Sidhartha Tan, M.D.

Sidhartha Tan, M.D.

Sidhartha Tan, M.D.

Log into NorthShoreConnect


General Information




NorthShore Medical Group



Academic Rank

Clinical Professor


Chinese, English, Hindi, Mandarin, Mandarin Chinese

Board Certified

Neonatal-Perinatal Medicine, Pediatrics

Clinical Service

Neonatal Medicine

Education, Training & Fellowships

Medical School

All India Institute of Medical Sciences, 1980


Columbus-Cabrini Medical Center, 1983


Columbus-Cabrini Medical Center, 1985
University of Chicago, 1986


University of Miami, Jackson Memorial Medical Center, 1989



NorthShore Medical Group

2650 Ridge Ave.
Walgreen 1505
Evanston, IL 60201
847.570.2033 847.570.0231 fax Get Directions This location is not wheelchair accessible.


Commercial Plans
  • Aetna Choice POS
  • Aetna Elect Choice EPO and EPO
  • Aetna Health Network Options
  • Aetna HMO
  • Aetna Managed Choice
  • Aetna Managed Choice POS
  • Aetna Open Choice PPO
  • Aetna Open Choice PPO (Aetna HealthFund)
  • Aetna QPOS
  • Aetna Savings Plus
  • Aetna Select
  • Beechstreet PPO Network
  • Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Advantage
  • Blue Cross Blue Shield HMOI
  • Cigna HMO
  • Cigna LocalPlus
  • Cigna Open Access Plus (OAP)
  • Cigna Open Access Plus with CareLink (OAPC)
  • Cigna POS
  • Cigna PPO
  • Cofinity PPO (an Aetna Company)
  • Coventry Health Care Elect Choice EPO
  • Coventry Health Care First Health PPO
  • Galaxy Health PPO Network
  • Great West PPO/POS
  • Healthcare's Finest Network (HFN)
  • Humana - All Commercial Plans (including Choice Care)
  • Humana - NorthShore Complete Care
  • Humana/ChoiceCare Network PPO
  • Medicare
  • Multiplan and PHCS PPO Network (Including PHCS Savility)
  • NorthShore Employee Network
  • Preferred Plan PPO
  • Three Rivers Provider PPO Network (TRPN)
  • Tricare
  • Unicare
  • United Healthcare - All Commercial Plans
    Not Contracted United Healthcare Core
    Not Contracted United Healthcare Navigate
Exchange Plans
  • Aetna Whole Health Chicago
  • Not Contracted Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Precision HMO
  • Coventry (PPO)
  • Harken Health - an Affiliate of United Healthcare
    Verify physician participation and out of pocket expenses with Harken
  • Land of Lincoln Health Traditional PPO
  • Not Contracted United Healthcare Compass
  • Illinois Department of Public Aid (IDPA)
  • Illinicare ICP
  • Community Care Partners
Medicare Advantage Plans
  • Aetna Medicare (SM) Plan (HMO)
  • Aetna Medicare (SM) Plan (PPO)
  • Blue Cross Blue Shield Medicare Advantage PPO Plan
  • Cigna-HealthSpring Advantage HMO
  • Cigna-HealthSpring Premier HMO-POS
  • Cigna-HealthSpring Primary HMO
  • Humana Gold Plus HMO
  • Humana Gold Plus PFFS
  • HumanaChoice PPO
  • United Healthcare - All Medicare Plans
Medicare Medicaid Alignment Initiative (MMAI) Plans
  • Blue Cross Blue Shield Community
  • HealthSpring
  • Humana
  • Illinicare Health Plan
  • Meridian Complete


  • Human Umbilical Cord Blood Cells Ameliorate Motor Deficits in Rabbits in a Cerebral Palsy Model.

    Developmental neuroscience 2015

    Authors: Drobyshevsky A, Cotten CM, Shi Z, Luo K, Jiang R, Derrick M, Tracy ET, Gentry T, Goldberg RN, Kurtzberg J, Tan S
    Cerebral palsy (CP) has a significant impact on both patients and society, but therapy is limited. Human umbilical cord blood cells (HUCBC), containing various stem and progenitor cells, have been used to treat various brain genetic conditions. In small animal experiments, HUCBC have improved outcomes after hypoxic-ischemic (HI) injury. Clinical trials using HUCBC are underway, testing feasibility, safety and efficacy for neonatal injury as well as CP. We tested HUCBC therapy in a validated rabbit model of CP after acute changes secondary to HI injury had subsided. Following uterine ischemia at 70% gestation, we infused HUCBC into newborn rabbit kits with either mild or severe neurobehavioral changes. Infusion of high-dose HUCBC (5 × 10(6) cells) dramatically altered the natural history of the injury, alleviating the abnormal phenotype including posture, righting reflex, locomotion, tone, and dystonia. Half the high dose showed lesser but still significant improvement. The swimming test, however, showed that joint function did not restore to naïve control function in either group. Tracing HUCBC with either MRI biomarkers or PCR for human DNA found little penetration of HUCBC in the newborn brain in the immediate newborn period, suggesting that the beneficial effects were not due to cellular integration or direct proliferative effects but rather to paracrine signaling. This is the first study to show that HUCBC improve motor performance in a dose-dependent manner, perhaps by improving compensatory repair processes.
    PMID: 25791742 [PubMed - as supplied by publisher]
  • A Critical Review of Models of Perinatal Infection.

    Developmental neuroscience 2015

    Authors: Dean JM, Shi Z, Fleiss B, Gunn KC, Groenendaal F, van Bel F, Derrick M, Juul SE, Tan S, Gressens P, Mallard C, Bennet L, Gunn AJ
    One of the central, unanswered questions in perinatology is why preterm infants continue to have such poor long-term neurodevelopmental, cognitive and learning outcomes, even though severe brain injury is now rare. There is now strong clinical evidence that one factor underlying disability may be infection, as well as nonspecific inflammation, during fetal and early postnatal life. In this review, we examine the experimental evidence linking both acute and chronic infection/inflammation with perinatal brain injury and consider key experimental determinants, including the microglia response, relative brain and immune maturity and the pattern of exposure to infection. We highlight the importance of the origin and derivation of the bacterial cell wall component lipopolysaccharide. Such experimental paradigms are essential to determine the precise time course of the inflammatory reaction and to design targeted neuroprotective strategies to protect the perinatal brain from infection and inflammation.
    PMID: 25720344 [PubMed - as supplied by publisher]
  • Elevated spinal monoamine neurotransmitters after antenatal hypoxia-ischemia in rabbit cerebral palsy model.

    Journal of neurochemistry 2015 Feb

    Authors: Drobyshevsky A, Takada SH, Luo K, Derrick M, Yu L, Quinlan KA, Vasquez-Vivar J, Nogueira MI, Tan S
    We hypothesized that a deficiency in the descending serotonergic input to spinal cord may underlie postnatal muscle hypertonia after global antenatal hypoxic-ischemic injury in a rabbit model of cerebral palsy. Neurotransmitter content was determined by HPLC in the spinal cord of newborns with and without muscle hypertonia after fetal global hypoxic-ischemic brain injury and naïve controls. Contrary to our hypothesis, serotonin levels in both cervical and lumbar expansions and norepinephrine in cervical expansion were increased in hypertonic kits relative to non-hypertonic kits and controls, with unchanged number of serotonergic cells in caudal raphe by stereological count. Serotonergic fiber length per unit of volume was also increased in hypertonic kits' cervical and lumbar spinal cord, both in dorsal and ventral horns. Gene expression of serotonin transporter was increased and 5-HTR2 receptors were decreased in hypertonic kits relative to controls in cervical and lumbar cord. Intrathecal administration of non-selective serotonin receptor inhibitor methysergide decreased muscle tone in hypertonic kits only. Conversely, intrathecal administration of serotonin solution increased muscle tone only in non-hypertonic kits. We speculate that maturation of serotonergic system in spinal cord may be directly affected by decreased corticospinal connectivity after antenatal hypoxic-ischemic brain injury. Following prenatal hypoxia-ischemia, newborn rabbits exhibit elevated levels of serotonin in the spinal cord that were linked to muscle hypertonia. Serotonergic terminal density was also increased in hypertonic newborns' spinal cord. Intrathecal administration of the non-selective serotonin receptor inhibitor methysergide decreased muscle tone in hypertonic newborns only. Elevated spinal serotonin thus suggests a novel pathophysiological mechanism of hypertonia in cerebral palsy.
    PMID: 25421613 [PubMed - as supplied by publisher]
  • Functional correlates of central white matter maturation in perinatal period in rabbits.

    Experimental neurology 2014 Nov

    Authors: Drobyshevsky A, Jiang R, Derrick M, Luo K, Tan S
    Anisotropy indices derived from diffusion tensor imaging (DTI) are being increasingly used as biomarkers of central WM structural maturation, myelination and even functional development. Our hypothesis was that the rate of functional changes in central WM tracts directly reflects rate of changes in structural development as determined by DTI indices. We examined structural and functional development of four major central WM tracts with different maturational trajectories, including internal capsule (IC), corpus callosum (CC), fimbria hippocampi (FH) and anterior commissure (AC). Rabbits were chosen due to perinatal brain development being similar to humans, and four time points were studied: P1, P11, P18 and adults. Imaging parameters of structural maturation included fractional anisotropy (FA), mean and directional diffusivities derived from DTI, and T2 relaxation time. Axonal composition and degree of myelination were confirmed on electron microscopy. To assess functional maturation, conduction velocity was measured in myelinated and non-myelinated fibers by electrophysiological recordings of compound action potential in perfused brain slices. Diffusion indices and T2 relaxation time in rabbits followed a sigmoid curve during development similar to that for humans, with active changes even at premyelination stage. The shape of the developmental curve was different between the fiber tracts, with later onset but steeper rapid phase of development in IC and FH than in CC. The structural development was not directly related to myelination or to functional development. Functional properties in projection (IC) and limbic tracts (FH) matured earlier than in associative and commissural tracts (CC and AC). The rapid phase of changes in diffusion anisotropy and T2 relaxation time coincided with the development of functional responses and myelination in IC and FH between the second and third weeks of postnatal development in rabbits. In these two tracts, MRI indices could serve as surrogate markers of the early stage of myelination. However, the discordance between developmental change of diffusion indices, myelination and functional properties in CC and AC cautions against equating DTI index changes as biomarkers for myelination in all tracts.
    PMID: 24997240 [PubMed - as supplied by publisher]
  • Magnesium is not consistently neuroprotective for perinatal hypoxia-ischemia in term-equivalent models in preclinical studies: a systematic review.

    Developmental neuroscience 2014

    Authors: Galinsky R, Bennet L, Groenendaal F, Lear CA, Tan S, van Bel F, Juul SE, Robertson NJ, Mallard C, Gunn AJ
    There is an important unmet need to further improve the outcome of neonatal encephalopathy in term infants. Meta-analyses of large controlled trials now suggest that maternal magnesium sulfate (MgSO4) therapy is associated with a reduced risk of cerebral palsy and gross motor dysfunction after premature birth, but that it has no effect on death or disability. Because of this inconsistency, it remains controversial whether MgSO4 is clinically neuroprotective and, thus, it is unclear whether it would be appropriate to test MgSO4 for treatment of encephalopathy in term infants. We therefore systematically reviewed the preclinical evidence for neuroprotection with MgSO4 before or after hypoxic-ischemic encephalopathy (HIE) in term-equivalent perinatal and adult animals. The outcomes were highly inconsistent between studies. Although there were differences in dose and timing of administration, there was evidence that beneficial effects of MgSO4 were associated with confounding mild hypothermia and, strikingly, the studies that included rigorous maintenance of environmental temperature or body temperature consistently suggested a lack of effect. On balance, these preclinical studies suggest that peripherally administered MgSO4 is unlikely to be neuroprotective. Rigorous testing in translational animal models of perinatal HIE is needed before MgSO4 should be considered in clinical trials for encephalopathy in term infants.
    PMID: 24854050 [PubMed - as supplied by publisher]
  • nNOS inhibition during profound asphyxia reduces seizure burden and improves survival of striatal phenotypic neurons in preterm fetal sheep.

    Neuropharmacology 2014 Aug

    Authors: Drury PP, Davidson JO, Mathai S, van den Heuij LG, Ji H, Bennet L, Tan S, Silverman RB, Gunn AJ
    Basal ganglia injury after hypoxia-ischemia remains common in preterm infants, and is closely associated with later cerebral palsy. In the present study we tested the hypothesis that a highly selective neuronal nitric oxide synthase (nNOS) inhibitor, JI-10, would improve survival of striatal phenotypic neurons after profound asphyxia, and that the subsequent seizure burden and recovery of EEG are associated with neural outcome. 24 chronically instrumented preterm fetal sheep were randomized to either JI-10 (3 ml of 0.022 mg/ml, n = 8) or saline (n = 8) infusion 15 min before 25 min complete umbilical cord occlusion, or saline plus sham-occlusion (n = 8). Umbilical cord occlusion was associated with reduced numbers of calbindin-28k-, GAD-, NPY-, PV-, Calretinin- and nNOS-positive striatal neurons (p < 0.05 vs. sham occlusion) but not ChAT-positive neurons. JI-10 was associated with increased numbers of calbindin-28k-, GAD-, nNOS-, NPY-, PV-, Calretinin- and ChAT-positive striatal neurons (p < 0.05 vs. saline + occlusion). Seizure burden was strongly associated with loss of calbindin-positive cells (p < 0.05), greater seizure amplitude was associated with loss of GAD-positive cells (p < 0.05), and with more activated microglia in the white matter tracts (p < 0.05). There was no relationship between EEG power after 7 days recovery and total striatal cell loss, but better survival of NPY-positive neurons was associated with lower EEG power. In summary, these findings suggest that selective nNOS inhibition during asphyxia is associated with protection of phenotypic striatal projection neurons and has potential to help reduce basal ganglia injury in some premature babies.
    PMID: 24726307 [PubMed - as supplied by publisher]
  • Unmyelinated axon loss with postnatal hypertonia after fetal hypoxia.

    Annals of neurology 2014 Apr

    Authors: Drobyshevsky A, Jiang R, Lin L, Derrick M, Luo K, Back SA, Tan S
    White matter (WM) injury due to myelination defects is believed to be responsible for the motor deficits seen in cerebral palsy. We tested the hypothesis that the predominant injury is to functional electrical connectivity in unmyelinated WM fibers by conducting a longitudinal study of central WM tracts in newborn rabbit kits with hypertonia in our model of cerebral palsy.
    Pregnant rabbits at 70% gestation underwent 40-minute uterine ischemia. Motor deficits in newborn kits, including muscle hypertonia, were assessed by neurobehavioral testing. Major central WM tracts, including internal capsule, corpus callosum, anterior commissure, and fimbria hippocampi, were investigated for structural and functional injury using diffusion tensor magnetic resonance imaging (MRI), electrophysiological recordings of fiber conductivity in perfused brain slices, electron microscopy, and immunohistochemistry of oligodendrocyte lineage.
    Motor deficits were observed on postnatal day 1 (P1) when WM tracts were unmyelinated. Myelination occurred later and was obvious by P18. Hypertonia was associated with microstructural WM injury and unmyelinated axon loss at P1, diagnosed by diffusion tensor MRI and electron microscopy. Axonal conductivity from electrophysiological recordings in hypertonic P18 kits decreased only in unmyelinated fibers, despite a loss in both myelinated and unmyelinated axons.
    Motor deficits in cerebral palsy were associated with loss of unmyelinated WM tracts. The contribution of injury to myelinated fibers that was observed at P18 is probably a secondary etiological factor in the motor and sensory deficits in the rabbit model of cerebral palsy.
    PMID: 24633673 [PubMed - as supplied by publisher]
  • Fault and blame, insults to the perinatal brain may be remote from time of birth.

    Clinics in perinatology 2014 Mar

    Authors: Tan S
    There is a certainty in malpractice cases that neurodevelopmental deficits are caused by preventable events at birth when the onset, nature, and timing of the insult in the antenatal and natal period are unknown. The biggest problem is determining timing. Electronic fetal monitoring is given excessive importance in legal cases. Before assigning fault on events at birth, a better understanding of developmental neurobiology and limitations of the present clinical biomarkers is warranted. The issues of single versus repeated episodes, timing of antenatal insults, pros and cons of legal arguments, interaction of various etiologic and anatomic factors are discussed.
    PMID: 24524449 [PubMed - as supplied by publisher]
  • Astrocytes and microglia in acute cerebral injury underlying cerebral palsy associated with preterm birth.

    Pediatric research 2014 Jan

    Authors: Mallard C, Davidson JO, Tan S, Green CR, Bennet L, Robertson NJ, Gunn AJ
    Cerebral palsy is one of the most devastating consequences of brain injury around the time of birth, and nearly a third of cases are now associated with premature birth. Compared with term babies, preterm babies have an increased incidence of complications that may increase the risk of disability, such as intraventricular hemorrhage, periventricular leukomalacia, sepsis, and necrotizing enterocolitis. The response to injury is highly dependent on brain maturity, and although cellular vulnerability is well documented, there is now evidence that premyelinating axons are also particularly sensitive to ischemic injury. In this review, we will explore recent evidence highlighting a central role for glia in mediating increased risk of disability in premature infants, including excessive activation of microglia and opening of astrocytic gap junction hemichannels in spreading injury after brain ischemia, in part likely involving release of adenosine triphosphate (ATP) and overactivation of purinergic receptors, particularly in white matter. We propose the hypothesis that inflammation-induced opening of connexin hemichannels is a key regulating event that initiates a vicious circle of excessive ATP release, which in turn propagates activation of purinergic receptors on microglia and astrocytes. This suggests that developing effective neuroprotective strategies for preterm infants requires a detailed understanding of glial responses.
    PMID: 24336433 [PubMed - as supplied by publisher]
  • Developmental susceptibility of neurons to transient tetrahydrobiopterin insufficiency and antenatal hypoxia-ischemia in fetal rabbits.

    Free radical biology & medicine 2014 Feb

    Authors: Yu L, Vásquez-Vivar J, Jiang R, Luo K, Derrick M, Tan S
    Tetrahydrobiopterin (BH4) is important for normal brain development as congenital BH4 deficiencies manifest movement disorders at various childhood ages. BH4 transitions from very low levels in fetal brains to higher "adult" levels postnatally, with the highest levels in the thalamus. Maternal supplementation with the BH4 precursor sepiapterin reduces postnatal motor deficits and perinatal deaths after 40-min fetal hypoxia-ischemia (HI) at 70% gestation, suggesting that brain BH4 is important in improving function after HI. We tested the hypothesis that the intrinsically low concentrations of BH4 made fetal neurons vulnerable to added insults. Brains were obtained from naïve fetal rabbits or after 40-min HI, at 70% (E22) and 92% gestation (E29). Neuronal cultures were prepared from basal ganglia, cortex, and thalamus, regions with different intrinsic levels of BH4. Cultures were grown with or without added BH4 for 48h. Cell survival and mitochondrial function were determined by flow cytometry. At E22, thalamic cells had the lowest survival rate in a BH4-free milieu, in both control and HI groups, whereas BH4 supplementation ex vivo increased neuronal survival only in HI cells. Neuronal survival was similar in all regions without BH4 at E29. BH4 supplementation increased cell survival and cells with intact mitochondrial membrane potential, from basal ganglia and cortex, but not thalamus. After E29 HI, however, the benefit of BH4 was limited to cortical neurons. We conclude that BH4 is important for fetal neuronal survival after HI especially in the premature thalamus. Supplementation of BH4 has a greater benefit at an earlier gestational age.
    PMID: 24316196 [PubMed - as supplied by publisher]