OBES SURG (2014) 24:1800–1807 DOI 10.1007/s11695-014-1376-x

REVIEW

Neurological Complications of Bariatric Surgery Anne Landais

Published online: 25 July 2014 # Springer Science+Business Media New York 2014

Abstract Obesity is reaching pandemic proportions, and the number of bariatric surgeries is increasing. Neurological complications of bariatric procedures are more and more frequently reported and physicians need to recognize and be able to manage them. Neurological complications may result from mechanical or inflammatory mechanisms, but mainly from nutritional deficiencies. Vitamin B12, folate, thiamine, vitamin D, and vitamin E are the most frequent deficiencies. Different patterns of complications can be observed that may differ from time to presentation. At an early stage, immediate peripherical nerve injury, Wernicke’s encephalopathy, and polyradiculoneuropathy are the most frequent. Late complications may appear after years and include optic neuropathy, myelopathy, peripherical neuropathy, and myopathy. Bariatric surgery patients should benefit from careful nutritional follow-up with routine monitoring of micronutrients at 6 weeks and 3, 6, and 12 months post-op and then annually after surgery, and multivitamin supplementation for life.

complicated obesity (BMI >35, with obesity-related complications such as hypertension, obstructive sleep apnea, diabetes mellitus, dyslipidemia, and disabling osteoarticular diseases), who have failed conservative treatment. In December 2010, FDA gave approval of laparoscopic adjustable gastric banding for people with a BMI of 35 or higher, or 30 to 35 with related health problems [3]. Sleeve gastrectomy is more and more popular, and may become the procedure of choice in the future as it is less invasive than gastric bypass and produces better weight loss than gastric banding. The number of bariatric procedures has grown during the last two decades and was evaluated at 120,000 in 2008 in the USA [4]. Such procedures have complications, among which neurologic complications are more and more described. We present in this article a thorough review of the neurological complications of bariatric surgery.

Illustrating Cases Keywords Bariatric surgery . Obesity . Neurological complications About one in three Americans is obese. Obesity is reaching pandemic proportions with more than 78 million adult Americans in 2010 with obesity (defined by body mass index (BMI) ≥30), and the impact of this condition is huge as it is associated with morbidity and mortality [1, 2]. Bariatric surgery (BS) is the most efficient long-term treatment concerning weight loss, comorbidities, quality of life improvement, and mortality reduction for morbid obesity (BMI >40) and A. Landais (*) Neurology Department, University Hospital of Pointe-à-Pitre/CHU de Pointe-à-Pitre, Route de Chauvel, Guadeloupe 97139 Abymes, France e-mail: [email protected]

Here are a few cases from our experience illustrating these neurological complications.

Case No. 1 A 52-year-old woman with morbid obesity underwent sleeve gastrectomy 4 months prior to presentation. Her operation was uncomplicated, but 1 month later she began to present deterioration of general condition, vomiting, asthenia, paresthesias of both legs, lower limb weakness, and gait disorders which progressively worsened. She used to fall down once a week. Ten days before presentation, paresthesias began to involve the upper limbs and she noted weakness in the upper limbs. She had lost 25 kg since her surgery. On admission, bilateral lower extremity proximal muscle weakness was noted from

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the thighs distally. Sensation to light touch from knees distally was decreased. Reflexes were absent in the lower limbs, diminished in the upper limbs. Cranial nerves were intact. The electromyogram showed a severe axonal sensorimotor neuropathy predominating in the lower limbs. Complete blood count, metabolic profile, and sedimentation rate were unremarkable. Vitamin levels revealed thiamine deficiency at 38.6 nmol/l (66–200) and vitamin B6 deficiency at12 nmol/l (15–73). Aggressive thiamine replacement therapy was immediately started with 500 mg of intravenous thiamine followed by 100 mg of intramuscular thiamine daily. After a few days, she felt slight improvement in gait disorders. Physical therapy was initiated. She slowly but progressively improved, and 6 months later, she had nearly completely recovered.

Case No. 2 We present a young patient who had a sleeve gastrectomy for morbid obesity. There were no immediate post-op complications. The patient left the clinic 3 days after surgery, and no supplemental vitamin therapy was prescribed. One and a half months later, he presented food intolerance, at first for solids then with liquids, with vomiting and regurgitation, leading to total anorexia 2 months after his surgery. No abnormalities were found neither on abdominal X-ray nor on barium swallow. Two months post-op, the patient was hospitalized with blurred vision, diplopia, and a progressive diminution of his visual acuity, with photophobia. His general health was altered on admission, with frequent vomiting. His visual acuity was markedly diminished (simple binocular light perception), with associated color-vision abnormalities and bilateral papillary edema on optic fundi examination. A CT head scan, both with and without injection was performed on the patient, and the results were found to be normal. An abdominal-thoracic CT scan was also within normal limits. The patient was transferred to the neurology ward a few days after his admission. His weight was 112 kg (a loss of 38 kg, or 25.3 % of his weight in 2 months). The subject was somnolent and confused (temporo-spatial disorientation, false recognitions and perceptions, inappropriate responses), presented anterograde amnesia, motor deficit of all four limbs, predominantly the lower limbs, making it impossible to stand (muscular force of 4/5 for the upper limbs and 3/5 for the lower limbs), an axial hypotonia rendering the sitting position impossible, ataxia of his upper limbs. Osteo-tendon reflexes were present but diminished for upper members and abolished in the lower limbs, with a normal sensitivity. A quasicomplete ophthalmoplegia with a diminished visual acuity was noted. A follow-up eye examination found the persistence of bilateral papillary edema with flame hemorrhages. A neuropsychological work-up found confabulations, temporo-

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spatial disorientation, attention deficit, severe impairment of recovery of information in verbal episodic memory, a faulty maintaining of active strategy research in semantic memory, perseverations, and a discrete trouble of abstract reasoning for verbal material. It was also noted anxiety symptoms with a diminished self-esteem. From a biological point of view, CBC showed a microcytosis without anemia, normal hemostasis findings, a sed rate of 37, and a hepatic work-up initially perturbed. Initial vitamin B1 was low at 55.9 nmol/l (normal 66.5–200), confirming the diagnosis of Gayet-Wernicke; the serum folate level was also low at 1 ng/ml (2.3–17). EMG studies noted a moderate sensitive-motor axonal polyneuropathy of the lower limbs. The MRI study noted T2 FLAIR hyper signals, and on the diffusion sequence, bithalamic, at the base of the fourth ventricle, in periacqueducal around the third ventricle, and in the mammillary tubercule region of the hypothalamic area, where the contrast enhancement was noted (see Fig. 1). The overall imagery exams were in favor of typical Gayet-Wernicke encephalopathy (WE). Gastroscopy revealed a grade 3 esophagitis, with a marked biliary reflux, erythematous gastric mucosa and of the anastomosis, with a tubular aspect of the stomach, without stenosis. The patient was started on IV vitamin B1—1 g/day. Two weeks later, he was transferred to the physical therapy ward. The clinical and radiological results were in favor of WE associated with Korsakoff’s syndrome. The diagnosis was confirmed by the measurement of vitamin B1, which showed the low serum level, and also by the clinical improvement of the neurological problems following vitamin B1 supplementation. The patient also presented axonal polyneuropathy and optic neuropathy. He was seen 5 months after the onset of clinical symptoms and was still involved with physical therapy. Visual acuity was practically normal. It was noted a bilateral horizontal nystagmus in the lateral regard, confusion and disorientation resolved, and improvement in memory problems despite persisting trouble with recent memory. Motor improvement was equally limited; the patient was able to stand and walk a few meters, but needed a wheelchair for longer distances.

Frequency In a review of longitudinal surgical series reporting experience and complications of bariatric surgery, only 1.3 % of 9,996 patients were reported to present neurologic complications [5]. In a large prospective (the only one) series, Abarbanel found 23 (4.6 %) neurologic complications among 500 patients who underwent gastric restrictive surgery for morbid obesity between 3 and 20 months [6]. But the prevalence of

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Fig. 1 Illustration of Wernicke’s encephalopathy case following a sleeve gastrectomy in one of our patients. Brain magnetic resonance imaging (MRI) represents the key tool to suspicion and diagnosis of Wernicke’s encephalopathy. Showing pathognomonic high signal intensity lesions in T2-weighted and fluid-attenuated inversion recovery (FLAIR) weighted

sequences, on either side of the third ventricle, extending forward to the mammillary bodies, and backward to the periacqueducal gray matter. The mammillary bodies lesions show contrast enhancement on T1 weighted axial and coronal sequences

neuropathy was of 16 % in a controlled retrospective study of peripheral neuropathy following bariatric surgery (BS) from the Mayo Clinic [7]. Most of the data relies on case reports or case series and retrospective studies, where micronutrient analyses were neither uniform nor consistent. The patients were rarely presented clinically. Electrophysiology studies and neuropsychological assessments were often lacking. There is a need for prospective studies in this field to assess the real prevalence of these complications with collaboration between neurologists and BS practitioners. More knowledge about the different complications related to nutrient deficiencies is provided by the observation of what can be observed in other fields, for example, after gastrectomy surgery for neoplasy, or in the case of vitamin B12 deficiency in Biermer’s disease.

3. But the most important factors in the pathogenesis of neurologic complications after BS are the nutritional deficiencies generally due to malabsorption or prolonged emesis that lead to neurologic dysfunction at different level of the neuraxis [7].

Mechanisms of Neurological Complications 1. Mechanisms of neural injury may include mechanical compression and entrapment in mononeuropathies. Rapid weight loss may make the nerves more susceptible to compression through loss of subcutaneous tissue, loss of protective fat pads or structural changes. Sometimes, injury from mechanical retractors, patients’ malpositioning, and use of radial or ulnar catheter at the wrist during surgery may participate to immediate complications after BS [7]. 2. Thaisetthawatkul has reported inflammatory infiltrates in nerve biopsies from patients who had bariatric-related neurological complications (polyneuropathy or radiculoplexus neuropathy with acute or subacute onset): a cachexia-like state with nutritional deficiencies may induce inflammatory changes and immune mechanisms of neuropathy [5, 7].

Obesity is, surprisingly, a preexisting risk factor of malnutrition, and 20–30 % obese patients would have micronutriment deficiencies before surgery [8, 9]. After surgery, these deficiencies can get worse because of prolonged vomiting, loss of absorptive surface, altered dietary patterns, bacterial overgrowth, loss of gastric acid, loss of intrinsic factor, and lead to malnutrition [9]. The deficiency risk depends of the importance of weight loss, of preexisting deficiencies, and of the type of surgical procedure used, growing from gastric banding, vertical banded gastroplasty, sleeve gastrectomy, Roux-en-Y gastric bypass, then partial biliopancreatic bypass [10]. In all types of procedures, there is a supply deficiency related to food restriction and possible intolerance for certain kind of food (meet, milk, fibers particularly). This supply deficiency is particularly important when weight loss is major, food intolerances numerous, and vomiting frequent [10]. This explains why nutritional deficiencies can be observed even after “predominantly restrictive” procedures, such as sleeve gastrectomy. In gastric bypass, there is a decrease in gastric acid secretion which is useful in certain micronutriments absorption, as iron and vitamin B12. There is also a duodenojejunal malabsorption (duodenum is the main absorption site of calcium, iron, and vitamin B1) [15]. In a review of eight studies evaluating micronutriments levels after BS in 957 patients, 25 % had vitamin B12 deficiency, 20 % serum vitamin B9 (folate) deficiency, and 1 % thiamine deficiency [5]. Most common nutritional deficiencies post-BS are vitamin B12, vitamin B9, and thiamine. Other

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Table 1 Clinical neurological presentations following bariatric surgery Wernicke’s encephalopathies

Ophtalmoplegia or nystagmus, gait ataxia, and consciousness disturbance or mental status changes (Hypothermia, vestibular dysfunction, ocular abnormalities and urinary incontinence) Korsakoff syndrome Severe memory loss, anterograde amnesia, retrograde amnesia, confabulations Acute polyradiculoneuropathies Pain in the lower limbs, weakness, ascending paralysis, areflexia Optic neuropathies Blurred vision with central scotoma, night blindness Myelopathies Disabling gait ataxia, spasticity in the legs, paresthesias, loss of proprioception and vibratory sensations in legs, limb weakness Peripherical neuropathies Polyneuropathy: symmetric, distal, sometimes painful paresthesias (“burning feet syndrome”), sometimes weakness, gait ataxia, loss of pinprick, vibratory and temperature sensation Mononeuropathy (carpal tunnel syndrome, ulnar neuropathy, radial neuropathy, peroneal neuropathy [foot drop] and lateral femoral cutaneous neuropathy [meralgia paresthesica]) Radiculoplexus neuropathy Small fibers neuropathies (neuropathic pain, hyperalgesia) Restless leg syndrome Myopathies Weakness, diffuse pain

deficiencies associated with neurological impairment include vitamin D, niacin, pyridoxine, vitamin E, and copper [5–11]. The physiopathology of neurologic complications of micronutriments deficiencies and malabsorption has been reviewed in detail by Chaudhry, Kumar, and Kazemi [12–14]. These mechanisms are beyond the goals of this article, and the reader will refer to the abovementioned articles. Table 1 presents the clinical neurological complications following bariatric surgery. Table 2 presents the main vitamin deficiencies after bariatric surgery and their clinical presentation.

Neurologic Complications Can Be Classified by Time to Presentation

given to positioning, padding during procedures to prevent nerve injury. There is also a risk of rhabdomyolysis that can be fatal and myopathies associated with compression injury. Meralgia paresthetica is caused by compression damage to lateral cutaneous nerve as it passes through the inguinal ligament, resulting in pain, paresthesias, or hypersensitivity in the anterior and lateral part of the thigh. This condition usually resolves spontaneously [7]. Vagal nerve injury can sometimes occur during BS, resulting in decreased mobility that may cause nausea and vomiting. Reinnervation may occur spontaneously [24]. Excessive vagal stimulation, resulting in vasovagal response, arrhythmia that may lead to death, has also been reported [25]. Encephalopathy

Early Complications They occur less than 1 year after BS. Immediate Peripherical Nerve and Muscle Injury Stretch injury of the brachial plexus and ulnar mononeuropathy are often reported after BS [9]. Careful attention should be Table 2 Important deficiencies and their clinical presentations

It is an early, acute complication that may develop within a few months, often within a few weeks. Encephalopathy is usually associated with thiamine deficiency [5]. Thiamine is essential for energy production and myelin formation in nerve cells. The B1 deficiency can cause lactic acidosis, reduced oxygen uptake, and depression of transketolase activity [16–18]. It alters mitochondrial function by impairing

Vitamin/nutrient

Neurological complications

Vitamin A Vitamin B1

Night blindness, optic neuropathy, (xerophthalmia) Wernicke’s encephalopathy, Korsakoff’s syndrome, acute polyradiculoneuropathy, neuropathy (dry beriberi), optic neuropathy Peripherical neuropathy, optic neuropathy, myelopathy Peripherical neuropathy, optic neuropathy, restless leg syndrome, (affective disorders?) Myelopathy, peripherical neuropathy, optic neuropathy, (dementia and mental disorders?) Myopathy Myelopathy, peripherical neuropathy Myelopathy, Peripherical neuropathy, optic neuropathy, myopathy Myopathy

Vitamin B6 Vitamin B9 (folate) Vitamin B12 Vitamin D Vitamin E Copper Global protein

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oxidative metabolism and alters vitamin B1 dependant enzymes, resulting in selective neuronal cell death [19]. It can lead to acute and chronic encephalopathies as Wernicke’s encephalopathy and Korsakoff’s syndrome. In Wernicke’s encephalopathy (WE), the classic triad (ophthalmoplegia or nystagmus, ataxia, and consciousness disturbance or mental status changes) is often incomplete. Hypothermia, vestibular dysfunction, ocular abnormalities, and urinary incontinence have also been reported. Ocular findings can vary widely in presentation and include convergent strabismus, bilateral sixth nerve palsy, conjugate gaze palsy, pupillary abnormalities, retinal hemorrhage, ptosis, and scotomata. Gait abnormalities vary from mild gait disturbances to not being able to bear weight. Untreated, Wernicke’s encephalopathy can lead to death, or to a chronic state of mental dysfunction with dramatic permanent impairment of anterograde and retrograde memory with confabulations (invented memories), known as Korsakoff’s syndrome. It can be associated with polyneuropathy (dry beriberi). Vitamin B1 (thiamine) deficiency has been reported as soon as 6 weeks after BS. Persistent vomiting is often noted weeks before. Wernicke’s encephalopathy (WE) is typically preceded by prolonged emesis, but sometimes by increased alcohol intake, or vitamin supplementation noncompliance. Determination of thiamine serum concentration can confirm a clinical suspicion of WE. MRI findings often provide diagnosis confirmation. MRI is the technique of first choice, as WE lesions do not appear on CT scans. MRI shows pathognomonic high signal intensity lesions in T2 weighted, fluid attenuated inversion recovery (FLAIR), and diffusion weighted sequences, in the bilateral dorsomedial thalami, both hypothalami, the mesencephalic tectum, and the periacqueducal gray matter. The thalamic and hypothalamic lesions can show contrast enhancement on T1-weighted MRI. Diffusion restriction can be noted. Hemorrhage involving the fornix and anterior thalami have also been reported [26–29]. But the MRI sensitivity for this diagnosis is only of 53 %, with a specificity of 93 %: the diagnosis of WE remains clinical and mainly supported by the dramatic response of neurological signs to parenteral thiamine. Treatment consists in intravenous thiamine administration: 500 mg IV three times a day during 3 days, followed by 250 mg IV daily until improvement ceases has been proposed. This dose must be followed by an oral dose of 50–100 mg daily [17, 18]. Patients with history of bariatric surgery and repeated postoperative vomiting should be given preventive thiamine supplementation by 250 mg IM once a day [17, 18]. Recovery may occur 3 to 6 months after therapy if diagnosis is made early. Chronic neurologic sequelae are not uncommon. Ophthalmoplegia usually resolves in a few hours and the global confusion typically improves within days. Some degree of cognitive dysfunction may be permanent. Persistent findings typically include nystagmus, gait ataxia, and Korsakoff’s syndrome.

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Acute Polyradiculoneuropathy Rapidly progressive, presenting as Guillain Barré syndrome, it has sometimes been associated with vitamine B1 deficiency [5, 11]. It can appear within a few weeks or months after surgery, beginning with pain in the lower limbs, then appear ascending paralysis, weakness beginning in the feet and hands, and migrating towards the trunk, ataxia, areflexia, and vibratory sensory loss. Weight loss is usually important and precedes symptoms. Protein level in CSF is normal. EMG confirms the diagnostic, showing axonal, sensorimotor polyradiculoneuropathy, more severe in the legs, characterized by axonal degeneration with no demyelinization. Parenteral supplementation with thiamine (100 mg daily) improves symptoms. Intravenous immunoglobulines must be discussed [30]. The occurrence of this polyradiculopathy is rare: Kofmann reports only 2 % among 96 patients with neurological complications [5]. Some more cases can be found in surgical series [31, 32].

Late Complications Optic Neuropathy Associated with copper, carotene and B12 deficiencies, optic neuropathy has been reported between 1.5 and 3 years after surgery [11]. In a literature review of 139 subjects with neurologic complications post-BS, Juhasz-Pocsine found five cases (3.5 %) of optic neuropathy after mean latency of 2.7 years, one with B12 deficiency, and she reported two own patients with optic neuropathy and low serum vitamin B12[11]. Clinical symptoms can be blurred vision with central scotoma, nyctalopia (night blindness). Koffman found eight (8 %) cases with optic neuropathy among 96 patients with neurologic complications of BS [5]. This complication is more frequent following jejuno-ileal bypass, or biliopancreatic bypass than after gastroplasty, enhancing the role of malabsorption. Vitamin B12 (cyanocobalamin) levels have been found to be reduced despite a theoretically adequate intake and supplementation 1 year after BS (gastric bypass) in 30 % of 20 patients [15]. Vitamin B12 deficiency after BS is related to inadequate intake, impaired hydrolysis of Vitamin B12 from dietary protein, defect in either the amount of intrinsic factor available, or the interaction between intrinsic factor and vitamin B12. Vitamin B12 plays a role in myelin synthesis and in methylation of RNA which slows RNA degradation, explaining the involvement of long axons in vitamin B12 deficiency. This deficiency can appear years after BS because of the importance of liver stores, sufficient to cover needs for several years. Vitamin B12 deficiency appears to be frequent after sleeve gastrectomy. Intramuscular vitamin B12 continues

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to be the gold standard of therapy for vitamin B12 deficiency, especially in symptomatic patients. Copper deficiency may also result in optic neuropathy [22, 23]. Several case reports of vitamin A deficiency after BS have been related [33–36]. Slater [37] has shown that vitamin A deficiency is present in 52 to 69 % of patients without supplementation in a delay of 1 and 4 years after malabsorptive surgery. Vitamin A is important in the constitution of the rods, nervous cells of the retina. [This deficiency can also lead to xerophthalmia with corneal and conjunctival xerosis that can lead to blindness if treatment is not introduced, hence the interest in detecting and treating such deficiencies]. Vitamin B1, B2 (riboflavin), B6 (pyridoxine), B3 (niacin), and B9 (folates) deficiencies are possible causes of optic neuropathies that may appear following BS, although no cases of such complications have been reported to our knowledge. Myelopathy (Subacute Combined Degeneration) Juhasz-Pocsine described 12 patients with posterolateral myelopathy, which started insidiously, with mean latency of 9.9 years [11]. Symptoms were disabling gait ataxia, spasticity in legs with pyramidal signs, paresthesias, loss of proprioception and vibratory sensations in legs, and limb weakness sometimes restricted to the legs. Some patients described loss of pin-prick and temperature sensation, eight had urinary urgency or incontinence. Most patients (9/12) had copper or vitamin B12 deficiency or both. Two of seven patients tested had low vitamin E levels. Subacute combined degeneration and myelopathy have been reported after BS mostly with vitamin B12 deficiency that can appear as we already said many years after BS [11]. Copper deficiency may result in myelopathy resembling to the one observed with vitamin B12 deficiency, as late as 24 years after bypass. Vitamin E (tocopherol) is essential for normal neurological functioning; protecting neural cells membranes from oxidative damage. Myelopathies have been described associated with vitamin E deficiency, and may be treatable [20, 21]. Vitamin B6 and folate deficiencies also have been evoked [5]. MRI can show high signal intensity lesions on T2weighted sequences of the spinal cord. Treatment consists in oral or parenteral correction of nutritional deficiencies and increase caloric intake. Despite this treatment, most patients, although somewhat improved, remained disabled because of gait ataxia after mean followup of 3 years. One patient achieved dramatic improvement after surgical revision to shorten the bypassed intestine [11]. Myelopathy is less frequently reported than other neurologic complications because of its long delay after BS (only five cases in three cases reports in 40 years reported by Juhasz-Pocsine [11]).

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Peripherical Neuropathy It is a late, slowly progressive complication that brings symmetric, distal, painful paresthesias (“burning feet syndrome”), sometimes weakness, gait ataxia, loss of pinprick and temperature sensation, and vibratory sensation loss. Vitamin deficiencies most commonly encountered in this case are vitamin B1 (thiamine) vitamin B12, vitamin B6 (pyridoxine), vitamin E (tocopherol), copper, niacin (also called vitamin B3, or vitamin PP), and possibly vitamin D and folate [5, 8, 20, 21]. Polyneuropathies in BS may be related to multiple vitamin and micronutrient deficiencies. EMG reveals sensorimotor axonal distal length dependent polyneuropathy. Sural nerve biopsies show prominent degeneration and perivascular inflammation. Nutritional supplementation can partially improve symptoms; physical therapy is also recommended [5]. In her Arkansas series, Juhasz-Pocsine noted five cases of polyneuropathy (19 %) among 26 patients. Her literature review found 46 cases of polyneuropathy published in 40 years [11]. Another case series of 96 patients with BS neurological complications reported 27 polyneuropathies (29.3 %) [5]. In a Mayo Clinic retrospective study, Thaisetthawatkul found among 435 BS patients 71(16 %) having a peripherical neuropathy: 39 (9 %) having a mononeuropathy, 27 (6 %) with sensory-predominant polyneuropathy, and 5 (1 %) with radiculo plexus neuropathy. Risk factors of polyneuropathies included rate and absolute amount of weight loss, prolonged gastrointestinal symptoms, not attending a nutritional clinic after BS, reduced serum albumin and transferrin after BS, postoperative surgical complications requiring hospitalization, and having jejunoileal bypass [7]. Mononeuropathies may occur after BS. Carpal tunnel syndrome is the most common, followed by ulnar neuropathy at the elbow, radial mononeuropathy, peroneal (with foot drop), and lateral femoral cutaneous (meralgia paresthesica) neuropathies [5, 7]. Lumbosacral plexopathies have also been described [7]. A French team recently reported small-fiber neuropathies, proven by skin biopsies and epidermal nerve fiber densities, with neuropathic pain, hyperalgesia, and allodynia, [30]. Folate (vitamin B9) deficiency after gastric bypass may lead to peripheral neuropathy or to restless legs syndrome (irresistible urge to move one’s legs to stop uncomfortable or odd sensations) [5, 20]. Vitamin B6 (pyridoxine) deficiency has been found in 17.6 and 14.2 % of patients at 1 and 2 years follow-up after bypass surgery [21]. Myopathy It has been reported mainly in patients with global protein, vitamin D, copper deficiencies, or hypokalemia. Other deficiencies (vitamins B1 and E, calcium, phosphate, and

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magnesium) have also been evoked [5, 20, 21, 38]. A literature review reports only three (2 %) cases of myopathy among 139 reviewed subjects with neurological complications of BS [11]. Symptoms may be weakness, diffuse pain. Electromyography shows a myopathic pattern. Myopathy may improve with treatment. Global protein deficiency has been described mostly after biliopancreatic diversion or duodenal switch, and there are few reports after gastric bypass, generally related to supply deficiency. These deficiencies most often appear in a context of surgical complications (stenosis, fistulas…). In the cases of restrictive surgery such as sleeve gastrectomy or gastric banding, protein deficiency can also occur if the weight loss is rapid and significant, or in case of complications or intercurrent illness [10]. Vitamin D deficiency with related hypocalcemia and secondary hyperparathyroidism can lead to myopathy that may improve with treatment [5, 8, 20]. A syndrome of osteomalacic myopathy with diffuse pain has been described. Myopathy attributedted to vitamin D deficiency after a gastrectomy procedure was found in three of 106 patients [39]. Copper-related myopathies have also been described [22, 23].

Conclusion The number of bariatric surgery procedures has increased. Neurological complications can result from this surgery. Clinicians need to recognize and learn to manage these complications that may develop within a few weeks to many years or decades after surgery, and can be irreversible. It is important to educate patients so that they may be able to consult in emergency in case of confusion, memory troubles, weakness, and gait ataxia. Vitamin levels should ideally be investigated very easily in BS patients. These patients should if possible be followed in multidisciplinary teams [40]. A systematic, multidisciplinary approach of intensive nutritional management before and after surgery with frequent follow-up and routine screening of selected nutrients (vitamins B6, B12, D, and E, folate, iron, thiamine, calcium) at 6 weeks and 3, 6, and 12 months, and then annually after BS, in addition to nutritional supplements may help to prevent these complications [40]. Guidelines from the American Association of Clinical Endocrinologists, the Obesity Society, and the American Society for Metabolic and Bariatric Surgery recommend that all BS patients should take multivitamin supplement twice daily, with further micronutriment supply when needed, particularly when a more malabsorptive procedure has been used as biliopancreatic diversion [41]. All patients who present neurological complications should be tested for thiamin, folate, vitamin B12, zinc, copper, vitamin A, and vitamin E deficiencies and be treated according to the results [41].

OBES SURG (2014) 24:1800–1807 Conflicts of Interest Author declared to have no conflicts of interest and no financial disclosure, to have no commercial or proprietary interest in any drug, device, or equipment mentioned in this article.

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Neurological complications of bariatric surgery.

Obesity is reaching pandemic proportions, and the number of bariatric surgeries is increasing. Neurological complications of bariatric procedures are ...
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