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fqtoxicity · 8 months

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New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/fluoroquinolone-associated-pseudotumor-cerebri/

Fluoroquinolone Associated Pseudotumor Cerebri

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What is pseudotumor cerebri?

Pseudotumor cerebri (PTC) literally means “false brain tumor.” Medical professionals also called PTC idiopathic intracranial hypertension (IIH). I would like to redefine PTC not only to include intracranial hypertension (IIH) but also intracranial hypotension as well. PTC occurs when there is a pressure abnormality inside the skull due to poor regulation of the cerebrospinal fluid (CSF) causing a buildup, reduction, or poor absorption of the CSF. Furthermore, I believe anecdotal data has shown that the fluoroquinolones (FQ) can induce either transient or chronic osmoregulatory dysfunction.

The IIH version of PTC is considered to be rare by medical professionals and the hypotension version of PTC is considered ‘uber’ rare. The latter being so rare that you would probably get laughed out of a doctor’s office for even suggesting it, despite the fact that it does show up in the medical literature. IIH, or the hypertension version, has more medically documented cases and causes therefore it is more known to the medical field, albeit still uncommon Intracranial hypotension, is almost always associated in the medical literature with a leak in the dura, and almost all medical professionals will not consider other causes such as osmoregulatory dysfunction.

However, one thing that has become abundantly clear to me over the last 15 years (sesquidecade) is that nothing with FQAD is actually that rare and PTC (hyper and hypo) is no exception. I have documented several anecdotal cases of PTC of both the hyper and hypo varieties.

Most cases of PTC do not get reported due to their transient nature, thus the reason for lack of awareness. Additionally, there have been patients with chronic symptoms who have gone years before getting any acknowledgement of the validity of their symptoms.

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What is Cerebrospinal Fluid?

CSF is a clear, colorless, watery fluid that flows in and around your brain and spinal cord. It is made by tissue called the choroid plexus in the ventricles (hollow spaces) in the brain.

CSF acts like a cushion that helps protect your brain and spinal cord from sudden impact or injury. The fluid also removes waste products from the brain and helps your central nervous system work properly. The CSF that is produced in the brain eventually is absorbed into the bloodstream at a rate that usually allows the pressure in your brain to remain constant in a finely balanced system that we take for granted.

If this delicate system becomes unbalanced several symptoms can appear.

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Symptoms of PTC can include:

Severe headaches and/or feelings of intense head pressure (hyper & hypo).

Abnormal pressure sensations in the ear, that can cause a whooshing sound (hyper).

Muffled hearing that may pulse with your heartbeat (hypo).

Nausea, vomiting or dizziness (hyper & hypo).

Vision loss (hyper)

Brief episodes of blindness, lasting a few seconds and affecting one or both eyes (hyper)

syncope (hyper & hypo)

Difficulty seeing to the side (hyper)

Double vision (hyper & hypo)

Seeing light flashes (hyper & hypo)

Neck, shoulder or back pain (hypo)

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PTC and Fluoroquinolones

PTC is associated with the members of the FQ family of pharmaceuticals. Although considered ‘rare’ by the medical community, anecdotal data suggests that this adverse event is not really that rare within the scope of the FQs and should probably be considered a class adverse event.

PTC was first reported in the quinolone family of drugs in 1966 when a nine-year-old girl, who was being treated by nalidixic acid, the grandfather drug of today’s fluoroquinolones, experienced the adverse event while being treated for a urinary tract infection subsequent to an automobile injury (1). In 1998 twenty cases of Nalidixic acid-induced PTC were documented in children who were being treated for acute dysentery (2).

A scholarly search will return numerous case reports of PTC associated with all members of the FQs, including the modern family members of levofloxacin, ciprofloxacin, ofloxacin, and others. The exact pathogenesis of PTC from FQs remains unclear just like many of the other adverse events from this family of antibiotics (3).

Recent studies such as “Oral fluoroquinolones and risk of secondary pseudotumor cerebri syndrome: Nested case-control study” from 2017 conclude that oral FQ usage poses a risk of PTC but it is very rare (5).

The problem with studies such as these is that they miss the non-reported cases which I believe account for the majority. Most doctors are very reluctant to report FQ-related adverse events and unfortunately, the burden falls back on the FQ community to keep track of events the best we can.

It is also unreasonable to limit the FQ’s ability to impact CSF too narrowly. Besides the more common intracranial hypertension, many cases of intracranial hypotension, and encephalopathy have been reported.

Cases of reversible encephalopathy have been reported as far back as 1966. In 2013 a 16-year boy who was being treated for pneumonia developed encephalopathy and CNS symptoms after starting Cipro. It was theorized that the pathogenesis of his adverse event was a failure of cerebral auto-regulation (6).

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Anecdotal Data

Over the years there have been numerous individuals who have experienced CSF pressure issues as just one of the many adverse event symptoms associated with FQ exposure. Thankfully, it appears that most cases of PTC seem to be of a transient nature and resolve on their own, still, there is a subset in the FQ community who are plagued with CSF pressure issues indefinitely, and some of the symptoms can be very incapacitating. Mayo Clinic’s data agree in an indirect fashion when on their website they state that PTC can resolve on its own but can also recur months or years later (4).

Over the last decade, anecdotal reports of CSF issues have included symptoms of intermittent diffuse headaches, some headaches worse in the evening or at night, and often aggravated by sudden movement. Visual disturbances include visual obscurations, blurred vision, double vision, and photophobia. Diplopia is sometimes reported as well and it is believed to be secondary to toxicity of the sixth cranial nerve.

Other symptoms reported are brain fog, lethargy, irritability, neck stiffness, tinnitus, dizziness, clumsiness, chronic fatigue, and paresthesia.

It should be noted that in anecdotal cases of FQ-induced intracranial hypertension, there have been more reports of optic disk nerve swelling (papilledema) as opposed to intracranial hypotension. It appears in FQ-induced hypertension cases visual acuity is usually preserved, helping to distinguish acute papilledema from optic neuritis, something else that can also be caused by FQ’s direct toxicity.

In FQ-induced intracranial hypotension, more noticeable auditory disturbances have been reported as opposed to FQ-induced hypertension.

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Craniocervical instability

Although not the direct subject of this article, it is necessary to mention craniocervical instability (CCI) due to the overlap and dovetailing of symptomatology between the CCI/CSF issues and the FQs.

CCI is a pathological condition of increased mobility at the craniocervical junction, the area where the skull meets the spine. In CCI the ligamentous connections of the craniocervical junction can be stretched, weakened, or ruptured impacting the brain and brainstem.

CCI is very complex and can cause a variety of serious symptoms including debilitating fatigue and weakness and is outside the diagnostic scope of most medical professionals. CCI has been implicated in certain forms of Chronic fatigue (ME). CSF pressure issues can also mimic some of these same symptoms and/or be directly related and connected to CCI. In other words, there is a large overlap in symptomatology in which pressure issues could be the result of CCI, or there could be an underlying/undiagnosed CCI condition in cases of brain pressure abnormalities.

In some cases of FQAD, symptoms of CCI are believed to be triggered by FQs causing connective tissue weakening. It has been shown in research and overwhelming anecdotal evidence that FQs upregulate matrix metalloproteinases (MMPs) and degrade collagen. This leads to increased collagen degradation and weakening of the tendons and connective tissue and could easily cause CCI (7). FQAD, CCI, and ME have overlapping symptomology and in some cases, all are present in certain cases.

In the near future, I will address CCI as it pertains to FQs.

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Choroid Plexus

Side view of head and brain showing cerebrospinal fluid.

The choroid plexus (CP) is a network of blood vessels and cells in the ventricles (fluid-filled spaces) of the brain. The blood vessels are covered by a thin layer of cells that make CSF.

Over the last decade, some conversations with FQAD-impacted individuals have led me to suspect a metabolic imbalance caused by the FQs impacting the CP. It is clearly known in academic research and in overwhelming community data that FQs negatively impact mitochondria. It is also known that without sufficient mitochondrial energy production, the active ion transporters in CP cannot operate normally and produce CSF properly (8). Researchers with Alzheimer’s disease have found that improper functioning CP cells are deficient in the mitochondrial enzyme cytochrome c oxidase and complex IV of the electron transport chain (9).

There are specific genes involved in the active transport of ions (along with the obligatory transport of H2O) from blood to the ventricular lumen of the CP. These are the final pathway of CSF production and are considered rate-limiting genes. In other words, these genes control how much or not enough CSF fluid is produced. The main genes that code for Na–K-ATPase and the Na–K–Cl cotransporter would be of interest final secretory pathway.

The work of the Na/K pump is the most fundamental process of life because it consumes 20% to 50% of the ATP produced. This regulation depends on the ability of the mitochondria to produce ATP which drives the Na/K pump. In the case of sustained oxidative stress initiated by the FQs, the NA/K pumps cannot function because ATP production is lowered. The normally operating cells switch states to a permanent stress adaptation and in turn, impact the final path of CSF production.

As I have pointed out time and time again, the FQs have the ability to reach every area of the body and the CP is no exception. Since a larger majority of PTC cases resolve on their own, it would stand to reason that these PTC cases are occurring during a spike in oxidative stress (ROS). However, the FQs can raise ROS for extended periods of time, in some cases for many years, or indefinitely. These long-term changes impact the methylation of DNA resulting in epigenetic changes. In some individuals, these changes could impact the CP.

The FQ’s ability to alter changes in CSF through impact on the CP is just one way, out of many, in which the FQs can brain physiology.

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Conclusion

If you believe you are suffering from one of these conditions options are currently limited. This is another one of those areas where there are very few experts and the patient usually becomes more well-versed in the medical condition than the doctor. There are patient groups where the members are making headway by seeing certain select doctors who specialize in these rare areas of healthcare.

Facebook Groups:

Tarlov Cysts – https://www.facebook.com/groups/971580869576257

ME/CFS+ Brain and Spine – https://www.facebook.com/groups/1353765701467793

Spinal Leak Support – https://www.facebook.com/SpinalCSFLeakSupport

Spinal Leak Foundation – https://www.facebook.com/Spinal.CSf.Leak.Foundation

Pseudotumor cerebri IIH – https://www.facebook.com/groups/247197510096871

Although I have had contact with several individuals with intracranial hypotension post FQs, there is no support group for this malady. Certain health centers like Mayo Clinic Rochester and Duke have specialists who deal with these issues, however, they will always approach the situation as if there is a CSF leak present. Intracranial hypotension caused by an mitochondrial or metabolic dysfunction is considered very, very rare, with Mayo Rochester having seen one case. That doesn’t mean they don’t exist however as logic would dictate if medical science sees cases of metabolic intracranial hypertension, then conversely cases of metabolic intracranial hypotension should exist as well, and they do.

Brain pressure abnormalities, both hyper and hypo, can sometimes be imaged with MRI and CT. Also, I will concede that a good local neurologist can probably aid with intracranial hypertension and PTC, but most cannot comprehend and/or deal with hypotension or CCI.

Let me throw in the caveat that most doctors/neurologists/surgeons only associate intracranial hypotension with trauma to the dura. Their training and experience don’t allow a differential diagnosis to include causes other than a noticeable leak in the dura such as Tarlov cysts, venous fistulae, metabolic imbalances, and especially epigenetic changes wrought by the FQs. Be careful, this is an area where an uninformed doctor can cause more harm than good, so proceed with absolute caution

PTC and the associated dovetailing conditions can be chronic or acute. Some cases can indeed be severe medical emergencies and require evaluation to rule out other causes such as tumors, acute trauma, etc. When in doubt consult with a trusted medical practitioner or advisor.

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References

1. Boréus LO, Sundström B. Intracranial hypertension in a child during treatment with nalidixic acid. Br Med J. 1967 Jun 17;2(5554):744-5. doi: 10.1136/bmj.2.5554.744. PMID: 6025983; PMCID: PMC1841777.

2. Riyaz A, Aboobacker CM, Sreelatha PR. Nalidixic acid induced pseudotumour cerebri in children. J Indian Med Assoc. 1998 Oct;96(10):308, 314. PMID: 10063299.

3. Fernando RR, Mehta NN, Fairweather MG. Pseudotumor cerebri and ciprofloxacin: a case report. J Med Case Rep. 2011 Mar 16;5:104. doi: 10.1186/1752-1947-5-104. PMID: 21410941; PMCID: PMC3069949. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069949/

4. https://www.mayoclinic.org/diseases-conditions/pseudotumor-cerebri/symptoms-causes/syc-20354031

5. Sodhi M, Sheldon CA, Carleton B, Etminan M. Oral fluoroquinolones and risk of secondary pseudotumor cerebri syndrome: Nested case-control study. Neurology. 2017 Aug 22;89(8):792-795. doi: 10.1212/WNL.0000000000004247. Epub 2017 Jul 28. PMID: 28754842.

6. Ali WH. Ciprofloxacin-associated posterior reversible encephalopathy. BMJ Case Rep. 2013 Apr 11;2013:bcr2013008636. doi: 10.1136/bcr-2013-008636. PMID: 23585504; PMCID: PMC3645815. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645815/

7. Tsai WC, Hsu CC, Chen CP, Chang HN, Wong AM, Lin MS, Pang JH. Ciprofloxacin up-regulates tendon cells to express matrix metalloproteinase-2 with degradation of type I collagen. J Orthop Res. 2011 Jan;29(1):67-73. doi: 10.1002/jor.21196. PMID: 20602464. https://pubmed.ncbi.nlm.nih.gov/20602464/

8. Kant, S., Stopa, E.G., Johanson, C.E. et al. Choroid plexus genes for CSF production and brain homeostasis are altered in Alzheimer’s disease. Fluids Barriers CNS 15, 34 (2018). https://doi.org/10.1186/s12987-018-0120-7

9. Cottrell D, Blakely E, Johnson M, Ince P, Turnbull D. Mitochondrial enzyme-deficient hippocampal neurons and choroidal cells in AD. Neurology. 2001;157:260–4. https://doi.org/10.1212/wnl.57.2.260.

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#Cerebrospinal Fluid #CFS/ME #FQAD

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