The neurologic complications of bariatric surgery

Berger, Joseph; Singhal, Divya

doi:10.1016/b978-0-7020-4087-0.00039-5

Cited by 12 publications

(9 citation statements)

References 75 publications

(78 reference statements)

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“…In other series, this complication was more frequent [11]. This entity is presumably autoimmune or inflammatory, and the direct relation to BS seems elusive [20]. In our study, there are two patterns of neurological complications after bariatric surgery, generalized polyneuropathy that can be explained by malabsorption and prolonged vomiting that leads to neurologic dysfunction in different levels of the neuraxis.…”

Section: Discussionmentioning

confidence: 45%

“…Obesity is in fact a risk factor for CTS, so mechanical rather than metabolic factors may be at play [11]. Peroneal and ulnar nerve involvement at the predilection sites seems easier to explain after weight loss, as the reduction of protective subcutaneous fat together with increased nerve vulnerability in malnutrition results in easier development of compression [20,23,24]. We observed 2 patients with bilateral peroneal palsy among 22 mononeuropathies, while the literature reports on bilateral peroneal palsy after BS are few [25,26].…”

Section: Discussionmentioning

confidence: 83%

“…Such cases may represent either an early [17] or a late [18] complication of BS, often combined with Wernicke's encephalopathy [19]. As these generalized neuropathies seem mostly due to thiamine deficiency resulting from malabsorption and postoperative vomiting [15,20], postoperative care for patients with refractory vomiting should be very close, with adequate thiamine replacement.…”

Section: Discussionmentioning

confidence: 99%

“…Our data indicate that poor nutritional status and non-compliance with treatment in patients with postbariatric neuropathy are quite frequent. The study is not controlled and does not allow us to indicate particular factors, but this clustering of malnutrition among cases of peripheral complications is well-described and likely multifactorial (malabsorption, vomiting, rapid weight loss, poor compliance) [11,15,20]. While some peripheral complications of BS are mild, others may be disabling and irreversible [20,30].…”

Section: Discussionmentioning

confidence: 99%

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Post-bariatric surgery peripheral neuropathies: Kuwaiti experience

Rashad

Youssry

Mansour

et al. 2019

Egypt J Neurol Psychiatry Neurosurg

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Background: Obesity is a major global health problem. Kuwait has a very high prevalence of obesity, and consequently, the number of bariatric surgeries is rising. Objectives: The aim of this study is to analyze the clinical presentation and electrodiagnostic features of peripheral nerve complications following bariatric surgery. Subjects and methods: We retrospectively involved a convenience sample of patients presenting at a tertiary referral center and analyzed the patterns and frequency of peripheral nerve involvement, correlations with operative techniques, perioperative complications, nutritional status, possible risk factors, and functional impairment. Results: Among the 58 cases, 23 presented with chronic distal symmetrical sensorimotor neuropathy, 10 suffered from small fiber neuropathy, 22 had mononeuropathies, 2 patients had acute axonal sensorimotor neuropathy, and only 1 patient had lumbar plexopathy. In 22 patients, we observed mononeuropathies (10 cases of carpal tunnel syndrome, 7 cases of peroneal compression at the knee, 4 cases of ulnar neuropathies at the elbow, and 1 case of meralgia paresthetica). Rapid weight loss and protracted postoperative vomiting tended to correlate with generalized neuropathies, while focal compression with loss of the protective subcutaneous tissue pad was associated with mononeuropathies. All patients suffered from a deficiency of at least 1 micronutrient. Compliance with supplementary therapy was poor. Some post-bariatric neuropathies interfere severely with patients' functional status. Conclusion: Prevention by close follow-up, nutritional intervention, and patient education to avoid habitual postures related to nerve compression is appropriate.

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Section: Discussionmentioning

confidence: 45%

Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Post-bariatric surgery peripheral neuropathies: Kuwaiti experience

Rashad

Youssry

Mansour

et al. 2019

Egypt J Neurol Psychiatry Neurosurg

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“…The acute neuropsychiatric consequence of thiamine (vitamin B1) deficiency, Wernicke’s encephalopathy (WE), is associated with conditions such as alcoholism, bariatric surgery for morbid obesity (Berger and Singhal, 2014; Merola et al, 2012), cancer, HIV/AIDS, and advanced age (Lee et al, 2000). Animal models support a contribution of classical sterile neuroinflammatory mechanisms (cf., Graeber et al, 2011) in thiamine deficiency related pathology.…”

Section: Introductionmentioning

confidence: 99%

Associations between in vivo neuroimaging and postmortem brain cytokine markers in a rodent model of Wernicke's encephalopathy

Zahr

Alt

Mayer

et al. 2014

Experimental Neurology

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Thiamine (vitamin B1) deficiency, associated with a variety of conditions, including chronic alcoholism and bariatric surgery for morbid obesity, can result in the neurological disorder Wernicke’s encephalopathy (WE). Recent work building upon early observations in animal models of thiamine deficiency has demonstrated an inflammatory component to the neuropathology observed in thiamine deficiency. The present, multilevel study including in vivo magnetic resonance imaging (MRI) and spectroscopy (MRS) and postmortem quantification of chemokine and cytokine proteins sought to determine whether a combination of these in vivo neuroimaging tools could be used to characterize an in vivo MR signature for neuroinflammation. Thiamine deficiency for 12 days was used to model neuroinflammation; glucose loading in thiamine deficiency was used to accelerate neurodegeneration. Among 38 animals with regional brain tissue assayed postmortem for cytokine/chemokine protein levels, three groups of rats (controls+glucose, n=6; pyrithiamine+saline, n=5; pyrithiamine+glucose, n=13) underwent MRI/MRS at baseline (time 1), after 12 days of treatment (time 2), and 3h after challenge (glucose or saline, time 3). In the thalamus of glucose-challenged, thiamine deficient animals, correlations between in vivo measures of pathology (lower levels of N-acetyle aspartate and higher levels of lactate) and postmortem levels of monocyte chemotactic protein-1 (MCP-1, also known as chemokine ligand 2, CCL2) support a role for this chemokine in thiamine deficiency-related neurodegeneration, but do not provide a unique in vivo signature for neuroinflammation.

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Neuroimaging in alcohol use disorder: From mouse to man

Fritz

Klawonn

Zahr

2019

J of Neuroscience Research

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This article provides an overview of recent advances in understanding the effects of alcohol use disorders (AUD) on the brain from the perspective of magnetic resonance imaging (MRI) research in preclinical models and clinical studies. As a noninvasive investigational tool permitting assessment of morphological, metabolic, and hemodynamic changes over time, MRI offers insight into the dynamic course of alcoholism beginning with initial exposure through periods of binge drinking and escalation, sobriety, and relapse and has been useful in differential diagnosis of neurological diseases associated with AUD. Structural MRI has revealed acute and chronic effects of alcohol on both white and gray matter volumes. MR Spectroscopy, able to quantify brain metabolites in vivo, has shed light on biochemical alterations associated with alcoholism. Diffusion tensor imaging permits microstructural characterization of white matter fiber tracts. Functional MRI has allowed for elucidation of hemodynamic responses at rest and during task engagement. Positron emission tomography, a non‐MRI imaging tool, has led to a deeper understanding of alcohol‐induced receptor and neurotransmitter changes during various stages of drinking and abstinence. Together, such in vivo imaging tools have expanded our understanding of the dynamic course of alcoholism including evidence for regional specificity of the effects of AUD, hints at mechanisms underlying the shift from casual to compulsive use of alcohol, and profound recovery with sustained abstinence.

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The neurologic complications of bariatric surgery

Cited by 12 publications

References 75 publications

Post-bariatric surgery peripheral neuropathies: Kuwaiti experience

Post-bariatric surgery peripheral neuropathies: Kuwaiti experience

Associations between in vivo neuroimaging and postmortem brain cytokine markers in a rodent model of Wernicke's encephalopathy

Neuroimaging in alcohol use disorder: From mouse to man

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