Age: 14.0
Sex: M
Vaccine: HEP
Symptoms: Peroneal nerve palsy, Polyneuropathy
Clinical narrative: Information has been received regarding a case in litigation concerning a 14 yr old male with attention deficit hyperactivity disorder (ADHD) and a history of speech delays as a result of chronic ear infections, who on 5/11/01 was vaccinated with a first dose of hep B virus vaccine rHBsAg (yeast) (manufacturer unk). Concomitant therapy included methylphenidate HC1 (Ritalin) taken for treatment of ADHD. He received his second hep B vaccination on 8/8/01. On 09/04/01 the pt's father told the physician that his son had no equilibrium and that he would stand up and then fall over. The pt had a positive Romberg sign, when he stood with his eyes closed and feet together, he swayed. It was reported that he had been normal six days previously. He was diagnosed with cere[[name]]ar ataxia. On 06Sep01 the pt was seen by another physician and it was noted that he was not as [[name]] on the right and had trouble getting up the stairs; though his mental status was clear as a [[name]]. He had no previous recent illness. The MRI done on 9/6/01 was normal. On 09/07/01 the physician questioned whether the pt had Guillain [[name]]e syndrome (GBS) and referred the pt to a neurologist on the same day. Upon the physical examination, the pt's deep tendon reflexes were absent in his lower extremities and the neurologist recommended admitting him for testing and wrote that his symptoms suggested GBS. The pt was admitted on 09/07/01 and underwent nerve conduction studies on the same day. Results were supportive of a diagnosis of demyelinating polyneuropathy. An Epstein [[name]] virus panel done on 09/08/01 was negative. His total protein in his CSF was 192 mg/dl (normal is 15-45) on 08Sep01. His eosinophil count was elevated at 1.55 (normal=0.00-0.70), indicative of an allergic type of reaction. The pt was discharged on 16Sep01 with a diagnosis of GBS. The pt received physical therapy in Sept01. On 03Oct01, the pt was seen by a pediatric neurologist who recommended a second course of intravenous immunoglobulin (IVIG). It was noted at that time that it was too early to talk about a diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP). Further nerve conduction studies were performed on 10/10/01 and demonstrated mild worsening of conduction velocities and decrease in motor amplitudes. The needle EMG showed evidence of Wallerian degeneration in the tested muscles. The physician concluded that the results were consistent with GBS with evidence of axonal loss and denervation. On 10/11/01 the pt was admitted for one day with a diagnosis of acute infective poly neuritis. He was weaker in his legs and unstable. He received repeated IVIG therapy. On 10/23/01, clear regression was noted in pt's gait. Eight [[name]] after pt's diagnosis of acute inflammatory demyelinating polyneuropathy, he was showing relapse which is unexpected with GBS. On 11/08/01, he was admitted with a two month history of distal muscle weakness and gait disturbance. Bilateral facial weakness was noted by the pt's father. The physicians suspected that the pt had CIDP with a problem at the T4 level. From 11/08/01 to 11/14/01 the pt was admitted for CIDP and new onset papilledema. Testing was performed: ANA-2.7 (normal<1.5), Epstein [[name]] virus IgG 305 (normal <18), sedimentation rate 26 increased gamma spike on protein electrophoresis. An MRI of the spine was repeated on 09Nov01 and it revealed a syrinx at the level of T5-T8 with no evidence of cord enlargement. there was peripheral enhancement of the distal thoracic cord and lumbar nerve roots following contrast media, suggesting an inflammatory process. It was noted that he had papilledema bilaterally. He was administered three days of methylprednisolone sodium succinate (Solu Medrol). His CSF protein on 11/12/01 was 198. The pt's condition was noted to have improved significantly as of 11/23/01 and by 01/04/02 the pt was walking without a [[name]] and was in physical therapy (PT) three days/week. His plantar reflexes were positive indicating a central nervous system problem and his deep tendon reflexes were negative. On 02/01/02 the pt was noted to have left foot drop that was improving by 05/31/02. The pt's CIDP was in remission as of 06/09/03, although he continued to suffer from persistent foot drop as noted on 11/12/03. One physician did not think that the pt had either GBS or CIDP, but that it was a monophasic process that abated under the influence of steroids. He called the pt's illness encephalomyeloradiculoneuritis.