E. Marano

Flunarizine in Prophylaxis of Childhood Migraine: A Double-Blind, Placebo-Controlled, Crossover Study

An 8-month, double-blind, placebo-controlled, crossover trial of flunarizine in the prophylaxis of migraine has been performed in 70 children. After 4 weeks of medication-free base-line observation, 35 children (group A) received flunarizine (5 mg/day) and 35 (group B) received placebo over a 12-week period. After a 4-week washout they crossed treatments for another 12 weeks. Sixty-three patients completed the trial. In both groups flunarizine significantly reduced the frequency and average duration of headache attacks. In group A efficacy was maintained after placebo crossover for the last 4 months of the study. Five subjects in group B stopped placebo because of ineffectiveness; two children in group A discontinued flunarizine treatment, one because of excessive daytime sedation and the other because therapy was ineffective. The main side effects were daytime sedation and weight gain. It is concluded that flunarizine is an effective drug for the treatment of childhood migraine. In a study of this length no serious side effects were discovered.

Sudden re-opening of collapsed transverse sinuses and longstanding clinical remission after a single lumbar puncture in a case of idiopathic intracranial hypertension. Pathogenetic implications

The aetiopathogenetic role of sinus venous obstructions carried by most idiopathic intracranial hypertension (IIH) patients is controversial. We report the case of a young woman diagnosed with IIH with papilloedema and narrowing of transverse sinuses, in which lowering of intracranial pressure by a single 20 ml cerebrospinal fluid (CSF) resulted in a strong dimensional increase of the transverse sinuses. Changes were followed by clinical remission and normalisation of optical nerve calibre, maintained after a 2-month follow-up. Our findings indicate that, although secondary to CSF hypertension, venous sinuses compression may have an important role in hypertensive status maintenance. Pathogenetic implications of venous sinus compression by hypertensive CSF in IIH are discussed.

Trigeminal Stimulation Elicits a Peripheral Vestibular Imbalance in Migraine Patients

Objective.—The study explored the hypothesis that spontaneous nystagmus (Ny) in migraine patients can be triggered or modulated by painful trigeminal stimulation, providing evidence of a functional connection between vestibular and trigeminal systems.

A clinical comparison of trigeminal neuralgic pain in patients with and without underlying multiple sclerosis.

Despite clinical similitude, there is a tendency to consider trigeminal pain in multiple sclerosis (MS) as a distinct condition. To evaluate clinical differences in trigeminal pain presentation in patients with and without underlying MS, we compared clinical characteristics of facial pain found in 15 consecutive MS patients with those reported by 13 consecutive subjects diagnosed with classical trigeminal neuralgia. The only significant difference between MS and non-MS neuralgic patients was the age of onset of pain (43.4±10.5 in MS vs. 59.6±11.50 in non-MS patients, p=0.000629, unpaired Student’s t-test). No differences were observed for side, duration and quality of pain, trigeminal branches involved, presence of trigger areas or factors, pain refractive period, remitting-relapsing or chronic course. There was only a trend without statistical significance in interval pain and trigeminal hypoesthesia, more frequent in MS population. Only one patient in the MS group presented with long-lasting episodes (45–60 min) of atypical odontalgia. Our findings support the view of a common pathogenetic mechanism underlying TN in the two groups, possibly related to demyelination of the trigeminal entry root in the pons. Typical TN in MS patients should be considered as “symptomatic trigeminal neuralgia”.

Hypnic headache: an update

Hypnic headache (HH) is a rare sleep-associated primary headache disorder, usually affecting aged people, first described by Raskin in 1988. The headache attacks, single or multiple in one night, occur exclusively during sleep and tend to present at a consistent time each night, sometimes during a dream. Compared to the original description, newly reported cases have expanded the clinical spectrum of the disorder to include unilateral forms (about 40%, half of which are side-locked), forms with a longer duration (up to 3 h) and cases with onset in juvenile/adult age. The male predominance found in Raskin’s series has not been confirmed by subsequent observations. To date the reported F/M ratio is 1.7/1. Pain is of severe intensity in less then one-third of cases and mild-moderate in about two-thirds. The location of pain is fronto-temporal in over 40% of cases; headache is throbbing in 38% of cases, dull in 57% and stabbing in less than 5%. Nausea is reported in 19% of cases; photophobia, phonophobia or both are present in 6.8%. Mild autonomic signs (lacrimation, nasal congestion, ptosis) may rarely be present. In 2004, HH was included in Group 4 of the International Classification of Headache Disorders—II (Other primary headaches). Sufficient evidence, mainly from polysomnographic studies, indicates that HH is a primary rapid eye movement (REM) sleep-related headache disorder of chronobiological origin. Lithium, melatonin, indomethacin and caffeine at bedtime are among the most effective therapeutic options. The pathophysiology of HH is still unclear. Available data allow speculation that, in predisposed subjects, an age-related impairment of suprachiasmatic nucleus could cyclically activate a disnociceptive mechanism leading to both a sudden awakening and headache. The mechanism may be precipitated by neurophysiologic events such as the strong reduction of firing occurring in the dorsal raphe nucleus during a REM sleep phase.

Multiple sclerosis and headache co-morbidity. A case-control study

The prevalence of primary headache (PH) in a multiple sclerosis (MS) sample vs. control healthy subjects was investigated at a neurological clinic in 2004–2005: 122 of 238 (51%) MS patients and 57 of 238 (23%) controls proved to be affected by headache. The groups did not differ for the rates of PH types. Headache types of MS patients were comparable to those of PH patients that were observed at the same institute in a case-control comparison. First symptoms of headache preceded those of MS in two thirds of cases. Headache features did not significantly change after MS onset. Comorbidity of MS and PH could be explained by some common clinical and biological traits.

Acetazolamide efficacy and tolerability in migraine with aura : A pilot study

The study was an open uncontrolled pilot trial to test the efficacy and the tolerability of acetazolamide in a group of 22 outpatients suffering from migraine with aura (MA) with at least one aura episode in the last 2 months.

HELLP syndrome with reversible posterior leukoencephalopathy.

Abstract. We report the case of a 30-year-old primipara who developed a triplet pregnancy after having received artificial insemination. At the end of the eighth month of pregnancy she had a generalized tonic-clonic seizure and at the same time blood chemistry was indicative of HELLP syndrome. Brain MRI and EEG were altered immediately after the episode but returned to normal during a 6-month follow-up period.

Source of pain and primitive dysfunction in migraine: an identical site?

Twenty common migraine patients received a one sided frontotemporal application of nitroglycerin (10 patients) or placebo ointment (10 patients) in a double blind study. Early onset migraine attacks were induced by nitroglycerin in seven out of 10 patients versus no patient in the placebo group. Subsequently 20 migraine patients, who developed an early onset attack with frontotemporal nitroglycerin, received the drug in a second induction test at other body areas. No early onset migraine was observed. Thus the migraine-inducing effect of nitroglycerin seems to depend on direct stimulation of the habitual site of pain, suggesting that the frontotemporal region is of crucial importance in the development of a migraine crisis. This is not consistent with a CNS origin of migraine attack.

Focal hypertrophic cranial pachymeningitis associated with temporal arteritis

Sirs: Cranial pachymeningitis may be a cerebral MRI finding in patients complaining of headache [11]. Meningeal thickening typically does not follow cortical sulci [12]. The inflammatory nature of pachymeningitis is disclosed by the dural enhancement following gadolinium-EDTA intravenous administration [3, 4]. Dural enhancement has been found in idiopathic hypertrophic cranial pachymeningitis [2, 5, 13] or it has been associated with benign intracranial hypotension [3], infectious diseases (syphilis, tuberculosis, fungi) [1], collagen diseases (Wegener granulomatosis, Churg-Strauss arteritis) [8], dural carcinomatosis or sarcoidosis [14]. Recently, a few cases have been reported, in which a multifocal dural enhancement was found in association with a non-giant cells temporal arteritis [6, 7]. The present report deals with a new case of this association. The patient is a 65-year-old housewife. Since June 2000 she complained of a daily throbbing pain on the right side of the head, associated with photophobia and mild phonophobia, transiently responsive to nimesulide. In August 2000 her basal temperature was slightly elevated. There were no other constitutional symptoms such as weight loss, muscle pain, malaise and anorexia. In September she took amitriptyline (35 mg/day) and pizotifen (1 mg/day) for one month, without benefit. In October 2000 she was hospitalised for persistent headache. Routine blood chemistry showed: increased ESR (98 mm/h at the first hour) and C-reactive protein (CRP) values (1.79 mg/dl, normal range 0–0.50). All remaining tests were normal including: red and white cells counts; serum ANA, c-ANCA, circulating immune complexes, rheumatoid factor, tumor markers, thyroid hormones, ACE, VDRL, TPHA, fungal antigens (Cryptococcus, Candida and Aspergyllus), antibodies versus Borrelia burgdorferi and Mycobacterium tuberculosis. Chest radiographs and abdomen ultrasonography were normal. Carotid ultrasonography revealed bilateral small plaques at the bifurcation level. Brain MRI, performed with contrast in October 2000, revealed some subcortical vascular lacunae, a venous angioma (developmental venous anomalies or DVA) in the right cerebellar hemisphere and thickening with positive enhancement of the right tentorium (Fig. 1a). The patient came to our observation in November 2000. Neurological examination revealed only brisk, symmetric reflexes at the four limbs. She was submitted to lumbar puncture: CSF pressure and chemistry were normal. Growth of bacteria or fungi, IgM antibodies to HSV 1 and 2, HZV, CMV, EBV, cryptococcal antigen were negative and no oligoclonal bands were found. Although there was no superficial temporal artery tenderness she underwent temporal artery biopsy in December 2000. The specimen revealed fibrous intimal thickening with vasculitis and obstruction of the vasa vasorum. There was destruction of the lamina elastica. Microscopically, wall thickening was observed with an abundant full thickness lymphocytic cells infiltrate (Fig. 2a) composed of mature CD45Ro + T cell population (Fig. 2b). Histopathological data, with clear T cell infiltration, even though giant cells were absent, were suggestive of Horton arteritis. Nimesulide was stopped and prednisone was started per os (50 mg/day) with sudden remission of headache. After five days of therapy ESR fell to 15 mm/h and CRP returned to normal. After fifteen days of therapy new cerebral MRI with contrast confirmed the right cerebellar DVA, but showed a marked reduction of the enhancement of the right tentorium (Fig. 1b). In this late-onset migraine-like headache with MRI finding of focal cranial pachymeningitis CSF examination excluded infectious illness and intracranial hypotension. The persistent increase of ESR and CRP values and the finding of transient hyperthermia were consistent with the hypothesis of a connective tissue disease. Lack of systemic organ involvement and negative cANCA test made diagnosis of Wegener or Churg-Strauss diseases improbable. Sarcoidosis was not supported by negative serum ACE test and chest radiographs. Biopsy of the temporal artery confirmed the clinical suspicion of temporal arteritis. Absence of giant cells does not exclude temporal arteritis [10]. The genesis of the headache from the dural inflammatory process was suggested by the pain presentation, which was homolateral to the tentorium thickening, and it was confirmed by the temporal correspondence between the headache resolution and the marked reduction of the tentorium enhancement. The tentorium is a LETTER TO THE EDITORS