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Tremor is a common and very disabling symptom in patients with essential tremor and Parkinson's disease. In the recent years, transcranial ablation of thalamic nuclei using magnetic resonance guided high-intensity focused ultrasound has emerged as a minimally invasive treatment for tremor. The aim of this review is to discuss, in the light of our single-center experience, the technique, current applications, results, and future perspectives of this novel technology.

Objective: To identify possible relevant factors contributing to tremor relapse after MRgFUS thalamotomy in patients with essential tremor (ET) and Parkinson’s disease (PD). Methods: We identified patients with tremor relapse from a series of 79 treatments in a single institution. The demographic and clinical characteristics of the study group patients were compared to those of patients who did not relapse in the same follow-up period. Imaging and procedural factors were compared using a control group matched for clinical and demographic characteristics. Results: Concerning clinical and demographic characteristics, we did not find statistically significant differences in gender and age. Seventy-three percent of patients with tremor relapse were Parkinson’s disease patients. Using MRI, we found larger thalamotomy lesions at the 1-year follow-up in the control group with stable outcomes, compared to patients with tremor relapse. In the tractography evaluation, we found a more frequent eccentric position of the DRTt in patients with tremor relapse. Conclusions: The most relevant determining factors for tremor relapse after MRgFUS thalamotomy appear to be tremor from Parkinson’s disease and inaccurate thalamic targeting. Size of the thalamotomy lesion can also influence the outcome of treatment.

Objective In the recent years the increase of methamphetamines (MTA) abusers women has become an emerging problem. Very little data has been published regarding the effects of prenatal MTA exposure. We describe a case of MTA related toxicity in a term newborn which have early onset of neonatal encephalopathy and liver failure. Case report A term infant born to a MTA abuser mother developed seizures and severe neurological symptoms shortly after birth. Methamphetamine was detected both in maternal and in neonatal urine. The laboratoristic tests revealed severe hepatic insufficiency, coagulopathy and thrombocytopenia. Due to neonatal encephalopathy the newborn underwent hypothermia. Phenobarbital, fresh frozen plasma, platelet transfusions and vitamin K were administered. Cranial ultrasonography and magnetic resonance imaging (MRI) showed diffuse white matter damage and two ischemic-hemorrhagic cerebral lesions. Gradually the clinical conditions improved, at 1 month MRI showed a stabilization of cerebral lesions with residual diffuse leukomalacia. Physiotherapy and neurological follow up is ongoing to evaluate the long term effects. Conclusions: although infrequent, MTA-related toxicity should be suspected in infants with neurologic and hepatic symptoms. Further studies are warranted to confirm our findings in order to identify newborns at high risk of acute MTA toxicity in time to provide them the appropriate support.

OBJECTIVE To examine the relationship between electrographic seizures and developmental outcome at 18 and 24 months in neonates with moderate and severe hypoxic-ischemic encephalopathy [HIE] treated with therapeutic hypothermia [TH]. STUDY DESIGN 30 term infants with moderate-severe HIE treated with TH were enrolled prospectively from June 2012 to May 2018. All had continuous single channel amplitude integrated EEG (aEEG) monitoring for a minimum of 72 h and brain MR within 4 weeks. The aEEG was classified by severity of background and seizure burden. MR images were graded by the severity of injury. Outcome (defined abnormal in case of death, dyskinetic or spastic quadriplegic cerebral palsy, epilepsy, or Bayley III score < 85 in all three subscales or < 70 in any individual subscale) was assessed at 18 and 24 months. RESULTS Seizures were recorded in 24 out of 30 [80 %] neonates and an abnormal outcome was observed in 7 [23 %] of infants. Patients with poor outcome had a statistically significant correlation with: high seizure burden (p = 0.0004), need for more than one antiepileptic drugs (p = 0.006), a persistent abnormal aEEG trace at 48 h (p = 0.0001) and moderate-severe brain injury at MRI (p = 0.0001). Moreover, infants with status epilepticus or frequent seizures reported a significantly association with abnormal MR imaging and poor outcome than patients with sporadic seizures (p = 0.0009). CONCLUSION The role of seizures in the pathogenesis of brain injury remains controversial. In our cohort the presence of seizures, per se, was not associated with abnormal outcome; however a high seizure burden as well as a persistent abnormal aEEG background pattern and MR lesions resulted significantly associated with poor prognosis.

Progressive multifocal leukoencephalopathy (PML) is a rare rapidly progressive demyelinating disease of the central nervous system caused by reactivation of latent John Cunningham (JC) polyomavirus (JCV) infection. We describe an unusual case of PML in a 54-year-old patient with follicular non-Hodgkin lymphoma who received rituximab plus cyclophosphamide, hydroxydaunorubicin, oncovicin and prednisolone (R-CHOP) therapy. She started to notice gradual progressive neurological symptoms about two months after completion of rituximab treatment and was therefore admitted to hospital. On admission, brain CT and MRI showed widespread lesions consistent with a demyelinating process involving the subcortical and deep white matter of the cerebral and cerebellar hemispheres. CT and MRI findings were suggestive of PML, and JC virus DNA was detected by polymerase chain reaction assay of the cerebrospinal fluid and serum. The patient was treated supportively but reported a progressive worsening of the clinical and radiological findings. Our report emphasizes the role of CT and MRI findings in the diagnosis of PML and suggests that PML should be considered in patients with progressive neurological disorders involving the entire nervous system and mainly the white matter, especially in the presence of previous immunomodulatory treatment or immunosuppression.

Central nervous system (CNS) vasculitis can affect both adults and children, but some of these occur almost exclusively in childhood. In children may develop as a primary condition or secondary to an underlying systemic disease. Cerebral vasculitis can be classified on the basis of the diameter of the involved vessels, although there is no univocal consensus. The diagnosis of CNS vasculitis is particularly difficult because the available investigative modalities have limited sensitivities and specificities. The most helpful diagnostic tests include cerebrospinal fluid analysis, MRI (MR angiography/venography (MRA/MRV) of the brain, and angiography. However, brain biopsy may be required to diagnose small vessel vasculitis in order to make differential diagnosis with a wide range of conditions, such as degenerative vasculopathies, embolic diseases, or coagulation disorders. This paper discusses on current understanding of most frequent primary and secondary central nervous system vasculitis in children in which are involved small vessel.

Background Reduction of apparent diffusion coefficient (ADC) values in white matter is not always ischaemic in nature. Methods We retrospectively analysed our MRI records featuring reduced ADC values in the centrum semiovale without grey matter involvement or significant vasogenic oedema. Results Several conditions showed the aforementioned MR findings: moose-horn lesions on coronal images in X-linked Charcot-Marie-Tooth disease; small fronto-parietal lesions in Menkes disease; marked signal abnormalities in the myelinised regions in the acute neonatal form of maple syrup urine disease; strip-like involvement of the corpus callosum in glutaric aciduria type 1; persistent periventricular parieto-occipital abnormalities in phenylketonuria; diffuse signal abnormalities with necrotic evolution in global cerebral anoxia or after heroin vapour inhalation; almost completely reversible symmetric fronto-parietal lesions in methotrexate neurotoxicity; chain-like lesions in watershed ischaemia; splenium involvement that normalises in reversible splenial lesions or leads to gliosis in diffuse axonal injury. Conclusion Neuroradiologists must be familiar with these features, thereby preventing misdiagnosis and inappropriate management.

The most important symptoms associated with schizophrenia are affective flattening, decreased expression of emotions, anhedonia and social isolation. The purpose of the present study was to investigate the neural response to disgusting and pleasant visual stimuli in healthy subjects and in patients with first-episode schizophrenia. Twelve subjects in the first episode of schizophrenia (DSM-IV-R, APA, 2000) with a normal IQ and 12 healthy volunteers selected for age and education underwent functional magnetic resonance imaging (fMRI) during observation of pleasant and disgusting visual stimuli. Analysis showed that in healthy subjects, the prefrontal cortex and limbic areas are activated in response to pleasant and disgusting visual stimuli, whereas this does not occur in subjects with schizophrenia since the first episode of illness.

This paper focuses on radiological approach in pediatric stroke including both ischemic stroke (Arterial Ischemic Stroke and Cerebral Sinovenous Thrombosis) and hemorrhagic stroke. Etiopathology and main clinical findings are examined as well. Magnetic Resonance Imaging could be considered as the first-choice diagnostic exam, offering a complete diagnostic set of information both in the discrimination between ischemic/hemorrhagic stroke and in the identification of underlying causes. In addition, Magnetic Resonance vascular techniques supply further information about cerebral arterial and venous circulation. Computed Tomography, for its limits and radiation exposure, should be used only when Magnetic Resonance is not available and on unstable patients.

Background. Cerebral amyloid angiopathy-related inflammation (CAA-ri) results from autoimmune response to beta-amyloid deposits in cerebral vessels. Its clinical course and complications have seldom been described in literature.Case Report. In a patient presenting with delirium and left hemiparesis the diagnosis of CAA-ri was supported by the finding of elevated anti-amyloid autoantibodies in the cerebrospinal fluid (CSF). Steroid therapy produced significant improvements in clinical and investigational assessments, but after two months, it caused Acute Respiratory Distress Syndrome. After steroid therapy discontinuation the patient presented a rapidly progressive dementia, Guillain-Barré syndrome, new cerebral ischemic lesions, and thrombosis of the right cephalic and subclavian veins that were treated with subcutaneous heparin. After a week the patient died because of brain hemorrhage.Conclusion. This case suggests caution in steroid therapy discontinuation and antithrombotic therapy administration in patients with CAA-ri. The CSF search of anti-amyloid autoantibodies could be helpful to support the diagnosis.

The extreme variability of clinical and MRI findings in the suspicion of Devic's disease always requires the detection of specific antibodies (AQP4). MRI scans were performed with a high-field MRI scanner (1.5T General Electric Signa Horizon): the MRI protocol of the brain employed axial DP, T2, T1, FLAIR and DWI weighted images (wi) and coronal T2-wi. After intravenous administration of contrast medium axial and sagittal T1-weighted images of the brain were repeated. The spine protocol employed after contrast medium included sagittal T2-wi, T2-wi with fat suppression and T1-wi. In May 2004, a 64-year-old healthy Caucasian woman began to suffer loss of motor and thermal sensitivity in the left lower limb. MRI showed nonspecific areas of abnormal signal intensity on the deep left frontal and right frontoparietal white matter with no pathological enhancement after contrast medium and a small intramedullary area of altered signal at metameric level C2–C4 with a diagnosis of post-viral transverse myelitis. The patient had two similar episodes years later so the neurologist decided to search for circulating IgG AQP4 with the definitive diagnosis of neuromyelitis optica. In this case, compared to a clinical presentation of atypical deficit neurological involvement, the neuroradiological results of a progressive diffuse involvement of the white matter were atypical.

The Intracranial Complications of infection of the paranasal sinuses are uncommon and subdural empyema is rarer still. Roughly half of the cases of subdural empyema are caused by sinusitis and the most common source of infection is the frontal sinuses. MR scan is the method of choice for the diagnosis and monitoring of subdural empyema, allowing prompt institution of appropriate treatment thereby reducing mortality. We describe a 15-year-old girl with interhemispheric subdural empyema caused by fronto-ethmoidal sinusitis. Clinical onset was characterised by high fever, severe headache, nausea, vomiting and diplopia. CT scan showed evidence of a left parafalcial hypodense collection. MR scan, especially after contrast administration, showed the exact extension and location of the interhemispheric subdural empyema, also displaying the associated leptomeningitis and fronto-ethmoidal sinusitis. Prompt medical treatment led to a remission of symptoms and sinus infection with associated leptomeningitis as documented by serial MR monitoring. However, the slow progressive increase in size of the subdural collection was deemed an indication for neurosurgical management (evacuation of the collection by ventricular drainage catheters inserted under stereotaxic control) leading to a complete resolution of the subdural empyema without neurological sequelae.

Serial magnetic resonance imaging findings are described in a patient with a sporadically occurring pilocytic astrocytoma that underwent spontaneous regression over 6 years. To the authors' knowledge, this is the first report in which spontaneous involution of a pilocytic astrocytoma not associated with neurofibromatosis type 1 has been described. A literature review regarding sporadic and syndrome-associated pilocytic astrocytoma was undertaken, with particular reference to treatment and natural history.

Patients with post-traumatic stress disorder (PTSD) exhibit exaggerated brain responses to emotionally negative stimuli. Identifying the neural correlates of emotion regulation in these subjects is important for elucidating the neural circuitry involved in emotional dysfunction. The aim of this study was to investigate the functional connectivity between the areas activated during emotional processing of negative stimuli in a sample of individuals affected by PTSD compared to a group of healthy subjects. Ten subjects with PTSD (who survived the L’Aquila 2009 earthquake) and ten healthy controls underwent fMRI during which the participants observed 80 images: 40 pictures with negative emotional valence and 40 neutral (scrambled) stimuli. A higher activation was found in the left posterior (LP) insula for PTSD group and in the ventromedial prefrontal cortex (vmPFC) for the healthy group. Two sets of Granger causality modeling analyses were performed to examine the directed influence from LP-insula and vmPFC to other brain regions. Activity in the vmPFC in the healthy group while observing negative stimuli predicted activity in several subcortical regions and insula, while in the PTSD group the LP-insula exerted a positive directed influence on several cortical regions. The hyperactivation in PTSD subjects of subcortical areas such as the insula would underlie the emotional, social, and relational difficulties of PTSD patients.

The "default mode", or baseline of brain function is a topic of great interest in schizophrenia research. Recent neuroimaging studies report that the symptoms of chronic schizophrenia subjects are associated with temporal frequency alterations as well as with the disruption of local spatial patterns in the default mode network (DMN). Previous studies both on chronic and medicated subjects with psychosis suffered from limitations; on this basis, it was hypothesized that the default mode network showed abnormal activation and connectivity in young and neuroleptic-naïve patients with first-episode psychosis. This study investigated emotional responses to pleasant and unpleasant/disgusting visual stimuli by a resting-state analysis of fMRI-data from 12 untreated first-episode psychosis patients with prevalently negative symptomatology versus 12 healthy subjects. We chose this experimental task to explore the functional link between default mode network and hedonic processing which has been proposed as a marker of cerebral dysfunction in psychotic disorder and implicated in its pathophysiology. Independent Component Analysis (ICA) was used to identify the default mode component. Both healthy and first-episode subjects showed significant spatial differences in the default mode network. In first-episode subjects, medial frontal hypoactivity and cerebellar hyperactivity were correlated with the severity of negative symptoms.

Rosai-Dorfman disease (RDD) was firstly described in 1969 as a benign proliferative disorder of histiocytes with systemic symptoms and lymphadenopathy. This disease is of uncertain pathogenesis and mostly occurs in children and young adults. The typical clinical features of RDD include bilateral painless cervical lymphadenopathy, but extranodal involvement may also be present. The most common extranodal sites include organs such as the respiratory tract, skin, nasal cavity, orbit and bone. Isolated central nervous system (CNS) manifestations are extremely rare. In case of CNS involvement, the commonest imaging findings are dural-based extra-axial enhancing masses. We describe a case of intracranial RDD mimicking multiple meningiomas both clinically and radiologically in a 57-year-old man presenting with a six-year history of progressive right visual and hearing loss and tinnitus. In cases of multiple extra-axial lesions it is worth bearing in mind the possible differential diagnosis for intracranial RDD and eventually propose to the patient further investigations.

The "Emotional Numbing" (EN) constitutes one of the core symptoms in PTSD although its exact nature remains elusive. This disorder shows an abnormal response of cortical and limbic regions which are normally involved in understanding emotions since the very earliest stages of the development of processing ability. The aim of our study, which included ten physically healthy subjects with PTSD, diagnosed according to DSM-IV-TR, who survived L'Aquila earthquake of April 6, 2009, and 10 healthy controls matching for age, sex and education, was to examine automatic perceptual sensitivity to facial affect in PTSD, through an affective priming task that was administered during functional magnetic resonance (fMRI). Behavioural data revealed in the PTSD group a higher sensitivity to negative facial affect on an automatic processing level. FMRI data analysis revealed that PTSD subjects showed a significantly higher activation in right insula and left amygdala that we did not observe in healthy subjects; on the contrary, healthy controls showed a greater activation of left lingual gyrus. Our data support the hypothesis that PTSD appears to be sensitive to negative affect on an automatic processing level and correlates with the activation of specific areas involved in processing emotions. An elevated activation of these areas may underlie the emotion dysregulation in PTSD and could explain the Emotional Numbing symptom associated with this disorder. The present study suffers of a number of limitations, for instance, the relatively small sample size did not allow the application of alternative statistical models.

Subjects with post-traumatic stress disorder (PTSD) present a diminished or blunted emotional response, sometimes called “emotional numbing” (EN), that constitutes one of the central symptoms in PTSD. Symptoms of EN include diminished interest in activities, feeling detached or estranged from others, and restricted range of affect (American Psychiatric Association, 2000). The present work studied the emotional components in individuals with PTSD with the principal aim of investigating subjects' functional alteration in the limbic regions, insula and frontal cortex during an emotional task compared with healthy subjects. Ten subjects with PTSD (survivors of the 6.3 magnitude earthquake of April 6, 2009 in L'Aquila) and ten healthy controls underwent fMRI. PTSD was diagnosed according to DSM-IV-R (APA 2000). All subjects underwent fMRI while viewing content-neutral and emotional stimuli. Data analysis revealed that PTSD subjects had significantly greater cerebral activation in particular in the right anterior insula and in bilateral inferior frontal gyrus. Our data suggest that there is a change in the activation of brain areas responsible for emotional processing in patients with PTSD and are consistent with previous findings demonstrating hyperactivation in frontolimbic structures during emotional tasks. Our study suggests that close personal experience may be critical in engaging the neural mechanisms underlying the emotional modulation of memory. Our findings provide evidence that significant alterations in brain function, similar in many ways to those observed in PTSD, can be seen shortly after major traumatic experiences, highlighting the need for early evaluation and intervention for trauma survivors.

Myxopapillary ependymoma is a rare variant of ependymoma, almost exclusively occurring in the region of the cauda equina and filum terminale. We describe a myxopapillary ependymoma located in the left cerebellopontine angle of a young man suffering from peripheral vertigo and left sensorineural hearing loss for years. The patient underwent surgical removal of the tumour. Microscopic examination showed histological and immunohistochemical features consistent with a diagnosis of myxopapillary ependymoma. Imaging studies of the spine yielded normal findings, confirming the lesion’s primary nature. To the best of our knowledge, this is the first case of primary intracranial myxopapillary ependymoma described in this location.

Aim of our study is to present the findings of parietal cortex alterations in patients affected by movement disorders. We observed 4 patients with movement disorders (3 parkinsonian syndromes, I diffuse dystonia) and MR evidence of cortical alterations, without additional cerebral lesions. MR was performed with a 0.5T unit, SE T1-w, TSE T2-w, and Turbo Fluid Attenuated Inversion Recovery (T-FLAIR) sequences on axial and coronal planes, contiguous slices and 5 mm slice thickness. In the parkinsonian patients, parietal atrophy was observed in 2 cases and fronto-parietal atrophy in I case; in all cases T-FLAIR sequences showed bilateral parietal cortex signal alteration. The patient with diffuse dystonia presented severe bilateral parietal atrophy with bilateral fronto-parietal signal alteration. Our findings are strongly suggestive for cortico-basal degeneration. The evidence of signal alteration within the cortex suggests a primary pathogenetic involvement of cortico-basal pathways.

The hand and wrist are common sites for trauma, resulting in various bony, capsular, ligamentous and tendinous injuries. Traumatic injuries of the wrist are very frequent and occur at every age. Some lesions happen characteristically in a specific decade of life. Bone mineralization, which could be considered age-related, and ligamentous resistance and compliance, together with the mechanism of the trauma determine the resulting lesion [1-5]. Thus, metaphyseal fractures and slipping epiphysis typically occur in children. Both carpal dislocations and fracture-dislocations typically occur in young adults. Fractures, dislocations and fracture-dislocations of the distal extremity of radius and ulna usually occur in the elderly.

Joint impingement is a painful syndrome caused by the friction of joint tissues, which is both the cause and the effect of altered joint biomechanics. From the anatomical and clinical viewpoints, these syndromes are classified as bone impingement, soft tissue impingement and entrapment neuropathy, depending on what joint portion impinges on the others. We considered the most important impingement syndromes of the upper and the lower limbs from the clinical viewpoint. As for the upper limb, supraspinatus impingement is a frequent cause of shoulder pain in both athletes and the normal population; the painful subacromial arch is a typical sign of the rotator cuff impingement syndrome and of outlet and non-outlet impingement as well. As for the elbow, we considered both medial and lateral impingement. The carpal tunnel syndrome is the most common peripheral entrapment neuropathy of the upper limb; it is caused by compression of the median nerve at the wrist. We considered the main causes of carpal tunnel narrowing and the relative clinical findings. As for the lower limb, we considered the iliotibial band friction syndrome, which is the most common overuse syndrome of the knee and the ankle impingement syndrome. The latter includes anterolateral impingement (with chronic anterolateral and lateral pain and ankle instability), sinus tarsi impingement, anterior impingement (with pain during foot dorsiflection and posterior impingement. The tarsal tunnel syndrome is the most important ankle entrapment neuropathy causing burn pain and paresthesias in the toes and sole of the foot.

Background Ultrasound (US), Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) are widely used in the clinical diagnosis of parotid gland tumors and their efficacy in identifying benign lesions is well documented. However, problems arise when facing some malignant lesions. Only few cases of salivary gland low grade malignant tumors have been previously reported in the literature complete with the radiological features. Case presentation We here describe a case of epithelial-myoepithelial carcinoma (EMC) of the parotid gland, a low grade malignant tumor, with spread to an intraparotid lymph node and with CT and MRI findings mimicking a benign lesion. Conclusion All the images revealed sharply outlined profiles and a homogeneous enhancement of the nodule, suggesting a benign tumor and demonstrating that a radiological evaluation of the lesion alone may be unsatisfactory and misleading in the diagnosis of salivary gland tumours, especially in the case of low grade malignant tumors, such as EMC.

We describe MR findings in patients with a clinical diagnosis of corticobasal degeneration (CBD). Five patients with different extrapyramidal symptoms were submitted to MRI. All patients were clinically followed-up for a minimum period of at least 12 months. MRI study was performed on a 0.5 T system (Philips NT 5 II), using conventional SE, TSE and t-FLAIR sequences on axial and coronal planes. In all cases MR showed bilateral parietal cortical atrophy. t-FLAIR sequences demonstrated cortical signal alteration on both parietal and frontal cortex in four cases and on the parietal cortex alone in 1 case. During the follow-up clinical evolution gave rise to the suspicion of CBD. MRI demonstrated parietal cortex atrophy even in those cases in which symptoms at onset were not specific for CBD, thus helping the diagnosis. Moreover MRI, using t-FLAIR sequences suggested CBD diagnosis even in the earlier phases of the disease, in which cortical damage has not yet become evident as atrophy.

Background Congenital cystic adenomatoid malformation (CCAM) of the lung is an uncommon fetal development anomaly of the terminal respiratory structures. The large cyst type usually occurs in stillborn infants or newborn infants with respiratory distress. Cases of CCAM have been previously described in adulthood, more often type I with multiloculated cystic lesions. Case presentation We report a case of type I CCAM presenting as a single, expansive cystic mass in the middle pulmonary lobe in a 38-year-old man, revealed by persistent cough and haemoptysis. Computed tomographic scan showed a single cyst with air fluid level, occupying the lateral segment of the lobe. When the type I CCAM is a single cyst, other cystic pulmonary lesions must be excluded. The intrapulmonary localization and the absence of cartilage in the cyst wall are conclusive findings of CCAM. The pathogenesis, management and differential diagnosis with other lung malformations are discussed along with a review of the literature. Conclusion The literature data confirm that surgical resection is the treatment of choice in all cases of CCAM and in the cases of cystic pulmonary lesions with uncertain radiological findings, in order to perform a histological examination of the lesion and to prevent infection and the potential neoplastic transformation.