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Thyroid-associated ophthalmopathy (TAO) is a well-known and frequent epiphenomenon of a hyperthyroid autoimmune disease that can present with proptosis, strabismus, and diplopia. Ophthalmopathy can occur in the absence of overt Graves’ disease, even in euthyroid patients. Cavernous sinus dural fistulas (CS-DAVF) are abnormal communications between the cavernous sinus (CS) and dural branches from internal carotid or external carotid arteries. They can often present with ocular symptoms that can mimic a thyroid-associated ophthalmopathy. CS-DAVF are usually successfully treated with an endovascular embolization that can be pursued both through a transvenous or transarterial approach. TAO and CS-DAVF can coexist especially when the ocular symptoms are unilateral. In those cases, an endovascular embolization is usually curative, but sometimes the procedure can fail. Our hypothesis is that some cases of CS-DAVF may be of secondary nature (i.e., caused by compression of the venous outlet by the hypertrophic ocular muscles); therefore, treating the ocular disease with medical therapy may solve the vascular problem as well. We present a case of a CS-DAVF in a patient with TAO successfully treated with sole medical therapy after the failure of a first-line endovascular treatment.

Background The clinical criteria for cluster headache (CH) are included in Chapter 3 of the International Classification of Headache Disorders, 3rd beta edition (ICHD-III). CH may sometimes be secondary to other pathologies. Case reports We report two patients in whom the clinical features of CH initially fulfilled the ICHD-III criteria, but who later presented some radical modifications in headache natural history as a result of a secondary pathology. The first case of CH was secondary to a pontine cavernous angioma and the second to a cerebral venous thrombosis. Conclusion We highlight the importance of clinical modifications of CH that could suggest clinical investigations should be performed or repeated to exclude a secondary pathology in a previously diagnosed cluster headache. Some of the pathological mechanisms of CH and brain lesions are discussed.

Cluster headache (CH) is a rare and disabling primary trigeminal autonomic cephalalgia which interests especially the male population with smoking and alcohol ingestion habits. CH typically occurs at the same time of the day, once to eight times per day, and in the same period of the year. CH is featured by severe unilateral peri-orbital and/or temporal pain lasting from 15 to 180 minutes if untreated, associated with at least one autonomic symptom (conjunctival injection, lacrimation, nasal congestion, rhinorrhea, facial sweating, miosis, ptosis and eyelid edema)[1]. CH secondary forms can be a manifestation of neurological pathologies such as brain tumor, cerebral venous thrombosis[2], arterial aneurisma or multiple sclerosis[3].

Although olfactory hallucination or phantosmia could occur in several neurological and non-neurological conditions, olfactory migrainous hallucination (OMH) is a rare and probably underestimated phenomenon, involving about 0.1% of migraine patients[1], and not considered among the migrainous aura manifestations according to the International Classification of Headache Disorders, 3th edition (ICHD-III beta version)[2]. Very few clinical studies on the topic have been published[3]; therefore, the clinical characterization of OMH is still lacking.

Materials and methods By compiling a headache diary, efficacy parameters (mean reduction of headache days and hours) were evaluated at 90 days after the first cycle. We analyzed also: 30% and 50% response rates and the percent of firsttime responders to II cycle; association with headache related symptoms and comorbidities (depression/anxiety disorders, hypertension, sleep disturbances, caffeine intake, BMI >30).

Migraine (M) is one of the most frequent diseases recognized as a cause of disability, with a relevant influence on the quality of life, particularly in women.

According to the International Classification of Headache Disorders (2004), trigeminal neuralgia (TN) can be divided into classical and symptomatic [1]. The symptomatic TNs represent about 2% of cases and typically are caused by extrinsic lesions that produce neuropathy, demyelination, and axonopathy. We report on an unusual case of symptomatic TN due to an expansile lesion in the Meckel’s cave. A 54-year-old man presented with repetitive, severe stabbing pain localized to the left first and second trigeminal branch territory (zygomatic arch and orbit) lasting 1–2 min with a frequency of about 10–15 attacks/day. Despite that this symptomatology had developed abruptly, a dull background of persistent pain in the same region had started about 15 days before. The background pain was associated with photo-phonophobia and worsened with physical exertion. His past medical history was unremarkable. The patient did not present any cerebrovascular risk factors such as smoking, diabetes, or high blood pressure. The neurologic examination revealed an absence of the left corneal reflex and numbness in the ophthalmic and maxillary divisions of the nerve. A contrast-enhanced brain MRI detected an expansile lesion of the Meckel’s cave (Fig. 1a–d) with a cisternal portion and consequent dumbbell appearance. The lesion was T1-hyperintense on non-enhanced images and did not disappear on fat-saturated diffusion-weighted imaging, thus suggesting the presence of blood degradation products; after contrast medium administration, a marked enhancement of the cisternal portion of the trigeminal nerve was noted. Routine blood tests and hemocoagulative screening were normal; conventional catheter angiography of cerebroafferent vessels was negative. The patient underwent surgery that found a swollen and hemorrhagic Gasserian ganglion. At histology, blood without other pathologic tissue or microarteriovenous malformation was evidenced. After surgery, the pain resolved almost completely, while a complete left trigeminal deficit still persisted. At 3-year contrast-enhanced brain MRI, no sign of tumor was found in the Meckel’s cave, whereas a severe left masticatory muscles fatty degeneration was noted (Fig. 1d–f). Indeed, the patient presented with evident facial asymmetry due to severe left temporal and masseter muscle atrophy, without severe functional impairment. Traditionally, secondary TN constitutes a clinical syndrome attributed to a distinct, structural, pathologic lesion such as tumor, aneurysm, or other vascular malformation. The description of the pain can be identical to that seen in primary TN, with the exception that it tends to be accompanied by a continuous dull pain in the background and by trigeminal hypoesthesia or depression of the corneal reflex [2]. The age of onset may be somewhat younger than in the idiopathic cases, but it depends on the type of the structural lesion. We highlight an unusual cause of symptomatic TN related to an unknown-origin bleeding of the Gasserian ganglion mimicking a lesion. In the literature, only one case of spontaneous hematoma of Meckel’s cave has been reported [3]. A differential diagnosis needed to be performed with a hemorrhagic trigeminal schwannoma [4] or bleeding due to microarteriovenous malformation in the Meckel’s cave. Sometimes the latter might be F. Maggioni (&) M. Bellamio M. Margoni G. Zanchin Department of Neurosciences, Headache Centre, University of Padua, Via Giustiniani 5, 35128 Padua, Italy e-mail: ferdinando.maggioni@unipd.it