased HRF without assumptions. We can accurately differentiate T2DM patients using a data-driven classification of the HRF. HRF differences hold promise as biomarkers and could contribute to a deeper understanding of neurophysiological changes associated with T2DM.

A Brazilian series utilizing the SMASH-U system for etiologic classification of intracerebral hemorrhage.

Understanding the causes of intracerebral hemorrhage (ICH) is crucial for effective treatment and preventing recurrences. The SMASH-U scale is a suggested method for classifying and predicting the outcomes of ICH. To describe the SMASH-U classification and outcomes by etiology in patients admitted to a comprehensive stroke center in São Paulo, Brazil. A retrospective analysis was conducted on patients admitted to the hospital or outpatient clinic between April 2015 and January 2018. Two stroke neurologists evaluated the SMASH-U classification, and patients with incomplete medical records were excluded. Out of the 2000 patients with a stroke diagnosis evaluated, 140 were included in the final analysis. The mean age was 57.9 (± 15.5) years, and 54.3% were male. Hypertension was the most frequent etiology, accounting for 41.4% of cases, followed by amyloid angiopathy (18.5%) and structural lesions (14.1%). Structural lesions were more common among women and patients under 45 years old. Favorable outcomes were observed in 61% of patients with structural lesions, compared to 10% of patients with medication-related etiologies. This study provides important evidence regarding the etiological classification of Brazilian patients with ICH. Hypertension and amyloid angiopathy were the most frequent causes, while structural lesions and systemic diseases were more common in younger patients.

Claw Hand in Parsonage Turner syndrome

An elderly patient with an extensive smoking history presented with acute severe right-hand pain and evolving weakness with patchy sensory deficit. He had minimal relief from multiple analgesics, gabapentin, and acupuncture. Motor deficits in his right-hand progressed. A nerve conduction study confirmed motor-predominant polyneuropathy and magnetic resonance imaging (MRI) of his C-spine and brachial plexus ruled out apical lung mass or other structural lesions. A positive GalNAc-GD1a ganglioside antibody (IgG) was noted. A diagnosis of immune mediated neuralgic amyotrophy or Parsonage-Turner Syndrome was made. Intravenous immune globulin (IVIG) was started with partial improvement in motor function, six months later. Although this patient did not have SARS-CoV-2 infection nor was he recently vaccinated, this case is of interest to hospital-based internists as the Covid pandemic has seen an increase in the in reported cases of neuralgic amyotrophy worldwide due to the virus itself as well as the associated COVID-19 vaccines.

Distinct characteristics and progression patterns of facet joint structural lesions in radiographic axial spondyloarthritis.

Both vertebral bodies and posterior elements of the vertebrae (facet joints, FJ) can engage in bone formation in radiographic axial spondyloarthritis (r-axSpA). However, little is known about the specific structural lesions and progression patterns of FJs in r-axSpA. To identify specific lesions related to r-axSpA and to investigate the distinct progression patterns by comparing the FJ changes of r-axSpA with that of diffuse idiopathic skeletal hyperostosis (DISH), osteoarthritis (OA), and control group (CG). Single-center, retrospective study. Longitudinal imaging data were retrieved and collected. Age- and sex-matched patients with complete thoracic and lumbar spine computed tomography (CT) data were included and their bilateral FJs were assessed. FJ changes were divided into erosions, ankylosis, joint-space narrowing, osteophytes, subchondral sclerosis, subchondral cysts, and vacuum phenomena. Average progressed year was defined as "number of changed vertebrae × interval years"/number of changed vertebrae. In all, 50 patients in each group were included. Subchondral cysts and vacuum phenomena were not observed. Bilateral FJ ankylosis (FJA)/erosions in the thoracic and lumbar spine, and unilateral ankylosis/erosions in T1-4, T9-12 were significantly more common in r-axSpA. Joint-space narrowing/osteophytes/subchondral sclerosis were significantly more common in DISH and OA. FJ lesions progressed in 56.34% of vertebrae of r-axSpA. The most common pattern was "FJ normal advanced to ankylosis" (17.54%) which required 2.63 years. It was followed by "erosions advanced to ankylosis" (12.3%) which took 2.05 years, and by "normal FJ advanced to erosions" (11.04%) which took 2.29 years, respectively. Degenerative changes could also progress to FJ erosions/ankylosis (24.83%). The majority pattern in DISH/OA was "FJ changes advanced to subchondral sclerosis/osteophytes/joint-space narrowing." Bilateral FJA/erosions are r-axSpA-specific lesions. The specific progression pattern for r-axSpA was "FJ changes advanced to ankylosis/erosions." Repeated CT examination in intervals of at least 2 years will be more appropriate for monitoring FJ progression.

Predictive and concurrent validity of pain sensitivity phenotype, neuropeptidomics and neuroepigenetics in the MI-RAT osteoarthritic surgical model in rats.

Micro-RNAs could provide great insights about the neuropathological mechanisms associated with osteoarthritis (OA) pain processing. Using the validated Montreal Induction of Rat Arthritis Testing (MI-RAT) model, this study aimed to characterize neuroepigenetic markers susceptible to correlate with innovative pain functional phenotype and targeted neuropeptide alterations. Functional biomechanical, somatosensory sensitization (peripheral-via tactile paw withdrawal threshold; central-via response to mechanical temporal summation), and diffuse noxious inhibitory control (via conditioned pain modulation) alterations were assessed sequentially in OA (n = 12) and Naïve (n = 12) rats. Joint structural, targeted spinal neuropeptides and differential expression of spinal cord micro-RNAs analyses were conducted at the sacrifice (day (D) 56). The MI-RAT model caused important structural damages (reaching 35.77% of cartilage surface) compared to the Naïve group (P < 0.001). This was concomitantly associated with nociceptive sensitization: ipsilateral weight shift to the contralateral hind limb (asymmetry index) from -55.61% ± 8.50% (D7) to -26.29% ± 8.50% (D35) (P < 0.0001); mechanical pain hypersensitivity was present as soon as D7 and persisting until D56 (P < 0.008); central sensitization was evident at D21 (P = 0.038); pain endogenous inhibitory control was distinguished with higher conditioned pain modulation rate (P < 0.05) at D7, D21, and D35 as a reflect of filtrated pain perception. Somatosensory profile alterations of OA rats were translated in a persistent elevation of pro-nociceptive neuropeptides substance P and bradykinin, along with an increased expression of spinal miR-181b (P = 0.029) at D56. The MI-RAT OA model is associated, not only with structural lesions and static weight-bearing alterations, but also with a somatosensory profile that encompasses pain centralized sensitization, associated to active endogenous inhibitory/facilitatory controls, and corresponding neuropeptidomic and neuroepigenetic alterations. This preliminary neuroepigenetic research confirms the crucial role of pain endogenous inhibitory control in the development of OA chronic pain (not only hypersensitivity) and validates the MI-RAT model for its study.

Perfil antierosivo de uma solução experimental baseada em antioxidantes da Passiflora edulis em lesões iniciais de erosão dentinária

Abstract Introduction The non-carious degradation of the dentin matrix is a natural process throughout life; however, when associated with the presence of excessive acidic substances, it leads to lesions in dental structures. Objective This study developed an experimental solution based on antioxidant polyphenols from the yellow passion fruit seed (Passiflora edulis) and assessed its preventive potential on eroded dentin. The experimental polyphenolic solution was obtained from passion fruit seeds through drying and cold pressing. Material and method Thirty samples of bovine cervical root dentin were acquired and randomized into three groups (n=10): G1 – distilled water; G2 – experimental solution of phenolic antioxidants from passion fruit; G3 – Commercial anti-erosion toothpaste. Erosive cycling and treatment were conducted over 3 days. Subsequently, non-contact 3D confocal microscopy was employed to measure volumetric (Sa) and linear (Ra) roughness, as well as erosive wear. A one-way ANOVA/Tukey test was performed (α=0.05). Result The G2 group had lower Ra and Sa values compared to the other groups and demonstrated the lowest erosive wear in µm compared to G1 and G3. Conclusion: The experimental solution based on antioxidant polyphenols from Passiflora edulis showed promising performance on eroded dentin in this investigation. Nevertheless, further research is required to establish its effectiveness and potential use in developing a new product.

Neurological involvement in patients with primary immunodeficiency.

Primary immunodeficiency diseases (PID) are defined by recurrent infections, allergies, autoimmunity, and malignancies. Neurologic symptoms are one of the major components of some immunodeficiency syndromes, such as Ataxia-Telangiectasia (AT), Nijmegen breakage syndrome (NBS), and Purine Nucleoside Phosphorylase (PNP) deficiency, which are considered as the primary involvement. Various pathological mechanisms, DNA repair disorders, metabolic abnormalities, and autoimmune phenomena have also been linked with neurological conditions. We retrospectively assessed the neurological involvement in 108 patients out of 6000 with PID in this study. The female/male ratio of the cases was 49/59, and the median age was 13 years (min = 1; max = 60). Neurological problems were detected at a median age of 7 years (min = 0.5; max = 30). Di George Syndrome (DGS) and CVID (common variable immunodeficiency) were the most common diseases in our cohort (n = 31, 30% and n = 30, 27%, respectively). The most frequent outcomes were cognitive delay (n = 63, 58%), epilepsy (n = 25, 23%), and ataxia (n = 20, 18%). Central nervous system involvement was found in 99% of the patients (n = 107), and peripheral nervous system complication was found in only one patient with CVID and chronic inflammatory demyelinating polyneuropathy (CDIP). Cranial MRI was found to be abnormal in 74% (n = 80) of the patients. MRI findings included cerebellar atrophy (n = 33, 34%), white matter lesion (n = 27, 28.4%), cerebral atrophy (n = 21, 22.3%), gray matter lesion (n = 6, 6.3%), hydrocephalus (n = 5, 5,3%), and pituitary gland lesion (n = 3, 3.2%), intracranial hemorrhage (n = 3, 3%), intracranial vasculitis (n = 3, 2.7%), and arterio-venous malformation (n = 1, 0,9%). Primary involvement (a component of the disease) was 60% (n = 65), and secondary (infection or autoimmunity) and tertiary involvements (structural or incidental lesions) contributed 20% (n = 20) each in the patients. In this study, we describe the various neurologic findings of patients with PID. The neurologic presentation may represent the initial manifestation of certain types of PID. Early diagnosis and treatment are essential to prevent or reduce further neurologic damages.

A brief review of the neuroimaging modalities in schizophrenia and their scope

Abstract Schizophrenia is a serious mental disorder characterized by diverse symptoms, including hallucinations, delusions, and disorders in thinking, behavior and cognition. Its etiology is multifactorial involving genetic, environmental, developmental, and neurobiological factors. Neuroimaging studies have significantly contributed to understanding the underlying neural abnormalities associated with this disorder. Reduced brain volume was observed in frontal and temporal lobes in most studies using structural imaging techniques. Hypofrontality was observed in functional studies. Neuroimaging also aids in differentiating structural lesions causing symptoms mimicking schizophrenia. However, challenges persist due to variables such as age, gender, comorbidities, therapy history, substance use, and coexisting psychiatric conditions, which are often insufficiently controlled for, in the literature. This review article comprehensively consolidates the diagnostic and prognostic potential of various neuroimaging techniques in schizophrenia.

A Case Report of an Isolated Calvarial Defect in the Region of the Lambdoid Suture: A Rare Bone Manifestation of Neurofibromatosis Type 1

The Calvarial bone defects in the lambdoid suture region are a rare bone manifestation of neurofibromatosis type 1. They may be isolated or associated with an adjacent structural lesion, such as a dural ectasia or plexiform neurofibroma. The underlying pathophysiology for the development of these types of skull defects is still unclear. We present the case of a Calvarial defect in the region of the lambdoid suture in a 7-year-old boy with a medical history of neurofibromatosis type 1 who was referred for a brain scan to explore a palpable skull defect in right parieto-occipital region , noticed by his doctor.

Microbleeds within Mitochondrial Stroke-Like Lesion Rather Result from Their Vulnerability Than from Microangiopathy

MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and stroke-like episode) is one of the most common syndromic mitochondrial disorders (MID) and is due to the variant m.3243A&gt;G in MT-TL1 in approximately 80% of cases. MELAS is a multisystem disorder with stroke-like episodes (SLEs) as a pathognomonic feature. The morphological correlate of SLEs in cerebral imaging are stroke-like lesions (SLLs). SLLs present on cerebral MRI with a T2, FLAIR, DWI, and PWI-hyperintense and OEF-hypointense lesion that is not confined to a vascular territory and extends to a nadir before disappearing or terminating as a structural lesion. Occasionally, these features are accompanied by microbleeds within the SLL, usually along the cortex. These microbleeds are thought to result from laminar cortical necrosis, and end-stage of a SLL or seizures, a common manifestation of SLEs.

Thyroid disfunction and chronic obstructive pulmonary disease: case report

Common concomitant endocrine diseases in chronic obstructive pulmonary disease (COPD) patients include both structural and functional lesions of the thyroid gland.The purpose of the study was to determine specific indicators for the differential diagnosis of thyroid storm and exacerbation of COPD. A clinical observation of a 60-year-old patient who received inpatient treatment in the therapeutic department of a city clinical hospital is presented. The diagnosis upon admission was COPD, mixed form, severe, exacerbation, and respiratory failure of the first degree.Results. In the hospital, the patient experienced an episode of difficulty breathing lasting 45 minutes. Increased shortness of breath alternated with normal breathing and was accompanied by tremor of the hands. The patient was agitated, refused to breathe oxygen through the mask, and was in orthopnea. The patient’s condition during the attack was assessed at 40 points according to the Burch – Wartofsky scale, which corresponds to a high probability of thyroid storm (TS). Pronounced ventilation disturbances of a mixed type were recorded based on the spirography results (forced expiratory volume in 1 second – 19%). Echocardiography revealed no signs of cor pulmonale or pulmonary hypertension. A low concentration of thyroid-stimulating hormone was recorded, the level of free thyroxine (T4) remained within the reference range. Serum levels of thyroid peroxidase antibodies did not increase, and no changes in the thyroid gland were detected during ultrasound examination.Conclusion. When thyroid abnormality manifests in a patient with COPD, certain difficulties may arise with the differential diagnosis of exacerbation of COPD and TS due to the similarity of their clinical manifestations.

Diagnostic and therapeutical approaches to H3K27M-altered diffuse midline glioma in children: a review

H3K27M-altered diffuse midline gliomas are the most devastating pediatric brain tumors. These tumors are characterized by lesion of central nervous system midline structures, diffuse infiltrative growth and fatal prognosis. The pathogenesis of H3K27M-altered diffuse midline glioma is based on unique epigenetic and genetic changes which are associated with histone 3 (H3) alterations. Clinical disease course usually is non-specific, that could hamper diagnosis establishment and defines high prevalence of disseminated tumor stages. Diagnostic approach includes neuroimaging, various laboratory and molecular methods, including high throughput sequencing, which allows finding potential targets for precise therapy. Despite the availability of anti-tumor technologies, including targeted therapy and immunotherapy, the standard of care for H3K27M-altered diffuse midline glioma is radiation therapy, which does not allow achieving long-term event-free survival. A dismal prognosis and absence of curative options for these tumors determine the necessity of new treatment methods search that could improve patients’ outcome. In this article we present current worldwide data of the diagnosis and treatment trends in H3K27M-altered diffuse midline glioma.

Motor fiber function in spinal muscular atrophy-analysis of conduction velocity distribution.

The motor neuron survival protein, which is deficient in spinal muscular atrophy (SMA), performs numerous cellular functions. Currently, SMA is believed to be a multi-organ disease, including lesion of various structures of the central and peripheral nervous systems. Motor nerve damage, especially in milder SMA types, is controversial. This prompted the conduct of the electrophysiological studies in adults with SMA types 2 and 3 presented in this paper. The study group consisted of 44 adult patients with SMA types 2 and 3. All patients underwent neurological examination with Hammersmith Functional Motor Scale-Expanded (HFMSE) assessment. Standard electrophysiological studies in the ulnar nerve and conduction velocity distribution (CVD) tests were performed in all patients and controls. A prolongation of the distal latency and lowering of the motor potential amplitude with no changes in CVD were found in the whole patient group. There were no dependencies on the number of gene copies. Patients with low HFSME value had slower standard conduction velocity, CVD in upper and median quartiles, and narrower CVD spread; in milder SMA, CVD spread was greater than in controls. The significant reduction in motor response amplitude in SMA seems to be primarily related to motor neuron loss and directly proportional to its severity. The coexisting rearrangement in the peripheral nerve structure is present in SMA, and this could be partially caused by a coexisting demyelinating process. Nerve remodeling mainly affects large fibers and occurs in more severe SMA types with significant disability.

Structural brain lesion in epilepsy patients: An experience from Northeast India

Structural brain lesion in epilepsy patients: An experience from Northeast India

COVID19 and cognitive impairment ‐ A follow‐up study with cognitive and neuroimaging evaluation of the Clinical Hospital of São Paulo

AbstractBackgroundPost‐COVID19 syndrome is characterized by signs and symptoms that occur within 3 months of the onset of COVID19 and last for at least 2 months. Cognitive impairment has frequently been associated with COVID19 with descriptions of attentional, executive, memory, and language disorders. Moreover, some morphological and metabolic changes have been described in MRI and FDG PET‐CT, respectively. There is no formal treatment for this condition.MethodWe selected patients less than 65 years of age with COVID19 at least 3 or more months of symptoms and no more than 6 months, no relevant structural brain lesions, no record of neurodegenerative disease. A cross‐over design study was performed with neuropsychological rehabilitation. They were evaluated 3 times by a neurologist (0, 3, and 6 months) with specific cognitive battery tests and questionnaires and then by a neuropsychologist for evaluation and training. Finally, most patients underwent neuroimaging with cranial MRI and FDG PET CT or MRI.Result44 patients performed the first baseline evaluation, 34 matched inclusion criteria and were referred to neuropsychological rehabilitation. 20 underwent functional and structural neuroimaging. This sample had a mean age of 44 (SD8.9) years, 61% of females, 16.1 (SD5.1) years of education, 17.6% of hypertension, 2.9% diabetes, 11.8% dyslipidemia and 23.5% obesity. Cognitive evaluation depicted that 90.6% had memory complaints; MMSE of 27.7 (SD1.8); delayed recall of 8.68 (SD1.6) out 10 in the brief cognitive screening battery; semantic verbal fluency of 18.24 (SD5.1); lexical fluency of 31.7 (SD11.7); forward digit span 6.62 (SD0.7); backward digit span 4.82 (SD 1.3); clock drawing test of 9.12 (SD1.6) and Boston naming test‐15 of 14.06 (SD1.5). 46.9% reported more than 5 points on the depression scale and 41.2% somnolence on the Epworth scale. 60% had abnormal findings (hypometabolism) in brain FDG PET, 16% with frontotemporal involvement, 33% basal ganglia, 8% frontoparietal, 41% cerebellum, 8% parietal only, 8% frontalmedial, and 25% temporal. Some (33%) had mixed patterns.Conclusionpost‐COVID19 syndrome and cognitive impairment are relatively common and we need prospective studies in low and middle‐income countries to understand the cognitive profile, structural and metabolic patterns in neuroimage, and the role of neuropsychological rehabilitation.

Brain metabolism during delirium

AbstractBackgroundAltered cerebral glucose metabolism manifested by increased cerebrospinal fluid (CSF) lactate and decreased neuron specific enolase during delirium has been found in CSF analyses in multiple settings, although without change in CSF or blood glucose. These changes correlate with markers of delirium severity and outcomes of delirium.However, patients with delirium are acutely unwell in hospital and have multiple comorbidities. The contribution of acute illness and dementia have not been excluded.MethodWe studied two groups of acutely unwell older people in hospital after excluding underlying dementia by history and the Informant Questionnaire on Cognitive Decline in the Elderly. The first group had delirium and the second group had no delirium. All patients underwent a 18F‐fluorodeoxyglucose positron emission tomography (FDG‐PET) scan in hospital while unwell, and during delirium for the first group. Confounders on FDG‐PET such as structural brain lesions and medications that affect brain metabolism were excluded.Then we also compared the delirium FDG‐PET scans to a group with Alzheimer’s dementia.ResultPatients with delirium demonstrated a unique, novel pattern of brain hypometabolism that reflected symptoms of delirium. The affected areas included: bilateral thalami; right posterior cingulate cortex (PCC); right superior frontal, right infero‐lateral anterior temporal and left superior parietal cortices. The areas highly negatively correlated with delirium severity scores (Spearman’s rank correlation coefficients between ρ = ‐0.39 and ‐0.71; p values from 0.089 to 0.001) and performance on a range of relevant neuropsychological tests, for example thalami and Trail Making Test B (Spearman’s ρ = ‐0.52; p = 0.028). Direct comparison to AD scans significant thalamic hypometabolism (p&lt;0.01) in delirium, but the PCC was not different.ConclusionIn patients with acute illness but without dementia, delirium is accompanied by regional cerebral hypometabolism in a distribution that is not consistent with any known pattern of dementia. While there is some overlap with AD, thalamic hypometabolism is atypical of AD and consistent with the clinical features of delirium.ReferencesNitchingham AR, Pereira JV‐B, Wegner EA, Oxenham V, Close J Caplan GA. Regional cerebral hypometabolism on 18F‐FDG PET/CT scan in delirium is independent of acute illness and dementia. Alzheimers &amp; Dementia 2022; 1‐10.

Investigating associations of multiple common infections with brain structure and white matter lesions: findings from prospective neuroimaging studies

AbstractBackgroundEvidence for a role of common infections in neurodegenerative and cerebrovascular diseases is conflicting, and the extent to which pathogen exposure associates with subclinical imaging markers of these diseases is unclear. We aimed to investigate associations between a panel of serological measures characterising exposure to common pathogens – selected based on their relevance to public health – and brain volume, hippocampal volume, and white matter lesions in two population‐based cohorts in the UK.MethodSerology and imaging data were available for 1371 participants across two studies: the UK Biobank (N = 935, mean age(SD)[years] = 55.3(7.7) at serology; 63.8(7.7) at imaging) and the Medical Research Council National Survey of Health and Development [N = 436, mean age(SD) [years] = 63.3(1.1) years at serology; 70.7(0.7) years at imaging). Serology measures included a) serostatuses of 17 pathogens, b) total proportion of 17 pathogens exposed to, and c) total proportion of 11 neurotropic pathogens exposed to (Table 1). Associations between serology measures and outcomes (brain volume, hippocampal volume, and white matter lesion volume) were tested using linear regression. Regression models included adjustments for total intracranial volume and clinic information (basic models), and age, sex, ethnicity, education, socioeconomic position and lifestyle factors (Figure 1). Findings across cohorts were meta‐analysed using random‐effects models. The present study will be expanded to include an additional cohort (Southall and Brent Revisited,N≤1200) to add more precision for identifying associations.ResultSeropositivity to seven pathogens associated with an outcome in basic models, and four in fully‐adjusted models: seropositivity to JC virus was associated with smaller brain volumes, Epstein‐Barr virus with larger brain volumes, Merkel cell virus with larger hippocampal volumes and fewer white matter lesions, and C.trachomatis with fewer white matter lesions (Figure 2). Neurotropic pathogen burden scores associated with smaller hippocampal volumes in basic models, but no associations were seen for either pathogen burden score in fully‐adjusted models.ConclusionWe found some evidence of both positive and negative associations between common infections and imaging markers of subclinical cerebrovascular disease and neurodegeneration, with no evidence of relationships with pathogen burden. This work highlights key relationships for further investigation, which may reveal novel pathways associated with brain structure and cerebrovascular pathology.

The impact of amyloid‐PET and FDG‐PET on the progression from amnestic MCI to AD dementia in clinical practice

AbstractBackgroundAlzheimer disease (AD) is the most common cause of dementia worldwide. It is known that cerebral amyloid aggregation and neurodegeneration are first steps in the physiopathology of AD. In the prodromal phase, a clinical diagnosis of amnesic mild cognitive impairment (aMCI) can be stablished, but not all subjects with MCI have a prodromal AD. The objective of this study was to determinate the impact of amyloid and FDG PET on the progression from aMCI to AD dementia.MethodsFrom October 2013 to March 2021, we prospectively selected 145 patients with a diagnosis aMCI. We excluded subjects older than 85 and those with structural brain lesion on brain MRI. Participants went through an amyloid and an FDG‐PET scans and were classified as positive or negative for amyloid and neurodegeneration. Patients were followed to stablish progression to AD dementia, 118 patients were followed up more than 36 months. Statistical analyses were done with STATA with significance set at p&lt;0.05. All analyses were adjusted by age, gender, and education.ResultsDemographics are shown on table 1. Sensibility, specificity, negative predictive value, and positive predictive value during the 4 years are shown on table 2. 88 patients were A+ and 74 patients were A‐. We divided the patients in 4 groups: A+/FDG+ (n:54), A+/FDG‐ (n:34), A‐/FDG‐ (40), A‐/FDG+(4). The mean of conversion were 39.95 months, this time depends on the result of the biomarkers. A‐ patients converted less and latter with a mean of 75.07 (IC 56.54→81) month, than A+ patients, that converted earlier (chi2 = 20.37 Pr&gt;chi2 = 0.0000). A+/FDG+ converted with a mean of 27.79 (20.40‐33.21) months while A+/FDG‐ converted earlier with a mean of 37.38 (20.73‐48.26) month. (chi2 = 4.16 Pr&gt;chi2 = 0.0415).ConclusionsAmyloid and FDG PET can help us to stablish prognosis in aMCI patients. We have observed that a positive amyloid PET is associated with an increased risk of progression to AD dementia. Even more, aMCI patients with both, amyloid PET and FDG, positive PETs progressed more often and earlier to AD dementia than those who have a positive amyloid PET but a negative FDG‐PET.