Starting Treatment for Late Stage Lyme Disease (Neuroborreliosis)

As most of my readers may know, I contracted Lyme disease in 2006 from an infected tick. It had crawled onto my scalp, and had a family member not seen it, I may have never known I’d been bitten. I’d always heard “there’s no Lyme in the South” so I didn’t think anything of it, but fast forward to 2009 and a Western Blot revealed possible exposure. Once the disease has advanced to the late stages, the bacteria hide in your organs and usually evade blood tests as well as the immune system, which is why regular labs didn’t yield results. Further testing via IGeneX, a specialty lab, gave confirmation.

The infection has spread many places due to my late diagnosis, but has attacked my nervous system in particular (neuroborreliosis) because Borrelia species really, really love the brain. The disease affects me–and many others in this situation–in ways similar to multiple sclerosis.

Late stage neuropsychiatric Lyme disease can best be conceptualized as a disseminated and progressive, (predominately sub-cortical), encephalopathy. Animal studies and autopsies have contributed to our understanding of the disease process. (25,26,27,28). As symptoms progress, additional symptoms occur and increase in severity.

These symptoms may be categorized in the following manner:

  1. Brain Stem
    • Cranial Nerve symptoms
    • Autonomic symptoms. Dysautonomia may be the result of involvement of brain stem, involvement of other parts of the autonomic nervous system, or end organ pathology – i.e.: migraine, temperature dysregulation, sexual dysfunction, bright light sensitivity, mitral valve prolapse, irregular pulse, neutrally mediated hypotension, asthma, non-ulcerative dyspepsia, irritable bowel, and irritable bladder
    • Hormonal symptoms: From the result of either hypothalamus or end organ involvement, i.e., thyroid disease, HPA axis dysregulation, decline of sex hormone functioning, hypoglycemia
    • Long track disconnection syndromes (very late in the progression of the disease)
    • Cerebellar symptoms
  2. Limbic system, greater limbic system, extended amygdala
    • Altered attention, emotional, and behavioral modulation
    • Pathological psychiatric syndromes
  3. Cortical (May be from either cortical or sub-cortical nuclei involvement)
    • Signature syndromes
    • Processing difficulties
  4. Peripheral Neuropathy”
The Neuropsychiatric Assessment of Lyme Disease, Robert Bransfield, M.D.

It is highly unlikely I will ever get rid of this disease, but today, I’ve begun the battle to keep whatever health I can.

My insurance is still trying to cover Tindamax, so until then (hopefully next next) I am on Flagyl. I took my first dose today, and I’m doing okay! The neuropathy I’ve experienced just being off my bartonella meds for one week (which were the only thing keeping the Lyme disease subdued enough so that it wouldn’t take over) is amazing. This disease truly is frightening, and I’m so glad to finally be on something to stop its progression!

[Update: January 1, 2013 – Edited some of the above because, well, things didn’t go as planned…]

a rainbow at night

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