Minimal Cognitive Impairment Research Articles

Comparing the Effect of Preoperative Administration of Melatonin and Passiflora incarnata on Postoperative Cognitive Disorders in Adult Patients Undergoing Elective Surgery.

BackgroundAnxiety is a preoperative complication, which most patients encounter. The use of a premedication to reduce preoperative anxiety with minimal cognitive impairment is crucial.ObjectivesThis study was conducted to compare the sedative effect of preoperative melatonin and Passiflora incarnata in patients undergoing elective surgery regarding their potential for postoperative cognitive disorders.MethodsIn this clinical trial, 52 patients American society of anesthesiologists grade (ASA) I and II of both genders were selected to receive either Passiflora incarnata (1000 mg nature made) (n = 26) or melatonin (6 mg) (n = 26) as premedication one hour before surgery. Post-operative pain was evaluated using the visual analogue scale (VAS). Patient’s anxiety and cognitive dysfunction was evaluated with the Ramsey score and the digital symbol substitution test (DSST), respectively. All tests were carried out and evaluated at arrival in the operating room, before induction and before discharge from the post anesthesia care unit (PACU).ResultsThere were no statistically differences between groups in VAS (P > 0.05). However, the mean score of pain was higher in the melatonin group compared to the Pssiflora incarnata group when discharged from the PACU (27.63 vs. 25.37). The anxiety scores were statistically significant in both drugs (P = 0.001), however higher sedation scores was caused by premedication with melatonin (P = 0.003 vs. 0.008). Regarding the DSST, there was a significant difference between the two groups one hour before the surgery (P = 0.04) and at the time of discharge from the PACU (P = 0.007). When evaluating each group, the Passiflora incarnata group revealed a significant difference (P = 0.003).ConclusionsOur findings show that premedication with Passiflora incarnata reduces anxiety as well as Melatonin. However, Melatonin causes less cognitive impairment compared to Passiflora incarnata.

"I Know that You Know that I Know": Neural Substrates Associated with Social Cognition Deficits in DM1 Patients.

Myotonic dystrophy type-1 (DM1) is a genetic multi-systemic disorder involving several organs including the brain. Despite the heterogeneity of this condition, some patients with non-congenital DM1 can present with minimal cognitive impairment on formal testing but with severe difficulties in daily-living activities including social interactions. One explanation for this paradoxical mismatch can be found in patients’ dysfunctional social cognition, which can be assessed in the framework of the Theory of Mind (ToM). We hypothesize here that specific disease driven abnormalities in DM1 brains may result in ToM impairments. We recruited 20 DM1 patients who underwent the “Reading the Mind in the Eyes” and the ToM-story tests. These patients, together with 18 healthy controls, also underwent resting-state functional MRI. A composite Theory of Mind score was computed for all recruited patients and correlated with their brain functional connectivity. This analysis provided the patients’ “Theory of Mind-network”, which was compared, for its topological properties, with that of healthy controls. We found that DM1 patients showed deficits in both tests assessing ToM. These deficits were associated with specific patterns of abnormal connectivity between the left inferior temporal and fronto-cerebellar nodes in DM1 brains. The results confirm the previous suggestions of ToM dysfunctions in patients with DM1 and support the hypothesis that difficulties in social interactions and personal relationships are a direct consequence of brain abnormalities, and not a reaction symptom. This is relevant not only for a better pathophysiological comprehension of DM1, but also for non-pharmacological interventions to improve clinical aspects and impact on patients’ success in life.

Brain metastases management paradigm shift: A case report and review of the literature.

Brain metastases are the most common intracranial tumors in adults, accounting for over half of all lesions. Whole-brain radiation therapy (WBRT) has been a cornerstone in the management of brain metastases for decades. Recently, stereotactic radiosurgery (SRS) has been considered as a definitive or postoperative approach instead of WBRT, to minimize the risk of cognitive impairment that may be associated with WBRT. This is the case report of a 74-year-old female patient who was diagnosed with lung cancer in November, 2002, and histopathologically confirmed brain metastases in January, 2005. The patient received 5 treatments with Gamma Knife SRS for recurring brain metastases between 2005 and 2014. The patient remains highly functional, with stable intracranial disease at 10 years since first developing brain metastases, and with stable lung disease. Therefore, Gamma Knife SRS is a safe and effective treatment modality for patients with recurrent intracranial metastases, with durable local control and minimal cognitive impairment.

Higher Brain Dysfunction in Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis and Stroke-Like Episodes (MELAS)

Stroke-like episodes are one of the cardinal features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS), and occur in 84-99% of the patients. The affected areas detected on neuroimaging do not have classical vascular distribution, and involve predominantly the temporal, parietal and occipital lobes. Thus, the neurological symptoms including higher brain dysfunction correlate with this topographical distribution. In association with the occipital lobe involvement, the most frequent symptom is cortical blindness. Other symptoms have been occasionally reported in case reports: visual agnosia, prosopagnosia, cortical deafness, auditory agnosia, topographical disorientation, various types of aphasia, hemispatial neglect, and so on. On the other hand, cognitive decline associated with more diffuse brain impairment rather than with focal stroke-like lesions has been postulated. This condition is also known as mitochondrial dementia. Domains of cognitive dysfunction include abstract reasoning, verbal memory, visual memory, language (naming and fluency), executive or constructive functions, attention, and visuospatial function. Cognitive functions and intellectual abilities may decline from initially minimal cognitive impairment to dementia. To date, the neuropsychological and neurologic impairment has been reported to be associated with cerebral lactic acidosis as estimated by ventricular spectroscopic lactate levels.

A Synthesis of Peer-Reviewed Literature on Team-Coordinated and Delivered Early Supported Discharge After Stroke.

This review aimed to summarize data from peer-reviewed studies of team-coordinated and delivered early supported discharge (ESD) for postacute, poststroke rehabilitation. A systematic review was performed in Medline, Embase, and CINAHL for appropriate studies. Information on program details and patient cohorts was synthesized. All programs sought patients with mild-to-moderate functional impairment and minimal cognitive impairment (often based on Barthel Index and Mini-Mental State Examination scores, respectively). All also included at least one subjective admission criterion related to rehabilitation suitability or the suitability of the home environment. Based on the identified studies, ESD programs can assume that 15% of patients screened for ESD will be eligible and care should be provided for 4 to 5 weeks postdischarge. Although the benefits of team-coordinated and delivered ESD poststroke have been well-documented, this review may be helpful for clinicians, administrators, and policy makers looking to establish or refine an ESD program for stroke.

Τhe pattern of relations between cognitive control and Theory of Mind in older adults having vascular risk factors and older adults with Mild Cognitive Impairment: are there any differences?

Τhe pattern of relations between cognitive control and Theory of Mind in older adults having vascular risk factors and older adults with Mild Cognitive Impairment: are there any differences?

Five items differentiate mild to severe dementia from normal to minimal cognitive impairment—Using the Global Deterioration Scale

Background/PurposeThe aim of our study is to develop a concise and effective dementia screening tool for use in primary care, wherein we selected five items from the Global Deterioration Scale (GDS) that were most predictive of dementia diagnosis. MethodsOur study population comprised 191 patients older than 60 years who visited four university hospitals between 2008 and 2011 for impaired memory or medical care. Our 5-item screening tool is an abbreviated version of the GDS. We compared the assessment results obtained through our model with those obtained through the GDS in order to evaluate the accuracy of our tool in detecting dementia. ResultsThe screening tool had a sensitivity of 91.2%, specificity of 75.0%, a cutoff value of 12.495, and an area under the curve of 0.911 (95% confidence interval, 0.862–0.948; p < 0.05). ConclusionWe anticipate that our abridged GDS, composed of five items, will facilitate a rapid, yet effective assessment of patients in primary care centers. Its use will benefit both patients and medical professionals by minimizing the length of time required to conduct the assessment, and by allowing early diagnosis and care of patients. However, further research with a larger population is required to verify its efficacy.

Preventing the spread of Alzheimer's disease neuropathology: a role for calcilytics?

The "amyloid cascade hypothesis" posits that an extracellular build-up of amyloid-β oligomers (Aβ-os) and polymers (fibrils) subsequently inducing toxic hyperphosphorylated (p)-Tau oligomers (p-Tau-os) and neurofibrillary tangles starts the sporadic late-onset Alzheimer's disease (LOAD) in the aged lateral entorhinal cortex. Conversely, mutated genes cause a diffuse cerebral Aβs/Aβ-os overproduction promoting early-onset familiar AD (EOFAD). Surplus exogenous Aβ-os exert toxic actions at several levels. They reach the nuclei of human astrocyte-neurons teams (ANTs) to enhance the transcription of Aβ precursor protein (APP) and β-secretase/BACE1 genes. The overexpressed APP and BACE1 proteins act in concert with γ-secretase to overproduce endogenous Aβs/Aβ-os, of which a few enter the nuclei to upkeep Aβs overproduction, while the rest gather in the cytoplasm, damage mitochondria, and are oversecreted. Simultaneously, extracellular Aβ-os bind the ANTs' calcium-sensing receptors (CaSRs) activating signalings that hinder the proteolysis and hence favor the surplus hoarding/secretion of Aβs/Aβ-os. Overreleased Aβ-os spread, reach growing numbers of adjacent ANTs to recruit them to overproduce/oversecrete further Aβ-os amounts via the just mentioned mechanisms. Alongside, Aβ•CaSR signalings elicit a noxious overproduction/overrelease of nitric oxide (NO) and vascular endothelial growth factor (VEGF)-A from ANTs' astrocytes. While astrocytes survive the toxic onslaught, neurons die. Thus, AD progression is driven by ceaselessly self-sustaining neurotoxic cycles, which engender first Aβ-os and later p-Tau-os that cooperatively destroy increasingly wider cognition-related cortical areas. Notably, a highly selective allosteric CaSR antagonist (calcilytic), like NPS 2143, does preserve human cortical postnatal HCN-1A neurons viability notwithstanding the presence of exogenous Aβ-os by suppressing the otherwise elicited oversecretion and spread of newly synthesized Aβ-os. Therefore, if given at minimal cognitive impairment or earlier stages, calcilytics could halt AD progression and preserve the patients' cortical neurons, cognitive abilities, and eventually life.

Summer Issue 2015.

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Yoga and mental health services.

Byline: B. Gangadhar, Kishan. Porandla United Nations and International community recognized our Indian National Wisdom - “Yoga” by declaring “June-21” as “International Day of Yoga.” The word Yoga means “union,” that is, union of one's personal consciousness with the cosmic consciousness. Yoga helps the evolution from “I” to “WE;” that is, from limited individual to global human being.[sup][1] For a psychiatrist, this “union” could also mean, the union of thought and affect as well as mind and body, which could have therapeutic potential. Yoga is a spiritual lifestyle that transcends all religions. Yoga is successfully applied in various psychiatric disorders over the globe with encouraging evidence coming from scientific publications in reputed journals, especially in last three decades. These reports suggest a need to integrate yoga in mental health services. Yoga has been used with success both in severe and less severe mental disorders as an intervention either with other conventional treatments or even solely. Different forms of yoga viz., Sudarashankriya, Sahajyoga, yogasanas, have been investigated with promising results in the treatment of depression.[sup][2],[3] These investigations were prompted by the observation that yoga led to a feeling of well-being and reduced dysphoria in clinically healthy subjects. Studies of varying research results indicate that patients benefited with regards to reduction in depression scores following yoga. In randomized comparisons, yoga fared nearly as well as an antidepressant drug (imipramine).[sup][4] Yogasana-based therapy alone too reduced depression to the level of remissions.[sup][5] In anxiety states too, yoga has proven benefits not only in the nonclinical population but also in clinical populations.[sup][6] Patients with the obsessive compulsive disorder have been treated with Kundalini yoga and the effects have been encouraging.[sup][7] Well-conducted clinical trials have confirmed the benefits of yoga added to ongoing, stabilized antipsychotic therapy in outpatients of schizophrenia. Benefits of Yoga on the negative and cognitive symptoms of the disorder are notable.[sup][8],[9] These two symptoms have been implicated in the functional outcome of schizophrenia patients. These promising findings of yoga in schizophrenia have led to an international guideline to recommend yoga in the treatment of schizophrenia along with medications.[sup][10] The chronic nature of this disease puts demands and on the caregivers, thus subjecting the latter to stress and burden. In a randomized trial, yoga has also shown promise in helping such caregivers of schizophrenia outpatients.[sup][11] Though there is no direct evidence of yoga helping patients of drug/alcohol dependence to remain abstinent, research indicates that depression symptoms during withdrawal in alcohol dependent subjects are reduced better if a yoga practice is added during such acute detoxification program.[sup][12] Isolated reports suggest a role for yoga in other conditions such as attention deficit hyperkinetic disorder and autism.[sup][13],[14] Chronic back pain, a condition for which psychiatric intervention is often sought, has been treated with yoga. A review on this subject supports a role for yoga.[sup][15] Success with yoga in reducing functional pain in somatoform disorders is recently reported.[sup][16] Senior citizens with minimal cognitive impairment (MCI) have experienced improvements in sleep, cognitive function, and quality of life following yoga practice.[sup][17],[18] It is known that MCI is a forerunner of later dementia. Would yoga delay the onset of dementia if applied as a lifestyle package in the elderly? Well-designed longitudinal trials comparing yoga with appropriate control intervention can provide an answer to this question. …

Neurodegeneration with brain iron accumulation: diagnosis and management.

Neurodegeneration with brain iron accumulation (NBIA) encompasses a group of inherited disorders that share the clinical features of an extrapyramidal movement disorder accompanied by varying degrees of intellectual disability and abnormal iron deposition in the basal ganglia. The genetic basis of ten forms of NBIA is now known. The clinical features of NBIA range from rapid global neurodevelopmental regression in infancy to mild parkinsonism with minimal cognitive impairment in adulthood, with wide variation seen between and within the specific NBIA sub-type. This review describes the clinical presentations, imaging findings, pathologic features, and treatment considerations for this heterogeneous group of disorders.

Brain "fog," inflammation and obesity: key aspects of neuropsychiatric disorders improved by luteolin.

Brain “fog” is a constellation of symptoms that include reduced cognition, inability to concentrate and multitask, as well as loss of short and long term memory. Brain “fog” characterizes patients with autism spectrum disorders (ASDs), celiac disease, chronic fatigue syndrome, fibromyalgia, mastocytosis, and postural tachycardia syndrome (POTS), as well as “minimal cognitive impairment,” an early clinical presentation of Alzheimer's disease (AD), and other neuropsychiatric disorders. Brain “fog” may be due to inflammatory molecules, including adipocytokines and histamine released from mast cells (MCs) further stimulating microglia activation, and causing focal brain inflammation. Recent reviews have described the potential use of natural flavonoids for the treatment of neuropsychiatric and neurodegenerative diseases. The flavone luteolin has numerous useful actions that include: anti-oxidant, anti-inflammatory, microglia inhibition, neuroprotection, and memory increase. A liposomal luteolin formulation in olive fruit extract improved attention in children with ASDs and brain “fog” in mastocytosis patients. Methylated luteolin analogs with increased activity and better bioavailability could be developed into effective treatments for neuropsychiatric disorders and brain “fog.”

Dangerous Leaks: Blood-Brain Barrier Woes in the Aging Hippocampus

A leaky blood-brain barrier has long been implicated in cognitive dysfunction in aging and neurodegeneration, but reliable human data were lacking. Here, Montagne et al. (2015) provide the first in vivo evidence of blood-brain barrier disruption in the aging hippocampus and in minimal cognitive impairment.

Thalamic-hippocampal-prefrontal disruption in relapsing-remitting multiple sclerosis.

BackgroundCortical, thalamic and hippocampal gray matter atrophy in relapsing–remitting MS (RRMS) is associated cognitive deficits. However, the role of interconnecting white matter pathways including the fornix, cingulum, and uncinate fasciculus (UF) is less well studied.ObjectiveTo assess MS damage to a hippocampal–thalamic–prefrontal network and the relative contributions of its components to specific cognitive domains.MethodsWe calculated diffusion tensor fractional anisotropy (FA) in the fornix, cingulum and UF as well as thalamic and hippocampal volumes in 27 RRMS patients and 20 healthy controls. A neuropsychological battery was administered and 4 core tests known to be sensitive to MS changes were used to assess cognitive impairment. To determine the relationships between structure and cognition, all tests were grouped into 4 domains: attention/executive function, processing speed, verbal memory, and spatial memory. Univariate correlations with structural measures and depressive symptoms identified potential contributors to cognitive performance and subsequent linear regression determined their relative effects on performance in each domain. For significant predictors, we also explored the effects of laterality and axial versus radial diffusivity.ResultsRRMS patients had worse performance on the Symbol Digit Modalities Test, but no significant impairment in the 4 cognitive domains. RRMS had reduced mean FA of all 3 pathways and reduced thalamic and hippocampal volumes compared to controls. In RRMS we found that thalamic volume and BDI predicted attention/executive function, UF FA predicted processing speed, thalamic volume predicted verbal memory, and UF FA and BDI predicted spatial memory.ConclusionsHippocampal–thalamic–prefrontal disruption affects cognitive performance in early RRMS with mild to minimal cognitive impairment, confirming both white and gray matter involvement in MS and demonstrating utility in assessing functional networks to monitor cognition.

Effects of Emotionally Charged Auditory Stimulation on Gait Performance in the Elderly: A Preliminary Study

ObjectivesTo evaluate the effect of a novel divided attention task—walking under auditory constraints—on gait performance in older adults and to determine whether this effect was moderated by cognitive status. DesignValidation cohort. SettingGeneral community. ParticipantsAmbulatory older adults without dementia (N=104). InterventionsNot applicable. Main Outcome MeasuresIn this pilot study, we evaluated walking under auditory constraints in 104 older adults who completed 3 pairs of walking trials on a gait mat under 1 of 3 randomly assigned conditions: 1 pair without auditory stimulation and 2 pairs with emotionally charged auditory stimulation with happy or sad sounds. ResultsThe mean age of subjects was 80.6±4.9 years, and 63% (n=66) were women. The mean velocity during normal walking was 97.9±20.6cm/s, and the mean cadence was 105.1±9.9 steps/min. The effect of walking under auditory constraints on gait characteristics was analyzed using a 2-factorial analysis of variance with a 1-between factor (cognitively intact and minimal cognitive impairment groups) and a 1-within factor (type of auditory stimuli). In both happy and sad auditory stimulation trials, cognitively intact older adults (n=96) showed an average increase of 2.68cm/s in gait velocity (F1.86,191.71=3.99; P=.02) and an average increase of 2.41 steps/min in cadence (F1.75,180.42=10.12; P<.001) as compared with trials without auditory stimulation. In contrast, older adults with minimal cognitive impairment (Blessed test score, 5–10; n=8) showed an average reduction of 5.45cm/s in gait velocity (F1.87,190.83=5.62; P=.005) and an average reduction of 3.88 steps/min in cadence (F1.79,183.10=8.21; P=.001) under both auditory stimulation conditions. Neither baseline fall history nor performance of activities of daily living accounted for these differences. ConclusionsOur results provide preliminary evidence of the differentiating effect of emotionally charged auditory stimuli on gait performance in older individuals with minimal cognitive impairment compared with those without minimal cognitive impairment. A divided attention task using emotionally charged auditory stimuli might be able to elicit compensatory improvement in gait performance in cognitively intact older individuals, but lead to decompensation in those with minimal cognitive impairment. Further investigation is needed to compare gait performance under this task to gait on other dual-task paradigms and to separately examine the effect of physiological aging versus cognitive impairment on gait during walking under auditory constraints.

Post-stroke fatigue: a deficit in corticomotor excitability?

The pathophysiology of post-stroke fatigue is poorly understood although it is thought to be a consequence of central nervous system pathophysiology. In this study we investigate the relationship between corticomotor excitability and self-reported non-exercise related fatigue in chronic stroke population. Seventy first-time non-depressed stroke survivors (60.36 ± 12.4 years, 20 females, 56.81 ± 63 months post-stroke) with minimal motor and cognitive impairment were included in the cross-sectional observational study. Fatigue was measured using two validated questionnaires: Fatigue Severity Scale 7 and Neurological Fatigue Index - Stroke. Perception of effort was measured using a 0-10 numerical rating scale in an isometric biceps hold-task and was used as a secondary measure of fatigue. Neurophysiological measures of corticomotor excitability were performed using transcranial magnetic stimulation. Corticospinal excitability was quantified using resting and active motor thresholds and stimulus-response curves of the first dorsal interosseous muscle. Intracortical M1 excitability was measured using paired pulse paradigms: short and long interval intracortical inhibition in the same hand muscle as above. Excitability of cortical and subcortical inputs that drive M1 output was measured in the biceps muscle using a modified twitch interpolation technique to provide an index of central activation failure. Stepwise regression was performed to determine the explanatory variables that significantly accounted for variance in the fatigue and perception scores. Resting motor threshold (R = 0.384; 95% confidence interval = 0.071; P = 0.036) accounted for 14.7% (R(2)) of the variation in Fatigue Severity Scale 7. Central activation failure (R = 0.416; 95% confidence interval = -1.618; P = 0.003) accounted for 17.3% (R(2)) of the variation in perceived effort score. Thus chronic stroke survivors with high fatigue exhibit high motor thresholds and those who perceive high effort have low excitability of inputs that drive motor cortex output. We suggest that low excitability of both corticospinal output and its facilitatory synaptic inputs from cortical and sub-cortical sites contribute to high levels of fatigue after stroke.

CLINICAL FEATURES AND IMAGING ANALYSIS OF 38 CASES OF BEHAVIORAL VARIANT FRONTOTEMPORAL DEMENTIA

monitoring of Alzheimer’s disease (AD) patients in clinical trials. It is easy to use, inexpensive and quantifies the cognitive impairment of subjects. The objective was to adapt and validate ADAS-Cog in Colombian populations. Methods: The ADAS-Cog was translate from English and adjusted for trans-linguistic and cross-cultural equivalences. For validation people with AD (Sporadic and AD E280A mutation), minimal cognitive impairment (MCI) and normal controls were tested. Content validity was established through a factor analysis by the principal components methods. Construct validity was determined by comparisons between the 3 groups with non-parametric statistics. Concurrent criterion validity was established comparing with MoCA and GDS, using Spearman correlations. Internal consistency was evaluated with the Cronbach’s alpha. R eproducibility was tested with intraclass correlation coefficient (ICC), and the accuracy was established with ROC curves. Results: We performed a translation from the original version, then it was discussed and by consensus the Colombian Spanish version was reached. We carried a back-translation to assure that our version did not lose its psychometric properties. Then, we did a pilot study for adjustment. Then we performed the necessary changes and obtained the final version of the test. Between 2010 and 2013 we evaluated 378 subjects, 132 normal controls, 127 with MCI (16 E280A) and 119 with AD (41 E280A). Factor analysis showed that 3 main factors explained 70.3% of the variance; Sphericity was 0.001 and KMO index was 0.936. Construct validity showed that all variables and the total score were significant for different in all groups. Concurrent validity revealed a good correlation with MoCA (-0.811) and GDS (0.892). The alpha for internal consistency was 0.916, a result that implies a slight over correlation. Reproducibility was performed an average of 12.2 6 7.7 months later, and showed an ICC of 0.91 (CI95%:0.76-0.97). Accuracy presented an AUC of 0.947(CI95% 0.923-0.971). Conclusions: We adapted and validated the ADAS-Cog for its use in our region, it will facilitate international comparisons and participation in multicenter clinical trials. It has the psychometric properties of the original test, and quantifies AD regardless of its genetic background, or presentation.

Melatonin Therapy in Patients with Alzheimer's Disease.

Alzheimer’s disease (AD) is a major health problem and a growing recognition exists that efforts to prevent it must be undertaken by both governmental and non-governmental organizations. In this context, the pineal product, melatonin, has a promising significance because of its chronobiotic/cytoprotective properties potentially useful for a number of aspects of AD. One of the features of advancing age is the gradual decrease in circulating melatonin levels. A limited number of therapeutic trials have indicated that melatonin has a therapeutic value as a neuroprotective drug in the treatment of AD and minimal cognitive impairment (which may evolve to AD). Both in vitro and in vivo, melatonin prevented the neurodegeneration seen in experimental models of AD. For these effects to occur, doses of melatonin about two orders of magnitude higher than those required to affect sleep and circadian rhythmicity are needed. More recently, attention has been focused on the development of potent melatonin analogs with prolonged effects, which were employed in clinical trials in sleep-disturbed or depressed patients in doses considerably higher than those employed for melatonin. In view that the relative potencies of the analogs are higher than that of the natural compound, clinical trials employing melatonin in the range of 50–100 mg/day are urgently needed to assess its therapeutic validity in neurodegenerative disorders such as AD.

Textaphrenia: An emerging silent pandemic

We read the article by Ramlall et al (2013) with great interest which presents one of the few studies conducted on African population for prevalence of Dementia and Minimal Cognitive Deficits. The study brings to the fore some important data regarding the prevalence of Minimal cognitive impairment (MCI) and dementia in the African population as well as their socio-demographic profiles. Additionally the authors have also detailed the associated medical problems with these disorders in the backdrop of the available literature. However, we would humbly like to point out an important lacuna in the diagnostic evaluations used in the study which is common to earlier prevalence studies of dementia and MCI.

Hyperhomocysteinemia and neurologic disorders: a review.

Homocysteine (Hcy) is a sulfur-containing amino acid that is generated during methionine metabolism. It has a physiologic role in DNA metabolism via methylation, a process governed by the presentation of folate, and vitamins B6 and B12. Physiologic Hcy levels are determined primarily by dietary intake and vitamin status. Elevated plasma levels of Hcy (eHcy) can be caused by deficiency of either vitamin B12 or folate, or a combination thereof. Certain genetic factors also cause eHcy, such as C667T substitution of the gene encoding methylenetetrahydrofolate reductase. eHcy has been observed in several medical conditions, such as cardiovascular disorders, atherosclerosis, myocardial infarction, stroke, minimal cognitive impairment, dementia, Parkinson's disease, multiple sclerosis, epilepsy, and eclampsia. There is evidence from laboratory and clinical studies that Hcy, and especially eHcy, exerts direct toxic effects on both the vascular and nervous systems. This article provides a review of the current literature on the possible roles of eHcy relevant to various neurologic disorders.