Forty-nine cases of dissection of the internal carotid and vertebral arteries are reported in our prospective multicenter study of 35 men and 14 women, with a mean age of 46.77 years. (range 17-60 years). We evaluated etiology, clinical manifestations, investigative techniques, and treatment. Thirty-one patients had so-called spontaneous dissections, although in the remaining 18 minimal or obvious trauma was considered as the etiological factor. Headache and neck pain occurred in 32 patients (65.3%). Local neurological manifestations were present in 15 patients (30.6%) and ischemic cerebral symptoms were present in 41 patients (83.6%). The most-relevant of the diagnostic tools are duplex sonography, magnetic resonance angiography, and angiography. Anticoagulation with heparin followed by warfarin was the treatment of choice in most of our patients. Complete recovery is reported in 14 patients (28.5%); 41 patients showed cerebral ischemic symptoms, of which 13 (26.5%) had good functional recovery. In 28 (57.1%), the NIHSS score decreased from 6.68 to 3.31 during hospitalization.

Posterior reversible encephalopathy is a distinctive syndrome associated with different diseases and drugs. Disease evolution is frequently favorable with an adequate treatment. Damage typically involves parietal-occipital lobes even if a more anterior diffusion has been described. Here, we report the case of a woman affected by Polyarteritis Nodosa, who suddenly complicated with decreased consciousness and seizures, during an acute hypertensive state. MRI imaging showed increased T2 and FLAIR signal in posterior regions. Her neurological evolution was positive, according to arterial pressure correction, although the systemic vasculitis was still ongoing, hence affecting final prognosis.

Various diseases are described as antecedents of Guillain-Barré syndrome (GBS), particularly gastroenteritis and respiratory infectious diseases, but epidemiological surveys are rare. This paper details a multicentre matched case-control study carried out within a well-defined Italian population. For each GBS case fulfilling the Asbury and Cornblath criteria, one control was recruited from a neurological (NC) ward and another from a non-neurological (NNC) ward, matched for age, sex, season of disease onset and area of residence. All cases and controls were administered a semistructured questionnaire. The OR was calculated according to the Mantel-Haenszel equation for triplets. Between 1 October 1996 and 30 September 1998, 75 triplets were included in the case-control study. The OR for flu-like syndrome was 7.14 (CI 95%, 3.28-15.52) and for gastroenteritis 3.57 (CI 95%, 1.31-9.72); no other factor reached significance. Our results, based on the clinical and anamnestic features of triplets of patients, support the possible role as risk factors for GBS of infectious diseases, particularly flu-like syndrome and gastroenteritis.

Familial hemiplegic migraine (FHM) type 1 is a rare monogenic dominant autosomal disease due to CACNA1A gene mutations. Besides the classical phenotype, mutations on CACNA1A gene are associated with a broader spectrum of clinical features including cerebellar ataxia, making FHM1 a complex channelopathy. We report the case of a patient carrying the p.Arg583Gln mutation affected by hemiplegic migraine and late onset ataxia and we performed a literature review about the clinical features of p.Arg583Gln. Although p.Arg583Gln mutations are associated with a heterogeneous phenotype, carriers present cerebellar signs which consisted generally in ataxia and dysmetria, with intention tremor appearing mostly in advanced age, often progressive and permanent. The heterogeneous spectrum of CACNA1A gene mutations probably causes sporadic hemiplegic migraine (SHM) to be misdiagnosed. Given the therapeutic opportunities, SHM/FHM1 should be considered in differential diagnosis of patients with cerebellar ataxia and migraine with aura.