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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. 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. Schytz, H. PACAP38 induces migraine-like attacks in patients with migraine without aura. Tuka, B. Peripheral and central alterations of pituitary adenylate cyclase activating polypeptide-like immunoreactivity in the rat in response to activation of the trigeminovascular system. Peptides ; Amin, F. Cephalalgia ; Investigation of the pathophysiological mechanisms of migraine attacks induced by pituitary adenylate cyclase-activating polypeptide Brain ; Neurology ; Alterations in PACAPlike immunoreactivity in the plasma during ictal and interictal periods of migraine patients.

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]. Barone et al. 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 Young-HUNT study. The relationship between sleep and headache in children: implications for treatment.

Headache and attention deficit and hyperactivity disorder in children: common condition with complex relation and disabling consequences. Epilepsy Behav. Migraine and psychiatric comorbidity: a review of clinical findings. Mol Med. Association of 5-HTT gene polymorphisms with migraine: a systematic review and meta-analysis.

J Neurol Sci ; : Headache and comorbidity in children and adolescents. J Headache Pain ; Genetic and environmental influences on migraine: a twin study across six countries.

Twin Res. Pain and emotion: a biopsychological review of recent research. J Clin Psychol ; 67 9 : Attachment styles in children affected by migraine without aura. Neuropsychiatr Dis Treat. Behavioural problems in children with headache and maternal stress: is children’s attachment security a protective factor?

Dev ; DOI: The role of attachment insecurity in the emergence of anxiety symptoms in children and adolescents with migraine: an empirical study. 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. To verify variations in headache frequency, we used as baseline the month before the first VLCD and the first transition 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.

Stovner LJ. Migraine prophylaxis with drugs influencing the renin- angiotensin system. Eur J Neurol. Prevalence of neck pain in migraine and tension-type headache: a population study.

Temporomandibular disorders is more prevalent among patients with primary headaches in a tertiary outpatient clinic. Arq Neuropsiquiatr. Prakash S, Rathore C. Side-locked headache: an algorithm based approach. The Journal of Headache and Pain ; doi International consensus on the most useful physical examination tests used by physiotherapists for patients with headache: A Delphi study. Man Ther. Musculoskeletal dysfunction in migraine patients.

The International Classification of Headache Disorders, 3rd edition beta version Jul;33 9 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 ; Cephalalgia, submitted. Diagnosis of primary headache in children younger than 6 years: A clinical challenge.

Cephalalgia ; Chronic Migraine in Children and Adolescents. Headache and comorbidities in childhood and adolescence.

Springer, 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.

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: an appetite suppression induced by proteins and maybe by ketone bodies KBs , or a modification in hormone secretion insulin, glucagon, ghrelin, adipokines.

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. 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: however the cross-sectional nature of the study does not allow to establish a cause and effect relationship between TrPs and central sensitization, as other variables may influence this association [9].

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: a documentation of headache prevalence and disability worldwide. Cephalalgia ;— Tension type 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: A systematic review.

Pain ; — Frequency of headache is related to sensitization: a population study. 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. J Pain. 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: literature review. 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 prospective observational study. 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: the pain as a symptom, filogenetically responsible for maintaining homeostasis of the organism against actual or potential damage, becomes unnecessary illness without any protective meaning.

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: specific sign and symptoms of a certain type of pain in a specific moment , which is an epiphenomenon of underlyng pathogenetic mechanism, instead of basing it on a etiologic criterion[5].

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. 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.

World Health Organization. International classification of functioning, disability and health ICF. Geneva, World Health Organization, Steiner T. 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: diagnosis, pathophysiological mechanisms, and treatment. Lancet Neurol. 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.

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. Headache neuroimaging: 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: i.

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. Prevalence of migraine sufferers who are candidates for preventive therapy: results from the American migraine study AMPP study.

Headache ; — 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. Comorbid neuropathologies in migraine. Migraine headache and ischemic stroke risk: an updated meta-analysis. Am J Med. Migraine and hemorrhagic stroke: a meta-analysis. Sacco S, Kurth T.

Migraine and the risk for stroke and cardiovascular disease. Curr Cardiol Rep. Migraine and risk of ischaemic heart disease: a systematic review and meta-analysis of observational studies. Conventional vascular risk factors: Their role in the association between migraine and cardiovascular diseases.

Migraine and body mass index categories: a systematic review and meta-analysis of observational studies. Tension-type headache and psychiatric comorbidity. Tension-type headache and systemic medical disorders. Differentiating patients with life-threatening headaches from the overwhelming majority with primary headaches eg migraine, tension or cluster headache is an important issue in emergency department ED. Patients with non-traumatic headaches are up to 4.

These numbers seem to remain constant in Western countries Ramirez-Lassepas, ; Kowalski, ; Cvetkovic, ; Gaughran, Primary headaches still pose an open challenge in the ED because the failure to recognize a secondary headache could cause potentially fatal consequences. Unfortunately, to date, there is still no a standard diagnostic procedure for headache in emergency conditions; although according to the diagnostic guidelines there are red flags that could help in the process, the positive predictive value of each severity indicator is not yet determined.

The problem of poor diagnostic sensitivity was attributed to IHCD-3 criteria rigidity in relation to primary headache diagnosis in emergency setting Dutto, , Swadron, Alternatively, a different standardized work-up has been proposed for the most frequent headache scenarios in ED Cortelli, ; Dutto, A careful history and physical examination remain the most important part of the assessment of the headache patient; they enable the clinician to determine whether the patient is at significant risk for a dangerous cause of their symptoms and what additional workup is necessary.

This presentation will discuss how to approach adults with headache in ED with an emphasis on those features that characterize high-risk headaches. Thus, the muscolokeletal contribution in Primary Headaches is still debate in the literature [5]. Moreover, recent knowledge suggests that different clinical headache phenotypes arising from a common pathophysiology rather than an independent disorder [6].

That is, in the most prevalent headaches disorders i. In this presentation, the role of the musculoskeletal inputs in primary headaches it will be provided. Moreover, evidences of the effectiveness of a manual therapy management provided by a physiotherapist and its integration in a multidisciplinary team it will be discussed.

Migraine prophylaxis with drugs influencing the renin-angiotensin system. The impact of headache in Europe: principal results of the Eurolight project. Pietrobon D, Striessnig J. Neurobiology of migraine. Nat Rev Neurosci. Cady RK.

The convergence hypothesis. Noseda R, Burstein R. Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain. Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain. The European Headache Federation recognized the value of OnabotulinumtoxinA suggesting that, before labeling a patient as affected by refractory CM, a proper treatment with this drug needs to be completed [1].

In the last years several real-life prospective studies provided further evidence in clinical setting of OnabotulinumtoxinA U efficacy for the headache prophylaxis in CM complicated by medication overuse headache MOH [2].

Recently we published the results of a prospective study on the long-term 2 years efficacy and safety of a single dose of OnabotulinumtoxinA or U in patients with CM plus MOH had failed previous preventative drugs and detoxification attempts [3]. Both the doses were effective and equally safe, but U was more effective than U in reducing headache days, migraine days, pain medication intake days and Headache Impact Test HIT -6 score.

Even more, the U dose superior efficacy was evident since the first injection and maintained over all the study period of 24 months. Interestingly we observed a progressive improvement in all the efficacy measures during the 2 years of follow-up with both the doses and significantly more with U. Sometime a response appears only after the second or third injections. For this reason in selected cases can be useful to temporarily continue an oral preventative agent. The NICE guidelines recommend OnabotulinumtoxinA only for patients who have already tried at least three different preventative drug treatments that have not worked.

The chance to use it as first-line preventative treatment may shorten the period of chronicity and eventually prevent the developing of MOH. Several studies conducted before OnabotulinumtoxinA approval shown that it is ineffective in patients with episodic migraine [4].

Those studies had important limitations as range doses and injection paradigm. Furthermore, the population enrolled was represented in the majority by patients with low frequency episodic migraine an average of attacks per month. Refractory chronic migraine: a consensus statement on clinical definition from the European headache federation. J Headache Pain ;28; A critical evaluation on MOH current treatments.

Curr Treat Options Neurol. A two years open-label prospective study of OnabotulinumtoxinA U in medication overuse headache: a real-world experience. J Headache Pain ; Efficacy of botulinum toxin type A for the prophylaxis of episodic migraine headaches: a meta-analysis of randomized, double-blind, placebo-controlled trials.

Pharmacotherapy ;— Trigeminal autonomic cephalalgias TACs are a group of primary headaches comprehending the following syndromes: episodic and chronic cluster headache CH , episodic and chronic paroxysmal hemicrania PH , short-lasting unilateral neuralgiform headache attacks, and hemicrania continua HC [1]. Their phenotypes are similar and attack duration is the main feature distinguishing the first three TACs. An accurate diagnosis is important because of their different response to treatments.

CH typically occurs at the same time of the day, from once to eight times per day, and in the same period of the year. Trigger factors can include alcohol, volatile chemicals or a warm environment 3.

Controlled trials have investigated the efficacy of subcutaneous sumatriptan, nasal sumatriptan, and nasal zolmitriptan. When a preventive medication is required, verapamil is the reference treatment. PH attack features are characterized by unilateral, often stabbing, headaches, shorter and more frequent than in cluster headaches.

PH is responsive to treatment with indomethacin. Indomethacin dosages ranges from 25 to 75 mg, three times a day. SUNCT-SUNA attacks are very short in duration seconds to minutes , triggered by touching the face or chewing, with associated autonomic features and occur up to hundreds of times per day. In HC, clinical attack features have been reported as unilateral, side-locked continuous pain although interrupted by frequent severe exacerbations , associated with autonomic symptoms and responsive to indomethacin.

Therapeutic options in TACs are limited. In many patients the preventive treatment does not help to control attack frequency, or the acute drugs are not well tolerated or are contraindicated. For these reasons, after the discovery of the central role of the hypothalamus in TACs pathogenesis, neuromodulation techniques started. After the results obtained with hypothalamic deep brain stimulation in CH, other peripheral neuromodulation targets occipital nerves, spinal cord, sphenopalatine ganglion, vagus nerve were tried in the management of refractory CH and other TACs.

Headache Classification Committee of the International Headache Society: The international classification of headache disorders: 3th edition beta version. Cephalalgia , Headache ; Chronic headaches are a relevant health problem characterized by significant disability, poor quality of life and high economic burden 1. The most common forms include chronic migraine CM and medication overuse headache MOH , which are frequently associated, given that the majority of CM sufferers do overuse acute medications CM with MO.

Chronic headaches represent a challenge for physicians, given their frequent resistance to therapies, risk of relapse and associated comorbidities. Their management includes several steps aimed to: 1 make a proper diagnosis excluding secondary forms; 2 identify exacerbating factors; 3 treat comorbidities; 4 identify and address medication overuse; 5 establish a therapeutic agreement with patient; 6 define an integrated care approach.

Patient-history collection is crucial for defining headache onset and its life-long course, chronicization factors, and outcomes of previous therapies acute and prophylactic. Overused drug discontinuation is the first approach for MOH and it can be achieved via multiple modalities – in-patient or out-patient withdrawal procedures, advice alone — depending on several headache-associated or patient-associated factors.

During withdrawal, adequate care is required to help the patient to go through the treatment phases, given the frequent occurrence of headache recrudescence. Headache diaries represent useful tools in monitoring attacks frequency, detecting medication overuse, checking therapies outcomes, and assessing disability improvements. A relevant problem in MOH is the risk of relapse into overuse after successful withdrawal.

There are only few controlled pharmacological trials on the management of MO in CM, which does not allow to derive precise figures on the risk of relapse into MO associated to specific therapies. Furthermore, the relapse risk is also influenced by psychological and clinical comorbidities. For instance, mood and personality disorders e.

Psychological factors indeed seem to play a crucial role in predicting the outcome e. The presence of other pain-syndrome comorbidities e. Such a management is not limited to the earliest stages of treatment diagnosis, therapies, detoxification , being very important also when the patients resume their everyday life 4.

It is important to prevent unrealistic expectations e. The cost of headache disorders in Europe: the Eurolight project. Changes in anxiety and depression symptoms associated to the outcome of MOH: A post-hoc analysis of the Comoestas Project.

Psychological factors associated to failure of detoxification treatment in chronic headache associated with medication overuse. A consensus protocol for the management of medication-overuse headache: Evaluation in a multicentric, multinational study.

Headache prevalence is age-dependent and decreases progressively over time, especially starting from the age of The incidence of primary headaches declines, whereas secondary headaches tend to occur more frequently with increasing age [1]. Although the prevalence of headache in the elderly is relevant, few studies have been conducted in patients over 65 so far. The clinical records of consecutive outpatients aged over 18 referred to our Headache Centre from to were reviewed.

Patients were diagnosed based on The International Classification of Headache Disorders, 3rd edition beta version criteria [2]. Out of patients, a total of 5. Primary headaches were diagnosed in patients In the primary headache group the most common disorders were migraine without aura As for patients with migraine and chronic tension-type headache, the onset of headache occurred in most cases before 45, in particular in chronic migraine Secondary headaches were represented above all by cervicogenic headache, frequently associated with tension-type headache.

Among cranial neuropathies, trigeminal neuralgia was by far the most commonly diagnosed headache. Do this for both DataFrames. In [15]:. How do the positive tweets look like? In [16]:. How do the negative tweets look like? In [17]:. Merging the DataFrames to have both, positive and negative tweets in one DataFrame. In [18]:. In [19]:. Adding the negative tweets to our new DataFrame “tweets”. In [20]:. In [21]:. Let’s visualize and verify that our data is consistent.

In [22]:. Engaging in text processing allows us to move onto more difficult tasks which are unique to dealing with text What is text processing? There are a whole host of powerful libraries dedicated to this, including: string and str. For an easier text manipulation we will convert any string to lowercase.

We will remove special characters and any strings that are not going to be needed for further analysis. String module Cleaning the tweets before going though any other text manipulation is helpful. In [23]:. Before we start, let’s create a copy of our data so we can compare all the changes later. Converting any uppercase string to lowercase. In [24]:. In [25]:. In [26]:. Reviewing the tweets that include URL’s. In [27]:. Looking at the datapoint with index 0 to confirm that it has an URL.

Removing URL’s from tweets. In [28]:. In [29]:. In [30]:. In [32]:. We will use the library emot, which is open source. In [33]:. In [34]:. In [35]:. Converting emojis into words.

In [36]:. Convert emoticons into words. In [37]:. In [38]:. Replacing emojis and emoticons from the tweets.

In [39]:. Removing mentions. For example mariacamila In [40]:. Removing any noise that might be left: Special characters. In [41]:. In [42]:. What are stopwords? What are the languages available? In [43]:. In [44]:. Tokenization consists of dividing a piece of text into smaller pieces.

We can divide paragraph into sentences, sentence into words or word into characters. How do we understand the meaning of a sentence? Why is important? It is important because before doing a text analysis we to identify the words that constitute a string of characters. It’s also important because we can identify the different type of words after obtaining the tokens. In [45]:. Let’s review an example before applying it to our DataFrames.

But this is absurd. Instead of attempting such a definition I shall replace the question by another, which is closely related to it and is expressed in relatively unambiguous words. In [46]:. In [47]:. We can check how many sentences we got from the first text we have used for this example: print “The number of sentences is” , len sentences. The number of sentences is 7. The patterns can be chosen from the regular expressions.

Click here to learn more. In [48]:. In [49]:. How many substrings did we get? The number of substrings is In [50]:. In [51]:. In [52]:. In [53]:. Let’s try the tokenizers for our tweets. Which one would be better for the following text processing steps?

Is the combination of some characters useful for analyzing tweets? In [54]:. Name: tweets, Length: , dtype: object. In [55]:. In [56]:. Before getting the tokens from our tweets, we will proceed to remove the stop words.

In [57]:. In [58]:. Let’s check how many tokens do we get from each tweet after the tokenization. In [59]:. After getting the length for each tweet, we can check the distribution for the tweet’s length. In [60]:. In [61]:. In [62]:. In [63]:. In [64]:. Counter A Counter is a container that tracks how many times equivalent values are added. It can be used to implement the same algorithms for which other languages commonly use bag or multi-set data structures.

In [65]:. In [66]:. In [67]:. Sentence: [‘I’, ‘was’, ‘thinking’, ‘about’, ‘geometry’, ‘while’, ‘I’, ‘was’, ‘enjoying’, ‘the’, ‘best’, ‘month’, ‘of’, ‘winter’] Sentence with stemming: i wa think about geometri while i wa enjoy the best month of winter. In [68]:. Lemmatization reduce words to their root form. For example, if the tag starts with NN, the token is assigned as a noun. In [69]:. Sentence: [‘I’, ‘was’, ‘thinking’, ‘about’, ‘geometry’, ‘while’, ‘I’, ‘was’, ‘enjoying’, ‘the’, ‘best’, ‘month’, ‘of’, ‘winter’] Sentence with lemmatizing: I wa thinking about geometry while I wa enjoying the best month of winter.

In [70]:. Run this cell to learn more about the tags nltk. In [71]:. In [72]:. In [73]:. In [74]:. In [75]:. In [76]:. In [77]:. In [78]:. Double checking the differences between Stemming and Lemmatization.

In [79]:.

 
 

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Criteria employed to define intractable headaches were given more than ten years ago 1. An ad hoc European Headache Federation expert board has reviewed these aspects 2. A still unsolved issue is the lack of adequate placebo to properly design randomized controlled trials in neurostimulation studies. In patients with chronic pain conditions interpretation of placebo effect is a challange particularly for headache specialists.

In chronic migraine and chronic cluster headache patients occurrence of psychiatric comorbidities is frequently encountered. Also, occurrence of medication overuse headache — seen as an addiction behavior – is frequently observed both in chronic migraine and chronic cluster headache. These factors are often a barrier when selecting patients for neurostimulation procedures. Long term experience with deep brain stimulation of the posterior hypothalamic area in chronic cluster headache has suggested that the generator of the attacks is not there 3.

Similarly other neurostimulation procedures tried in migraine and cluster headache have shown poor, unsatisfactory ability to stop ongoing attacks. Towards a definition of intractable headache for use in clinical practice and trials. Neuromodulation of chronic headaches: position statement from the European Headache Federation. J Headache Pain. Success, failure and putative mechanisms in hypothalamic stimulation for drug resistant chronic cluster headache. Pain ; 1 : An underlying concept in the new ICHD-3 classification of trigeminal neuralgia is the postulation that clinical presentations matter because they reflect distinct pathophysiological mechanisms.

Previous attempts to establish the connection between the two have yielded uncertain results as the authors have paid limited attention to individual clinical symptoms and signs. Yet, the relatively strict criteria for trigeminal neuralgia and its subgroups yield homogenous populations that allow advantage to be taken of the advances in neurophysiological and imaging methods.

It is now possible to conduct subgroup-specific pathophysiological studies aimed at biomarkers that pave the way for precision diagnosis of TN and individualised therapy. An example of how this might be done comes from recent studies based on sensory profiling of peripheral neuropathic pain. In a large group of patients with three different diagnoses, cluster analysis of detailed sensory testing revealed three main sensory phenotypes [1], with the potential to allocate individual patients to these sensory groups [2].

In my presentation I will suggest a pathway as to how to accomplish this. I will start by arguing that the existing data are sufficient to recommend preferred treatment in selected cases. I will then highlight a number of clinically relevant research questions that can be answered by large-population multi-centre studies applying established methods ranging from QST and evoked potentials to structural and functional neuroimaging of the trigeminal system and linking them with clinical signs and symptoms.

Alongside this, I will discuss the challenges of phenotype profiling that could guide pharmacotherapy with, e. Peripheral neuropathic pain: a mechanism-related organizing principle based on sensory profiles. Pain ; Stratifying patients with peripheral neuropathic pain based on sensory profiles: algorithm and sample size recommendations.

Mild head injury is associated with good recovery in most patients, but with a small risk of poor outcomes. Headache is the most common complication that occurs as an isolated symptom or can be a part of the post-concussion syndrome which can also include dizziness, fatigue, reduced ability to concentrate, psychomotor slowing, mild memory problems, insomnia, anxiety, personality changes and irritability Following head injuries, children may develop headache for the first time or have their previously experienced headache getting worse in severity or frequency.

Post head injury headache is referred to as acute posttraumatic headache if it evolves within one week of the injury and resolves within 3 months and it is called chronic posttraumatic headache CPTH if it persisted for over 3 months. The pathophysiology of posttraumatic headache is not well understood, but likely to involve several mechanisms and factors.

It is suggested that even minor head injury may cause a widespread stretching or shearing injuries to the axonal network. Psychosocial factors may also play a role in the pathogenesis of CPTH. The clinical features of CPTH are similar to primary headache disorders phenotypes with the majority of children presenting with migraine-like headache and probable tension-type headache.

Some children may have mixed or unclassified headache disorders. In the majority of children no investigations are necessary. However, neuroimaging and other investigations may be necessary in children with red flags or abnormal findings on neurological examination.

The management of children with CPTH should include reassurances, adequate pain relief and preventative treatment as appropriate. Multidisciplinary approach is necessary and should include support from clinical psychology and education to help the child achieve normal school attendance and education. The prognosis of CPTH is generally good, but long term data are needed.

The interaction between enzyme inductive antiepileptics EiAED like carbamazepine, phenytoin, primidone, phenobarbitone, rufinamide, lamotrigine, topiramate and COCs is well-known. Therefore, while taking this medication, the risk of contraceptive failure is quite high. The mechanism of action of enzyme-inductors is to modify the metabolism of the sexual steroids in the liver.

Moreover, ethinylestradiol EE might modify the metabolism of certain antiepileptic drugs glucuronization of lamotrigine. Therefore, the gynaecologist has to be careful when prescribing the pill or administering other types of hormonal contraceptives for WWE.

Knowing the interaction between antiepileptics and contraceptives is important to find the most effective medication with fewer side effects. Nowadays, women with epilepsy do not always get the right information; thus, it is necessary to improve the cooperation and consultation between the epileptologist and the gynaecologist.

The information is also needed even if the patient is sexually inactive. Migraine is a complex neuronal disorder where the cortex has a key importance and characteristic headache attack is associated with multiple sensorial disturbances.

A cerebral cortical phenomenon known as cortical spreading depression CSD was linked to lateralized headache. CSD is an intrinsic brain phenomenon to a noxious stimulus such as high potassium or trauma, and manifests as an extreme excitability state of the gray matter with massive depolarization of neuronal and glial membranes and redistribution of ions.

Propagating depolarization in the brain parenchyma leads to a release of various vasoactive and nociceptive ions and molecules. Vascular compartment reacts with initial hyperemia followed by long-term oligemia.

It occurs in many species from rodents to primates, though it is hard to initiate and sustain its propagation in gyrencephalic brains. Spreading depression wave involves neuronal, glial and vascular cells, and leads remarkable effects on those compartments and overlying meningeal membranes with capability of triggering peripheral trigeminal fibers and second order trigeminal neurons in the brainstem nucleus, though its effect on subcortical structures are less known.

CSD is implicated in the development of inflammatory response and releasing CGRP and nitric oxide from trigeminal nerve endings. Animal studies investigating the mechanisms of migraine and CSD are usually conducted under anesthesia, despite the fact that pain is a conscious experience.

Anesthesia have profound effects on the mechanisms by which CSD is initiated and propagated, and clearly prevents observation of any associated behavioral response. Therefore CSD studies in awake animals are crucial for translational migraine research.

Cerebral cortex and thalamus are inseparable in sensory processing and thalamic reticular nucleus TRN is the gatekeeper of sensory outflow to the cortex. Electrocorticographic recordings demonstrated the direct propagation of CSD waves in to thalamic reticular nucleus.

It was dependent on full conscious experience and highly vulnerable to anesthetics. MK did not exert any effect on CSD induced amygdala activation and anxiety behavior.

TRN is also involved in discrimination of sensory stimulus and transient disruption of sensorial perception during migraine headache attacks was reported Boran et al, Involvement of a strategic subcortical thalamic structure by a cortical event is important to explain several clinical features of migraine such as 1 Dysfunction of the GABAergic neurons in TRN would result in enhanced transmission of sensory information to the cortex and disruption of sensory discrimination 2 Photophobia and visual hallucinations of aura may reflect dysregulation of visual stimuli by the TRN, 3 TRN could play a role in either termination or initiation of an attack as sleep is closely related with migraine, attacks are often associated with the circadian cycle and are typically relieved by sleep, 4 Thalamo-cortical gating could be a novel target in migraine as valproate, triptans and CGRP antagonists MK suppressed CSD induced TRN activation.

Common misdiagnoses for TN include dental pathology, other regional neuralgias, short-lasting neuralgiform headaches with autonomic signs SUNHA , cluster headache and theoretically an atypical shorter cluster-tic syndrome CTS. More rarely there may be more sinister underlying disorders tumors, multiple sclerosis that induce TN-like syndromes. We will outline and highlight the salient features across disorders that will ensure correct diagnosis.

Trigeminal neuralgia TN is a neurological disease which is peculiar under several respects. The diagnosis of TN, in its typical presentation, in unmistakable on clinical grounds alone. Pain manifests with intense bursts that occur and end abruptly and usually last few seconds only. This type of pain is paradigmatic of what pain scholars call paroxysmal pain. The most common verbal descriptors are electric-shock like or stabbing. Unique to TN is the trigger mechanism.

The attacks are evoked by innocuous stimuli in tiny zones of the extra- or intraoral trigeminal territories. The most frequent trigger maneuvers include activities of the daily life such as washing, cleaning, brushing the teeth or talking.

Although the trigger zones shared by most patients are confined between the nostril and the lateral perioral region, any area innervated by the trigeminal nerve may do. One aspect of pathophysiology is supported by established neurophysiologic, neuroimaging, and histologic evidence: the primary mechanism is focal demyelination of primary afferents near the entry extra- or intra-axial of the trigeminal root into the pons.

A second pathophysiologic theory, admittedly more debatable, is that hyperexcitable primary afferents, in the area of focal demyelination, become a source of ectopic generation of impulses and ephaptic transmission cross talk from close, healthy nerve fibers. More supported by evidence from animal models is the generation of high-frequency discharges. A third potential step, with so far almost no sound evidence at all, is that the hyperactivity of primary afferents secondarily induces central sensitization of wide dynamic range neurons in the spinal trigeminal nucleus or even more central changes.

Finally, TN is unique also for its pharmacological and surgical treatment. TN is highly sensitive to voltage-gated, frequency-dependent sodium-channels blockers and almost nothing else , and is the neuropathic pain condition that respond best to surgical lesions of the postganglionic primary sensory afferents.

The speaker will present an overview of the methodological potentials and challenges of the HUNT survey. Results will be displayed regarding prevalences of the common headache disorders and their trends over time.

Most importantly, the HUNT-survey enables risk factor analyses. Findings will be reviewed for factors of life such as physical activity, substance use, head traumas, insomnia, and mortality.

Finally, associations between intracranial abnormalities and headache disorders are now beginning to be published from a neuroimaging sub-study HUNT MRI.

SD is widely accepted as the pathophysiological event underlying migraine aura, and may play a role in headache pathogenesis in secondary headache disorders such as ischemic stroke, subarachnoid or intracerebral hemorrhage, traumatic brain injury, and epilepsy.

Here, we provide an overview of the pathogenic mechanisms and propose plausible hypotheses on the involvement of SD in primary and secondary headache disorders. SD can activate downstream trigeminovascular nociceptive pathways to explain the cephalgia in migraine, and possibly in secondary headache disorders as well. In healthy, well-nourished tissue such as migraine , the intense transmembrane ionic shifts, the cell swelling, and the metabolic and hemodynamic responses associated with SD do not cause tissue injury; however, when SD occurs in metabolically compromised tissue e.

Recent non-invasive technologies to detect SDs in human brain injury may aid in the investigation of SD in headache disorders in which invasive recordings are not possible. SD explains migraine aura and progression of neurological deficits associated with other neurological disorders. Studying the nature of SD in headache disorders might provide pathophysiological insights for disease and lead to targeted therapies in the era of precision medicine.

The proportion of adult patients reporting non-traumatic headache as their major complaint at ER access ranges from 0. The main objective is to identify the patients who require urgent investigations besause of a suspected serious secondary cause. The crucial step in the diagnosis is the initial interview.

Most patients presenting with headache as the chief complaint have a primary headache disorder, such as migraine or tension-type headache, the diagnosis of which relies on strict diagnostic criteria in the absence of any objective marker.

Secondary headache disorders manifest as new-onset headaches that arise in close temporal association with the underlying cause. Secondary headache should be suspected in any patient without a history of primary headache who reports a new onset headache and in any patient with a new unusual headache that is clearly distinct from their usual primary headache attacks.

Since many serious disorders, such as subarachnoid haemorrhage, can present with isolated headache and a normal clinical examination, diagnosis is reliant on clinical investigation. Subarachnoid hemorrhage should be suspected in anyone with a sudden or a thunderclap headache. Diagnosis is based on plain brain computed tomography and, if tomogram is normal, on lumbar puncture. Reversible cerebral vasoconstriction syndrome should be suspected in anyone with recurrent thunderclap headaches over a few days.

Cervical artery dissection, cerebral venous thrombosis, reversible cerebral vasoconstriction syndrome and pituitary apoplexy may present with isolated headache and normal physical examination, normal cerebral computed tomography and normal cerebrospinal fluid.

When computed tomography and lumbar puncture are normal, other investigations are needed, including cervical and cerebral vascular imaging and brain magnetic resonance imaging. Treatment of headaches in the ER should be based on the etiology.

The treatment of secondary headaches requires the treatment of the underlying cause and a symptomatic treatment based on intravenous acetaminophen or on opiates depending on the pain intensity. In women migraine prevalence peaks during reproductive years. Menstruation is a significant risk factor for migraine with attacks most likely to occur between 2 days before the onset of menstruation and the first three days of bleeding.

The pathophysiology of menstrual attacks involves estrogen withdrawal and potentially abnormal release of prostaglandins triggered by the end-cycle drop in estrogen level. Reproductive year are the life span during which many women require effective contraception. Migraine with aura MA and to a lesser extent migraine without aura MO increase the risk for cardiovascular events, especially for stroke.

There is a substantial elevation of these risks in migraineurs using combined contraceptive pills COC. Several clinical trials report improvements in migraine frequency and intensity in users of the progestin-only pill POP with desogestrel 75microgram. Both, inhibition of ovulation and ist continous use contribute to reduce hormone flucutations during ist use. The positive impact of this pill has been shown in MA and MO patients.

In women with chronic migraine, the reduction in pain medications used contributes to prevent medication overuse headaches. The existing nosology of cranial-nerve pains does not fully portray the subtle differences between various conditions. However, rather than abandoning many long-established diagnostic terms, this classification retains them, providing detailed definitions for differential diagnoses and their types, subtypes and subforms.

There are several axes of classification: a syndomology neuralgia vs. The authors of the classification tried to incorporate the existing literature into the IHS classification system. The current version defines the trigeminal neuralgia and trigeminal neuropathy. Trigeminal neuralgia is subdivided into classical due to nerve-vascular compression, not purely a nerve vascular contact , idiopathic unknown cause or nerve vascular contact, because the value of a nerve vascualr contact is unclear and secondary due to other disease.

Base don the clinical presentation it is further characterised as TN with and without concomitant facial pain indicating pure response to treatment. The cut-line for distinguishing between an acute and persistent headache is defined to be 3 months: resolution of headache within this period complies with an acute, persistence for the longer time — with a persistent headache.

Headache attributed to the injury to the head is further subclassified based on the severity of preceding trauma. Probably one of the most debated diagnostic criterions of this chapter is the time of onset of headache after a traumatic event. For the main classification it is agreed that causative relation between trauma and development of headache should be within 7 days after the trauma.

However based on a data derived from reports of everyday clinical practice alternative criteria published under the Appendix allow the delayed onset of headache, reaching up to 30 days following the injury. Clinical phenotypes of post-traumatic headache are varying from mild tension-type-like to severe migrainous.

Pathophysiological mechanisms of post-traumatic headaches remain largely unclear as a reason to the epidemiological data suggesting, that mild injury to the head represents a greater risk of developing persistent headache. The latter one causes a considerable reduction of health related quality of life and frequently is challenging in terms of treatment, requiring pharmacological preventative medications and non-pharmacological cognitive behavioural treatment, physical therapy, counselling etc approaches.

For treatment resistant cases interventional procedures, usage of onabotulinum toxin A and neurostimulation have been reported to be potentially effective. To determine persistence of and transitions between episodic migraine EM and chronic migraine CM and to describe and model the natural variability of self-reported frequency of headache days.

Relatively little is known about the stability of headache days per month in persons with EM or CM over time. Within person variability in headache day frequency has implications for the diagnosis of CM, assessing treatment in clinical practice and for the design and interpretation of clinical trials.

We modelled longitudinal transitions between EM and CM and, separately, headache day frequency per month using negative binomial repeated measures regression models NBRMR.

Among the 5, respondents with EM at baseline providing 4 or 5 waves of data, 5, Among respondents with CM at baseline providing 4 or 5 waves of data, had CM in every wave Individual plots revealed striking within-person variations in headache days per month.

Follow-up at 3 month intervals reveals a high level of short-term variability in headache days per month. Nearly three forths of persons with CM at baseline drop below this diagnostic boundary at least once over the course of a year. These findings my influence case definitions of migraine subtypes, the design and interpretation of epidemiologic studies and clinical trials as well as the interpretation of change in headache days in clinical practice.

Impairment of brain solute clearance through the recently described glymphatic system has been linked with traumatic brain injury, sleep deprivation, and aging. This lecture will summarize new data showing that cortical spreading depression CSD , the neural correlate of migraine aura, closes the paravascular space and impairs glymphatic flow. This closure holds the potential to define a novel mechanism for regulation of glymphatic flow.

It also implicates the glymphatic system in altered cortical and endothelial functioning of the migraine brain, which can explain the increased risk of stroke among migraine aura patients. Many patients report that their need to avoid light is driven mainly by how unpleasant it makes them feel. This lecture will attempt to explain why is light unpleasant. The data presented will show that during migraine, light can trigger the perception of a hypothalamic-mediated autonomic responses such as chest tightness, throat tightness, shortness of breath, fast breathing, faster than usual heart rate, light-headedness, dizziness, nausea, vomiting, dry mouth, salivation, rhinorrhea, stuffy sinuses and lacrimation; b hypothalamic mediated non-autonomic responses such as thirst, hunger drowsiness, tiredness, sleepiness, fatigue, and yawning; c negative emotions such as intense, irritable, angry, nervous, hopeless, needy, agitated, sad, scared, cranky, upset, depressed, disappointed, jittery, worried, stressed, anxious, panic and fear; and d positive emotions such as happy, relaxing, soothing, and calming.

By defining better the aversive nature of light, the findings suggest that the retina and hypothalamus play a critical role in migraine-type photophobia and that photophobia may not depend on hyperexcitable visual cortex, as traditionally thought. We have recently described a macroscopic pathway in the central nervous system — the glymphatic system that facilitates the clearance of interstitial waste products from neuronal metabolism.

Glymphatic clearance of macromolecules is driven by cerebrospinal fluid CSF that flows in along para-arterial spaces and through the brain parenchyma via support from astroglial aquaporin-4 water channels.

The glymphatic circulation constitutes a complete anatomical pathway; para-arterial CSF exchanges with the interstitial fluid, solutes collect along para-venous spaces, then drain into the vessels of the lymphatic system for ultimate excretion from the kidney or degradation in the liver. As such, this may after circulation represent a novel and unexplored target for prevention and treatment of neurodegenerative diseases.

We aimed to investigate the prevalence of headache in General Population adults years old in Greece. A quantitative study, using the form of computer-assisted telephone interviews C.

A draft questionnaire consisting of 37 questions was delivered in headache sufferers in a pre-study work to evaluate the diagnosis of the primary headache disorder according to ICH-3beta diagnostic criteria. After the analysis of this questionnaire the specific item questionnaire was decided. The one-year prevalence of Migraine that reduces activity was 8.

Females tend to suffer more from migraines and TTH as well as ages The average patients has been suffering from headaches for 12 years. Headaches typically occur once a month or more frequently, 8 days per month on average.

Although patients rarely misss work due to headaches, they do report headache-induced reductions in performance around 3 days per month.

About one fifth of patients seek professional treatment for headaches, most of them in the private sector. The most popular specialty for headache treatment is neurologist, followed by internist. Regarding both prophylactic and acute treatment, patients prefer oral medication to injection, even if the former is administered more frequently.

The stimulation device seems to be more attractive to males. Painkillers also are by far the most common acute treatment for headaches and the vast majority of patients have never taken prophylaxis for headaches. Only a small fraction have stopped taking a prophylactic treatment due to adverse effects. Calcitonin gene-related peptide CGRP , a neuropeptide previously known only by specialists interested in neurogenic inflammation, is now discussed throughout the communities of migraine researchers, headache therapists and even migraine patients.

The reason for this surprising career of CGRP awareness is evident. CGRP is the main neuropeptide of a major part of nociceptive trigeminal afferents and is released upon their activation. Thus CGRP release is characteristic, though in no way specific, for the trigeminovascular system, which is regarded as the structural basis for headache generation.

In fact, CGRP has been found at elevated concentrations in the cranial outflow during attacks of migraine and some trigemino-autonomic headaches; infusion of CGRP into patients suffering from primary headaches can cause head pain mimicking their spontaneous headache attacks; inhibiting CGRP or its receptors or its release can be preventive or therapeutic in those types of primary headaches.

However, looking behind the curtain of impressive significance of this biomarker, broad gaps in our knowledge are visible concerning the sites of CGRP release, its flow through the meningeal compartments, the sites and mechanisms of actions and its elimination. With preclinical experiments we are only at the beginning to study these issues, which are increasingly important in the light of new pharmacological developments targeting CGRP and its receptors by antagonists or monoclonal antibodies, and keeping in mind possible risks of a long-term treatment with these substances.

Trigeminal activity controlled by CGRP receptor activation could indeed be a pivot point in headache generation and therapy. However, measurable circulating concentrations of CGRP are far too low to explain any receptor effects, while it is difficult to assess its real concentrations near the likely release sites, namely the meningeal terminals of trigeminal afferents, the trigeminal ganglion and the central terminals in the trigemino-cervical brainstem complex.

The central effects of CGRP as a synaptic neuromodulator could explain neuronal CGRP effects to some extent but big molecules like monoclonal antibodies are unlikely to pass the blood-brain barrier and may not be able to act there. Peripheral effects of CGRP are largely confined to its well-known vascular functions, while fast neuronal effects are not established so far in the trigeminal system.

The trigeminal ganglion is a possible point of CGRP action but only few experiments have shown an impact on the signalling or metabolic changes of ganglion neurons.

Therefore new experimental approaches are needed to uncover the secrets of the nociceptive CGRP signalling system and its therapeutic control. Medical management of headache disorders, for the vast majority of people affected by them, can and should be carried out in primary care.

It does not require specialist skills. Nonetheless, it is recognised that non-specialists throughout Europe may have received limited training in the diagnosis and treatment of headache. This publication, in the Journal of Headache and Pain , provides a combination of educational materials and practical management aids. It is a product of the Global Campaign against Headache, a programme of action for the benefit of people with headache conducted by the UK-registered non-governmental organization Lifting The Burden LTB in official relations with the World Health Organization.

It updates the first edition [1], published 10 years ago. It has undergone review by a wider consultation group of headache experts, including representatives of the member national societies of EHF, primary-care physicians from eight countries of Europe, and lay advocates from the European Headache Alliance.

While the focus is Europe, the inclusion in the consultation group of members from all six world regions has aimed for cross-cultural relevance of all content so that it is useful to a much wider population. The European principles of management of headache disorders in primary care , laid out in 11 sections, are the core of the content.

Each of these is more-or-less stand-alone, in order to act as practical management aids as well as educational resources. There is a set of additional practical management aids. An abbreviated version of the International Classification of Headache Disorders, 3rd edition ICHD-3 , provides diagnostic criteria for the few headache disorders relevant to primary care.

A headache diary further assists diagnosis and a headache calendar assists follow-up. A measure of headache impact the HALT index can be employed in pre-treatment assessment of illness severity, and an outcome measure the HURT questionnaire is a guide to follow-up and need for treatment-review.

Five patient information leaflets are included, which may be offered to patients to improve their understanding of their headache disorders and their management. We hope for benefits for both physicians and patients.

Several data indicate that migraine, especially migraine with aura, is associated with an increased risk of ischemic stroke and other vascular events.

Of concern is whether the risk of ischemic stroke in migraineurs is magnified by the use of hormonal contraceptives HCs. As migraine prevalence is high in women of reproductive age, it is common to face the issue of migraine and HC use in clinical practice. The document pointed out that evidence addressing the risk of ischemic stroke associated with the use of HCs is generally poor.

All information relies on observational data, which may carry the risk of potential bias. Available studies had different settings and used different groups for comparing risks, limiting reliable comparison of studies as a pooled analysis of data. Most of the available studies were published several years ago and used compounds which are different from those available today. Additionally, in most studies not enough information is available regarding the type of HC considered and in most cases results are not provided according to migraine type.

Despite those limitations, available data pointed toward an increased risk of ischemic stroke associated with the use of HCs in women with migraine. Literature indicated that, whereas combined HCs carry a certain risk of arterial ischemic events this does not happen for progestogens-only HCs which are considered safe in terms of cardiovascular risk even in the presence of associated risk factors.

Considering those data, and unless studies will prove safety of the use of combined HCs in women with migraine, the recommendations from the Consensus Group gave priority to safety and suggested several limitations in the use of combined HCs in women with migraine. There are alternative methods to combined HCs which provide similar contraceptive benefits but that are much safer in terms of risks.

Further research is need to address safety of newer compounds in women with migraine. J Headache Pain ;in press. Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system. The term lesion is refers to nervous system damage demonstrated by imaging, neurophysiology, biopsies or surgical evidence. 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.

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.

Schytz, H. PACAP38 induces migraine-like attacks in patients with migraine without aura. Tuka, B. Peripheral and central alterations of pituitary adenylate cyclase activating polypeptide-like immunoreactivity in the rat in response to activation of the trigeminovascular system.

Peptides ; Amin, F. Cephalalgia ; Investigation of the pathophysiological mechanisms of migraine attacks induced by pituitary adenylate cyclase-activating polypeptide Brain ; Neurology ; Alterations in PACAPlike immunoreactivity in the plasma during ictal and interictal periods of migraine patients. 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]. Barone et al.

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 Young-HUNT study. The relationship between sleep and headache in children: implications for treatment. Headache and attention deficit and hyperactivity disorder in children: common condition with complex relation and disabling consequences.

Epilepsy Behav. Migraine and psychiatric comorbidity: a review of clinical findings. Mol Med. Association of 5-HTT gene polymorphisms with migraine: a systematic review and meta-analysis.

J Neurol Sci ; : Headache and comorbidity in children and adolescents. J Headache Pain ; Genetic and environmental influences on migraine: a twin study across six countries. Twin Res. Pain and emotion: a biopsychological review of recent research.

J Clin Psychol ; 67 9 : Attachment styles in children affected by migraine without aura. Neuropsychiatr Dis Treat. Behavioural problems in children with headache and maternal stress: is children’s attachment security a protective factor?

Dev ; DOI: The role of attachment insecurity in the emergence of anxiety symptoms in children and adolescents with migraine: an empirical study. 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. To verify variations in headache frequency, we used as baseline the month before the first VLCD and the first transition 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. Stovner LJ. Migraine prophylaxis with drugs influencing the renin- angiotensin system. Eur J Neurol. Prevalence of neck pain in migraine and tension-type headache: a population study.

Temporomandibular disorders is more prevalent among patients with primary headaches in a tertiary outpatient clinic. Arq Neuropsiquiatr. Prakash S, Rathore C. Side-locked headache: an algorithm based approach. The Journal of Headache and Pain ; doi International consensus on the most useful physical examination tests used by physiotherapists for patients with headache: A Delphi study. Man Ther. Musculoskeletal dysfunction in migraine patients. The International Classification of Headache Disorders, 3rd edition beta version Jul;33 9 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 ; Cephalalgia, submitted. Diagnosis of primary headache in children younger than 6 years: A clinical challenge.

Cephalalgia ; Chronic Migraine in Children and Adolescents. Headache and comorbidities in childhood and adolescence. Springer, 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.

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: an appetite suppression induced by proteins and maybe by ketone bodies KBs , or a modification in hormone secretion insulin, glucagon, ghrelin, adipokines.

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. 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.

We’ll add tags for each kind of tweet. Positive tweets: pos and negative tweets: neg. Steps: Create a new column to identify both, positive and negative tweets. Call this new column sentiment.

Do this for both DataFrames. In [15]:. How do the positive tweets look like? In [16]:. How do the negative tweets look like? In [17]:. Merging the DataFrames to have both, positive and negative tweets in one DataFrame. In [18]:. In [19]:. Adding the negative tweets to our new DataFrame “tweets”. In [20]:. In [21]:. Let’s visualize and verify that our data is consistent. In [22]:. Engaging in text processing allows us to move onto more difficult tasks which are unique to dealing with text What is text processing?

There are a whole host of powerful libraries dedicated to this, including: string and str. For an easier text manipulation we will convert any string to lowercase. We will remove special characters and any strings that are not going to be needed for further analysis. String module Cleaning the tweets before going though any other text manipulation is helpful. In [23]:. Before we start, let’s create a copy of our data so we can compare all the changes later.

Converting any uppercase string to lowercase. In [24]:. In [25]:. In [26]:. Reviewing the tweets that include URL’s. In [27]:. Looking at the datapoint with index 0 to confirm that it has an URL. Removing URL’s from tweets. In [28]:. In [29]:. In [30]:. In [32]:. We will use the library emot, which is open source. In [33]:. In [34]:. In [35]:. Converting emojis into words. In [36]:. Convert emoticons into words. In [37]:. In [38]:. Replacing emojis and emoticons from the tweets.

In [39]:. Removing mentions. For example mariacamila In [40]:. Removing any noise that might be left: Special characters. In [41]:. In [42]:. What are stopwords? What are the languages available?

In [43]:. In [44]:. Tokenization consists of dividing a piece of text into smaller pieces. We can divide paragraph into sentences, sentence into words or word into characters. How do we understand the meaning of a sentence? Why is important? It is important because before doing a text analysis we to identify the words that constitute a string of characters. It’s also important because we can identify the different type of words after obtaining the tokens. In [45]:. Let’s review an example before applying it to our DataFrames.

But this is absurd. Instead of attempting such a definition I shall replace the question by another, which is closely related to it and is expressed in relatively unambiguous words. In [46]:. In [47]:. We can check how many sentences we got from the first text we have used for this example: print “The number of sentences is” , len sentences.

The number of sentences is 7. The patterns can be chosen from the regular expressions. Click here to learn more. In [48]:. In [49]:. How many substrings did we get? The number of substrings is In [50]:. In [51]:. In [52]:. In [53]:. Let’s try the tokenizers for our tweets. Which one would be better for the following text processing steps? Is the combination of some characters useful for analyzing tweets? In [54]:. Name: tweets, Length: , dtype: object.

In [55]:. In [56]:. Before getting the tokens from our tweets, we will proceed to remove the stop words. In [57]:. In [58]:. Let’s check how many tokens do we get from each tweet after the tokenization.

In [59]:. After getting the length for each tweet, we can check the distribution for the tweet’s length. In [60]:. In [61]:. In [62]:. In [63]:. In [64]:. Counter A Counter is a container that tracks how many times equivalent values are added.

It can be used to implement the same algorithms for which other languages commonly use bag or multi-set data structures. In [65]:. In [66]:. In [67]:. Sentence: [‘I’, ‘was’, ‘thinking’, ‘about’, ‘geometry’, ‘while’, ‘I’, ‘was’, ‘enjoying’, ‘the’, ‘best’, ‘month’, ‘of’, ‘winter’] Sentence with stemming: i wa think about geometri while i wa enjoy the best month of winter. In [68]:. Lemmatization reduce words to their root form. For example, if the tag starts with NN, the token is assigned as a noun.

In [69]:. Sentence: [‘I’, ‘was’, ‘thinking’, ‘about’, ‘geometry’, ‘while’, ‘I’, ‘was’, ‘enjoying’, ‘the’, ‘best’, ‘month’, ‘of’, ‘winter’] Sentence with lemmatizing: I wa thinking about geometry while I wa enjoying the best month of winter. In [70]:. Run this cell to learn more about the tags nltk. In [71]:. In [72]:. In [73]:. In [74]:. In [75]:.

In [76]:.