Neurologic disability: a hidden epidemic for India.
ABSTRACT India, the world's second most populous country, is facing the emergence of a hitherto "hidden" epidemic: neurologic disability. The rapid economic, demographic, and social transformation of India in recent decades has already resulted in the double burden of unresolved epidemics of infectious diseases (e.g., malaria, tuberculosis) coupled with rising rates of chronic diseases (e.g., cardiovascular diseases). Neurologic disability is likely to join these public health concerns as a third epidemic, largely due to 3 emerging health trends: 1) an increase in traumatic brain injuries (TBI) from road traffic accidents (RTA); 2) an increase in the incidence of age-related dementia; and 3) an increase in the stroke incidence. Without adequate preparation, the treatment and long-term care for an increasing population of neurologically disabled people will strain India's health care system and economy in the coming years in unprecedented ways.
Full-textDOI: · Available from: Abhijit Das, Jul 15, 2015
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ABSTRACT: "Healthy citizens are the greatest asset any country can have."-Sir Winston Churchill.Neurology 01/2014; 82(4):366-7. DOI:10.1212/WNL.0000000000000053 · 8.30 Impact Factor
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ABSTRACT: The paper presents a point of care testing device for neurovascular coupling (NVC) from simultaneous recording of electroencephalogram (EEG) and near infra red spectroscopy (NIRS) during anodal transcranial direct current stimulation (tDCS). Here, anodal tDCS modulated cortical neural activity leading to hemodynamic response can be used to identify impaired cerebral microvessels functionality. The impairments in the cerebral microvessels functionality may lead to impairments in the cerebrovascular reactivity (CVR) where severely reduced CVR predicts the chances of transient ischemic attack (TIA) and ipsilateral stroke. The neural and hemodynamic responses to anodal tDCS were studied through joint imaging with EEG and NIRS where NIRS provided optical measurement of changes in tissue oxy-( ) and deoxy-( ) haemoglobin concentration and EEG captured alterations in the underlying neuronal current generators. Then, a cross-correlation method for the assessment of neurovascular coupling (NVC) underlying the site of anodal tDCS is presented. The feasibility studies on healthy subjects and stroke survivors showed detectable changes in the EEG and NIRS responses to a 0.526A/m2 of anodal tDCS. The NIRS system was bench tested on 15 healthy subjects that showed a statistically significant (p<0.01) difference in the signal to noise ratio (SNR) between the on and off states of anodal tDCS where the mean SNR of the NIRS device was found to be 42.33±1.33dB in the on state and 40.67±1.23dB in the off state. Moreover, the clinical study conducted on 14 stroke survivors revealed that the lesioned hemisphere with impaired circulation showed significantly (p<0.01) less change in than the non-lesioned side in response to anodal tDCS. The EEG study on healthy subjects showed a statistically significant (p<0.05) decrease around "individual alpha frequency" in the Alpha band (8-13Hz) following anodal tDCS. Moreover, the joint EEG-NIRS imaging on 4 stroke survivors showed an immediate increase in the Theta band (4Hz-8Hz) EEG activity after the start of anodal tDCS at the non-lesioned hemisphere. Furthermore, cross-correlation function revealed a significant (95 percent confidence interval) negative cross-correlation only at the non-lesioned hemisphere during anodal tDCS where the log-transformed mean-power of EEG within 0.5Hz-11.25Hz lagged response in one of the stroke survivors with white matter lesions. Therefore, it was concluded that anodal tDCS can perturb local neural and vascular activity (via NVC) which can be used for assessing regional NVC functionality where confirmatory clinical studies are required.12/2014; DOI:10.1109/JTEHM.2015.2389230
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ABSTRACT: Functional neuroimaging studies in mild traumatic brain injury (mTBI) have been largely limited to patients with persistent post-concussive symptoms, utilizing images obtained months to years after the actual head trauma. We sought to distinguish acute and delayed effects of mild traumatic brain injury on working memory functional brain activation patterns < 72 hours after mild traumatic brain injury (mTBI) and again one-week later. We hypothesized that clinical and fMRI measures of working memory would be abnormal in symptomatic mTBI patients assessed < 72 hours after injury, with most patients showing clinical recovery (i.e., improvement in these measures) within 1 week after the initial assessment. We also hypothesized that increased memory workload at 1 week following injury would expose different cortical activation patterns in mTBI patients with persistent post-concussive symptoms, compared to those with full clinical recovery. We performed a prospective, cohort study of working memory in emergency department patients with isolated head injury and clinical diagnosis of concussion, compared to control subjects (both uninjured volunteers and emergency department patients with extremity injuries and no head trauma). The primary outcome of cognitive recovery was defined as resolution of reported cognitive impairment and quantified by scoring the subject's reported cognitive post-concussive symptoms at 1 week. Secondary outcomes included additional post-concussive symptoms and neurocognitive testing results. We enrolled 46 subjects: 27 with mild TBI and 19 controls. The time of initial neuroimaging was 48 (+22 S.D.) hours after injury (time 1). At follow up (8.7, + 1.2 S.D., days after injury, time 2), 18 of mTBI subjects (64%) reported moderate to complete cognitive recovery, 8 of whom fully recovered between initial and follow-up imaging. fMRI changes from time 1 to time 2 showed an increase in posterior cingulate activation in the mTBI subjects compared to controls. Increases in activation were greater in those mTBI subjects without cognitive recovery. As workload increased in mTBI subjects, activation increased in cortical regions in the right hemisphere. In summary, we found neuroimaging evidence for working memory deficits during the first week following mild traumatic brain injury. Subjects with persistent cognitive symptoms after mTBI had increased requirement for posterior cingulate activation to complete memory tasks at 1 week following a brain injury. These results provide insight into functional activation patterns during initial recovery from mTBI and expose the regional activation networks that may be involved in working memory deficits.PLoS ONE 05/2015; 10(5):e0126110. DOI:10.1371/journal.pone.0126110 · 3.53 Impact Factor