Cephalalgia

Headache (HA) following traumatic brain injury (TBI) is common, but predictors and time course are not well established, particularly after moderate to severe TBI.

A prospective, longitudinal cohort study of HA severity post-TBI was conducted on 450 participants at seven participating rehabilitation centers. Generalized linear mixed-effects models (GLMMs) were used to model repeated measures (months 3, 6, and 12 post-TBI) of two outcomes: HA density (a composite of frequency, duration, and intensity) and HA disruptions to activities of daily living (ADL).

Although HA density and ADL disruptions were nominally highest during the first three months post-TBI, neither showed significant changes over time. At all time points, history of pre-injury migraine was by far the strongest predictor of both HA density and ADL disruptions (odds ratio (OR) = 8.0 and OR = 7.2, averaged across time points, respectively). Furthermore, pre-injury non-migraine HA (at three and six months post-TBI), penetrating-type TBI (at six months post-TBI), and female sex (at six and 12 months post-TBI) were each associated with an increase in the odds of a more severe HA density. Severity of TBI (post-traumatic amnesia (PTA) duration) was not associated with either outcome.

Individuals with HA at three months after moderate-severe TBI do not improve over the ensuing nine months with respect to HA density or ADL disruptions. Those with pre-injury HA, particularly of migraine type, are at greatest risk for HA post-TBI. Other independent risk factors are penetrating-type TBI and, to a lesser degree and post-acutely only, female sex. Individuals with these risk factors should be monitored and considered for aggressive early intervention.

To explore a possible differential effect of sumatriptan on extracerebral versus cerebral arteries, we examined the superficial temporal (STA), middle meningeal (MMA), extracranial internal carotid (ICA_extra), intracranial internal carotid (ICA_intra), middle cerebral (MCA) and basilar arteries (BA).

The arterial circumferences were recorded blindly using high-resolution magnetic resonance angiography before and after subcutaneous sumatriptan injection (6 mg) in 18 healthy volunteers.

We found significant constrictions of MMA (16.5%), STA (16.4%) and ICA_extra (15.2%) (p ≤ 0.001). Smaller, but statistically significant, constrictions were seen in MCA (5.5%) and BA (2.1%) (p ≤ 0.012). ICA_intra change 1.8% was not significant (p = 0.179). The constriction of cerebral arteries was significantly smaller than the constriction of extracerebral arteries (p < 0.000001).

Sumatriptan constricts extracerebral arteries more than cerebral arteries. We suggest that sumatriptan may exert its anti-migraine action outside of the blood–brain barrier.

While cross-sectional studies have shown associations between migraine and depression, few studies have been able to evaluate the association between migraine and incident depression.

A prospective cohort study among 36,016 women without a history of depression enrolled in the Women's Health Study who provided information about migraine and headache at baseline. Women were classified as either having nonmigraine headache, migraine with aura, migraine without aura, past history of migraine or no history of headache. Cox proportional hazards models were used to evaluate the association between migraine and headache status and incident depression.

At baseline, 5115 women reported a history of nonmigraine headache, 1805 reported migraine with aura, 2723 reported migraine without aura, and 1896 reported a past history of migraine. During 13.8 mean years of follow-up, 3833 new cases of depression occurred. The adjusted relative risks of incident depression were 1.44 (95% CI: 1.32, 1.56) for nonmigraine headache, 1.53 (95% CI: 1.35, 1.74) for migraine with aura, 1.40 (95% CI: 1.25, 1.56) for migraine without aura, and 1.56 (95% CI: 1.37, 1.77) for past history of migraine compared to no history of headache.

Middle-aged women with migraine or nonmigraine headache are at increased risk of incident depression. Frequent migraine attacks (weekly or daily) were associated with the highest risk for developing depression.

The aim of this study was to evaluate the angiotensin II receptor antagonist candesartan as prophylactic medication in patients with episodic cluster headache.

This study comprised a prospective, placebo-controlled, double-blind, parallel-designed trial performed in seven centres in Scandinavia. Forty (40) patients with episodic cluster headache (ICHD-2) were recruited and randomised over a five-year period to placebo or 16 mg candesartan in the first week, and placebo or 32 mg candesartan in the second and third week.

The number of cluster headache attacks (primary efficacy variable) during the three-week treatment period was reduced from 14.3 ± 9.2 attacks in week 1 to 5.6 ± 7.0 attacks in week 3 (−61%) in the candesartan group and from 16.8 ± 14.1 attacks in week 1 to 10.5 ± 11.3 attacks in week 3 (−38%) in the placebo group. The difference between the candesartan and placebo group was not significant with the pre-planned non-parametric ranking test, but a post-hoc exact Poisson test, which takes into account the temporal properties of the data, revealed a significant result (p < 0.0001).

This was a negative trial. Post-hoc statistics suitable to describe the temporal changes in cluster headache indicate that conduction of future larger studies may be justified.

In a previous study we demonstrated that high-frequency oscillations (HFOs) elicited by median nerve stimulation are significantly correlated to clinical fluctuations of migraine. We aimed at verifying whether clinical fluctuations and HFO changes are correlated to N20 somatosensory evoked potential (SEP) recovery cycle, which is likely to reflect the functional refractoriness of primary somatosensory cortex neurons.

We analysed both HFOs and N20 SEP recovery cycle to paired stimulation in 21 migraine patients and 18 healthy volunteers.

Shortened recovery cycle correlated with low-amplitude HFOs as well as with clinical worsening. By contrast, prolonged recovery cycle correlated with enhanced HFOs, as well as with spontaneous clinical improvement.

In our migraine patients the strict relationship between presynaptic HFO amplitude and N20 recovery function suggests that changes of both parameters might be caused by modifications of the thalamo-cortical drive. Our findings suggest that the thalamo-cortical drive during interictal stages could fluctuate from abnormally high to abnormally low levels, depending on mechanisms which reduce cortical excitability in spontaneously improving patients, and increase cortical excitability in spontaneously worsening ones.

Supraspinal activity-dependent neuroplasticity may be important in the transition from acute to chronic pain. We examined neuroplasticity in a cortical region not considered to be a primary component of the central pain matrix in chronic tension-type headache (CTTH) patients. We hypothesised that neuroplasticity would be exaggerated in CTTH patients compared to healthy controls, which might explain (in part) the development of chronic pain in these individuals.

Neuroplasticity was examined following a ballistic motor training task in CTTH patients and control subjects (CS). Changes in peak acceleration (motor learning) and motor-evoked potential (MEP) amplitude evoked by single-pulse transcranial magnetic stimulation were compared.

CTTH patients showed significantly less motor learning on the training task than CS (mean acceleration increase 87% CTTH, 204% CS, p < .05), and CS but not CTTH patients showed a significant increased MEP amplitude following training (CS: F = 2.9, p < .05; CTTH: F = 1.6, p > .05).

These findings suggest a deficit in use-dependent neuroplasticity within networks responsible for task performance in CTTH patients which might reflect reciprocal influences between primary motor cortex and interconnected pain processing networks. These findings may help explain the positive effects of facilitatory non-invasive brain stimulation targeting motor areas on chronic pain and help elucidate the mechanisms mediating chronic pain.

Migraine attacks exclusively felt in the face are very rare, the pain involving the territories supplied by the second and third branches of the trigeminal nerve.

Two patients suffering from heminasal pain attacks accompanied with typical migrainous features and responsive to oral or intranasal triptans – but not to intranasal lidocaine or oxymetazoline. In one patient, the attacks could be precipitated upon slight touching on the tip of the nose, in the other attacks were preceded by the nasal sensation typically heralding sneezing.

Migraine pain mostly develops within the innervation territory of the first branch of the trigeminal nerve, which includes the nose. Therefore, episodes of unilateral nasal pain with migrainous features could be considered a migraine with unusual topography (nasal migraine). Painful nasal attacks occasionally preceded by stimulation of trigeminal afferents in the nose, could be conceived of as migraine-tic syndrome.