Anatomy and Pathology of Cluster Headaches



Anatomy and Pathology of Cluster Headaches


Jan Erik Hardebo

Norihiro Suzuki



The location of maximal pain in cluster headache (CH) is strikingly similar in almost every sufferer: it is felt deep in or behind the orbit on one side. The signs of disturbed autonomic function in the eye, nose, and facial skin are also closely linked to the pain, both spatially and temporally. This points to deep orbital or retro-orbital structures as being affected in the disease. The tendency to develop CH on the other half of the face is 200 times higher than for an individual to develop the disease at all (33). This indicates that a structure with anatomic connections over the midline is involved.

CH persists, and may also arise, after ipsilateral enucleation (18). Likewise, CH may even arise after ipsilateral orbital exenteration (6,23). This demonstrates that CH may arise after an operation in this area but that the pain of CH does not originate in the eye and that intact structures in the orbit are not necessary for the formation of attacks. Thus, pain appears to originate from retro-orbital structures, except in cases with referred pain (see below).


PATHOLOGY OF IDIOPATHIC CASES

Epidemiologic studies reveal a marked correlation between CH and prior head trauma (5,6). Narrow nasal passages, such as a deviated nasal septum, are often found on the painful side in CH sufferers (7,8). Surgical resections in this area, to eliminate narrow conditions, are sometimes beneficial (7). Craniometric measures in CH suggest narrowness of the cavernous sinus/hypophyseal fossa region (8). These findings may represent constitutional predisposing factors for CH. Investigations with magnetic resonance imaging (MRI) of the cavernous sinus region outside of CH attacks has not revealed any pathologic changes (9).

By the aid of voxel-based morphometric analysis of MRI scans, an increase in tissue volume within the posterior hypothalamic area has been found in CH sufferers (10). This finding was bilateral, remained outside periods of attacks, and was interpreted as an increase in neuronal density. The area is similar or identical to local findings during attacks of an ipsilateral increase in blood flow (see neuroimaging of cluster headache), as a cause or a consequence of pain.


PATHOLOGY OF SYMPTOMATIC CASES

Several symptomatic cases have been described in which CH-like attacks have evolved secondary to the growth of an intracranial expansive process, ipsilaterally, or in the midline: orbitosphenoidal aspergillus infection (11), parasellar meningioma (12), adenoma of the pituitary gland (12,13), calcified lesion in the region of the third ventricle (14), aneurysm of the anterior or posterior communicating artery (15,16), dilated ipsilateral and aneurysmatic contralateral internal carotid artery (ICA) intracranially (15), granulomatous tissue in the cavernous sinus (17) epidermoid tumor in the clivus expanding rostrally to the suprasellar cistern (18), large arteriovenous malformations in the ipsilateral frontal, temporal, parietotemporal, or occipital lobes (19, 20, 21, 22), meningioma or inflammatory myofibroblastic tumor on the undersurface of the tentorium cerebelli (23,24), and upper cervical meningioma (2).

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Jun 21, 2016 | Posted by in PAIN MEDICINE | Comments Off on Anatomy and Pathology of Cluster Headaches

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