Reported findings from the blink reflex in MFS are diverse and additional data is required to see whether certain findings are more predominant than others. her first entrance revealed comparatively decreased sensory nerve actions potentials (SNAPs) and a standard blink reflex. Her SNAPs improved on the next admission, nevertheless, the EMG was performed just 2 days following the onset of her symptoms, restricting some early results that may have not matured electrophysiologically. She was treated with IVIG on both occasions with quick recovery within 5 days. This case highlights the fact that MFS can be recurrent. It also provides further evidence that anti-GAD antibodies may be associated with MFS. Reported findings of the blink reflex in MFS are diverse and further data is needed to determine if certain findings are more predominant than others. Treatment typically consists of IVIG, though steroids may also be considered for recurrence. Prognosis is generally favorable, regardless of treatment. strong class=”kwd-title” Keywords: miller fisher syndrome, Guillain barre syndrome, autoimmune disorders, neuromuscular disease, neurophysiology Introduction The Miller Fisher Syndrome (MFS) is usually a variant of Guillain-Barre Syndrome (GBS) that is characterized by ataxia, areflexia and ophthalmoplegia. It was first explained clinically in 1956. 1 Anti-GQ1b antibodies are positive in at least 85% of patients. 2 Treatment usually consists of intravenous immunoglobulin (IVIG) or plasmapheresis. However, treatment with corticosteroids may be considered for cases with recurrence. 3 Here is described a case statement of recurrent MFS along with a literature and Electromyography (EMG) and Nerve Conduction Study (NCS) review. Case Statement A 32-year-old female with a history of hypothyroidism in the beginning presented to our institution in 2018 with a 2-day history of diplopia, lower extremity weakness and distal paresthesias. She experienced a preceding sinusitis for 2 months that eventually improved 2 weeks prior to admission. On exam, she experienced ophthalmoplegia, ataxia, reduced lower extremity reflexes and bilateral nystagmus. Her MRI Brain showed no acute abnormalities. She received a lumbar puncture on hospital day 2. Her cerebrospinal fluid (CSF) protein was borderline elevated at 47 mg/dL and her white blood cells (WBCs) were less than 3. These results may have been secondary to obtaining the CSF early into her presentation. Her infectious workup was unfavorable. Her anti-GQ1b antibody was positive. Her anti-GAD65 antibody was elevated at 0.17 nmol/L, an increase from normal of 8.5 fold. She experienced an EMG performed 8 days after her symptoms, which showed relative to baseline decreased sensory nerve action potential (SNAP) amplitude. She was given 5 doses of IVIG 0.4 g/kg with rapid improvement in her symptoms within 5 days. On follow up a month later, she was at her baseline. About a 12 months later, she developed diplopia, distal weakness and paresthesias again. She experienced an episode of sinusitis a few weeks prior. Her symptoms progressed rapidly to the point where she could not walk within a day. She experienced ophthalmoplegia, ataxia and areflexia on exam. MRI Rabbit polyclonal to UGCGL2 brain, cervical, thoracic and lumbar spine with and without contrast showed no acute abnormalities. She received a lumbar puncture on hospital day 2. Her CSF protein was 47 mg/dL and her WBCs were less than 3. Her anti-GAD65 antibody was elevated at 0.13 nmol/L, this time a 6.5 fold increase from normal. Her EMG experienced R1 responses that were upper limit of normal. The sensory and motor amplitudes in the limbs were also normal (though that could have been an artifact of being only 2 days into symptoms prior to the evolution of those electrophysiologic findings). The H reflexes were absent Elbasvir (MK-8742) bilaterally. Table 1 shows a summary of her EMG/NCS findings for both admissions. She was treated with IVIG and again experienced significant improvement within 5 days. On follow up a month later, most of her symptoms experienced resolved. However, she still experienced some residual ophthalmoplegia and diplopia. Table 1. Nerve Conduction Studies. thead th colspan=”2″ rowspan=”1″ Sensory NCS /th th colspan=”3″ rowspan=”1″ First evaluation (8 days after symptom onset) /th th colspan=”3″ rowspan=”1″ Second evaluation (2 days after symptom onset) /th th colspan=”2″ rowspan=”1″ Nerve/Sites /th th rowspan=”1″ colspan=”1″ SNAP Amp /th th colspan=”2″ rowspan=”1″ Velocity m/s /th th rowspan=”1″ colspan=”1″ SNAP Amp /th th colspan=”2″ rowspan=”1″ Velocity m/s /th /thead L Median ?Dig II11.651.349.559.1?Palm54.354.912456.9L Ulnar ?Dig V13.152.424.458.8?Palm20.456.956.764.0L Sural ?Calf22.355.634.357.1 Motor NCS First evaluation Second evaluation Nerve/Sites Amp mV Velocity m/s Amp mV Velocity m/s L MedianAPB ?Wrist14.9 17.8 ?Elbow14.054.717.359.2L UlnarADM ?Wrist12.8 14.0 ?B. Elbow12.465.112.762.4?A. Elbow10.860.012.160.0L PeronealEDB ?Ankle5.9 9.1 ?FibHead5.547.17.350.3?Knee5.059.17.154.9L TibialAH ?Ankle27.7 25.1 Blink Reflex First evaluation Elbasvir (MK-8742) Second evaluation Nerve/Sites Muscle R1 (ms) R2: Ipsi (ms) R2: Cont (ms) R1 (ms) R2: Ipsi (ms) R2: Cont (ms) Supraorbital ?Stim L Rec IpsiL Orb Elbasvir (MK-8742) Oculi11.3*31.3512.2428.39?Stim L Rec ContR Orb.