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  1. Idris Z, Ghani AR, Mar W, Bhaskar S, Wan Hassan WN, Tharakan J, et al.
    J Clin Neurosci, 2010 Oct;17(10):1343-4.
    PMID: 20620064 DOI: 10.1016/j.jocn.2010.01.054
    A 24-year-old male patient with refractory Tourette syndrome was treated with deep brain stimulation (DBS) and developed subsequent bilateral subcortical haematomas. Additional blood tests revealed abnormalities of plasma factor XIIIA and tryptophan levels, which may be associated with Tourette syndrome. Neurosurgeons who perform DBS surgery on patients with Tourette syndrome must be aware of possible disastrous complications resulting from factor XIIIA disorders of blood haemostasis. Routine screening for this condition is not typically performed prior to surgery in these patients.
    Matched MeSH terms: Deep Brain Stimulation/adverse effects*
  2. Lim LW, Prickaerts J, Huguet G, Kadar E, Hartung H, Sharp T, et al.
    Transl Psychiatry, 2015;5:e535.
    PMID: 25826110 DOI: 10.1038/tp.2015.24
    Deep brain stimulation (DBS) is a promising therapy for patients with refractory depression. However, key questions remain with regard to which brain target(s) should be used for stimulation, and which mechanisms underlie the therapeutic effects. Here, we investigated the effect of DBS, with low- and high-frequency stimulation (LFS, HFS), in different brain regions (ventromedial prefrontal cortex, vmPFC; cingulate cortex, Cg; nucleus accumbens (NAc) core or shell; lateral habenula, LHb; and ventral tegmental area) on a variety of depressive-like behaviors using rat models. In the naive animal study, we found that HFS of the Cg, vmPFC, NAc core and LHb reduced anxiety levels and increased motivation for food. In the chronic unpredictable stress model, there was a robust depressive-like behavioral phenotype. Moreover, vmPFC HFS, in a comparison of all stimulated targets, produced the most profound antidepressant effects with enhanced hedonia, reduced anxiety and decreased forced-swim immobility. In the following set of electrophysiological and histochemical experiments designed to unravel some of the underlying mechanisms, we found that vmPFC HFS evoked a specific modulation of the serotonergic neurons in the dorsal raphe nucleus (DRN), which have long been linked to mood. Finally, using a neuronal mapping approach by means of c-Fos expression, we found that vmPFC HFS modulated a brain circuit linked to the DRN and known to be involved in affect. In conclusion, HFS of the vmPFC produced the most potent antidepressant effects in naive rats and rats subjected to stress by mechanisms also including the DRN.
    Matched MeSH terms: Deep Brain Stimulation/methods*
  3. Khairuddin S, Ngo FY, Lim WL, Aquili L, Khan NA, Fung ML, et al.
    J Clin Med, 2020 Oct 12;9(10).
    PMID: 33053848 DOI: 10.3390/jcm9103260
    Major depression contributes significantly to the global disability burden. Since the first clinical study of deep brain stimulation (DBS), over 406 patients with depression have now undergone this neuromodulation therapy, and 30 animal studies have investigated the efficacy of subgenual cingulate DBS for depression. In this review, we aim to provide a comprehensive overview of the progress of DBS of the subcallosal cingulate in humans and the medial prefrontal cortex, its rodent homolog. For preclinical animal studies, we discuss the various antidepressant-like behaviors induced by medial prefrontal cortex DBS and examine the possible mechanisms including neuroplasticity-dependent/independent cellular and molecular changes. Interestingly, the response rate of subcallosal cingulate Deep brain stimulation marks a milestone in the treatment of depression. DBS among patients with treatment-resistant depression was estimated to be approximately 54% across clinical studies. Although some studies showed its stimulation efficacy was limited, it still holds great promise as a therapy for patients with treatment-resistant depression. Overall, further research is still needed, including more credible clinical research, preclinical mechanistic studies, precise selection of patients, and customized electrical stimulation paradigms.
    Matched MeSH terms: Deep Brain Stimulation
  4. Goh CH, Abdullah JY, Idris Z, Ghani ARI, Abdullah JM, Wong ASH, et al.
    Malays J Med Sci, 2020 May;27(3):53-60.
    PMID: 32684806 DOI: 10.21315/mjms2020.27.3.6
    Background: Deep brain stimulation (DBS) was pioneered by Neuroscience team of Hospital Universiti Sains Malaysia (HUSM) nearly a decade ago to treat advanced medically refractory idiopathic Parkinson's disease (IPD) patients.

    Objectives: Brain volume reduction occurs with age, especially in Parkinson plus syndrome or psychiatric disorders. We searched to define the degree of volume discrepancy in advanced IPD patients and correlate the anatomical volumetric changes to motor symptoms and cognitive function.

    Methods: We determined the magnetic resonance imaging (MRI)-based volumetry of deep brain nuclei and brain structures of DBS-IPD group and matched controls.

    Results: DBS-IPD group had significant deep nuclei atrophy and volume discrepancy, yet none had cognitive or psychobehavioural disturbances. Globus pallidus volume showed positive correlation to higher mental function.

    Conclusion: The morphometric changes and clinical severity discrepancy in IPD may imply a more complex degenerative mechanism involving multiple neural pathways. Such alteration could be early changes before clinical manifestation.

    Matched MeSH terms: Deep Brain Stimulation
  5. Hooi LL, Fitzrol DN, Rajapathy SK, Chin TY, Halim SA, Kandasamy R, et al.
    Malays J Med Sci, 2017 Mar;24(2):87-93.
    PMID: 28894408 MyJurnal DOI: 10.21315/mjms2017.24.2.11
    Deep brain stimulation (DBS) was first introduced in 1987 to the developed world. As a developing country Malaysia begun its movement disorder program by doing ablation therapy using the Radionics system. Hospital Universiti Sains Malaysia a rural based teaching hospital had to take into consideration both health economics and outcomes in the area that it was providing neurosurgical care for when it initiated its Deep Brain Stimulation program. Most of the patients were from the low to medium social economic groups and could not afford payment for a DBS implant. We concentrated our DBS services to Parkinson's disease, Tourette's Syndrome and dystonia patients who had exhausted medical therapy. The case series of these patients and their follow-up are presented in this brief communication.
    Matched MeSH terms: Deep Brain Stimulation
  6. Low HL, Ismail MNBM, Taqvi A, Deeb J, Fuller C, Misbahuddin A
    Clin Neurol Neurosurg, 2019 Oct;185:105466.
    PMID: 31466022 DOI: 10.1016/j.clineuro.2019.105466
    OBJECTIVE: To compare posterior subthalamic area deep brain stimulation (PSA-DBS) performed in the conventional manner against diffusion tensor imaging and tractography (DTIT)-guided lead implantation into the dentatorubrothalamic tract (DRTT).

    PATIENTS AND METHODS: Double-blind, randomised study involving 34 patients with either tremor-dominant Parkinson's disease or essential tremor. Patients were randomised to Group A (DBS leads inserted using conventional landmarks) or Group B (leads guided into the DRTT using DTIT). Tremor (Fahn-Tolosa-Marin) and quality-of-life (PDQ-39) scores were evaluated 0-, 6-, 12-, 36- and 60-months after surgery.

    RESULTS: PSA-DBS resulted in marked tremor reduction in both groups. However, Group B patients had significantly better arm tremor control (especially control of intention tremor), increased mobility and activities of daily living, reduced social stigma and need for social support as well as lower stimulation amplitudes and pulse widths compared to Group A patients. The better outcomes were sustained for up to 60-months from surgery. The active contacts of Group B patients were consistently closer to the centre of the DRTT than in Group A. Speech problems were more common in Group A patients.

    CONCLUSION: DTIT-guided lead placement results in better and more stable tremor control and fewer adverse effects compared to lead placement in the conventional manner. This is because DTIT-guidance allows closer and more consistent placement of leads to the centre of the DRTT than conventional methods.

    Matched MeSH terms: Deep Brain Stimulation/methods*
  7. Fox SH, Katzenschlager R, Lim SY, Barton B, de Bie RMA, Seppi K, et al.
    Mov Disord, 2018 08;33(8):1248-1266.
    PMID: 29570866 DOI: 10.1002/mds.27372
    OBJECTIVE: The objective of this review was to update evidence-based medicine recommendations for treating motor symptoms of Parkinson's disease (PD).

    BACKGROUND: The Movement Disorder Society Evidence-Based Medicine Committee recommendations for treatments of PD were first published in 2002 and updated in 2011, and we continued the review to December 31, 2016.

    METHODS: Level I studies of interventions for motor symptoms were reviewed. Criteria for inclusion and quality scoring were as previously reported. Five clinical indications were considered, and conclusions regarding the implications for clinical practice are reported.

    RESULTS: A total of 143 new studies qualified. There are no clinically useful interventions to prevent/delay disease progression. For monotherapy of early PD, nonergot dopamine agonists, oral levodopa preparations, selegiline, and rasagiline are clinically useful. For adjunct therapy in early/stable PD, nonergot dopamine agonists, rasagiline, and zonisamide are clinically useful. For adjunct therapy in optimized PD for general or specific motor symptoms including gait, rivastigmine is possibly useful and physiotherapy is clinically useful; exercise-based movement strategy training and formalized patterned exercises are possibly useful. There are no new studies and no changes in the conclusions for the prevention/delay of motor complications. For treating motor fluctuations, most nonergot dopamine agonists, pergolide, levodopa ER, levodopa intestinal infusion, entacapone, opicapone, rasagiline, zonisamide, safinamide, and bilateral STN and GPi DBS are clinically useful. For dyskinesia, amantadine, clozapine, and bilateral STN DBS and GPi DBS are clinically useful.

    CONCLUSIONS: The options for treating PD symptoms continues to expand. These recommendations allow the treating physician to determine which intervention to recommend to an individual patient. © 2018 International Parkinson and Movement Disorder Society.

    Matched MeSH terms: Deep Brain Stimulation
  8. Hescham S, Jahanshahi A, Meriaux C, Lim LW, Blokland A, Temel Y
    Behav Brain Res, 2015 Oct 1;292:353-60.
    PMID: 26119240 DOI: 10.1016/j.bbr.2015.06.032
    Deep brain stimulation (DBS) has gained interest as a potential therapy for advanced treatment-resistant dementia. However, possible targets for DBS and the optimal stimulation parameters are not yet clear. Here, we compared the effects of DBS of the CA1 sub-region of the hippocampus, mammillothalamic tract, anterior thalamic nucleus, and entorhinal cortex in an experimental rat model of dementia. Rats with scopolamine-induced amnesia were assessed in the object location task with different DBS parameters. Moreover, anxiety-related side effects were evaluated in the elevated zero maze and open field. After sacrifice, we applied c-Fos immunohistochemistry to assess which memory-related regions were affected by DBS. When comparing all structures, DBS of the entorhinal cortex and CA1 sub-region was able to restore memory loss when a specific set of stimulation parameters was used. No anxiety-related side effects were found following DBS. The beneficial behavioral performance of CA1 DBS rats was accompanied with an activation of cells in the anterior cingulate gyrus. Therefore, we conclude that acute CA1 DBS restores memory loss possibly through improved attentional and cognitive processes in the limbic cortex.
    Matched MeSH terms: Deep Brain Stimulation*
  9. Tan SZK, Temel Y, Chan AY, Mok ATC, Perucho JAU, Blokland A, et al.
    Brain Struct Funct, 2020 Sep;225(7):1957-1966.
    PMID: 32594260 DOI: 10.1007/s00429-020-02102-w
    Electrical stimulation of the dorsolateral periaqueductal gray (dlPAG) in rats has been shown to elicit panic-like behaviour and can be a useful as an unconditioned stimulus for modelling anticipatory fear and agoraphobia in a contextual fear conditioning paradigm. In this study, we further analysed our previous data on the effects of escitalopram (a selective serotonin reuptake inhibitor, SSRI) and buspirone (a 5-HT1A receptor partial agonist) on dlPAG-induced anticipatory fear behaviour in a rat model using freezing as a measure. We then attempted to unravel some of the interactions with dopamine signalling using tyrosine hydroxylase (TH) immunohistochemistry to probe the effects on dopaminergic neurons. We showed that acute treatment of escitalopram, but not buspirone, was effective in reducing anticipatory freezing behaviour, while chronic administrations of both drugs were effective. We found that the dlPAG stimulation induced increase number of dopaminergic neurons in the ventral tegmental area (VTA) which was reversed in both chronic buspirone and escitalopram groups. We further found a strong positive correlation between the number of dopaminergic neurons and freezing in the VTA and showed positive correlations between dopaminergic neurons in the VTA and substantia nigra pars compacta (SNpc) in escitalopram and buspirone groups, respectively. Overall, we showed that chronic treatment with an SSRI and a 5-HT1A agonist reduced anticipatory freezing behaviour which seems to be associated, through correlative studies, with a reversal of dlPAG stimulation induced increase in number of dopaminergic neurons in the VTA and/or SNpc.
    Matched MeSH terms: Deep Brain Stimulation
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