Age: 21.0
Sex: F
Vaccine: HPVX
Symptoms: Alanine aminotransferase normal, Antinuclear antibody negative, Arthralgia, Aspartate aminotransferase normal, Asthenia
Clinical narrative: Information has been received from an investigator concerning a 21 year old female patient with migraine headaches who entered the study. On 16-OCT-2009, the patient was randomized and was vaccinated with the first dose of 0.5 ml intramuscular (IM) blinded therapy of HPV vaccine or placebo. On 16-DEC-2009 and on 14-APR-2010, the patient was vaccinated with the second and third dose of 0.5 ml blinded therapy or placebo respectively. Concomitant therapy included CYCLEN. On 01-MAY-2010, the patient experienced bilateral numbness to extremities. It was reported that the patient reported bilateral numbness/generalized weakness that started on May 2010. Peripheral numbness was noted with numbness to fingers and toes fluctuated in frequency/duration, episodic in nature. The patient's mother had Multiple Sclerosis (MS). The patient was seen by her general practitioner (GP) on 07-SEP-2010 and was referred to the neurologist. The patient was treated with ALEVE for joint pain. On 29-DEC-2010, a neurological physician report stated that the patient described '3 main weird symptoms'. She described symptoms of episodic burning and paresthesias involving the perioral area, fingers and toes. These symptoms lasted less than 1 minute. The symptoms were not triggered or exacerbated by activity or other factors. She also described joint pain in multiple areas including wrist, fingers, ankles and knees; they felt swollen and were tender to palpation. These symptoms also fluctuated and were episodic in nature. The patient also described multiple areas of muscle soreness and stiffness, and occasional blurred vision of the right eye. She denied Lhermitte's phenomena or Uhthoff's phenomena, other than those symptoms the patient was healthy. The patient did not smoke, she drank alcohol on occasion. The patient denied illicit drug use and she was not pregnant. The patient's cognitive function was unremarkable. The blood pressure was 100/80 with a pulse of 70 and regular. Her vision was 20/20 bilaterally uncorrected. She had mild binocular diplopia with medial and downward gaze. There was no evidence of an internuclear ophthalmoplegia (INO) or a relative afferent pupillary defect (RAPD). The cranial nerve examination was otherwise unremarkable. Carotid bruits were not present. The examination of the upper and lower extremities revealed no atrophy, fasciculations or abnormal movements. The strength was graded as 5/5 and equal bilaterally. The tone was normal bilaterally and the reflexes were graded as 2/2 and equal bilaterally. Plantar responses were down going bilaterally and clonus was not present. Sensory and coordination examination were normal bilaterally. The gait was normal, with a negative Romberg's test. Symptoms were uncertain in etiology. There was no evidence of an underlying neurological cause to account for her symptoms. The patient's symptoms seem to be consistent with a musculoskeletal cause. The patient was recommended further blood work including ESR, Na+, K+, CL-, Ca++, Mg++, PO4, ANA, Rh factor, C3, C4, Quant. immune elect, extractable nuclear ant, C-reactive protein, TSH, Lyme disease, urea, creatinine, LDH, SGPT, SGOT and MRI to rule out evidence of demyelination and if the MRI showed a significant abnormality, the physician would arranged a follow-up appointment. On 29-DEC-2010, the patient was performed following laboratory tests: erythrocyte sedimentation rate (ESR) 5; Biochemistry workup electrolytes: serum calcium 2.35, serum chloride 103, serum magnesium 0.97; serum phosphate 0.91; serum potassium 4.6 (normal); serum sodium 142; enzymes: serum alanine aminotransferase (ALT) 18, serum aspartate aminotransferase (AST) 20, serum LD (lactate dehydrogenase) 163; serum TSH 1.9 and Immunological workup including serum antinuclear antibodies (ANA), nuclear anti C reactive protein, serum quantative immune C3 1.24; serum quantative immune C4 0.21; C reactive protein negative; serum albumin 42; serum creatinine 70; latex rheum factor (serum rheumatoid factor test) negative; serum Urea 5.4. Result of serum Borrelia burgdorferi on 29-DEC-2010 was negative. Symptoms had decreased in frequency and duration since January 2011. On 07-FEB-2011, patient had magnetic resonance imaging (MRI) cervical spine for diagnoses which showed cervical spine: mild central spinal canal prominence with no evidence of cord compression and no evidence of syrinx; mild posterolateral disc protrusion to left at the C5-C6 level, some loss of spinal lordosis at this level, no other abnormality noted. MRI brain was performed on 07-FEB-2011 with a result of brain: Sagittal FLAIR, axial proton-denalty and T2 images of the brain were obtained. An intracranial mass lesion, intracranial hemorrhage, area of infarction or area of demyelination was not identified. Lab work up was all negative. Laboratories values were within normal range. No course of treatment for this event. The patient had no clinical course and she was advised to contact general practitioner (GP) office if symptoms worsen in frequency and severity. No working diagnosis to report at this time. The patient's symptoms was less in frequent. The patient was being followed by GP. The neurologist suggested repeat serum protein electrophoresis to be redrawn 6-12 months. Neurology availed for consult if symptoms worsen. The neurologist and the patient reported symptoms improving in severity and frequency. She was currently well and denied any new symptoms or focal neurological deficits. The patient reported resolution of all symptoms. No definitive evidence of underlying neurological cause for symptoms reported by neurologist. On 11-MAR-2011, the neurologist saw the patient for a follow up appointment regarding numbness and reported that she was currently well and her symptoms had improved since he saw her the last time. The patient denied any new symptoms or focal neurological deficits. She denied again Lhermitte's phenomena. The site received her MRI results and there was no evidence of MS. There was a mild prominence of her central cord at the C5-7 region, but no definite evidence of syrinx. There were mild degenerative changes at the C5-6 region. Her blood work was unremarkable but showed a mildly elevated IgM level, which was likely an aberration. The neurologist was happy to saw that the patient's symptoms had improved. Her cervical spine findings were likely incidental in nature. However if she developed new symptoms down the road, then she should had a repeat MRI of her spine to re-evalute. The neurologist also suggested repeating a serum protein electrophoresis in 6-12 months time. The neurologist had not set up another appointment, but would be happy to do so at the request. On 01-JAN-2012, the patient recovered from bilateral numbness to extremities. The patient completed the study medication and was continuing into next trial segment. The reporting investigator left that bilateral numbness to extremities was related to study therapy. Bilateral numbness to extremities was considered to be an other important medical event by the reporting investigator. The patient was placed on the following therapies during study protocol: vitamin D (unspecified) (01-MAY-2011) as prophylaxis, omega 3 marine triglycerides (December 2010) and calcium (unspecified) (December 2010) as prophylaxis. Additional information has been requested. Narrative was updated. The record for this patient was broken on 03-Sep-2013.