Age: 50.0
Sex: F
Vaccine: FLUX, FLUX
Symptoms: White blood cell count
Clinical narrative: This case was reported in a literature article and described the occurrence of a sensory ataxic variant of Guillain-Barre syndrome in a 50 year-old female subject who had received an unspecified influenza vaccine (manufacturer unknown). No information regarding the subject's medical history, concurrent medical condition or concomitant medications was provided. On an unspecified date, the subject received a dose of an unspecified influenza vaccine (dose, route and injection sites unknown; batch number not provided). On an unknown date, 7 days after vaccination with the unspecified influenza vaccine the subject presented with symmetric sensory paresthesias. Upon examination she was noted to have areflexia, a marked loss of joint position sense in both the proximal and distal areas of her arms and legs. She also had involuntary limb movements that were present at rest but that they became exacerbated when she closed her eyes and was unaware of them. These movements were classified as pseudochoreoathetosis. This case was considered as medically serious by GSK. Serum protein electrophoresis was normal, anti-Hu antibodies were negative and anti-nuclear antibodies were abnormal with a titer of 1:40 and a diffuse pattern. Cerebrospinal fluid albuminocytological dissociation was noted with a protein level of 196 mg/dl and a white blood cell count of 1. Electrodiagnostic studies were performed on days 5 and 10 after symptom onset and they showed a loss of sensory action potential amplitude with preservation of compound muscle action potentials and F-waves. On day 5, her sensory nerve action potential amplitude for the left median nerve (digit II) was 14uV, 13uV for the left ulnar nerve (digit V), 18 uV for the left radial nerve (snuffbox) and there was no response for the left sural nerve (lateral malleolus). On day 10, there was no longer any response for any of these nerves. The muscle action potential for the left ulnar (abductor digiti minimi) was 8.8 uV on day 5 and 9.3 uV on day 10; and for the left tibial (abductor hallucis) was 5.0 uV on day 5 and 6.7 uV on day 10. The F waves for both were normal in both occasions. The treatment was unknown. At the time of reporting, the outcome of the events was unspecified. The authors did not comment on any possible casual relationship between the event and the unspecified influenza vaccine. The authors' conclusion stated that pseudochoreoathetosis resulted from impaired proprioception. The appearance of the movements was indistinguishable from true choreoathetosis, where there is no sensory loss. Subjects could be unaware of the movements when their eyes are closed, and the loss of visual input could or could not exacerbate movements. The lesion responsible for pseudochoreoathetosis could be located anywhere along the sensory pathways. This led to the hypothesis that pseudochoreoathetosis results from failure of the striatum to properly integrate cortical sensory and motor inputs.   [Due to memory limitations, the remainder of this text could not be compared.]  nputs Peripheral sensory disturbances with localization at or distal to the dorsal root ganglia due to Guillain-Barre syndrome variance and paraneoplastic or Sjogren syndrome-associated sensory neuropathy have been described as rare causes for pseudochoreoathetosis.