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The Journal of Headache and Pain Dec 2016The differential diagnosis of strictly unilateral hemicranial pain includes a large number of primary and secondary headaches and cranial neuropathies. It may arise from... (Review)
Review
The differential diagnosis of strictly unilateral hemicranial pain includes a large number of primary and secondary headaches and cranial neuropathies. It may arise from both intracranial and extracranial structures such as cranium, neck, vessels, eyes, ears, nose, sinuses, teeth, mouth, and the other facial or cervical structure. Available data suggest that about two-third patients with side-locked headache visiting neurology or headache clinics have primary headaches. Other one-third will have either secondary headaches or neuralgias. Many of these hemicranial pain syndromes have overlapping presentations. Primary headache disorders may spread to involve the face and / or neck. Even various intracranial and extracranial pathologies may have similar overlapping presentations. Patients may present to a variety of clinicians, including headache experts, dentists, otolaryngologists, ophthalmologist, psychiatrists, and physiotherapists. Unfortunately, there is not uniform approach for such patients and diagnostic ambiguity is frequently encountered in clinical practice.Herein, we review the differential diagnoses of side-locked headaches and provide an algorithm based approach for patients presenting with side-locked headaches. Side-locked headache is itself a red flag. So, the first priority should be to rule out secondary headaches. A comprehensive history and thorough examinations will help one to formulate an algorithm to rule out or confirm secondary side-locked headaches. The diagnoses of most secondary side-locked headaches are largely investigations dependent. Therefore, each suspected secondary headache should be subjected for appropriate investigations or referral. The diagnostic approach of primary side-locked headache starts once one rule out all the possible secondary headaches. We have discussed an algorithmic approach for both secondary and primary side-locked headaches.
Topics: Algorithms; Cluster Headache; Cranial Nerve Diseases; Diagnosis, Differential; Facial Pain; Headache; Headache Disorders, Primary; Humans; Neck Pain; Neuralgia; Paroxysmal Hemicrania; Referral and Consultation; Trigeminal Autonomic Cephalalgias
PubMed: 27770404
DOI: 10.1186/s10194-016-0687-9 -
Journal of Neurosciences in Rural... 2016Alcoholic drinks (ADs) have been reported as a migraine trigger in about one-third of the migraine patients in retrospective studies. Some studies found that ADs trigger... (Review)
Review
Alcoholic drinks (ADs) have been reported as a migraine trigger in about one-third of the migraine patients in retrospective studies. Some studies found that ADs trigger also other primary headaches. The studies concerning the role of ADs in triggering various types of primary headaches published after the International Headache Society classification criteria of 1988 were reviewed, and the pathophysiological mechanisms were discussed. Many studies show that ADs are a trigger of migraine without aura (MO), migraine with aura (MA), cluster headache (CH), and tension-type headache (TH). While data on MO and CH are well delineated, those in MA and TH are discordant. There are sparse reports that ADs are also triggers of less frequent types of primary headache such as familial hemiplegic migraine, hemicrania continua, and paroxysmal hemicrania. However, in some countries, the occurrence of alcohol as headache trigger is negligible, perhaps determined by alcohol habits. The frequency estimates vary widely based on the study approach and population. In fact, prospective studies report a limited importance of ADs as migraine trigger. If ADs are capable of triggering practically all primary headaches, they should act at a common pathogenetic level. The mechanisms of alcohol-provoking headache were discussed in relationship to the principal pathogenetic theories of primary headaches. The conclusion was that vasodilatation is hardly compatible with ADs trigger activity of all primary headaches and a common pathogenetic mechanism at cortical, or more likely at subcortical/brainstem, level is more plausible.
PubMed: 27114660
DOI: 10.4103/0976-3147.178654 -
SpringerPlus 2016Linear headache (LH) has recently been described as a paroxysmal or continuous fixed head pain restricted in a linear trajectory of 5-10 mm in width, linking one...
BACKGROUND
Linear headache (LH) has recently been described as a paroxysmal or continuous fixed head pain restricted in a linear trajectory of 5-10 mm in width, linking one endpoint in occipital or occipitocervical region with another endpoint in ipsilateral nasion or forehead region. For some patients, this headache had some features resembling migraine without aura.
METHODS
We made a prospective search of patients presenting with a clinical picture comprised under the heading of LH and we have accessed eight new cases. A detailed clinical feature of the headache was obtained in all cases to differentiate with cranial neuralgia, paroxysmal hemicrania, cervicogenic headache, nummular headache and migraine.
RESULTS
The eight LH patients complained of a recurrent moderate to severe, distending, pulsating, or pressure-like pain within a strictly unilateral line-shaped area. The headache duration would be ranged from 1 h to 2 days or persistent for 1-6 months with recurrent worsening of headaches. For some patients, this headache had couple of features similar to that of migraine pattern, such as accompaniments of nausea, vomiting, and phonophobia, diziness, triggering factors of noise, bright night, resting after physical activity, fatigue, menstruation, and response to anti-migraine therapy.
CONCLUSIONS
This description reinforces the proposal of LH as a new headache syndrome or a new variant of a previously known headache syndrome, probably of migraine.
PubMed: 27057481
DOI: 10.1186/s40064-016-1991-1 -
SpringerPlus 2016The trigeminal autonomic cephalagias (TACs) are short-lasting unilateral headaches associated with autonomic features. Even if coexistence of different ipsilateral TACs...
INTRODUCTION
The trigeminal autonomic cephalagias (TACs) are short-lasting unilateral headaches associated with autonomic features. Even if coexistence of different ipsilateral TACs in the same patient has been previously reported in few papers, the simultaneous occurrence of contralateral TACs is not described previously.
CASE DESCRIPTION
A 50 years old working man complained, at the end of his cluster period, a new TAC, fitting the criteria for probable paroxysmal hemicrania. The dramatic improvement of this last cephalalgia with indomethacin treatment confirmed the diagnosis.
DISCUSSION EVALUATION AND CONCLUSION
There is a clear overlap in clinical diagnosis between cluster headache (CH) and paroxysmal hemicrania (PH) and similarities are somewhat greater than differences. The originality of this report is the coexistence of contralateral TACs in the same patients at the same moment. According neuroimaging studies, CH hypothalamic activation occurs ipsilateral to the side of the headache while in PH hypothalamic activation occurs contralateral to the side of headache. It could be suggested that a continuous hypothalamic activation give a maladaptive plasticity recruiting closed neuronal aggregates responsible for the developing of PH after a long period of CH, confirming the central origin of both CH and PH. Further studies need to confirm this hypothesis.
PubMed: 27047722
DOI: 10.1186/s40064-016-2000-4 -
Current Neuropharmacology 2015Trigeminal autonomic cephalalgias (TACs) are a group of primary headaches including cluster headache (CH), paroxysmal hemicrania (PH) and short-lasting unilateral... (Review)
Review
Trigeminal autonomic cephalalgias (TACs) are a group of primary headaches including cluster headache (CH), paroxysmal hemicrania (PH) and short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT). Another form, hemicrania continua (HC), is also included this group due to its clinical and pathophysiological similarities. CH is the most common of these syndromes, the others being infrequent in the general population. The pathophysiology of the TACs has been partly elucidated by a number of recent neuroimaging studies, which implicate brain regions associated with nociception (pain matrix). In addition, the hypothalamic activation observed in the course of TAC attacks and the observed efficacy of hypothalamic neurostimulation in CH patients suggest that the hypothalamus is another key structure. Hypothalamic activation may indeed be involved in attack initiation, but it may also lead to a condition of central facilitation underlying the recurrence of pain episodes. The TACs share many pathophysiological features, but are characterised by differences in attack duration and frequency, and to some extent treatment response. Although alternative strategies for the TACs, especially CH, are now emerging (such as neurostimulation techniques), this review focuses on the available pharmacological treatments complying with the most recent guidelines. We discuss the clinical efficacy and tolerability of the currently used drugs. Due to the low frequency of most TACs, few randomised controlled trials have been conducted. The therapies of choice in CH continue to be the triptans and oxygen for acute treatment, and verapamil and lithium for prevention, but promising results have recently been obtained with novel modes of administration of the triptans and other agents, and several other treatments are currently under study. Indomethacin is extremely effective in PH and HC, while antiepileptic drugs (especially lamotrigine) appear to be increasingly useful in SUNCT. We highlight the need for appropriate studies investigating treatments for these rare, but lifelong and disabling conditions.
Topics: Animals; Cluster Headache; Headache; Humans; Neuropharmacology; Paroxysmal Hemicrania; SUNCT Syndrome; Trigeminal Autonomic Cephalalgias
PubMed: 26411963
DOI: 10.2174/1570159x13666150309233556 -
BMC Research Notes Jun 2015Transient or permanent neurological symptoms occur in 17-40% of patients with aortic dissection. They can distract from or even mask the underlying life-threatening...
BACKGROUND
Transient or permanent neurological symptoms occur in 17-40% of patients with aortic dissection. They can distract from or even mask the underlying life-threatening condition.
CASE PRESENTATION
We present the case of a young Caucasian man who consulted for recurrent episodes of stereotyped right-sided sudden-onset severe headache. Upon questioning, he also reported a dull chest pain. Clinical examination and brain magnetic resonance imaging were unremarkable. The concomitant presence of chest pain made us consider aortic dissection. Contrast-enhanced cervico-thoraco-abdominal computerized tomography revealed type A aortic dissection. The patient underwent surgical replacement of the ascending aorta and reported no further episode of headache thereafter. Differential diagnosis of headache in this case includes paroxysmal hemicrania, cluster headache, migraine, trigeminal neuralgia and short lasting unilateral neuralgiform headache with conjunctival injection and tearing. Failure to match diagnostic criteria for any of these primary headache disorders and the resolution of pain episodes following surgery led us to postulate that these new-onset hemicrania episodes were symptomatic of aortic dissection. We hypothesize that aortic wall ischemia could have activated the trigeminovascular system and thereby caused hemicranial pain. Such an effect might be mediated by two different pathways that can be referred to as anatomical and humoral. The humoral hypothesis would posit that ischemia results in synthesis of pro-inflammatory mediators released from the aortic wall into the blood stream, such that they reach the central nervous system and directly stimulate specific receptors. The anatomical hypothesis would imply that pain signals generated by nociceptors in the aortic wall are transferred to the trigeminal ganglion via the cardiac plexus, the first cervical ganglion and the internal carotid nerve such that pain perception is referred to related cranio-cervical dermatomes.
CONCLUSION
In cases of isolated headache that does not match key diagnostic criteria for a primary headache entity; a thorough review of systems should be performed to look for symptoms that may indicate symptomatic headache from potentially life-threatening conditions. Neurologists should consider aortic dissection in patients presenting with acute headache and chest pain. Further clinical or experimental studies are required to refute or validate the pathophysiological hypothesis discussed here.
Topics: Adult; Angioplasty; Aorta; Aortic Aneurysm, Thoracic; Chest Pain; Diagnosis, Differential; Headache; Humans; Male; Migraine Disorders; Paroxysmal Hemicrania; Trigeminal Neuralgia
PubMed: 26082134
DOI: 10.1186/s13104-015-1223-8 -
Revista de Neurologia Oct 2014Hemicranias are an uncommon type of headache characterised by strictly unilateral pain, either as a continuous, although fluctuating, headache in hemicrania continua...
INTRODUCTION
Hemicranias are an uncommon type of headache characterised by strictly unilateral pain, either as a continuous, although fluctuating, headache in hemicrania continua (HC) or in the form of recurring attacks in paroxysmal hemicrania (PH). In both types of headache, an absolute response to indomethacin is reported. AIMS. To analyse the fulfilment of current diagnostic criteria for HC and PH and the recent introduction of HC within the group of trigeminal-autonomic cephalgias.
PATIENTS AND METHODS
The clinical and therapeutic characteristics of patients diagnosed with HC or PH were evaluated retrospectively. Demographic and symptomatological information as well as data regarding the analogical pain scale and response to indomethacin were included.
RESULTS
A sample of 12 HC (four males and eight females) was evaluated from a total of 520 cases (2.3%). Mean age at onset: 47.1 ± 16.4 years. Baseline pain intensity: 3.3 ± 1,9. Exacerbations: 9.2 ± 1.1. Eight cases (66.7%) presented autonomic symptoms, four (33.3%) followed a time pattern, and two (16.7%) did not respond to indomethacin. We evaluated a sample of 11 PH (100% females) from 520 cases (2.1%). Mean age at onset: 37.0 ± 13.9 years. Pain intensity: 8.7 ± 2.7. Nine cases (81.8%) presented autonomic symptoms, three (27.3%) followed a time pattern and one (9.1%) did not respond to indomethacin.
CONCLUSIONS
Hemicranias are not frequently diagnosed in day-to-day clinical practice. Their diagnosis requires the fulfilment of certain criteria that are sometimes not fully satisfied. We believe that the criteria need revising and we also support the recent inclusion of HC within the group of trigeminal-autonomic cephalgias.
Topics: Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal; Autonomic Nervous System; Female; Headache Disorders; Humans; Indomethacin; Male; Middle Aged; Paroxysmal Hemicrania; Retrospective Studies
PubMed: 25297475
DOI: No ID Found -
Anales de Pediatria (Barcelona, Spain :... Nov 2014
Topics: Child; Diagnosis, Differential; Humans; Lacrimal Apparatus Diseases; Male; Migraine Disorders; Paroxysmal Hemicrania
PubMed: 24380776
DOI: 10.1016/j.anpedi.2013.11.020