The Role of the Trigemino Cervical Complex in Chronic Whiplash Associated Headache: A Cross Sectional Study

Abstract

Objective To investigate signs of central sensitization in a cohort of patients with chronic whiplash associated headache (CWAH). Background Central sensitization is one of the mechanisms leading to chronicity of primary headache, and thus might contribute to CWAH. However, the pathophysiological mechanism of CWAH is poorly understood and whether it is simply an expression of the primary headache or has a distinct pathogenesis remains unclear. Thus, the factors involved in the genesis of CWAH require further investigation. Methods Twenty‐two patients with CWAH (20 females, 2 males; age 25–50 years, mean age 36.3 years) and 25 asymptomatic participants (13 females, 12 males; age 18–50 years, mean age 35.6 years) rated glare and light‐induced discomfort in response to light from an ophthalmoscope. Hyperalgesia evoked by a pressure algometer was assessed bilaterally on the forehead, temples, occipital base, and the middle phalanx of the third finger. The number, latency, area under the curve, and recovery cycle of nociceptive blink reflexes elicited by a supraorbital electrical stimulus were also recorded. Results Eight and 6 CWAH patients had migrainous and tension‐type headache (TTH) profiles, respectively; the remainder had features attributable to both migraine and TTH. Patients in the whiplash group reported significantly greater light‐induced pain than controls (8.48 ± .35 vs 6.66 ± .43 on a 0–10 scale; P = .001). The CWAH patients reported significantly lower pressure pain thresholds at all sites. For stimuli delivered at 20 second intervals, whiplash patients were more responsive than controls (4.8 ± .6 blinks vs 3.0 ± .6 blinks in a block of 10 stimuli; P = .036). While R2 latencies and the area under the curve for the 20 second interval trials were comparable in both groups, there was a significant reduction of the area under the curve from the first to the second of the 2‐second interval trials only in controls (99 ± 8% of baseline in whiplash patients vs 68 ± 7% in controls; P = .009). The recovery cycle was comparable for both groups. Conclusions Our results corroborate previous findings of mechanical hypersensitivity and photophobia in CWAH patients. The neurophysiological data provide further evidence for hyperexcitability in central nociceptive pathways, and endorse the hypothesis that CWAH may be driven by central sensitization.

The tongue after whiplash: case report and osteopathic treatment

“…We know that there is a mechanical hypersensitivity after whiplash, with hyperexcitability in central nociceptive pathways via trigeminal reflex (the lingual nerve is part of the trigeminal system, and the hypoglossal nerve is connected to the trigeminal system). 14 We can speculate that the osteopathic treatment improves the receptorial mechanical response, reducing the hyperexcitability that leads to pain.…”

Misperception of Visual Verticality in Patients with Primary Headache Disorders: A Systematic Review with Meta-Analysis

“…Patients with TTH are known to present with oculomotor disturbances, including a reduction in the speed of smooth pursuit and saccadic eye movements [ 13 ]. These oculomotor disturbances are related to dysfunction in the upper cervical structures [ 62 ], which may cause headaches owing to the convergence of cervical and trigeminal afferent fibers at the trigeminal–cervical complex [ 17 ]. The integrity of the oculomotor system is essential for correctly estimating verticality, as tilts of the visual vertical are often associated with the components of an ocular tilt reaction (OTR) [ 63 ].…”

“…Furthermore, vestibular dysfunction and non-specific balance disturbances have also been widely linked to headaches, despite the origin of their concomitance being unknown [ 14 , 15 , 16 ]. It is possible that a sensitization process at the trigeminal level may be the link that allows observation of the concomitance previously mentioned [ 9 , 17 , 18 ].…”

Post-traumatic cephalalgia

“…Epidural hematoma with expansion 5 days to 3 weeks post-trauma have also been described (Illingworth and Shawdon, 1983) This likely explains why cervicalgia following whiplash must be evaluated and treated to prevent secondary activation of the TCC which may cause aggravation of headache disorders such as migraine (Bartsch, Goadsby, 2003) due to promulgation of trigeminal system hypersensitivity as well as spread and referral of pain. Trauma that may occur with cervical whiplash may also induce migraine headaches through a yet unknown mechanism that may involve the trigeminocervical complex (Watson, Drummond, 2016). Whiplash injuries to the cervical spine also (Tyburski, Cheng, Assari, et al, 2017;Zasler, Etheredge, 2020).…”