Handbook of Clinical Neurology, Vol. 120 (3rd series) Neurologic Aspects of Systemic Disease Part II Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved

Chapter 39

The neurologic complications of bariatric surgery JOSEPH R. BERGER* AND DIVYA SINGHAL Department of Neurology, University of Kentucky College of Medicine, Lexington, KY, USA

OBESITY: AN OVERVIEW Weight is a national obsession. In 1999, Americans spent over $300 million on prescription medications for obesity (Wilhelm, 2000) and at the end of the 20th century 2.5% of the adult population reported using such preparations (Khan et al., 2001). By some estimates, the medical costs of obesity have risen to $147 billion per year as of 2008. Obesity is now officially recognized by the US Surgeon General as a significant health risk factor. Current prevalence of obesity is estimated to be over 30% in the US (Flegal et al., 2010), and another third are overweight. Obesity increases the risk for numerous medical illnesses, among them diabetes mellitus, hypercholesterolemia, hypertension and other cardiovascular disorders, pulmonary disease, chronic diseases, including osteoarthritis, liver and kidney disease, asthma, chronic back pain, sleep apnea, and depression and some forms of cancer (Fisher and Schauer, 2002; Mokdad et al., 2003). Obesity also increases the risk of death from all causes; it is estimated that 300 000 adults in the US die from obesityrelated causes annually (Allison et al., 1999). Given the increasing prevalence of obesity, it has been postulated that obesity may soon become the leading cause of death in the US (Mokdad et al., 2004). Furthermore, the average obese person costs society more than $7000 a year in lost productivity and as much as $30 000 in added medical costs over a lifetime (Freedman, 2011). The problem of obesity is a global phenomenon consequent on the ready availability of food with high caloric content and the reduction of daily energy expenditure. While the percentage of overweight adults in most Western European countries has not surpassed that of the US, their numbers are increasing rapidly. The number of obese children in many of these countries, such as, England, is growing rapidly (Lobstein et al., 2003) and

has outstripped that in the US. In major population centers of developing countries, obesity is also seen with increasing frequency. For medical purposes, obesity is defined by body mass index (BMI), which is derived by dividing an individual’s weight in kilograms by their height in meters square. Normal weight is defined as a BMI of 18.5–24.9 (National Heart, Lung, and Blood Institute, 1998). A BMI exceeding this value is regarded as overweight. BMIs of 30 or greater are considered obese and those equal to or exceeding 40 as morbidly obese (National Heart, Lung, and Blood Institute, 1998). Prevalence data from the CDC (US Centers for Disease Control and Prevention) indicates that in 1999–2000, 64.5% of US adults were overweight, 30.5% were obese, and 4.7% were morbidly obese (Flegal et al., 2002). Despite the billions of dollars spent on diets, dietary supplements, exercise programs, and other nonsurgical modalities for weight reduction, long-term success rates have been quite variable. Increasing numbers of people are, therefore, resorting to bariatric surgery for control of their weight problem. The increasing popularity of these procedures may, in part, be attributable to media attention provided by television personalities who have undergone surgery for their own weight reduction. From 1990 to 2000, the national annual rate of bariatric surgery increased nearly sixfold, from 2.4 to 14.1 per 100 000 adults (Trus et al., 2005). Population-adjusted rates of bariatric surgery in the overall sample increased more than sevenfold in the study period, from 3.5 per 100 000 US population in 1996 to 24.0 per 100 000 in 2002 (Davis et al., 2006).

BARIATRIC SURGERY National guidelines reserves bariatric surgery for individuals who have failed attempts of nonsurgical weight

*Correspondence to Dr. Joseph R. Berger, Department of Neurology, University of Kentucky College of Medicine, Kentucky Clinic L-445, 740 S. Limestone Street, Lexington, KY 40536-0284, USA. Tel: þ1-859 218-5039, Fax: þ1-859 323-5943, E-mail: [email protected]

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loss and have a BMI  35 with an obesity-related comorbidity or a BMI > 40 with or without a comorbidity (National Institutes of Health, 1992). A number of different surgical procedures have been employed for achieving weight reduction (Deitel and Shikora, 2002). Gastroplasties rely on the mechanical restriction of food passage through the stomach, whereas gastric bypass is considered to result in weight loss by a more physiologic mechanism (Livingston, 2002). Gastric bypass, typically the Roux-enY gastric bypass, is now performed more commonly than gastroplasties (Pope et al., 2002). Many of these surgical procedures can be performed laparoscopically (Azagra et al., 1999; Higa et al., 2000; Schauer et al., 2000). Average excess weight loss following laparoscopic Roux-en-Y gastric bypass has been reported to approach 70% at 12 months (Higa et al., 2000) and 83% at 24 months (Schauer et al., 2000), with excellent control of comorbidities (Buchwald et al., 2004). Although success rates have been variable, persistent, long-term weight loss of 10 or more years following these procedures has been documented (Yale, 1989; Pories et al., 1992). Studies of costeffectiveness support the value of bariatric surgery (Clegg et al., 2003; Fang, 2003). The complications of bariatric surgery are not insignificant, in part related to the problems inherent in operating on the obese person. In one series (Schauer et al., 2000), major complications occurred in 3.3% and the in-hospital mortality was 0.4%. Reoperation may be necessitated by bleeding, abscess, and wound dehiscence. A variety of late complications are recognized, generally the consequence of nutritional deficiency (Table 39.1). Mineral deficiencies include iron, calcium, phosphate, and magnesium, and vitamin deficiencies include thiamine (B1), cyanocobalamin (B12), folate, vitamin D, vitamin E. Iron, folate, and vitamin B12 deficiency have been reported to be the most common nutritional deficiencies observed following gastric bypass (Halverson, 1992; Skroubis et al., 2002; Bal et al., 2010). Table 39.1 Micronutrient deficiencies following bariatric surgery ● ● ● ● ● ● ● ● ● ● ●

Thiamine (B1) Cyanocobalamin (B12) Vitamin D Vitamin E Folate Iron Calcium Magnesium Phosphate Copper Selenium

Neurologic complications of bariatric surgery A broad spectrum of neurologic complications has been reported to occur in association with bariatric surgery (Table 39.2). No part of the neuraxis is exempt from these complications. To date, all studies addressing the neurologic complications occurring in the setting of bariatric surgery have been retrospective in nature. In 1987, Abarbanel and colleagues reported that 23 of 500 (4.6%) patients undergoing bariatric surgery experienced neurologic complications (Abarbanel et al., 1987). Of the 500 patients, 457 had a Roux-en-Y procedure and 43 had gastroplasty (Abarbanel et al., 1987). The neurologic complications became manifest 3–20 months after surgery and all affected patients experienced protracted vomiting, a symptom that may occur in up to one-third of all patients undergoing gastric bypass (Halverson, 1992; Bal et al., 2010). The constellation of neurologic complications included chronic and subacute peripheral neuropathy (52%), acute peripheral neuropathy (4%), burning feet (9%), meralgia paresthetica (9%), myotonic syndrome (4%), posterolateral myelopathy (9%), and Wernicke’s encephalopathy (9%) (Abarbanel et al., 1987). In this series, individuals with burning feet and Wernicke’s encephalopathy responded to thiamine administration (Abarbanel et al., 1987). In a retrospective review of 556 patients undergoing bariatric surgery at the Mayo Clinic from 1980 through 2003, Thaisetthawatkul and colleagues observed 48 patients (8.6%) with complications affecting the peripheral nervous system (Thaisetthawatkul, 2003). Of these 48 patients, 23 (48%) developed mononeuropathies with carpal tunnel syndrome, the most common accounting for 74% of the total (Thaisetthawatkul, Table 39.2 Neurologic complications of bariatric surgery ● ● ● ● ● ● ● ● ●

● ● ● ●

Encephalopathy Behavioral abnormalities Seizures Cranial nerve palsies Ataxia Myelopathy Plexopathies Peripheral neuropathy Mononeuropathies ● Carpal tunnel syndrome ● Meralgia paresthetica Compartment syndromes Myopathy Myotonia Restless legs syndrome

THE NEUROLOGIC COMPLICATIONS OF BARIATRIC SURGERY 589 2003). Peripheral neuropathies were observed in 20 Ranne, 1984; Oczkowski and Kertesz, 1985). Although (41.7%), plexopathies in 4 (17.4%), and myopathy in 1 some authors had previously considered Wernicke’s (4.3%) (Thaisetthawatkul, 2003). Perhaps the most debilencephalopathy a “very rare complication” of gastric itating of the neurologic consequences of bariatric sursurgery for morbid obesity (Bozbora et al., 2000), there gery are those occurring from vitamin deficiency, are at least 104 cases in the world’s literature and the particularly vitamins B1 and B12, as these may result in number of cases after bariatric surgery is substantially permanent neurologic disability. higher than previously reported (Aasheim et al., 2009). This complication is almost always associated with severe intractable vomiting. It may be seen relatively Thiamine deficiency (vitamin B1) soon after surgery, usually within 4–12 weeks (Kramer Thiamine deficiency alters mitochondrial function, and Locke, 1987) but occasionally as late as 18 months impairs oxidative metabolism, and causes selective after the procedure. neuronal death by diminishing thiamine-dependent Peripheral neuropathy often, but not invariably, enzymes (Ke et al., 2003). A deficiency of thiamine accompanies Wernicke’s encephalopathy following surresults in peripheral neuropathy, ophthalmoplegia and gery for morbid obesity. Peripheral neuropathy with or nystagmus, ataxia, encephalopathy and may lead to perwithout Wernicke’s encephalopathy that is attributable manent impairment of recent memory. This constellato thiamine deficiency and has occurred following surtion is referred to as Wernicke’s encephalopathy. The gery for morbid obesity has been referred to as “bariatric diagnostic criteria of Wernicke’s encephalopathy require beriberi” (Gollobin and Marcus, 2002). It appears to be two of the following four features: (1) dietary deficiency; more common than encephalopathy and may also occur (2) oculomotor abnormality; (3) cerebellar dysfunction; within 6 weeks of surgery (Chaves et al., 2002), although (4) confusion or mild memory impairment. These criteria intervals exceeding 3 years have been reported (Koike have a very high inter-rater reliability for the diagnosis et al., 2001). The neuropathy predominantly affects (Caine et al., 1997). This condition is most commonly the lower limbs and is both sensory and motor, with described in the setting of alcohol abuse when the individvariable involvement of each. While it may progress ual has had insufficient dietary intake of thiamine over a over years when untreated, rapid progression over long period of time. However, it is important to recall one intervals as short as 3 days may mimic Guillain–Barre´ of the three cases in the initial description in 1881 by Carl syndrome (Koike et al., 2001; Chang et al., 2002). ElecWernicke was the consequence of esophageal damage trophysiologic studies reveal that this neuropathy is axofrom sulfuric acid ingestion with associated refractory nal in nature with markedly reduced amplitudes of emesis (Wernicke, 1881). The mechanism by which compound motor action potential and sensory nerve bariatric surgery leads to thiamine deficiency, whether action potentials, especially in the lower extremities resulting in an encephalopathy or peripheral neuropathy, (Koike et al., 2001). is almost certainly inadequate vitamin repletion attending Thiamine deficiency can be confirmed by assessing persistent, intractable vomiting. the thiamine pyrophosphate effect in erythrocyte transIn 1977, Printen and Mason reported four patients ketolase studies (Boni et al., 1980). The clinical constelwho developed peripheral neuropathy and protracted lation coupled with the response to parenteral thiamine, emesis following gastric operations for obesity especially with the features of the encephalopathy, may (Printen and Mason, 1977). In this and other early reports prove sufficiently diagnostic. Additionally, magnetic of the neurologic complications occurring with gastric resonance imaging (MRI) of the brain may show characbypass, the specific cause of the neurologic disorder teristic abnormalities, in particular, hyperintense signal remained uncertain. In 1981, Ayub and colleagues abnormalities on T2-weighted images in the dorsomedial described confusion, slurred speech, and unsteadiness thalamic nuclei, periaqueductal gray matter, and mamin seven of 110 patients undergoing bariatric surgery millary bodies (Cirignotta et al., 2000; Toth and Voll, (Ayub et al., 1981). The authors listed several potential 2001). Both the encephalopathy and peripheral neuropaetiologies, including nutritional disturbances, metabolic thy of thiamine deficiency may occur despite oral supabnormalities, medication side-effects, lactic acidosis, plementation with thiamine as emesis may preclude or potential “toxic” bowel product attributable to a effective absorption. Substantial functional recovery micro-organism (Ayub et al., 1981). Some, if not all, of typically occurs within 3–6 months of the initiation of these cases were likely due to thiamine deficiency. Over therapy (Koike et al., 2001); however, neurologic recovthe past three decades, several reports linked the appearery may be incomplete (Salas-Salvado et al., 2000), parance of Wernicke’s encephalopathy with surgery for ticularly if the nature of the disorder is not recognized morbid obesity (Rothrock and Smith, 1981; Haid et al., promptly. Physical therapy for the peripheral neuropathy 1982; MacLean, 1982; Milius et al., 1982; Villar and is also recommended (Chaves et al., 2002).

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J.R. BERGER AND D. SINGHAL hematologic manifestations may not accompany the Copper deficiency myelopathy neurologic syndrome (Kumar et al., 2003, 2004b). Copper deficiency myelopathy (CDM) was first reported Serum copper and serum ceruloplasmin levels have in 2001 and over the last decade, it has become an consistently been found to be low and of statistical sigincreasingly recognized myelopathy that most comnificance. Urinary copper level excretion is frequently monly occurs as a consequence of prior gastrointestinal low (when dietary copper is low). For assessment of surgery. The clinical and radiologic picture is usually metabolically active copper stores, activity of copper indistinguishable from subacute combined degeneration enzymes such as erythrocyte superoxide dismutase (SCD) (Kumar et al., 2004) due to vitamin B12 (cobalamin) and platelet or leukocyte cytochrome c oxidase may be deficiency, and the two may coexist (Juhasz-Pocsine et al., utilized (Kumar and Weimar, 2010). Electrophysiologic 2007). Other, less frequently reported and less clearly tests reveal an axonal sensorimotor peripheral causally related neurologic associations of acquired copneuropathy (to varying degrees). Somatosensory per deficiency include isolated peripheral neuropathy, potentials are abnormal with impaired central conducmotor neuron disease, myopathy, cerebral demyelination, tion being a key finding (Jaiser and Winston, 2010). cognitive dysfunction, and optic neuropathy. Spinal MRI shows an augmented T2 signal involving Jaiser and Winston (2010) reviewed 55 cases in the the dorsal column in posterior cervical or thoracic literature – previous upper gastrointestinal surgery was cord in nearly half of the cases with no contrast enhancethe commonest reported cause, being implicated in almost ment (22 cases) (Kumar, 2006); rarely, signal changes half the cases. Of these, nine cases were attributable to involving the lateral column may be seen (Kumar bariatric surgery. The interval between upper gastrointeset al., 2003). tinal surgery and symptom onset ranged from 5 to 26 Although there have been no studies that address the years in the bariatric group (mean 11.4 years). Likely cause most appropriate dose and duration of copper supplefor copper deficiency is greater reduction in the effective mentation, based on a review of all articles addressing absorption area for copper (postoperatively, food this subject, oral copper supplementation is the preferred bypasses most of the stomach and the entire duodenum). route of supplementation. Oral supplementation equivCopper is a component of numerous metalloenzymes alent to doses ranging from 2 to 8 mg of elemental copand proteins that have a key role in maintaining the per per day have been recommended by different structure and function of the nervous system. It is a constitauthors (Kumar, 2006; Jaiser and Winston, 2010). Pracuent of cytochrome oxidase (oxidative phosphorylation), tice at Mayo Clinic involves 6 mg/day of elemental copsuperoxide dismutase (antioxidant defense), ceruloplasmin per orally for a week, 4 mg/day for the second week, and (iron metabolism), tyrosinase (melanin synthesis), and 2 mg/day thereafter. Periodic assessment of serum copdopamine b-monooxygenase (catecholamine synthesis) per is essential to determine adequacy of replacement (Kumar et al., 2004a). Based on similarities to SCD due and the most appropriate long-term administration stratto vitamin B12 deficiency and copper deficiency myelopaegy is recommended (Winston and Jaiser, 2008). Since thy, it has been hypothesized that methionine synthase zinc can interfere with copper absorption, care must be and S-adenosylhomocysteine hydrolase (another enzyme taken to avoid copper preparations containing significant involved in the cycle) may depend on copper. Dysfunction quantities of zinc, such as multivitamin tablets. As the in the methylation cycle and associated failure of myelin underlying risk factor of decreased copper absorption maintenance could therefore explain the clinical and cannot be eliminated in cases of bariatric surgery, a short radiologic congruence between CDM and SCD, but it 5 day course of parenteral therapy (to facilitate rapid norremains to be proven with direct biochemical evidence malization of body copper stores) followed by indefinite (Kumar et al., 2006; Kumar and Weimar, 2010). oral copper supplementation has been recommended. Most common neurologic manifestation in adults is a Whilst treatment causes prompt and full resolution of myeloneuropathy with gait difficulties (primarily due to hematologic abnormalities, the neurologic deficits merely sensory ataxia due to dorsal column dysfunction), spasstabilize (51% of cases) or partially improve (49% cases). tic gait and lower limb paresthesias; urinary symptoms Hence, it is crucial to avoid delays in diagnosis and treatare infrequent. Examination usually shows a spastic ment to avert potentially irreversible neurologic deterioraparaparesis or tetraparesis with a truncal sensory level tion (Jaiser and Winston, 2010). for dorsal column modalities. A sensory/motor neuropImprovement when present is often subjective and athy frequently coexists and manifests as depression of preferentially involves sensory symptoms. There are distal reflexes and superimposed sensory impairment in some reports of definite improvement in the neurologic a glove and stocking distribution. Although the hematodeficits, nerve conduction studies, evoked potential logic hallmark of copper deficiency is anemia and neustudies, and MRI T2 cord signal changes with normalitropenia, it is being increasingly recognized that zation of serum copper (Kumar, 2006).

THE NEUROLOGIC COMPLICATIONS OF BARIATRIC SURGERY 591 colleagues (2009) have reported that the risk of vitamin Other nutritional and metabolic disorders deficiencies differs significantly based on the type of Absorption of vitamin B12 is complex and requires the bariatric surgery – compared with gastric bypass, duodepresence of intrinsic factor derived from gastric parietal nal switch may be associated with a greater risk of thiacells, acid gastric pH, and absorption in the ileum. mine, vitamin A and D deficiencies in the first year after Bariatric surgery may interfere with several of these the procedure. Hence, patients who undergo these two mechanisms. As liver stores of cyanocobalamin are sufsurgical interventions may require different monitoring ficient to allow for years of dietary insufficiency, these and supplementation regimens in the first year after surfeatures may not appear for long periods of time. A low gery. In addition to vitamin D, patients undergoing gasserum vitamin B12 level has been observed in as many as tric bypass may also be at risk of depletion of another 70% patients undergoing gastric bypass, and vitamin B12 fat-soluble vitamin, vitamin E (Provenzale et al., 1992), deficiency in more than 30% (Amaral et al., 1985). which is also associated with neurologic manifestations The prototypical neurologic disorder occurring with (Satya-Murti et al., 1986). cyanocobalamin deficiency is subacute combined degenBoldery and colleagues have reported two cases eration in which the peripheral nerves and posterior colimplicating selenium deficiency as a cause of heart failumns of the spinal cord are chiefly affected. A large ure in patients after gastric bypass surgery; selenium number of neurologic symptoms and signs have been deficiency is recognized as a cause of Keshan associated with cyanocobalamin deficiency, including, disease, also known as nutritional cardiomyopathy. paresthesias, loss of cutaneous sensation, weakness, However, in postbypass surgery patients with heart faildecreased reflexes, spasticity, ataxia, incontinence, loss ure, obstructive sleep apnea and thiamine deficiency of vision, dementia, psychoses, and altered mood must also be considered as potential explanations (Healton et al., 1991). Subacute combined degeneration (Boldery et al., 2007). has been reported after partial gastrectomy (Weir and Neurologic disorders consequent to rapid fat metabGatenby, 1963; Williams et al., 1969). The infrequency olism or the result of multiple nutritional and metabolic of disorders related to vitamin B12 has suggested to some factors have been reported, but remain unproven. Feit investigators that vitamin B12 deficiency is seldom clinand colleagues reported two patients who developed a ically relevant in the postgastric bypass patient (Brolin severe polyneuropathy chiefly affecting position et al., 1998); however, Bloomberg and colleagues sense associated with ataxia and pseudochorea within (2005) reviewed the literature and reflected on the need 3 months of gastric partitioning for morbid obesity for further studies to evaluate the clinical significance of (Feit et al., 1982). In one patient who died, autopsy nutritional deficiencies and establish guidelines for revealed extensive demyelination associated with extensupplementation. sive accumulation of lipofuscin in anterior horn cells Low plasma folate is seen in up to 42% of persons and dorsal root ganglia and lipid in Schwann cells (Feit undergoing gastric bypass followed for 3 years et al., 1982). The authors suggested that a toxin from (Halverson, 1986). Folate deficiency with an attendant rapid fat catabolism or loss of carnitine were responsible peripheral neuropathy would not be unexpected. Howrather than thiamine or another vitamin deficiency ever, the literature does not suggest that it is a common (Feit et al., 1982). Similarly, Paulson and colleagues problem and some investigators argue that it is not clinireported six patients with a clinical picture characterized cally relevant (Brolin et al., 1998). As with vitamin B12, oral by confusion, abnormal behavior, profound leg weakfolate supplementation appears effective in maintaining ness, diminished or absent muscle stretch reflexes, and levels within the normal range (Brolin et al., 1991). in three, ophthalmoplegia, or nystagmus (Paulson Niacin deficiency and pellagra has occurred after et al., 1985). While thiamine deficiency was considered gastroplasty (Lopez et al., 2000). This syndrome is charin the differential diagnosis, the authors believed that acterized by a symmetrical rash on sun-exposed areas this disorder was likely the consequence of rapid with hyperkeratosis, hyperpigmentation, and desquamametabolism of fat in obesity (Paulson et al., 1985). tion. Glossitis, diarrhea, fatigue, hallucinations, and Other investigators have proposed that some of the neuencephalopathy are also features of the disorder. rologic complications which follow bariatric surgery, Symptomatic hypocalcemia secondary to vitamin D such as the peripheral neuropathy or psychosis, arise deficiency after gastric bypass has been described from multifactorial causes (Seehra et al., 1996; (Marinella, 1999). Marinella reported a patient who Thaisetthawatkul et al., 2004). developed carpopedal spasms, intermittent facial twitchRecurrent spells of encephalopathy characterized by ing and ophthalmoplegia in association with hypocalceconfusion, behavioral abnormalities, weakness, lethargy, mia years after gastric bypass who responded to calcium ataxia, and dysarthria occurring with lactic acidosis may repletion (Marinella, 1999). Interestingly, Aasheim and occur after jejunoileostomy for morbid obesity (Dahlquist

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et al., 1984). This same disorder has been described in individuals with short bowel syndrome (Stolberg et al., 1982). It is precipitated by high carbohydrate diets. The neurologic symptoms occur in association with elevated concentrations of D-lactate in blood, urine, and stool (Dahlquist et al., 1984). The elevated levels of D-lactate are believed to result from fermentation of carbohydrates in the colon or bypassed segment of the small bowel (Dahlquist et al., 1984). Minerals (calcium, phosphorus, and magnesium) and trace elements (zinc, iodine, copper, manganese, fluoride, chromium, molybdenum, selenium, and iron) have seldom been studied in patients following gastric bypass (Bal et al., 2010).

Miscellaneous disorders Some of neurologic complications of bariatric surgery that are not ascribable to micronutrient insufficiency, although not exclusive to this setting, remain relatively unique. Unilateral lower compartment syndrome occurring in the immediate postoperative period may be observed (Gorecki et al., 2002). This syndrome arises from ischemic injury to tissues in the anterior compartment with progressive increase in pressure and ultimately nerve injury. Prompt recognition and fasciotomy are essential for a favorable outcome (Gorecki et al., 2002). Lumbosacral plexopathy with an asymmetric peripheral neuropathy has been reported following gastric partitioning (Harwood et al., 1987). The specific pathogenesis of this disorder have not been addressed (Harwood et al., 1987) and whether it is due to a micronutrient deficiency or other cause remains uncertain. Similarly, Thaisetthawatkul noted plexopathy in five of his 435 patients (Thaisetthawatkul, 2003). A wide variety of musculoskeletal symptoms have been reported to occur in association with gastric bypass (Ginsberg et al., 1979). Ginsberg and colleagues reported 13 patients who developed a constellation of arthritis, polyarthalgias, myalgias, and morning stiffness 3 weeks to 48 months after undergoing jejunoileal shunt surgery (Ginsberg et al., 1979). These symptoms tended to be transient in nature and the demonstration of circulating immune complexes suggested an autoimmune process (Ginsberg et al., 1979).

CONCLUSIONS In summary, neurologic complications occurring in the setting of bariatric surgery are not uncommon. These complications have been reported in as many as 5–10% of patients undergoing surgery for obesity (Berger, 2004). Any part of the neuraxis, including brain, cerebellum, spinal cord, peripheral nerve, and muscle, may

be involved by these complications. Most of these neurologic complications are the consequence of micronutrient deficiency. Following bariatric surgery, at 6 month intervals during the first 3 years, then once yearly ferritin, zinc, copper, magnesium, total 25-hydroxyvitamin D, folate, whole blood thiamine, vitamin B12 and 24 h urinary calcium levels should be checked (Bal et al., 2010). Physicians need to be particularly alert to Wernicke’s encephalopathy developing after bariatric surgery as it is a medical emergency and demands rapid diagnosis and intervention. Copper deficiency is an increasingly recognized complication (Jaiser and Winston, 2010) (and expected to become even more frequent with increase in number of bariatric surgeries) – early recognition and treatment is of utmost importance because it can prevent neurologic deterioration (VidetGibou et al., 2010). Physicians caring for patients who have undergone bariatric surgery should be familiar with the constellation of neurologic disorders that may occur.

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