Daily persistent headache after viral illness during a worldwide pandemic ...: Lessons from 1890 Russian/Asiatic flu, 2020, Rosen

Dolphin

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https://journals.sagepub.com/doi/full/10.1177/0333102420965132

New daily persistent headache was first documented in the medical literature in the 1980s. The leading trigger is a viral illness. As we navigate our way thru the current SARS-CoV-2 pandemic, looking back at past viral epidemics may help guide us for what to expect in the near future in regard to headaches as a persistent manifestation of the SARS-CoV-2 infection. The 1890 viral pandemic known as the “Russian or Asiatic flu”, has extensive documentation about the neurologic sequelae that presented months to years after the pandemic ended. One of the complications was daily persistent headache. There are actually many similarities between the viral presentation of the 1890 pandemic and the current SARS-CoV-2 pandemic, which may then suggest that not only will NDPH be part of the neurological sequelae but a possible key consequence of the SARS-CoV-2 infection.

Keywords New daily persistent
headache
, viral pandemic, Russian flu, SARS-CoV-2, neurasthenia, headache
 
As stated, one of the main neurologic sequelae of influenza was the syndrome of neurasthenia. Typically, the neurasthenic symptoms would start along with or just after resolution of the acute phase of influenza and could last for months to years after the onset of the infection (12,17). Multiple treatises were written on this condition from the late 1890s through the mid-1900s. In Cobb’s (12) text from 1920, he remarked that the majority of individuals with neurasthenia give a history of this “dread disease, often in a severe form. It [influenza] is so common a precursor that we can say that this malady maybe regarded as an extremely frequent and potent source of Neurasthenia.” He points to the 1890 pandemic as the first time influenza was connected to neurasthenia, or post-influenza debility as it was also called.
The majority of NDPH sufferers have hypermobility issues (20). Recent studies in patients with Ehlers-Danlos syndrome (the most common form of hypermobility) have demonstrated an alteration in inflammatory/pain modulation genes including CFD, AQP9, COLEC12, KCNG5, PRLR; thus, a possible predisposing factor for an abnormal immune response in the hypermobile population to infections (21). Fascinatingly, sufferers who developed chronic daily headache after the 1890 viral pandemic may also have demonstrated hypermobility. Bouveret (22), Cobbs (12) and others noted two physical subtypes who suffered from post influenza debility. One group was tall and thin and who had low blood pressure, while a second group was well-fed and robust. The former group was the one who developed frequent headaches, lethargy, insomnia and had signs of hyperalgesia on exam (“any pain he suffers is out of proportion to its cause”) after the viral infection (12). Thus, there is the tall, lanky appearance that is noted in the majority of the hypermobile NDPH patients and their predisposition for hypotension and autonomic dysfunction, which is a hallmark of patients with joint hypermobility/Ehlers-Danlos syndrome (20,23).
 
The majority of NDPH sufferers have hypermobility issues (20)

Reference

Rozen, TD, Roth, JM, Denenberg, N. Cervical spine joint hypermobility: A possible predisposing factor for new daily persistent headache. Cephalalgia 2006; 26: 1182–1185.

The objective of this study was to suggest that joint hypermobility (specifically of the cervical spine) is a predisposing factor for the development of new daily persistent headache (NDPH). Twelve individuals (10 female, 2 male) with primary NDPH were evaluated by one of two physical therapists. Each patient was tested for active cervical range of motion and for the presence of excessive intersegmental vertebral motion in the cervical spine. All patients were screened utilizing the Beighton score, which determines degree of systemic hypermobility. Eleven of the 12 NDPH patients were found to have cervical spine joint hypermobility. Ten of the 12 NDPH patients had evidence of widespread joint hypermobility with the Beighton score. Based on our findings we suggest that joint hypermobility, specifically of the cervical spine, may be a predisposing factor for the development of NDPH.

Obviously the citation is misleading, as 12 patients with no controls can't define the majority of ndph sufferers, probably over-reps women and will all have come through the same clinic (rozen). But, I wil have to find a sci-hub to read this full paper. I was aware of a vague link of hEDS to NDPH, though obviously much weaker than what is suggested here, not the cci reference.
 
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Rozen summarizes more of his ideas here. https://sci-hub.se/https://doi.org/10.1111/head.13624 (2019 publication)

The suggestion is that in some cases there is "cervicogenic irritation" due to cervical hypermobility in some subset. However, he does not reference fusion surgery as a treatment.

Their headache is speculated to be the result of an exacerbation of this underlying upper cervical facet syndrome induced by the cervical hyperextension occurring during intubation and the neck positioning during surgery. In younger patients who develop this subtype of NDPH, they are more likely to have an underlying cervical hypermobility syndrome and thus secondary underlying cervical facet irritation and/or atlantoaxial irritation going into their procedure. The same situation occurs with dental and otolaryngology procedures and even at the hairdresser where neck extension for prolonged periods leads to trigeminocervical activation in those individuals who already have baseline cervical facet/atlantoaxial irritation.

Interestingly, he frequently references intubation surgeries as a cause of some ndph, which reminded of Brea's thyroid surgery and development of CCI symptoms.

This NDPH subtype on examination should demonstrate significant upper cervical facet, GON, and sometimes C1-2-based irritation. This NDPH subtype has shown a significant improvement with cervicogenic-based treatments including: medications (muscle relaxants combined with anti-inflammatories), onabotu-linum toxin A injections, and directed high cervical spine-based pain anesthesia procedures including: upper cervical facet injections (C2-4), C2 dorsal root ganglia injections, and C1-2 localized injections.1

Other subsets are thought to include post-viral that does not respond to treatment as well as increased/decreased CSF or cerebral hypovlemia which can be treated accordingly.

Not that most neurologist still treat ndph as the headache type it most resembles (migraine/tension) and use the drugs accordingly, with a generally low success rate.

Rozen does claim here that
he majority of NDPH patients have cervical and systemic hypermobility,
but his reference is the same 2006 study.
 
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I've had a diagnosis of NDPH from a number of years ago, as I developed a new-onset headache with the infection that led to my developing ME, and the headaches were serious enough for me to request a neurology referral. After an MRI to exclude secondary headache and after trying a number of standard migraine treatments, I was referred to one of the UK's few headache centres where that diagnosis was replaced by one of NDPH.

Interestingly, the headache-specialist neurologist I've seen - before I became housebound - has told me on more than one occasion that he suspects an overlap between NDPH and "CFS". Apparently, he has a number of patients with a history of novel headache of post-infectious onset with both ME/CFS and NDPH diagnoses being made. Perhaps this is just a curio of referral bias - an artifact of unusual cases being referred to tertiary-care clinics - or perhaps there is something more to it.

It seems that NDPH is not usually diagnosed outside specialist headache clinics, ordinarily being attributed by GPs or general neurologists to chronic migraine or (if mild and lacking in migrainous features) chronic tension-type headache.

For me, headache is merely one of the many - and definitely not the most serious - symptoms of ME, and I've always associated headaches more with the PEM state. I was surprised by the seriousness with which the NDPH diagnosis was treated in the clinic I attended.

As far as I know, the location, character, nature and duration of headaches in ME - although anecdotally severe headaches are very common for us - is not particularly well-surveyed save for this Ravindran et al. paper. NDPH is not mentioned in that paper, but it is from 2011, and the previous ICHD-2 criteria for NDPH (that were in use prior to 2013) were far more restrictive and excluded patients with headaches that had migrainous features.

I'd be interested to know how many ME and long-COVID patients have developed headaches that meet the current ICHD-3 criteria for NDPH.
 
The 1890 viral pandemic known as the “Russian or Asiatic flu”, has extensive documentation about the neurologic sequelae that presented months to years after the pandemic ended. One of the complications was daily persistent headache.

It's not clear to me whether by "neurologic sequelae that presented months to years after the pandemic ended" they mean "continued to present" or "first presented" - months to years after the pandemic ended.

I developed really severe daily persistent headaches beginning only several months after the infection that led to the onset of ME/CFS. It was part of the continuing decline during the first six months after onset. It's hard to describe how relentless and intense these headaches were. They seemed to shrug off any pain relievers that I threw at them. It was probably the most torturous period of the initial decline. It lasted about two months and then it just let up and stopped as mysteriously as it had begun.

I don't have any hypermobility issues so far as I know, although I can lock my thumb joints (but not my finger joints) as in this admittedly disturbing image.

hand.jpg
https://en.wikipedia.org/wiki/Hypermobility_(joints)
 
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