Instruction: Generate impression based on findings.

Input: Evaluate depth of scalp melanoma. Brain: There is an enhancing nodular lesion involving the epidermis and dermis of the left parietal scalp that measures up to 12 mm in width and 9 mm in depth. There is also mild thickening and hyperenhancement of the periosteum deep to the lesion, but there is no discernible signal abnormality in the underlying calvarium. The superficial aspect of the lesion is slightly indented, which may be related to prior biopsy. There is a prominent left occipital scalp lymph node that measures up to 10 mm in length. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma and pituitary gland appear unremarkable. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits are grossly unremarkable.Neck: There is no evidence of measurable mass lesions or significant cervical lymphadenopathy. The thyroid and major salivary glands are unremarkable. The osseous structures are unremarkable.

Output: 1. A left parietal scalp lesion that corresponds to the biopsied melanoma measures up to 12 mm in width and 8 mm in depth and involves both the epidermis and dermis. While there is nonspecific mild periosteal reaction deep to the lesion, the underlying calvarium appears to be grossly intact. 2. A prominent left occipital scalp lymph node is nonspecific.3. No evidence of cervical lymphadenopathy.


Instruction: Generate impression based on findings.

Input: Female, 60 years old, with back pain and history of breast cancer. Evaluate for metastases. Spinal alignment is anatomic. Vertebral body height and morphology are within normal limits. No evidence of pathologic marrow replacement or edema is seen. No abnormal enhancing lesions are detected. The visualized spinal cord shows normal signal intensity and morphology and is also free of pathologic enhancement. No epidural lesions are seen.Disc degeneration is seen at C6-7 with loss of disc height and mild posterior disc-osteophyte complex formation. No significant spinal canal stenosis is evident at this level, though there may be mild right foraminal narrowing. No interval change is seen. The other intervertebral discs are preserved and no areas of significant spinal canal or foraminal stenosis are detected.

Output: 1.No evidence of metastatic disease in the cervical spine.2.Mild disc degeneration at C6-7 is unchanged.


Instruction: Generate impression based on findings.

Input: 15 years old female with a giant vertebrobasilar aneurysm. Please provide endovascular treatment. Left subclavian artery: There is no evidence for arteriovenous fistula. No pseudoaneurysms in the V1-V3 segments of the LVA. There is aneurysmal dilation of the LVA at the V4 segment.Right subclavian artery: There is no evidence for arteriovenous fistula. There is no evidence for evidence for vertebral dissection. There is no stenosis at the origin of the right vertebral artery. No pseudoaneurysms in the V1-V3 segments of the RVA.Left vertebral artery:There is a giant vertebrobasilar aneurysm present. LVA is displaced laterally. There is a partially thrombosed 42x34x34 mm giant aneurysm at the distal left vertebral artery and vertebrobasilar junction. The LVA ends in the aneurysm. There is a vascular tunnel through the thrombosed aneurysm. The LVA is the dominant supply to the aneurysm. There is extracranial left PICA origin.Right vertebral artery: There is filling of the distal aspect of the giant vertebrobasilar aneurysm. RVA is displaced laterally. There is a 18 mm dilated segment of the RVA of which the distal 10mm open into the aneurysm. The RVA is the dominant supply to the basilar artery. There is reverse filling of the left PCOMA with partial opacification of the left middle cerebral artery. There is an inflow jet of unopacified blood entering via the LVA. The RVA is fenestrated at the level of the extracranial right PICA. The PICA originates from the larger loop.The anterior spinal artery has a dominant right C5 segmental artery supply which also supplies medulla.Right common carotid artery: There is no stenosis at the carotid bifurcation on the basis of NASCET criteria. There is no evidence for carotid dissection or pseudoaneurysm. Right internal carotid artery: There is opacification of the right anterior and middle cerebral arteries. Venous and parenchymal phases were within normal limits. There is no angiographic evidence for vasculitis. There is partial opacification of he left anterior cerebral artery.Left common carotid artery: There is no evidence for carotid stenosis on the basis of NASCET criteria. There is an aneurysm measuring approximately 16x26mm at the C1 vertebral body level along the lateral aspect of the left ICA which displaces the LICA medially and mildly narrows it. Approximately 12 mm distal to the LICA origin there is an approximately 4.5x3mm sessile aneurysm present.Left internal carotid artery: There is opacification of the left anterior and middle cerebral arteries. Venous and parenchymal phases were within normal limits. There is a large aneurysm at the C1 vertebral body level along the lateral aspect of the left ICA which displaces the LICA medially and mildly narrows it. Approximately 20 mm distal to the LICA origin there is a 7x5mm sessile aneurysm present. There is opacification of some of the distal right ACA vasculature (superior internal parietal artery).Left external carotid artery: There is no evidence for arteriovenous fistula. There is no evidence for AVM. There is no angiographic evidence for vasculitis. No aneurysms are identified.Intraprocedural angiograms:Serial arteriograms performed the during the LVA occlusion demonstrate progressive occlusion of the LVA. Serial arteriograms performed the during the stent assisted aneurysm coiling demonstrate serial occlusion of the aneurysm. At the end of the procedure there is opacification of the base of the aneurysm. Presumably the stents extend into the base.Right vertebral artery: There is opacification of the base of the aneurysm. Presumably the stents extend into the base. The RVA is displaced laterally. There is a 18 mm dilated segment of the RVA of which the distal 10mm open into the aneurysm. The stents are deployed from the basilar artery just below AICA origin to the more normal appearing RVA distal to the PICA. The RVA is the exclusive supply to the basilar artery. There is some unopacified blood entering via the left PCOMA. There is transient reverse filling of the left PCOMA with partial opacification of the left middle cerebral artery. The RVA is fenestrated at the level of the extracranial right PICA. The PICA originates from the larger loop.The anterior spinal artery has a dominant right C5 segmental artery supply which also supplies medulla.Right common iliac artery: The right profunda femoris artery originates proximal to the puncture site.Left common iliac artery: No anatomic contraindications to closure device.

Output: 1.Vertebrobasilar giant aneurysm primarily involving the LVA but also involving V-B junction and RVA.2.There are two dissecting aneurysms along the left cervical ICA. A larger one measuring is at the C1 level and a smaller one is just distal to the carotid bulb.3.Embolic coil occlusion of left vertebral artery (LVA) distal to the PICA.4.Stent assisted coiling of vertebrobasilar junction giant aneurysm using Neuroform stent system. These are MRI compatible devices up to 3 T.5.Findings were discussed with Dr Awad and Dr Ardelt at the end of the procedure.


Instruction: Generate impression based on findings.

Input: 38 year old female with right breast cancer and gene mutation, status post neoadjuvant chemotherapy. Minimal parenchymal enhancement is noted bilaterally. The background breast consists of symmetric heterogeneously dense glandular tissue.The mass in the central right breast with adjacent Hydromark clip artifact now measures 0.5 cm AP x 0.6 cm CC x 0.4 cm TV (previously 1.5 x 1.7 x 1.3 cm). No other suspicious enhancing mass or suspicious non-mass enhancement is evident in either breast. No abnormal axillary lymph nodes are identified in either axillary region. A left chest port is noted.

Output: Decreased size of the right breast mass, representing imaging response to therapy.BIRADS: 6 - Known cancer.RECOMMENDATION: T - Take Appropriate Action - No Letter.


Instruction: Generate impression based on findings.

Input: Multiple sclerosis, follow up for progression. Motion artifacts degraded exam quality.There are multiple bihemispheric high signal intensity lesions on FLAIR images.The lesions involve right frontal lobe, right parietal lobe, right occipital lobe, left frontal lobe, left parietal lobe, left occipital lobe and periventricular white matter and bilateral trigone areas. The ventricles, sulci and cisterns are symmetric and unremarkable. There is no mass, mass effect, edema, midline shift, intra or extra-axial fluid collection/hemorrhage, or restricted diffusion/acute ischemia. The midline structures and cranial-cervical junction are normal. Normal flow voids are identified in the major intracranial vessels. The paranasal sinuses and mastoid air cells are clear.

Output: Multifocal bihemispheric abnormal FLAIR high signal lesions which are consistent with MS lesions as described above.No comparison was made since there is no prior exam available.


Instruction: Generate impression based on findings.

Input: Female, 41 years old, with pain and radiating symptoms through C8 to T1. Alignment is anatomic. Vertebral body height and morphology are within normal limits. No marrow replacement or edema is seen. The visualized spinal cord demonstrates normal signal intensity and morphology throughout. No epidural abnormalities are suspected.C2-3: No spinal canal or foraminal stenosis. C3-4: Right facet arthropathy. Minimal posterior disc-osteophyte complex formation. No spinal canal stenosis. Mild right foraminal narrowing. C4-5: Minimal posterior disc-osteophyte complex formation. No spinal canal or foraminal stenosis. C5-6: Mild facet arthropathy. Minimal posterior disc-osteophyte complex formation. No spinal canal or foraminal stenosis. C6-7: Mild facet arthropathy. No spinal canal or foraminal stenosis. C7-T1: No spinal canal or foraminal stenosis.

Output: Minimal degenerative findings are seen. At most, the right C3-4 neural foramen is mildly narrowed. No areas of significant spinal canal compromise are seen.


Instruction: Generate impression based on findings.

Input: BRAIN:The ventricles and sulci are normal in size. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. There is no evidence for intracranial hemorrhage or acute cerebral, brainstem or cerebellar infarction. No diffusion-weighted abnormalities are identified. There are no extraaxial fluid collections or subdural hematomas. Flow voids are present within the major vessels indicating patency. The mastoid air cells are clear. There is a minimal air-fluid level in the right maxillary sinus. The ethmoids are partially opacified.There is a partial empty sella. There is no correlative evidence for optic sheath ectasia, optic nerve sheath dilatation, flattening of the optic disc, or a "pinched" appearance of the lateral ventricle frontal horns.MR VENOGRAM:Internal jugular veins, sigmoid sinuses, transverse sinuses, and sagittal sinus are normal in caliber. No evidence of stenosis or occlusion.

Output: 1.There is a minimal air-fluid level in the right maxillary sinus and the ethmoids are partially opacified.2.A partially empty sella is present, which in a patient of stated age 35 years can be seen in the presence of idiopathic intracranial hypertension (a.k.a. pseudotumor cerebri) or idiopathic partially empty sella. As there is no evidence of optic nerve sheath ectasia, optic nerve sheath dilatation, flattening of the optic disc, or a "pinched" appearance of the frontal horns, idiopathic partially empty sella is felt to be most likely.3.Normal MRV of the brain.


Instruction: Generate impression based on findings.

Input: 44 year old with newly diagnosed right breast cancer. There is heterogeneous amount of fibroglandular tissue in both breasts.Mild parenchymal enhancement is noted bilaterally.The biopsy proven cancer in the posterior depth of the right breast at the 12:30 position is seen as a 1.1 x 1.4 x 1.2 cm enhancing mass with internal artifact from the biopsy clip. Located immediately inferior to this mass (3 mm inferior) is a 4 mm enhancing focus. The CC extent inclusive of the adjacent focus is 2.2 cm. A clear fat plane is maintained between the mass, focus and the pectoralis. The mass and focus are both within 4 mm of the pectoralis. No abnormal enhancement is seen in the left breast. A stable normal sized intramammary lymph node in the outer breast is also visible on multiple prior mammograms. No abnormal lymph nodes are identified in either axillary region.A few scattered non-specific high T2 hepatic lesions are noted. These are most likely benign cysts.

Output: Biopsy proven right breast malignancy with an adjacent focus immediately inferior to the proven cancer. No evidence of contralateral disease or axillary metastasis. BIRADS: 6 - Known cancer.RECOMMENDATION: T - Take Appropriate Action - No Letter.


Instruction: Generate impression based on findings.

Input: Reason: R knee patellar instability. Measure TT-TG, assess for chondral injury, assess MPFL. History: R knee patellar instability MENISCI: The medial and lateral menisci are normal.ARTICULAR CARTILAGE AND BONE: There is lateral translation of the patella with respect to the femoral trochlea. The femoral trochlea is shallow, indicating femoral trochlear dysplasia. The tibial tubercle to the trochlear groove distance measures 21 mm which is abnormally increased. The Insall-Salvati ratio is 1.5, indicating patella alta. Note is made of a supratrochlear spur. There is no abnormal bone marrow signal. The articular cartilage of the knee is intact.LIGAMENTS: The cruciate and collateral ligaments are normal. EXTENSOR MECHANISM: The quadriceps and patellar tendons are normal.ADDITIONAL

Output: 1. Mild femoral trochlear dysplasia and lateral translation of the patella with respect to the femoral trochlea. Abnormally increased tibial tubercle trochlear groove distance.2. Patella alta.


Instruction: Generate impression based on findings.

Input: BRCA 1 mutation. High-risk screening. There is extreme amount of fibroglandular tissue in both breasts.Minimal parenchymal enhancement is noted bilaterally.Again noted are a few enhancing foci in the far posterior left breast. Ultrafast sequence imaging did not demonstrate suspicious early enhancement. No suspicious enhancing lesions are noted in either breast. No enlarged axillary or internal mammary lymph nodes.

Output: Stable examination without MR evidence of malignancy.BIRADS: 2 - Benign finding.RECOMMENDATION: T - Take Appropriate Action - No Letter.


Instruction: Generate impression based on findings.

Input: Reason: eval plexiform neurofibroma History: pt with nf-1 and large plexiform tumor causing pain The patient returned on April 5th for additional scans of the right lower extremity to include the patient's entire plexiform neurofibroma. Please see the original report from 2/24/2016 (accession #15868965), regarding the detailed description of the larger discrete masses of the patient's extensive plexiform neurofibroma. Overall the plexiform neurofibroma extends from approximately 12 to 13 cm above the knee joint to approximately 29 to 30 cm below the level of the knee joint.

Output: Large plexiform neurofibroma. Please refer to the MRI right tibia/fibula examination dated 2/24/2016 for additional details.


Instruction: Generate impression based on findings.

Input: Left sided proptosis; history of left eyelid melanoma excision. Orbit: There is mild left proptosis associated with bowing of the posterolateral wall of the orbit secondary to an arachnoid cyst in the anterior portion of the left middle cranial fossa. Otherwise, there is no evidence of intraorbital mass lesions and the globes and ocular adnexa are intact. Brain: The arachnoid cyst in the anterior portion of the left middle cranial fossa measures up to 18 mm in width with associated remodeling of the overlying skull. There is no evidence of acute intracranial hemorrhage or abnormal enhancement. There is a 9 mm wide left choroid fissure cyst. The ventricles are otherwise normal in size and configuration. There is no midline shift or herniation. There is moderate right maxillary sinus mucosal thickening and a left sphenoid sinus retention cyst. There is minimal fluid signal in the right mastoid air cells.

Output: Mild left proptosis associated with bowing of the posterolateral wall of the orbit secondary to an arachnoid cyst in the anterior portion of the left middle cranial fossa. No evidence of intraorbital or intracranial tumors otherwise.


Instruction: Generate impression based on findings.

Input: Left-sided paresthesias, word finding difficulties, concern for MS, previous MRI due to left-sided paresthesia for weeks with T2 FLAIR hyperintensities. No diffusion restriction is seen to suggest acute ischemia. No susceptibility weighted artifact is seen to suggest intracranial hemorrhage. Scattered T2/FLAIR hyperintense foci are seen in the periventricular and subcortical white matter, unchanged from the prior study. No enhancement is seen associated with these lesions. No lesions are seen within the posterior fossa. No new lesions are identified. No abnormal areas of enhancement are seen. The CSF spaces are appropriate for the patient's stated age with no midline shift. Prominent perivascular spaces are seen in the right inferior basal ganglia. Normal vascular flow voids are present in the major intracranial vasculature.The imaged portions of the paranasal sinuses are clear. The imaged portions of the mastoid air cells are clear. The imaged portions of the orbits are intact.

Output: Nonspecific T2/FLAIR hyperintense foci are unchanged. Differential diagnosis most likely includes demyelinating disease, migraine sequela, diffuse axonal injury, and small vessel ischemic disease.


Instruction: Generate impression based on findings.

Input: 64 year-old female history of left hepatectomy for multiple hepatic adenoma now with elevated alkaline phosphatase and fever. The study is limited due to patient motion.ABDOMEN:LIVER, BILIARY TRACT: Status post recent extended left hepatectomy and segment 6 segmentectomy with adjacent surgical drain present. Small amount of perihepatic ascites. No drainable fluid collections. No intra or extra hepatic biliary ductal dilatation.Scattered, smaller, presumed hepatic adenomas, are grossly unchanged compared to the prior CT.Status post cholecystectomy.SPLEEN: No significant abnormality noted.PANCREAS: 8 mm cystic lesion at the body/head junction likely represents an IPMN. Additional similar appearing cystic focus present near the inferior aspect of the uncinate process measuring 6 mm.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Small renal cysts.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: Small right pleural effusion with associated basilar atelectasis/consolidation. Mild subsegmental atelectasis left lower lobe. Anasarca.

Output: 1. Postoperative changes in the liver as above with no evidence of drainable fluid collections. Small volume ascites.2. No intra or extrahepatic biliary ductal dilation.3. Small right pleural effusion and basilar atelectasis/consolidation.4. Small hepatic lesions presumably representing adenomas are unchanged from prior CT.5. Two small cystic lesions in the pancreas as above likely representing IPMNs.


Instruction: Generate impression based on findings.

Input: Left buttock to left lower extremity pain and numbness since LP on 8/31. Examination is slightly technically degraded related to motion and patient's body habitus. Five lumbar type vertebral bodies are presumed to be present. Vertebral body heights are within normal limits. Alignment is within normal limits. Bone marrow signal is benign. The conus medullaris is normal in position. Cauda equina nerve roots appear unremarkable. No abnormal enhancement.Individual levels as described below:L1-L2: No significant disc disease. No spinal canal or neural foraminal stenosis.L2-L3: No significant disc disease. No spinal canal or neural foraminal stenosis. There is a benign-appearing subcentimeter focus of T2 hyperintensity involving the right sided facet joint which may represent a tiny subchondral cyst.L3-L4: No significant disc disease. No spinal canal or neural foraminal stenosis.L4-L5: No significant disc disease. No spinal canal or neural foraminal stenosis.L5-S1: No significant disc disease. No spinal canal or neural foraminal stenosis.Paraspinous soft tissues are within normal limits.

Output: Examination is slightly technically degraded due to motion and patient's body habitus. There is however no significant disc disease or spinal canal or neural foraminal stenosis at any level. No evidence of intraspinal hematoma or abscess.


Instruction: Generate impression based on findings.

Input: Diagnosis: Benign neoplasm of meninges, unspecifiedClinical question: meningioma f/u, compare w/ priorComments: Meningioma resection 7/2012 | The CSF spaces are appropriate for the patient's stated age with no midline shift. The patient is status post right-sided craniotomy. A small focus of encephalomalacia is present along the right frontal lobe along the lateral aspect of the right precentral gyrus extending to the subcentral lobule. No abnormal enhancing lesion is appreciated to suggest local recurrence.There is a T1 hyperintense mass present along the perivertebral musculature at the C1-2 level measuring 41 x 26 mm axial dimensions which is bright on T1-weighted imaging and suppresses on the fat suppressed images suggesting that this is a lipoma. It is unchanged since the prior exam.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.

Output: 1.No evidence for local recurrence of meningioma status post right parietal bone craniotomy for removal of the meningioma.2.Lipoma in the left upper neck is stable.


Instruction: Generate impression based on findings.

Input: Again seen are postsurgical changes of Chiari decompression including suboccipital craniectomy and resection of the posterior arch of C1. Again seen are foci of deformity of the posteroinferior aspect of the cerebellum, with tenting towards the overlying dura and unchanged. There is a retroflexed dens with associated narrowing of the column of cerebrospinal fluid flow across the anterior neo-foramen magnum. Biphasic flow anteriorly at the foramen magnum is otherwise preserved. There is diminished CSF flow and diminished CSF space dorsal to the cervical cord, not significantly changed since 2/11/2016, allowing for slight differences in technique. Biphasic flow at the foramen Magendie appears preserved.There appears to be slight further decrease in size of the thoracic syrinx with minimal residual prominence of the central canal measuring 1 to 2 mm seen at T5-T6 and in the mid to lower thoracic cord more inferiorly. Previous seen tiny syrinx which is less visible on the current study is likely partly related to motion degradation on the current study. No new cord signal abnormality. Vertebral body heights and alignment are grossly unremarkable aside from mild straightening. Conus is in normal position at the upper L2 level. No spinal canal or neural foraminal stenosis is evident.

Output: Postoperative findings related to Chiari decompression again seen. Compared to 2/11/2016, there is no significant change in the appearance of the posterior fossa including retroflexed dens with associated narrowing of the anterior column of CSF flow as well as tenting of cerebellar tissue towards the overlying dura posteriorly, which may represent an adhesion. Motion degradation limits comparison, however, the residual tiny mid thoracic syrinx seen previously on 2/11/2016 is stable to slightly further decreased. Syrinx is markedly decreased when compared to 10/22/2015.


Instruction: Generate impression based on findings.

Input: Status post femoral access attempts. Rule out retroperitoneal bleeding. ABDOMEN: Bilateral small pleural effusions. Cardiomegaly. Independent atelectasis lung bases.LIVER, BILIARY TRACT: Liver is nodular in contour with hypertrophic left lobe suggestive of chronic liver disease. Cholelithiasis without evidence of cholecystitis. No biliary dilatation.SPLEEN: No significant abnormality noted.PANCREAS: Pancreas is atrophic. Lack of IV contrast severely limits evaluation of the pancreas. If there is any clinical concern for pancreatic pathology MRI is recommended.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Both kidneys demonstrate retained contrast likely from previous contrast enhanced study. Bilateral large stones mostly in the lower pole of the collecting system of the kidneys are again noted. Large left-sided renal cyst and small bilateral renal cysts.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.PELVIS:UTERUS, ADNEXAE: No significant abnormality noted.BLADDER: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: Small left-sided inguinal hematoma. No extension to the retroperitoneum.OTHER: Right-sided femoral venous catheter extends to the right ventricle.

Output: No evidence of retroperitoneal hemorrhage. Cholelithiasis and bilateral nephrolithiasis unchanged.Cardiomegaly bilateral small pleural effusions. Possible chronic liver disease. If there is a clinical concern for pancreatic pathology MR of the liver is recommended. This study is extremely limited for evaluation of the pancreas.


Instruction: Generate impression based on findings.

Input: There is stable minimal thickening and enhancement of the left tentorial leaflet without adjacent mass effect or vasogenic edema. There is no other suspicious intracranial enhancement, acute infarct, mass effect or midline shift. The ventricles are sulci are unchanged. There is no hydrocephalus. The cerebellar tonsils remain above the foramen magnum. There is a mucus retention cyst in the left maxillary sinus.

Output: Stable minimal nonspecific thickening and enhancement of the left tentorial leaflet without mass-effect. Otherwise, unremarkable examination.


Instruction: Generate impression based on findings.

Input: Diagnosis: Altered mental status, unspecifiedClinical question: altered mental status , Hx of endometrial cancer R/o Encephalitis/ meningitis / infarctionSigns and Symptoms: Altered mental status The CSF spaces are appropriate for the patient's stated age with no midline shift. No foci of diffusion restriction are present within the brain parenchyma.There is a mild degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images. Some patchy T2 and FLAIR signal hyperintensities are present in the pons and the lower midbrainNo abnormal enhancing mass lesions are appreciated intracranially. No intracranial hemorrhage is identified. No edema is identified within the brain parenchyma.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact. The eyeball lenses are thin.

Output: 1.Periventricular and subcortical white matter changes and patchy lesions in the brainstem of a mild degree are nonspecific. At this age they are most likely vascular related. 2.There is no evidence for acute ischemic cerebral infarction. 3.There is no evidence for intracranial mass lesion. 4.There is no MR evidence for meningitis. Please note that lack of MR evidence for meningitis does not exclude meningitis.


Instruction: Generate impression based on findings.

Input: Redemonstrated is decreased volume of the left cerebral hemisphere and asymmetry of the basal ganglia, thalamus and cerebral peduncles. Again noted is abnormal signal around the ventricles. The corpus callosum is fully formed, although appears somewhat blunted on the anterior most genu, with the midline falx present. Asymmetric prominence of the right lateral ventricle, but is slightly decreased in size along with the third ventricle. There is interval decrease in the size of the subarachnoid spaces. Evaluation of the posterior fossa again demonstrates fourth ventricular enlargement with communication of the the fourth ventricle with a posterior fossa space, hypoplasia of the vermis, mild superior displacement of the fourth ventricle and vermis, and mild enlargement of the posterior fossa. There is no mass effect. There are no areas of abnormal signal. There is no diffusion abnormality. No extra-axial fluid collection is identified. Normal flow-voids are demonstrated in the major intracranial vascular structures. Incidentally noted is a prominent node of Rouviere on the right measuring 12 mm, which is likely reactive.The inadvertently performed CSF flow sequence demonstrates biphasic flow ventral and dorsal to the cervicomedullary junction as well as flow in the aqueduct and 4th ventricle.

Output: 1. Unchanged constellation of posterior fossa findings suggestive of a Dandy-Walker variant/spectrum.2. Generalized decreased volume of the left cerebral hemisphere in comparison to the contralateral side including similar asymmetry of the basal ganglia, thalami, and left cerebral peduncle. 3. Abnormal signal findings around the ventricles, favoring delayed myelination and/or gliosis, and less likely heterotopia.4. Prominence of the right lateral ventricle and third ventricle is slightly decreased in extent as well as the previously noted prominence of the subarachnoid spaces, likely relating to resolving benign external enlargement of subarachnoid spaces which usually resolves by two years of age.


Instruction: Generate impression based on findings.

Input: History of new ulcerative sigmoid colon mass seen on colonoscopy, evaluation of hepatic lesion seen on prior CT imaging ABDOMEN:LIVER, BILIARY TRACT: Corresponding to hypodensity seen on prior CT imaging is hepatic segment II focus of abnormal signal measuring 1.8 x 1.2 cm, which demonstrates mildly increased T2 signal and restricted diffusion as well as postcontrast rim enhancement (pattern of enhancement appears to be continuous and somewhat nodular). Although postcontrast enhancement difficult to delineate due to small size, additional smaller adjacent foci demonstrating similar signal characteristics otherwise seen, measuring up to 0.7 x 0.5 cm, image 27 series 401, suspicious for additional nearby metastatic foci. Another tiny focus of restricted diffusion seen in right hepatic dome, image 328 series 501, difficult to assess for postcontrast enhancement and T2 signal abnormality due to small size, nonspecific but a metastatic lesion not entirely excluded. Best seen in the portal venous phase of imaging is a 1.3 x 1.2 cm left hepatic dome focus, hypointense compared to background liver during this phase (image 364 series 901), indeterminate, no corresponding restricted diffusion delineated. A T2 hyperintense focus lateral to gallbladder fossa located in hepatic segment 5 may be a cyst, image 274 series 901.SPLEEN: Multiple soft tissue signal lesions in expected region of spleen/splenic bed, suggestive of splenosis.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Right upper pole renal cyst. Multifocal left renocortical scarring.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.

Output: 1. Hepatic lesions as described, demonstrating imaging characteristics consistent with metastases.


Instruction: Generate impression based on findings.

Input: 12 years, Female, episode of uncontrolled left are lasting 37 minutes, concern for seizure. There is no restricted diffusion to suggest acute ischemia. There is no intracranial hemorrhage. No intracranial mass or mass-effect. The ventricles are within normal limits in size and configuration. The hippocampi appear symmetric. The hypothalamus is normal in appearance. There is no evidence of cortical dysplasia.There is no abnormal parenchymal or meningeal enhancement. Major flow-voids are preservedSella and orbits are grossly within normal limits. There are minimal retained secretions within the maxillary sinuses. Bone marrow signal and extracranial soft tissues are within normal limits.

Output: No evidence of intracranial hemorrhage, mass, or acute infarction. There are no MRI findings to explain the clinical symptoms.


Instruction: Generate impression based on findings.

Input: Bilateral lower extremity weakness, unable to ambulate, known T12 compression fracture. Metastatic renal cell cancer. Compared to 6/25/2015, there has been worsening of vertebral body height loss involving the T12 vertebral body. There is increased osseous retropulsion and development of severe spinal canal stenosis at this level. Compared to prior, the posterior thecal sac is now effaced. Increased kyphosis is also noted at this level.There is evidence of diffuse osseous metastatic disease with multiple additional levels of bone marrow signal abnormality noted including the T1, T3, T8, and T9, and multiple lumbar vertebral bodies. No significance spinal canal stenosis is seen aside from the T12 level.

Output: Evidence of osseous metastatic disease at multiple levels in the thoracolumbar spine with interval worsening of the severe pathologic compression fracture involving the T12 vertebral body with worsened spinal canal stenosis, deformity of the lower thoracic cord, and kyphosis at this level.Please note limited sequences were obtained for this exam per acute cord compression protocol.Dr. Ali discussed findings with Dr. Jelinek at 0908 hours on 8/6/2015.


Instruction: Generate impression based on findings.

Input: There are artifacts from the right parietal approach shunt valve which limits interpretation of the diffusion and the susceptibility images.There is redemonstration of ventriculostomy catheter with the left frontal horn, revised since prior MR. The ventricles are slitlike and decompressed. Compared to the previous CT, there is grossly stable fourth ventricular dilatation, measuring approximately 28 x 19 mm in transaxial view. The right foreman of Luschka is widened.There is dysmorphic appearance of the brain. There is diffuse white matter volume loss with also prominence of the sulci.In the visualized portion of the susceptibility images, low signal is seen in the left thalamus and in the right centrum semiovale. The left thalamic cyst that was seen in the previous study is still present but has significantly decreased in size from 22 mm to 7 mm CC. There is greater extent of the T2/FLAIR high signal in the periventricular white matter with involvement of the centrum semiovale.The falx is dysplastic and there is a focal leftward herniation of the medial posterior right frontal lobe through the falcine deficiency.There is an abnormal cleft perhaps along the spectrum of schizencephaly of the left frontoparietal region, versus severe gliosis and loss of white matter with abnormal sulcation. However, no definite abnormal gyral thickening or polymicrogyria is detected.The anterior body and the genu of the corpus callosum are seen with small rostrum. The posterior body and splenium are not as well visualized, suggesting hypoplasia.

Output: 1. Persistent slitlike lateral and third ventricles with significantly dilated fourth ventricle and widened right foramen of Luschka, unchanged from the previous CT. Stable right parietal approach ventriculostomy catheter.2. The left thalamic cyst has significant decreased in size, likely in communication with the lateral ventricles.3. Greater extent of the T2/FLAIR high signal in the periventricular and deep white matter, which may relate to areas of gliosis perhaps relating to underlying periventricular leukomalacia. Extensive volume loss, especially of white matter.4. Dysplastic anterior falx with leftward herniation of the right medial posterior frontal lobe.5. Hypoplastic posterior corpus callosum.6. Abnormal deep sulcus along left frontoparietal region, with questionable schizencephaly spectrum abnormality vs. gliosis and abnormal sulcation. No definite migrational abnormality appreciated.


Instruction: Generate impression based on findings.

Input: History of hemoglobin SC with confusion, dizziness, failing grades. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma and pituitary gland appear unremarkable. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, and scalp soft tissues are grossly unremarkable. There is mild scattered paranasal sinus mucosal thickening and hyperenhancement, suggestive of inflammation.

Output: No evidence of intracranial hemorrhage, mass, or acute infarct.


Instruction: Generate impression based on findings.

Input: Acute myeloblastic leukemia, not having achieved remission [C92.00], Reason for Study: ^Reason: cause of erosions noted on CT max facial, cause of arachnoid granulations History: leukemia, previous Head CT max/facial showed erosions The left sphenoid greater wing shows inner table of skull erosion with extension of arachnoid space (series 901, image 10/30) with crossing blood vessel signal intensities. Inferior aspect of bilateral sphenoid greater wing show indistinctive bony cortical margins especially on axial T2 images, however, these could be artifactual. There is no evidence of definitive mass on this MR scan. These findings are non specific. Contrast enhancement MR study may help for further imaging evaluation. There is no evidence of acute ischemic or hemorrhagic lesion.The ventricles, sulci and cisterns are symmetric and unremarkable. There is no mass, mass effect, edema, midline shift, intra or extra-axial fluid collection/hemorrhage, or restricted diffusion/acute ischemia. The midline structures and cranial-cervical junction are normal. Normal flow voids are identified in the major intracranial vessels. The mastoid air cells are clear.Mucosal thickening of the left maxillary sinus, left ethmoid sinus and left middle turbinate concha bullosa.

Output: 1. No definitive mass along bilateral sphenoid greater wing. Contrast enhanced MRI can be considered for further imaging evaluation.2. No evidence of acute ischemic or hemorrhagic lesion.


Instruction: Generate impression based on findings.

Input: For the purposes of numbering, the most inferior well-defined disc space is labeled L5-S1. There is minimal grade 1 retrolisthesis of L5 on S1, and minimal grade 1 anterolisthesis of L4 on L5, as before. The remainder of the spine shows normal alignment. There is loss of T2 signal in all visualized disks with moderate loss of disk height at L4-5 and L5-S1 with vacuum phenomena. There is diffusely heterogeneous marrow signal which is nonspecific. There are type II endplate degenerative changes at L4-5 and L5-S1. There is minimal edema in the right-sided L4 and L5 articulating facets and pedicles which is nonspecific, likely reflecting degenerative process with similar to prior. The conus terminates at L1-2 and shows normal caliber and signal.Individual levels as below:T12-L1: No significant disc disease. No spinal canal or neural foraminal stenosis.L1-2: No significant disc disease. No spinal canal or neural foraminal stenosis.L2-3: No significant disc disease. No spinal canal or neural foraminal stenosis.L3-4: Minimal disk bulge and bilateral facet arthropathy contributing to mild to moderate left and mild right neural foraminal stenosis. No spinal canal stenosis.L4-5: Diffuse disk bulge, bilateral facet arthropathy and ligamentum flavum thickening causing moderate right and mild left neural foraminal stenosis and no significant central spinal stenosis. Disk material encroaches upon the right greater than left subarticular zones without significant central canal stenosis.L5-S1: Diffuse disk bulge asymmetric to the left with a left foraminal protrusion causing up to moderate left and mild right neural foraminal narrowing. There is also an osteophyte component more laterally abutting the left L5 nerve root. There is bilateral facet arthropathy. No significant spinal canal stenosis.

Output: 1. Multilevel degenerative changes in the lumbar spine not significantly changed since 2/28/2015. There is no significant central spinal canal stenosis at any level. There is up to moderate left L5-S1 neural foraminal stenosis where there may be impingement of the left L5 nerve root, similar to prior.2. Facet arthropathy at L3-4, L4-L5, and L5-S1, which may be contributing to patient's low back pain. There is bone marrow edema involving the posterior elements at the right L4-L5 and L5-S1 levels similar to prior.


Instruction: Generate impression based on findings.

Input: Female, 47 years old, with multiple sclerosis presenting with paresthesias. Evaluate for progression. Brain:As on the prior examination, approximately five T2 hyperintense lesions are seen involving the periventricular and juxtacortical regions of the cerebral hemispheres. There has been no significant interval change in the size or morphology of these lesions and no new lesions are detected. Lesions in the left superior frontal gyrus and in the bilateral periatrial regions demonstrate corresponding marked T1 hypointensity, similar to prior.No significant parenchymal edema or mass effect is detected. No abnormal extra-axial fluid collections are identified. The ventricles remain normal in size and morphology.C-spine:Patchy spinal cord T2 hyperintensity is seen at the cervico-medullary junction, at the C3-4 level, at the C6-7 level, at the T1-2 level, and perhaps also at the T3-4 level, partially visualized. The lesion at T1-2 is associated with mild cord volume loss indicating chronicity. No prior cervical spine MRI is available for comparison, but the lesions at T1-T2 and T3-4 appear similar to prior.Mild degenerative reversal of the normal cervical lordosis is seen. Sagittal alignment is otherwise unremarkable. Vertebral body heights and morphology are unremarkable allowing for degenerative endplate collapse at C5 and C6. Corresponding degenerative endplate signal change is also seen. No concerning marrow replacement is detected.C2-3: No spinal canal stenosis or neuroforaminal narrowing. C3-4: Minimal posterior disc-osteophyte complex formation. No significant spinal canal or foraminal stenosis. C4-5: No spinal canal stenosis or neuroforaminal narrowing. C5-6: Loss of disc height. Minimal posterior disc-osteophyte complex formation. No significant spinal canal stenosis. Very mild left foraminal narrowing. C6-7: Minimal posterior disc-osteophyte complex formation. No significant spinal canal stenosis. Mild left foraminal narrowing. C7-T1: No spinal canal stenosis or neuroforaminal narrowing.

Output: 1.Approximately five white matter lesions are demonstrated within the cerebral hemispheres showing no significant interval change. No new lesions are detected.2.Patchy spinal cord signal abnormality is identified in the cervical region and in the visualized upper thoracic region. No prior cervical spine MR images are available for adequate comparison, but the upper thoracic cord lesions appear similar to prior.


Instruction: Generate impression based on findings.

Input: 58 years Male (DOB:12/8/1957)Reason: 58 yo M with metastatic SCC of H\T\N to brain s/p whole brain RT, eval for progression/response History: nonePROVIDER/ATTENDING NAME: STEVEN J CHMURA STEVEN J CHMURA There is redemonstration of multiple enhancing lesions within the brain parenchyma which have decreased in size since the prior exam. One located in the left frontal lobe currently measures 17 x 12 mm and previously measured 30 x 27. One located in the left middle frontal gyrus currently measures 8 x 7 mm axial dimensions and previously measured 22 x 16 mm axial dimensions. One in the left cuneus previously measured 13 x 16 mm and currently measures 9 x 11 mm axial dimensions. One in the right temporal lobe previously measured 23 x 16 mm and currently measures 15 x 10 mm axial dimensions. There are numerous other lesions are simple also decreased in size compared to the prior exam.There is redemonstration of a encephalomalacia in the right frontal lobeNormal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells demonstrate some opacities in the right mastoid air cells probably related to retained secretions which were not present on the prior exam.. The visualized portions of the orbits are intact.

Output: 1.Since prior examination lesions within the brain parenchyma compatible with metastatic disease have decreased in size but have not disappeared.2.There is encephalomalacia redemonstrated in the right frontal lobe.3.Retained secretions in the right mastoid air cells is nonspecific finding. Please correlate with clinical history and symptoms.


Instruction: Generate impression based on findings.

Input: History of cholecystectomy and vertical banding gastroplasty with postprandial epigastric pain. Endoscopic ultrasound findings suggestive of benign ampullary stenosis. ABDOMEN:LIVER, BILIARY TRACT: The liver is normal in morphology, signal intensity, size and enhancement. There is significant extrahepatic and moderate intrahepatic diffuse biliary ductal dilatation to the level just proximal to the ampulla. The common bile duct measures up to 13 mm (series 10/26). No focal liver lesion. The vessels are patent.Status post cholecystectomy.SPLEEN: The spleen is normal in morphology and size.PANCREAS: The pancreas is normal in morphology and enhancement. There are several punctate pancreatic tail subcentimeter cystic foci which appear to communicate with the main pancreatic duct likely representing side branch type IPMNs. The main pancreatic duct is dilated up to 7 mm to the level just proximal to the ampulla where both the main pancreatic duct and common bile duct taper abruptly with mild shouldering (series 5 image 75). Postcontrast images demonstrate very subtle irregularly marginated enhancing focus at the ductal transition point (series 14 image 156 through 161). There is no significant distal pancreatic parenchymal atrophy. Following secretin administration there is no significant caliber change in the main pancreatic duct.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Right minimally complex septated cyst. No hydroureteronephrosis or suspicious lesion. Punctate left renal probable simple cysts.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: Post-surgical changes from vertical banding gastroplasty. BONES, SOFT TISSUES: L1 hemangioma.OTHER: No significant abnormality noted.

Output: Biliary and main pancreatic ductal dilatation to the level just proximal to the ampulla where there is a subtle subcentimeter irregularly marginated focus of enhancement, suspicious for an underlying obstructive lesion. Correlation with repeat ERCP/EUS is advised.


Instruction: Generate impression based on findings.

Input: Knee pain MENISCI: There is a bucket-handle type tear of the medial meniscus with displacement of the medial fragment beneath the PCL. There is additional horizontal tearing of the body of the meniscus with extension to the tibial articular surface.The lateral meniscus is intact.ARTICULAR CARTILAGE AND BONE: There is partial-thickness degeneration of the articular cartilage of the both the medial and lateral facets of the patella and more focal degeneration of articular cartilage along the medial facet of the trochlea inferiorly. The articular cartilage of the medial and lateral compartments is preserved.LIGAMENTS: The ACL appears unusually thinned. Although there are no bony contusions or other secondary findings to suggest an acute injury, these findings could represent a remote single bundle tear. The remaining ligaments are intact.EXTENSOR MECHANISM: No significant abnormality noted.ADDITIONAL

Output: Bucket-handle type tear of the medial meniscus with other findings described above.


Instruction: Generate impression based on findings.

Input: Female, 35 years old, with headache and hydrocephalus. A midline cystic lesion is evident centered on the midbrain and measuring up to 29 mm AP, 19 mm CC, and 17 mm TV. Inferiorly, the lesion contains multiple septations or cystic loculations, and this portion of the lesion appears to be intraparenchymal within the midbrain tegmentum. Superiorly, the dominant portion of the cyst projects into the posterior aspect of the third ventricle, elevating and stretching the midbrain tectum, and likely obstructing outflow through the cerebral aqueduct. No clear evidence of any solid or enhancing tissue is seen within the lesion.The lateral and third ventricles are enlarged with evidence of mild transependymal CSF flow. The fourth ventricle is within normal limits. Incidental note is made of descent of the cerebellar tonsils approximately 10 mm below the level of the foramen magnum.

Output: A cystic lesion is evident centered on the midbrain which projects into the third ventricle and likely effaces the cerebral aqueduct. Consequently, hydrocephalus involving the lateral and third ventricles is seen. The lesion appears to be at least partly intraparenchymal within the midbrain tegmentum, and this portion of the lesion demonstrates multiple septations or loculations. The differential diagnosis would include a neuroglial cyst, with arachnoid cyst a somewhat less likely consideration given location and imaging features. A cystic neoplasm is felt to be unlikely due to lack of solid or enhancing tissue.Inferior herniation of the cerebellar tonsils is seen which technically meets criteria for a Chiari I malformation. However, this finding should be assessed after correction of hydrocephalus as the appearance may change.


Instruction: Generate impression based on findings.

Input: Unprovoked seizure. The images are markedly degraded by patient motion. There is gyriform T1 hyperintensity and encephalomalacia along the margins of the left parieto-occipital sulcus. There are also small areas of surrounding high signal on DWI with what may correspond to mildly low ADC values, although these areas are too small to accurately characterize. The previously demonstrated scattered punctate foci of cortical, subcortical, corpus callosal, bilateral basal ganglia, and left cerebellar restricted diffusion have evolved into chronic infarcts. There is also patchy cerebral white matter T2 hyperintensity in the bilateral cerebral hemispheres and pons. The hippocampi appear to be grossly unremarkable. There is no evidence of intracranial hemorrhage or mass. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. There is a left lamina papyracea defect with herniation of orbital fat. There is a small left maxillary sinus retention cyst.

Output: 1. No evidence of acute intracranial hemorrhage or mass, although the images are markedly degraded by patient motion.2. Prior infarction along the margins of the left parieto-occipital sulcus with evidence of cortical laminar necrosis. 3. Small areas of surrounding high signal on DWI may represent superimposed recent infarction. Likewise, the previously demonstrated scattered punctate foci of cortical, subcortical, corpus callosal, bilateral basal ganglia, and left cerebellar restricted diffusion have evolved into chronic infarcts.4. Patchy areas of cerebral white matter T2 hyperintensity in the bilateral cerebral hemispheres and pons are nonspecific, but may represent chronic small vessel ischemic disease.


Instruction: Generate impression based on findings.

Input: Radiculopathy, cervical region [M54.12], Reason for Study: ^Reason: left C7 radiculopathy on EMG History: pain and weakness There is normal cervical lordosis. The cranial-cervical junction is normal. The spine alignment is anatomic. The vertebral body height is preserved. The bone marrow and end plates demonstrate a normal MR appearance. The cord signal is normal. The paraspinal soft tissues and musculature are unremarkable.Degenerative changes are specified by the intervertebral level as follows: C2-C3: no neuroforaminal narrowing or spinal stenosis. C3-C4: no neuroforaminal narrowing or spinal stenosis. C4-C5: no neuroforaminal narrowing or spinal stenosis. C5-C6: There is a broad-based central to left disc protrusion, however, no blood compression or spinal canal stenosis is not evident. C6-C7: Broad-based disc bulging associated with the focal disc protrusion towards left side lateral recess which abuts thecal sac and narrows left lateral recess stenosis (series 1001, image 11/11, series 701, image 20/48). Mild disc desiccation.C7-T1: Minimal bulging of disc central to right no evidence of spinal canal or neuroforaminal stenosis..

Output: 1. Left lateral recess stenosis due to disc protrusion at the level of C6-7 as described above.2. Disc bulging at the level of C5-6 and C7-T1 as described above.


Instruction: Generate impression based on findings.

Input: The risks (including, but not limited to, those of bleeding, infection, allergic reaction, temporary nerve block, pain, and inability to access the joint) and benefits of the procedure were explained to the patient, and informed written consent was obtained. A pre-procedural “time-out” form was completed.The patient was placed supine on the fluoroscopy table. The right hip was localized fluoroscopically, and a spot radiograph was obtained. The course of the femoral artery was noted on the patient's skin using an ink marker. The skin was cleansed and covered with a sterile drape. The skin and subcutaneous tissues were anesthetized with 1% lidocaine using 25-gauge and 22-gauge needles.Under fluoroscopic guidance, a 20-gauge spinal needle was advanced into the joint. Attempted aspiration yielded no fluid. Next, 2 ml of a 50/50 mixture of Omnipaque 240 (to confirm the intra-articular position of the needle) and dilute Multihance (0.1 cc in a 10 cc vial of saline, for subsequent MR imaging) were injected into the joint. Contrast opacified the joint in the expected manner. A spot radiograph was obtained for documentation. The needle was withdrawn. Blood loss was negligible (<1cc), and patient tolerated the procedure well without immediate complication. An adhesive bandage was placed on the patient’s skin. Routine post procedure instructions were communicated to the patient. The patient was escorted to the MRI suite for further imaging in stable condition. Please refer to the subsequent MRI report for further information.Exposure time: 21 secondsEntrance dose: 7.20 mGy

Output: Successful steroid injection of the right hip under fluoroscopic guidance.


Instruction: Generate impression based on findings.

Input: Evaluate for recurrence of meningioma. Patient had two seizures today. There is no evidence of intracranial hemorrhage. A hyperdense region is identified along the superior falx. Adjacent to an area of encephalomalacia in the left frontal lobe is a density along the inner table of the left skull that likely represents cerebral cortex. However, an MRI is needed for further evaluation of these areas.White matter hypodensity in the right frontal lobe is more prominent than on the prior study. Correlate with any history of radiation therapy.The ventricles and basal cisterns are normal in size and configuration.Postsurgical findings of a craniotomy are noted. The visualized paranasal sinuses and mastoid air cells are normally pneumatized.

Output: Hyperdense region is identified along the superior falx. Further evaluation with MRI is recommended. White matter hypodensity in the right frontal lobe is more prominent than on the prior study.


Instruction: Generate impression based on findings.

Input: Cognitive impairment: Memory decline. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There are mild scattered foci of cerebral white matter T2 hyperintensity, which may represent chronic small vessel ischemic disease. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull is grossly unremarkable. There are bilateral lens implants. There is mild mucosal thickening in the maxillary sinuses.

Output: No evidence of acute intracranial hemorrhage, mass, or acute infarct.


Instruction: Generate impression based on findings.

Input: 49 year-old female with low back pain. Additional history per chart, prior L3-L4 discectomy. 5 lumbar type vertebral bodies are presumed. Vertebral body heights are maintained. There is minimal retrolisthesis of L5 on S1 as well as straightening of the lumbar curvature similar to prior. Again seen is fatty infiltration involving the filum terminale with more focal lipoma along the filum measuring 4 mm at the L2 level, inferior to the conus which terminates normally at the L1-L2 level.Slightly prominent epidural fat in the distal sacral spinal canal is felt to represent an anatomic variant. Marrow signal is benign. Multilevel degenerative changes as described below:L1-L2: No significant disc disease. No spinal canal or neural foraminal stenosis.L2-L3: Previously seen left paracentral disc extrusion has resolved. There remains a mild disc bulge without significant spinal canal or neural foraminal stenosis.L3-L4: Asymmetric disk bulge to the right with loss of disk height. There is mild bilateral, right greater than left, neural foraminal stenosis and also contact of the right extraforaminal L3 nerve root. This finding is stable to minimally worse since 7/15/2013. Again seen is atrophy of the right paraspinous musculature likely reflective of prior surgery for discectomy. No significant central spinal canal stenosis.L4-L5: Disc bulge with an eccentric portion involving the left extraforaminal segment and mild bilateral facet arthropathy. Disc height loss appears minimally worse. Mild to moderate left and mild right neural foraminal stenosis, minimally worse in the interval. No significant central spinal canal stenosis.L5-S1: Disc bulge and mild bilateral facet arthropathy. There is partial effacement of the lateral recesses without significant central spinal canal stenosis. There is mild to moderate right and mild left neural foraminal stenosis stable to minimally worse (on the right) since prior. There is contact and mild lateral displacement of the extraforaminal right L5 nerve root. Conjoined right S1 and S2 nerve roots incidentally noted.

Output: 1. Mild to moderate multilevel degenerative changes in the lumbar spine have overall minimally changed from MRI from 7/15/2013. No significant central spinal canal stenosis at any level. Please see additional details above. 2. Lipomatous infiltration of the filum terminale again seen, measuring up to 4 mm in thickness at L2. Conus is in normal position at the L1-L2 level but would suggest correlation with clinical signs of cord tethering.


Instruction: Generate impression based on findings.

Input: Left sided weakness. There is a defect in the right thalamus that measures up to 12 mm. Otherwise, there no evidence of intracranial hemorrhage, mass, or acute infarct. There is diffuse mild cerebral volume loss. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: Chronic right thalamus lacunar infarct. Otherwise, no evidence of acute infarct, intracranial hemorrhage, or mass.


Instruction: Generate impression based on findings.

Input: Neurofibromatosis type II. Sensory changes in the right hand and decreased thenar eminence. Decreased hearing and more balance problems. BRAIN MRI:Numerous intracranial meningiomas are present, compatible with the known diagnosis of neurofibromatosis type II. Few have increased in size, while most of the lesions remain unchanged. The largest of these is a right-sided anterior falcine meningioma which measures axially 2.3 cm x 2.1 cm compared to 1.8 cm x 1.6 cm. A convexity meningioma overlying the left sylvian fissure remain unchanged and measures in the axial plane 2.2 cm x 1.2 cm compared to 2.2 cm x 1.1 cm previously. A meningioma at the level of foramen Magendie has very minimally increased in size, if any. In the sagittal plane, it measures 1.3 cm x 0.6 cm compared to 1.0 cm x 0.6 cm. A right occipital parasagittal meningioma that previously measured 1.7 cm now measures 1.8 cm. It does mildly compress the adjacent posterior part of the superior sagittal sinus though it remains patent. Multiple other similar parasagittal meningiomas are also present and do mildly compress the superior sagittal sinus without occluding it. An apparent filling defect in the lateral aspect of the right transverse sinus is unchanged and likely represents incidental arachnoid granulation. Apart from mild mass-effect by the meningiomas, the brain parenchyma is unremarkable. There is no acute infarct or intracranial hemorrhage. There is no ventricular dilatation. There is no midline shift or brain herniation. There is an unchanged, small mass involving the right orbital apex, which probably represents an optic sheath meningioma. .INTERNAL AUDITORY CANAL MRI:Lobulated contrast enhancing masses expanding the internal auditory canals remain not significantly changed since the previous examination, including the previous MRI of the IAC from October 2012. The involvement is much more extensive on the right. Involvement of the genu of the facial nerve is also not significantly changed, more pronounced on the right.CERVICAL SPINE MRI:Multiple contrast enhancing lesions within the cervical spinal cord have progressed since November 2013. The lesion at C3 level shows the most significant size progression and now measures up to 1.5 cm, compared to 0.8 cm. The adjacent lesion at C4 level, which was previously the largest and shows cystic change, has not significantly changed in size and still measures up to 1.2 cm but most of the other smaller lesions have increased in size. For example, the one at C6 level measures 8 mm compared to 5 mm previously. The associated cord expansion and central T2-hyperintensity has also progressed and now extends from C1-C2 level to the C5-C6 level. The small left posterolateral extramedullary lesion at the level of C2 has not changed. A small extramedullary mass at the left dorsal C6 levels also unchanged. There is sagittal straightening. Shallow ventral indentation of the thecal sac by the C6-C7 disc-osteophyte complexes is not significantly changed. The spinal canal is otherwise preserved.

Output: 1.Numerous intracranial meningiomas. Few have increased in size but most of them remain unchanged as described above. The parasagittal meningiomas mildly narrow the superior sagittal sinus, but it remains patent. 2.Mild progression of the multiple cervical spine intramedullary masses, most likely ependymomas.3.Unchanged cervical extramedullary intraspinal masses at C2 and C6 levels, which may represent schwannomas. I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Female, 77 years old, with history of parotid cancer status post induction chemotherapy. Please note that comparison will be made largely with reference to the prior CTA dated 3/18/2015 as the field of view of the prior MRI is not adequate for accurate comparison.An extensive infiltrative tumor is redemonstrated, centered on and involving nearly the entirety of the right parotid and masticator spaces. Tumor infiltrates the hemimandible from the level of the condyle as far anteriorly as the mentum. Tumor extends laterally almost to the skin surface, and medially to the level of the parapharyngeal and pharyngeal spaces. Superiorly, tumor appears to infiltrate into the temporalis muscle.Tumor infiltrates into the pterygopalatine fossa, the sphenoid sinuses, the clivus and the sella. Meckel's cave and the right cavernous sinus are nearly completely infiltrated as well. The right ICA flow void is moderately narrowed as a result. Tumor encroaches upon the right prepontine cistern and tracks along the petrous bone to very nearly enter the right IAC.Tumor erodes through the bony floor of the right middle cranial fossa and invades and thickens the dura in this area. Tumor tracks along the anterior clinoid process and may slightly encroach upon the right orbital apex. The right mastoid air cells demonstrate fluid signal intensity likely indicating outflow obstruction.On comparison to the prior exam, it does appear that the lesion is overall larger and more widely infiltrative throughout. As a very rough estimate, the maximal dimension of this lesion at the level of the masticator space is at least 77 mm, and on the prior CT the same dimension is probably no more than 60 mm.Intracranially, despite the extensive tumor erosion into the right middle cranial fossa and infiltration/thickening of the regional dura, no definite evidence of parenchymal edema or pathologic parenchymal enhancement is seen to suggest frank brain invasion.No restricted diffusion is seen within the brain. A few scattered small foci of nonspecific T2 hyperintensity are evident within the cerebral hemispheres. No significant mass effect is detected. No evidence of significant intracranial hemorrhage or any abnormal extra-axial collection is seen. The ventricles are normal in size and morphology. Loss of the T2 flow void of the right transverse and sigmoid sinus is seen, likely indicating slow flow as the sinus does appear to enhance normally on postcontrast images.

Output: A diffusely infiltrative tumor is redemonstrated centered upon the right parotid and masticator spaces. As on the prior exam, this lesion extensively invades the regional structures and spaces including the pterygopalatine fossa, sphenoid bone, clivus and sella, Meckel's cave and cavernous sinus, extending even into the prepontine cistern. Tumor also extensively invades through the floor of the right middle cranial fossa with infiltration and thickening of the regional dura. Accurate comparison is complicated by lack of prior MRI with an adequate field of view, but despite this, it does appear that the lesion has become at least moderately more extensive than previously.Although there is extensive intracranial invasion as above, no definite evidence of brain parenchymal involvement is seen.


Instruction: Generate impression based on findings.

Input: Reason: assess for medial meniscal tear s/p twisting injury History: pain and swelling MENISCI: There is deformity of the posterior horn of the medial meniscus which may represent degeneration and superficial fraying. There is no fluid-filled unstable tear identified. The lateral meniscus appears intact.ARTICULAR CARTILAGE AND BONE: There is a full-thickness articular cartilage defect along the weightbearing surface of the medial femoral condyle above the body of the meniscus. There is also full-thickness articular cartilage degeneration along the weightbearing surface of the medial femoral condyle above the posterior horn of the meniscus. The lateral tibiofemoral articular cartilage appears relatively spared. There is a full-thickness articular cartilage cleft along the lateral facet of the femoral trochlea, centrally. There is subjective thinning of the patellofemoral articular cartilage.LIGAMENTS: The cruciate and collateral ligaments appear intact. EXTENSOR MECHANISM: The extensor mechanism appears intact.ADDITIONAL

Output: 1. Full-thickness articular cartilage degeneration and defects most pronounced along the medial tibiofemoral compartment.2. Deformity of the posterior horn of the medial meniscus likely represents a combination of degeneration and superficial fraying. No fluid-filled unstable tear is identified.3. Moderate size joint effusion. Other findings as described.


Instruction: Generate impression based on findings.

Input: Reason: acl tear? Meniscal pathology? History: pain after popping injury on 4/14 MENISCI: There is globular signal without a discrete linear component seen in the posterior horn of the lateral meniscus, consistent with intrasubstance degeneration. The medial meniscus is intact.ARTICULAR CARTILAGE AND BONE: There is patchy red marrow signal within the distal femur and proximal tibia, which appears appropriate for the patient's age. There is a partial-thickness tear of the articular cartilage at the apex of the patella. There is thinning and heterogeneous signal within the articular cartilage of the medial femoral condyle with underlying bone changes. More pronounced thinning is seen along the anterior aspect of the lateral femoral condyle. Multiple well-defined cystic areas are seen within the lateral femoral condyle and proximal tibia, which likely represent subchondral cysts. Edema-type signal is seen within the lateral tibial plateau, consistent with a bone contusion.LIGAMENTS: There is complete disruption of the ACL with retraction. Thickening of the MCL with surrounding fluid signal is consistent with a sprain. Otherwise, the remaining ligaments are intact.EXTENSOR MECHANISM: No significant abnormality noted.ADDITIONAL

Output: 1. Complete tear of the ACL with moderate joint effusion and bone contusion.2. MCL sprain. 3. Moderate to near severe osteoarthritis of the knee.


Instruction: Generate impression based on findings.

Input: 21-year-old female with a history of lupus and knee avascular necrosis. Fell down stairs on 9/15/2015 now with pain, swelling and limited mobility. MENISCI: Note is made of a discoid lateral meniscus. No definite increased signal abnormality is identified within the meniscus to suggest a tear. The medial meniscus appears intact.ARTICULAR CARTILAGE AND BONE: There is deformity of the weightbearing surface of the lateral femoral condyle. There are multiple ossicles identified along the lateral aspect and weight bearing surface of the lateral femoral condyle likely representing osteochondral defect/loose bodies within the joint space. The largest measures 2.3 cm in the AP dimension (image 7; series 8). There are multiple additional fragments along the weightbearing surface of the medial aspect of the lateral femoral condyle which also likely represent osteochondral fragments which are surrounded by fluid signal intensity measuring up to 15 mm in AP dimension (image 11; series 9). There is increased signal abnormality within the lateral femoral condyle and posterior aspect of the lateral tibial plateau.There is partial-thickness articular cartilage degeneration along the medial facet of the femoral trochlea. There is subjective thickening of the articular cartilage along the medial facet of the patella. The articular cartilage along the medial tibiofemoral compartment appears relatively spared.LIGAMENTS: The cruciate and collateral ligaments appear intact. EXTENSOR MECHANISM: The extensor mechanism appears intact.ADDITIONAL

Output: 1. Multiple osteochondral fragments/loose bodies along the lateral aspect and weightbearing surface of the lateral femoral condyle as described above. There is also deformity of the weightbearing surface of the lateral femoral condyle which presumably represents the sequela of the patient's stated history of avascular necrosis.2. Discoid lateral meniscus without convincing evidence of a meniscal tear.


Instruction: Generate impression based on findings.

Input: Headaches, CNS white matter lesions, cortical atrophy No diffusion restriction is seen to suggest acute ischemia. No susceptibility weighted artifact is seen to suggest intracranial hemorrhage. Periventricular and subcortical foci of T2/FLAIR hyperintensity are nonspecific and unchanged. No mass lesion is seen within the brain parenchyma. The CSF spaces are appropriate for the patient's stated age with no midline shift. Normal vascular flow voids are present in the major intracranial vasculature.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.

Output: No change in nonspecific white matter signal abnormality.


Instruction: Generate impression based on findings.

Input: Female, 52 years old, with pain, history of Chiari decompression. Suboccipital craniectomy and resection of the posterior arch of C1 are again seen. The CSF spaces at the foramen magnum are well expanded. The cerebellar tonsils demonstrate a normal round morphology. On CSF flow imaging, biphasic flow is demonstrated both dorsally and ventrally through the surgically widened foramen magnum.Spinal alignment is anatomic. Vertebral body height and morphology are within normal limits. No evidence of edema or marrow replacement is seen. The visualized spinal cord shows normal signal characteristics throughout. There is no evidence of any spinal cord syrinx or other focal signal abnormality. No epidural lesions are suspected.C2-3: No spinal canal stenosis or neuroforaminal narrowing. C3-4: No spinal canal stenosis or neuroforaminal narrowing. C4-5: No spinal canal stenosis or neuroforaminal narrowing. C5-6: Minimal posterior disc-osteophyte complex formation. Minimal ligamentum flavum thickening. No significant spinal canal or foraminal stenosis. No interval changes. C6-7: Posterior disc-osteophyte complex formation and ligamentum flavum thickening. Mild generalized spinal canal stenosis. Moderate left and mild right foraminal narrowing due to projecting disc osteophyte. C7-T1: No spinal canal stenosis or neuroforaminal narrowing.

Output: 1.Redemonstrated findings compatible with prior Chiari decompression. The neo-foramen magnum appears to be well expanded with adequate space and flow both dorsally and ventrally.2.Degenerative findings are again seen in the cervical spine, most notably affecting C5-6 and C6-7. These have not significantly changed.


Instruction: Generate impression based on findings.

Input: Female, 13 years old, lower back pain and leg pain, follow-up pseudomeningocele. The vertebral body naming scheme will remain unchanged relative to prior examinations. As such, the last rib bearing vertebral body will be considered T12. There are 5 lumbar type vertebral bodies with a transitional S1, and a rudimentary disk between S1 and S2.Postoperative findings are again seen compatible with tethered cord repair. The laminae and spinous processes are absent from L3 through the sacrum region.The spinal cord continues to terminate at an abnormally low level, continuing at least to the L4-5 level with placode potentially extending much further inferiorly. The distal cord remains deformed and closely opposed to the posterior right aspect of the thecal sac. The quantity and morphology of fatty material seen along the inferior dorsal thecal sac is similar to the prior examination.The lower thecal sac remains ectatic, perhaps slightly more so than on the prior examination.Spanning the L4 through S1 levels, there remains a fluid collection with CSF signal characteristics immediately dorsal to the deformed distal spinal cord. On sagittal images, this collection measures 65 x 15 mm (image 6 of series 201), previously 69 x 21 mm. A second collection is also seen just above and superficial to the first measuring up to 45 x 15 mm on sagittal images (image 7 series 201), previously only a thin sliver of fluid. These two collections are separated by a thin membrane which may represent dura or duraplasty material, less likely an adhesion (see image 27 series 501).A large subcutaneous collection seen previously overlying the paraspinal musculature has resolved.Multicystic ovaries are partially visualized.

Output: 1. Redemonstration of findings compatible with tethered cord and tethered cord repair.2. Interval resolution of the previously seen large superficial subcutaneous fluid collection overlying the paraspinal musculature.3. Slight decrease in size of a CSF-like fluid collection immediately dorsal to the distal spinal canal, with interval increase in size of a second collection superficial to and above the first. These two collections are separated by a thin membrane which may represent dura, duraplasty or less likely an adhesion.


Instruction: Generate impression based on findings.

Input: Family history of pancreatic cancer presents with nausea and vomiting. ABDOMEN:LIVER, BILIARY TRACT: The liver is normal morphology, size, signal intensity and enhancement. Right hepatic dome simple cyst. No intra or extrahepatic biliary ductal dilatation. The patient is status post cholecystectomy.SPLEEN: Normal splenic size without a focal lesion.PANCREAS: Normal main pancreatic duct without a focal lesion. The pancreas is normal in intrinsic T1-weighted signal intensity and demonstrates homogeneous enhancement. No peripancreatic inflammatory changes.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: Small non-specific peri-esophageal lymph node, likely reactive.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: Normal MRCP without a pancreatic lesion or other findings to account for the patient's nausea and vomiting.


Instruction: Generate impression based on findings.

Input: 31-year-old male with a history of metastatic testicular cancer status post SRS. There is a new T1 hyperintense lesion in the right frontal lobe with susceptibility effect peripherally, measuring at least up to 13 mm. There are also new subcentimeter lesions with susceptibility effect in the left precentral gyrus, right occipital lobe, and right superior parietal lobe. There is redemonstration of two enhancing masses within the left frontal lobe. The left postcentral gyrus mass measures approximately up to 25 mm, which has slightly increased in size. However, the associated vasogenic edema has markedly improved. Likewise, there has been slight interval increase in size of the subcentimeter lesion with susceptibility effect within the left frontal lobe centrum semiovale, now with prominent central T1 hyperintensity, but decreased surrounding edema. There is T1 shortening and susceptibility within the metastatic lesions indicating intratumoral hemorrhage/hemosiderin. There is no evidence of acute infarct. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: 1. New hemorrhagic metastatic lesions in the left precentral gyrus, right frontal lobe, right occipital lobe, and right superior parietal lobe. 2. The treated left postcentral gyrus and left frontal centrum semiovale lesions are slightly larger, perhaps due to interval hemorrhage, but the associated vasogenic edema has diminished.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Brain MRI appears within normal limits for age. There is no diffusion abnormality to suggest infarct. No significant parenchymal signal abnormality. No evidence of hemorrhage. No intracranial mass or mass effect. The ventricles and sulci are within normal limits for age. Normal flow-voids are demonstrated in the major intracranial vascular structures. The midline structures and craniocervical junction are within normal limits. High-resolution 3-D T2 images of the internal auditory canals also demonstrates no mass at the cerebellopontine angles or internal auditory canals. Sella and orbits are grossly unremarkable. Paranasal sinuses and mastoid air cells are clear. Calvarium and extracranial soft tissues are also grossly unremarkable.MRA NECK

Output: 1. Brain MRI appears within normal limits. Specifically, no evidence of infarct or intracranial mass.2. No significant stenosis in the major arterial vasculature in the neck.


Instruction: Generate impression based on findings.

Input: Reason: 74F with non-healing worsening ulcer over her lateral right ankle. Concern for osteo History: worsening pain and size of ulcer 2 skin markers overlie the lateral aspect of the ankle. Note is made of soft tissue irregularity along the lateral aspect of the distal tibia consistent with patient's known history of ulceration. There is subcutaneous edema in the underlying area likely representing cellulitis. There is interval development of periosteal reaction along the lateral aspect of the distal fibula as well as interval increase in bone marrow signal abnormality in the underlying fibula with associated decreased signal abnormality on T1-weighted images. While some of this new bone marrow signal abnormality may reflect reactive bone marrow edema, the presence of periosteal reaction and decreased T1 signal abnormality indicates osteomyelitis. There is heterogeneous bone marrow signal abnormality likely representing residual islands of red marrow. There is increased signal abnormality within the anterior calcaneus about the calcaneocuboid articulation likely representing degenerative changes. The peroneal tendons appear intact. The anterior tendons appear intact. There is a small amount of circumferential fluid within the tendon sheaths of the posterior tibialis, flexor digitorum longus and flexor hallucis longus which may represent a very mild tenosynovitis. There is nonspecific increased signal abnormality within the plantar musculature of the foot which can be seen in diabetic patients.

Output: Interval development of increasing bone marrow signal abnormality and periosteal reaction within the distal fibula suspicious for osteomyelitis. Other findings as described above.


Instruction: Generate impression based on findings.

Input: 60-year-old man with history of known IPMN. ABDOMEN:LIVER, BILIARY TRACT: The liver is cirrhotic in morphology with overall decreased signal. No focal hepatic lesion identified.SPLEEN: No significant abnormality noted.PANCREAS: There is a 59 x 40 mm well-defined T2 hyperintense lesion within the head of the pancreas, not clearly communicating with the pancreatic duct. The common bile duct is displaced by this cystic lesion and the pancreatic duct is nondilated. This lesion contains 2 small septations, but there is no enhancement. ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: Subsegmental atelectasis noted in the left lung base.

Output: Cystic lesion in the head of the pancreas increasing in size over multiple exams, most likely a macrocystic serous cystadenoma or IPMN (although communication with the pancreatic duct is not seen).


Instruction: Generate impression based on findings.

Input: Reason: blinotumomab toxicity? CNS involvement of ALL? History: expressive dysphasia, ALL The CSF spaces are appropriate for the patient's stated age with no midline shift. There is a mild degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images.No abnormal enhancing mass lesions are appreciated intracranially. No intracranial hemorrhage is identified. No edema is identified within the brain parenchyma.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.Exam is somewhat compromised by patient motion.

Output: 1.Periventricular and subcortical white matter changes of a mild degree are nonspecific. At this age they are most likely vascular related. This is stable compared to the November exam.2.Exam is somewhat compromised by patient motion which may obscure more subtle abnormalities.


Instruction: Generate impression based on findings.

Input: 57 year old female. Sacroiliac pain. No edema or pathologic enhancement of the sacroiliac joints. No sacral fracture is evident. Bone marrow signal intensity is within normal limits. The visualized musculature of the pelvis is unremarkable.

Output: No evidence of sacroiliitis or sacral fracture.


Instruction: Generate impression based on findings.

Input: Female 36 years old with P53 syndrome and a history of bilateral breast cancer. Evaluate for pancreatic mass. ABDOMEN:LIVER, BILIARY TRACT: The liver has a smooth contour. Some loss of signal is seen on out of phase imaging suggesting mild fatty infiltration. There are no suspicious hepatic lesions. The hepatic and portal veins are patent. No intra or extrahepatic biliary ductal dilatation.SPLEEN: No significant abnormality noted. There are two splenules.PANCREAS: Normal caliber pancreatic duct. The pancreas enhances homogeneously and is without suspicious lesion.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: There is susceptibility artifact from surgical clips in the right axilla. Bone marrow signal intensity is within normal limits.OTHER: A small amount of pleural fluid is seen bilaterally.

Output: No measurable pancreatic mass.


Instruction: Generate impression based on findings.

Input: Brain MRI:There are a few scattered foci of T2 hyperintensity within periventricular and subcortical white matter. Two lesions within periventricular white matter also demonstrate central T1 hypointensity, and there is no associated susceptibility abnormality or mass effect. There are no similar appearing foci within posterior fossa structures.The ventricles and sulci are normal in size. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. The pituitary gland is normal in size. There is no evidence for intracranial hemorrhage or acute cerebral, brainstem or cerebellar infarction. No diffusion-weighted abnormalities are identified. There are no extraaxial fluid collections or subdural hematomas. The paranasal sinuses and mastoid air cells are clear. Brain MRA: There is antegrade flow within the distal bilateral vertebral arteries, within the basilar artery, distal bilateral internal carotid arteries and carotid siphons and bilateral anterior, middle and posterior cerebral arteries. Incidental note is made of persistent left fetal PCA circulation as well as a right ophthalmic origin infundibulum. No arterial stenoses, occlusions or aneurysms are identified. No arteriovenous malformations are identified and there is no evidence for cerebral vasculitis. Neck MRA:There is conventional takeoff of the great vessels from the aortic arch without evidence for stenosis of the origin of the great vessels or of the bilateral vertebral arteries which are codominant. There are no stenoses of the bilateral common, internal or external carotid arteries or of the bilateral carotid bifurcations. There is no evidence for vasculitis, fibromuscular dysplasia or dissection of the carotid or vertebral arterial systems within the neck. There are no vascular masses identified.

Output: 1.There are a few scattered foci of T2 hyperintensity within periventricular and subcortical white matter. Two lesions within periventricular white matter also demonstrate central T1 hypointensity, and there is no associated susceptibility abnormality or mass effect. There are no similar appearing foci within posterior fossa structures. These are nonspecific in appearance, and the differential diagnosis would most likely include chronic small vessel ischemic disease, although given lesional appearance and patient age, demyelination is also a consideration.2.Negative MRA of the brain.3.Negative MRA of the neck.


Instruction: Generate impression based on findings.

Input: Renal cell carcinoma status post right partial nephrectomy. ABDOMEN:LIVER, BILIARY TRACT: No significant abnormality noted.SPLEEN: No significant abnormality noted.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Postsurgical changes from right partial nephrectomy. There is surrounding fat necrosis and fascial thickening. There is no evidence of local recurrence. No regional lymphadenopathy.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: No evidence of locoregional recurrence or metastatic disease in the upper abdomen.


Instruction: Generate impression based on findings.

Input: headache, altered mental status, known cerebellar ICH, IVH and SAH evaluation. There is 40mm x 20mm x 20mm sized cerebellar ICH (subacute) located on the vermis and right side hemisphere. The hemorrhages are extended toward 4th ventricle and perimesencephalic cistern.However, there is no other hemorrhagic lesion identified. There is no acute ischemic lesion either.There are patchy scattered high signal intensities on FLAIR images on bilateral centrum semiovale indicating non specific small vessel ischemic disease. Left eyeball is artificial one with air-fluid level.Ventriculostomy tube has been inserted via right frontal burr hole and the tip is located at the right side foramen of Monroe.There is no abnormal enhancement.The ventricles, sulci and cisterns are symmetric and unremarkable. The paranasal sinuses and mastoid air cells are clear.

Output: 1. Vermian and right cerebellar hemispheric ICH, IVH and SAH with surrounding edema as described above.2. Non specific small vessel ischemic disease.3. Ventriculostomy tube inserted via right frontal horn and the tip located at the right side foramen of Monroe.4. No abnormal enhancement seen.5. No acute ischemic lesion.


Instruction: Generate impression based on findings.

Input: 30-year-old male patient with instability and concern for ACL tear. MENISCI: Posterior horn of the medial meniscus is diminutive in size, which may be due to prior meniscectomy, and contains abnormal increased intrasubstance signal intensity. There is a complex undersurface tear of the posterior horn of the lateral meniscus as well as capsular separation at the periphery. There is increased intrasubstance signal intensity within the anterior horn of the lateral meniscus, compatible with degeneration.ARTICULAR CARTILAGE AND BONE: There is subjective mild thinning of the articular cartilage of the medial patellar facet. There are no fluid-filled cartilage defects in the patellofemoral compartment. There is mild thinning of the weightbearing portions of the medial and lateral compartments without focal fluid-filled cartilage defects. Abnormal signal intensity within the lateral condyle may be secondary to patient's prior arthroscopy. Medial and lateral compartment osteophyte formation is noted.There are at least three screws in the proximal tibial metaphysis, one screw and multiple staples in the distal metaphysis of the femur, and one screw in the proximal lateral fibula.LIGAMENTS: The anterior cruciate ligament graft is thinned, compatible with at least partial tearing. There is mild buckling of the posterior cruciate ligament. The medial collateral ligament, lateral collateral ligament complex, and patellar retinacula are intact. There is perhaps atrophy of the biceps femoris, greater than expected for patient's age.EXTENSOR MECHANISM: The extensor mechanism appears intact.ADDITIONAL

Output: 1.Thinning of the anterior cruciate ligament graft and mild buckling of the posterior cruciate ligament is suggestive of at least a partial tear.2.Postsurgical changes from prior surgeries as described above.3.Complex undersurface tearing of the posterior horn of the lateral meniscus with capsular separation. 4.Diminutive posterior horn of the medial meniscus may be from prior meniscectomy.5.Osteoarthritis most prominent in the weight bearing portions of the knee.


Instruction: Generate impression based on findings.

Input: Left knee pain and effusion MENISCI: The medial meniscus is intact. The body of the lateral meniscus appears mildly prominent suggesting a slight discoid configuration but we see no discrete meniscal tear.ARTICULAR CARTILAGE AND BONE: There is mildly increased signal intensity of the articular cartilage of the lateral patellar facet suggesting chondromalacia but there is no focal fluid-filled cartilage defect identified. The articular cartilage of the medial and lateral compartments is preserved. The bone marrow signal of the knee is normal.LIGAMENTS: The cruciate and collateral ligaments are intact. EXTENSOR MECHANISM: No significant abnormality noted.ADDITIONAL

Output: Moderate joint effusion with mild nonspecific posterior soft tissue edema. The possibility of a ruptured Baker's cyst is considered. There is perhaps mild chondromalacia of the lateral patellar facet but otherwise there are no findings to suggest internal derangement.


Instruction: Generate impression based on findings.

Input: 79-year-old female patient with failure to thrive, altered mental status. Question of leptomeningeal disease. There are no new foci of restricted diffusion to suggest acute ischemia. Multiple nodular enhancing parenchymal lesions, some of which have intrinsic high T1 signal, within the bilateral hemispheres and left cerebral hemisphere appear unchanged in distribution compared to the prior study. Some of these lesions demonstrate mildly decreased enhancement. Two previously noted lesions within the right superior frontal gyrus and the right pars marginalis demonstrate decreased T2 signal abnormality compared to the prior study. Gyriform enhancement of the right temporal lobe is not significantly changed. Encephalomalacia of the right precentral gyrus is unchanged. No new enhancing lesion is identified. There is interval increase in right parieto-occipital and right temporal white matter T2 signal abnormality, which is presumably related to posttreatment change.There is mild interval increase in size of the lateral and third ventricles as well as the sulci suggesting parenchymal volume loss. The basal cisterns are patent. There is no midline shift or herniation. The major cerebral flow voids are intact. There are postsurgical changes within the right parietal bone. The orbits, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: 1. Overall, stable distribution of metastatic lesions within the bilateral cerebral hemispheres and left cerebellar hemisphere without new lesion identified or definite progression of existing lesions. 2. Decreased edema within the right frontal lobe and right pars marginalis, compared to the prior study.3. Increased T2 signal abnormality within the white matter of the right parieto-occipital and right temporal lobes which likely represents posttreatment change.4. Mildly increased size of the lateral and third ventricles likely secondary to volume loss.


Instruction: Generate impression based on findings.

Input: 48 years, Female, multiple sclerosis and gait disorder. Brain: There is a moderate burden of T2/FLAIR hyperintense lesions in the periventricular and subcortical white matter with distribution consistent with known demyelinating disease. There is extensive confluent signal abnormality in the periventricular and pericallosal region. There is mild to moderate burden of T1 hypointense lesions. There is also brain parenchymal volume loss which is advanced for age with diffuse thinning of the corpus callosum. There is fairly mild involvement of the posterior fossa but with abnormal signal in the bilateral paramedian midbrain including along the medial longitudinal fasciculus, the paramedian ventral medulla, and along the right aspect of the cerebellar vermis with associated volume loss. No intracranial mass effect, midline shift, or herniation. No hydrocephalus or extra-axial collections. Visualized calvarium and extra cranial soft tissue structures are grossly unremarkable.Cervical spine:There is a T2 hyperintense lesion involving the dorsal paramedian cervical cord at the mid C2 level. There are more subtle tiny lesions suspected involving the left dorsolateral C2 and left lateral C3 levels as seen on the axial T2 and mFFE sequence as well as one involving the right dorsolateral C6 level. Vertebral body heights and alignment are maintained. Bone marrow signal is benign. There is a small central disc protrusion at the C5-C6 level There is no significant spinal canal or neural foraminal stenosis.

Output: 1. Findings consistent with known demyelinating disease with moderate burden of supratentorial lesions and to a lesser degree in the infratentorial brain as described above.2. Few small T2 hyperintense lesions in the cervical cord are suspected as described above.