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Articles by M. K Singh
Total Records ( 2 ) for M. K Singh
  I. H Gotlib , J. P Hamilton , R. E Cooney , M. K Singh , M. L Henry and J. Joormann

Context  Deficits in reward processing and their neural correlates have been associated with major depression. However, it is unclear if these deficits precede the onset of depression or are a consequence of this disorder.

Objective  To determine whether anomalous neural processing of reward characterizes children at familial risk for depression in the absence of a personal history of diagnosable disorder.

Design  Comparison of neural activity among children at low and high risk for depression as they process reward and loss.

Setting  University functional magnetic resonance imaging facility.

Participants  Thirteen 10- to 14-year-old never-disordered daughters of mothers with recurrent depression ("high risk") and 13 age-matched never-disordered daughters with no family history of depression ("low risk").

Main Outcome Measure  Neural activity, as measured using functional magnetic resonance imaging, in key reward and attention neural circuitry during anticipation and receipt of reward and loss.

Results  While anticipating gains, high-risk participants showed less activation than did their low-risk counterparts in the putamen and left insula but showed greater activation in the right insula. When receiving punishment, high-risk participants showed greater activation in the dorsal anterior cingulate gyrus than did low-risk participants, who showed greater activation in the caudate and putamen.

Conclusions  Familial risk for depression affects neural mechanisms underlying the processing of reward and loss; young girls at risk for depression exhibit anomalies in the processing of reward and loss before the onset of depressive symptoms. Longitudinal studies are needed to examine whether these characteristics predict the subsequent onset of depression.

  H. K Anuradha , R. K Garg , A Agarwal , M. K Sinha , R Verma , M. K Singh and R. Shukla

Background: Stroke is a devastating complication of tuberculous meningitis and is an important determinant of its outcome.

Aim: To prospectively evaluate the predictive factors for stroke in patients with tuberculous meningitis and to assess the impact of stroke on the overall prognosis and outcome.

Methods: We evaluated and followed 100 patients of tuberculous meningitis for 6 months. Magnetic resonance imaging was performed at inclusion and after 6 months. We evaluated the predictors of stroke and also assessed the effect of stroke on the outcome. Outcome was defined with the help of modified Rankin scale.

Results: Of the 100 patients, 6 lost to follow-up. Thirty patients had stroke, 27 of them had stroke at inclusion. Three patients developed stroke during follow-up. In most of the patients, stroke was a manifestation of advanced stages of tuberculous meningitis. Internal capsule/basal ganglia were the most frequently involved sites. Infarcts commonly involved the middle cerebral arterial territory. On univariate analysis, predictors of stroke were aged >25 years (P < 0.001), cranial nerve involvement (P < 0.001), sylvian fissure exudates (P = 0.026), posterior fossa exudates (P = 0.016), optic chiasmal exudates (P = 0.04) and vision impairment (P = 0.004). Stage III tuberculous meningitis (P < 0.001) was also a predictor of stroke. On multivariate analysis aged >25 years was found a significant predictor of stroke. Strokes in patients with tuberculous meningitis were associated with poor prognosis.

Conclusions: Stroke occurred in 30% of cases with tuberculous meningitis. Advanced stage of tuberculous meningitis, basal exudates, optochiasmatic arachnoiditis and vision impairment were significant predictors of stroke. Stroke independently predicted the poor outcome of tuberculous meningitis.

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