Fábio Henrique de Gobbi Porto

Effects of Aerobic Training on Cognition and Brain Glucose Metabolism in Subjects with Mild Cognitive Impairment

BACKGROUNDnAerobic training (AT) is a promising intervention for mild cognitive impairment (MCI).nnnOBJECTIVEnTo evaluate the effects of AT on cognition and regional brain glucose metabolism (rBGM) in MCI patients.nnnMETHODSnSubjects performed a twice-a-week, moderate intensity, AT program for 24 weeks. Assessment with ADAS-cog, a comprehensive neuropsychological battery, and evaluation of rBGM with positron emission tomography with 18F-fluorodeoxyglucose ([18F]FDG-PET) were performed before and after the intervention. Aerobic capacity was compared using the maximal oxygen consumption VO2max (mL/Kg/min). [18F]FDG-PET data were analyzed on a voxel-by-voxel basis with SPM8 software.nnnRESULTSnForty subjects were included, with a mean (M) age of 70.3 (5.4) years and an initial Mini-Mental State Exam score of 27.4 (1.7). Comparisons using paired t-tests revealed improvements in the ADAS-cog (M difference: -2.7 (3.7), pu200a< u200a0.001) and VO2max scores (M difference: 1.8 (2.0) mL/kg/min, pu200a< u200a0.001). Brain metabolic analysis revealed a bilateral decrease in the rBGM of the dorsal anterior cingulate cortex, pFWEu200a=u200a0.04. This rBGM decrease was negatively correlated with improvement in a visuospatial function/attentional test (rhou200a=-0.31, pu200a=u200a0.04). Several other brain areas also showed increases or decreases in rBGM. Of note, there was an increase in the retrosplenial cortex, an important node of the default mode network, that was negatively correlated with the metabolic decrease in the dorsal anterior cingulate cortex (ru200a=-0.51, pu200a=u200a0.001).nnnCONCLUSIONnAT improved cognition and changed rBGM in areas related to cognition in subjects with MCI.

Catatonia in obsessive-compulsive disorder: etiopathogenesis, differential diagnosis, and clinical management.

ObjectiveWe describe the case of a patient who developed an episode of catatonia during the course of her life-long obsessive-compulsive disorder (OCD) and discuss issues related to the etiopathogenesis, differential diagnosis, and therapeutic management of this association. BackgroundCatatonia is conventionally considered a heterogeneous syndrome of motor dysregulation characterized by mutism, immobility, negativism, posturing (catalepsy), stereotypies, and echophenomena. The relationship between OCD and catatonia is still misunderstood and poses significant challenges to the diagnosis and treatment of patients with both conditions. MethodNaturalistic follow-up of a single case. ResultsA patient with OCD developed catatonia in concert with deteriorating mood, thought, and behavior. This atypical clinical presentation of individuals with OCD and the list of differential diagnosis raised during the patients clinical assessment are discussed on 3 different levels: symptomatic presentation, comorbidity pattern, and pharmacodynamic mechanisms involved. ConclusionsThe development of a systematic therapeutic plan for patients with OCD and comorbid catatonia includes: the fine-tuning of the antiobsessional treatment; management of comorbid disorders that may engender catatonia; prompt discontinuation, and subsequent slow reintroduction of drugs deemed to trigger toxic reactions or to worsen comorbid disorders and, ultimately, the catatonia; and the implementation of specific anticatatonia measures.

Brain metabolism and cerebrospinal fluid biomarkers profile of non-amnestic mild cognitive impairment in comparison to amnestic mild cognitive impairment and normal older subjects

IntroductionMild cognitive impairment (MCI) is classically considered a transitional stage between normal aging and dementia. Non-amnestic MCI (naMCI) patients, however, typically demonstrate cognitive deficits other than memory decline. Furthermore, as a group, naMCI have a lower rate of an eventual dementia diagnosis as compared to amnestic subtypes of MCI (aMCI). Unfortunately, studies investigating biomarker profiles of naMCI are scarce. The study objective was to investigate the regional brain glucose metabolism (rBGM) with [18F]FDG-PET and cerebrospinal fluid (CSF) biomarkers in subjects with naMCI as compared to a control group (CG) and aMCI subjects.MethodsNinety-five patients were included in three different groups: naMCI (N = 32), aMCI (N = 33) and CG (N = 30). Patients underwent brain MRI and [18F]FDG-PET. A subsample (naMCI = 26, aMCI = 28) also had an assessment of amyloid-β, tau, and phosphorylated tau levels in the CSF.ResultsBoth MCI groups had lower rBGM in relation to the CG in the precuneus. Subjects with naMCI showed decreased right prefrontal metabolism as well as higher levels of CSF amyloid-β relative to aMCI subjects.ConclusionWhile amnestic MCI subjects showed a biomarker profile classically related to MCI due to Alzheimer’s disease, naMCI patients illustrated a decrease in both prefrontal hypometabolism and higher CSF amyloid-β levels relative to the aMCI group. These biomarker findings indicate that naMCI is probably a heterogeneous group with similar precuneus hypometabolism compared to aMCI, but additional frontal hypometabolism and less amyloid-β deposition in the brain. Clinical follow-up and reappraisal of biomarkers of the naMCI group is needed to determine the outcome and probable etiological diagnosis.

The Syndrome of Irreversible Lithium-Effectuated Neurotoxicity (SILENT) : One-year follow-up of a single case

In this article, we report the case history of a 44-year-old female patient with bipolar disorder who developed the so-called Syndrome of Irreversible Lithium-Effectuated Neurotoxicity (SILENT). A detailed description of our patients neurologic status is provided at baseline (i.e. during lithium intoxication) and after one year of follow-up, confirming the persistency of cerebellar signs and symptoms. Although rare, our report - which shows a severe and disabling form of SILENT - underscores the need to perform a strict control of the putative risk factors argued to be associated with the development of this syndrome. In our case, the presence of fever and the administration of multiple doses of antipsychotics may have contributed to the poor outcome exhibited by the patient.

Hemimedullary infarct with ipsilateral hemiplegia: A vertebral artery dissection syndrome? ☆

BACKGROUNDnHemimedullary syndrome is very rare and combines the clinical features of lateral and medial medullary infarctions. In patients with hemimedullary syndrome, the presence of ipsilateral, rather than contralateral hemiplegia, is rare.nnnOBJECTIVEnTo describe a patient with an infarction in the right hemimedulla with an ipsilateral motor deficit due to dissection of the right vertebral artery (VA) and to assess whether the ipsilateral hemiplegia may be the result of a specific stroke mechanism.nnnMETHODSnWe reviewed the reports of hemimedullary syndrome in the literature and compared the characteristics of patients with dissection of the VA with those with VA atherosclerotic disease.nnnRESULTSnIn our patient, magnetic resonance angiography showed dissection of the right VA to be the cause of the stroke. In a review of the literature (including our case), hemiplegia was ipsilateral to the infarction in four of the five patients with VA dissection, but contralateral in all six patients with atherosclerotic disease of the VA (p=0.01). In all five cases of VA dissection, the right hemimedulla was involved, while, in the six cases of atherosclerotic disease, the left side of the medulla oblongata was affected in five instances and the right side in one (p=0.01).nnnCONCLUSIONnDissection of the VA may provoke a hemimedullary lesion at a lower level than atherosclerosis, thus affecting medullary-penetrating branches that irrigate the medulla immediately below the pyramidal decussation. Hemimedullary syndrome accompanied by ipsilateral motor deficit should raise suspicion of dissection of the VA.

Prevalence of Cognitive Impairment Without Dementia and Dementia in Tremembé, Brazil.

Background:The prevalence of cognitive impairment is insufficiently determined in developing countries. The aim of this study was to ascertain the prevalence of cognitive impairment without dementia and dementia in community-dwelling elderly in Brazil. Methods:This was a single-phase cross-sectional survey of the elderly (aged 60 years and above) living in the municipality of Tremembé, Brazil. Twenty percent of the households with elderly persons were randomly selected from urban and rural areas, to obtain a homogenous representation of all socioeconomic and cultural levels. Results:We assessed 630 individuals [mean age, 71.3 y (±7.99); mean years of education, 4.9 (±4.54)] and found prevalence rates of 17.5% (95% confidence interval, 14.6-20.6) for dementia and 19.5% (95% confidence interval, 16.6-22.8) for cognitive impairment without dementia. These prevalence rates were influenced by age (P<0.001) and by educational level (P<0.001). There was no significant sex difference among diagnostic groups (P=0.166). The prevalence of dementia was higher in relatively younger individuals (below 70 y) when compared with other studies. Besides, dementia was associated with low socioeconomic status, stroke, previous psychiatric disorder, alcoholism, and epilepsy. Conclusions:The prevalence of dementia in this study was higher than in other studies, particularly among younger elderly.

Motor neuron disease and acquired axonal neuropathy association in HIV infection: case report and update.

BACKGROUNDnA possible viral etiology has been documented in the genesis of motor neuron disorders and acquired peripheral neuropathies, mainly due to the vulnerability of peripheral nerves and the anterior horn to certain viruses. In recent years, several reports show association of HIV infection with Amyotrophic Lateral Sclerosis - Syndrome, Motor Neuron Diseases and peripheral neuropathies.nnnOBJECTIVEnTo report a case of an association between Motor Neuron Disease and Acquired Axonal neuropathy in HIV infection, and describe the findings of neurological examination, cerebrospinal fluid, neuroimaging and electrophysiology.nnnMETHODSnThe patient underwent neurological examination. General medical examinations were performed, including, specific neuromuscular tests, analysis of cerebrospinal fluid, muscle biopsy and imaging studies.nnnRESULTS AND DISCUSSIONnThe initial clinical presentation of our case was marked by cramps and fasciculations with posterior distal paresis and atrophy in the left arm. We found electromyography tracings with deficits in the anterior horn of the spinal cord and peripheral nerves. Dysphagia and release of primitive reflexes were also identified. At the same time, the patient was informed to be HIV positive with high viral load. He received antiretroviral therapy, with load control but with no clinical remission.nnnCONCLUSIONnMotor Neuron disorders and peripheral neuropathy may occur in association with HIV infection. However, a causal relationship remains uncertain. It is noteworthy that the antiretroviral regimen may be implicated in some cases.

ANHIDROSIS AS THE FIRST SIGN OF ROSS SYNDROME

Resident in Dermatology, Federal Fluminense University, Antônio Pedro Hospital, Department of Dermatology, Niteroi RJ, Brazil; Resident in Neurology, Federal Fluminense University, Antônio Pedro Hospital, Department of Neurology, Niterói RJ, Brazil; Professor of the Dermatology Department, Federal Fluminense University, Antônio Pedro Hospital, Department of Dermatology, Niteroi RJ, Brazil; Chair of the Neurology Department, Federal Fluminense University, Antônio Pedro Hospital, Department of Neurology, Niteroi RJ, Brazil.

Addenbrooke's cognitive examination-revised: normative and accuracy data for seniors with heterogeneous educational level in Brazil

BACKGROUNDnSeveral cognitive tools have been developed aiming to diagnose dementia. The cognitive battery Addenbrookes Cognitive Examination - Revised (ACE-R) has been used to detect cognitive impairment; however, there are few studies including samples with low education. The aim of the study was to provide ACE-R norms for seniors within a lower education, including illiterates. An additional aim was to examine the accuracy of the ACE-R to detect dementia and cognitive impairment no dementia (CIND).nnnMETHODSnData originated from an epidemiological study conducted in the municipality of Tremembé, Brazil. The Brazilian version of ACE-R was applied as part of the cognitive assessment in all participants. Of the 630 participants, 385 were classified as cognitively normal (CN) and were included in the normative data set, 110 individuals were diagnosed with dementia, and 135 were classified as having CIND.nnnRESULTSnACE-R norms were provided with the sample stratified into age and education bands. ACE-R total scores varied significantly according to age, education, and sex. To distinguish CN from dementia, a cut-off of 64 points was established (sensitivity 91%, specificity 76%) and to differentiate CN from CIND the best cut-off was 69 points (sensitivity 73%, specificity 65%). Cut-off scores varied according to the educational level.nnnCONCLUSIONSnThis study offers normative and accuracy parameters for seniors with lower education and it should expand the use of the ACE-R for this population segment.

Thalamic alexia with agraphia

Alexia with agraphia is defined as an acquired impairment affecting reading and writing ability. It can be associated with aphasia, but can also occur as an isolated entity. This impairment has classically been associated with a left angular gyrus lesion In the present study, we describe a case involving a patient who developed alexia with agraphia and other cognitive deficits after a thalamic hemorrhage. In addition, we discuss potential mechanisms of this cortical dysfunction syndrome caused by subcortical injury. We examined a patient who presented with alexia with agraphia and other cognitive deficits due to a hemorrhage in the left thalamus. Neuropsychological evaluation showed attention, executive function, arithmetic and memory impairments. In addition, language tests revealed severe alexia with agraphia in the absence of aphasia. Imaging studies disclosed an old thalamic hemorrhage involving the anterior, dorsomedial and pulvinar nuclei. Tractography revealed asymmetric thalamocortical radiations in the parietal region (left <right), and single photon emission computed tomography demonstrated hypoperfusion in the left thalamus that extended to the frontal and parietal cortices. Cortical cognitive deficits, including alexia with agraphia, may occur as the result of thalamic lesions. The probable mechanism is a diaschisis phenomenon involving thalamic tract disconnections.