pattismith
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Update in the understanding of new daily persistent headache - Kuan-Po Peng, Todd D Rozen, 2023 (sagepub.com)
Triggers:
Triggers:
Common triggers include infectious episodes or stressful life events
The earliest record of NDPH-like headache after an infectious episode can be traced back to 1890 after the Russian/Asiatic flu.
Headache was a complaint in 75–83% of the patients during the acute stage, and some of the patients (the exact number unknown) developed a long time subsequent headache that mimics NDPH (26).
Infectious episodes as triggers, such as Epstein-Barr virus or Salmonella/E. Coli infection has been mentioned in the early NDPH series before the introduction of the S-L Criteria when both primary and secondary causes were not differentiated (4,5).
The infectious triggers are not restricted to specific pathogens. Bordini and Valença (27) reported three possible cases of NDPH in 450 patients with Dengue fever.
More recently, approximately half of the patients infected with COVID-19 developed headaches during the acute stage (28).
Some patients developed persistent headaches after the resolution of the acute episodes, (29,30), among which some fulfilled the ICHD-3 diagnostic criteria of NDPH (29).
The second most reported trigger is stressful life events, up to 26% in some series (8).
However, stress is even more often reported as a trigger for migraine attacks (31) and is highly unspecific and easily falsely attributed.
On the contrary, some NDPH triggers are not common but highly specific and remain rarely reported in other headache disorders.
These triggers suggest a possible link to the mechanism that triggers persistent headache.
In a large NDPH-series (n = 97), Rozen (18) reported nine patients with NDPH-like headaches after surgical interventions that required intubation.
Cervical spine joint hypermobility was reported in 11 of 12 NDPH patients in another earlier report (32).
Both combined suggest a possible cervicogenic etiology in a subset of NDPH patients.
Valsalva event as a trigger has been reported in another seven NDPH patients.
None of them had papilledema, and four had a normal weight.
Therefore, idiopathic intracranial hypertension is less likely, but idiopathic intracranial hypertension without papilledema can only be excluded with a proper cerebrospinal fluid (CSF) pressure monitor, while a single spinal tap may fall in the normal range (<25 cm CSF) in 40% of these patients (33).
Typical treatment options for intracranial hypertension, such as acetazolamide, reduced the headache frequency by more than 90% in five of seven patients (34), suggesting an abnormal distribution or equilibrium of CSF may also link to typical NDPH phenotypes.
All the distinct triggers, each accounting for a small proportion of NDPH patients, suggest that NDPH is probably a syndrome with various mechanisms, instead of a homogenous disease (see below).