The aim of our study was to evaluate the etiopathogenesis and the vascular risk factors in a consecutive series of patients with juvenile ischemic stroke. We enrolled 273 patients (158 males and 115 females), aged between 16 and 49 years, with ischemic cerebrovascular events (ICVE), including transient ischemic attack (TIA) or stroke, referred to our neurology ward between January 1994 and December 2001. Our protocol included medical history, cardiac and neurological examinations, assessment of risk factors and laboratory tests. The instrumental assessment included transthoracic echocardiography (70%), transesophageal echocardiography (60%), conventional angiography (30%), MR angiography (30%), cranial computed tomography (100%) and brain MRI (48%). The ICVE was a stroke in 60% of the cases, a reversible ischemic neurologic deficit in 14% and a TIA in 26%. Thirty-three patients were aged less than 29, 59 were aged between 30 and 39 and 181 between 40 and 49. The percentage of females was higher in patients aged less than 29 while males were prevalent in the 4th and 5th decade. The patients were subtyped according to etiopathogenesis. A large-vessel disease (LVD) was diagnosed in 43 patients (16% of the cases), mostly in patients aged more than 40 years (36 cases). A small-vessel disease (SVD) was found in 48 patients (17% of cases), mostly in patients aged more than 40 years (41 cases). A cardioembolic stroke (CE) was diagnosed in 66 patients (24% of the cases). In the majority of the cases, the cardiopathies were at low-uncertain embolic risk: patent foramen ovale (PFO, 39 cases, in 8 patients associated with an atrial septal aneurism), atrial septal aneurism (12 cases) and myxomatous mitral valve prolapse (3 cases). Stroke due to other causes was found in 51 patients (19% of the cases). Arterial dissection, more frequently involving the carotid region, was diagnosed in 35 patients. Coagulopathies and vasculitis were found in 5 and 6 patients, respectively. Stroke of unknown etiology was found in 65 patients (24% of the cases) with a homogeneous distribution among decades. Our study highlights the role of minor cardiac sources of embolism and arterial dissection in the etiology of juvenile ischemic stroke, whereas coagulopathies and vasculitis are less relevant. LVD and SVD were relevant only in the 5th decade.

Sirs: Occipital neuralgia (ON) (Arnold's neuralgia) is characterized by jabbing pain attacks in the territory of occipital nerves associated to hypesthesia/dysesthesia in the same area [1,2]. Pain frequently radiates to the frontal region and may be associated with tenderness over the affected nerve at the superior nucal line. ON can be caused by trauma, injury, inflammation, or compression of the greater occipital nerve somewhere along its course from the C2 dorsal root to the peripheral territory.A 59-year-old woman was referred to us in May 1999 because of a five-year history of pain involving the right occipito-parietal scalp, often radiating to frontal and retroauricular regions. The pain was sharp and burning with paroxysms triggered by pressure at the emergence of the greater occipital nerve and hyperalgesia for brush, touch and pinprick stimuli in the right occipital as well as in the auricular and retroauricular region. Skin rubbing at those levels caused paroxysmal attacks (for example when she held the telephone receiver over the right ear or put the right side of her head on a cushion). She complained of almost continuous uncomfortable paresthesias in the occipito-nucal area. Head and neck trauma were not reported. No clinical or laboratory evidence of rheumatologic disorders were present. Neurologic examination revealed only a slight hyperreflexia in the right limbs, without other signs of myelopathy. MRI showed a right intramedullary multilobated lesion at C1-C2 level (Figs. 1, 2) with a mild contrast enhancement. The lesion was slightly hyperdense on CT. Angiography of vertebral, common carotid and cervical branches from the subclavian arteries was normal . Therefore a diagnosis of intramedullary cavernous angioma was hypothesized. Amitryptiline and carbamazepine but not NSAIDs and greater occipital nerve anesthetic blockade were useful in reducing the pain. No change was evident on MRI performed 6 months later and the clinical picture was unchanged at the last visit in July 2001.The present case broadens the spectrum of causes of ON and suggests that spinal cord imaging may be useful also without clinical evidence of myelopathy. Indeed, in our patient ON was the unique symptom of an intramedullary cavernous angioma.About 5-10 % of central nervous system cavernous angiomas arise within the spinal cord and the cervical level is the most frequent after the thoracic [3]. They usually cause a progressive myelopathy through gradual enlargement and repeated microhemorrhages [3]. In ON pain and sensory symptoms involve the distribution of the branches derived from C2 spinal nerve. Just immediately after the origin the C2 spinal nerve gives rise to a ventral and a dorsal ramus. The greater occipital nerve raises from the dorsal ramus, enters the scalp through the trapezius aponeurosis at the superior nucal line and innervates the skin of the occipital area up to the coronal suture [1][2][3][4][5]. The lesser occipital nerve emerges from the C2 ventral ramus and supplies the scalp over the mastoid and the p...

We report a case of a 75-year-old female with pheochromocytoma of the bladder. Clinical evaluation included ultrasonography, intravenous pyelography, CT scan, I-MIBG scintiscan. A transurethral resection was performed for a exophytic tumor of 2 cm diameter. The histological result indicated the diagnosis of bladder pheochromocytoma. Three years later the patient remains disease free. Preoperative diagnosis is established by determination of blood and urine levels of catecholamines and their metabolites is a nonspecific diagnostic tool. The sensitivity of CT scan is 82%. Iodine-methyliodobenzylguanidine (I-MIBG), used by scintiscanning, specifically accumulates in pheochromocytomas. Life-long follow-up is necessary to diagnose late recurrences.

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Background: Studies have indicated that apolipoprotein E (ApoE)-ε4 is a risk factor for ischemic cerebrovascular diseases (ICVD), but the existence of this association is still controversial. The aims of this study were: (1) to compare ApoE genotype and allele frequencies in Italian cases with ICVD and in healthy control subjects and (2) to compare ApoE allele frequencies among ischemic stroke subtypes. Methods: A hospital-based cohort of 302 Italian subjects with ICVD and 228 healthy subjects have been recruited to investigate the role of ApoE polymorphisms as risk factors for ICVD. TOAST criteria were employed to stratify ICVD cases by subtypes. Results: No significant differences in ApoE genotype and allele frequencies were found between cases and control subjects. The frequency of ApoE-ε4 was lower in cases than in control subjects (6% vs. 10.1%), although not significantly. No differences in ApoE genotype and allele frequencies were evident among ICVD subtypes. However, out of 36 ApoE-ε4 alleles 23 (3.7%) were found in subjects with ICVD related to primary degenerative arterial disease related to large vessel disease and small vessel disease, and 13 (2.1%) in remaining subjects. Using logistic regression analysis we assessed whether ApoE-ε4 allele was independently associated with risk of ICVD related to a primary degenerative arterial disease compared to other ICVD subtypes. While classical risk factors were significantly associated with higher risk for ICVD due to large vessel disease and small vessel disease than other ICVD subtypes, the role of ApoE-ε4 allele was not significant (OR 1.25, 95% CI 0.57–2.74). Conclusion: Our study shows similar ApoE-ε4 genotype and allele frequencies in patients with ICVD and in control subjects. No differences were found among different ICVD subtypes either.

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Background-Various sensory syndromes in lateral medullary infarctions are described. A small variation in the location of a lesion may lead to very different clinical features, owing to the complex anatomy of the medulla oblongata. MRI may identify the location and extent of the ischemic lesions, allowing a clear clinical-anatomical correlation. Case Description-We describe a man with an ischemic lesion in the right portion of the lower medulla that presented a contralateral impairment of spinothalamic sensory modalities and an ipsilateral impairment of lemniscal modalities with a restricted distribution (left forearm and hand, right hand and fingers, respectively). The restricted and dissociated sensory abnormalities represent the only permanent neurological consequence of that lesion. Conclusions-The

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