Dr Balaji Anvekar FRCR

Time 2020-09-17 03:02:25

Web Name: Dr Balaji Anvekar FRCR

WebSite: http://www.neuroradiologycases.com

ID:49331

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Balaji,Dr,FRCR,

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A linear low signal running transversely in L1 vertebral body through its whole sagittal diameter without marrow odema on STIR.It's a "Hahn cleft or canal", a normal anatomical variation of no clinical significance and is secondary to persistent nutrient artery and its canal, should not be mistaken for fracture.COVID 19 stands for Corona virus disease 2019.It s a highly contagious disease caused by severe acute respiratory syndrome corona virus 2, SARS COV 2, a race of corona virus.Initial cases were seen in Wuhan of China in late December 2019 with the rapid spread of disease globally and came up as a pandemic affecting more than 10 million people worldwide.Non-symptomatic carriers and asymptomatic transmission is a major cause of poor control over the disease.Disease transmission is primarily human-to-human as of now, transmitted similarly as the common cold, via contact with droplets of infected individuals during sneezing, coughing or even speaking.The suggested incubation period of the disease is approximately five days, almost all developing symptoms typically 14th day after the exposure to the virus. Fortunately, the death rate of the disease is only 2 to 3%. Furthermore, it is speculated that the death rate is much lower than that because asymptomatic or mildly symptomatic cases are not being tested and included in the statistics, apparently showing the high death rate.It is interesting to mention that 60% of patients affected are male with high predominance between 45 to 60 years of age. Older age is known for increased mortality. Children across the globe relatively found spared by the disease. However, critically ill children under 12 years of age and infants are known as well in certain corners of the world with a shorter incubation period of about two days compared to adults.Clinical presentation is typically systemic or respiratory. Gastrointestinal or cardiovascular symptoms are very uncommon. Common symptoms in the descending order are fever 85-90%, cough 65-70%, fatigue, shortness of breath, body pain, headache, sore throat, shivering with associated nausea vomiting.Patients presenting with palpitations, chest tightness, urinary tract infection, diarrhoea are also known.RT-PCR Swab testA positive RT-PCR test needed for a definitive diagnosis of disease.Its real-time reverse transcriptase-polymerase chain reaction (RT-PCR) test, is highly specific, but with sensitivity reported as low as 60-70%. Thus, false negatives are a real clinical problem so several negative tests might be required to be confident about excluding the disease.A false-negative rate of 100% on the first day after exposure, dropping to 67% on the fourth day. On the day of symptom onset approximately 4 days after exposure, the false-negative rate remains at 40 %, and it reaches its lowest to 20% at around three days after symptoms during which test has the highest accuracy. After this again the false-negative rate increases reaching 66% on day 21 after exposure.Role of CT chestCT findings were not part of the diagnostic criteria for COVID-19. However, CT findings have been used controversially as a surrogate diagnostic test by few including me being fast and highly sensitive.I would like to mention that CT is not recommended for follow-up imaging to assess disease progression. Chest X-ray is considered to be the best for bedside follow-up in this regard. However, chest Xray is much less sensitive than chest CT, so its very common to have normal chest Xray in early or mild disease.CT Chest with typical GGONormal Chest Xray of the same patientCT protocol is non-contrast spiral chest CT. Iodinated contrast medium is only indicated when one need to do CT pulmonary angiogram (CTPA) for suspected pulmonary thromboembolism.Primary findings of COVID-19 on chest radiograph and CT are those of atypical pneumonia or organizing pneumonia. The most frequent is airspace opacities, often described as consolidation and ground-glass opacity, often bilateral, peripheral, and lower zone predominant. Fibrotic bands and traction bronchiectasis can be seen when the disease is resolving.Pleural effusion and lymphadenopathy are rare, rather they are not the features of the disease.Other common ancillary lab tests which are performed in a hospitalised patient are CBC for lymphopenia, increased prothrombin time (PT), increased lactate dehydrogenase, CRP, ESR, D-dimer, serum amylase. Mildly deranged liver function tests are common, primarily elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Alkaline phosphatase (AKP) and gamma glutamyl transferase (GGT) levels remain normal.Complications during the disease which contributes in mortality are acute respiratory distress syndrome (ARDS), acute thromboembolic disease, pulmonary embolism, acute cardiac injury due to elevated troponin levels, myocardial ischemia, cardiac arrest, myocarditis. These complications are more common when there are associated comorbidities like obesity, older age, and diabetes.Rx, no definitive treatment or vaccine exists as of now however, dexamethasone, a kind of steroid has a crucial role in changing the outcome of clinically bad patients. Antiviral therapy such as Tab Fabiflu recently launched in the market and is available with a prescription.A benign bone tumour, typically occurs in children and adolescents, more common in males. Characteristically present with night pain which is relieved by the use of salicylate analgesia such as aspirin.They are a classic cause of painful scoliosis when occurring in spine, concave on the side of the lesion. Soft tissue swelling and oedema may occur and if close to a growth plate, accelerated growth may be evident, may be related to hyperemia.Most osteoid osteomas occur in long tubular bones of the limbs such as femur and tibia.The femur is the most common location especially the neck of femur. The mid-tibial diaphysis is the next common location.Osteoid osteomas are usually cortical lesions with adjacent sclerosis which is reactive and does not represent the lesion itself.The nidus is usually less than 2 cm in diameter and is typically ovoid in shape. Associated solid periosteal reaction with cortical thickening on x-ray or CT. The nidus is sometimes visible as a well-circumscribed lucent region, occasionally with a central sclerotic dot.CT is excellent at characterizing the lesion and is the modality of choice.Nuclear medicine, skeletal scintigraphy will show typical focal uptake and at times will show a double density sign.MRI is sensitive, but is non-specific and is often unable to identify the nidus due to associated bone marrow and adjacent soft tissue oedema.The lesion is benign and treatment has traditionally been with surgical resection.General imaging differential considerations include:osteomyelitis, Brodie abscessosteoblastoma more than 2 cm in sizestress fracturecortical desmoidosteochondromaosteosarcomaenostosislocalized cortical thickeningintracortical hemangiomaClinically: patient presented with low back pain.No posterior mediastinal symptoms or signs.MRI DORSAL SPINE shows:A well-defined unilocular cystic lesion measuring approximately 20 mm in posterior mediastinum adjacent to the dorsal spine at D4 D5 level at 11 o'clock position on axial sections. No obvious adjacent osseous involvement or intraspinal extension.Rest of the MRI WHOLE SPINE screening unremarkable.Imaging diagnosis:Appears an incidental non-tumoural posterior mediastinal cyst-like Mullerian cyst.DDs:No associated vertebral anomaly to suggest Neuroenteric cyst. The lesion is not close to trachea or oesophagus to suggest duplication cyst. Rest of the sag T2w screening MRI study of the Whole spine shows no significant abnormality in cord or cauda equina.Cystic lesions found in the mediastinum are typically included bronchogenic cysts, esophageal duplication cysts and Neuroenteric cysts.But typical Mullerian cysts of this kind also needs consideration which is often overlooked.The reason may be Mullerian cysts in locations outside of the female pelvis are rare. Some reported locations include the skin and retroperitoneum. The etiology of Mullerian cysts arising in the mediastinum is unclear. Batt suggested that the lesion is derived directly from the primary Mullerian apparatus.While only 14 cases of mediastinal cysts with Mullerian differentiation have been described in the literature, it is likely that they are much more common than presumed in older females and often misdiagnosed as either bronchial or oesophagal cysts.The fourteen definitive mediastinal cysts with Mullerian differentiation have been identified, have occurred in females 40-60 years old. These patients typically presented with cough or were asymptomatic. All cysts were paravertebral in location, occurring between T3-T8 vertebrae. All of the cysts were positive for either ER or PR. Our report is the first to show expression of PAX8 and WT1, both markers of Mullerian differentiation, in these cysts.The other DDs for cystic masses of the posterior mediastinum include: bronchogenic cyst esophageal duplication cyst neuroenteric cyst meningocele lymphangioma mediastinal thoracic duct cyst mediastinal pancreatic pseudocyst.This CT and MRI study of brain shows:Multiple dense nodular calcifications along enpendymal lining of bilateral lateral ventricle best seen on CT. Cortical tubers seen as small multi focal cortical and sub cortical white matter patchy hypodensities on CT and T2 hyper intensities on MRI. No obvious obstructive hydrocephalus.The lesion at right caudo thalamic groove not calcified on CT but shows avid enhancement on post contrast, needs follow up imaging as it may turn out to be a sub ependymal giant cell astrocytoma leading to obstructive hydrocephalus. However as of now there is not obvious obstructive hydrocephalus.Imaging diagnosis : Tuberous Sclerosis.TUBEROUS SCLEROSISSyn: Tuberous sclerosis complex (TSC), Bourneville-Pringle Syndrome.A inherited tumor disorder with multi-organ Hamartomas.In CNS characterized by Subependymal nodules, Subependymal giant cell astrocytoma, Cortical/subcortical tubers.Abnormal differentiation/proliferation of germinal matrix cells, Migrational arrest of dysgenetic neurons appears to be the pathogenesis behind the lesions.Histopathology and microscopic features are Balloon cells, Myelin loss, vacuolation and gliosis, Ectopic neurons.ImagingCT and MRI both are equally sensitive but MRI often shows more number of lesions.Subependymal nodulesSeen in ~ 98%. Commonest and specific site is caudothalamic groove followed by atrial and temporal lobe white matter.~ 50% them shows an associated calcification best depicted on CT. calcification is often progressive after 1 yr.30-80% of SEN shows mild enhancement on post contrast study, appreciated better on MRI than CT.SEN at foramen of Monro needs close follow. If its enlarging it is equivalent to Subependymal giant cell astrocytoma (SGCA) and can cause obstructive hydrocephalus.Subependymal giant cell astrocytoma (SGCA)Seen in ~15%.Cortical/subcortical tubers, WM lesionsSeen in ~ 70-95% common in Fronto parietal followed by temporo occipital regions and Cerebellum.Ill defined patchy hypodensites on CT +/- calcification.Hypo intense on T1 hyper intense on T2 and FLAIR on MRI. No restricted diffusion. May show low signal intensity on T2*GRE if an associated calcification.~12% cortical/subependymal tubers show faint enhancement on post contrast T1.Cyst-like white matter lesions as focal lacune best seen on MRI T2w images, common in corona radiata.An associated thickened cortex, enlarged gyri.MRS: decreased NAA/Cr, increased ml/Cr in subcortical tubers, SENs.Associated abnormalitieso Renal: Angiomyolipoma and cysts 40-80%o Cardiac: Rhabdomyomas 50-65%; majority involute over timeo Lung: Cystic lymphangiomyomatosis/fibrosiso Solid organs: Adenomas; leiomyomaso Skin: Ash-leaf spots (majority) including scalp/hair; facial angiofibromas; shagreen patches 20-35% post pubertalo Extremities: Subungual fibromas 15-20%; cystic bone lesions; undulating periosteal newbone formationo Ocular: "Giant drusen" (50%)o Dental pitting permanent teeth in most adults with TSCDDs:Subependymal heterotopia : Isointense to GM, don't enhance or Ca++.TORCH : Periventricular Ca++ , White matter lesions, Cortical dysplasia common with Cytomegalovirus (CMV).Taylors dysplasiaGeneticsDe novo = spontaneous mutation/germ-line mosaicismAutosomal dominant, high but variable penetrance. Approximately 50% of TSC cases are inherited.Clinical presentationClassic clinical triad1. Facial angiofibromas 90%;2. Mental retardation 50-80%;3. Seizures / Epilepsy 80-90%All three ("epiloia") seen in ~ 30% of cases.More the number lesion ~ high the neurologic symptoms.Diagnosed at any age.First year of life commonly present with seizures, Infantile spasms like episodes.Child present with Autistic-like behavior, mental retardation, seizures, or skin lesions.Adult may present for first time due to a symptomatic SGCA.TreatmentTreat seizures.Resect isolated tubers if seizure focus or if able to identify seizure focus among many tubers.SGCAs resected if obstructing foramen of Monro.Reference :Diagnostic imaging Osborn.Clinically: youngfemale patient with short history of drowsiness, brought unconscious.MRI brain shows bilateral fronto parietal, temporo parietalcortical T2 hyperintensity with restricted diffusion. Lab report mentions Patient s serum ammonia was high.Imaging diagnosis:Hyperammonaemia.Differential diagnosis considered were Posterior reversibleencephalopathy, CJD (Creutzfeldt-Jakob disease). Possibility of posterior reversible encephalopathy, PRES wasruled out as blood pressure was normal and there was no intra or postpartumhistory of seizures, eclampsia.Absence of dementia, very short clinical history and absenceof cerebral cortical atrophy on MRI was against CJD.Clinically: 35 year old female with sudden onset slurred speech since two days with associated giddiness, fever.On neurological examination there was facial Palsy. No signs of internuclear ophthalmoplegia.MRI BRAIN shows:Bilateral symmetric abnormal T2 hyperintensity with mild focal parenchymal swelling involving dorsum of Pons at the floor of fourth ventricle.Area of involvement corresponds to facial colliculus.Imagingwise differential diagnosis:Bilateral facial colliculus syndrome due to demyelinating lesion.Viral infection,Rhombencephalitis.Suggested CSF for oligoclonal band and serum immunoglobulin in view of Multiple sclerosis.Antinuclear antibodies in view of autoimmune disease.Routine CSF forviral infection.Facial colliculus and facial follicle syndromeFacial colliculus is an elevation on the floor of fourth ventricle in Pons under which there is a presence No nucleus is located with facial nerve axons traversing over it giving of bump like appearance.Lesion involving facial colliculus present with Internuclear ophthalmoplegia, abducens nerve, lower motor neuron type of facial nerve palsy with an associated features of medial longitudinal fascicles involvement.There is important to make note that not symptomsand signs will be present in each and every patient.Causes of facial colliculus syndrome include demyelination for example multiple sclerosis,viral infection like Rhombencephalitis, tumourwhereas it can be secondary to ischaemicinfarct in old age patient.Facial colliculus syndrome secondary to Stroke going to be uni lateral whereas demyelinating lesionwill be more or less bilateral.Clinical details: A 2 y/o female child, h/o inability to maintain posture, inability to walk, delay in developmental milestones.Enlarged head on inspection.CHOROID PLEXUS PAPILLOMAThe most benign tumor of choroid plexus.Vast majority of choroid plexus papilloma occur in the lateral and fourth ventricle. Atrium is the most common site, usually solitary tumours varying in size from small to large. Occasionally multiple non contigious lesions are seen. Most of the are well circumscribed papillary or cauliflower like masses may adhere but usually do not invade through the ventricular wall.Histologically the architecture of C.P.Ps closely resemble that of non-neoplastic choroid plexus. A core of fibrovascular connective tissue covered by a single layer of benign appearing epithelial cells is typical. Cytokeratins,Vimentins,and Podoplanin are expressed virtually by all C.P.Ps.Choroid plexus papillomas are W.H.O grade 1 neoplasm.C.P.Ps account for less than 1 % of all primary intracranial neoplasm but represent 13% of brain tumors occurring in 1st yr of life. Median age of presentation for lateral and third ventricular C.P.Ps is 1.5 yrs, for 4th ventricular C.P.Ps it is 22.5 yrs. There is slight male preponderance.Headache,nausea, vomiting with enlarged head size may be seen in children and infants.IMAGING FINDINGS:Intra ventricular mass isodense to hyperdense compared to brain parenchyma on CT. Intense homogenous enhancement on post contrast.A well defined , lobulated intraventricular mass with frond like papillary excression, iso to slightly hypointense compared to brain parenchyma is seen on T1W1, iso-to hyperintense on T2W1 and FLAIR. Linear and branching internal flow voids reflects the increased vascularity within choroid plexus papillomas. T2w images may show hypointense foci secondary to calcification.Associated hydrocephalus due to overproduction of c.s.f.Elevated myoinositol on MR spectroscopy.Dr Prasad JagdaleRadiology ResidentCNS Hospital, SolapurMRI brain shows:1. Moderate grade diffuse cerebellar atrophy. No associated Brainstem or cerebral cortical atrophy.2. Multiple punctate low signal intensity foci on GRE in bilateral cerebral white matter.Imaging diagnosis: Ataxia-telangiectasia.Ataxia TelangiectasiaA rare multisystem condition with autosomal recessive inheritance, incidence at around 1:40,000-300,000 live births, sometimes classified as a phakomatosis.Characterized by multiple telangiectasias, cerebellar ataxia, pulmonary infections and immunodeficiency.Diagnostic clue on MRI brain is diffuse cerebellar atrophy, compensatory enlargement of the fourth ventricle, micro hemorrhages secondary to capillary telangiectasia.Main clinical features include cerebellar ataxia progressive and present in all cases, associated oculomucocutaneous telangiectasias, susceptibility to pulmonary infection due to immunodeficiency.Genetics, results from a defective gene located on chromosome 11q22 23.Treatment is generally supportive.Clinical Details : 42 yo female, sometime in May 2019 suffered from an episode of un responsivity associated with no features to suggest a seizure. There was no excessive perspiration. She however regains consciousness spontaneously after about 15 minutes. Thereafter she was well but on the 9th of August abruptly lost consciousness, had abnormal tonic posturing of the limbs, hyper salivation but no tongue bite or incontinence. SHe however had excessive profuse perspiration.Present clinical examination is entirely normal.BP 130/90MR study of brain reveals multicystic changes clustered in the gyrus rectus of right frontal lobe.Clinical significance is doubtful in this case.However this is a rare finding so far reported only with tourette syndrome in literature.Ref :Tourette syndrome associated with unilateral cystic changes in the gyrus rectus.McAbee GN1, Wark JE, Manning A Department of Pediatrics (Neurology), University of Medicine and Dentistry of New Jersey, Children's Regional Hospital at Cooper Hospital/University Medical Center, Camden 08103, USA. Dr Balaji Anvekar s Neuro and MSK Cases. Awesome Inc. theme. 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