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Obesity

see Obesity in spinal surgery.

Concern exists for increased complications due to surgical challenges posed by obese patients and their often-prevalent comorbidities.

In a study involving a nationwide administrative database, milder obesity was not significantly associated with increased mortality rates, neurological complications, or poor outcomes after SAH. Morbid obesity, however, was associated with increased odds of venous thromboembolic, renal, and infectious complications, as well as of a nonroutine hospital discharge. Notably, milder obesity was associated with decreased odds of some medical complications, primarily in patients treated with coiling 1).

Obesity is a major risk factor globally and it is associated with an increased risk of severe vision loss due to idiopathic intracranial hypertension (IIH). There has been an increase in obesity prevalence in the Middle East countries mainly affecting the Gulf Council Countries (GCC), which parallels increased industrial development. This rise may be contributing to the increasing incidence of IIH in these countries. Other risk factors may also be contributing to IIH in Middle East countries and the differences and similarities to Western IIH merit further study 2).

Types

see Hypothalamic obesity

Severe obesity: body mass index (BMI ≥ 35)

Deep brain stimulation for obesity

Sixteen Sprague-Dawley rats were maintained on a high-fat diet. Daily food intake and weight gain were measured for 7 days, at which time the animals underwent stereotactic placement of 0.25-mm-diameter bipolar stimulating electrodes bilaterally in the LH. On postoperative Day 7, eight animals began to receive continuous stimulation of the LH. The remaining eight animals were left unstimulated as the control group. Individual animal weight, food intake, and water intake were monitored daily and continuously throughout the experiment until postoperative Day 24.

There was a decreased rate of weight gain after surgery in all animals, but the unstimulated group recovered and resumed a linear weight gain curve. The stimulated group, however, failed to show weight gain and remained below the mean baseline for body mass. There was a significant weight loss between the stimulated and unstimulated groups. On postoperative Day 24, compared with the day of surgery (Day 0), the unstimulated group had a mean weight gain of 13.8%, whereas the stimulated group had a 2.3% weight loss on average (p = 0.001), yielding a 16.1% weight difference between the two groups 3).


The lateral hypothalamus and ventromedial hypothalamus are the appetite and satiety centers in the brain, respectively. Substantial data support targeting these regions with DBS for the purpose of appetite suppression and weight loss. However, reward sensation associated with highly caloric food has been implicated in overconsumption as well as obesity, and may in part explain the failure rates of conservative management and bariatric surgery. Thus, regions of the brain's reward circuitry, such as the nucleus accumbens, are promising alternatives for DBS in obesity control 4).


Several studies have shown involvement of the nucleus accumbens in these and other addictive behaviors. In a case report, a patient who quit smoking and lost weight without any effort.

A 47-year-old woman presented with chronic treatment-refractory obsessive-compulsive disorder, nicotine dependence, and obesity.

The patient was treated with deep brain stimulation of the nucleus accumbens for obsessive-compulsive disorder. Unintended, effortless, and simultaneous smoking cessation and weight loss were observed.

This study supports the idea of compulsivity with common circuitry in the processing of diverse rewards and suggests that deep brain stimulation of the nucleus accumbens could be a possible treatment of patients with a dependency not responding to currently available treatments 5).


Deep brain stimulation must achieve a success rate of 83% to be equivalent to bariatric surgery. This high-threshold success rate is probably due to the reported success rate of LRYGB, despite its higher complication rate (33.4%) compared with DBS (19.4%). The results support further research into the role of DBS for the treatment of obesity 6).


Appetite modulation in conjunction with enhancing metabolic rate with hypothalamic lesions has been widely documented in animal and even in humans. It appears these effects can be reproduced by DBS, and the titratability and reversibility of this procedure, in addition to well established safety profile, make DBS an appealing option for obesity treatment. Targeting the hypothalamus with DBS has already been shown to be feasible and potentially effective in managing patients with intractable chronic cluster headache [26]. The surgical risk however must be cautiously taken into account when targeting the hypothalamus, where some mortality cases have been reported when targeting the posterior part [34]. The development of new surgical approach will probably reduce this surgical risk. Moreover, the role of functional neurosurgery in obesity is not a new idea. In fact, LH was targeted in obese humans with electrocoagulation more than 30 years ago, resulting in significant yet transient appetite suppression and slight weight reduction [36]. All those elements have made possible the recent regain of interest in DBS for morbid obesity and open an exciting new area of research in neurosurgery and endocrinology 7).


Ho et al. present a review of the evidence of the neuroanatomical basis for obesity, the potential neural targets for deep brain stimulation (DBS), as well as a rationale for DBS and future trial design. Identification of an appropriate patient population that would most likely benefit from this type of therapy is essential. There are also significant cost and ethical considerations for such a neuromodulatory intervention designed to alter maladaptive behavior. Finally, the authors present a consolidated set of inclusion criteria and study end points that should serve as the basis for any trial of DBS for obesity 8).

Dupré et al. review the history of deep brain stimulation (DBS) in patients for treating obesity, describe current DBS targets in the brain, and discuss potential DBS targets and nontraditional stimulation parameters that may improve the effectiveness of DBS for ameliorating obesity. Deep brain stimulation for treating obesity has been performed both in animals and in humans with intriguing preliminary results. The brain is an attractive target for addressing obesity because modulating brain activity may permit influencing both sides of the energy equation-caloric intake and energy expenditure 9).

Tumor

Findings highlight obesity as a risk factor for overall brain/CNS tumors, meningiomas and gliomas among females, as well as for meningiomas among males 10).

For Niedermaier et al adiposity is related to enhanced risk for meningioma but is unassociated with risk for glioma. Based on a limited body of evidence, physical activity is related to decreased risk of meningioma but shows little association with risk of glioma 11).

1)
Dasenbrock HH, Nguyen MO, Frerichs KU, Guttieres D, Gormley WB, Ali Aziz-Sultan M, Du R. The impact of body habitus on outcomes after aneurysmal subarachnoid hemorrhage: a Nationwide Inpatient Sample analysis. J Neurosurg. 2016 Jul 15:1-11. [Epub ahead of print] PubMed PMID: 27419827.
2)
Almarzouqi SJ, Morgan ML, Lee AG. Idiopathic intracranial hypertension in the Middle East: A growing concern. Saudi J Ophthalmol. 2015 Jan-Mar;29(1):26-31. doi: 10.1016/j.sjopt.2014.09.013. Epub 2014 Sep 28. Review. PubMed PMID: 25859136; PubMed Central PMCID: PMC4314590.
3)
Sani S, Jobe K, Smith A, Kordower JH, Bakay RA. Deep brain stimulation for treatment of obesity in rats. J Neurosurg. 2007 Oct;107(4):809-13. PubMed PMID: 17937228.
4)
Halpern CH, Wolf JA, Bale TL, Stunkard AJ, Danish SF, Grossman M, Jaggi JL, Grady MS, Baltuch GH. Deep brain stimulation in the treatment of obesity. J Neurosurg. 2008 Oct;109(4):625-34. doi: 10.3171/JNS/2008/109/10/0625. Review. PubMed PMID: 18826348.
5)
Mantione M, van de Brink W, Schuurman PR, Denys D. Smoking cessation and weight loss after chronic deep brain stimulation of the nucleus accumbens: therapeutic and research implications: case report. Neurosurgery. 2010 Jan;66(1):E218; discussion E218. doi: 10.1227/01.NEU.0000360570.40339.64. PubMed PMID: 20023526.
6)
Pisapia JM, Halpern CH, Williams NN, Wadden TA, Baltuch GH, Stein SC. Deep brain stimulation compared with bariatric surgery for the treatment of morbid obesity: a decision analysis study. Neurosurg Focus. 2010 Aug;29(2):E15. doi: 10.3171/2010.5.FOCUS10109. Review. PubMed PMID: 20672917.
7)
Torres N, Chabardès S, Benabid AL. Rationale for hypothalamus-deep brain stimulation in food intake disorders and obesity. Adv Tech Stand Neurosurg. 2011;36:17-30. doi: 10.1007/978-3-7091-0179-7_2. Review. PubMed PMID: 21197606.
8)
Ho AL, Sussman ES, Pendharkar AV, Azagury DE, Bohon C, Halpern CH. Deep brain stimulation for obesity: rationale and approach to trial design. Neurosurg Focus. 2015 Jun;38(6):E8. PubMed PMID: 26030708.
9)
Dupré DA, Tomycz N, Oh MY, Whiting D. Deep brain stimulation for obesity: past, present, and future targets. Neurosurg Focus. 2015 Jun;38(6):E7. PubMed PMID: 26030707.
10)
Sergentanis TN, Tsivgoulis G, Perlepe C, Ntanasis-Stathopoulos I, Tzanninis IG, Sergentanis IN, Psaltopoulou T. Obesity and Risk for Brain/CNS Tumors, Gliomas and Meningiomas: A Meta-Analysis. PLoS One. 2015 Sep 2;10(9):e0136974. doi: 10.1371/journal.pone.0136974. eCollection 2015. PubMed PMID: 26332834; PubMed Central PMCID: PMC4558052.
11)
Niedermaier T, Behrens G, Schmid D, Schlecht I, Fischer B, Leitzmann MF. Body mass index, physical activity, and risk of adult meningioma and glioma: A meta-analysis. Neurology. 2015 Sep 16. pii: 10.1212/WNL.0000000000002020. [Epub ahead of print] Review. PubMed PMID: 26377253.
obesity.txt · Last modified: 2017/04/03 08:48 by administrador