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Retrieved 3 May Retrieved 30 January Archived from the original on 9 February Retrieved 14 December Retrieved 19 May Retrieved 18 December Retrieved 6 June The term disease is used when the nervous system damage is due to a neurological disorder such as stroke or peripheral diabetes neuropathy.

In peripheral neuropathic pain there is usually a mixture of damaged and undamaged axons within the peripheral nerve, leading to the clinical presentation with ongoing pain, sensory loss and sensory gain hyperalgesia, allodynia. The clinical presentation in central neuropathic pain is similar, but the mechanisms are less well understood.

Mechanisms of peripheral neuropathic pain include ectopic impulse generation, peripheral sensitization of undamaged nerve fibers, and central sensitization; the latter includes altered signal processing in the CNS due to changes in descending pain modulation. For this reason the exact prevalence of neuropathic pain is not yet known, but is expected to be high due to the high prevalence of the underlying neurological disorders. A range of clinical neurophysiological and functional imaging studies have suggested that migraine might be associated with cerebellar dysfunction.

These studies all had methodological short-comings to a greater or lesser extent. Therefore, it is still uncertain whether migraine is associated with cerebellar dysfunction, and, if so, to what extent and why. Recent anatomical studies demonstrated that the output of the cerebellum targets multiple non-motor areas in the prefrontal and posterior parietal cortex. Neuro-anatomy and functions of the cerebellum will be reviewed as well as the evidence of cerebellar infarcts in migraineurs.

During the last decades, the methods of neurophysiology proved to be very effective in disclosing subtle functional abnormalities of the brain of patients affected by primary headache disorders. These methods received several refinements during the last years, further improving our understanding of headaches pathophysiology. Abnormal increased responsivity was several times revealed with almost all the sensory modalities of stimulation in migraine between attacks, with its normalization during the attacks.

Recently, authors observed that the degree of some neurophysiological abnormalities might depends on the distance from the last attack, i. Somatosensory cortex lateral inhibition, gating, and interhemispheric inhibition were altered in migraine, and may contribute to cortical hyperresponsivity and clinical features. Cluster headache patients are characterized by a deficient habituation of the brainstem blink reflex during the bout, outside of attacks, on the affected side.

Evidence for sensitization of pain processing was disclosed by studying temporal summation threshold of the nociceptive withdrawal reflex, which was less modulated by supraspinal descending inhibitory controls. In conclusion, much has been discovered and much more needs to be investigated to better understand what causes, how it triggers, keeps and runs out recurrent primary headaches.

Clarifying some of these mechanisms might help in the identification of new therapeutic targets. Within the brain, neuropeptides can modulate the strength of synaptic signaling even at a relatively large distance from their site of release. Given the evidence for CGRP in migraine and potential roles for other hypothalamic peptides, it seems likely that altered neuropeptide actions may be a general theme underlying the heightened sensory state of migraine.

Towards this point, I will briefly discuss our preclinical CGRP and optogenetic studies using light aversive behavior in mouse models as a surrogate for migraine-associated photophobia. I will describe how both the brain and the periphery are susceptible to elevated CGRP and how CGRP appears to act by distinct mechanisms in these sites. These ideas will be tied together in a speculative model that integrates peripheral and central CGRP actions in photophobia. Classical trigeminal neuralgia TN is a unique neuropathic facial pain disorder. As there are no diagnostic tests to confirm the diagnosis, it relies on a thorough history and exam.

MRI is used to exclude symptomatic trigeminal neuralgia, not to confirm the diagnosis of TN. Knowing how to interpret MRI findings is of importance with respect to surgical treatment options and their expected chance of a successful outcome. TN is characterized by paroxysms of unilateral intense pain usually in the 2 nd and 3 rd trigeminal branch.

The pain quality is stabbing and the pain is typically evoked by sensory stimuli like light touch, brushing teeth, cold wind or eating. Up to half of the patients also have concomitant persistent pain. A smaller proportion of patients may have sporadic autonomic symptoms. The average age of disease onset is in the early fifties and TN is slightly more prevalent in women than in men. As a general rule, the neurological exam is normal in TN patients. As objective signs of TN, patients may wince at pain paroxysms and may avoid shaving or brushing their teeth on the affected side.

Some studies argue that a proportion of TN patients have subtle sensory abnormalities at bedside exam, primarily hypoesthesia. Studies using quantitative sensory testing also documented sensory changes in TN. Rather than indicating nerve damage, the findings may be explained by functional changes of the nervous system in response to severe pain. There is widespread consensus that TN is associated to a neurovascular contact between the trigeminal nerve and a blood vessel in the prepontine course of the nerve. Emerging advanced imaging studies confirms that at the site of a neurovascular contact on the ipsilateral side of pain, there is of demyelination — a process that seems to be reversible in some patients after successful surgery.

Imaging studies also consistently show that TN is strongly associated to a neurovascular contact with morphological changes of the trigeminal nerve, i.

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Meanwhile, only half of TN patients have morphological changes of the trigeminal nerve and there may be other unknown etiological factors causing TN. The pearls and pitfalls of TN diagnosis and neuroimaging is discussed from both a clinical and a scientific perspective. The first evidence for potential role of PACAP in pathomechanism of migraine was the intravenous administration of PACAP caused headache and vasodilatation in healthy subjects as well as in migraineurs, and lead to delayed-type migraine-like attacks [2].

Preclinical experiments revealed that both PACAP and PACAP were found elevated in the trigeminal nucleus caudalis of rats following electrical stimulation of the trigeminal ganglion or chemical stimulation by nitroglycerin of the trigeminovascular system [3]. A magnetic resonance imaging MRI angiographic study demonstrated that PACAPinduced headache was associated with prolonged dilatation of the middle meningeal arteries, but not of the middle cerebral arteries in healthy volunteers [4]. The recent functional imaging study pointed that intravenous PACAPinduced migraine attacks was associated with alterations in brain network connectivity [6].

Clinical investigation provided evidence of a clear association between migraine phases during a spontaneous migraine attack versus pain-free period and the alteration of plasma PACAP level [7]. The activation and sensitization of the trigeminovascular system by vasoactive neuropeptides might be crucial factors of the migraine pathogenesis [8]. The recent preclinical and clinical studies suggest the importance of PACAP as a future biomarker of migraine headache.

PACAP38 induces migraine-like attacks in patients with migraine without aura. Peripheral and central alterations of pituitary adenylate cyclase activating polypeptide-like immunoreactivity in the rat in response to activation of the trigeminovascular system. Investigation of the pathophysiological mechanisms of migraine attacks induced by pituitary adenylate cyclase-activating polypeptide A resting-state functional MRI study.

Alterations in PACAPlike immunoreactivity in the plasma during ictal and interictal periods of migraine patients.

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Several studies are found a relationship between headache and psychiatric comorbidity in both children and adolescents []. The most frequently described comorbidities include anxiety, mood disorders [1], sleep disorder [2] and attention hyperactive disorder [3]. The association between headache and comorbidities has been interpreted in the light of different possible causal pathways.

Psychiatric comorbidity may represent the consequence of a link between neurotransmitter systems involved in migraine and psychiatric disorder, such as depression and anxiety [4]. A central role is thought to be played by serotonergic receptors, adrenergic and dopaminergic D2 receptor genotype, that seem to be associated with migraine, major depression, generalized anxiety disorder, panic attacks and phobia [5].

It has been suggested that the patient's vulnerability to anxiety disorders and affective disorders as well as migraine might be attributed to the dysregulation of the serotonergic system [6]. Furthermore, it is possible that each disorder increases the risk of the other [4;7]. Therefore, the relevance of other mediating factors for the co-occurrence of headache and psychiatric comorbidity has to be taken into consideration.

Recent research found that an insecure attachment may be a risk factor for an outcome of poor adaptation that includes chronic pain [9] and that pain perception may change in relation with specific attachment styles. The ambivalent attachment seems to be the most common style among patients reporting high attack frequency and severe pain intensity and in children with this attachment style there is a relationship between high attack frequency and high anxiety levels [10].

Although more studies are needed in order to detect the biological, genetic and environmental mechanisms underlying the relationship between headache and comorbidities, attachment styles can be regarded as one of the factors mediating this association [12]. Anxiety, depression and behavioral problems among adolescents with recurrent headache: The relationship between sleep and headache in children: Headache and attention deficit and hyperactivity disorder in children: Migraine and psychiatric comorbidity: Association of 5-HTT gene polymorphisms with migraine: J Neurol Sci ; Headache and comorbidity in children and adolescents.

J Headache Pain ; Genetic and environmental influences on migraine: J Clin Psychol ; 67 9: Attachment styles in children affected by migraine without aura. Behavioural problems in children with headache and maternal stress: The role of attachment insecurity in the emergence of anxiety symptoms in children and adolescents with migraine: J Headache Pain In Press.

Metabolic syndrome and overweight are highly prevalent among migraineurs and the weight-loss was suggested as a useful strategy to improve both migraine and metabolic syndrome. Recently, we have observed that a particular version of VLCD characterized by very low-carbohydrate intake and Ketone bodies KBs production, named very low-calorie ketogenic diet VLCKD , was able to induce a rapid improvement of headache in migraineurs.

To assess if the favorable outcome on migraine was due to the caloric restriction, instead of KBs, we performed a double blind crossover study to compare headache modifications during a VLCD and a VLCKD in a population of overweighed and obese migraineurs. Among patients referred to the Sapienza University Obesity Clinic, a neurologist specializing in headache recruited 35 migraineurs.

Randomly patients started with one of the two diets according to the following scheme: To verify variations in headache frequency, we used as baseline the month before the first VLCD and the first transition diet. Out 35 enrolled patients, six dropped at the first month of diet: Headaches are one of the most disabling disorders [1]. Moreover, recent knowledge have suggested that physical examination for provocative procedures should be done on each patient with side- locked headaches as many of these headaches may closely mimic primary headaches [4].

There have been identified eleven physical tests to properly assess cervical disorders. When these dysfunctions are present, they support a reciprocal interaction between the trigeminal and the cervical systems as a trait symptom in migraine [6, 7]. In this presentation, an evidence based physical protocol of specific tests it will be provided by a physiotherapist to assess musculoskeletal disorders in the most common primary headaches as Migraine and Tension Type Headache.

Moreover, the integration of this examination in a multidisciplinary team it will be discussed. Migraine prophylaxis with drugs influencing the renin- angiotensin system. Prevalence of neck pain in migraine and tension-type headache: Temporomandibular disorders is more prevalent among patients with primary headaches in a tertiary outpatient clinic. Prakash S, Rathore C. The Journal of Headache and Pain ; International consensus on the most useful physical examination tests used by physiotherapists for patients with headache: Musculoskeletal dysfunction in migraine patients.

Headache represents the most common neurological symptom in pediatric age. Among the primary headaches, migraine is far more prevalent than tension-type headache and cluster headache. Though extremely rare at this age, also trigeminal autonomic cephalgias have been reported. The most frequent causes of pediatric secondary headaches are represented by respiratory tract infections, while potentially life-threatening diseases, such as brain tumors, are less common.

However, especially in the emergency setting, the possibility that a headache attack is due to a brain tumor must be always considered. To avoid missing these cases, some headache characteristics red flags have been identified [1]. However, while the most recent ICHD criteria improved the possibility to classify some patients, such as children with migraine with aura [2], they turned out to be unsuitable for others, such as young patients with primary headache. Several studies have shown the primary role played by psychological factors in determining the severity of migraine in children [4].

Therefore, a psychological examination is often mandatory, as part of the initial assessment of the patient. Lastly, when assessing a child with primary headache, possible comorbidities should be never forgotten, since addressing them can represent a crucial point for the treatment [5]. Headache as an emergency in children and adolescents. Curr Pain Headache Rep ; Diagnosis of primary headache in children younger than 6 years: Chronic Migraine in Children and Adolescents.

Headache and comorbidities in childhood and adolescence. Whether medication-overuse headache MOH represents a distinct biological entity within the concept of chronic daily headache with specific neurobiological and genetic background is still a matter of debate. A great deal of interest has been directed at understanding the neurophysiological mechanisms that underlie MOH pathogenesis.

Currently, two main, non-mutually exclusive hypotheses have been proposed. The first, stems from the apparent compulsive use of headache medications by MOH patients, and considers this disorder a sort of addiction to symptomatic remedies. The second shifts the focus from drug addiction to neural sensitization, claiming that triptan overuse triggers adaptations of the trigeminovascular system, thereby facilitating pain transmission and leading to a state of latent sensitization. Answering these questions might be relevant to better understand the neurochemical mechanisms prompted by acute headache medications that underlie the pathophysiology of MOH and of chronic headache in general.

In this presentation, preclinical data will be presented showing that chronic exposure to eletriptan or indomethacin alter trigeminal ganglion gene expression patterns broadly and to a similar extend. Remarkably, qualitative transcriptomic analysis reveals that prolonged exposure to the two different symptomatic drugs triggers almost identical, increased expression of various genes coding for proteins involved in headache pathogenesis such as neuropeptides, their cognate receptors, TRP channels, prostanoid and NO synthesizing enzymes.

These findings will be correlated with the clinical aspects of MOH.

The dramatic caloric restriction promotes the fat metabolism, mimicking the starvation, even if meals replacements ad hoc developed accounts for essential nutrients, avoiding the malnutrition. Because of the extreme caloric restriction, this type of diet is very effective in weight loss, however, that characteristic also is the main limit of VLCD, since it is possible to follow this kind of dietetic regimen for a very limited period usually weeks. According to macronutrients intake, it is possible to divide all the VLCDs in two sub-groups: Salads are allowed ad libitum dressed with a spoonful of olive oil.

Also in this kind of diet, there are meals per day, mainly consisting in meal replacement products. There is a growing interest in the ketogenic form of the VLCD because several studies have shown a higher compliance of patients with this diet. The reason of this higher adherence to the diet is still under scrutiny but several reasons are called in cause: The real impact of ketogenic diets in weight loss is still disputed; in fact, on the long period there are not differences between low-carb and low-fat diets in terms of weight reduction and regain of lost weight after the diet.

However, thanks to the higher compliance and the drastic caloric restriction, the VLCKDs seem to be a promising approach in the early management of obesity and in the preparation phase for patients that must undergo to bariatric or other types of surgical procedures. Temporomandibular disorders TMD represent the main cause of orofacial pain of non-dental origin and comprehend several disturbances of the masticatory system characterized by myofascial pain of masticatory muscles or articular pain localized in the pre-auricular area.

Moreover, TMD patients show temporomandibular joint sounds and deviation or limitation of the opening of the mouth.

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Myofascial pain is a probable consequence of central nervous system mechanisms of convergence and activation of second order neurons with enlargement of the receptive field, reduced pain threshold and allodinia. Often there are accompanying symptoms like facial pain and headaches. Headache is the most prevalent neurologic disorder, third most diffused health disturbance and the seventh cause of disability in the world.

It can be primary, without apparent organic cause, or secondary to other pathologies. Some epidemiological studies indicates that headache is more prevalent in TMD patients and TMD is more prevalent in subjects affected by headache. A stronger association exists between TMD and chronic migraine in comparison with other types of headache. Nevertheless the methodological quality of the available studies is not optimal and many of them classify patients with anamnestic questionnaire that tend to overestimate the values of prevalence.

A growing body of literature suggests that the association between headache and TMD may be a manifestation of a central sensitization mechanism. Temporomandibular joint and muscles receive the sensitive innervation of the trigeminal nerve that supply also the cranial vascular structures likely involved in the etiology of the headache. The sensitization of the trigeminal caudate nucleus by the TMD symptoms can favor the triggering of migraine episode.

Beside the epidemiological studies and the neurophysiologic hypothesis, there are some initial clinical evidence that show how severity of TMD symptoms parallels an increase of frequency and intensity of migraine and the simultaneous treatment of both conditions results in better outcomes.

From a clinical perspective, a comprehensive assessment based on a biopsychosocial approach can provide relevant information to plan a contemporaneous treatment of TMD and headache, together with an intervention targeted to the reduction of psychosocial conditions that can elicit and maintain mechanisms of central sensitization likely responsible of the comorbidity of TMD and headache. The exact pathophysiology is still unknown, but evidence supporting both peripheral and central mechanisms i. In fact, the frequency of headache attacks has found to be related to the level of central sensitization [4].

However, not all TTH patients present with the same level of central sensitization and clinical presentation, but subgroups need to be identified in order to offer specific therapeutic programs [5]. Prolonged peripheral nociceptive input from the pericranial, neck, and shoulder regions e. In fact, it has been found that sustained stimulation of TrPs may induce central sensitization in healthy participants [7].

The number of TrPs seems to be associated with the degree of widespread pressure pain hypersensitivity in TTH patients, supporting the role of TrPs on central sensitization: Physical therapy may be helpful for the management of TTH patients [10,11], as it may decrese the peripheral nociceptive input. The global burden of headache: Curr Rheumatol Rev ; Pressure pain thresholds assessed over temporalis, masseter, and frontalis muscles in healthy individuals, patients with tension- type headache, and those with migraine: Frequency of headache is related to sensitization: Pain ; Identification of subgroups of patients with tension type headache with higher widespread pressure pain hyperalgesia.

J Headache Pain ; 18 1: The role of muscles in tension-type headache. Curr Pain Headache Rep. Sustained nociceptive mechanical stimulation of latent myofascial trigger point induces central sensitization in healthy subjects. Myofascial trigger points and sensitization: An updated pain model for tension-type headache. Trigger Points are associated with widespread pressure pain sensitivity in people with tension-type headache.

Cephalalgia [Epub ahead of print]. Muscle trigger point therapy in tension-type headache. Expert Rev Neurother ; 12 3: Effectiveneess of physical therapy in patients with tension-type headache: J Jpn Phys Ther Assoc ; 17 1: Migraine is related to the highest disability among headaches. Great efforts are faced to improve the outcome of forthcoming treatments. However, still now, many patients regard as unsatisfactory the low responder rate about the half of patients and adverse effects that current treatments account.

Therefore, waiting for innovative, more tolerated and effective treatments, there is a large request for non-pharmacological approaches that in many cases have specific pathophysiological targets. Among these treatments, nutraceuticals has a leading role. Several nutraceutical products are proposed for migraine and sold around the world, but researchers adequately study only few compounds. Among studied nutraceuticals compounds, only few of them have studies of good quality in support. Moreover, also interactions among different molecules are not studied.

We have reviewed literature data in order to find researches that support the use of nutraceutical molecules in migraine management. Available good quality data support the use of certain nutraceuticals, in particular riboflavin, coenzyme Q10, magnesium, butterbur, feverfew, and omega-3 polyunsaturated fatty acids. Even if not supported by double blind studies, recently some prospective observational studies about fixed combination of nutraceuticals were performed. For instance, it is the case of a combination of coenzyme Q10, feverfew and magnesium for migraine prophylaxis: A double blind versus placebo study about the effect of a fixed combination of riboflavin, coenzyme Q10, feverfew, andrographis and magnesium for migraine prophylaxis is currently in progress.

Usually patients appreciate nutraceuticals more than traditional drugs, since they are regarded as safe and of efficacy not inferior to other pharmacological products. Available data seem to support this widespread belief, but some concerns about the regulation of nutraceuticals and quality of some products, still remain. Contrary to what is generally thought of, headaches and algology pain therapy share many aspects. Headaches and chronic non-oncological pain are two paradigms of chronic illness capable of generating enormous individual and social impact by disabling the sick person not only in the biological, but also in the psychological, professional, social and relational spheres.

Both cause alterations in psychological equilibrium, secondary depression, loss of social and professional roles, which, in the most serious cases, can cause loss of work. Literature documents in both cases, headaches and chronic pain, a rise in direct costs but above all of the indirect ones with a huge burden of disease. Both are capable of generating a marked drop in the quality of life associated with a serious bio-psycho-social disability. Headaches and chronic pain, although distinct according to a topographical criterion, share many mechanisms and physiopathogenetic steps.

One of the most current fields in which neurologists and pain therapists converge is the focus on neuroinflammation [3] and central sensitization[4], two key mechanism for triggering, maintaining, and subsequent perpetuation of pain: Another important shared pathogenetic passage is that of neuroimmune mechanisms, which interlink the immune system with the central nervous system[4].

Furthermore, numerous contribution to the scientific international literature highlight the need to modify the therapeutic approach, directing it towards a semeiotic criterion pain phenothype: This would enable a more appropriate prescription and greater efficiency, taking into primary consideration the possibility of getting back to everyday life rather than obtaining complete analgesia. All the above mentioned aspects are equally important but one of them can prevail over the others depending on patient characteristics and background.

From that derives another shared aspect: In conclusion it can be stated that the aspects of sharing between headaches and chronic non-oncological pain are significantly greater than those that clearly divide them. International classification of functioning, disability and health ICF.

Geneva, World Health Organization, J Lifting the burden: The global campaign against headache. Ru-Rong Ji Emerging targets in neuroinflammation-driven chronic pain. Nat Rev Drug Discov. Baron R Neuropathic pain: Edwards RR Patient phenotyping in clinical trials of chronic pain treatments: Headache is a common clinical feature in neurological patients. Usually, neuroimaging is unnecessary in patients with episodic migraine or tension type headache with typical headache features and with a normal neurological examination. These patients do not have a higher probability of a relevant brain pathology compared to the general population.

A recent study, however, reported that neuroimaging is routinely ordered in outpatient headache even if guidelines specifically recommend against their use. Brain MRI with detailed study of the pituitary area and cavernous sinus, is recommended for all trigeminal autonomic cephalalgias TACs. Neuroimaging should be considered in patients presenting with atypical headache features, a new onset headache, change in previously headache pattern, headache abruptly reaching the peak level, headache changing with posture, headache awakening the patient, or precipitated by physical activity or Valsalva manoeuvre and abnormal neurological examination.

Other condition for which MRI is recommended are: A recent consensus recommends brain MRI for the case of migraine with aura that persists on one side or in brainstem aura. According the same consensus, fFor primary cough headache, exercise headache, headache associated with sexual activity, thunderclap headache and hypnic headache apart from brain MRI additional tests may be required [3].

Particularly in emergency room it is mandatory to exclude a secondary headache that requires special attention and further diagnostic workup. CT scan is the first line neuroimaging examination. MRI offers a greater resolution and discrimination and might therefore be the preferred method of choice in non acute headache. In addition, radiation due to CT scanning may be avoided.

Neuroimaging non conventional techniques are of little or no value in the clinical setting. Routine testing when guidelines recommend against them. European Headache Federation consensus on technical investigation for primary headachedisorders. Migraine frequency fluctuates over time. In the literature, the most important recognized factors associated to chronic migraine are overuse of acute migraine medication, ineffective acute treatment, obesity, depression, presence of allodynia and stressful life events. Other factors reported in studies are age, female sex and low educational status.

Very recently, a large population study suggested that the presence of additional noncephalic pain site is a risk factor for migraine chronification. For many of these factors the relationship with migraine chronification may however be bi-directional. For instance, in the case of depression, it is possible that depression may negatively affect the response of migraine to acute and prophylactic treatments, but it is also true the opposite: In the case of obesity, the association with chronic migraine may simply be ascribed to the effect of fat tissue in drug distribution.

Beside and beyond the putative biological factors that may cause a worsening of disease, several lines of evidence suggest that the progression from episodic to chronic migraine is associated to a progressive increase and stabilization of functional and anatomical changes associated to chronic sensitization. In this frame, it appears obvious that an additional cause for chronic migraine is quite likely represented by the low rate of prescription of preventive medications.

The underutilization of preventive drugs has several explanations ranging from drug-associated issues limited efficacy, poor tolerability profile to education of practitioners, pharmacists and patients, and it also involve the limited access to qualified care.

Underutilization of preventative drugs also translate into a higher recourse to acute drugs, thus feeding on a vicious cycle that leads to negative consequences. CT has participated in advisory boards for Allergan and electroCore; she has lectured at symposia sponsored by Allergan; she is PI or collaborator in clinical trials sponsored by Alder, electroCore, Eli-Lilly and Teva.

Comorbid pain and migraine chronicity: Prevalence of migraine sufferers who are candidates for preventive therapy: The added value of an electronic monitoring and alerting system in the management of medication-overuse headache: A controlled multicentre study. To date, the majority of clinical studies concerning primary headaches and their comorbidities are focused on migraine. Comorbidities of migraine may include neurological and psychiatric conditions, as mood disorders depression, mania, anxiety, panic attacks , epilepsy, essential tremor, stroke, and the presence of white matter abnormalities [2].

Particularly, a complex and bidirectional relation between migraine and stroke has been described, including migraine as a risk factor for cerebral ischemia, migraine caused by cerebral ischemia, migraine mimicking cerebral ischemia, migraine and cerebral ischemia sharing a common cause, and migraine associated with subclinical vascular brain lesions [2]. A recent meta-analysis pointed out that migraine is associated with increased ischemic stroke risk [3], and according to a systematic review and meta-analysis [4] the risk of hemorrhagic stroke in migraineurs is increased with respect to non-migraineurs.

Besides, the risk of transient ischemic attack seems to be increased in migraineurs, although this issue has not been extensively investigated [5]. A recent systematic review and meta-analysis also describes an increased risk of myocardial infarction and angina in migraineurs compared to non-migraineurs [6]. Concerning the association between migraine and vascular risk factors arterial hypertension, diabetes mellitus, dyslipidemia, obesity, alcohol consumption, family history of cardiovascular disease , a recent review [7] showed no solid evidence of an increased burden of conventional vascular risk factors in migraineurs, with the only exceptions of dyslipidemia and cigarette smoking, while a systematic review and meta-analysis regarding migraine and body mass index categories [8] found an increased risk of having migraine in underweight subjects and in obese women as compared with normal-weight subjects.

Few studies investigated the comorbidities of tension-type headache TTH , despite the fact that tension-type headache TTH is highly prevalent, and may be as debilitating as migraine [9]. It is noteworthy that, according to a review, TTH is associated with increased rate of affective distress [9]. Furthermore, some medical disorders may worsen a preexisting TTH, and it has been described the comorbidity of TTH with psychiatric disorders and fibromyalgia [10].

The International Classification of Headache Disorders, 3 rd edition beta version.

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