Several clinical variants of GBS have been recognized which can present with?extremity, facial, respiratory, or bulbar muscle involvement .?Asymmetry in peripheral nerve involvement is atypical and has been only rarely described in the literature [2-6]. treatable disease. strong class=”kwd-title” Keywords: guillain-barre syndrome, asymmetry, asymmetric, hyporeflexia, facial diplegia Introduction Guillain-Barre syndrome (GBS) is an acute paralytic polyneuropathy resulting from an autoimmune response directed towards peripheral nerves leading to heterogeneous forms of demyelinating and axonal damage. Several clinical variants of GBS have been recognized which can present with?extremity, facial, respiratory, or bulbar muscle involvement .?Asymmetry in peripheral nerve involvement is atypical and has been only rarely described in the literature [2-6]. To our knowledge, combined facial diplegia and asymmetric lower extremity hyporeflexia is a unique presentation of GBS that our following case will serve to highlight. Case presentation A 53-year-old female patient?with a history?of type II?diabetes and hypertension?presented with a one-week history?of?abdominal pain, constipation, nausea, and vomiting. She?reported?a single episode?of?bright red blood?per rectum a Ubiquitin Isopeptidase Inhibitor I, G5 few days prior to admission. Two days following the presentation the patient?started complaining of?perioral numbness,?progressive?bilateral?facial weakness, and difficulty?of swallowing?initiation.? On?examination,?vital signs were within normal limits. The patient was?conscious, alert, and oriented.?Cranial nerves?exam was notable for diminished facial muscles’ strength bilaterally (unable to smile or puff her cheeks, unable to maintain eyelid closure against resistance and unable to raise eyebrows bilaterally).?Strength was preserved (5/5)?in?all proximal and distal?bilateral?upper and lower extremity muscle groups. The patient had?an?absent left patellar reflex but otherwise?had 2+ (normal) right patellar, and bilateral biceps, triceps, brachioradialis, and Achilles reflexes. The sensory exam was intact. The exam was also notable for? a mildly distended?abdomen?but was otherwise unremarkable. Constipation shortly resolved with laxatives and computerized tomography (CT) of the abdomen was unremarkable. With regard to the solitary?episode of bloody stool, it was decided to proceed with colonoscopy as an outpatient.?A Ubiquitin Isopeptidase Inhibitor I, G5 stool culture was not sent as the patient presented with constipation rather than a diarrhea illness. Concerning her new neurological findings, CT and?magnetic?resonance?imaging (MRI) (Figure ?(Figure1)1) of?the?brain?were obtained and were unremarkable except for?changes of?chronic small vessel ischemic disease.?Neurology was consulted?who raised the concerns of an atypical presentation of?Guillain-Barr syndrome?and recommended cerebrospinal fluid (CSF) examination. Same day lumbar puncture (LP)?demonstrated increased protein (93 mg/dL) with absent?white and red blood?cells.?No microorganisms were?visible on gram stain.?Due to the high suspicion of?GBS, the patient was urgently?started?on intravenous?immunoglobulins (IVIG) with a dose of?400?mg/kg/day. The level of care Ubiquitin Isopeptidase Inhibitor I, G5 was escalated to the progressive care unit where the patient underwent frequent negative?inspiratory force (NIF) and forced vital capacity (FVC) monitoring which remained within normal limits. Open in a separate window Figure 1 Magnetic resonance imaging of the brain.Mild nonspecific scattered subcortical and deep periventricular?T2 FLAIR hyperintensities (arrows)?suggestive of chronic small vessel ischemic disease. The patient completed?a?five-day course?of IVIG?during which she had?no worsening of symptoms but only a slight improvement.?On day 9 of hospitalization, the patient decided to leave against medical advice (AMA) and did not show up for her follow-up appointment. Discussion Guillain-Barr syndrome is an autoimmune demyelinating disorder usually heralded by a? gastrointestinal or respiratory tract?infection that incites an abnormal immune response targeting peripheral nerves?[1,7].?Among the first clinical SCDO3 manifestations of GBS are pain, numbness, paresthesia, and/or weakness in the limbs. Weakness usually presents in the distal extremities in a rapidly progressive, ascending, and symmetric fashion. However, it can also begin more proximally in the legs or arms. Many patients develop reduced tendon reflexes in the affected limbs?[8-10]. About half of the patients present with cranial nerve deficits, particularly bilateral facial weakness, swallowing difficulties (bulbar symptoms), and/or oculomotor dysfunction,?which might afterwards extend to involve the limbs?[8,11]. The mix of intensifying symmetrical weakness with or without sensory disruptions quickly, hyporeflexia, or areflexia in the lack of a CSF mobile response but raised protein level continues to be the hallmark for the scientific medical diagnosis of GBS. Id of symptoms and building diagnosis have to be produced promptly in order to avoid the damaging sequelae of neglected disease that may Ubiquitin Isopeptidase Inhibitor I, G5 result in respiratory system muscle paralysis. The correct level of treatment with close observation and?regular monitoring of detrimental?inspiratory drive (NIF) and forced essential capacity (FVC) are essential once the medical diagnosis is manufactured . Early administration of intravenous immunoglobulins (IVIG) or initiating plasma exchange (PLEX) will be the mainstay treatment, in sufferers with quickly progressive weakness particularly?. With no treatment, symptoms continue steadily to progress for fourteen days and gradually plateau over 2-4 weeks with following continuous recovery of function in nearly all sufferers. Disease-modifying treatment assists shorten this timeline?[13,14]. Our defined case illustrates how adjustable GBS presentation could be. Asymmetry.