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New Game Info. Post your extra beta codes here. Office vs. How to run 16 bit DOS. Its bad news for Audio 8 2 owners. Medialink Bluetooth 4. Nice Post Really enjoyed this post. Really thank you! 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.

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