Posterior hypothalamic activation in paroxysmal hemicrania

Matharu, Manjit; Cohen, Anna; Frackowiak, R. S. J.; Goadsby, Peter J.

doi:10.1002/ana.20763

Cited by 187 publications

(139 citation statements)

References 71 publications

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“…Finally, we observed significant unilateral activation in the RN after heat stimulus to the V2A (Fig. 4), similar to that reported after experimental visceral and somatic pain in healthy subjects (Bingel et al, 2002;Dunckley et al, 2005) and in paroxysmal hemicrania (Matharu et al, 2006). A role for the RN in neuropathic pain is unknown, but it has been suggested to be involved in withdrawal behavior or execution of movements (Keifer and Houk, 1994) and the sensorimotor integration of nociceptive information involves via a spino-rubral circuit (Steffens et al, 2000).…”

Section: Thalamus and Cortex (Si)supporting

confidence: 85%

Trigeminal Neuropathic Pain Alters Responses in CNS Circuits to Mechanical (Brush) and Thermal (Cold and Heat) Stimuli

Becerra

Morris²,

Bazes³

et al. 2006

J. Neurosci.

172

140

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Functional magnetic resonance imaging was used to study patients with chronic neuropathic pain involving the maxillary region (V2) of the trigeminal nerve in patients with spontaneous pain and evoked pain to brush (allodynia). Patients underwent two functional scans (2-3 months apart) with mechanical and thermal stimuli applied to the affected region of V2 and to the mirror site in the unaffected contralateral V2 region, as well as bilaterally to the mandibular (V3) division. Patients were stimulated with brush, noxious cold, and noxious heat. Significant changes were observed in regions within and outside the primary trigeminal sensory pathway. Stimulation to the affected (neuropathic) side resulted in predominantly frontal region and basal ganglia activation compared with the control side. The differences were consistent with the allodynia to brush and cold. A region of interest-based analysis of the trigeminal sensory pathway revealed patterns of activation that differentiated between the affected and unaffected sides and that were particular to each stimulus. Activation in the spinal trigeminal nucleus was constant in location for all pain stimuli. Activation in other brainstem nuclei also showed differences in the blood oxygenation level-dependent signal for the affected versus the unaffected side. Thus, sensory processing in patients with trigeminal neuropathic pain is associated with distinct activation patterns consistent with sensitization within and outside of the primary sensory pathway.

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Section: Thalamus and Cortex (Si)supporting

confidence: 85%

Trigeminal Neuropathic Pain Alters Responses in CNS Circuits to Mechanical (Brush) and Thermal (Cold and Heat) Stimuli

Becerra

Morris²,

Bazes³

et al. 2006

J. Neurosci.

172

140

View full text Add to dashboard Cite

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“…Although cluster headaches have been reported to respond to indomethacin, 8 this feature usually suggests paroxysmal hemicrania 2 and raises the possibility that this phenomenon may be relevant to the trigeminal autonomic cephalgias (TAC) as a group, all of which are associated with the posterior hypothalamus. 9 The sympathetic nervous system is believed to be associated with TAC in a passive manner 1 ; however, in some cases, there is evidence of sympathetic dysfunction before the onset of TAC, 10 suggesting that sympathetic underactivity may underlie TAC pathogenesis. If TAC pain is dependent on low sympathetic tone, theoretically the episode could be reversed by the increase in sympathetic activity accompanying sexual activity and, specifically, orgasm.…”

Section: Discussionmentioning

confidence: 99%

Now dear, I have a headache! Immediate improvement of cluster headaches after sexual activity

Guillaume

Steiner

Biran

2006

Journal of Neurology, Neurosurgery & Psychiatry

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“…It is noteworthy that a previous PET study found significant activation of the contralateral posterior hypothalamus in untreated PH, 13 whereas ipsilateral posterior hypothalamic activation has been demonstrated during a cluster headache attack. 11 Nevertheless, ipsilateral hypothalamic stimulation was effective in the patient with PH, as already noted, 64 just as it is in cluster headache.…”

Section: Sunct Syndrome and Paroxysmal Hemicraniamentioning

confidence: 87%

“…11 This latter area was initially thought to be activated only in cluster headache, and was proposed as the cluster generator. 11 It was subsequently shown, however, that this hypothalamic area is also activated during SUNCT, 12 PH, 13 and hemicrania continua. 14 Hemicrania continua is a strictly unilateral headache accompanied by ipsilateral oculofacial autonomic symptoms not now considered to be a trigeminal autonomic cephalalgia, because of its long-lasting pain.…”

Section: Rationale For Hypothalamic Stimulation In Headachementioning

confidence: 99%

Deep brain stimulation for trigeminal autonomic cephalalgias

Messina

Broggi

Levi

et al. 2018

Expert Review of Neurotherapeutics

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Summary:Cluster headache (CH), paroxysmal hemicrania (PH), and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT syndrome) are primary headaches grouped together as trigeminal autonomic cephalalgias (TACs). All are characterized by short-lived unilateral head pain attacks associated with oculofacial autonomic phenomena. Neuroimaging studies have demonstrated that the posterior hypothalamus is activated during attacks, implicating hypothalamic hyperactivity in TAC pathophysiology and suggesting stimulation of the ipsilateral posterior hypothalamus as a means of preventing intractable CH. After almost 10 years of experience, hypothalamic stimulation has proved successful in preventing pain attacks in approximately 60% of the 58 documented chronic drug-resistant CH patients implanted at various centers. Positive results have also been reported in drug-resistant SUNCT and PH. Microrecording studies on hypothalamic neurons are increasingly being performed and promise to make it possible to more precisely identify the target site. The implantation procedure has generally proved safe, although it carries a small risk of brain hemorrhage. Long-term stimulation is proving to be safe: studies on patients under continuous hypothalamic stimulation have identified nonsymptomatic impairment of orthostatic adaptation as the only noteworthy change. Studies on pain threshold in chronically stimulated patients show increased threshold for cold pain in the distribution of the first trigeminal branch ipsilateral to stimulation. When the stimulator is switched off, changes in sensory and pain thresholds do not occur immediately, indicating that long-term hypothalamic stimulation is necessary to produce sensory and nociceptive changes, as also indicated by clinical experience that CH attacks are brought under control only after weeks of stimulation. Infection, transient loss of consciousness, and micturition syncope have been reported, but treatment interruption usually is not required.

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Posterior hypothalamic activation in paroxysmal hemicrania

Abstract: These activated subcortical structures may play a pivotal role in the pathophysiology of this syndrome.

Cited by 187 publications

References 71 publications

Trigeminal Neuropathic Pain Alters Responses in CNS Circuits to Mechanical (Brush) and Thermal (Cold and Heat) Stimuli

Trigeminal Neuropathic Pain Alters Responses in CNS Circuits to Mechanical (Brush) and Thermal (Cold and Heat) Stimuli

Now dear, I have a headache! Immediate improvement of cluster headaches after sexual activity

Deep brain stimulation for trigeminal autonomic cephalalgias

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