The journal of headache and pain
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Review Meta Analysis
New daily persistent headache: a systematic review on an enigmatic disorder.
New daily persistent headache (NDPH) presents with a sudden onset headache which continues without remission within 24 h. Although rare, NDPH is important because it is one of the most treatment refractory primary headache disorders and can be highly disabling to the individuals. In this structured review, we describe the current knowledge of epidemiology, clinical features, trigger factors, pathophysiology, diagnosis and therapeutic options of NDPH to better understand this enigmatic disorder. The prevalence of NDPH estimated to be 0.03% to 0.1% in the general population and is higher in children and adolescents than in adults. Individuals with NDPH can pinpoint the exact date their headache started. The pain is constant and lacks special characteristics but in some has migraine features. The exact pathogenic mechanism of NDPH is unknown, however pro-inflammatory cytokines and cervicogenic problems might play a role in its development. The diagnosis of NDPH is mainly clinical and based on a typical history, but proper laboratory investigation is needed to exclude secondary causes of headache. Regarding treatment strategy, controlled drug trials are absent. It is probably best to treat NDPH based upon the predominant headache phenotype. For patients who do not respond to common prophylactic drugs, ketamine infusion, onabotulinum toxin type A, intravenous (IV) lidocaine, IV methylprednisolone and nerve blockade are possible treatment options, but even aggressive treatment is usually ineffective. ⋯ NDPH remains poorly understood but very burdensome for the individual. Multi-center randomized controlled trials are recommended to gain better understanding of NDPH and to establish evidence based treatments.
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Review Meta Analysis
New daily persistent headache: a systematic review on an enigmatic disorder.
New daily persistent headache (NDPH) presents with a sudden onset headache which continues without remission within 24 h. Although rare, NDPH is important because it is one of the most treatment refractory primary headache disorders and can be highly disabling to the individuals. In this structured review, we describe the current knowledge of epidemiology, clinical features, trigger factors, pathophysiology, diagnosis and therapeutic options of NDPH to better understand this enigmatic disorder. The prevalence of NDPH estimated to be 0.03% to 0.1% in the general population and is higher in children and adolescents than in adults. Individuals with NDPH can pinpoint the exact date their headache started. The pain is constant and lacks special characteristics but in some has migraine features. The exact pathogenic mechanism of NDPH is unknown, however pro-inflammatory cytokines and cervicogenic problems might play a role in its development. The diagnosis of NDPH is mainly clinical and based on a typical history, but proper laboratory investigation is needed to exclude secondary causes of headache. Regarding treatment strategy, controlled drug trials are absent. It is probably best to treat NDPH based upon the predominant headache phenotype. For patients who do not respond to common prophylactic drugs, ketamine infusion, onabotulinum toxin type A, intravenous (IV) lidocaine, IV methylprednisolone and nerve blockade are possible treatment options, but even aggressive treatment is usually ineffective. ⋯ NDPH remains poorly understood but very burdensome for the individual. Multi-center randomized controlled trials are recommended to gain better understanding of NDPH and to establish evidence based treatments.
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To systematically review studies quantifying the association between primary chronic headaches and persistent low back pain (LBP). ⋯ We identified a positive association between persistent LBP and primary headache disorders. The quality of the review findings is limited by diversity of populations, study designs and uncertainly about headache and LBP definitions.
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To systematically review studies quantifying the association between primary chronic headaches and persistent low back pain (LBP). ⋯ We identified a positive association between persistent LBP and primary headache disorders. The quality of the review findings is limited by diversity of populations, study designs and uncertainly about headache and LBP definitions.
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Mouse models of rare monogenic forms of migraine provide a unique experimental system to study the cellular and circuit mechanisms of the primary brain dysfunctions causing a migraine disorder. Here, we discuss the migraine-relevant phenotypes and the migraine-relevant functional alterations in the brain of five genetic mouse models of migraine, four of which carry mutations derived from patients with familial hemiplegic migraine (FHM) and the fifth carry a mutation from patients with both phenotypically normal MA and familial advanced sleep phase syndrome (FASPS). We focus on the latter mouse model, in which a ubiquitous serine-threonine kinase is mutated, and on two mouse models of pure FHM, in which a voltage-gated calcium channel controlling neurotransmitter release at most brain synapses and a Na/K ATPase that is expressed mainly in astrocytes in the adult brain are mutated, respectively. ⋯ Third, we review the alterations in the trigeminovascular pain pathway and discuss possible implications for migraine pain mechanisms. Finally, we discuss the insights into migraine pathophysiology obtained from the genetic models of migraine, in particular regarding the mechanisms that make the brain of migraineurs susceptible to the ignition of "spontaneous" CSDs. Although the reviewed functional studies support the view of migraine as a disorder of the brain characterized by dysfunctional regulation of the excitatory/inhibitory balance in specific neuronal circuits, much work remains to be done in the genetic mouse models e.g. to identfy the relevant dysfunctional circuits and to establish whether and how the alterations in the function of specific circuits (in the cerebral cortex and/or other brain areas) are state-dependent and may, in certain conditions, favor CSD ignition and the migraine attack.