Brainstem Influences on the Cephalic Circulation: Experimental Data From Cat and Monkey of Relevance to the Mechanism of Migraine

Lance, James W.; Lambert, Geoffrey; Goadsby, Peter J.; Duckworth, J. W.

doi:10.1111/j.1526-4610.1983.hed2306258.x

Cited by 159 publications

(81 citation statements)

References 15 publications

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“…Lance et al (11) suggested that brainstem centres such as the locus coeruleus and raphe nuclei influence the vascular changes and pain of migraine; heightened activity of the locus coeruleus might also facilitate sensory processing. The cerebral cortex is densely innervated by noradrenergic fibres from the locus coeruleus.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Increased Sensitivity to Noise and Light in Migraine Headache

Woodhouse

Drummond

1993

Cephalalgia

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Cephalalgia Woodhouse A, Drummond PD. Mechanisms of increased sensitivity to noise and light in migraine headache. Cephalalgia 1993;13:417-21. Oslo. ISSN 0333-1024 To determine whether phonophobia is a manifestation of loudness recruitment, the hearing and auditory discomfort thresholds to an 8000 Hz tone were measured during the headache-free interval and again during an attack of migraine in 16 migraine sufferers. The visual discomfort threshold was also determined. For comparison, measures were taken in 10 non-headache controls of similar age and sex distribution. Auditory and visual discomfort thresholds decreased substantially during attacks of migraine. Increases (three subjects) or decreases (three subjects) in hearing threshold during attacks of migraine were significantly greater than the variation recorded in control subjects from Session I to Session 2. The findings do not support the view that phonophobia in migraine is a manifestation of loudness recruitment, although cochlear disturbances might mediate hearing loss in some cases. Disruption of central sensory processing mechanisms during migraine could increase sensitivity to quiet sounds, and contribute to phono-and photophobia. € Loudness recruitment, migraine, phonophobia, photophobia Peter Drummond, Psychology Section, Murdoch University, 6150, Western Australia. Received 18 May 1993, accepted 30 July 1993 Most migraine sufferers develop an intolerance to light (photophobia) and sound (phonophobia) during headache, preferring to wait out their attack in a quiet, dark room. Kayan and Hood (1) suggested that phonophobia in migraine might have the same pathology as loudness recruitment (an abnormally rapid increase in loudness with increase in intensity of sound), which accompanies cochlear disturbances. Patients with loudness recruitment dislike loud noise because it sounds distorted. In patients with unilateral cochlear hearing loss, loudness in the recruiting ear generally catches up with and matches loudness in the normal ear at high sound levels (2). Thus, there is a reduced dynamic range between the hearing threshold and the level at which sounds become uncomfortably loud.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of Increased Sensitivity to Noise and Light in Migraine Headache

Woodhouse

Drummond

1993

Cephalalgia

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“…Such an effect could account for both the neurological symptoms of migraine and the observed changes in blood flow and vascular reactivity. 6 In fact, it has been shown that extracranial blood flow is increased by 50% during migraine headache compared with that of normal subjects. 7 Thus, an increase in blood flow at the site of the migraine may result from alterations in sympathetic tone.…”

Section: Commentsmentioning

confidence: 99%

“…The reason this temporary sympathetic blockade may have triggered migraine headaches 24 hours later can only be postulated from data obtained from previous studies. [5][6][7][8] Abnormalities in autonomic nervous system control have been well documented in migraine, even during the headache-free interval. This autonomic imbalance in migraine consists of markedly enhanced sympathetic sensitivity with nonsignificantly reduced parasympathetic activity during headache-free periods.…”

Section: Commentsmentioning

confidence: 99%

Migraine Headache Following Stellate Ganglion Block for Reflex Sympathetic Dystrophy

Lehmann¹,

Warfield²,

Bajwa³

1996

Headache

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The alteration of extracranial blood flow in conjunction with clinical signs of autonomic nervous system dysfunction have led to various explanations concerning the pathophysiology of migraine headache.Reflex sympathetic dystrophy, a painful disorder of the sympathetic nervous system, can be treated by blocking the sympathetic nerves located in the stellate ganglion, resulting in vasodilation, ptosis, miosis, and anhydrosis. In theory, these changes could trigger a migraine headache attack secondary to autonomic dysfunction reflecting an imbalance between sympathetic and parasympathetic nervous systems. This may be especially true in a patient with a previous history of meningitis that may have resulted in a disorder of cerebrovescular regulation. We report a 56-year-old man with no previous history of migraine who developed migraine with aura after a stellate ganglion block. Those episodic headaches occurred with decreasing frequency end severity for over 6 months, with eventual complete resolution. This interesting phenomenon has not been reported in the English literature and may help to better understand the pathophysiology of migraine.Key words: migraine, meningitis, stellate ganglion block, reflex sympathetic dystrophy, oculosympathetic paresis (Horner's syndrome), sumatriptan (Headache 1996;36:335-337) The International Headache Society (IHS) defines a typical attack of migraine without aura as a moderate to severe throbbing, usually unilateral headache associated with nausea, anorexia, phonophobia, and photophobia which occurs one to four times per month lasting 4 to 72 hours (untreated or unsuccessfully treated), aggravated by physical activity, and usually improved with sleep. This definition of migraine is comprehensive and requires five previous attacks and is often familial. The definition of migraine with aura requires two attacks and concentrates on the details and timing of the aura. 1,2 Three of the following four characteristics must be noted (1) one or more fully reversible symptoms, (2) at least one aura symptom develops gradually over 4 minutes or two or more symptoms occur in succession, (3) no aura symptom lasts more than 60 minutes, and (4) headache follows aura with a free interval of less than 60 minutes.There is some evidence that an increase in extracranial blood flow contributes to pain in some migraine sufferers, particularly in patients with clear signs of ocular sympathetic deficit on the usual side of the headache. 3 We report a case of apparent migraine headache with aura following a stellate ganglion block. To our knowledge, this is the first case report describing this phenomena. CASE HISTORYA 56-year-old right-handed man was evaluated at our pain management center for symptoms consistent with the diagnosis of reflex sympathetic dystrophy (RSD) involving his left upper extremity. Two years previously, the patient was injured when a piece of glass penetrated the skin between the second and third metacarpals of his left hand. This area was explored and a 3 to 4 mm piece of gl...

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“…The brainstem became a focus of attention for migraine research about 20 years ago in several laboratories including ours [Lance et al, 1983] and there is increasing evidence that a ''perturbation'' [Raskin et al, 1987] of the brainstem may lead to migraine. Two brainstem centers have been implicated in this defect-the periaqueductal gray matter (PAG) [Welch et al, 2001] and the nucleus raphe magnus (NRM) [Ellrich et al, 2001]-through which the PAG may relay.…”

Section: Brainstemmentioning

confidence: 99%

“…It is fair to say that most neural theories have adhered to Liveling's idea that some form of increased activity, somewhere in the CNS, is the ultimate cause of migraine pain. Brain areas or nuclei that have come under suspicion include the cortex [Hardebo, 1991], the periaqueductal gray matter (PAG) [Welch et al, 2001], the raphe nuclei, including the nucleus raphe magnus (NRM) [Lance et al, 1983;MacKenzie et al, 1985], the locus coeruleus [Goadsby et al, 1982], the superior salivatory nucleus [Burstein and Jakubowski, 2005], and the thalamus [Shields and Goadsby, 2005].…”

Section: Neural Theoriesmentioning

confidence: 99%

Looking in the wrong place? The search for an ideal migraine preventative

Lambert¹

2007

Drug Development Research

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The cause of migraine headache is still unknown, although triggers for it are often apparent. There are, in consequence, no reliable migraine headache preventative drugs that act through an influence on known causal pathways. This review discusses the pathophysiology of migraine, the link between migraine triggers and the consequent headache and the putative mode of action of different classes of migraine drugs in the light of a number of pathophysiological models. It advances the idea that migraine triggers produce headache because they increase cortical excitability and discharge, which in turn reduces the inhibitory drive of the descending pain control system, selectively for trigeminovascular sensation. Supporting evidence for such a mechanism is presented and suggestions made as to the modes and sites of action of future improved migraine preventative agents. Drug Dev Res 68: 376-388, 2007.

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Brainstem Influences on the Cephalic Circulation: Experimental Data From Cat and Monkey of Relevance to the Mechanism of Migraine

Cited by 159 publications

References 15 publications

Mechanisms of Increased Sensitivity to Noise and Light in Migraine Headache

Mechanisms of Increased Sensitivity to Noise and Light in Migraine Headache

Migraine Headache Following Stellate Ganglion Block for Reflex Sympathetic Dystrophy

Looking in the wrong place? The search for an ideal migraine preventative

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