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Copyright of Oncolog-Hematolog is the property of MEDICHUB MEDIA, S.R.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Oncolog-Hematolog is the property of MEDICHUB MEDIA, S.R.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Tumefactive demyelinating lesions (TDL) are large (usually more than 2 cm) demyelinating lesions, that can present with perilesional edema, mass effect, and different enhancement patterns mimicking tumor, infection, or acute vascular diseases of the brain. Magnetic resonance imaging (MRI) is the most useful diagnostic tool that can help set the proper course of treatment, follow-up and avoid unnecessary invasive procedures. We present a pictorial review of pseudotumoral demyelinating lesions from a series of cases diagnosed in our clinic and we discuss the most important differential diagnostics. We reviewed the magnetic resonance investigations of the patients with known or suspected multiple sclerosis or other inflammatory demyelinating lesions over a period of three years (2018-2020). Out of the 187 reviewed cases, 11 presented TDL, representing 5.88%. The mean age at the time of diagnosis was 38 years old, with a net female predominance. The main common element of TDL was the incomplete ring enhancement pattern, essential for positive and differential diagnosis. [ABSTRACT FROM AUTHOR]

Copyright of Oncolog-Hematolog is the property of MEDICHUB MEDIA, S.R.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Diabetic striatopathy is an uncommon complication of diabetes mellitus, usually characterized by hemichorea-hemiballismus with T1-high signal intensities involving the contralateral striatum. We present the case of an 81 years-old woman with poorly controlled type 2 diabetes mellitus, who was rushed to the hospital for acute-onset right-sided hemiparesis, somnolence and aphasia. Blood analysis revealed hyperglycemia (412 mg/dl) and raised level of glycated hemoglobin (14.5%), while head CT examination showed a spontaneous hyperdensity involving the left caudate and lenticular nuclei, with no edema. Brain MRI was also performed and highlighted T1-hyperintensities at the level of the same structures, with no diffusion restriction. The patient improved significantly under adjustment of insulin therapy. Based on these observations, a diagnosis of diabetic striatopathy was established. We present a short review of the literature regarding this condition and its main characteristics. [ABSTRACT FROM AUTHOR]

Copyright of Oncolog-Hematolog is the property of MEDICHUB MEDIA, S.R.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Oncolog-Hematolog is the property of MEDICHUB MEDIA, S.R.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A 53 years-old male, diagnosed with ulcerative colitis and liver cirrhosis due to HCV infection, was hospitalized at the Gastroenterology Department for paraclinical workup, prior to inclusion on the liver transplantation waiting list. The patient was known with a gigantic arachnoid cyst and presented a transient ischemic attack one year prior, for which treatment with aspirin was initiated. Consequently, we performed a brain MRI examination, which disclosed a left-sided gigantic arachnoid cyst with mass effect, midline shift of 9 mm and subfalcine herniation. No focal neurologic deficits or signs of increased intracranial pressure were found on neurological examination. Following neurosurgical evaluation, the presence of the cyst was not deemed to be a contraindication for liver transplantation. [ABSTRACT FROM AUTHOR]

Prostate cancer is one of the most common malignancies in men, generally with a slow growth rate and early detection is essential for a complete treatment. Multiparametric magnetic resonance imaging (MP MRI) lead to a better choice of therapy by improving detection and staging of prostate cancer. Conventional sequences are useful to evaluate prostate cancer in the peripheral zones; functional acquisitions, represented by DWI and DCE, extent the MR diagnostic accuracy particularly in central and anterior fibromuscular stroma zones. This technique also improves the differential diagnosis of prostate cancer. [ABSTRACT FROM AUTHOR]

Cryptogenic strokes represent a category of ischemic strokes in which there is no well-defi ned cause identifi ed. For that matter, choosing between antiplatelet and anticoagulant therapy can be challenging. We present the case of a 44 year old Caucasian male with a history of multiple ischemic strokes, with thrombophilia, but no atrial fi brillation or known cardio-embolic sources, who initially received anticoagulant treatment, which was switched in 2015 with Clopidogrel. Aspirin was added in 2017 after having a TIA in the left MCA territory. Despite dual antiplatelet therapy, the patient developed ischemic stroke in the left MCA territory, for which re-initiation of anticoagulant treatment was decided. Holter ECG, transthoracic and transesophageal echocardiography were performed, but failed to identify a cause. [ABSTRACT FROM AUTHOR]

Tuberous sclerosis complex (TSC) is an autosomal dominant disorder with multisystemic involvement usually resulting from mutations in the tuberous sclerosis 1 (TSC1) or TSC2 genes. However, 10 to 25% of patients do not exhibit these mutations. Cerebral cavernous malformations (CCMs) are capillary-venous malformations that can be asymptomatic or cause variable neurological manifestations, including seizures. Familial CCMs are recognized. In both conditions, specific dermatological lesions are associated. We present the case of a 31-year-old female with TSC diagnosed at the age of 18 years who presented with negative genetic testing. She was admitted to our department in 2019 for a sudden increased frequency of focal seizures. Patient examination revealed multiple facial and intraoral angiofibroma, diplopia, right hemihypoesthesia, brisk deep tendon reflexes, and distal leg paresthesia. VideoEEG indicated a frontal paramedian epileptogenic focus. Cerebral magnetic resonance imaging (MRI) and angioMRI identified multiple fronto-parietal cortical tubers, as well as multiple CCMs, with evidence of bleeding in one. Under antiepileptic drug (AED) and mTOR inhibitor treatment, the seizure frequency significantly improved in a short period of time. This is the first reported case of tuberous sclerosis with negative genetic testing associated with multiple cerebral cavernoma. Such complex patients require multidisciplinary management and detailed genetic testing for increasing knowledge on neuro-cutaneous disorders. [ABSTRACT FROM AUTHOR]

The acute confusional state is one of the most common reasons for neurologic consultation in the hospital setting and the plethora of causes can truly be daunting. The etiology can vary from structural, metabolic, toxic to systemic infections. Our purpose is to present a rare case of acute confusional state in a patient with bilateral thalamic ischemic stroke due to occlusion of the artery of Percheron (AOP). A 79-year-old woman with a history of hypertension and surgery for lumbar disc herniation, managed on antiplatelet therapy, angiotensin receptor blocker and diuretics, was admitted for acute confusion and paresthesia of all four limbs. She had disorientation in time and space, abnormal behavior, decreased muscle strength in both lower limbs (paraparesis 2/5 MRC since the surgery), paresthesia in all four limbs and was unable to walk due to generalized weakness. Laboratory analysis showed high blood levels of cholesterol and glucose. Both head CT and cerebral MRI showed bilateral ischemic changes in the thalami, suggesting an infarct along the artery of Percheron territory. However, no clear cause for the stroke could be identified. Screening for coagulation abnormalities and autoimmune disorders (lupus anticoagulant, anti-beta-2 glycoprotein, anti-cardiolipin, anti-nuclear and anti-ds DNA antibodies) came back negative. There were no pathological finds on the echocardiogram and electrocardiogram, while cervical Doppler ultrasound showed atherosclerosis without stenosis. [ABSTRACT FROM AUTHOR]

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary disease caused by mutations in NOTCH3 gene, characterized by accumulation of a toxic protein in the small and medium size arterioles. Clinical manifestations of CADASIL include lacunar infarcts or, less frequently, large artery ischemic strokes, transient ischemic attacks, dementia, migraine and psychiatric disorders. Brain magnetic resonance imaging (MRI) usually shows multiple lacunar infarcts, diffuse leukoencephalopathy and cerebral microbleeds. The authors report the case of a 39-year-old Romanian woman who presented two transient ischemic attacks manifested with aphasia, headache and mild cognitive impairment. Brain MRI showed multiple isolated and confluent bilateral supratentorial hyperintense fluid-attenuated inversion recovery (FLAIR) and apparent diffusion coefficient (ADC) areas involving the subcortical and deep white matter, but also lenticular and caudate regions and normal aspects of the brain arteries on magnetic resonance angiography (MR-angiography). Differential diagnosis with other disorders affecting small cerebral vessels was performed. Transesophageal echocardiography showed presence of patent foramen ovale (PFO), with right-to-left shunt and contrast passage at Valsalva maneuver. Genetic testing revealed a pCys194Arg heterozygous mutation with C580T>C nucleotide's change on exon 4 of NOTCH 3 gene. The authors discuss the association of CADASIL to PFO and mild cognitive impairment as well as ongoing research for a therapeutic strategy. [ABSTRACT FROM AUTHOR]

We present the case of a 69-year-old male, alcohol consumer, who was brought in by the ambulance for language impairment with onset two days prior to presentation in our hospital. Medical history revealed therapeutically neglected gout and colchicine allergy. On neurological exam, the patient presented predominantly motor aphasia with poor verbal fluency and anomic elements, mild right-sided hemiparesis 4/5 MRC and right-sided Babinski sign. Still, he was conscious and cooperative, and denied any recent head trauma or headache. Based on clinical picture, an acute cerebrovascular event was suspected, and the patient was hospitalized. However, brain CT revealed a late subacute subdural hematoma in the left hemisphere, with maximum thickness of 20 mm and displacement of median structures by 12 mm to the right (subfalcine herniation). The patient was then rapidly transferred to a Neurosurgical department for appropriate treatment and care. [ABSTRACT FROM AUTHOR]

Objectives: Hepatic encephalopathy is a complex of neuropsychiatric manifestations in patients with acute or chronic liver insufficiency and/or porto-systemic shunts. Material and methods: The diagnostic can be sustained by various elements, clinical and paraclinical. Selected patients with hepatic encephalopathy have been investigated by Magnetic Resonance, in parallel with specific biochemical analysis. Outcomes: This paper emphasizes the importance of Magnetic Resonance Imaging in an accurate diagnosis and patient monitoring after treatment. Conclusions: Magnetic Resonance Spectroscopy has a substantial role, showing even minute metabolite ratio changes, with a potential in investigating minimal hepatic encephalopathy. [ABSTRACT FROM AUTHOR]

Minimal Hepatic Encephalopathy (MHE) is a potentially reversible spectrum of neuro-psychiatric alterations in patients with acute or chronic liver disease, in the presence of a normal neurological examination. Studies demonstrated that early diagnosis and treatment of this complication increases the quality of life of the patients and leads to an overall better liver disease management. Currently, a practical method of diagnosing MHE is through psychological tests, with modest accuracy. A highly sensible and specific non-invasive method of diagnosis is Magnetic Resonance Spectroscopy (MRS) which identifies the key neuro-biochemical profile of hepatic encephalopathy. In selected cases of equivocal psychological test results, MRS is justified and adequate according to the authors' opinion. [ABSTRACT FROM AUTHOR]

Hematopoietic cell transplantation (HCT) is widely performed for neoplastic and non-neoplastic diseases. HCT involves intravenous infusion of hematopoietic progenitor cells from human leukocyte antigen (HLA)-matched donor (allogeneic) or from the patient (autologous). Before HCT, the patient is prepared with high dose chemotherapy and/or radiotherapy to destroy residual malignant cells and to reduce immunologic resistance. After HCT, chemotherapy is used to prevent graft rejection and graft versus host disease (GvHD). Neurological complications are related to the type of HCT, underlying disease, toxicity of the conditioning regimens, immunosuppression caused by conditioning regimens, vascular complications generated by thrombocytopenia and/or coagulopathy, GvHD and inappropriate immune response. In this review, neurological complications are presented according to time of onset after HCT: (1) early complications (in the first month) - related to harvesting of stem cells, during conditioning (drug toxicity, posterior reversible encephalopathy syndrome), related to pancytopenia, (2) intermediate phase complications (second to sixth month) - central nervous system infections caused by prolonged neutropenia and progressive multifocal leukoencephalopathy due to JC virus, (3) late phase complications (after sixth month) - neurological complications of GvHD, second neoplasms and relapses of the original disease., Competing Interests: None declared

State-of-the-art magnetic resonance (MR) imaging using tissue specific contrast media facilitates detection and characterization in most cases of hepatic nodules. According to the currently used nomenclature, in liver cirrhosis there are only two major types of hepatocellular nodular lesions: regenerative lesions and dysplastic or neoplastic lesions. The purpose of this clinical imaging review is to provide information on the properties of tissue-specific MR contrast agents and on their usefulness in the demonstration of the pathologic changes that take place at the level of the hepatobiliary and reticuloendothelial systems during the carcinogenesis in liver cirrhosis.

Budd-Chiari syndrome is caused by the obstruction of the hepatic venous outflow at the level of the hepatic venules, large hepatic veins, and inferior vena cava up to the confluence with the right atrium. When it is untreated, the mortality rate for patients is high. Because the clinical presentation of this syndrome is nonspecific, imaging investigation--computed tomography and magnetic resonance--are important diagnostic steps. Contrast-enhanced multiphase spiral computed tomography (CT) and magnetic resonance (MR) angiography permits morphologic and functional assessment of parenchymatous liver changes in this particular entity. In this review, we present the spectrum of vascular and hepatic parenchymal abnormalities in Budd-Chiari syndrome observed on multiphase contrast enhanced spiral CT and MR angiography.