Report 2001003273-1 describes pain in an adult (age not provided) who received an injection of Lyme disease vaccine (Lymerix). This report was received from news service reports and has not been verified by a physician or other health care professional. The pt has tested (+) (NOS) for HLA-DR4. The pt received the 1st and 2nd doses of Lymerix on 4/13/00 and 5/11/00. At some later, unspecified time, he experienced intense pain, the site where the pain occurred was not specified. The patient's spouse stated "everything that's part of your day to day functioning is taken away from you." This report is considered SB medically serious because the patient reportedly could not perform his usual day-to-day functions. The report did not provide the outcome of this event. Follow-up dx: chronic inflammatory demylinating polyneuropathy. He underwent bi-weekly plasmapheresis. He also developed "a lot of atrophy, insulin dependence, depression, yeast infections, compression fractures, edema and tremors". As of 1/31/01, the pt was able to walk with a walker and is now profoundly disabled. Follow-up, states that in 7/00, he began to experience neurological symptoms and weakness. The pt was hospitalized for 5 days, then discharged for outpt physical therapy. He continued to grow weaker. His spouse stated that, "in September, when he was not responding, but continuing to deteriorate" the dx was changed from Guillain-Barre syndrome to chronic inflammatory demyelinating polyneuropathy. The pt was hospitalized for 9 days and underwent bi-weekly plasmapharesis. He continued to deteriorate. Within a 6 month period, he was hospitalized a total of 4 times. He received a total of 25 plasmapharesis treatments. He reportedly experienced intense pain; the site where the pain occurred was not specified. He also developed "a lot of atrophy, insulin dependence, depression, yeast infections, compression fractures, edema, tremors". Information received from the pt's spouse on 2/23/01, states that as of 1/31/01, the pt was able to walk with the assisstance of a walker. The pt's spouse stated that the pt "is now profoundly disabled". The report did not provide the outcome of the pain, atrophy, edema or tremors. The most recent information was received on 7/11/01 from an article posted on the internet. This article did not provide an outcome for any of the reported events. The pt had a history of non-insulin dependent diabetes mellitus since 1995. Pharmacy records from 1998 through 02/10/2002 indicates that he received two vials of human regular insulin, one on 12/21/2000 and one on 03/22/2001. The pharmacy records also indicated that he received mystatis suspension on 12/05/2000 and 01/09/2001. The pt was seen by a neurologist on 11/20/2000 "for an additional opinion concerning a polyneuropathy. The pt dates the onset of his problem to July and August of this year. On 05/11 and then again about one month later he received the LYMErix vaccine, which he tolerated well. However, in mid July he became aware of pain radiating downt the right leg reminiscent of the sciatica he had previously, over the next month or so he developed progressive tingling, numbness and weakness in all four limbs. On August 11 he fell twice at home and was seen the following day. An EMG wsa consistent with a demyelinating polyneuropathy. He was admitted to a hospital, diagnosed as having Guillain Barre and admitted to the intensive care unit. He received IV immunoglobulin on four occasions and seemed to plateau. On 08/17 he was sent home with physical therapy. Over the following month he seemed to become weaker. On 09/19 he ws seen by a physician who felt a more appropriate diagnosis would be CIDP and recommended steroids. The following day he was seen by another physician and was admitted to another hospital where he had plasmapheresis x 5 and was started on prednisone 30 mg daily, which he has been on up until now. At the time he was put on Prilosec prophlactically additional cycle. Since then he had additional plasmaphareses between 10/13 and 27. he is currently in the middle of an additional cycle, having had one pharesis on 11/13. He finds that within two weeks of the pheresis he starts to have increasing paresthesias and weakness. He was treated with Neurontin 900 mg at one point, which did not seem to have much impact. He has had no sphinetor difficulty or bulbar trouble. He also has had paresthesias on the anterior chest from the anterior axillary line to the midline, from about his low thoracic level down and not above that area. He had noticed increased tramulousness with this illness. He has had some pedal edema on the steroids as well as a lot of atrophy." The neurologist stated that review of systems was "notable for decreasing hearing, which he relates to noise exposure, with tinnitus, particularly in the right ear." The pt takes occasional diasepen for sleep." On physical examinations, he appeared "cushingpoid. VIII is cedreased bilaterally. He has mild dysmetria on finger to nose with eyes closed, but not with eyes opened. Heel knee shin is accurate but limited by weakness. There is hand interosseous wasting. There is substantial diminution of vibratory and temperature perception to the knees, mild in the fingersn and diminished temperature perception on the anterior abdominal and chest wall. He is areflexic, flanteux withdraw bilaterally. He cannot walk, but can transfer from wheelchair to examining table." The neurologist reviewed prior diagnostic evaluations and noted cerebrospinal fluid protein 125 mg/dL in August 2000. An EMG "demonstrated multi-focal demyelination with mild distal prolongation and no clear conduction block." The neurologist's impression was "The pt probably does have CIDP. The possible relation to LYMErix vaccine is interesting, but perhaps coincidental. At this point, his weakness appears to be a combination both of his underlying neuropathy and his steroid use." The neurologist decreased the prednisone dosage to 70 mg daily. Serum protein electrophoresis performed on 12/08/2000 revealed hypogammaglobulinemia. No monoclonal band was identified on immunofixation. The pt underwent magnetic resonance imaging of the lumbar spine, with contrast, on 12/19/2000. The radiologists impressions were "In comparisonto a screening evaluation of the lumbar spine obtained on 08/13/2000, there is a new finding of milc compression deformity of the superior and plate of T12 and more subtly involving the anterosuperior end plate of Ld. Associated band-like signal abnormality is suggestive of a non-specific marrow edema pattern. There is diffuse lumbar spondylosis which is not significantly changed form the prior examination. There is straightening of the normal lumbar lordosis. There is no abnormal enhancement ot suggest an infectious or inflammatory process. Specifically, there is no evidence for thickening or abnormal enhancement of the nerve roots." The pt was seen by the neurologist on 12/20/2000, after having his fifth pheresis session that morning. "The pt is minimally stronger in his upper extremities after the pheresis, but feels better overall. He recently has ha dcompression fractures at two levels in the back. I encouraged him to take calcium and vitamin D. He is developing a lot of pedal edema and I suggested he start on Dyazide twice a day for three or four days." The neurologist noted that the pt had been taking prednisone 50 mg daily for the previous two weeks. The neurologist lowered the dosage to 50 mg daily. Lyme nerology performed on 12/22/2000 was non-reactive. The pt returned to the neurologist on 03/27/2001. At that time, he was receiving plasmapheresis on Monday, Wednesday, and Friday approximately every six weeks. Medications included prednisone 30 mg alternating with 20 mg, calcium, vitamin D, dyazide one capsule twice daily, and Neurontin 300 mg three times daily. The neurologist noted, "He does have some leg restlessness at night with a lot of cramping. However, he has been getting increasingly active doing multiple chores around the house, gardening, and exercising. He is able to lift eight pounds. He has noticed continued easy bruising and bleeding. He continues to have severe tingling in hands and feet, which he finds quite distracting. On exam he is able to walk, which he could not do previously. He is just barely able to rise on toes. He can walk a few steps with the toes lifted off the ground. There is marked diminution of vibratory sense at the great toe, mild to moderate at the ankles. He is aroflexic. He has a mild foot drop on walking, but he is able to compensate for this." The neurologist's impression was "The pt is doing much better. He continues to have some steroids related side effects." The neuralogist reduced the prednisone dosage to 30 mg alternating with 10 mg, asked the pt to reduce plasmapheresis to two times every six weeks, and increased the Neurontin dosage. The pt returned to the neurologist on 05/22/2001. "He generally is doing well. He is now able to walk and finds his hands have improved significantly. He has a dull sensation in the hands, tingling and paresthesias in the calves and feet and occasional shooting pain in the feet." On examination, "He does walk with a waddling gait and a tendency to a foot drop,but he is able to walk clearing the floor with his toes or walk on his heels. He is areflexic. There is significant less of vibratory sense at the left great toe and ankle, as well as the right great toe. Sensation at the right ankle is almost normal." The neurologist reduced the prednisone dosage to 30 mg alternating with 0 mg, and increased the neurontin dosage to 300 mg three times daily. The pt was seen by the neurologist on 08/02/2001. "He has been doing quite well, although he stillneeds plasmapheresis at roughly four weeks intervals. His strength overall is improving steadily. he notes a lot of numbness and pins and needles paresthesias in the feet, as well as occasional lancinating pain. He has been diagnosed as having rheumatoid arthritis." The pt was seen by neurologist on 10/16/2001. "He feels he has been doing well. On his last visit I started him on Klavil 25 g. He now sleeps soundly and is relatively pain free until about noon." The most recent report info received on 02/19/2002, indicated that the chronic inflammatory demyelinating polyneuropathy had improved "substantially," but persisted as of 12/18/2001. Foot discomfort also persisted. Pharmacy records indicated that the pt had not received insulin for 11 months. He had not received treatment for yeast infectons for 13 months. The outcomes of the atrophy, depresion, compressionfractures, and edema were not specified. The most recent info, received on 03/22/2002, indicated that leg pain, weakness, loss of function, and decreased sensation persisted as of 02/13/2002. The follow-up states that there were no known drug allergies. To the vaccinee's knowledge, there was no family history of Parkinson's disease, Alsheimer's disease, motor neuron disease, myasthenia gravis, multiple sclerosis, neuromuscular diseases, thyroid disease, lupus or rheumatoid arthritis. On 04/03/2002, medical records were received from a neurologist at a care center, who evaluated the vaccinee as on unspecified date. This neurologist indicated thatt he vaccinee "is seeing me as a second opinion. In mid-July 2000, the pt awoke with low back pain. He says that several days later he noted that there was tingling and cold in his feet and the back pain continued. He noted the onset of floppiness of his feet, right being worse than left. He says that this followed in mid-August by tingling in his hands. He fell several times about 08/12/2000 and was seen by a neurologist. He was hospitalized, and the diagnosis of Guillain Barre was made and was given intravenous immunoglobulin. The pt states that the numbness in the feet gradually spread proximally to the knees over approximately a week. This then ascended to the hip level after a following week and after that, it went up to the mid-abdominal level. There was weakness gradually progressive in teh legs, and he had problems arising from the toilet and getting out of a sofa. Following the intravenous immunoglobulin, he was no worse although he did not notice any improvement. He began to use a walker at that time for ambulation. He has had rehabilitation, however, the tingling and weakness have remained about the same, but he thinks perhaps they may have actually worsened. Despite the rehab, his strength has lessened especially in his legs and his endurance has gotten significantly worse. He also has ha dproblems with grip strength which may have improved with exercise although he is not clear about this. The leg strength he believes is clearly worse. The pt denies problems with bowel or bladder functions, and he has been quite depressed. He uses Serzone 200 mg per day for the depression." Later in the document, the neurologist listed the nefazodone dosage as 200 mg twice daily. The neurologist wrote, "on neurological examination, the mental status shows an emotional lability and anxiety. He is otherwise normal. On motor examinations, there is weakenss of the back flemors and extensors. There is also some ataxia noted on finger-nose-figner testing, however, it is even hard for him to hold his arms up therefore making the ataxia testing somewhat unreliable. Rapid alternating movements as judged by finger tapping is normal, and toe tapping is relatively normal though limited by weakness. The range of motion is markedly decreased because of weakness. The gait shows bilateral foot drops, and the pt uses a walker, and he has problems with back support and seems to be falling somewhat forward. The pt is unalbe to tendon walk as he needs a walker, and he has na unsteady gait and some tremor which is probably related to his weakness. There are Habinski sings noted, and the deep tendon reflexes are absent throughout. There is decreased vibration in soft tissue up to the thighs and to the wrists soft tissue. Pin and cold are normal. Proprioception is decreased in the fingers and abnormal to the level of the ankles. There are after sensations noted to the mid-shin level and also to the level of the wrists. On muscle strength testing, there is moderate weakness proximally and somewhat more exaggerated distally although this is somewhat spotty in the upper extremities. They are relatively symmetrical in the lower extremities. The weakness, again is more proximally although it is somewhat spotty. The worst areas appear to be the hip flaxors which are 3 to 4/5 bilaterally and also the finger and wrsit extensors which again are -4. The ankle dorsiflexors are also -4 as are the knee flexors and extensors. There are no fasciculations noted, and there is no atrophy noted. The reflexes are absent throughout. Neck flexion is weak as is extension although this is only mild. The facial muscles are normal strength. The impression is that the pt has CIDF or chronic inflammatory demyelinaitng polyradiculoneuropathy. On 04/03/2002, did not provide the outcome or the reported events. The pt was evaluated at a pain management center on 11/16/2001. Medications at that time included prednisone 15 mg every other day, Glucotrol XL 10 mg daily. Actos 30 mg daily, Celexa 30 mg twice daily, Prinivil 5 mg daily, neurontin 800 mg daily, Dyaside once daily, Mumulin R sliding scale as needed, desipramine 10 mg daily, anitriptyline 25 mg daily, multivitamin and mineral supplement, vitamin E, and calcium carbonate. The pain psecialist's impression was "painful polyneuropathy secondary to a number of otiologics including his history of diabetes and CIDP." The physician recommended discontinuation of desipramine, tapering of Neurontin until it was discontinued, increasing the amitriptyline dossage to 50 mg at night, consolidation of antidepressant medications and the application of lidocaine patches to the soles of both foot two to four times daily. On 12/19/2001, the pain specialist recommended tha tLidodern patches tbe applied at night and that lidocaine/prilocaine cream be applied to the soles and dorsol aspects of the feet four times daily. The amitriptyline dosage was increased to 75mg daily at bedtime. The vaccinee returned to the pain specialist on 03/06/2002. The pt reported that "raising his amitriptyline dosage to 75 mg only made him sleepy without any additional benefit from a pain control point of view. Therefore, I am going to start him on Lamictal 25 mg twice daily." The pt was to take amitriptyline 50mg daily at bedtime. The most recent info received on 04/11/2002, indicated that painful polyneuropathy persisted as of 03/04/2002. Info received on 03/22/2002 indicated that leg pain, weakness, loss of function, and decreased sensation persisted as of 02/13/2002. Of the thoracic spine MRI, the radiologist wrote, " Screening thoracic spine MRI shows no evidence of cord compression or central spinal stenosis. No definite focal disc herniation is identified. There are degenerative disc changes." Of the lumber spine MRI, the radiologist wrote, "Screening lumber spine examination shows diffuse lumbar spaadylosis, most marked at the L4-5 and L5-S1 levels, where there may be mild central spinal stenosis. There are diffuse degenerative disc changes. No definite focal disc herniation is identified." Bilateral sensorineural hearing loss, that was "mild sloping to severe" (01/25/1999) and palmar fasciectomy of the right palm and ring finger(1999). The most recent info, received 05/28/02, did not specify the outcome of the reported events. On 08/24/01, the pt was seen by the pediatrist for a chief complaint of thick and elongated toenails. His current medications included prednisone, Glucotrol, Actos, Celexa, Prinivil, dyazide, Neurontin, Humulin and Fosamax. The pt was not physically active. The neurologic examination revealed diminished sharp/dull and two-point discrimination, but the pt does have 5.07 monofilament wire sense. pt had cavus foot type with rearfoot valgus noted upon weight bearing. biomechanical examination revealed muscle strength testing was 5 out of 5 in all cardinal planes. There were noted some contractures to all lesser digits of the right lower extremity. X-ray examination revealed severe degenerative joint disease to the first metatarsophalangeal joint and the proximal interphalangeal joint of the hallux noted bilaterally. The impression was diabetes mellitus and anychomyocosis. The pt's nails were debrided. *Follow-up report on 10/10/02: The vaccinee was evaluated by an oncologist/hematologist on 9/26/01 "regarding a possible monoclonal gammopathy". The MD stated that serum protein clactrophoresis and immunoclectrophoresis were performed in July 01, and "revealed the presence of an IgG lambda gammopathy. IgG was 337, IgA 113, and IgM 94. I saw him in consultation on Sept. 26, 01. He felt well. Paresthesias in his feet persisted. He noted no fever, swollen glands, abdominal pain, weight loss, nor night sweats. He has had chronic low back pain due to vertebral compression fractures. He stated he is pherosod once per month. His last pherosis was 3 weeks previously." The MD noted that the vaccinee's "medical history was notable for... rheumatoid arthritis (but his rheumatoid factor is negative)." Medications included prednisone 20 mg every other day, glipizide (Glucotrol XL), pioglitazone (Actos), citalopram (Celexa), lisinopril (Prinivil), gabapentin (Neurontin), triamtorone/ hydrochlorethieside (Dryside), regular human insulin (Rumulin R), naproxan (Neprosyn), alendronate (Posamax), amitriptyline, multivitamin, vitamin E, bioflavinoids/ vitamin C (Ester? C), mathyloebalamino, calcium carbonate/ cholecalciferol (OsCal 500 + D), and ferrous sulfate (slowFe). Serum protein electrophoresis and serum protein immunoelectrophoresis were repeated. The MD stated, "I could not confirm the presence of monoclonal gammopathy upon re-evaluation in [the facility's] lab. His IgG level is minimally depressed. This may well be related to his steroid therapy and pharesis." On 10/11/01, a variety of merologies for Lyme disease were performed. The lab's overall interpretation was "no evidence of seroreactivity beyond that expected from Lyme vax." The PT was seen by the 2nd neurologist on 10/16/01. "He feels he has been doing well. On his last visit I started him on Elavil (amitriptyline) 25 q hs [at bedtime]. He now sleeps soundly and is relatively pain free until about noon." Other medications included prednisone 20 mg every other day, Neurontin 800 mg twice daily, and Dyazide. The PT "has been able to stretch his pheresis to every 5 wks. However, by that point he had developed a lot of pain, tingling and progressive weakness." On exam, he was able to walk on heels and toes, as well as, tandem. "Romberg is quite unsteady." The neurologist reduced the prednisone dosage to 15 mg every other day, reduced the Neurontin dosage to 400 mg twice daily, and added nortriptyline (Pamelor) 10 mg at mid-day. On 11/16/01 the vaccinee was seen by a 2nd rheumatologist. The rheumatologist reported that the PT's complaint was "diffuse joint pains" (this event was not reported as an adverse event due to vax admin, but was found during the course of review of the vaccinee's medical records). The PT had informed the rheumatologist that "this has been going on for approx 1-1.5 yrs and had started in his kness, hands, and feet". The PT had seen another rheumatologist who Dx'd him w/"possible rheumatoid arthritis and concomitant osteoarthritis". The other rheumatologist had "treated him w/delecoxib (Celebrex) which was not helpful and then was treated w/prednisone which did help to some degree. The MD exam revealed "a fair appearing male w/a slow gait". Exam of the "KEENT" was unremarkable. His visit showed pain w/flexion and palpation. There was slight arepitus of the knees. The feet revealed some downward protrusion of the matatersal heads. Lab data included a negative rheumatoid factor, normal C-reactive protein (CRP) and sedimentation rate." The rheumatologist believed "this PT has multifactorial pain. There is some degree of osteoarthritis, particularly in the knees. His neuropathic disease is also contributing, but there seems to be no evidence of an inflammatory connective tissue disease. At this time, I would recommend continued pain control w/his Neurontin as well as tricyclics. He is also on prednisone 15 mg every other day, which does seem to be helping. He should, or course, continue the Focamax to prevent steroid-induced osteoperosis". The rheumatologist requested that he return approximately 2 mts to follow up on his pain. The PT was evaluated at a pain management center on 11/16/01. Medications at that time included prednisone 15 mg every other day, Glucotrol XL 10 mg daily, Actos 10 mg daily, ditalopram (Celexa) 30 mg twice daily (initiated by the PT's internist for the treatment of depression). Prinivil 5 mg daily, Neurontin 800 mg daily, Dyaride once dailly, Kumulin R sliding scale s needed, desipramine 10 mg daily, amitriptyline 25 mg daily, multivitamin and mineral supplement, vitamin E, and oslolum carbonato. The pain specialist's impression was "Painful polyneuropathy secondary to a number of etiologies including his history of diabetes and CIDF." The MD recommended discontinuation of dosipramine, tapering of Neurontin until it was discontinued, increasing the amitriptyline dosage to 50 mg at night, consolidation of antidepressant medications, and the application of lidocaine (Lidoderm) patches to the soles of both feet two to 4 times daily. The PT returned to the 2nd neurologist on 12/18/01. "He has been on 15 mg of prednisone every other day since Oct. and has been getting 3 pharceci 6 wks which he has tolerated well. He feels he is steadily improving. Last Christmas he was in a wheelchair. He is now quite ambulatory. He still has considerable foot discomfort... He was tried on a lidocaine patch, but he finds this bunches up in his shoes and is awkward to use. The Flavil? was doubled from 25 to 50 mg at night which he has tolerated, but it has not yet had an impact on his Sx's. He continues on Neurontin 800 mg daily... On sensory testing there is a significant loss of temperature perception to mid calf, a little worse in the right leg than the left. There is a marked, but incomplete loss of vibratory perception at the great toe bilaterally, mild to moderate at the ankles. Upper extremity reflexes are 1+ and symmetric, as are knee jerks. Ankle jerks are absent. Plantars are flexor. He is able to walk on heels and toes. Hamberg is quite unsteady. IMPRESSION & PLAN: The PT is doing substantially better than he was previously. He will drop his prednisone to 12 mg every other day and plan to drop it to 10 mg in about 4 wks. He will drop his Neurontin to 400 mg daily for the next week or 2. If his Sxs are no worse, he will continue to taper it off." On 12/19/01, the pain specialist recommended that Lidoderm patches he applies at night, and that lidocaine/prilocaine cream (EMLA cream) be applied to the soles and dorsal aspects of the feet four times daily during the day. The amitriptyline dosage was increased to 75 mg daily at bedtime. The vaccinee underwent physical therapy evaluation on 2/12/02. The vaccinee reported that "He received therapy last yr for strengthening and conditioning and was feeling better. He is currently ambulating around the house in short distances w/out assisted device. However, he does use a walker for outside or long term walking. His chief complaint is that of constant pain in the legs, weakness and loss of function. He states he has decreased sensation which gets worse distally. He cannot feel the bottom of his feet." The vaccinee was to receive physical therapy 3 times / week for 6-8 wks to "Increase flexibility, increase strength, increase endurance." The vaccinee stopped going to physical therapy after 7 sessions. The vaccinee returned to the pain specialist on 3/6/02. The PT reported that "Raising his amnitriptyline? dosage to 75 mg only made him sleepy w/out any add'l benefit from a pain control point of view. Therefore, I am going to start him on Lamictal [lamotrigine] 25 mg twice daily." The PT was to also take amitriptyline 50 mg daily at bedtime. Pharmacy records indicate that the PT was also treated w/zolpidem (Ambien) and taleplon (Sonata). On 4/3/02, medical records were received from a neurologist at a tertiary care center, who evaluated the vaccinee on an unspec'd date. This neurologist indicated that the vaccinee "is seeing me as a 2nd opinion. In mid-July 00, the PT awoke w/low back pain. He says that several days later he noted that there was tingling and cold in his feet and the back pain continued. He noted that onset of floppiness on his feet, right being worse than left. He says that this followed in mid-August by tingling in his hands. He fell severall times about 8/12/00 and was seen by a neurologist. He was hospitalized, and the Dx of Quillain-Barre was made and was given intravenous immunoglobulin... The PT states that the numbness in the feet gradually spread proximally to the knees over approx a week. This then ascended to the hip level after a following week, and after that, it went up to the mid-abdominal level. There was weakness gradually progressive in the legs, and he had prob's arising from the toilet and getting out of a sofa. Following the intravenous immunoglobulin, he was no worse although he did no notice any improvement. He began to use a walker at that time for ambulation. He has had rehab, however, the tingling and weakness have remained about the same, but he thinks perhaps they may have actually worsened. Despite the rehab, his strength has lessened especially in his legs and his endurance has gotten significantly worse. He also has had prob's w/grip strength which may have improved w/exercise although he is not clear about this. The leg strength he believes is clearly worse. The PT denies prob's w/bowel or bladder function, and he has been quite depressed. He uses Serzone [nafazadone] 200 mg per day for the depression." Later in the document, the neurologist listed the nefazadone dosage as 200 mg twice daily. Other medications at the time of the evaluation included naproxen 500 mg twice daily, omeprazole 20 mg daily, gabapantin 400 mg three times daily, amlodipino 5 mg twice daily, glipizide 10 mg daily, and lisinopril 5 mg daily. The neurologist wrote, "On neurological exam, the mental status shows an emotional lability and anxiety. He is otherwise normal... On motor examination, there is weakness of the neck flexors and extensors. There is also some staxia noted on finger-nose-finger treating, however it is even hard for him to hold his arms up therefore making the ataxis testing somewhat unreliable. Rapid alternating movements as judged by finger tapping is normal, and toe tapping is relatively normal though limited by weakness. The range of motion is markedly decreased because of weakness. The gait shows bilateral foot drops, and the PT uses a walker, and he has prob's w/back support and seems to be falling somewhat forward. The PT is unable to tandem walk as he needs a walker, and he has an unsteady gait and some tremor which is probably related to his weakness. There are Babinski signs noted, and the deep tendon reflexes are absent throughout. There is decreased vibration in soft tissue up to the thighs and to the wrists soft tissue. Pin and cold are normal. Proprioception is decreased in the fingers and abnormal to the level of the ankles. There are alter sensations noted to the mid-shin level and also to the level of the wrists. On muscle strength testing, there is moderate weakness proximally and somewhat more exaggerated distally although this is somewhat spotty in the upper extremities. They are relatively symmetrical in the lower extremities. The weakness, again, is more proximally although it is somewhat spotty. The worst areas appear to be the hip flexors which are 3 to -4/5 bilaterally and also the finger and wrist extensors which, again, are -4. The ankle dorsiflexors are also -4 as are the knee flexors and extensors. There are no fasciculations noted, and there is no atrophy noted. The reflexes are absent throughout. Neck flexion is weak as ix extension although this is only mild. The facial muscles are normal strength. The impression is that the PT has CIDP or chronic inflammatory damyelinating polyradiouloneuropathy." On 5/17/02, the PT was seen by the pediatrist. The PT c/o'd of "blueness of right leg" and was sent for vascular evaluation "as soon as possible." The most recent info, received 9/24/02, did not specify the outcome of the reported events. Info. received on 4/11/01 indicated that painful polyneuropathy persisted as of 3/6/02. Info received on 3/22/02 indicated that leg pain, weakness, loss of function, and decreased sensation persisted as of 2/13/02. Info received from the PT's spouse on 2/23/01 indicated that, as of 1/31/01, the PT was "profoundly disabled." Info received on 2/19/02 indicated that the chronic inflammatory demyalinating polyneuropathy had improved "substantially", but persisted as of 12/18/01. Pharmacy records indicated that the PT had not received insulin for 11 mts. He had not received treatment for yeast infections for 13 mts. The most recent info, received on 10/1/03, indicated that the pt was "stable" and "has very little pain" as of 3/6/03. Information received from the pt's spouse on 2/23/01 indicted that, as of 1/31/01, the pt was "profoundly disabled." Pharmacy records indicated that the pt had not received insulin for 11 months. He had not received treatment for yeast infections for 13 months. Report 2001003273-1 describes chronic inflammatory demyelinating polyneuropathy in 60-year-old male who received from news service reports, the patient's spouse, and as part of lit