Cognitive dysfunction

The majority of chronic Lyme patients suffer with some degree of cognitive dysfunction.  The term “brain fog” is commonly used. Patients don’t feel as sharp. It becomes difficult to think clearly. Short term memory and working memory are poor. Finding words, completing sentences becomes difficult. Patients feel like they have the sudden onset of ADD (attention deficit disorder). Patients frequently experience disorientation and confusion and a long list of other symptoms. 

It has been suggested that all patients with “neuro-lyme” should be given IV antibiotics. This is not realistic since most patients have brain symptoms. Spirochetes may cross the blood brain barrier within days of infection.

Coinfections alter the clinical p

icture and must be dealt with separately, in specific ways.

Cognitive changes may correlate with white matter spots seen on brain MRI or with poor blood perfusion on nuclear medicine SPECT scans.  

Cognitive symptoms for the most part are due to inflammation, not permanent structural damage; so, in most cases, these symptoms are reversible with appropriate therapy. 

In most cases I like to start with oral antibiotics, ones that are effective against the pleomorphic forms of Borrelia (round body forms and others), and ones that pass the blood brain barrier.  I will talk about treatment in a subsequent BLOG. 

Unfortunately many patients get worse with treatment: we refer to this as a brain Herxheimer reaction. 

The best thing to do may be to hold antibiotics for several days and then restart at a lower dose, as tolerated.    Intravenous glutathione, (only IV), and I have tried all other forms, liposomal, oral, intranasal and even rectal is the only form that works. Glutathione (GTH) when it works, can seem like magic.  HBOT, hyperbaric oxygen therapy can be very effective. I have also found that Welchol works for some patients. 

Welchol is interesting. Being in the field (of chronic Lyme doctors), early on I was told that Welchol and related drugs remove biotoxins.  This is plainly incorrect. The important biotoxin, quinolinic acid (QUIN), does not cross the blood brain barrier. QUIN binds to NMDA receptors, it promotes action of the neurotransmitter NMDA. Drugs that antagonize NMDA are well known to many. These drugs include phencyclidine (angel dust and others). In the Lyme brain the opposite is happening. Excessive activation of NMDA receptors causes (glutamate-excito-toxicity) with increased cell death, associated with a wide spectrum of neurodegenerative disorders, including Alzheimer’s disease.

It turns out that bile acids, thought to be detergents to emulsify fat have neuro-regulatory function. Cholesterol also has neuro-regulatory effects. Welchol may help neuro-inflammation by unanticipated mechanisms.

Other drugs which help moderate the effects of QUIN include the mood stabilizer Lamictal and the Alzheimer’s drug Namenda. Both have a role in the treatment of QUIN toxicity.

It is perfectly OK to treat symptoms as the patient heals. A word of caution with depression: SSRIs, typically used for depression may have a paradoxical effect in the “Lyme brain.” Lamictal, discussed above may be effective. Also, Wellbutrin may be better tolerated. 

Stimulants are very effective for ADD symptoms as well as for fatigue, including: Ritalin, Adderall and others. 

Brain fog and cognitive problems (a patient told me she felt her brain is broken) hopefully improve, incrementally, over time, with active treatment, supportive therapies with an active effort not to make sure the patient does not become worse.  (Do no harm)

Although I do not like to start with IV antibiotics, if patients show no improvement after 4-6 months, and I am sure the diagnosis is correct, it is time to consider IV antibiotic therapy.