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In normal old (Nold) and Alzheimer's disease (AD) persons, a high cognitive reserve (CR) makes them more resistant and resilient to brain neuropathology and neurodegeneration. Here, we tested whether these effects may affect neurophysiological oscillatory mechanisms generating dominant resting state electroencephalographic (rsEEG) alpha rhythms in Nold and patients with mild cognitive impairment (MCI) due to AD (ADMCI). Data in 60 Nold and 70 ADMCI participants, stratified in higher (Edu+) and lower (Edu-) educational attainment subgroups, were available in an Italian-Turkish archive. The subgroups were matched for age, gender, and education. RsEEG cortical sources were estimated by eLORETA freeware. As compared to the Nold-Edu- subgroup, the Nold-Edu+ subgroup showed greater alpha source activations topographically widespread. On the contrary, in relation to the ADMCI-Edu- subgroup, the ADMCI-Edu+ subgroup displayed lower alpha source activations topographically widespread. Furthermore, the 2 ADMCI subgroups had matched cerebrospinal AD diagnostic biomarkers, brain gray-white matter measures, and neuropsychological scores. The current findings suggest that a high CR may be related to changes in rsEEG alpha rhythms in Nold and ADMCI persons. These changes may underlie neuroprotective effects in Nold seniors and subtend functional compensatory mechanisms unrelated to brain structure alterations in ADMCI patients.
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Ritmo alfa/fisiologia , Doença de Alzheimer/fisiopatologia , Amnésia/fisiopatologia , Córtex Cerebral/fisiopatologia , Disfunção Cognitiva/fisiopatologia , Escolaridade , Idoso , Doença de Alzheimer/psicologia , Amnésia/psicologia , Disfunção Cognitiva/psicologia , Eletroencefalografia/métodos , Feminino , Humanos , Masculino , Testes Neuropsicológicos , Descanso/fisiologia , Descanso/psicologiaRESUMO
AIMS: The aims of this study were to assess vascular dysfunction in patients with Alzheimer disease (AD) by investigating cerebral vasomotor reactivity using transcranial Doppler ultrasound (TCD) and to evaluate any correlations between cerebral vasoreactivity and endothelium dysfunction. Moreover, the frequency of circulating progenitor cells (CPCs) and the blood concentration of vascular/inflammatory markers were evaluated. MATERIALS AND METHODS: We recruited 35 AD subjects and 17 age-matched, sex-matched, and education-matched healthy control subjects. Cerebral vasomotor reactivity was assessed by means of the TCD-based breath-holding index test (BHI). The level of CPCs was evaluated by means of flow cytometry from venous blood samples, while blood vascular/inflammatory markers were measured by means of enzyme-linked immunosorbent assay. RESULTS: Both cerebral assay blood flow velocity in the middle cerebral artery (MCAFV) and BHI values were significantly lower in AD subjects than in healthy controls (P<0.05). A positive trend was found between MCAFV and BHI values and Mini-Mental State Evaluation (MMSE) scores. Moreover, the hematopoietic progenitor cells' count was found to be lower in patients with AD than in controls (P<0.05). Finally, a significantly higher expression of the plasma chemokine CCL-2 was observed in AD patients than in healthy controls. CONCLUSIONS: Our results confirm that cerebral hemodynamic deterioration may be a critical marker of cognitive decline. Further studies are needed to investigate the role of circulating CPCs and chemokines as potential contributors to neurovascular dysfunction.
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Doença de Alzheimer , Biomarcadores/sangue , Artéria Cerebral Média , Ultrassonografia Doppler Transcraniana , Idoso , Doença de Alzheimer/diagnóstico por imagem , Doença de Alzheimer/fisiopatologia , Suspensão da Respiração , Circulação Cerebrovascular , Quimiocina CCL2/sangue , Feminino , Humanos , Masculino , Testes de Estado Mental e Demência , Artéria Cerebral Média/diagnóstico por imagem , Artéria Cerebral Média/fisiopatologia , Células-Tronco/imunologiaRESUMO
Complementary alternative medicine, such as shiatsu, can represent a suitable treatment for primary headaches. However, evidence-based data about the effect of combining shiatsu and pharmacological treatments are still not available. Therefore, we tested the efficacy and safety of combining shiatsu and amitriptyline to treat refractory primary headaches in a single-blind, randomized, pilot study. Subjects with a diagnosis of primary headache and who experienced lack of response to ≥2 different prophylactic drugs were randomized in a 1:1:1 ratio to receive shiatsu plus amitriptyline, shiatsu alone, or amitriptyline alone for 3 months. Primary endpoint was the proportion of patients experiencing ≥50%-reduction in headache days. Secondary endpoints were days with headache per month, visual analogue scale, and number of pain killers taken per month. After randomization, 37 subjects were allocated to shiatsu plus amitriptyline (n = 11), shiatsu alone (n = 13), and amitriptyline alone (n = 13). Randomization ensured well-balanced demographic and clinical characteristics at baseline. Although all the three groups improved in terms of headache frequency, visual analogue scale score, and number of pain killers (p < 0.05), there was no between-group difference in primary endpoint (p = ns). Shiatsu (alone or in combination) was superior to amitriptyline in reducing the number of pain killers taken per month (p < 0.05). Seven (19%) subjects reported adverse events, all attributable to amitriptyline, while no side effects were related with shiatsu treatment. Shiatsu is a safe and potentially useful alternative approach for refractory headache. However, there is no evidence of an additive or synergistic effect of combining shiatsu and amitriptyline. These findings are only preliminary and should be interpreted cautiously due to the small sample size of the population included in our study. Trial registration 81/2010 (Ethical Committee, S. Andrea Hospital, Sapienza University, Rome, Italy).
Assuntos
Acupressão , Amitriptilina/uso terapêutico , Analgésicos não Narcóticos/uso terapêutico , Transtornos da Cefaleia Primários/terapia , Adolescente , Adulto , Amitriptilina/efeitos adversos , Analgésicos não Narcóticos/efeitos adversos , Terapia Combinada , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Medição da Dor , Projetos Piloto , Método Simples-Cego , Resultado do Tratamento , Adulto JovemRESUMO
Although a large number of studies have examined possible differences in cognitive performance between Alzheimer's disease (AD) and vascular dementia (VaD), the data in the literature are conflicting. The aims of this study were to analyze the neuropsychological pattern of subjects affected by degenerative dementia without evidence of small vessel pathology (DD) and small vessel VaD subjects in the early stages and to investigate differences in the progression of cognitive impairment. Seventy-five patients with probable VaD and 75 patients with probable DD were included. All the subjects underwent a standard neuropsychological evaluation, including the following test: Visual Search, Attentional matrices, Story Recall, Raven's Coloured Progressive Matrices, Phonological and Semantic Verbal Fluency, Token, and Copying Drawings. The severity of cognitive impairment was stratified according to the MMSE score. Fifteen subjects with probable DD and 10 subjects with probable VaD underwent a 12-month cognitive re-evaluation. No significant difference was found between DD and VaD subjects in any of the neuropsychological tests except Story Recall in the mild cognitive impairment (P < 0.001). The re-test value was significantly worse than the baseline value in the MMSE (P = 0.037), Corsi (P = 0.041), Story Recall (P = 0.032), Phonological Verbal Fluency (P = 0.02), and Copying Drawings (P = 0.043) in DD patients and in the Visual Search test (P = 0.036) in VaD subjects. These results suggest that a neuropsychological evaluation might help to differentiate degenerative dementia without evidence of small vessel pathology from small vessel VaD in the early stages of these diseases.
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Cognição/fisiologia , Demência Vascular/psicologia , Demência/psicologia , Doenças Neurodegenerativas/psicologia , Idoso , Idoso de 80 Anos ou mais , Demência/patologia , Demência Vascular/patologia , Progressão da Doença , Feminino , Humanos , Masculino , Doenças Neurodegenerativas/patologia , Testes NeuropsicológicosRESUMO
We report a case of neurosyphilis presenting with meningitis and subacute multicranial neuropathy in a young immune-competent man. Signs of primary and secondary stages of syphilitic infection occurred almost contemporarily in our patient. MRI revealed the involvement of several cranial nerves. CSF examination proved to be diagnostic. Syphilitic meningitis should be considered among the differential diagnoses of subacute, multicranial neuropathy, or skull base meningitis. The clinical course of this patient shows that early diagnosis and treatment warrant a good neurological outcome.
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Nervos Cranianos/patologia , Neurossífilis/diagnóstico , Polineuropatias/diagnóstico , Adulto , Diagnóstico Diferencial , Humanos , Masculino , Neurossífilis/líquido cefalorraquidianoRESUMO
BACKGROUND AND PURPOSE: Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a rare autosomal dominant disorder caused by NOTCH3 mutations, is characterized by vascular smooth muscle and endothelial cells abnormalities, altered vasoreactivity, and recurrent lacunar infarcts. Vasomotor function may represent a key factor for disease progression. Tetrahydrobiopterin, essential cofactor for nitric oxide synthesis in endothelial cells, ameliorates endothelial function. We assessed whether supplementation with sapropterin, a synthetic tetrahydrobiopterin analog, improves endothelium-dependent vasodilation in CADASIL patients. METHODS: In a 24-month, multicenter randomized, double-blind, placebo-controlled trial, CADASIL patients aged 30 to 65 years were randomly assigned to receive placebo or sapropterin 200 to 400 mg BID. The primary end point was change in the reactive hyperemia index by peripheral arterial tonometry at 24 months. We also assessed the safety and tolerability of sapropterin. Analysis was done by intention-to-treat. RESULTS: The intention-to-treat population included 61 patients. We found no significant difference between sapropterin (n=32) and placebo (n=29) in the primary end point (mean difference in reactive hyperemia index by peripheral arterial tonometry changes 0.19 [95% confidence interval, -0.18, 0.56]). Reactive hyperemia index by peripheral arterial tonometry increased after 24 months in 37% of patients on sapropterin and in 28% on placebo; however, after adjustment for age, sex, and clinical characteristics, improvement was not associated with treatment arm. The proportion of patients with adverse events was similar on sapropterin and on placebo (50% versus 48.3%); serious adverse events occurred in 6.3% versus 13.8%, respectively. CONCLUSIONS: Sapropterin was safe and well-tolerated at the average dose of 5 mg/kg/day, but did not affect endothelium-dependent vasodilation in CADASIL patients. CLINICAL TRIAL REGISTRATION URL: https://www.clinicaltrialsregister.eu. Unique identifier: 2007-004370-55.
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Biopterinas/análogos & derivados , CADASIL/tratamento farmacológico , Endotélio Vascular/efeitos dos fármacos , Vasodilatação/efeitos dos fármacos , Adulto , Idoso , Biopterinas/farmacologia , Método Duplo-Cego , Feminino , Humanos , Hiperemia/tratamento farmacológico , Masculino , Pessoa de Meia-IdadeRESUMO
The role of interleukin-6 (IL-6) as a risk factor for developing depressive symptoms, neuropsychological impairment, and related functional and neurological symptom severity during the acute phase of ischemic stroke is still underexplored. Here, the authors assessed this issue, in 48 patients without significant clinical history for major medical illnesses or other factors that promote inflammation, 72 hours after a first-ever acute ischemic stroke. In the acute phase of ischemic stroke, increased IL-6 plays a key role in the onset of depressive disorders, apathy/amotivation, somatic symptoms of depression, and neurological/functional symptoms, resulting in higher disability and poor outcome of stroke patients.
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Depressão/complicações , Interleucina-6/sangue , Acidente Vascular Cerebral/sangue , Acidente Vascular Cerebral/psicologia , Avaliação de Sintomas , Idoso , Biomarcadores/sangue , Isquemia Encefálica/sangue , Isquemia Encefálica/complicações , Isquemia Encefálica/psicologia , Depressão/sangue , Feminino , Humanos , Masculino , Testes Neuropsicológicos , Escalas de Graduação Psiquiátrica , Índice de Gravidade de Doença , Acidente Vascular Cerebral/complicaçõesRESUMO
Cognitive alterations accompany or follow motor disorders in subjects with Parkinsonism. The canonical phenotypeof the Parkinson's disease Dementia (PD-D) or Lewy Body Dementia (LBD) includes deficit of attention, executiveand visuospatial functions, and presents often with apathy, hallucinations, delusions, excessive daytime sleepiness,or sleep disorders. However, the clinical expression may overlap with other neurodegenerative diseases associatedwith cognitive disorders. Thus, while clinicians rely on phenomenological patterns to infer the disease causing thecognitive impairment, the inference is weakened by the heterogeneous clinical expression of the disease. In addition,recent post-mortem studies seem to undermine the supposed pathology-phenotype coherence, making it moreand more unreliable the diagnosis based on symptoms. The lack of coherence between phenotype and pathologymay support the speculation about a common mechanism underlying the progression of the disease. While it is verylikely that a distinct, specific causal event determines the disease itself, the progression might well follow commonpatterns. A number of observations suggest that progressive diseases, which cause cognitive impairment, share aprion-like mechanism. A seeding process is supposed to account for the spreading of the lesion.
RESUMO
BACKGROUND: Transient ischemic attacks (TIAs) bear a presumed high risk of early recurrence of stroke. Data in the literature, however, are inconsistent, as recurrence rates range from 9.5 to 20%, at 90 days. AIMS: The study was designed to determine the risk of stroke after TIA. METHODS: 94 consecutive patients referred to a Stroke Unit for TIA or minor stroke, within 24 h of symptom onset, were recruited. Eleven of the 94 patients (12%, 95% CI: 7-20%) had a relapse within 90 days. The relapse consisted of a TIA for 9 patients (10%, 95% CI: 5-17%), or of a stroke for 2 subjects (1%, 95% CI: 0-8%). More than a quarter of the relapses occurred within 1 week from the first TIA. ABCD(2), ABCD(2)-I and ABCD-E+ scores were similar among people with or without relapse. CONCLUSIONS: The data seem to confirm previous reports on the relatively low relapse rate for stroke, when TIA patients are promptly assisted in dedicated structures. The findings stress the potential benefit of early intervention in subjects with TIA.
Assuntos
Ataque Isquêmico Transitório/diagnóstico , Acidente Vascular Cerebral/diagnóstico , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Hospitalização , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Recidiva , Risco , Medição de RiscoRESUMO
CADASIL is a hereditary disease characterized by cerebral subcortical microangiopathy leading to early onset cerebral strokes and progressive severe cognitive impairment. Until now, only few studies have investigated the extent and localization of grey matter (GM) involvement. The purpose of our study was to evaluate GM volume alterations in CADASIL patients compared to healthy subjects. We also looked for correlations between global and regional white matter (WM) lesion load and GM volume alterations. 14 genetically proved CADASIL patients and 12 healthy subjects were enrolled in our study. Brain MRI (1.5 T) was acquired in all subjects. Optimized-voxel based morphometry method was applied for the comparison of brain volumes between CADASIL patients and controls. Global and lobar WM lesion loads were calculated for each patient and used as covariate-of-interest for regression analyses with SPM-8. Compared to controls, patients showed GM volume reductions in bilateral temporal lobes (p < 0.05; FDR-corrected). Regression analysis in the patient group revealed a correlation between total WM lesion load and temporal GM atrophy (p < 0.05; uncorrected), not between temporal lesion load and GM atrophy. Temporal GM volume reduction was demonstrated in CADASIL patients compared to controls; it was related to WM lesion load involving the whole brain but not to lobar and, specifically, temporal WM lesion load. Complex interactions between sub-cortical and cortical damage should be hypothesized.
Assuntos
CADASIL/patologia , Substância Cinzenta/patologia , Adulto , Atrofia/patologia , Estudos de Casos e Controles , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Análise de Regressão , Lobo Temporal/patologiaRESUMO
The delayed conditioned eyeblink reflex, in which an individual learns to close the eyelid in response to a conditioned stimulus (e.g. a tone) relies entirely on the functional integrity of a cerebellar motor circuitry that involves the contingent activation of Purkinje cells by parallel and climbing fibres. Molecular changes that disrupt the function of this circuitry, in particular a loss of type-1 metabotropic glutamate receptors (mGlu1 receptors), occur in Purkinje cells of patients with multiple sclerosis and in mice with experimental autoimmune encephalomyelitis as a result of neuroinflammation. mGlu1 receptors are required for cerebellar motor learning associated with the conditioned eyeblink reflex. We propose that the delayed paradigm of the eyeblink conditioning might be particularly valuable for the detection of subtle abnormalities of cerebellar motor learning that are clinically silent and are not associated with demyelinating lesions or axonal damage. In addition, the test might have predictive value following a clinically isolated syndrome, and might be helpful for the evaluation of the efficacy of drug treatment in multiple sclerosis.
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Piscadela/fisiologia , Doenças Cerebelares/fisiopatologia , Condicionamento Clássico/fisiologia , Esclerose Múltipla/diagnóstico , Animais , Doenças Cerebelares/metabolismo , Diagnóstico Precoce , Humanos , Camundongos , Esclerose Múltipla/metabolismo , Esclerose Múltipla/fisiopatologia , Receptores de Glutamato Metabotrópico/metabolismoRESUMO
BACKGROUND: In relaxed adults, staying in quiet wakefulness at eyes closed is related to the so-called resting state electroencephalographic (rsEEG) rhythms, showing the highest amplitude in posterior areas at alpha frequencies (8-13âHz). OBJECTIVE: Here we tested the hypothesis that age may affect rsEEG alpha (8-12âHz) rhythms recorded in normal elderly (Nold) seniors and patients with mild cognitive impairment due to Alzheimer's disease (ADMCI). METHODS: Clinical and rsEEG datasets in 63 ADMCI and 60 Nold individuals (matched for demography, education, and gender) were taken from an international archive. The rsEEG rhythms were investigated at individual delta, theta, and alpha frequency bands, as well as fixed beta (14-30âHz) and gamma (30-40âHz) bands. Each group was stratified into three subgroups based on age ranges (i.e., tertiles). RESULTS: As compared to the younger Nold subgroups, the older one showed greater reductions in the rsEEG alpha rhythms with major topographical effects in posterior regions. On the contrary, in relation to the younger ADMCI subgroups, the older one displayed a lesser reduction in those rhythms. Notably, the ADMCI subgroups pointed to similar cerebrospinal fluid AD diagnostic biomarkers, gray and white matter brain lesions revealed by neuroimaging, and clinical and neuropsychological scores. CONCLUSION: The present results suggest that age may represent a deranging factor for dominant rsEEG alpha rhythms in Nold seniors, while rsEEG alpha rhythms in ADMCI patients may be more affected by the disease variants related to earlier versus later onset of the AD.
Assuntos
Envelhecimento/fisiologia , Ritmo alfa/fisiologia , Doença de Alzheimer/diagnóstico por imagem , Amnésia/diagnóstico por imagem , Cognição/fisiologia , Disfunção Cognitiva/diagnóstico por imagem , Idoso , Idoso de 80 Anos ou mais , Envelhecimento/psicologia , Doença de Alzheimer/fisiopatologia , Doença de Alzheimer/psicologia , Amnésia/fisiopatologia , Amnésia/psicologia , Disfunção Cognitiva/fisiopatologia , Disfunção Cognitiva/psicologia , Eletroencefalografia/métodos , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Descanso/fisiologia , Descanso/psicologiaRESUMO
Recent studies suggest strong interactions between cerebrovascular and Alzheimer's disease (AD) pathology. These conditions share common risk factors and individuals having both frequently show greater cognitive impairment than those affected by only one disease. Many studies point to early vascular dysregulations in AD. The exchange between vascular and neural cells occurs through mechanisms not completely understood, involving interactions among endothelial, glial, neuronal and smooth muscle cells within the neurovascular unit. Studies suggest that the dysregulation of the unit is likely associated with hypertension and other systemic diseases. Associations between hypertension and cognitive decline are not established, but other variables associated with hypertension could create a causal link. Many studies have lacked a consistent, quantitative neuropsychological approach for assessing cognitive functions. This approach is reductive, as the need for a formal neuropsychological assessment has gained broad recognition, and the definition of dementia has gone through revision processes, which are in progress.
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Doença de Alzheimer/fisiopatologia , Endotélio Vascular/fisiopatologia , Encéfalo/irrigação sanguínea , Encéfalo/fisiopatologia , Transtornos Cognitivos/fisiopatologia , Humanos , Hipertensão Intracraniana/fisiopatologiaRESUMO
Despite the large body of data available, chronic cerebral hypoperfusion lacks an operative definition. In a tautological way, the term hypoperfusion is being referred to conditions of "inadequate blood flow", "defects of perfusion" or "dysfunction of autoregulation". The chronicity refers to sustained conditions or wavering states characterized by repeated phases of inefficient functional hyperemia. The phenomenon may affect the whole brain or defined areas. A few defined clinical disorders, including heart failure, hypotension, atherosclerosis of large or small vessels and carotid stenosis are thought to cause progressive brain disorders due to chronic hypoperfusion. The clinical relevance manifests mostly as neurocognitive disorders associated with neuroimaging changes.The available data support a conceptual framework that considerschronic cerebral hypoperfusiona likely, relevant pathogenic mechanism for the neurodegeneration-like progression of the neurocognitive disorders. The relationship between neuropathology, cerebral perfusion, and symptoms progression is, however, elusive for several aspects. Typical microangiopathy findings, such as MRI white matter hyperintensities, may appear in individuals without any cerebrovascular risk or vascular lesions. Pathology features of the MRI changes, such as demyelination and gliosis, may result from dysfunction of the neuro-vascular unit not directly associated withvascular mechanisms. In this review, we aim to overview the most common clinical conditions thought to reflect chronic hypoperfusion.
Assuntos
Encéfalo/irrigação sanguínea , Encéfalo/diagnóstico por imagem , Circulação Cerebrovascular/fisiologia , Transtornos Neurocognitivos/diagnóstico por imagem , Transtornos Neurocognitivos/fisiopatologia , Animais , Encéfalo/patologia , Isquemia Encefálica/diagnóstico por imagem , Isquemia Encefálica/fisiopatologia , Doença Crônica , Progressão da Doença , Homeostase/fisiologia , Humanos , Imageamento por Ressonância Magnética/métodosRESUMO
[This corrects the article DOI: 10.3389/fnana.2020.00017.].
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Most neurological disorders seemingly have heterogenous pathogenesis, with overlapping contribution of neuronal, immune and vascular mechanisms of brain injury. The perivascular space in the brain represents a crossroad where those mechanisms interact, as well as a key anatomical component of the recently discovered glymphatic pathway, which is considered to play a crucial role in the clearance of brain waste linked to neurodegenerative diseases. The pathological interplay between neuronal, immune and vascular factors can create an environment that promotes self-perpetration of mechanisms of brain injury across different neurological diseases, including those that are primarily thought of as neurodegenerative, neuroinflammatory or cerebrovascular. Changes of the perivascular space can be monitored in humans in vivo using magnetic resonance imaging (MRI). In the context of glymphatic clearance, MRI-visible enlarged perivascular spaces (EPVS) are considered to reflect glymphatic stasis secondary to the perivascular accumulation of brain debris, although they may also represent an adaptive mechanism of the glymphatic system to clear them. EPVS are also established correlates of dementia and cerebral small vessel disease (SVD) and are considered to reflect brain inflammatory activity. In this review, we describe the "perivascular unit" as a key anatomical and functional substrate for the interaction between neuronal, immune and vascular mechanisms of brain injury, which are shared across different neurological diseases. We will describe the main anatomical, physiological and pathological features of the perivascular unit, highlight potential substrates for the interplay between different noxae and summarize MRI studies of EPVS in cerebrovascular, neuroinflammatory and neurodegenerative disorders.
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Extending Basar's theory of event-related EEG oscillations, here we hypothesize that even in quiet wakefulness, transient increases in delta rhythms may enhance global cortical arousal as revealed by the desynchronization of alpha rhythms in normal (Nold) seniors with some derangement in Alzheimer's disease dementia (ADD). Clinical and EEG datasets in 100 ADD and 100 Nold individuals matched as demography, education, and gender were taken from an international archive. Standard delta (< 4 Hz) and alpha1 (8-10.5 Hz) bands were used for the main analysis, while alpha2 (10.5-13 Hz), theta (4-8 Hz), beta1 (13-20 Hz), beta2 (20-35 Hz), and gamma (35-40 Hz) served as controls. In the interpretation, the higher the alpha1 power (density), the lower that arousal. As expected, when compared to the Nold group, the ADD group showed higher global (scalp) power density at the delta-theta band and lower global power density at the alpha-beta bands. As novel findings, we observed that: (1) in the Nold group, the global delta and alpha1-2 power were negatively and linearly correlated; (2) in the ADD group, this correlation was just marginal; and (3) in both Nold and AD groups, the EEG epochs with the highest delta power (median value for stratification) were associated with the lowest global alpha1 power. This effect was related to eLORETA freeware solutions showing maximum alpha1 source activations in posterior cortical regions. These results suggest that even in quiet wakefulness, delta and alpha rhythms are related to each other, and ADD partially affects this cross-band neurophysiological mechanism.
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Doença de Alzheimer , Córtex Cerebral , Ritmo Delta , Eletroencefalografia , Humanos , Descanso , VigíliaRESUMO
Compared with Alzheimer's disease (AD), Parkinson's disease (PD) shows peculiar clinical manifestations related to vigilance (i.e., executive cognitive deficits and visual hallucinations) that may be reflected in resting-state electroencephalographic rhythms. To test this hypothesis, clinical and resting-state electroencephalographic rhythms in age-, sex-, and education-matched PD patients (N = 136) and Alzheimer's disease patients (AD, N = 85), and healthy older participants (Nold, N = 65), were available from an international archive. Electroencephalographic sources were estimated by eLORETA software. The results are as follows: (1) compared to the Nold participants, the AD and PD patients showed higher widespread delta source activities (PD > AD) and lower posterior alpha source activities (AD > PD); (2) the PD patients with the most pronounced motor deficits exhibited very low alpha source activities in widespread cortical regions; (3) the PD patients with the strongest cognitive deficits showed higher alpha source activities in widespread cortical regions; and (4) compared to the PD patients without visual hallucinations, those with visual hallucinations were characterized by higher posterior alpha sources activities. These results suggest that in PD patients resting in quiet wakefulness, abnormalities in cortical neural synchronization at alpha frequencies are differently related to cognitive, motor, and visual hallucinations. Interestingly, parallel PD neuropathological processes may have opposite effects on cortical neural synchronization mechanisms generating cortical alpha rhythms in quiet wakefulness.