Hypothalamic activation after stimulation of the superior sagittal sinus in the cat: a Fos study

Benjamin, Laura; Levy, Miles; Lasalandra, Michele P; Knight, Yolande E.; Akerman, Simon; Classey, John; Goadsby, Peter J.

doi:10.1016/j.nbd.2004.03.015

Cited by 100 publications

(57 citation statements)

References 35 publications

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“…The fi ndings indicate a complex relationship between nociceptive trigeminal neuronal activation and suppression of food intake at the level of the hypothalamus, consistent with clinical observations of loss of appetite in primary headaches [23]. Stimulation of the superior sagittal sinus in the cat has also demonstrated hypothalamic activation in the supraoptic and posterior hypothalamic nucleus, consistent with a role for hypothalamic structures in modulation of nociceptive processing [24].…”

Section: Experimental Evidence For Hypothalamic Involvement In Clustesupporting

confidence: 79%

Cluster headache, hypothalamus, and orexin

Holland

Goadsby²

2009

Current Science Inc

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Cluster headache (CH) is a highly disabling condition resulting in severe, recurrent unilateral bouts of pain and accompanying autonomic symptoms. This review describes some current views regarding the underlying pathophysiology covering the pain and cranial autonomic (parasympathetic) activation, and highlights the potential importance of the hypothalamus in CH. The hypothalamus is known to modulate many functions and has been shown to be involved in the pathophysiology of a variety of primary headaches, including CH. Hypothalamic structures are likely to underlie the circadian and circannual periodicity of attacks and contribute to the pain and autonomic disturbances. We discuss the hypothalamic involvement in CH and modulation of trigeminovascular processing and examine the emerging involvement of the hypothalamic orexinergic system as a possible key pathway in CH pathophysiology.

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Section: Experimental Evidence For Hypothalamic Involvement In Clustesupporting

confidence: 79%

Cluster headache, hypothalamus, and orexin

Holland

Goadsby²

2009

Current Science Inc

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“…Although animal experiments suggest the lateral hypothalamus to be involved in pain modulation (Dafny et al, 1996;Workman and Lumb, 1997), serving as a relay station for nociceptive transmission and autonomic function (Randich and Gebhart, 1992), electrical stimulation of the hypothalamus to produce analgesia has only been used in experimental animals (Lopez et al, 1991). Conversely, electrical stimulation of the superior sagittal sinus activates the supra-optic nucleus and posterior hypothalamic area (Benjamin et al, 2004) [a monosynaptic pathway connecting the hypothalamus and trigeminal nucleus has been documented (Malick et al, 2000)]. The posterior hypothalamus is able to both decrease and enhance nociceptive responses in the trigeminal nucleus caudalis (Bartsch et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic Deep Brain Stimulation in Positron Emission Tomography

May¹,

Leone²,

Boecker³

et al. 2006

J. Neurosci.

163

101

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Recently, functional imaging data have underscored the crucial role the hypothalamus plays in cluster headache, one of the most severe forms of primary headache. This prompted the application of hypothalamic deep brain stimulation. Yet, it is not apparent how stimulation of an area that is thought to act as a pace-maker for acute headache attacks is able to prevent these attacks from occurring. We addressed this issue by examining 10 operated chronic cluster headache patients, using H 2 15 O-positron emission tomography and alternately switching the hypothalamic stimulator on and off. The stimulation induced activation in the ipsilateral hypothalamic gray (the site of the stimulator tip), the ipsilateral thalamus, somatosensory cortex and praecuneus, the anterior cingulate cortex, and the ipsilateral trigeminal nucleus and ganglion. We additionally observed deactivation in the middle temporal gyrus, posterior cingulate cortex, and contralateral anterior insula. Both activation and deactivation are situated in cerebral structures belonging to neuronal circuits usually activated in pain transmission and notably in acute cluster headache attacks. Our data argue against an unspecific antinociceptive effect or pure inhibition of hypothalamic activity. Instead, the data suggest a hitherto unrecognized functional modulation of the pain processing network as the mode of action of hypothalamic deep brain stimulation in cluster headache.

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“…One plausible explanation for sensitisation in migraine would be dysfunction of known sub-cortical trigeminal modulatory nuclei, i.e., disinhibitory sensitisation rather than sensitisation due to abnormal afferent traffi c [58] . Most prominent among these inhibitory systems are projections from brainstem structures, such as the periaqueductal gray (PAG), nucleus raphe magnus (NRM) and the rostroventral medulla (RVM), which have a profound antinociceptive effect on these neurons [59] , but other structures such as the hypothalamus [60] , thalamus [61] and cortical regions seem also to be involved. Recent fi ndings emphasize the role of the ventrolateral division of the PAG (vlPAG) in trigeminal nociception as stimulation of the vlPAG modulates dural nociception and receives input from trigeminovascular afferent [62][63][64] .…”

Section: Disinhibitory Sensitisation -Disordered Modulation Of Trigemmentioning

confidence: 99%

Migraine, Allodynia, Sensitisation and All of That ...

Goadsby¹

2005

Eur Neurol

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Migraine is the most common form of disabling primary headache. One common and often troublesome feature of the disorder is an abnormal sensory state where normally innocuous stimuli are felt as painful: allodynia. This occurs in about two-thirds of patients and manifests as common complaints, such as pain when touching the hair. The neurophysiological correlate of allodynia is sensitisation, an increased afferent barrage for an unchanged peripheral stimulus. Sensitisation may be peripheral, central or disinhibitory. The potential mechanisms of each of these and their possible manipulation by treatments of the acute attack are considered.

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Hypothalamic activation after stimulation of the superior sagittal sinus in the cat: a Fos study

Cited by 100 publications

References 35 publications

Cluster headache, hypothalamus, and orexin

Cluster headache, hypothalamus, and orexin

Hypothalamic Deep Brain Stimulation in Positron Emission Tomography

Migraine, Allodynia, Sensitisation and All of That ...

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