Guillain-Barré-like Syndrome after Bariatric Surgery

| July 1, 2015 | 0 Comments

by Natalia Bodunova, MD; Daniil Degterev, MD, PhD; Natalia Suponeva, MD, PhD; Evgeniy Zorin, MD, PhD

Dr. Natalia Bodunova is a Scientific Associate at the Moscow Clinical Scientific Center in Moscow, Russia. Dr. Daniil Degterev is from the Department of Neurology, Moscow Clinical Scientific Center. Dr. Natalia Suponeva is Head of Neurology Unit for the Moscow Scientific Neurology Center in Moscow, Russia. Dr. Evgeniy Zorin is a surgeon at the Clinical Rehabilitation Center in Moscow, Russia.

Bariatric Times. 2015;12(7):16–18.

Macro- and micronutritional deficiencies may occur in some bariatric patients post surgery, which can result in serious neurological complications. In this article, the authors describe the case of a patient who developed polyradiculoneuropathy, a variation of acute inflammatory demyelinating polyneuropathy or Guillain-Barré syndrome, following Roux-en-Y gastric bypass surgery. They discuss the importance of identifying symptoms of polyradiculoneuropathy after bariatric surgery and give recommendations for treatment.

Bariatric surgery has been shown to be the most effective treatment for obesity in the long term, with the gold standard being the Roux-en-y gastric bypass (RYGP), a malapsorptive procedure that has consistently shown excess bodyweight loss (eBWL) of 70 to 80 percent.[1] Macro- and micronutritional deficiencies, however, may occur in some bariatric patients post surgery, which can result in serious neurological complications.[1] Acute post-gastric reduction surgery (APGARS) neuropathy is a term used to describe such complications that have been linked to bariatric surgery.[3] We present a case of a patient who developed polyradiculoneuropathy (PRN) following RYGP surgery that resembled Guillain-Barré syndrome.

PRN Etiology
PRN is a condition in which polyneuropathy and polyradiculopathy occur together.[2,3] Polyneuropathy is a general degeneration of peripheral nerves that spreads toward the center of the body. Polyneuropathy is a serious neurological complication that has been associated with bariatric surgery with a frequency varying between 0.06 and 6.2 percent.[4–6] Polyradiculopathy is an inflammatory disorder that affects the spinal nerve roots.

Symptoms of PRN after bariatric surgery include pain in the feet or lower back with ascending paresthesias that may progress to leg weakness associated with ataxia, areflexia, and vibration and proprioceptive sensory loss.[7] These symptoms resemble acute inflammatory demyelinating polyneuropathy (AIDP), the most common form of GBS—a disorder in which the body’s immune system attacks part of the peripheral nervous system—with the exception that patients with PRN tend to have axonal degeneration, rather than demyelination, and normal CSF protein levels.[7] In the bariatric patient, the onset of PRN is believed to be associated vitamin B1 deficiency.[7] Changes in the immune system after bariatric surgery have also been linked to the development of PRN, and in most cases, incidents of PRN occur 2 to 4 weeks after an episode of acute viral or bacterial infection in postsurgery bariatric patients.[8]

Case Report
A 34-year-old man with morbid obesity (body mass index [BMI] 46.2kg/m2) underwent laparoscopic RYGB in February 2014 (Table 1). The operation and initial postoperative period were uneventful. Within two months postoperatively, his weight loss amounted to 43kg. In early April 2014, the patient reported feeling influenza-like symptoms with a low-grade fever. He was treated with doxycycline. Three weeks later, he developed nausea and vomiting after meals. He was admitted to the hospital, and work-up that included blood and urine analysis revealed no abnormalities. An upper gastrointestinal (GI) study showed gastroenteroanastomosis patent with good flow of contrast. The patient was given sulpiride 200mg daily, and in a week, symptoms regressed. The patient’s health improved and he was discharged from the hospital after two weeks.

One week after hospital discharge, he developed new onset of numbness in the abdomen and a sense of “cooling” in his feet. He also reported leg weakness with numbness spreading up his legs that required him to use a walking aid. The patient ceased to move independently five days after onset of these neurological symptoms. Two weeks later, he developed numbness in the lower third portion of his forearms on both sides of his body. He was readmitted to the hospital. A neurological examination was performed using the Medical Research Council (MRC) scale for muscle testing strength.[9] The MRC for muscle effort grades movement from 0 to 5, with 0 representing “no movement” and 5 representing “muscle contracts against full resistance.” The patient’s MRC results were as follows: lower paraparesis with decreased muscle strength in the legs proximal (2.5/5 MRC) and in the dorsal flexors of the toes of both feet (3/5 MRC). Deep reflexes of the legs were absent, and carporadial reflexes were decreased. Pain sensitivity in the feet and hands was decreased. Assessment of vibratory sensations was done with a 128 Hz tuning fork with two scaled dampers ranging from 0 to 8 points (reference value ≥ 6 points). Vibration sensitivity was reduced more proximally (spina iliaca anterior superior 2.5/8 points, patella 2/8 points, ankles 5.5/8 points) on both sides of the patient’s body. There was a decrease of painful, tactile sensation on the surface of the abdomen and on the lower third portion of the chest. His hip muscles were nearly symmetrical (left side: 49cm, right side: 47cm). His bladder and bowel functions were good.

Blood and urine tests showed normal levels of iron, calcium, magnesium, potassium, sodium, total protein, total bilirubin, and creatinine levels. Magnetic resonance imaging (MRI) scans of the brain and cervical and upper thoracic levels were without pathological changes. There were increased levels of alanine transaminase (ALT [206 U/l]), aspartate aminotransferase (AST [86 U/l]), and glucose (7.7mmol/L). Analysis of the cerebrospinal fluid showed the following: white blood cells were 2 cells/mm3 and total protein was 1.2g/L (normal range=0.15–0.45g/L). The level of thiamine was a decreased. Other vitamins (cyanocobalamine, pyridoxine, folic acid) were been normal. Antiganglioside antibodies were not examined.

Assessment of nerve conduction velocity (NCV)10 indicated the motor fibers of tibials and peroneals nerve M-waves were not affected. NCV assessment also showed tachycardia and chrono-dispersion of F-wave latency and the disappearance of afferent components of the H-reflex in the soleus muscles. NCV in upper extremities was normal. A needle electromyography (EMG) of quadriceps femoris and iliolumbal muscles on both sides of the patient’s body was performed, which indicated increased insertion activity, which increased the neuropathic recruitment ratio (>10Hz) and the average duration and aximal amplitude of polyphasic and pseudopolyphasic motor unit action potentials (MUAPs). Spontaneous denervation activity  was the only fasciculation (++) present.
Based on medical history, clinical, laboratory, electrophysiological data, and the revised diagnostic criteria by Dimachkie and Barohn,11  we diagnosed the patient with acute postgastroplastic PRN. We treated the patient with vitamin B complex (milgamma) 4mL per day, thiamine 500mg per day, pyridoxine 3mL per day, and ferrous sulfate 640mg per day. We decided not to treat the patient with plasma exchange and intravenous immunoglobulin (IVIG) due to the disease’s mild course and lack of respiratory disturbances.

After nine days of treatment in the hospital, the patient’s neurological symptoms stabilized. After two weeks of treatment, the patient reported feeling a release from numbness in his hands and pain in his feet. His muscle strength increased to 3.5/5 MRC in the proximal muscles of the legs, and vibration sensation improved in spinal iliaca anterior superior and patella (3/8) and ankles (6/8).

We discharged the patient from the hospital after three weeks, and following discharge, the patient reported successfully walking 10 meters without support two weeks after discharge. EMG assessments were repeated five weeks after patient presented with symptoms. NCV was normal. The needle EMG of the quadriceps femoris and tibialis anterior muscles on both sides of the body showed spontaneous denervation activity like fibrillations (++), positive sharp waves (++), and fasciculations (++).

Over the next several months, the patient’s symptoms gradually improved; however, he required the assistance of a walker for six months before his symptoms completely resolved.

Neurological complications of bariatric interventions are mainly attributed to deficiencies in vitamins A, B1, B2, B6, folic acid, B12, D, E) and the minerals copper, and zinc.[7] Depending on the nature of nutritional deficiency, any part of the nervous system may be involved. Neurological complications may emerge with symptoms of encephalopathy, optic neuritis, myelopathy, radiculopathy, and neuropathy.[7]

Disturbances of the peripheral nervous system are observed in 16 percent of bariatric patients during the first year following weight loss surgery.6 Risk factors for developing peripheral neuropathy (especially polyneuropathy) are relative to absolute weight loss, duration of gastrointestinal disorders, reduced levels of albumin and transferrin after surgery, and postoperative complications requiring hospitalization.[6] Based on the clinical, electrophysiological, and histological findings, there are several forms of peripheral neuropathies after bariatric surgery: isolated small fiber neuropathy, axonal polyneuropathy, and demyelinating PRN.[12]

Polyneuropathy within the post-gastroplastic syndrome is generally characterized by the development numbness and paresthesia in the distal first and then in the proximal parts of the lower extremities. Occasionally, disturbances in consciousness, amnestic syndrome, oculomotor disturbances, psycho-emotional disorders, and/or myelopathy may occur. NCV/needle EMG has revealed signs of axonopathy.[5] The appearance of polyneuropathy is predominantly associated with a lack of vitamin B1 (thiamine) and vitamin B12.[13,14] The vitamin B1 deficiency polyneuropathy is characterized by a combination with Wernicke-Korsakoff encephalopathy. Usually, Wernicke-Korsakoff syndrome is observed 4 to 12 weeks after bariatric surgery.[15] It is characterized by severe cognitive and psychotic disorders, confusion, and dysfunction of the cranial nerves (especially in the oculomotor group), and ataxia.[16] In a study by Aasheim,17 brain MRIs identified lesions characteristic of Wernicke-Korsakoff in 47 percent of cases. Polyneuropathy in patients with B1 deficiency may experience signs of autonomic (orthostatic hypotension) dysfunction, and heart failure.[5,18] Violations of protein-cell ratio in the analysis of the cerebrospinal fluid is not characteristic of deficiency of B vitamins.[19] It is important to note that the deficiency of other vitamins and minerals can make a significant contribution to the development of postbariatric polyneuropathy as well (Table 2).[20–23]

It is not always possible to detect the direct connection between nutritional deficiency and the development of neurological complications in postsurgery bariatric patients.[24,25] The exception is myelopathy that develops from vitamin B12 and copper deficiency.[26] Chang et al[4] conducted a retrospective study of 168,010 patients who underwent bariatric surgery and found that out of 109 cases of postoperative polyneuropathy, specifically APGARS neuropathy, only 40 percent were deficient in vitamin B1 and/or B12. Similar observations were made with the Wernicke-Korsakoff syndrome. In one out of three cases, the level of vitamin B1 in the blood plasma and the activity of erythrocyte tiamintransketolazy remained normal.[27]

An interpretation of clinical data creates difficulties in diagnosis of PRN and other bariatric postsurgery polyneuropathies due to their polymorphism. For example, Aluka et al[19] described the case of a 40-year-old woman who developed lower paraparesis and neuropathic pain five months after undergoing bariatric surgery. EMG study of this patient determined spontaneous denervation activity in the calf muscles. The condition was regarded by the researchers as axonal variant of Guillain-Barré syndrome. Specific treatment was not carried out and the symptoms completely regressed after six months. Paulson et al[28] and Chang et al[4] also reported similar cases.

Identifying symptoms of PRN after bariatric surgery
Occurrences of bariatric postsurgery neurological disorders usually occur within the first six months (usually 3–5 months) after the surgery. Dysfunction of the upper gastrointestinal tract usually precedes PRN symptoms, which can progress rapidly (i.e., in days). Symptoms of PRN include paresis, which is predominantly observed in the lower extremities, pain, demyelination, and axonopathy. Recovery can be extended and symptoms can regress with or without therapy.[25]

In this case, our patient exhibited all of these symptoms, and the presence of protein-cell dissociation in the cerebrospinal fluid two weeks after the appearance of neurological symptoms confirmed the acute inflammatory nature of this condition. However, the detected deficiency of vitamins B1 and B6 may be the cause of peripheral neuropathy.

According to Philippi et al,[12] pathogenesis of postbariatric polyneuropathy is represented by a combination of malnutrition, inflammatory, and immunodeficiency disorders. In our patient, we believe the anatomical positioning of the GI tract after surgery, lack of strict adherence by the patient to the nutritional recommendations post surgery, and the occurrence of an acute infection shortly after surgery likely contributed to the autoimmune aggression against the peripheral nerves, which resulted in PRN. The Guillain-Barré-like syndrome in our patient (with dysfunction of the walk) was not accompanied by a disruption to his vital functions. The symptoms began and increased over a nine-day period and then began to diminish after two weeks, without specific therapy other than nutritional supplementation. The patient was able to walk, with the help of a walking aid, one month after onset.

We hope this report underscores the important of thoroughly examining and observing bariatric patients after surgery, particularly during the first year postsurgery. Early identification and intervention of nutritional deficiencies may help to reduce the occurence of disruptions to the nervous system. We recommend the following daily regimen to all of our patients after RYGB: 100mg of thiamine, 10mg of vitamin B6, 5mg of vitamin B9, 2,000mg of calcium, 3,000IU vitamin D, and 200mg of iron.

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Funding: No funding was provided.

Disclosures: The authors report no conflicts relevant to the content of this article.

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