Purposeto investigate the factors affecting survival and toxicity in patients treated with stereotactic radiosurgery (SRS), with special attention to volumes of brain receiving a specific dose (V10 - V16 Gy) as predictors for brain radionecrosis.Patients and MethodsTwo hundred six consecutive patients with 310 cerebral metastases less than 3.5 cm were treated with SRS as primary treatment and followed prospectively at University of Rome La Sapienza Sant'Andrea Hospital. Overall survival, brain control, and local control were estimated using the Kaplan-Meier method calculated from the time of SRS. Univariate and multivariate analysis using a Cox proportional hazards regression model were performed to determine the predictive value of prognostic factors for treatment outcome and SRS-related complications.ResultsMedian overall survival and brain control were 14.1 months and 10 months, respectively. The 1-year and 2-year survival rates were 58% and 24%, and respective brain control were 43% and 22%. Sixteen patients recurred locally after SRS, with 1-year and 2-year local control rates of 92% and 84%, respectively. On multivariate analysis, stable extracranial disease and KPS >70 were associated with the most significant survival benefit. Neurological complications were recorded in 27 (13%) patients. Severe neurological complications (RTOG Grade 3 and 4) occurred in 5.8% of patients. Brain radionecrosis occurred in 24% of treated lesions, being symptomatic in 10% and asymptomatic in 14%. On multivariate analysis, V10 through V16 Gy were independent risk factors for radionecrosis, with V10 Gy and V12 Gy being the most predictive (p = 0.0001). For V10 Gy >12.6 cm3 and V12 Gy >10.9 cm3 the risk of radionecrosis was 47%.ConclusionsSRS alone represents a feasible option as initial treatment for patients with brain metastases, however a significant subset of patients may develop neurological complications. Lesions with V12 Gy >8.5 cm3 carries a risk of radionecrosis >10% and should be considered for hypofractionated stereotactic radiotherapy especially when located in/near eloquent areas.

Although classical trigeminal neuralgia (CTN) is frequently caused by neurovascular contact (NVC) at the trigeminal root entry zone (REZ), both anatomical and MRI studies have shown that NVC of the trigeminal nerve frequently occurs in individuals without CTN. To assess the accuracy of MRI in distinguishing symptomatic from asymptomatic trigeminal NVC, we submitted to high-definition MRI the series of CTN patients referred to our outpatient service between June 2011 and January 2013 (n=24), and a similar number of age-matched healthy controls. Two neuroradiologists, blinded to the clinical data, evaluated whether the trigeminal nerve displayed NVC in the REZ or non-REZ, whether it was dislocated by the vessel or displayed atrophy at the contact site, and whether the offending vessel was an artery or a vein. Our data were meta-analyzed with those of all similar studies published from January 1970 to June 2013. In our sample, REZ contact, nerve dislocation and nerve atrophy were independently associated with CTN (P=.027; P=.005; P=.035 respectively). Compared to a rather low sensitivity of each of these items (alone or in combination), their specificity was high. When REZ contact and nerve atrophy coexisted, both specificity and positive predictive value rose to 100%. Meta-analysis showed that REZ NVC was detected in 76% of symptomatic and 17% of asymptomatic nerves (P<.0001), whereas anatomical changes were detected in 52% of symptomatic and 9% of asymptomatic nerves (P<.0001). In conclusion, trigeminal REZ NVC, as detected by MRI, is highly likely to be symptomatic when it is associated with anatomical nerve changes.

Injuries of vertebral endplates in porcine discs were found to cause degenerative changes in the disc tissue on MRI, histologic, and biochemical investigations. The severity of such degenerative changes was related to the severity of endplate injuries. Injuries of vertebral endplate may be one of the pathomechanisms leading to early changes in the disc matrix and eventually to abnormal biomechanical behavior of the whole disc. The present animal model seems to be a suitable experimental model for disc degeneration.

The classification proposed on the basis of radiological findings allows sufficient clinical differentiation of AO and evaluation of the possibilities for surgical treatment. The latter is conditioned by the type of arachnoiditis, degree of neurological involvement, and presence of any concomitant pathological findings.

A patient with relapsed B cell non-Hodgkin lymphoma (NHL) infiltrating the Central nervous system (CNS) and resistant to chemotherapy was treated with intrathecal Rituximab (IT RTX), administered weekly for eight weeks at increasing doses, from 10 to 40 mg. After the second administration the patient showed significant clinical improvement and Cerebro spinal fluid (CSF) clearance of lymphomatous cells. A MRI scan performed after 30 days from the start of therapy showed full regression of lymphomatous infiltration. This report confirms the efficacy and safety of IT RTX in the treatment of CNS B-cell NHL.

Brain magnetic resonance imaging (MRI) was performed in 17 late-detected PKU patients (aged 2.8-25 years). Twelve subjects had been treated late (0.7-4.5 years), and 5 not at all. Four were still on diet when the study was performed. Mental development was normal in 4 subjects, mildly retarded in 6, and moderately or severely retarded in 7. None had exhibited mental or neurological deterioration. On MRI examination a symmetrical increase of T2-weighted signal in the periventricular white matter was found in all patients, although to different degrees. Concomitant signal decrease on the T1-weighted sequences was detected in 9 patients. Ten subjects showed focal white-matter abnormalities. A variable degree of cortical and subcortical atrophy was found in 12 subjects, and asymmetry of lateral ventricles in 4. White-matter involvement correlated with phenylalanine concentrations during the year preceding (rs = 0.5706; p < 0.02) and at the time of (rs = 0.6182, p < 0.01) the investigation. Cortical and subcortical atrophy correlated with the patient's age (rs = 0.5889, p < 0.02, and rs = 0.5929, p < 0.02, respectively). We conclude that late-detected PKU patients showed the same MRI abnormalities reported in early-treated subjects and in subjects who underwent neurological deterioration; white-matter abnormalities possibly result from the recent exposure to high phenylalanine concentrations; in late-detected PKU subjects cerebral atrophy could be the late result of chronic exposure to high phenylalanine concentrations.

A clinical, biochemical and neuroradiological (MRI) study was performed in 22 hyperphenylalaninemic patients detected by neonatal screening and early treated (Group A; 5-23 years old, 13 females and 9 males) and in 5 late detected, symptomatic subjects (Group B; 9-23 years old, 3 females and 2 males). The screening subjects were clustered in a Group A1 (10 on diet patients), and a Group A2 (12 after end of diet patients). On MRI examination (1.5-T magnet, SE T1-weighted 530/22/2, T2-weighted 2400/15-90/1 sequences, SL 6 mm, gap 1.8) a symmetrical increase of the T2-weighted signal in the periventricular white matter was found in all patients. The periatrial white matter was always involved, the occipital region was affected in 22 cases, the frontal region in 16. Concomitant signal decrease on the T1-weighted sequences in the same areas with the highest signal intensity on the T2-weighted scans was found in 7 patients (in 3 out of 12 Group A2 and in 4 out of 5 Group B patients). In 6 Group A and in 3 Group B subjects a variable degree of cortical and subcortical atrophy was detected. A significantly positive correlation was found between white matter involvement and the degree of recent exposition to high PHE values. This correlation was also confirmed when only Group A was examined. Moreover, a significant difference in neuroradiological involvement was found between Group A1 and Group A2 subjects, but not between Group A2 and Group B subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is a rare hereditary stroke disease. The gene has been recently mapped, in two French families, on chromosome 19q12 between two highly polymorphic genetic markers. We report on a new large Italian family affected with this disease, which is characterized by recurrent stroke episodes, focal neurological deficits progressing to pseudo-bulbar palsy, and dementia. Multiple deep infarcts and diffuse leucoencephalopathy were revealed by MRI and brain histopathology showed abnormalities of arterial media. A genetic study performed with microsatellite markers from region 19q12 showed that the disease locus lies in an interval largely overlapping that already described and is closely linked to two microsatellite markers, D19S212 and D19S222. A joint analysis of genotypic and phenotypic data shows that diffuse leucoencephalopathy is a reliable sign of the disease in otherwise normal 50%-risk subjects over the age 30 years and that penetrance of stroke episodes or dementia is most likely complete around age 60 years.