Materiały źródłowe

• #1 Chronic Headaches – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559083/

  Chronic headache is not a single disease entity but an umbrella term that encompasses all chronic headaches. The International Headache Society defines chronic daily headaches (CDH) as „15 or more headache episodes per month for at least three months.” A chronic daily headache can be divided into primary and secondary headache disorders depending upon its etiology. Primary chronic headache disorders do not have secondary organic etiology. Within the primary headache categories, a headache duration of fewer than 4 hours is labeled as a 'short headache.’ More than 4 hours is known as a 'long headache.’ Long headaches more commonly include chronic migraine and chronic tension headaches. […] Chronic headaches are not an official class in the International Classification of Headache Disorders (ICHD). CDH is rather a descriptive term that most encompasses five subtypes of primary and secondary headaches defined by ICHD-3: Chronic migraine headache, Chronic tension-type headache, Medication overuse headache (MOH), Hemicrania continua, New daily persistent headache.

• #2 Chronic Headaches | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/93576

  Chronic headache is not a single disease entity but an umbrella term that encompasses all chronic headaches. The International Headache Society defines chronic daily headaches (CDH) as „15 or more headache episodes per month for at least three months.” […] A chronic daily headache can be divided into primary and secondary headache disorders depending upon its etiology. Primary chronic headache disorders do not have secondary organic etiology. […] It is important to realize that chronic headaches are often caused by a multifactorial combination of the causes mentioned above and can occur along a continuum. […] Although the pathophysiology of each type of chronic headache varies, shared features include sensitization of the trigeminal system, alterations in brain structure and function, and environmental factors. Most chronic headaches result from the transformation of an episodic headache disorder.

• #3 Chronic Headaches – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559083/

  Secondary headaches can occur due to secondary causes such as medication overuse, intracranial tumors, central nervous system (CNS) infections, raised intracranial pressure, metabolic abnormalities, post-traumatic, vascular, and structural pathologies. It is important to realize that chronic headaches are often caused by a multifactorial combination of the causes mentioned above and can occur along a continuum. […] Although the pathophysiology of each type of chronic headache varies, shared features include sensitization of the trigeminal system, alterations in brain structure and function, and environmental factors. Most chronic headaches result from the transformation of an episodic headache disorder. Modifiable risk factors, including sleep disorders, obesity, and high caffeine consumption, increase the chance of headache transformation from episodic to chronic headaches.

• #4 Chronic Headaches | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/93576

  Chronic headache is not a single disease entity but an umbrella term that encompasses all chronic headaches. The International Headache Society defines chronic daily headaches (CDH) as „15 or more headache episodes per month for at least three months.” […] A chronic daily headache can be divided into primary and secondary headache disorders depending upon its etiology. Primary chronic headache disorders do not have secondary organic etiology. […] It is important to realize that chronic headaches are often caused by a multifactorial combination of the causes mentioned above and can occur along a continuum. […] Although the pathophysiology of each type of chronic headache varies, shared features include sensitization of the trigeminal system, alterations in brain structure and function, and environmental factors. Most chronic headaches result from the transformation of an episodic headache disorder.

• #5 Frequent Headaches: Evaluation and Management | AAFP

  https://www.aafp.org/pubs/afp/issues/2020/0401/p419.html

  Most frequent headaches are typically migraine or tension-type headaches and are often exacerbated by medication overuse. […] Repeated headaches can induce central sensitization and transformation to chronic headaches that are intractable, are difficult to treat, and cause significant morbidity and costs. […] Biochemical, metabolic, and other changes induced by frequent headaches and/or medication are thought to cause central sensitization and neuronal dysfunction that results in inappropriate response to innocuous stimuli, lowered thresholds to trigger pain response, exaggerated response to stimuli, and persistence of pain after removal of inciting factors. […] Each year, 3% to 4% of patients with episodic migraine or tension-type headaches (TTH) escalate to chronic forms. […] An estimated 2% to 4% of U.S. adults have chronic headaches, and more than 30% of these report daily symptoms.

• #6 Chronic Headaches | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/93576

  Modifiable risk factors, including sleep disorders, obesity, and high caffeine consumption, increase the chance of headache transformation from episodic to chronic headaches. […] Serotonin, which has vasoconstrictive and anti-inflammatory effects, is a therapeutic target of triptans in migraines. […] Calcitonin gene-related peptide is abundant in trigeminal ganglion neurons. It is released from the peripheral and central nerve terminals and secreted within the trigeminal ganglion. […] Medication overuse headaches share much of the pathophysiology of migraine and tension headaches as functional and structural changes in the central nervous system. […] Trigeminal autonomic cephalalgias, cluster headache, SUNCT, SUNA, and hemicrania continua, have complex pathogenesis. Severe pain and autonomic symptoms are attributed to the trigeminal autonomic reflex via pain-producing innervation and cranial parasympathetic activation.

• #7 Pathophysiology of chronic daily headache – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11676888/

  Despite no clear explanation of the mechanism underlying chronic daily headache, sensitization of central nociceptive neurons is one possibility. Either prolonged activation of peripheral nociceptors or any factors that can alter the endogenous pain control system can trigger this process. A decrease in platelet serotonin has been observed in patients with chronic tension-type headache as well as migraine patients with medication-induced headache. It was also shown that chronic analgesic exposure led to changes in the serotonin content and the density of the 5-HT(2A) receptor in the cerebral cortex. The plasticity of the serotonin-dependent pain control system may facilitate the process of sensitization and results in the development of chronic daily headache.

• #8 Frequent Headaches: Evaluation and Management | AAFP

  https://www.aafp.org/pubs/afp/issues/2020/0401/p419.html

  Once central sensitization occurs, headaches are difficult to treat and cause substantial morbidity. […] Chronic pain, especially musculoskeletal pain, and obesity are strongly associated with chronification. […] Cutaneous allodynia is strongly associated with chronification and may be a marker of central sensitization. […] About 30% to 50% of patients who develop chronic headaches have MOH, which is defined as headache on 15 or more days per month in a patient with preexisting primary headache, developing as a consequence of regular overuse of acute or symptomatic headache medication for more than three months. […] MOH usually resolves after stopping overuse, but this is no longer required for diagnosis. […] MOH develops almost exclusively in patients with migraine or TTH. […] The optimal strategy for medication withdrawal is unclear. […] In about 75% of patients with MOH, discontinuing the overused medication results in reversion to episodic migraine or TTH; however, the relapse rate is about 30% per year.

• #9 Tension Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/792384-overview

  In chronic THH, stimuli that are normally painless are misinterpreted as pain. This continuous painful input induces central sensitization. The increased nociceptive stimulation of supraspinal structures results in increased facilitation and decreased inhibition of pain transmission at the level of the spinal dorsal horn/trigeminal nucleus, and in increased pericranial muscle activity. […] A study by Kiran et al indicated that patients with chronic tension headaches for longer than 5 years tended to have lower cortisol levels. […] More recently it is believed that there is increased myofascial pain sensitivity caused by central factors such as sensitization of neurons in the supraspinal region as well as second order neurons in the spinal dorsal horn/trigeminal nucleus. […] Another mechanism of pain is decreased antinociception or inability of the body to stop painful stimuli to the supraspinal structures.

• #10

  https://link.springer.com/article/10.1007/s11916-001-0071-5

  Despite no clear explanation of the mechanism underlying chronic daily headache, sensitization of central nociceptive neurons is one possibility. […] A decrease in platelet serotonin has been observed in patients with chronic tension-type headache as well as migraine patients with medication-induced headache. […] It was also shown that chronic analgesic exposure led to changes in the serotonin content and the density of the 5-HT2A receptor in the cerebral cortex. […] The plasticity of the serotonin-dependent pain control system may facilitate the process of sensitization and results in the development of chronic daily headache. […] The relationship between these biochemical changes and the development of CDH was discussed.

• #11 Chronic Headaches – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559083/

  Serotonin, which has vasoconstrictive and anti-inflammatory effects, is a therapeutic target of triptans in migraines. […] Calcitonin gene-related peptide is abundant in trigeminal ganglion neurons. It is released from the peripheral and central nerve terminals and secreted within the trigeminal ganglion. When released from the peripheral terminals, it initiates an increased synthesis of nitric oxide and later sensitization of trigeminal nerves. […] Medication overuse headaches share much of the pathophysiology of migraine and tension headaches as functional and structural changes in the central nervous system. Changes in the serotonergic neuromodulatory system and upregulation of vasoactive and pro-inflammatory mediators also contribute. […] Trigeminal autonomic cephalalgias, cluster headache, SUNCT, SUNA, and hemicrania continua, have complex pathogenesis. Severe pain and autonomic symptoms are attributed to the trigeminal autonomic reflex via pain-producing innervation and cranial parasympathetic activation.

• #12 chronic daily headache | PPT

  https://www.slideshare.net/slideshow/chronic-daily-headache/1446543

  Pathophysiology of Chronic Daily Headache The nucleus caudalis (NC) of the trigeminal complex, the major relay nucleus for head and face pain, receives nociceptive input from cephalic blood vessels and pericranial muscles, as well as inhibitory and facilitatory supraspinal input. Recent evidence suggests that central pain facilitatory neurons (on-cells) are present in the ventromedial medulla. […] Pathophysiology of Chronic Daily Headache Abnormal excitation of peripheral nociceptive afferent fibers (perhaps due to chronic neurogenic inflammation). Enhanced responsiveness of NC neurons (central sensitization). Decreased pain modulation. Spontaneous central pain. Combination of these. […] Pathogenesis Release of vasoactive neuropeptides, including calcitonin gene related peptides (CGRP), substance P, and neurokinin A from the nerve terminals. Mast cell activation. Sensitization of the nerve terminals. Extravasation of fluid into the perivascular space around the dural blood vessels. Intense neuronal stimulation causes induction of c-fos (an immediate-early gene product) in the trigeminal NC of the brain stem. Substance P and CGRP further amplify the trigeminal terminal sensitivity by stimulating the release of bradykinin and other inflammatory mediators from non-neuronal cells (Moskowitz, 1992).

• #13 Mechanisms of migraine as a chronic evolutive condition | The Journal of Headache and Pain | Full Text

  https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-1066-0

  The physiological mechanisms that underlie the development of chronic migraine from its episodic form are not understood. […] Inflammation and central sensitization play a significant role in the evolutive mechanisms of chronic migraine. […] The continuous changes in migraine phenotype and pathophysiology during a migraine attack between episodic and chronic migraine and during the patient lifespan, make migraine, even in its episodic form, a chronic evolutive disease.

• #14 chronic daily headache | PPT

  https://www.slideshare.net/slideshow/chronic-daily-headache/1446543

  Pain Modulation Off-cells In the rostroventromedial medulla which inhibit on-cells, which facilitate nociception. Enhanced neuronal activity in the NC as a result of enhanced on-cell or decreased off-cell activity. Long-term potentiation of nociceptive neurons and decreased activity in the antinociceptive system could cause primary CDH. […] Drug-Induced Headache Mechanisms Overuse of analgesics, opioids, barbiturates, ergotamine-containing compounds, or triptans may contribute to the transformation of episodic into chronic migraine. Drug-induced primary CDH is due to a rebound effect wherein medication withdrawal triggers the next headache, which in turn leads to the consumption of more drug. This may produce a vicious cycle, resulting in more frequent drug use and drug-induced primary CDH (Post and Silberstein, 1994).

• #15

  https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/neurology/headache-syndromes/

  The pathophysiology of migraine is a complex process that begins with primary neuronal dysfunction. The dural vascular structures are innervated by neurons arising from the trigeminal nucleus and dorsal portions of the upper cervical roots. These structures project onto second order neurons in the trigeminal cervical complex and trigeminal nucleus caudalis (TNC). Fibers then ascend to the thalamus and sensory cortex. Pain is felt in the head and neck due to convergence of fibers from the trigeminal nerve via the TNC and upper cervical roots. Pain can be modulated by both descending fibers from the hypothalamus, periaqueductal grey, locus coerulus and nucleus raphe magnus onto the TNC and by ascending fibers from the hypothalamus, locus coerulus, and periaqueductal grey. […] […] Cortical spreading depression, originally only thought to occur in migraine with aura occurs in all migraines. This is a slow, self-propagating wave of cellular depolarization across the cerebral cortex that is associated with depression of neuronal activity and altered brain metabolism. This process also activates neurons in the TNC and causes the inflammatory process in the meningeal vascular structures to begin causing pain and headache. Brain matrix metalloproteinase is upregulated and this alters the permeability of the blood brain barrier. […]

• #16 Evidence for chronic headaches induced by pathological changes of myodural bridge complex | Scientific Reports

  https://www.nature.com/articles/s41598-024-55069-7

  Clinical studies have shown that there may be a certain relationship between pathological changes of the myodural bridge complex (MDBC) and chronic headaches of unknown cause. […] This study aims to further confirm this relationship between MDBC and chronic headaches and explore its potential occurrence mechanism in rats. […] The current study further confirms the view that there is a relationship between pathological changes of MDBC and chronic headaches of unknown cause. This study may provide anatomical and physiological explanations for the pathogenesis of some chronic headaches of unknown cause. […] These findings suggested a possible role for the MDBC in the pathogenesis of chronic headaches. […] It has been reported that hyperplastic changes of the MDBC in this model resulted in increased stiffness of the SDM and reduced compliance of various structures within the cranio-cervical junction.

• #17 Evidence for chronic headaches induced by pathological changes of myodural bridge complex | Scientific Reports

  https://www.nature.com/articles/s41598-024-55069-7

  The MDBC plays important functions, particularly serving as a significant contributor to CSF circulation. […] It had been well documented that the pathological changes of the MDBC might be relevant to the onset of chronic headaches. […] Therefore, these behavioral findings preliminarily indicated that the MDBC hyperplastic rats have headache-related symptoms. […] These findings further supported the relationship between hyperplastic changes of the MDBC and chronic headaches. […] According to the above discussions, increased expression levels of neurotransmitters in the present study were observed in the emotional and behavioral nuclei or regions of rats with MDBC hyperplastic changes. […] These changes may also have triggered the headache. […] In conclusion, the current study provides further support for the view that pathological changes in the MDBC are one of the causes of chronic headaches.

• #18 Chronic Daily Headache: Diagnosis and Management | AAFP

  https://www.aafp.org/pubs/afp/issues/2014/0415/p642.html

  Most patients with long-duration chronic daily headaches have migraines or tension-type headaches. […] Chronic migraines occur in patients with a history of migraines who have a rapid or gradual progression to chronic daily headache. […] Overuse of abortive medication, including acetaminophen, nonsteroidal anti-inflammatory drugs, triptans, butalbital, caffeine, and narcotics, is found in two-thirds of patients, further complicating any treatment regimen. […] It is important to work with patients to change the type, dosing, or timing of pharmacotherapy to maximize compliance and help prevent overuse of abortive therapies.

• #19 Chronic daily headache |

  https://sydneynorthneurology.com.au/chronic-daily-headache/

  The mechanism through which migraine medications cause habituation is not well understood and differs depending on the type of medication. NSAIDs, paracetamol, codeine and dihydrocodeine are thought to cause rebound headaches through altering the neurological pathways involved in pain responses, while combination analgesics containing codeine or caffeine appear to cause such headaches due to their addictive properties. […] Individuals with chronic migraine experience 20 headache days per month on average, and on 15 of these days a migraine-type headache is experienced.

• #20

  https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/neurology/headache-syndromes/

  Central sensitization occurs during this process. Neurons become upregulated and sensitized to both nociceptive and non-nociceptive stimuli. This in turn causes peripheral sensitization where pain receptor fields are enlarged causing increased sensitivity to both noxious and non-noxious stimuli. Allodynia and exacerbation of pain by physical activity is thought to be caused by this process. […] […] Although poorly understood, input from myofascial trigger points in the pericranial areas appear to be responsible for episodic tension-type headache. With prolonged nociceptive activation of the pericranial myofascia, central pain pathways are activated and may be responsible for conversion to chronic tension-type headache. […] […] The pathophysiology of cluster headache is poorly understood, but is believed to be caused by activation of the posterior hypothalamus with secondary activation of the trigeminal autonomic reflex through the trigeminal-hypothalamic pathway. Severe, unilateral pain is mediated by activation of the first division of the trigeminal nerve (V1). The autonomic symptoms associated with cluster headache (lacrimation, miosis, sweating) are thought to be due to parasympathetic outflow from the superior salivatory nucleus via the pterygopalatine (sphenopalatine) ganglion. […]

• #21 Tension Headache: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/792384-overview

  The pathogenesis of tension type headaches is multifactorial. Given the wide variation in frequency and intensity in TTH, not only between individuals but also within individuals over time, it is likely that the underlying pain mechanisms in TTH are dynamic. It is suggested that the mechanisms vary from one individual to another, and potentially from one attack to another in the same individual. […] These factors include environmental and genetic factors. Environmental factors influence the development of episodic TTH more than chronic TTH, while genetic factors appear to play an important role in the development of chronic TTH. […] It is postulated that peripheral activation or sensitization of myofascial nociceptors play a major role in episodic TTH. Extended nociceptive stimuli from pericranial myofascial tissues seems to be responsible for the conversion of episodic to chronic TTH.

• #22 New daily persistent headache: a systematic review on an enigmatic disorder | The Journal of Headache and Pain | Full Text

  https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-1022-z

  New daily persistent headache (NDPH) presents with a sudden onset headache which continues without remission within 24h. […] The exact pathogenic mechanism of NDPH is unknown, however pro-inflammatory cytokines and cervicogenic problems might play a role in its development. […] A significant portion of NDPH patients describe that they experienced infection or a flu-like illness at the onset of headache. […] Considering that a certain percentage of patients appear to develop NDPH after an infection, Rozen and Swidan proposed that NDPH might develop in response to the release of pro-inflammatory cytokines during persistent systemic or CNS inflammation and looked at Tumor necrosis factor alpha (TNF-) levels in the cerebrospinal fluid (CSF) and serum of NDPH patients to discover whether increased level of pro-inflammatory cytokines due to CNS inflammation might lead to NDPH evolution.

• #23 New daily persistent headache – UpToDate

  https://www.uptodate.com/contents/new-daily-persistent-headache

  New daily persistent headache (NDPH) is a type of chronic daily headache that begins one day and typically does not remit. Many patients can pinpoint the exact date their headache started. NDPH may occur spontaneously or after a systemic trigger such as infection or a stressful life event. For some patients, NDPH can be refractory to treatment and may endure for many years or even decades. […] The pathophysiology of NDPH is poorly understood. NDPH is characterized by a specific date of onset that may be associated with a triggering event, but pathophysiologic correlates are largely speculative. […] The observation that headache onset can occur in relation to infection or flu-like illness suggests a possible microbial etiology. Several viral infections have been associated with NDPH in observational studies, including Epstein-Barr virus (EBV), herpes simplex virus (HSV), cytomegalovirus (CMV), dengue virus, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). […] An activated autoimmune response that may lead to persistent neurogenic inflammation has been hypothesized to account for NDPH, but the potential causal role of viral or other infection in the pathogenesis remains to be determined.

• #24 New Daily Persistent Headache

  https://practicalneurology.com/articles/2022-may/new-daily-persistent-headache

  The biologic causes of NDPH may be similar to other primary headache disorders (eg, migraine), considering symptoms can be fairly similar with the exception of onset. […] The relationship of several viruses with NPDH supports the concept of NDPH as a postinfectious immune-mediated disorder, which is also supported by elevated markers of CNS inflammation (eg, tumor necrosis factor ).

• #25 Chronic Daily Headache: Diagnosis and Management | AAFP

  https://www.aafp.org/pubs/afp/issues/2014/0415/p642.html

  Chronic daily headache is defined as the presence of a headache on 15 days or more per month for at least three months. The most common types of chronic daily headache are chronic migraines and chronic tension-type headaches. […] Several prophylactic treatments for chronic daily headache can reduce headache frequency and severity, as well as improve overall quality of life. […] Chronic daily headache is diagnosed in approximately 3% to 5% of patients presenting with acute headache. […] For patients with migraine, modifiable risk factors for progression to chronic migraine include obesity, medication overuse, stressful life events, snoring, caffeine overuse, and other causes of chronic pain. […] The most pervasive secondary cause of chronic daily headache, medication overuse, often coexists with a primary headache syndrome.

• #26

  https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/neurology/headache-syndromes/

  A clinic-based study on the development of chronic daily headache (CDH) over the course of 1 year showed that the risk of developing chronic daily headache increased dramatically with the frequency of migraine. The odds ratios for developing CHD was 6.2 (95% confidence interval [CI] 1.726.6) for patients with headache 10 to 14 days a month compared with patients with headache 0 to 4 days per month.

• #27 Constant or Chronic Headaches: Symptoms, Causes, and More

  https://www.healthline.com/health/constant-headache

  Chronic daily headaches are when you have a headache for 15 days or more per month during a 3-month period. […] Experts currently believe that constant, or chronic, headaches result when an episodic headache disorder transforms into a chronic one. While the mechanisms behind this change are poorly understood, some risk factors for the transition from episodic to chronic headache include: overuse of pain medication, obesity, disrupted sleep, high caffeine intake, persistently high stress levels. […] Regardless of the exact mechanism, its known that headaches are often triggered by lifestyle or environmental factors. A few examples include: stress, lack of sleep, skipped meals, physical exertion, changes in weather, caffeine or alcohol use, feelings of anxiety or depression, certain types of medications.

• #28 Chronic daily headaches – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/chronic-daily-headaches/symptoms-causes/syc-20370891

  Most people have headaches from time to time. But if you have a headache more days than not, you might have chronic daily headaches. […] The constant nature of chronic daily headaches makes them one of the most disabling headache conditions. Aggressive initial treatment and steady, long-term management might reduce pain and lead to fewer headaches. […] By definition, chronic daily headaches occur 15 days or more a month, for longer than three months. True (primary) chronic daily headaches aren’t caused by another condition. […] The causes of many chronic daily headaches aren’t well-understood. True (primary) chronic daily headaches don’t have an identifiable underlying cause. […] Conditions that might cause nonprimary chronic daily headaches include: Inflammation or other problems with the blood vessels in and around the brain, including stroke, Infections, such as meningitis, Intracranial pressure that’s either too high or too low, Brain tumor, Traumatic brain injury. […] If you have chronic daily headaches, you’re also more likely to have depression, anxiety, sleep disturbances, and other psychological and physical problems.

• #29 Chronic Daily Headache in Children and Adolescents: A Multi-Faceted Syndrome | Canadian Journal of Neurological Sciences | Cambridge Core

  https://www.cambridge.org/core/journals/canadian-journal-of-neurological-sciences/article/chronic-daily-headache-in-children-and-adolescents-a-multifaceted-syndrome/AEB5B6E67210B82E6DE042C5A12F1462

  Chronic daily headache (CDH) is a multi-faceted, often complex pain syndrome in children and adolescents. Chronic daily headache may be primary or secondary. Chronic migraine and chronic tension-type are the most frequent subtypes. Chronic daily headache is co-morbid with adverse life events, anxiety and depressive disorders, possibly with other psychiatric disorders, other pain syndromes and sleep disorders; these conditions contribute to initiating and maintaining CDH. […] Hence, early management of episodic headache and treatment of associated conditions are crucial to prevention. There is evidence for the benefit of psychological therapies, principally relaxation and cognitive behavioral, and promising information on acupuncture for CDH. […] The multifaceted nature of CDH makes it a good candidate for a multi-axial classification system. Such an approach should facilitate biopsychosocial management and enhance consistency in clinical research.

• #30 Chronic daily headache: I. Diagnosis and pathophysiology

  https://www.imrpress.com/journal/RN/40/2/10.33588/rn.4002.2004284

  Chronic daily headache (CDH), or headache more than 15 days/month or over 180 days/year, is one of the main reasons for visits to specialised headache centres and accounts for up to 5% of primary headaches. […] The pathophysiology of CDH is multifactorial; it has been suggested that genetic factors, peripheral and central neuronal dysfunction derived from the alteration of protein and receptor synthesis, inadequate release of inhibitory and excitatory neuropeptides, imbalance, excitatory and inhibitory neuropeptides concentration imbalance, in association with abuse of analgesics, high comorbidity with psychiatric disorders (anxiety, depression and panic) and sleep disorders may all be involved. […] Pathophysiology is multifactorial; there is a strong association with analgesic abuse, high comorbidity with psychiatric disorders and sleep disorders.

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