Imperial College London

DrDipankarNandi

Faculty of MedicineDepartment of Brain Sciences

Professor of Practice (Neurosurgery)
 
 
 
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Contact

 

+44 (0)20 3311 1182d.nandi

 
 
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Location

 

Lab BlockCharing Cross Campus

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Summary

 

Publications

Publication Type
Year
to

96 results found

Marcus HJ, Darzi A, Nandi D, 2013, Surgical Simulation to Evaluate Surgical Innovation: Preclinical Studies With MARTYN, Bulletin of The Royal College of Surgeons of England, Vol: 95

Journal article

Marcus HJ, Hughes-Hallett A, Cundy TP, Nandi D, Yang GZ, Darzi Aet al., 2013, Robotic Surgery. Not everything that counts can be easily counted., BMJ, Vol: 346

Journal article

Marcus H, Nandi D, Darzi A, Yang G-Zet al., 2013, Surgical Robotics Through a Keyhole: From Today's Translational Barriers to Tomorrow's "Disappearing" Robots, IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING, Vol: 60, Pages: 674-681, ISSN: 0018-9294

Journal article

Marcus H, Vakharia V, Kirkman MA, Murphy M, Nandi Det al., 2013, Practice Makes Perfect? The Role of Simulation-Based Deliberate Practice and Script-Based Mental Rehearsal in the Acquisition and Maintenance of Operative Neurosurgical Skills, NEUROSURGERY, Vol: 72, Pages: A124-A130, ISSN: 0148-396X

Journal article

Yousif N, Pavese N, Naushahi MJ, Nandi D, Bain PGet al., 2012, Reversing the polarity of bipolar stimulation in DBS for essential tremor – a theoretical explanation for a useful clinical intervention., Neurocase: The Neural Basis of Cognition

Journal article

Camp SJ, Roncaroli F, Apostolopoulos V, Weatherall M, Lim S, Nandi Det al., 2012, Intracerebral multifocal Rosai-Dorfman disease, JOURNAL OF CLINICAL NEUROSCIENCE, Vol: 19, Pages: 1308-1310, ISSN: 0967-5868

Journal article

Gupta K, Bhattacharya S, Nandi D, Dhar A, Maity A, Mukhopadhyay A, Chattopadhyay DJ, Ray NR, Sen P, Ghosh UCet al., 2012, Arsenic(III) sorption on nanostructured cerium incorporated manganese oxide (NCMO): a physical insight into the mechanistic pathway., J Colloid Interface Sci, Vol: 377, Pages: 269-276

Arsenic(III) sorption was investigated with nanostructured cerium incorporated manganese oxide (NCMO). The pH between 6.0 and 8.0 was optimized for the arsenic(III) sorption. Kinetics and equilibrium data (pH=7.0±0.2, T=303±1.6 K, and I=0.01 M) of arsenic(III) sorption by NCMO described, respectively, the pseudo-second order and the Freundlich isotherm equations well. The sorption process was somewhat complicated in nature and divided into two different segments, initially very fast sorption followed by slow intraparticle diffusion process. Sorption reaction of arsenic(III) on NCMO was endothermic (ΔH°=+13.46 kJ mol(-1)) and spontaneous (ΔG°=-24.75 to -30.15 kJ mol(-1) at T=283-323 K), which took place with increasing entropy (ΔS°=+0.14 kJ mol(-1)K(-1)) at solid-liquid interface. Energy of arsenic(III) sorption estimated by analyzing the equilibrium data using the D-R isotherm model was 15.4 kJ mol(-1), indicating the ion-exchange type mechanism. Raman, FT-IR, pH effect, desorption, etc. studies indicated that arsenic(III) was oxidized to arsenic(V) during the sorption process.

Journal article

Yousif N, Borisyuk R, Pavese N, Nandi D, Bain Pet al., 2012, Spatiotemporal visualisation of deep brain stimulation induced effects in the subthalamic nucleus, European Journal of Neuroscience

Journal article

Marcus H, Nandi D, 2011, C-reactive protein in neurosurgery: valuable marker of post-operative infection or unnecessary over-investigation?, BRITISH JOURNAL OF NEUROSURGERY, Vol: 25, Pages: 788-788, ISSN: 0268-8697

Journal article

Pereira EAC, Nandi D, Jenkinson N, Stein JF, Green AL, Aziz TZet al., 2011, Pedunculopontine stimulation from primate to patient., J Neural Transm (Vienna), Vol: 118, Pages: 1453-1460

Deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) is a novel neurosurgical therapy developed to address symptoms of gait freezing and postural instability in Parkinson's disease and related disorders. Here we summarise our non-human primate investigations of relevance to our surgical targeting of the PPN and relate the primate research to initial clinical experience of PPN DBS.

Journal article

Bhatia R, Dalton A, Richards M, Hopkins C, Aziz T, Nandi Det al., 2011, The incidence of deep brain stimulator hardware infection: the effect of change in antibiotic prophylaxis regimen and review of the literature., Br J Neurosurg, Vol: 25, Pages: 625-631

The complication of hardware infection related to deep brain stimulator implantation (or revision) varies between 0 and 15.2% in the literature. However, no national guidelines exist at present to define an average or acceptable rate of infection associated with, nor the preferred antibiotic prophylaxis required for, this procedure. The aim of this study was to examine the effect of changing the antibiotic prophylaxis regimen used in a single neurosurgical centre on the incidence and outcome of hardware infection. A prospective cohort of 38 patients undergoing deep brain stimulation (DBS) implantation or internal pulse generator (IPG) replacement and receiving perioperative vancomycin (including intravenous gentamicin on induction) and pouch-installed gentamicin, was compared to a historical cohort of 35 patients receiving perioperative cefuroxime in the same unit. The infection rate over 2 years in the prospective group for DBS surgery was 0 compared to 1 (5.6%) in the historical cohort (p = 0.11, χ(2)); the infection rate for IPG replacements was 1(3.6%) in the prospective cohort, versus 3 (17.6%) in the historical (p = 0.44, χ(2)). In this article, we have also systematically reviewed the literature to date and derived an average infection rate of 4.7% (PI 0.9-22%, Random Effects Meta-analysis, Stata) for 35 studies comprising 3550 patients. There is no significant difference in infection rates between DBS procedures that are primarily internalised (n = 9) compared to those in which there is a period of electrode externalisation (n = 23) (p = 0.9, Meta-regression analysis, Stata).

Journal article

Nandi D, Mishra MK, Basu A, Bishayi Bet al., 2010, Effects of IL-18 and IL-10 pre-treatment on the alteration of endogenous cytokines in liver and spleen of mice with experimental endotoxemia., Indian J Exp Biol, Vol: 48, Pages: 1103-1110, ISSN: 0019-5189

Mechanisms of interleukin-18 (IL-18) and interleukin-10 (IL-10) in lipopolysaccharide (LPS) induced endotoxemia are not clear; their protective role is being investigated so that they may effectively modulate the host cytokine levels during endotoxemia. The aim of the study was to evaluate protective effects of IL-18 and IL-10 in experimentally induced endotoxemia in mice correlating the changes in tissue anti-oxidant enzymes and circulating cytokines. Liver injury was determined by estimation of serum glutamate oxalate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT), serum nitric oxide (NOx), hepatic anti-oxidant enzyme and cytokine content in LPS (250 microg/kg) induced endotoxemic mice receiving either IL-18 (500 ng/mouse) or IL-10 (600 ng/mouse) treatment. Mice (87% of IL-10 treated and 74% of IL-18 treated) survived when administered prior to LPS challenge. Pre-treatment of mice with either IL-10 or IL-18 followed by LPS, lead to reduction in SGPT and SGOT level, serum NOx, and altered hepatic anti-oxidant enzymes activity and myeloperoxidase activity than the only LPS treated group. Marked reduction in the amounts of LPS-induced hepatic and splenic TNF-u content has been observed after IL-10 pre-treatment. Results suggested that attenuating the induction of TNF-alpha and IFN-gamma and subsequent induction of nitric oxide formation in response to LPS may in part account for efficient protection by IL-18 and IL-10 in the reduction of LPS-induced liver injury.

Journal article

Nandi D, Mishra MK, Basu A, Bishayi Bet al., 2010, Protective effects of interleukin-6 in lipopolysaccharide (LPS)-induced experimental endotoxemia are linked to alteration in hepatic anti-oxidant enzymes and endogenous cytokines., Immunobiology, Vol: 215, Pages: 443-451

Endogenous interleukin-6 has been considered as an important anti-inflammatory cytokine controlling both local and systemic acute inflammatory responses; the usefulness of IL-6 in endotoxemia aiming to block the production of reactive oxygen species and the release of inflammatory cytokines is under discussion The aim of the study was to evaluate the protective effects of IL-6 in experimentally induced endotoxemia in mice correlating the changes in tissue anti-oxidant enzymes and circulating cytokines. Liver injury in low-dose bacterial lipopolysaccharide (5 microg/mouse)-induced endotoxemic mice receiving IL-6 (300 ng/mouse) treatment either before or after LPS injection was detected by the estimation of serum oxaloacetate transaminase and serum glutamate pyruvate transaminase. This finding supports that liver injury during experimental endotoxemia could be lowered by IL-6. Current data also demonstrate the critical role of IL-6 in inducing SOD in liver, whereas IL-6 prior and after LPS challenge group showed reduced PMN infiltration in the liver as evident by decreased hepatic MPO content in those mice. IL-6 treatment also showed higher IL-10 production in serum than endotoxic group as IL-10 is a potent and pleiotropic anti-inflammatory cytokine that inhibits the synthesis of pro-inflammatory cytokines and also has a suppressive effect on pro-inflammatory cytokine like TNF-alpha, IFN-gamma and IL-12. It is also directly involved in the modulation of other aspects of inflammation, particularly cytokine responses and inflammatory cell infiltration.

Journal article

Yousif N, Purswani N, Bayford R, Nandi D, Bain P, Liu Xet al., 2010, Evaluating the impact of the deep brain stimulation induced electric field on subthalamic neurons: A computational modelling study, JOURNAL OF NEUROSCIENCE METHODS, Vol: 188, Pages: 105-112, ISSN: 0165-0270

Journal article

Homapour B, Bowen JE, Want EJ, O'Neill K, Apostolopoulos V, Nandi D, Van Dellen JR, Roncaroli Fet al., 2010, Intra-operative, real-time, three-dimensional ultrasound assisted positioning of catheters in the microdialysis of glial tumours, JOURNAL OF CLINICAL NEUROSCIENCE, Vol: 17, Pages: 506-510, ISSN: 0967-5868

Journal article

Naushahi MJ, Nandi D, Chir M, 2009, Re: Diathermy training and usage trends among surgical trainees - will we get our fingers burnt? Assiotis A, Christofi T, Raptis DA et al. Surgeon 2009; 7 (3): 132-36, SURGEON-JOURNAL OF THE ROYAL COLLEGES OF SURGEONS OF EDINBURGH AND IRELAND, Vol: 7, Pages: 381-381, ISSN: 1479-666X

Journal article

Ray NJ, Jenkinson N, Brittain J, Holland P, Joint C, Nandi D, Bain PG, Yousif N, Green A, Stein JS, Aziz TZet al., 2009, The role of the subthalamic nucleus in response inhibition: Evidence from deep brain stimulation for Parkinson's disease, NEUROPSYCHOLOGIA, Vol: 47, Pages: 2828-2834, ISSN: 0028-3932

Journal article

Bain PG, Aziz T, Liu X, Nandi Det al., 2009, Deep brain stimulation, Publisher: Oxford Univ Pr, ISBN: 9780199543717

Book

Jenkinson N, Nandi D, Muthusamy K, Ray NJ, Gregory R, Stein JF, Aziz TZet al., 2009, Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus., Mov Disord, Vol: 24, Pages: 319-328

The pedunculopontine nucleus is composed of cholinergic and non-cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post-mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man.

Journal article

Nandi D, ORiordan S, Bain PG, 2009, Deep brain stimulation for dystonia., European Neurological Review, Vol: 4(2), Pages: 79-82

Journal article

Pereira EAC, Green AL, Nandi D, Aziz TZet al., 2008, Stereotactic neurosurgery in the United Kingdom: the hundred years from Horsley to Hariz., Neurosurgery, Vol: 63, Pages: 594-606

The history of stereotactic neurosurgery in the United Kingdom of Great Britain and Northern Ireland is reviewed. Horsley and Clarke's primate stereotaxy at the turn of the 20th century and events surrounding it are described, including Mussen's development of a human version of the apparatus. Stereotactic surgery after the Second World War is reviewed, with an emphasis on the pioneering work of Gillingham, Hitchcock, Knight, and Watkins and the contributions from Bennett, Gleave, Hughes, Johnson, McKissock, McCaul, and Dutton after the influences of Dott, Cairns, and Jefferson. Forster's introduction of gamma knife radiosurgery is summarized, as is the application of computed tomography by Hounsfield and Ambrose. Contemporary contributions to the present day from Bartlett, Richardson, Miles, Thomas, Gill, Aziz, Hariz, and others are summarized. The current status of British stereotactic neurosurgery is discussed.

Journal article

Yousif N, Bayford R, Nandi D, Bain PG, Liu Xet al., 2008, Computational visualisation of the effect of stimulation contact parameters on the induced electric field in deep brain stimulation, 12th Congress of the European-Federation-of-Neurological-Societies, Publisher: WILEY-BLACKWELL, Pages: 123-124, ISSN: 1351-5101

Conference paper

Liu X, Wang S, Yianni J, Nandi D, Bain PG, Gregory R, Stein JF, Aziz TZet al., 2008, The sensory and motor representation of synchronized oscillations in the globus pallidus in patients with primary dystonia, BRAIN, Vol: 131, Pages: 1562-1573, ISSN: 0006-8950

Journal article

Demetriades AK, Zilidis G, Nandi D, Aziz TZet al., 2008, Fatal cerebral ischaemia by embolization of a gunshot fragment from an extracranial penetrating injury., Br J Neurosurg, Vol: 22

Journal article

Nandi D, Jenkinson N, Stein J, Aziz Tet al., 2008, The pedunculopontine nucleus in Parkinson's disease: primate studies., Br J Neurosurg, Vol: 22 Suppl 1, Pages: S4-S8

Gait freezing and poor balance are two of the most disabling symptoms of advanced Parkinson's disease (PD), and also of other untreatable progressive neurological disorders, such as multi-system atrophy (MSA) and progressive supranuclear palsy (PSP). In PD, these symptoms are currently inadequately managed by drugs and also the present surgical treatment of deep brain stimulation (DBS) of the sub-thalamic nucleus (STN) and the globus pallidus internus (GPi). The pedunculopontine nucleus (PPN) has been implicated in these symptoms. The PPN is in the upper brain stem. The major inhibitory input is from the GPi and substantia nigra reticulata (SNr), and bilateral output is to the substantia nigra compacta (SNc), thalamus and spinal cord. Stimulation of the PPN in the decerebrate rat, cat and dog induced gait-like movements. In autopsy studies in PD, MSA, PSP and the DYT-1 dystonic brain, the PPN is degenerate. Autoradiography of the MPTP-Parkinsonian primate shows excessive inhibition in the PPN. Lesions of the PPN in the normal primate induced PD-type bradykinesia, which was persistent with bilateral lesions. In the MPTP-primate model, microinjections of the gamma aminobutyric acid A (GABA) antagonist bicuculine into the PPN reversed Parkinsonian akinesia implying that stimulation of this region might have a therapeutic role in drug resistant PD. Low frequency (5-10Hz) stimulation of the PPN in the same model reversed akinesia independently of L-dopa; moreover, l-dopa and stimulation effects were additive, implying the involvement of non-dopaminergic pathways.

Journal article

Pereira EAC, Green AL, Nandi D, Aziz TZet al., 2007, Deep brain stimulation: indications and evidence., Expert Rev Med Devices, Vol: 4, Pages: 591-603, ISSN: 1743-4440

Deep brain stimulation is a minimally invasive targeted neurosurgical intervention that enables structures deep in the brain to be stimulated electrically by an implanted pacemaker. It has become the treatment of choice for Parkinson's disease, refractory to, or complicated by, drug therapy. Its efficacy has been demonstrated robustly by randomized, controlled clinical trials, with multiple novel brain targets having been discovered in the last 20 years. Multifarious clinical indications for deep brain stimulation now exist, including dystonia and tremor in movement disorders; depression, obsessive-compulsive disorder and Tourette's syndrome in psychiatry; epilepsy, cluster headache and chronic pain, including pain from stroke, amputation, trigeminal neuralgia and multiple sclerosis. Current research argues for novel indications, including hypertension and orthostatic hypotension. The development, principles, indications and effectiveness of the technique are reviewed here. While deep brain stimulation is a standard and widely accepted treatment for Parkinson's disease after 20 years of experience, in chronic pain it remains restricted to a handful of experienced, specialist centers willing to publish outcomes despite its use for over 50 years. Reasons are reviewed and novel approaches to appraising clinical evidence in functional neurosurgery are suggested.

Journal article

Sivan M, Nandi D, Cudlip S, 2006, Intramedullary spinal metastasis (ISCM) from pituitary carcinoma., J Neurooncol, Vol: 80, Pages: 19-20, ISSN: 0167-594X

Journal article

Yianni J, Wang SY, Liu X, Bain PG, Nandi D, Gregory R, Joint C, Stein JF, Aziz TZet al., 2006, A dominant bursting electromyograph pattern in dystonic conditions predicts an early response to pallidal stimulation, JOURNAL OF CLINICAL NEUROSCIENCE, Vol: 13, Pages: 738-746, ISSN: 0967-5868

Journal article

Yianni J, Wang SY, Liu X, Bain PG, Nandi D, Gregory R, Joint C, Stein JF, Aziz TZet al., 2006, A dominant bursting electromyograph pattern in dystonic conditions predicts an early response to pallidal stimulation., J Clin Neurosci, Vol: 13, Pages: 738-746, ISSN: 0967-5868

Although chronic pallidal deep brain stimulation (DBS) is effective in the treatment of medically intractable dystonia, there is no way of predicting the variations in clinical outcome, partly due to our limited understanding of the pathophysiological mechanisms underlying this condition. We recorded electromyographic (EMG) activity from the most severely affected muscle groups in seven dystonia patients before and after pallidal DBS. Patient EMG recordings could be classified into two groups: one consisting of patients who at rest demonstrated a dominant low frequency component of activity on power spectral analysis (ranging from 2 to 5 Hz), and one group in which this dominant pattern was absent. Early postoperative improvements (within 2-3 days) were observed in the former group, whereas the latter group benefited more gradually (over several months). Analysis of EMG activity may provide a sensitive means of identifying dystonic patients who are likely to be most responsive to functional neurosurgical intervention.

Journal article

Jenkinson N, Nandi D, Oram R, Stein JF, Aziz TZet al., 2006, Pedunculopontine nucleus electric stimulation alleviates akinesia independently of dopaminergic mechanisms., Neuroreport, Vol: 17, Pages: 639-641, ISSN: 0959-4965

The symptom of Parkinson's disease that is most disabling and difficult to treat is akinesia. We have previously shown that low-frequency stimulation of the pedunculopontine nucleus can alleviate such akinesia in a macaque rendered Parkinsonian using 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine. Here, we have extended that study to show that adding stimulation of the pedunculopontine nucleus to levodopa treatment in this Parkinsonian monkey increased its motor activity significantly more than levodopa alone. This additivity suggests that pedunculopontine nucleus stimulation may improve movement by acting at a site downstream from where levodopa therapy affects the basal ganglia.

Journal article

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