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Unremitting head and neck pain (UHNP) is a commonly encountered phenomenon in Headache Medicine and may be seen in the setting of many well-defined headache types. The prevalence of UHNP is not clear, and establishing the presence of UHNP may require careful questioning at repeated patient visits. The cause of UHNP in some patients may be compression of the lesser and greater occipital nerves by the posterior cervical muscles and their fascial attachments at the occipital ridge with subsequent local perineural inflammation. The resulting pain is typically in the sub-occipital and occipital location, and, via anatomic connections between extracranial and intracranial nerves, may radiate frontally to trigeminal-innervated areas of the head. Migraine-like features of photophobia and nausea may occur with frontal radiation. Occipital allodynia is common, as is spasm of the cervical muscles. Patients with UHNP may comprise a subgroup of Chronic Migraine, as well as of Chronic Tension-Type Headache, New Daily Persistent Headache and Cervicogenic Headache. Centrally acting membrane-stabilizing agents, which are often ineffective for CM, are similarly generally ineffective for UHNP. Extracranially-directed treatments such as occipital nerve blocks, cervical trigger point injections, botulinum toxin and monoclonal antibodies directed at calcitonin gene related peptide, which act primarily in the periphery, may provide more substantial relief for UHNP; additionally, decompression of the occipital nerves from muscular and fascial compression is effective for some patients, and may result in enduring pain relief. Further study is needed to determine the prevalence of UHNP, and to understand the role of occipital nerve compression in UHNP and of occipital nerve decompression surgery in chronic head and neck pain.

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The presence of extracranial fibers arising from meningeal nociceptors, and the demonstration of extracranial pathology in the form of inflammation, may address the question as to why centrally-directed treatment for migraine are so often ineffective. The standard pharmacological treatment for CM or CTTH has traditionally been centrally acting agents that reduce neuronal excitability, such as anti-convulsants and anti-depressants [8]; however, adherence to such treatment regimens is low, indicating low efficacy, at least for some patients [16, 17]. Similarly, behavioral interventions such as Cognitive Behavioral Therapy, while highly effective for some individuals [18, 19], often do not provide adequate and prolonged headache reduction. As a result of inadequate efficacy of these centrally-directed treatments, several treatments directed at the extracranial portion of the head and neck have been increasingly incorporated into the practice of headache medicine over the last decade. Such treatments include occipital nerve blocks [20], trigger point injections [20], botulinum toxin injections [21], and more recently, the use of monoclonal antibodies targeting the calcitonin gene related peptide pathway acting mostly outside of the blood-brain barrier [22].

We speculate that while triptan agents may be effective for the acute exacerbations of frontal, trigeminally-mediated pain, the unremitting pain in the neck and occiput often does not respond to such acute interventions; nor does the UHNP generally respond well to centrally directed, membrane stabilizing agents such as anti-convulsants. Peripherally directed treatments such as steroid injections to the occiput in the form of trigger point injections or occipital nerve blocks, as well as botulinum toxin and monoclonal antibodies directed at CGRP, may provide temporary benefit for the UHNP caused by occipital nerve compression. Surgical decompression of the occipital nerves may provide more enduring relief of pain.

It is important and helpful to distinguish the symptoms of UHNP associated with ON compression from the condition of Occipital Neuralgia as defined in the ICHD [3]. Occipital Neuralgia is defined as pain that has two of the following three characteristics: [1] recurring in paroxysmal attacks lasting from seconds to minutes; [2] severe in intensity; [3] shooting, stabbing or sharp in quality. The pain is associated with dysesthesia and/or allodynia, and either tenderness to palpation of the nerve or its branches, or the presence of tender trigger points at the emergence of the GON. The pain must also be temporarily eased by an anesthetic block of the GON.

Longitudinal studies can provide stronger evidence of causality than cross-sectional studies. However, the longitudinal studies reviewed were generally short in duration, usually with only two measurement points, one or two years apart [35, 40, 44, 50, 58]. They were all observational in nature, with no control groups, and with limited measurement of the level of participation and frequency or duration of sport activities. All studies were based on surveys conducted through schools, with participation in sport and other extracurricular activities reported mainly in binary categories.

Transverse relaxation can be understood by remembering that the net magnetisation is the result of the sum of the magnetic moments (spins) of a whole population of protons. Immediately after the rf pulse they rotate together in a coherent fashion, so that as they rotate they continuously point in the same direction as each other within the xy plane. The angle of the direction they point at any instant is known as the phase angle and the spins having similar phase angles are said at this initial stage to be 'in phase' (Figure 4). Over time, for reasons explained in a moment, the phase angles gradually spread out, there is a loss of coherence and the magnetic moments no longer rotate together and they are said to move 'out of phase'. The net sum of the magnetic moments is thus reduced, resulting in a reduction in the measured net (transverse) magnetisation. The signal that the receiver coil detects (if no further rf pulses or magnetic field gradients are applied) is therefore seen as an oscillating magnetic field that gradually decays (known as a Free Induction Decay or FID). There are two causes of this loss of coherence. Firstly, the presence of interactions between neighbouring protons causes a loss of phase coherence known as T2 relaxation.

This arises from the fact that the rate of precession for an individual proton depends on the magnetic field it experiences at a particular instant. While the applied magnetic field Bo is constant, it is however possible for the magnetic moment of one proton to slightly modify the magnetic field experienced by a neighbouring proton. As the protons are constituents of atoms within molecules, they are moving rapidly and randomly and so such effects are transient and random. The net effect is for the Larmor frequency of the individual protons to fluctuate in a random fashion, leading to a loss of coherence across the population of protons. i.e. the spins gradually acquire different phase angles, pointing in different directions to one another and are said to move out of phase with one another (this is often referred to as de-phasing). The resultant decay of the transverse component of the magnetisation (Mxy) has an exponential form with a time constant, T2, hence this contribution to transverse relaxation is known as T2 relaxation (Figure 4). As it is caused by interactions between neighbouring proton spins it is also sometimes known as spin-spin relaxation. Due to the random nature of the spin-spin interactions, the signal decay caused by T2 relaxation is irreversible.

Gradient echoes are generated by the controlled application of magnetic field gradients. Magnetic field gradients are used to produce a change in field strength and hence a corresponding change in Larmor frequency along a particular direction. When a magnetic field gradient is switched on it causes proton spins to lose coherence or de-phase rapidly along the direction of the gradient as they precess at different frequencies. This de-phasing causes the amplitude of the FID signal to rapidly drop to zero (Figure 5). The amount of de-phasing caused by one magnetic field gradient can however be reversed by applying a second magnetic field gradient along the same direction with a slope of equal amplitude but in the opposite direction. If the second gradient is applied for the same amount of time as the first gradient, the de-phasing caused by the first gradient is cancelled and the FID re-appears. It reaches a maximum amplitude at the point at which the spins de-phased by the first gradient have moved back into phase, or 're-phased'. If the second gradient then continues to be applied, the FID signal de-phases and disappears once more. The signal that is re-phased through the switching of the gradient direction is known as a gradient echo. The time from the point at which the transverse magnetisation (the FID) is generated by the rf pulse, to the point at which the gradient echo reaches it's maximum amplitude is known as the echo time (abbreviated TE). This can be controlled by varying the timing of the applied magnetic field gradients. If the echo time is chosen to be longer, more natural T2* de-phasing occurs and the maximum echo amplitude becomes smaller. In practice, the TE is set by the MR system operator (in milliseconds) as it determines, amongst other things, the influence of T2* on the image contrast.

First, the resonance of protons is confined to a slice of tissue. This is done by applying a gradient magnetic field at the same time as the rf excitation pulse is transmitted (Figure 7). The frequency of the rf pulse corresponds to the Larmor frequency at a chosen point along the direction of the applied gradient. The result is for resonance only to occur for protons in a plane that cuts through that point at right angles to the gradient direction, effectively defining a slice of tissue. This process is known as slice selection and the gradient is known as the slice selection gradient, GS. The orientation of the slice is determined by the direction of the applied gradient known as the slice selection direction (in the example of Figure 7 this is the z-direction). Rather than just a single frequency, the transmitted rf pulse is comprised of a small range of frequencies, known as the transmit bandwidth of the rf pulse. This gives the slice a thickness. The thickness of the slice is determined by the combination of the rf pulse bandwidth and the steepness (or strength) of the gradient. 041b061a72

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