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A diagnosis of idiopathic intracranial hypertension with- out papilledema (IIHWOP) should be considered in unresponsive chronic daily headache (CDH) patients [1]. A CSF opening pressure (OP) above 200 mm H2O has been detected in chronic migraine patients with conflict-ing result, ranging from 10% to 86% of patients [1,2]. Moreover, controversies ex ist regarding the OP cut-off value greater than 200 or 250 mm H2O and the role of transverse sinus stenosis (TSS) [3,4].

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Background: No valid biomarkers are available to detect among patients who suffer from Episodic (EM) and Chronic migraine (CM) those at greatest risk of develop a Medication Overuse Headache (MOH). Several evidences confirmed that pain vulnerability and attitude to chronic pain sensitivity are heritable via genetic but also epigenetic pathways though changes in DNA expression. Epigenetic mechanisms would have the potential to link early life events, neuro-inflammation and brain plasticity in the aetiology of migraine chronification. Method: The aim of this pilot study was to identify changes in DNA methylation associated with headache chronification comparing controls without headache (HC), episodic migraineurs and patients suffering from MOH. In all selected subjects, genome-wide DNA methylation levels were characterized longitudinally at baseline and during follow-up using the Infinium HumanMethylationEPIC Bead-Chip. Results: A total of 25 patients with MOH were enrolled at baseline (T0), of these 18 completed the 6 months follow up (T3). In the group of EM, 20 patients were enrolled and completed the 6-month follow up (T1). 13 HC subjects were enrolled at T0, and 11 completed study. Comparing MOH vs HC group at T0, none differentially methylated regions (DMRs) reached statistical significance. Nevertheless 29 DMRs had a delta of at least 0.05 in at least one CpG site. One of the most significant CpG site identified was at the chr10:76993892 island, which maps in the COMT (catechol-O-methyltransferase) gene and resulted hypermethylated in MOH. Discussion: These preliminary data suggest a role in MOH of epigenetic processes involved in aberrant immune-inflammatory responses and deregulation of dopaminergic neurotransmission theoretically implied in mechanisms of brain plasticity which control drug addiction and cognitive-emotional processes. However, all these data are preliminary and require replication and validation in a larger sample.

Background and purpose Adult-onset autosomal dominant leukodystrophy (ADLD) is a rare progressive neurological disorder caused by Lamin B1 duplication (LMNB1). Our aim was to investigate longitudinally the pattern of the autonomic dysfunction and the degree of neuropsychological involvement. Methods Three related ADLD patients and one asymptomatic carrier of LMNB1 duplication underwent a standardized evaluation of autonomic nervous system, including cardiovascular reflexes, pharmacological testing, microneurography, skin biopsy, Metaiodobenzylguanidine scintigraphy and a complete neuropsychological battery. Results An early neurogenic orthostatic hypotension was detected in all patients and confirmed by a low rise in noradrenaline levels on Tilt Test. However infusion of noradrenaline resulted in normal blood pressure rise as well as the infusion of clonidine. At the insulin tolerance test the increase in adrenaline resulted pathological in two out three patients. Microneurography failed to detect muscle sympathetic nerve activity bursts. Skin biopsy revealed a poor adrenergic innervation, while cardiac sympathetic nerves were normal. None of ADLD patients showed a global cognitive deficit but a selective impairment in the executive functions. Conclusion Autonomic disorder in ADLD involves selectively the postganglionic sympathetic system including the sympatho-adrenal response. Cognitive involvement consisting in an early impairment of executive tasks that might precede brain MR abnormalities.

Introduction adult-onset autosomal dominant leukodystrophy (ADLD) is a rare inherited disorder due to a duplication of lamin-B1 (LMNB1) gene. The aim of this study was to investigate brain metabolic and microstructural alterations by using advanced MR techniques. Methods we performed brain MR scans including single-voxel proton-MR Spectroscopy ( 1 H-MRS) of the lateral ventricles and parietal white matter and diffusion tensor imaging (DTI) in 4 subjects with LMNB1 gene duplication, 6 non-mutated relatives and 7 unrelated healthy controls. Cervical and thoracic spinal cord MR was performed in three symptomatic subjects with LMNB1 mutation. All participants underwent clinical and neuropsychological evaluation. Results all subjects with LMNB1 gene duplication presented pathological accumulation of lactate in lateral ventricles CSF and no alterations of brain white matter absolute metabolites concentrations or metabolites/Cr ratios. We found increased white matter intra- and extracellular water transverse relaxation times. Tract-based spatial statistics analysis detected a significantly reduced fractional anisotropy in the genu of the corpus callosum in mutated cases compared to unrelated healthy controls and non-mutated relatives. Moreover, we detected different degrees of the typical white matter signal intensity alterations and brain and spinal atrophy at conventional MRI in symptomatic subjects with LMNB1 mutation. A mild impairment of executive functions was found in subjects with LMNB1 gene mutation. Conclusion in subjects with LMNB1 gene duplication, we found a pathological increase in CSF lactate, likely due to active demyelination along with glial activation, and microstructural changes in the genu of the corpus callosum possibly underpinning the mild neuropsychological deficits.

Headache-related healthcare system utilization. Number of consultations per year are categorizes into 4 groups, and shown as percentage of the student population. 1Missing data on 3 patients from Germany and 5 patients from Spain, respectively. (PDF 55 kb)

Medication overuse headache sub-diagnosis and duration of medication overuse. The table characterizes the medication overuse headache (MOH) sub-diagnosis. Results are shown as percent of patients with a specific MOH sub-diagnosis. Numbers in brackets presents the proportion of the patient population that used a specific analgesics 30 days/month. p-values correspond to comparison of MOH sub-diagnosis between Europe and Latin America. *p

Multiple medication overuse headache sub-diagnoses and specific combination of medication overuse. The table characterizes the proportion of patients with multiple medication overuse headache (MOH) sub-diagnoses and the specific medication overuse profile. The data are shown as percentages. (PDF 66 kb)

Multiple medication overuse headache sub-diagnoses and specific combination of medication overuse. The table characterizes the proportion of patients with multiple medication overuse headache (MOH) sub-diagnoses and the specific medication overuse profile. The data are shown as percentages. (PDF 66 kb)

According to International Headache Classification (ICHD-3), migraine is classified in episodic migraine (EM) and chronic migraine (CM) based on the frequency of attacks. Medication overuse headache (MOH) is a secondary chronic headache disorder defined as a frequent headache (15 days per month or more) induced by the overuse of analgesics. Currently, the best treatment options include a detoxification programme based on the abrupt withdrawal of overused painkillers and eventually a preventive treatment. Despite these therapeutic efforts, the relapse rate of MOH is high, and no valid biomarkers are available to detect among patients who suffer from EM and CM those at greatest risk of develop MOH. According to available data, certain groups of people are more vulnerable to develop chronic pain conditions and poor adaptation to stress.

Background: Drug withdrawal still remains the key element in the treatment of Medication Overuse Headache (MOH), but there is no consensus about the withdrawal procedure. Still debated is the role of the steroid therapy. The aim of this study was to evaluate the effectiveness of methylprednisolone or paracetamol in the treatment of withdrawal headache in MOH. Methods: We performed a pilot, randomized, single-blinded, placebo controlled trial. MOH patients, unresponsive to a 3 months prophylaxis, underwent withdrawal therapy on an inpatient basis. Overused medications were abruptly stopped and methylprednisolone 500mg i.v (A) or paracetamol 4g i.v. (B) or placebo i.v. (C) were given daily for 5days. Patients were monitored at 1 and 3months. Results: Eighty three consecutive MOH patients were enrolled. Fifty seven patients completed the study protocol. Nineteen patients were randomized to each group. Withdrawal headache on the 5th day was absent in 21.0% of group A, in 31.6% of group B and in 12.5% of group C without significant differences. Withdrawal headache intensity decreased significantly after withdrawal without differences among the groups. Rregardless of withdrawal treatment, 52% MOH patients reverted to an episodic migraine and 62% had no more medication overuse after 3 months. Conclusions: This study suggests that in a population of severe MOH patients, withdrawal headache decreased significantly in the first 5 days of withdrawal regardless of the treatment used. Methylprednisolone and paracetamol are not superior to placebo at the end of the detoxification program.

Background: Depression-related gray matter changes in Parkinson disease (PD) patients have been reported, although studies investigating cortical thickness in early-stage disease are lacking. Objective: We aimed to evaluate cortical changes related to depression in early-stage PD patients with an extensive neuropsychological evaluation. Methods: 17 PD patients and 22 healthy controls underwent a 1.5-T brain MR protocol, and voxel-wise differences in cortical thickness among patients with (n = 6) and without (n = 11) depression and controls were evaluated using FreeSurfer software. Results: Cortical thickness was increased in the precuneus bilaterally in PD patients with depression compared to the other groups (number of vertices >100; p < 0.001, uncorrected) with a direct correlation with the Beck Depression Inventory score (p < 0.001, uncorrected). Conclusion: Precuneal cortical thickening is evident in PD patients with mild-moderate depression even in the early stages of the disease. This finding may reflect the early involvement of this region in the development of PD-related depression.

Colloid cysts are rare congenital benign tumors accounting for 0.2-2% of all intracranial neoplasms. They usually occur in the front part of the third ventricle. The clinical presentation is related to the increased intracranial pressure and is widely variable; sudden death associated with acute hydrocephalus can occur, therefore recognition of this rare condition is important in order to select an appropriate surgical treatment. We report a case of new onset headache secondary to a colloid cyst of the third ventricle. Case report A 44-year-old woman with unremarkable medical history was admitted to our clinic for recurrent attacks of pressing headache, with abrupt onset and brief duration, accompanied by nausea, transient hearing loss and tinnitus. These symptoms were relieved by supine position. The clinical picture progressively worsened, with episodes of vomiting during headache. Neurological examination was negative. A magnetic resonance imaging (MRI) scan showed a spherical mass lesion with lipid signal at the intraventricular foramina of Monro causing compression of the third ventricle and expansion of the ventricular system, suggestive of hydrocephalus. After neurosurgical evaluation the patient underwent an endoscopic removal of the lesion. Histological findings were compatible with colloid cyst of the third ventricle. After surgical treatment the patient recovered completely from symptoms and the follow-up MRI demonstrated the complete excision of the lesion. Conclusions Colloid cysts are congenital, slow growing, benign intraventricular lesions usually arising in the third ventricle. They may cause obstruction of the foramen of Monro with blockage of cerebrospinal fluid (CSF) flow, producing progressive or intermittent elevated intracranial pressure with chronic or acute hydrocephalus [1]. The onset of symptoms is usually between 20 to 50 years of age, often with paroxismal attacks of severe headache associated with nausea and vomiting [2]. Presentations with thunderclap headache have also been described [3]. Headache can resolve or reduce in supine position, suggesting that the colloid cyst moves in and out of the foramen of Monro with intermittent obstruction of CSF. Colloid cysts, if left untreated, may lead to serious complications such as visual loss, memory difficulties, acute disturbances of consciousness and even sudden death as a consequence of acute obstructive hydrocephalus with brain herniation or cardiovascular failure due to abrupt disturbance of hypothalamic function. The risk of sudden neurologic deterioration cannot be predicted, therefore surgical treatment is recommended [1, 2]. Our case highlights the importance of early detection and prompt treatment of this potentially life-threatening cause of headache.