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Monday, April 6, 2009

Long term follow up of patient treated by IDSA standards and then ILADS standards

A 15 year old female was seen in August 2007. She complained of pain and swelling of the knees. She recalled a recent tick bite with a rash behind one knee. She had effusion of both knees. There was a previous history of Lyme disease presenting as acute monoarticular arthritis of a knee treated in 2003. Since 2004 she had been treated for ADD. At the time of this presentation other symptoms included fatigue- for years, numbness and tingling and decreased concentration (ADD).

She has been a patient in our practice since 2002 for general primary care.
In 2003 she she complained of right knee pain for 5 days. She had been growing rapidly at that time and running at school. The patient and her mother suggested this is a cause of her knee pain. Her right knee had effusion, increased temperature and painful range of motion. Laboratory tests for the known causes of monoarticular arthritis were obtained.

The Lyme ELISA test showed an index of 5.8.(normal below 1.1). Lyme WB showed 10/10 IgG bands and 0/3 IgM bands. A colleague prescribed 14 days of Ceftin. She did not follow up as instructed. 5 weeks later she returned with ear pain and was treated with Amoxicillin for 10 days for otitis media. Two days into the Amoxicillin therapy she returned with recurrent knee pain. She was treated with Naproxyn for "post-Lyme" residual joint pain. Six months later she received a course of Zithromax for bronchitis. I think it is of interest that many children with Lyme disease receive courses of antibiotics for various other infections such as ear infections, sore throats and sinusitis in short bursts over a period of months and years. It is not known how these therapies impact the natural history of the illness.

Three months later the patient requested a referral to a psychiatrist for evaluation and counseling. I have no follow data regarding that treatment.

A month later an associate prescribed low dose Minocin for acne. She took it for about one month.

Five months later she was prescribed a Z-pack for a respiratory infection.

10 months later she had received no further antibiotics. She returned for a routine physical at age 14. It was noted that the psychiatrist had prescribed Ritalin for ADD and that this had been helpful. It was also noted that there was a family history of ADD.

Over the next several months she was prescribed brief courses of Zithromax and Augmentin for respiratory infections. And then she saw me with recurrent knee pain as discussed above. Lab work obtained at that time showed: Lyme WB 10/10 IgG bands, IgM positive 23 band (previously absent). B12 was 259- on the low side and folate was 5.0- low. Vitamin D ratio was reversed 32/60. The C6 peptide index was very elevated- 9.6.

She was initially treated with Cipro and Ceftin. She improved and then got worse. She described more pain, tingling, fatigue and memory loss. She was treated with Amoxicillin, Biaxin and Plaquenil. After 6 weeks of oral antibiotic therapy she developed new neurological symptoms which caused a great deal of alarm. She had a loss of sensation from the knees down and was having difficulty walking. The exam confirmed a dense peripheral neuropathy and weakness of the lower limbs.
The picture was that of an evolving acute autoimmune demyelinating neuropathy of the Guillain Barre type. She was immediately started on IV Rocephin. The oral Biaxin and Plaquenil were continued.

Two weeks later she was improved. She had improved sensation in her legs and the weakness had resolved. The exam showed only mild abnormalities.
I cannot explain the rapid improvement. I can propose theories: 1) Neurotoxins caused the deficits and rapidly dissipated with therapy (seems unlikely) or 2) The autoantibodies generated by Lyme infection had not yet caused structural damage to the myelin sheath of neurons- the autoimmune, inflammatory process had caused only temporary dysfunction in neurons at risk; the process was aborted before permanent or long term damage could occur.(I like this theory). She received 30 days of IV antibiotics and was then converted to oral antibiotics. She continued to slowly improve over the next 4 months and was then "lost to follow up".

She returned 5 months later with a full blown relapse. Now she had increased numbness and tingling, pain and the forgetfulness and cognitive dysfunction which had become much worse. This is a strange phenomenon. Patients who stop therapy prematurely can present with cognitive deficits which appear significantly worse than those present before the initiation of treatment. I cannot propose a theoretical basis for this effect. Now the SPECT showed hypoperfusion of the left frontal lobe.

Over the next 4 months she was treated with a panoply of oral medications covering the spectrum of Lyme and TBD co-infections. Everything was better except her cognitive dysfunction.

She had severe global cognitive deficits. She was doing very poorly at school. Her short term memory was severely impaired. Her "processing" was severely impaired and she was very inattentive.

IV Rocephin was begun again. This was combined with oral Minocin.

Now- after 9 weeks, her cognitive functions have returned 100%. An amazing result.

The Rocephin will be continued for a total of at least 12 weeks- and then followed with courses of potent oral anti-Borrelia antimicrobial therapy. This time she has agreed to fully comply with my instructions.

It also looks like the "ADD" is large gone. She is weaning off stimulants. A future SPECT scan will hopefully show normalization.

As previously noted: ADD and Lyme neuroborreliosis are both classically associated with hypo-functioning of the frontal lobes. I makes sense that the symptoms of both disorders would overlap.

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