Instruction: Generate impression based on medical findings.

Input: 30 year-old male with a history of osteochondral defect in the lateral femoral condyle presents with knee pain. MENISCI: Poorly defined increased signal intensity within the inner fibers of the posterior horn and body of the lateral meniscus likely represents intrasubstance degeneration and free edge fraying. These findings appear slightly more prominent compared to the prior study; this may represent progression of fraying or simply differences in technique (3T versus 1.5 T scanner).Again seen is poorly defined signal intensity within the anterior horn of the lateral meniscus suggesting additional intrasubstance degeneration. No fluid signal intensity is identified in the lateral meniscus. The medial meniscus is intact.ARTICULAR CARTILAGE AND BONE: Again seen is a linear focus of metallic susceptibility artifact in the lateral femoral condyle, compatible with an orthopedic screw that presumably affixes the patient's known osteochondral defect based on prior reports. Focal depression of the overlying subchondral bone plate appears similar to the prior study. Small cysts in the subchondral bone of the lateral femoral condyle, just above the free edge of the anterior horn of the lateral meniscus, also appear similar to the prior study. Thinning/heterogeneity of the overlying articular cartilage is not significantly changed, likely representing chronic degeneration. No large fluid-filled gaps are seen. Increased signal intensity within the articular cartilage of the lateral tibial plateau, just anterior to the free edge of the posterior horn of the lateral meniscus, appears more prominent; this finding suggests progression of full thickness cartilage degeneration. Abnormal increased signal intensity within the lateral tibial spine appears similar to previous MRI. Articular cartilage of the medial tibiofemoral compartment is intact. The patellar cartilage is also intact, but new increased signal intensity within the articular cartilage of the femoral trochlea suggests focal degeneration at this site. Tricompartmental osteophytes are again noted.LIGAMENTS: The cruciate and collateral ligaments are intact.EXTENSOR MECHANISM: The extensor mechanism is intact. Minimal thickening of the patellar tendon and scarring within Hoffa's fat pad are consistent with prior surgery.ADDITIONAL

Output: 1.Postoperative changes s/p lateral femoral condyle osteochondral defect fixation as described above, appearing similar to the prior MRI. However, there appears to have been progression of focal degeneration of the articular cartilage overlying the adjacent lateral tibial plateau.2.Degeneration and free edge fraying of the lateral meniscus, which may have slightly progressed since the prior MRI. However, no fluid-filled lateral meniscal tear is identified.3.New focal degeneration of the articular cartilage overlying the femoral trochlea and other findings as described above.


Instruction: Generate impression based on medical findings.

Input: NSCLC brain metastases status post WBRT in 11/2014. There is interval decrease in size of multiple subcentimeter enhancing supratentorial and infratentorial lesions. For example, a right anterior frontal lobe lesion measures up to 4 mm, previously 8 mm and a left cerebellar hemisphere lesion measures up to 3 mm, previously 5 mm. There is also negligible residual vasogenic edema associated with the lesions. There is a punctate focus of susceptibility effect in a left precentral gyrus lesion, which may represent hemorrhage or calcification. In addition, the enhancing component within the pineal gland has decreased in size. There is minimal patchy cerebral white matter T2 hyperintensity. There is no evidence of intracranial hemorrhage or acute infarct. The ventricles and basal cisterns are unchanged in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull, paranasal sinuses, and scalp soft tissues are unremarkable. There is patchy fluid signal within the bilateral mastoid air cells.

Output: Interval decrease in size of multiple subcentimeter enhancing supratentorial and infratentorial metastases.


Instruction: Generate impression based on medical findings.

Input: CTLA4 deficiency autoimmune disease, inflammatory arthritis, AIHA status post splenectomy on Rapamune, pulmonary nodules, now presenting with new onset severe headache and nausea/vomiting. There are multiple infiltrative cortical and white matter enhancing lesions with high T2 signal within the right frontal lobe, bilateral parietal lobes, occipital lobes, left insula, and right cerebellum, which are generally more prominent. In addition, there is a newly apparent subcortical enhancing lesion in the left middle frontal lobe. The lesions display minimal mass effect and there is no midline shift. There are no associated susceptibility or restricted diffusion. There is an unchanged linear T2 hyperintense lesion in the superior right frontal white matter without associated enhancement. The ventricles and basal cisterns are normal in size and configuration. There is diffuse paranasal sinus mucosal thickening and fluid levels in the maxillary sinuses. There are partially-imaged prominent cervical lymph nodes, particularly on the left side. The orbits are unremarkable.

Output: 1. Slightly increased prominence of multiple supratentorial and infratentorial lesions may represent lymphocytic infiltration associated with CTLA4 deficiency rather than conventional central nervous system lymphoma. 2. Partially-imaged prominent cervical lymph nodes, particularly on the left side may also be related to the autoimmune disorder.3. Findings suggestive of acute sinusitis.


Instruction: Generate impression based on medical findings.

Input: Cervical radiculopathy Craniovertebral junction appears within normal limits. The cervical vertebral bodies are appropriate in height. Alignment is maintained. Bone marrow signal is within normal limits. There is no definite cord signal abnormality at any level aside from punctate focus involving the left aspect of the cord at the C5-C6 level.There is developmental narrowing of the cervical spinal canal with significant superimposed degenerative changes as detailed below: C2-3: Central disc protrusion with mild indentation on the ventral cord and ligamentum flavum thickening. There is overall moderate spinal canal stenosis at this level. Neural foramina are patent.C3-4: There is a disc osteophyte complex and ligamentum flavum thickening contributing to moderate spinal canal stenosis at this level and mild cord deformity. There is uncovertebral hypertrophy and mild facet arthropathy contributing to moderate bilateral neural foraminal stenosis, right greater than left.C4-5: There is disc osteophyte complex and ligamentum flavum thickening contributing to moderate spinal canal stenosis with mild cord deformity. There is uncovertebral hypertrophy and mild facet arthropathy contributing to moderate to severe right and moderate left neural foraminal stenosis.C5-6: There is disc osteophyte complex and ligamentum flavum thickening contributing to moderate to severe spinal canal stenosis with cord deformity, particularly on the left. There is uncovertebral hypertrophy and mild facet arthropathy contributing to moderate to severe right and moderate left neural foraminal stenosis. There is abnormal T2 signal involving the left lateral aspect of the cord at this level.C6-7: There is disc osteophyte complex which effaces the ventral thecal sac and contributes to mild to moderate spinal canal stenosis. There is minimal narrowing of the neural foramina related to uncovertebral hypertrophy.C7-T1: No significant compromise to the spinal canal or neural foramina.The vertebral artery flow voids appear to be intact. Multinodular goiter is noted and better assessed on recent ultrasound. Right submandibular gland is not definitively seen and may be absent or diminutive.

Output: 1. Developmental narrowing of the cervical spinal canal with superimposed degenerative changes resulting in significant multilevel spinal canal stenoses from the C2-C3 to the C6-C7 level with mild cord flattening, worst at the C5-C6 level. There is also significant neural foraminal stenoses from the C3-C4 to the C5-C6 levels as detailed above. 2. Focal cord signal abnormality involving the left aspect of the cord at the C5-C6 level favored to represent sequela of compressive myelopathy.


Instruction: Generate impression based on medical findings.

Input: Brain: Again seen are postoperative changes of suboccipital decompressive craniectomy and C1 laminectomy related to resection of small meningioma at the C1-C2 level. Again seen is a fluid collection in the suboccipital craniectomy surgical bed which is slightly smaller in the interval and likely represents a pseudomeningocele. The heterogeneously enhancing mass with cystic changes involving the medulla and upper cervical cord appears similar in size and configuration, measuring 2.4 x 3.5 cm in the AP and craniocaudal dimensions. There is clear enlargement of this mass compared to more remote MRI spine from 6/18/2012 when it measured 1.5 x 2.5 cm in the sagittal dimension. The other known intracranial masses also are not significantly changed including a left cavernous sinus mass which extends superiorly into the lateral aspect of the suprasellar cistern and posteriorly into the Meckel's cave; mass is compatible with a meningioma or schwannoma. Bilateral vestibular schwannomas involving the internal auditory canals are unchanged measuring approximately 9 mm bilaterally. Enhancing extra-axial lesion measuring approximately 7 mm in the right suprasellar cistern abutting the right optic nerve is also unchanged. Small areas of extra-axial enhancement along the falx are also unchanged and likely related to tiny meningiomas.Evaluation of the orbits on the brain sequences again demonstrates an enhancing mass in the left orbit extending from the orbital apex to just posterior to the globe likely representing an optic nerve sheath meningioma. No significant change in diffuse thickening, T2 hyperintensity and enhancement involving the left upper eyelid as well as the left temporalis muscle.No evidence of acute ischemia or hemorrhage. No new mass effect. No hydrocephalus. There is a small left maxillary sinus mucosal retention cyst. Fatty denervation changes are noted involving the right hemitongue and present previously since at least 4/1/2015.Cervical Spine: Minimal dural based enhancement is seen along the dorsal C1-C2 level without evidence of recurrence of previously resected meningioma at this level. Cervicomedullary enhancing mass as described above is not significantly changed since 2/23/2015 and likely represents an ependymoma. Smaller intramedullary cord masses at the C3 and the T3 level also appear similar. More punctate intramedullary enhancing foci at the C4 and C6 levels are also unchanged since 2/23/2015. Compared to 6/18/2012, there is clear enlargement of the cervical medullary junction mass as mentioned above and also of the T3 lesion which measures approximately 8 mm in the craniocaudal dimension.Extra-axial enhancing lesion consistent with meningioma at the at the T1-T2 level which mildly impresses the dorsal aspect of the upper thoracic cord also is not significantly changed. Otherwise no significant spinal canal or neural foraminal stenosis is appreciated.Vertebral body heights in the cervical and upper thoracic spine are normal. Alignment is maintained aside from loss of cervical lordosis. No significant disc disease.

Output: 1. Continued evolution of postsurgical changes of suboccipital decompression and resection of small C1-C2 meningioma. There is minimal dural based enhancement without evidence of meningioma recurrence at this location. Mild decrease in size of fluid collection in the surgical bed is seen, which likely represents a pseudomeningocele. 2. No significant change in left orbital mass which likely represents an optic nerve sheath meningioma when compared to most recent study. There is mild enlargement when compared to more remote studies dating back to 6/15/2012 with mild compression of the left optic nerve. 3. Additional stigmata of neurofibromatosis type 2 with additional masses including a left cavernous sinus meningioma, small falcine meningiomas, and bilateral vestibular schwannomas which are not significantly changed. Multiple enhancing masses in the cervical and visualized thoracic cord are not significant changed since 2/23/2015 cervical spine MRI. Compared to 6/18/2012, however, there is enlargement of the large cervicomedullary and smaller T3 intramedullary enhancing masses which likely represent ependymomas.4. Mild impression on the right dorsal aspect of the thoracic cord at the T1-T2 level related to meningioma, minimally worse since 6/18/2012. Otherwise no significant spinal canal or neural foraminal stenosis is appreciated in the cervical or imaged upper thoracic spine.


Instruction: Generate impression based on medical findings.

Input: Other disorders of psychological development [F88] / Other symptoms and signs involving the musculoskeletal system [R29.898], Reason for Study: ^Reason: Please evaluate for abnormality to explain hypotonia, or for Chiari History: Global developmental delay. No evidence of acute ischemic or hemorrhagic lesion.No evidence of intra-axial or extra-axial mass lesion.The ventricles, sulci and cisterns are symmetric and unremarkable. The gray-white matter differentiation is normal. 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: No evidence of acute ischemic or hemorrhagic lesion.No mass lesion.No evidence of Chiari malformation.


Instruction: Generate impression based on medical findings.

Input: 4-year-old male with a prolonged seizure, history VPS. Intracranial VP shunt catheter tubing is intact. Catheter tubing traverses the right parietal lobe, through the atria of the right lateral ventricle, and terminates with tip in the body of a mildly dilated left lateral ventricle. No change in the position or course of the catheter compared to previous examination. The right lateral ventricle remains collapsed and unchanged from previous exam, and the left ventricle also appears grossly unchanged compared to most recent brain MRI allowing for differences in the two modalities. Significant brain volume loss consistent with periventricular leukomalacia as well as abnormal callosal thinning. There is no evidence of periventricular edema to suggest elevated ventricular pressures. There is no evidence of intracranial hemorrhage, mass, or edema. The bones of the calvaria are thin and there is triangulated appearance of the skull, consistent with mild trigonocephaly. The brain may be small for age, correlate clinically for microcephaly. The visualized paranasal sinuses and mastoid air cells are normally pneumatized.

Output: 1.No significant change in ventricular size or configuration allowing for difference in technique between CT and MRI.2.PVL and callosal abnormality. refer to most recent MRI for further morphologic description.3.trigonocephaly with possible small size to the brain. Clinically correlate for microcephalus.


Instruction: Generate impression based on medical findings.

Input: Pressure and pain. History of left occipital occipital scalp hemangioma resection. Rule out recurrence. There are unchanged postoperative changes in the left posterior scalp and underlying skull spanning the proximal, occipital and suboccipital regions. In addition, the multilobulated, T2-hyperintense, intensely contrast enhancing residual left suboccipital scalp mass is unchanged. In the axial plane, the largest, left suboccipital component of the lesion measures 5.9 cm x 1.2 cm (series #1301, image #13) compared to 6.0 cm x 1.2 cm previously. The smaller left parietal scalp lesion is minimally larger and now measures in the axial plane 1.2 cm x 0.7 cm (series #1301, image #24) compared to 1.1 cm x 0.5 cm in May 2012. A similar right parieto-occipital scalp lesion that measures in the axial plane 1.4 mm x 0.6 mm is new since May 2012 examination. The prominent left parietal cortical veins remain unchanged.Focal encephalomalacia involving the posterior left parietal lobe remain unchanged. The remainder of the brain is unremarkable without acute infarct or intracranial hemorrhage. The ventricles and other CSF-containing spaces are unchanged. There is no midline shift or brain herniation.There is no gross orbital abnormality. Mastoid air cells are clear.

Output: 1.Unchanged residual left suboccipital scalp hemangioma and associated postoperative change.2.The small left parietal scalp hemangioma is minimally larger than on the previous examination as above.3.A similar small lesion has developed in the right parieto-occipital scalp since the previous examinations. 4.Unchanged small left parietal encephalomalacia and other posttreatment findings.


Instruction: Generate impression based on medical findings.

Input: 45-year-old female with severe pain and history of avascular necrosis. Evaluate for avascular necrosis. There is a curvilinear band of abnormal signal within the right femoral head indicating avascular necrosis. The band extends from the medial aspect of the femoral head just above the fovea to the lateral aspect of the femoral head indicating involvement of the majority of the weight-bearing surface. Mild edema of the adjacent bone on T2 weighted images is noted; the majority of the necrotic segment maintains fat signal on the T1-weighted images. There is a tiny step off along the anterior/superior aspect of the femoral head suggestive of minimal articular surface collapse that we suspect is chronic. Otherwise the shape of the femoral head is maintained. Small right hip joint effusion, which is not uncommon in patients with avascular necrosis. Mild degeneration of the articular cartilage along the anterior/superior aspect of the acetabulum. The anterior labrum is partially separated from the underlying acetabulum from the 3 to 4 o'clock position just superior to the transverse acetabular ligament. We suspect this represents normal variant recess rather than a tear.On the large field of view images, evaluation of the left hip is limited due to metallic susceptibility artifact from the total hip arthroplasty. Note is made of residual red marrow but no focal abnormalities are seen. The musculature is within normal limits.

Output: Avascular necrosis and other findings as above.


Instruction: Generate impression based on medical findings.

Input: Status post surgery and radiotherapy for left carotid cancer (carcinoma ex pleomorphic adenoma with perineural invasion), with left neck pain and spasm. There are post-treatment changes related to the left parotidectomy and radiotherapy, which may account for the persistent signal abnormality within the left mandible bone marrow. However, there are no mass lesions in this region suggestive of residual/recurrent disease. There is no significant lymphadenopathy in the neck. There is a small right upper lip skin excrescence. The remaining salivary glands, nasopharynx, oropharynx, hypopharynx, and larynx are unremarkable. There are unchanged nodules within the thyroid. There is a carious tooth number 19. The imaged intracranial structures are orbits are unremarkable. There is anterior surgical fusion of C4-6 and degenerative spondylosis of the cervical spine.

Output: Post-treatment findings related to left parotidectomy and radiation with no evidence of measurable locoregional tumor recurrence of significant cervical lymphadenopathy, although the assessment is limited by the lack of intravenous contrast. Persistent signal abnormality within the left mandible bone marrow may be treatment-related, such as osteonecrosis.


Instruction: Generate impression based on medical findings.

Input: An intra-axial, predominately cystic lesion is present in the right frontal lobe measuring approximately 6.5 AP x 5.8 ML x 5.2 CC cm with surrounding confluent T2 signal abnormality. There is substantial mass effect on the right lateral ventricle with partial effacement, and 8mm midline shift to the left. There is mild left lateral ventricular dilatation compatible with entrapment. The lesion is dominated by two large cystic components. Anteromedial to them, there is an elongated ovoid region of near CSF signal intensity through which it appears that small vessels may pass and which may also be a part of the lesion. The walls of the cystic components enhance, as does the solid nodular portion which is located more laterally. The solid portions of the lesion demonstrate mildly increased diffusion signal and subtle susceptibility effect suggesting hemorrhage and/or mineralization. The solid nodular portions of this tumor are inseparable from the right frontal opercular gyri which are thickened and heterogeneous, further supporting that the mass is intra-axial, and possibly originating from the cortex. The internal cystic components show no restricted diffusion.

Output: Large intra-axial cystic and solid mass with enhancing nodular components in the right frontal region with extensive mass effect, and midline shift as described above. Although the point of origin of this lesion is not entirely clear, it may originate from the cortex of the right frontal operculum as described above. A primary brain tumor is the favored diagnosis. Certainly atypical or parasitic infectious processes can present similarly, but given the findings detailed above, this is considered much less likely.


Instruction: Generate impression based on medical findings.

Input: History of cervicothoracic laminectomy for metastases/debulking. Evaluate for changes/recurrence. Surveillance. Again seen are postoperative findings related to multilevel laminectomies in the lower cervical and upper thoracic spine. Vertebral body heights in the cervical spine are normal. Alignment of cervical spine is maintained. Mild degenerative changes are present including small disc osteophyte complexes at the C3-C4 to C5-C6 levels with ligamentum flavum thickening contributing to mild spinal canal stenosis. No high-grade spinal canal stenosis in the cervical spine. There is also fairly mild neural foraminal narrowing without high-grade neural foraminal stenosis at any level. Cervical cord signal is unremarkable.Again seen is severe compression fracture involving the T2 vertebral body (previously described as T1) with near complete loss of height and osseous retropulsion which is grossly similar to prior. Again noted is grade 2 anterolisthesis of T1 on T2 which appears similar to prior. There is resulting effacement of the ventral thecal sac and mild flattening of the ventral cord at the T2 level which is also similar to prior. Subtle T2 signal abnormality in the thoracic cord is again seen and extends into the left aspect of the cord to the T3-T4 level likely representing Wallerian degeneration along the left corticospinal tract. Posterior paraspinous enhancement in the laminectomy bed which is at least predominantly postsurgical is similar to prior without new or enlarging lesions to suggest tumor progression.Aside from T2, remaining thoracic vertebral body heights are maintained. Alignment is maintained. Focal signal abnormality involving the right T3 posterior elements is nonspecific but not significantly changed. Right T12-L1 lesion (previously described as T11-T12) demonstrates continued decrease in size compared to 5/24/2016 and 2/20/2016. No new metastatic lesions are appreciated. No evidence of epidural tumor. No cord signal abnormality involving the mid or lower thoracic cord. Spinal canal and neural foramina below the T2 level are also patent.

Output: 1. No evidence of progression of metastatic disease in the spine. 2. No significant change in severe compression fracture of the T2 vertebral body with osseous retropulsion and grade 2 anterolisthesis of T1 on T2. Associated indentation of the ventral cord at the T2 level is also not significantly changed. Subtle associated chronic cord signal abnormality involving the left aspect of the cord is also not significantly changed and may represent sequela of prior compression.3. Continued decrease in size of right T12-L1 lesion. Nonspecific focal signal abnormality involving the right T3 posterior elements which may represent treated lesion is not significantly changed. No new osseous lesion, new pathologic fracture, or epidural tumor.


Instruction: Generate impression based on medical findings.

Input: History of prostate cancer status post robotic-assisted laparoscopic prostatectomy on 5/27/2016. His final pathology revealed Gleason 4+5 disease with positive margins at the L peripheral and L apex, 2/19 node involvement on the right with largest lymph node tumor being 15 mm with extranodal invasion, tumor volume 65%, pT3bN1MxR1. Recent PSA is 0.29, post-operatively was 0.11. Preoperatively PSA=11.85 ng/ml PELVIS:PROSTATE:Prostate Size: Patient is status post prostatectomy.Peripheral Zone: Patient is status post prostatectomy.Central Gland: Patient is status post prostatectomy.Seminal Vesicles: Patient is status post prostatectomy.Extracapsular Extension: Patient is status post prostatectomy.BLADDER: No significant abnormality noted.LYMPH NODES: Left external iliac T2 hyperintense lesion measuring 2.4 x 1.1 cm (series 1901 image 95). This lesion has no internal enhancement and favor lymphocele. Previously seen right external iliac lymph node is not definitely seen on current study and may have been surgically removed. Tiny nonspecific periprostatic lymph node.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: 1.Left external iliac T2 hyperintense lesion without internal enhancement, favor lymphocele. 2.Tiny nonspecific periprostatic lymph node, but no specific evidence of disease recurrence.PI-RADS™ v2 Assessment Categories:PIRADS 1 – Very low (clinically significant cancer is highly unlikely to be present) PIRADS 2 – Low (clinically significant cancer is unlikely to be present)PIRADS 3 – Intermediate (the presence of clinically significant cancer is equivocal)PIRADS 4 – High (clinically significant cancer is likely to be present) PIRADS 5 – Very high (clinically significant cancer is highly likely to be present)https://www.acr.org/~/media/ACR/Documents/PDF/QualitySafety/Resources/PIRADS/PIRADS%20V2.pdf


Instruction: Generate impression based on medical findings.

Input: Male, 40 years old, lumbar pain and radiculopathy. Spinal alignment is anatomic. Vertebral body height and morphology are within normal limits. No evidence of pathologic marrow replacement or edema is seen.The visualized distal spinal cord and conus are within normal limits. The nerve roots of the cauda equina disperse evenly through the thecal sac. No epidural abnormalities are suspected.Mild loss of disc height and disc bulging are seen in the lower thoracic spine as visualized on sagittal images. Additional level specific findings are as follows:L1-2: Unremarkable. L2-3: Unremarkable. L3-4: Mild facet arthropathy. Small right foraminal disc protrusion which contacts the exiting right L3 nerve root. No significant spinal canal stenosis is seen. The right neural foramen is mildly narrowed. L4-5: Mild facet arthropathy, left more than right. No significant spinal canal stenosis. Mild left foraminal narrowing. L5-S1: Moderate facet arthropathy. Mild bulging disc with a superimposed left foraminal annular fissure/protrusion. No significant spinal canal stenosis. Moderate left and mild right foraminal narrowing.

Output: 1.A small foraminal disc protrusion on the right at L3-4 contacts the exiting L3 nerve root but causes only mild generalized narrowing of the foramen.2.A left foraminal protrusion at L5-S1, along with facet arthropathy, causes moderate narrowing of the neural foramen.3.No areas of significant spinal canal stenosis are seen


Instruction: Generate impression based on medical findings.

Input: Some images are degraded by motion artifact.Brain MRI: The ventricles and sulci are normal in size. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. No abnormal enhancing lesion is identified. The pituitary gland is normal in size. There is no evidence for intracranial hemorrhage or acute infarction. The paranasal sinuses and mastoid air cells are clear. There is left temporal lobe developmental venous anomaly, which is a normal variant. Bilateral prominent perivascular spaces are noted with focal prominence in the left periatrial white matter. Brain MRA: There is normal flow related enhancement of the basilar artery, distal bilateral internal carotid arteries and carotid siphons and bilateral anterior, middle and posterior cerebral arteries. There is central lack of flow related enhancement of the anterior communicating artery, which may be artifactual versus a tiny fenestration. Left A1 segment and bilateral P1 segments are hypoplastic, which are normal variants. No arterial narrowing, occlusions or aneurysms are identified. No arteriovenous malformations are identified.Brain MRV: There is normal venous flow demonstrated within the internal cerebral veins, straight sinus, superior sagittal sinus and within the bilateral transverse and sigmoid sinuses. No dural venous sinus thromboses or occlusions are identified.

Output: 1.No acute intracranial abnormality.2.No intracranial arterial narrowing, occlusion, or aneurysms are identified.3.No intracranial venous sinus thromboses or occlusions are identified.


Instruction: Generate impression based on medical findings.

Input: Ms. Stefanski is a 56year old female with a personal history of left breast lumpectomy in 2013 for triple negative IDC followed by neoadjuvant chemotherapy and radiation. Personal history of BRCA2 mutation and two biopsy-proven fibroadenomas in the left breast. She has no current breast related complaints. There is heterogeneous amount of fibroglandular tissue in both breasts. Mild parenchymal enhancement is noted bilaterally.Susceptibility artifact is seen in the left medial breast and left axillary region, corresponding to the surgical clips from patient's prior lumpectomy. Two stable lobulated masses are present in the left breast, compatible with biopsy proven fibroadenomata. No abnormal enhancement is seen in either breast. No abnormal axillary lymph nodes are identified in either axillary region.

Output: Stable postsurgical changes of the left breast and axilla. No MRI evidence for malignancy. BIRADS: 2 - Benign finding.RECOMMENDATION: ND - Routine Diagnostic Mammogram.


Instruction: Generate impression based on medical findings.

Input: 68 year old female with possible right patellar tendon tear on plain film. MENISCI: The medial meniscus appears intact. There is globular increased signal abnormality within the body of the lateral meniscus consistent with intrasubstance degeneration. Some of this signal extends to the femoral articular surface consistent with degenerative tearing/superficial fraying.ARTICULAR CARTILAGE AND BONE: There is a focal full thickness articular cartilage cleft along the medial facet of the patella with underlying degenerative subchondral signal abnormality and cyst formation. There is subjective thinning of the lateral tibiofemoral compartment articular cartilage. There is a focal full-thickness articular cartilage degeneration along the lateral tibial plateau with underlying subchondral signal abnormality. There is full-thickness articular cartilage degeneration along the posterior aspect of the medial femoral condyle with underlying degenerative subchondral signal abnormality.LIGAMENTS: The cruciate and collateral ligaments appear intact. EXTENSOR MECHANISM: The extensor mechanism appears intact. There is increased signal abnormality within the distal fibers of the patellar tendon indicating mild patellar tendinosis.ADDITIONAL

Output: 1. Findings consistent with mild patellar tendinosis. The patellar tendon appears intact.2. Full-thickness articular cartilage cleft and degeneration as described above.3. Intrasubstance degeneration/degenerative tearing of the lateral meniscus.4. Nonspecific subcutaneous edema along the anterior aspect of the patellar tendon.


Instruction: Generate impression based on medical findings.

Input: Ankle pain and swelling TENDONS: There is redemonstration of enlargement and increased signal of the peroneus tendons, the extent of which appears similar to the prior exam. Further distally, the peroneus brevis tendon continues to appear thickened with increased signal although the peroneal longus tendon appears normal in caliber. Trace amount of fluid is seen within the peroneal sheath, similar to the prior exam.The Achilles tendon appears normal in caliber and signal. The medial ankle tendons appear normal; a small amount of fluid in the tibialis posterior tendon sheath is of doubtful significance. There is a type I accessory navicular. The anterior ankle tendons appear normal.LIGAMENTS: The anterior talofibular and calcaneofibular ligaments appear slightly thickened which may reflect prior sprain injury, however this is similar to the prior exam. The posterior talofibular ligament appears normal. The remaining ligaments appear similar to the prior exam.ARTICULAR SURFACES AND BONE: There is mild deformity of the posterior aspect of the distal tibial meta-epiphysis, likely representing an old healed fracture. Small osteophytes indicate mild osteoarthritis at the ankle and midfoot however there is no osteochondral defect of the talar dome. ADDITIONAL

Output: Essentially unchanged exam when compared to the prior study of 7/3/2014. There is persistent enlargement and increased signal of the peroneus tendons reflecting tendinopathy although no full-thickness tear is identified. Additional findings are described above.


Instruction: Generate impression based on medical findings.

Input: 77-year-old female with history of aneurysm, surveillance imaging. History of right MCA stroke and thrombectomy on Jun 8 2012 Brain MRI:No evidence of acute ischemia. Redemonstrated is FLAIR hyperintensity and volume loss involving the right frontal, parietal, and temporal lobes as well as the posterior insula consistent with prior right MCA infarct. Small infarcts involving the right frontal corona radiata and anterior caudate also again seen. Mild FLAIR hyperintensity involving the bilateral periventricular white matter is compatible with chronic small vessel ischemic changes. Chronic right inferior cerebellar infarct is also again seen. These findings are unchanged.Again seen are foci of susceptibility effect adjacent to the central sulcus in the region of the chronic infarct and unchanged indicative of chronic blood products. Additional scattered foci of chronic microhemorrhages in the right frontal lobe and in the right parietal periatrial white matter also unchanged. No intracranial mass or mass-effect. No extra-axial collections. No hydrocephalus. As before, there is diffuse opacification of the left mastoid air cells as well as mucosal thickening involving the right maxillary sinus.Brain MRARedemonstrated is a left PCOM artery aneurysm measuring 3.2 mm at the neck and 6 mm in length. No evidence of interval enlargement. The left posterior communicating artery arises in its medial and inferior aspect. Aneurysm projects posteriorly and inferiorly.There is bulbous appearance at the right superior cerebellar artery origin which is unchanged. There are atherosclerotic changes involving the cavernous and supraclinoid internal carotid arteries with ectasia of the anterior genu of the left cavernous carotid artery. The anterior communicating and bilateral posterior communicating arteries are patent. No additional aneurysmal dilatations or flow-limiting stenoses are evident in the anterior-posterior circulation.

Output: 1.Stable encephalomalacia involving the right frontal, temporal, and parietal lobes consistent with chronic right MCA territory infarct. No new infarcts. 2.Stable multiple foci of chronic microhemorrhage including within the area of prior infarct are unchanged.3.No significant change in left posterior communicating artery aneurysm measuring up to 6 mm in length and 3 mm at the base.4.Persistent opacification of the left mastoid air cells as well as mucosal thickening involving the right maxillary sinus.


Instruction: Generate impression based on medical findings.

Input: Diabetes, alcohol abuse, 40lbs weight loss, CT showed soft tissue infiltration around head of pancreas, evaluate for underlying neoplasm ABDOMEN:LIVER, BILIARY TRACT: No significant biliary duct dilatation. SPLEEN: No significant abnormality noted.PANCREAS: Dilatation of main pancreatic duct, measuring up to 7 mm, seen to level of ampulla, no evidence of obstructing mass. Intraductal stones/debris seen. No definite obstructing lesion seen. Marked pancreatic parenchymal atrophy with relative sparing of head. Curvilinear T2 hyperintensity at level of pancreatic head likely the cystic duct, image 14 series 501.ADRENAL GLANDS: 1 cm right adrenal nodule demonstrating signal loss on opposed phase imaging, consistent with adrenal adenoma, image 47 series 901.KIDNEYS, URETERS: Mild perinephric stranding. 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: 1. Findings compatible with chronic pancreatitis with ductal dilatation, secondary to stones. No definite obstructing lesion seen.2. Right adrenal adenoma.


Instruction: Generate impression based on medical findings.

Input: There is T1 and T2 linear hypointensity within the left precentral gyrus and precentral sulcus most compatible with chronic blood products as well as a small focus of T2 hyperintensity within the adjacent left superior frontal gyrus most compatible with gliosis. There is no evidence of acute infarct. There are a few scattered punctate foci of T2 hyperintensity within the supratentorial white matter that are most compatible with chronic small vessel ischemic disease. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is a prominent cisterna magna. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull, paranasal sinuses, and scalp soft tissues are unremarkable. There is minimal fluid within left mastoid air cells.

Output: 1.Findings most compatible with chronic blood products and minimal adjacent gliosis centered within the left pre-central and superior frontal gyri given the history of prior hemorrhage. 2.Minimal nonspecific fluid within left mastoid air cells.


Instruction: Generate impression based on medical findings.

Input: Encephalomalacia with gliosis and a rim of susceptibility hypointensity is present involving the posterior right frontal lobe (precentral gyrus). There is no associated restricted diffusion or enhancement.There are scattered punctate foci of T2 hyperintensity within periventricular and subcortical white matter without restricted diffusion, mass effect, or enhancement.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. Flow voids are present within the major vessels indicating patency. Mucosal thickening is present within posterior right ethmoid air cells and the left sphenoid sinus. The remaining paranasal sinuses and mastoid air cells are clear. There is no abnormal enhancement within the brain.

Output: 1.Remote right MCA territory infarct.2.Mild chronic small vessel ischemic disease.3.No MRI evidence of metastatic disease.


Instruction: Generate impression based on medical findings.

Input: 33-year-old male with history of seizures. There no areas of restricted diffusion to suggest acute ischemia. There is no evidence of acute intracranial hemorrhage. No mass or mass effect. No areas of parenchymal edema. The ventricles and sulci are symmetric. Specifically the medial temporal lobes are unremarkable. Normal flow voids are appreciated in the major intracranial vessels. There are mucous retention cysts in bilateral maxillary sinuses, left larger than right. There is a small amount of fluid in the left petrous bone which likely represents trapped fluid. The mastoid air cells are clear. The orbits are unremarkable.

Output: No evidence of mass or clear etiology of seizures.


Instruction: Generate impression based on medical findings.

Input: 53-year-old male with right shoulder and neck pain/radiculopathy. The vertebral body heights are preserved. There is mild loss of intervertebral disc height and disc signal throughout the cervical spine related to with degenerative disease. There is a small focus of increased T2 marrow signal in the C5 vertebral body may represent an atypical intraosseous hemangioma. Reactive marrow signal is present along the vertebral body endplates at C3-4. There is mild straightening of the cervical lordosis, but no spondylolisthesis. At C2-C3, there is a small disc osteophyte complex asymmetric to the left, but no significant spinal canal or neural foraminal stenosis. At C3-C4, there is asymmetric hypertrophy of the right uncovertebral joint with moderate right neural foraminal stenosis and mild spinal canal stenosis. At C4-C5, there is a small disc-osteophyte complex with trace right neural foraminal stenosis, but no significant spinal canal or left neural foraminal stenosis. At C5-C6, there is minimal uncovertebral joint hypertrophy, but no significant spinal canal or neural foraminal stenosis. At C6-C7, there is a small disc-osteophyte complex with minimal right neural foraminal narrowing, but no significant left neural foraminal or spinal canal stenosis. At C7-T1, there is no disc bulge, spinal canal stenosis, or neuroforaminal narrowing.

Output: Multilevel spondylosis, which is most pronounced at C3-4, where there is moderate right neural foraminal stenosis and mild spinal canal narrowing.


Instruction: Generate impression based on medical findings.

Input: 24 year old female with seizure history. Again seen is encephalomalacia in the left temporal lobe, compatible with prior temporal lobe resection and unchanged since the prior examination.There is crowding of the foramen magnum. This is compatible with mild cerebellar tonsillar ectopia which was seen on the prior MRI dated 7/3/08No evidence of acute hemorrhage. No evidence of mass or midline shift. The gray-white differentiation is preserved. There are surgical changes compatible with prior left frontotemporal craniotomy. The visualized paranasal sinuses and mastoid air cells are normally pneumatized.

Output: Postsurgical and other chronic changes as above. No evidence of acute hemorrhage or midline shift.


Instruction: Generate impression based on medical findings.

Input: Glioblastoma treatment planning. There are postoperative findings related to prior right frontal craniotomy. There is redemonstration of a heterogeneous mass that measures up to approximately 9 cm, centered within the right frontal lobe, with midline shift and extension across the midline and into the basal ganglia. There is effacement of most of the right lateral ventricle, but dilatation of portions of the third and left lateral ventricles. There is also heterogeneous tumor in the left cerebellar hemisphere and vermis with extension into the fourth ventricle, with diffuse surrounding high T2 signal in the cerebellum and brainstem.

Output: Treatment planning MRI redemonstrates a large mass centered in the right frontal lobe, with associated ventricular entrapment, and tumor in the posterior fossa.


Instruction: Generate impression based on medical findings.

Input: Knee pain MENISCI: There is deformity of the posterior horn of the medial meniscus likely relating to an overlying osteochondral lesion however there is no discrete tear identified. The lateral meniscus is intact.ARTICULAR CARTILAGE AND BONE: An osteochondral lesion is seen involving the medial femoral condyle measuring 1.6 cm in both the AP and transverse dimensions. There is loss of the overlying articular cartilage with increased marrow signal within the femur suggesting some component of instability. The lateral compartment is normal. There is mild irregularity of the articular cartilage of the medial patellar facet without full-thickness defect. LIGAMENTS: No significant abnormality noted. EXTENSOR MECHANISM: No significant abnormality noted.ADDITIONAL

Output: Osteochondral defect within the medial femoral condyle measuring approximately 1.6 cm. There is slightly increased marrow signal surrounding the lesion which may suggest a component of instability however there is no fluid signal undercutting the lesion and no evidence of detachment.


Instruction: Generate impression based on medical findings.

Input: Male, 41 years old, with problems walking and history of multiple sclerosis. Assess for changes from prior MRI. Brain:Numerous patchy areas of T2 hyperintensity are seen within the periventricular and juxtacortical white matter of the cerebral hemispheres. The cerebellum is also involved to a lesser degree. Since the prior examination, and accounting for differences in imaging technique, no significant interval change in the size or number of these lesions is appreciated.The above-mentioned lesions exert no significant mass effect. They are associated with no susceptibility effect or pathologic enhancement. No abnormal extra-axial collections are seen. The ventricular system is stable and within normal limits for size and morphology.Cervical spine:Abnormal T2 signal intensity is again observed at several locations in the cervical spinal cord. At C2, this signal abnormality is predominantly dorsal and extends for about 10 mm in the craniocaudal dimension. An additional area of signal abnormality is seen spanning from approximately C3 where the signal abnormality is holocord, down to approximately C4-5 where it is more right-sided. Evidence of cord volume loss is also seen at the C3 level. There has been no significant or convincing change in the appearance of these findings relative to the prior examination, again accounting for differences in imaging technique.Spinal alignment is anatomic. Vertebral body heights are preserved. No worrisome marrow signal replacement or marrow edema is seen. No significant disc herniation, spinal canal or neuroforaminal stenosis is identified.Thoracic spine:Areas of cord T2 signal abnormality are again observed on the right at T1, on the left at T3, on the right at T7-8, on the right at T9-10, and centrally at T11-12. Accounting for differences in imaging technique, and motion artifact on the present examination, no significant or convincing interval change is seen.Spinal alignment is anatomic. Vertebral body heights are preserved. Vertebral body hemangiomas are seen at T8 and T9. Marrow signal characteristics are otherwise unremarkable. No significant disc herniation, spinal canal or neuroforaminal stenosis is seen.

Output: Numerous periventricular and juxtacortical white matter lesions are reidentified in the brain compatible with the stated history of multiple sclerosis. There has been no significant interval change in the size, number or distribution of these lesions.Multiple areas of pathologic spinal cord signal abnormality are identified in the cervical and thoracic regions, again without significant or convincing interval change.


Instruction: Generate impression based on medical findings.

Input: Paresthesia of skin [R20.2] / Anesthesia of skin [R20.0], Reason for Study: ^Reason: eval for stenosis, herniation History: b/l foot numbness Cervical Spine MRILoss of normal cervical lordosis with straightening of cervical spine.There is no evidence of abnormal spinal cord signal intensity.Vertebral body height is preserved and MR signal intensity is normal.Degenerative changes are as follow;C23: Within normal limits.C34: Broad-based central to left disc protrusion which minimally narrows right lateral recess. Otherwise unremarkable.C45: Minimal bulging of disc otherwise unremarkable.C56: Broad based disc protrusion which abuts thecal sac with evidence of annular fissure. In addition, associated focal protrusion of disc narrows right lateral recess. C67: Within normal limitsC7T1: Within normal limitsLumbar spine MRIFor the purpose of this dictation, the lowest visualized intervertebral disc space is labeled L5-S1. The lumbar lordosis appears to be lessen than normal, unchanged since prior scan. The spine alignment is anatomic. The vertebral body height is preserved. The signal of the visualized cord is normal. The conus medullaris terminates at the L1 level. Degenerative changes are specified by the intervertebral level as follows: T12-L1: no neuroforaminal narrowing or spinal stenosis. L1-L2: Broad based disc bulging which indents thecal sac results mild to moderate spinal canal stenosis. Disc dessication is seen. Unchanged since prior scan. L2-L3: Diffuse bulging of disc with disc dessication which abuts thecal sac results minimal spinal canal stenosis, unchanged since prior scan. L3-L4: Interval development od broad based disc bulging which abuts thecal sac results mild to moderate spinal canal stenosis.no neuroforaminal narrowing or spinal stenosis. L4-L5: Disc dessication, otherwise unremarkable. L5-S1: no neuroforaminal narrowing or spinal stenosis.

Output: 1. Multilevel various degree disc degenerations as described above. 2. Disc herniation at the level C56 and interval disc bulging of L34 are noted. 3. Unchanged disc bulging with mild to moderate spinal canal stenosis at the level of L12 and L23 since prior scan.4. Normal spinal cord signal intensity.


Instruction: Generate impression based on medical findings.

Input: Unspecified convulsions [R56.9], Reason for Study: ^Reason: lesion that might produce seizures? History: seizure, h/o developmental delay during childhood There is no evidence of acute ischemic or hemorrhagic lesion on the scan.The ventricles, sulci and cisterns are symmetric and unremarkable. The gray-white matter differentiation is normal. 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: Normal brain MRI


Instruction: Generate impression based on medical findings.

Input: 47 years, Female, Reason: solid mass seen in left adnexa on ultrasound PELVIS: FemaleUTERUS, ADNEXA: Anteverted retroflexed uterus. Intramural T2 hypointense lesion within the posterior uterus measuring 1.1 x 1.4 cm (4/23) likely represents an intramural fibroid.There is a minimally complex left adnexal cystic lesion with a single septation measuring 4.8 x 2.6 x 4.4 cm (5/30 and 3/13). There are no enhancing components to this lesion. An ovarian location is favored given the acute angles of the lesion in relation to the ovary and apparent "claw sign." However, a paraovarian cystic structure such as a hydrosalpinx is among the differential considerations. The left ovary is enlarged, likely due to aforementioned cyst, compared to the right measuring 4.6 x 2.6 cm. Additional small follicles are noted.No significant pelvic ascites.BLADDER: No significant abnormality notedLYMPH NODES: No lymphadenopathy.BOWEL, MESENTERY: No significant abnormality notedBONES, SOFT TISSUES: No significant abnormality noted

Output: Minimally complex cystic lesion in the left adnexa with a thin nonenhancing septation and no suspicious solid or enhancing nodular components. An ovarian location is favored given the acute angles of the lesion in relation to the ovary and apparent "claw sign." However, a paraovarian cystic structure such as a hydrosalpinx is among the differential considerations. Correlation with prior ultrasound exams is recommended to assess for interval increase in size.


Instruction: Generate impression based on medical findings.

Input: 69 years Male (DOB:3/9/1946)Reason: Eval for acute infarct in R internal capsule vs pons History: L face/arm/Leg weaknessPROVIDER/ATTENDING NAME: ROBERT A MULLIKEN CHRISTOPHER M GOMEZ There is a new focus of diffusion restriction present in the right pons.The CSF spaces are appropriate for the patient's stated age with no midline shift. There is a moderate degree of periventricular and subcortical confluent hyperintense white matter lesions present identified on the FLAIR and T2 images.Small foci of T2 hyperintensity are present in the right internal capsule, right basal ganglia and thalami bilaterally. These were also present on the prior exam. There are patchy foci of T2 and FLAIR signal hyperintensity in the brainstem. The right cerebral peduncle is low but smaller than the left cerebral peduncle. There is signal hyperintensity within the right cerebral peduncle on T2 and FLAIR MR imaging.Susceptibility imaging is degraded by motion artifact as are many of the pulse sequences. There are punctate signal hypointensity is redemonstrated in the left middle cerebellar peduncle. In isolation these are of unknown clinical significance.No abnormal mass lesions are appreciated intracranially.Normal vascular flow voids are present in the distal left 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 right internal carotid artery flow-void is not readily visualized. This is a finding also present on the prior exam.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 demonstrate elongation the AP dimension of the right eye. The lens of the left eye is thin.

Output: 1.Findings are compatible with an acute right pontine lacunar infarct.2.Findings are compatible with old lacunar infarcts in the right basal ganglia, thalami and brainstem.3.Findings are suggestive of occlusion of the right internal carotid artery.4.Periventricular and subcortical white matter signal changes are nonspecific. At this age they are most likely vascular related though they could be related to a neurodegenerative process such as nonspecific leukoencephalopathy of aging. 5.Right eye staphyloma.6.The examination is degraded by patient motion which can obscure more subtle abnormalities.


Instruction: Generate impression based on medical findings.

Input: 52-year-old female. CT scan OSH with small calcifications in head of pancreas. Please use gadolinium and secretin to rule out chronic pancreatitis. Persistent nausea. ABDOMEN:LIVER, BILIARY TRACT: Small left hepatic lobe cyst. Small wedge shaped intrinsically T1 hyperintense area adjacent to the falciform ligament likely represents a perfusion abnormality. No suspicious hepatic mass. No biliary dilatation.SPLEEN: No significant abnormality noted.PANCREAS: Pancreatic divisum is noted. No pancreatic ductal dilatation and appropriate physiologic response of the pancreas to secretin. T1 signal intensity of the pancreas is normal. No focal mass is identified.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: Mild degenerative changes in the spine.OTHER: No significant abnormality noted.

Output: No specific evidence of chronic pancreatitis. Pancreatic divisum. Appropriate physiologic response of the pancreas to secretin.


Instruction: Generate impression based on medical findings.

Input: Female, 70 years old, history of sphenoid wing meningioma status post CyberKnife. Surveillance imaging. Findings related to right-sided craniotomy and tumor resection are redemonstrated. Mild encephalomalacia affecting the right orbital gyrus is unchanged. No evidence of new or concerning enhancement is seen in the operative bed to suggest residual or recurrent tumor.A 15 x 12 mm dural based enhancing mass along the left superior frontal gyrus is unchanged. No new enhancing or nonenhancing intracranial lesions are seen. A few scattered foci of white matter T2 hyperintensity are stable and nonspecific. No restricted diffusion is seen. No mass effect or parenchymal edema is detected.No evidence of intracranial hemorrhage or any abnormal extra-axial fluid collection is seen. The ventricles are normal in size and morphology.

Output: 1.Stable postoperative findings related to resection of a right sphenoid wing meningioma. No evidence of residual or recurrent tumor is seen.2.Stable left frontal convexity meningioma.


Instruction: Generate impression based on medical findings.

Input: Female 86 years old Reason: h/o cirrhosis and hcc, evaluate progression of liver disease History: elevated lfts ABDOMEN: Liver has a cirrhotic morphology with a nodular contour. There is now severe hepatic biliary ductal dilatation with bile duct irregularity. The left hepatic lobe shows progressive atrophy and biliary ductal dilatation. There is a focal area of narrowing about the Klatskin point with findings suggestive of a mass. Patient is status post cholecystectomy. Distal common bile duct is normal in caliber.Hepatic vessel patency cannot be evaluated due to the lack of intravenous contrast. The left portal vein flow void is not well visualized.SPLEEN: No significant abnormality noted.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: Multiple portacaval and upper abdominal lymph nodes which are borderline enlarged.BOWEL, MESENTERY: Bowel wall thickening which may be due to hypoalbuminemia.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: Large volume upper abdominal ascites.

Output: 1.Progression of biliary ductal dilatation with suggestion of a mass near the Klatskin point. Further evaluation with ERCP as previously suggested is recommended.


Instruction: Generate impression based on medical findings.

Input: History of HIV. History of regional enteritis. Evaluate for active inflammation. 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: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: The bowel is adequately distended with oral contrast. The small bowel fold pattern is maintained.The terminal ileum is well visualized. The small bowel is normal in caliber wall thickness and without adjacent inflammatory changes. There is no abnormal T2-weighted signal intensity, restricted diffusion or postcontrast enhancement of the small bowel wall to suggest active inflammation.No fixed luminal narrowing or upstream dilatation to suggest a flow-limiting stricture.No evidence of sinus tract or fistula formation.No free fluid or loculated fluid collection.The colon is normal caliber, wall thickness and without adjacent inflammatory changes.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.PELVIS:UTERUS, ADNEXA: No significant abnormality noted.BLADDER: No significant abnormality noted.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 active small bowel inflammation, flow-limiting stricture or sinus-fistulous disease.


Instruction: Generate impression based on medical findings.

Input: There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is a nonspecific punctate focus of susceptibility effect in the left parietal lobe, which may represent chronic hemorrhage. The brain parenchyma otherwise appears unremarkable. There is a partially empty sella. The ventricles and basal cisterns are otherwise 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 complete opacification of the left sphenoid sinus and sphenoethmoidal recess, extending into the left posterior ethmoid air cells. There is also a small amount of fluid signal in the bilateral mastoid air cells. There is persistent mild right greater than left exophthalmos.

Output: 1. A partially empty sella may represent pseudotumor cerebri.2. No evidence of intracranial hemorrhage, mass, or acute infarct. 3. Nonspecific small amount of fluid signal in the bilateral mastoid air cells may represent mastoiditis.4. Persistent left sphenoid sinus and posterior ethmoid sinusitis.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on medical findings.

Input: Clinical question:? Intracranial hemorrhage. Signs and symptoms: Seizures. CT of brain without infusion:Large area of vasogenic edema is noted in the right frontal lobe causing significant effacement of adjacent cortical sulci. A subtle mass effect on the right lateral ventricle. Within the area of vasogenic edema a partially cystic and partially solid mass is present. The larger cystic component of the mass measures 28 mm x 32-mm in transaxial dimensions (axial image 14. This finding is highly suspect of a neoplasm. There is no evidence of hemorrhage associated with this finding. There is a single small focus of low attenuation in the subcortical white matter of left posterior frontal (axial image 18). This finding is nonspecific and may represent an additional foci of neoplasm/metastases or a small foci of ischemic change. Further evaluation with an infused MRI examination is recommended. There is no evidence of hemorrhage, midline shift or hydrocephalus.Calvarium, limited paranasal sinuses and mastoid air cells are unremarkable.

Output: 1.Large area of vasogenic edema containing a partially cystic and partially solid mass highly concerning for malignancy. Follow-up with an MRI examination with infusion is recommended.2.Small foci of subcortical low attenuation is nonspecific however it may represent a second foci of malignancy or small vessel disease.3.No areas of hemorrhage, midline shift or hydrocephalus.4.Calvarium is intact.


Instruction: Generate impression based on medical findings.

Input: Clinical question: Incidental finding on head CT. Sclerotic changes of right parietal calvarium, MRI follow up for further evaluation was commented. Signs and symptoms: Patient is a status post fall on ice, hit head on the left side. Incidental finding of a sclerotic bony changes head CT. Pre-and post brain MRI:No acute intracranial process.Examination demonstrates a irregular focus of T1, T2 and T2 flair hypointensity without enhancement arising from the inner table of the right parietal bone corresponding to region of sclerotic bony change on head CT. This finding measures approximately at 19 x 21 mm in transaxial dimensions.Findings results in very subtle flattening deformity of the descending cerebral cortex however is without causing edema or abnormal enhancement.Findings to represent a calvarial osteoma. Possibility of a totally calcified/burned out meningioma cannot be entirely excluded.Examination otherwise demonstrate normal anatomical morphology and signal intensity brain parenchyma on all MRI sequences.Unremarkable cerebral cortex, cortical sulci, ventricular system, CSF spaces and myelination of brain.No detectable abnormal parenchymal, leptomeningeal enhancement. No evidence of calvarial or soft tissues of the scalp enhancement.Unremarkable images through the orbits and including axial fat sat post enhanced series.All paranasal sinuses and bilateral mastoid air cells and middle ear cavities demonstrate normal sacrum intensity.

Output: 1.A benign calvarial osteoma in the right parietal region as detailed. The less likely totally calcified/burned out meningioma cannot be entirely excluded.2.Unremarkable pre-and post enhanced brain MRI otherwise.


Instruction: Generate impression based on medical findings.

Input: Left hip pain Note that the patient terminated the exam prematurely and only coronal T1, coronal STIR, and axial T1 sequences were obtained.Within the limits of the exam, the marrow signal of the left hip is normal. The surrounding musculature of the left hip and pelvis is normal in caliber and signal.

Output: Limited examination demonstrates no obvious marrow or soft tissue abnormality of the left hip.


Instruction: Generate impression based on medical findings.

Input: Newly diagnosed prostate cancer. 3+4 disease right middle lobe PELVIS:PROSTATE:Prostate Size: 2.4 x 4.2 x 2.0 cmPeripheral Zone: Mild patchy increased T1-weighted signal intensity of the peripheral zone likely represents recent biopsy. This limits evaluation.There is an approximately 8 x 6 mm focus of restricted diffusion (series 703/184) associated with T2 weighted hypointensity (series 501/10) in the right lateral base/mid gland, suspicious for prostatic adenocarcinoma.Additional smaller foci of T2 weighted hypointensity are noted without definite associated restricted diffusion or abnormal enhancement.Central Gland: Mild changes of benign prostatic hyperplasia.Seminal Vesicles: No evidence of seminal vesicle invasion.Extracapsular Extension: No evidence of extracapsular extension.BLADDER: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: 8 mm focus in the right base/mid gland is suspicious for prostatic adenocarcinoma.No evidence of extraprostatic extension or enlarged pelvic lymphadenopathy.


Instruction: Generate impression based on medical findings.

Input: Reason: Cholestasis, rule out biliary obstruction History: bili 20. ABDOMEN:LIVER, BILIARY TRACT: Moderate to severe intrahepatic biliary ductal dilatation, greater in the left lobe than right lobe. Associated left lobe atrophy. There is soft tissue expansion of the main hepatic duct with extension into the right and left hepatic ducts, greater into the left hepatic duct. Left portal vein is not visualized, likely thrombosed. SPLEEN: No significant abnormality noted.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: No lymphadenopathy.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: Findings compatible with cholangiocarcinoma at the portal hepatis (Klatskin tumor). Extension into the left hepatic duct greater than right with associated left greater than right biliary ductal dilatation, left hepatic lobe atrophy and left portal vein thrombosis.


Instruction: Generate impression based on medical findings.

Input: 61-year-old female with altered mental status and elevated filling pressures on tap. Evaluate for metastasis, edema, or hydrocephalus. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is mild periventricular and subcortical white matter T2 hyperintensity which is nonspecific but likely related to chronic small vessel ischemic disease. There is no evidence of abnormal enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: Limited exam secondary to motion from patient discomfort and early termination of the study. Within these limitations, there is no evidence of acute intracranial hemorrhage, mass, acute infarct or hydrocephalus. Mild chronic likely small vessel ischemic disease is seen.


Instruction: Generate impression based on medical findings.

Input: Right breast IDC; New lytic lesion in the T12 vertebral body seen on CT scan for which bone biopsy recommended Serial CT images obtained during the biopsy procedure demonstrate the needle placement within the lytic T12 vertebral lesion. Post biopsy images demonstrate no complications.

Output: T12 vertebral bone biopsy under CT guidance. A total of two core samples were delivered to pathology for analysis. Touch preps were positive for neoplasm consistent with suspected breast cancer metastasis.


Instruction: Generate impression based on medical findings.

Input: Clinical question: Rule-out acute intracranial bleed. Signs and symptoms: Acute altered mental status. CT of brain without infusion:Large vessel intracranial vascular calcification of carotids and vertebral arteries are again identified. Very minimal scattered patchy areas of low-attenuation in the periventricular and subcortical white matter of bilateral cerebral hemispheres are concerning for minimal small vessel disease. Age of these is strokes cannot be determined on CT. Precise comparison with the prior examination for detection of new or small vessel stroke is not possible. Small vessel disease was noted on prior CT and MRI exam.No evidence of hemorrhage, edema, mass effect, midline shift or hydrocephalus is detected. Calvarium, paranasal sinuses and mastoid air cells are unremarkable.

Output: Findings consistent with small vessel disease of indeterminate age.


Instruction: Generate impression based on medical findings.

Input: Reason: right knee pain, evaluate for meniscus tearing History: above MENISCI: There is a full-thickness radial tear of the posterior horn of the lateral meniscus near its root with extension into the body of the meniscus. The posterior root of the lateral meniscus appears thickened which may represent a flipped meniscal fragment (image 17; series 7). There is intrasubstance degeneration of the posterior horn and deformity which may reflect degenerative tearing. There is a horizontal tear of the anterior horn of the lateral meniscus with small parameniscal cyst formation. The medial meniscus appears intact.ARTICULAR CARTILAGE AND BONE: There is full-thickness articular cartilage degeneration along the weightbearing surface of the lateral femoral condyle above the posterior horn of the meniscus with degenerative subchondral signal abnormality. There is full thickness degeneration of the lateral tibial plateau as well with underlying degenerative subchondral signal abnormality. There is subjective thinning of the medial tibiofemoral compartment. There is a full-thickness articular cartilage cleft along the medial facet of the patella with underlying subchondral signal abnormality. There are tricompartmental osteophytes.LIGAMENTS: The cruciate and collateral ligaments appear intact. EXTENSOR MECHANISM: The extensor mechanism appears intact.ADDITIONAL

Output: 1. Tearing of the lateral meniscus as described above.2. Osteoarthritis of the right knee including full-thickness articular cartilage degeneration most pronounced along the lateral tibiofemoral compartment as described above.3. Moderate size joint effusion with a lobulated Baker's cyst which may reflect a synovitis.


Instruction: Generate impression based on medical findings.

Input: Altered mental status. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is scattered cerebral white matter T2 hyperintensity. There are also small areas of encephalomalacia in the bilateral basal ganglia and corona radiata. There is prominent low T2 signal in the bilateral basal ganglia. The ventricles and basal cisterns are unchanged in size and configuration. There is diffuse cerebellar volume loss. 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 minimal fluid signal in the left mastoid air cells. There is diffuse paranasal sinus mucosal thickening. There is leftward nasal septal deviation with spur.

Output: 1. No evidence of acute intracranial hemorrhage, mass, or acute infarct.2. Probable chronic small vessel white matter ischemic disease and chronic bilateral basal ganglia and corona radiata lacunar infarcts. 3. Nonspecific diffuse cerebellar volume loss.


Instruction: Generate impression based on medical findings.

Input: Female, 41 years old, with back pain. Spinal alignment is anatomic. Vertebral body height and morphology are within normal limits. No evidence of marrow edema or marrow replacement is seen.The visualized distal spinal cord and conus are within normal limits. The nerve roots of the cauda equina are generally somewhat crowded which likely reflects a congenitally slender spinal canal. Additional superimposed degenerative findings are as follows:L1-2: Unremarkable. L2-3: Mild facet arthropathy. No significant spinal canal or foraminal stenosis. L3-4: Mild disc bulging, slightly progressed from prior. Mild generalized spinal canal narrowing. Mild bilateral foraminal narrowing. L4-5: Facet arthropathy, ligamentum flavum thickening, and disc bulging, progressed from prior. Mild generalized spinal canal stenosis, progressed from prior. Mild bilateral foraminal narrowing. L5-S1: Facet arthropathy, ligamentum flavum thickening, and mild spinal canal stenosis, progressed from prior. Moderate bilateral foraminal narrowing.

Output: Relatively mild but progressive disc and posterior element degeneration is seen from L3-4 through L5-S1. Superimposed upon a congenitally narrow spinal canal, these findings contribute to mild spinal canal and foraminal stenosis as detailed above.


Instruction: Generate impression based on medical findings.

Input: 28-year-old male with right shoulder instability ROTATOR CUFF: The muscles and tendons of the rotator cuff are intact. Contrast is contained within the glenohumeral joint.SUPRASPINATUS OUTLET: The acromioclavicular joint is within normal limits.GLENOHUMERAL JOINT AND GLENOID LABRUM: Normal glenohumeral alignment. There is a small defect within the mid posterior labrum containing contrast consistent with a nondisplaced labral tear. There is flattening of the posterior humeral head with bone marrow edema consistent with contusion from prior dislocation. BICEPS TENDON: Normally situated within the bicipital groove. ADDITIONAL

Output: 1. Hill-Sachs deformity with associated marrow edema.2. Small nondisplaced tear of the mid posterior labrum.


Instruction: Generate impression based on medical findings.

Input: 30 year old woman with breast cancer s/p resection, NSVT, concern for possible LV dysfunction and effusion on technically difficult echocardiogram, referred for cardiac MR to evaluate for infiltrative disease. Left VentricleThe left ventricle is mildly dilated with mildly reduced systolic function. The overall LV ejection fraction is 46%, the LV end diastolic volume index is 94 ml/m2 (normal range: 65+/-11), the LVEDV is 165 ml (normal range 109+/-23), the LV end systolic volume index is 51 ml/m2 (normal range 18+/-5), the LVESV is 89 ml (normal range 31+/-10), the LV mass index is 31 g/m2 (normal range 67+/-11), and the LV mass is 55 g (normal range 114+/-24). There is global hypokinesis. There is no late gadolinium enhancement to suggest the presence of an underlying fibrosing, infiltrative, or inflammatory process. There is no evidence of myocardial edema.The native T1 myocardial relaxation time is normal (<1100ms).There is no LV thrombus. Left AtriumThe left atrium is normal in size.Right VentricleThe right ventricle is normal in size with normal systolic function. The overall RV ejection fraction is 50%, the RV end diastolic volume index is 88 ml/m2 (normal range 69+/-14), the RVEDV is 156 ml (normal range 110+/-24), the RV end systolic volume index is 45 ml/m2 (normal range 22+/-8), and the RVESV is 79 ml (normal range 35+/-13). Right AtriumThe right atrium is normal in size. Aortic ValveThe aortic valve opens widely and there is no significant aortic regurgitation.Mitral ValveThe mitral valve opens widely and there is no significant mitral regurgitation.Pulmonic ValveThe pulmonic valve opens widely. There is no significant pulmonic regurgitation.Tricuspid ValveThe tricuspid valve opens widely. There is no significant tricuspid regurgitation.AortaThere is a left sided aortic arch with a normal brachiocephalic branching pattern. The aortic root is normal in size.Pulmonary VeinsAll four pulmonary veins drain normally into the left atrium.Pulmonary ArteryThe main pulmonary artery is normal in size. Venous AnatomyThe SVC and IVC drain normally into the right atrium. PericardiumThere is a trivial pericardial effusion.Extracardiac FindingsBilateral breast implants are present. Remnant thymus tissue noted. This study is not designed for the specific evaluation of extra-cardiac findings; therefore, the differentiation between artifacts and real extracardiac pathology may be difficult. If clinically indicated, a separate dedicated evaluation should be considered.

Output: 1. Mildly dilated left ventricle with mildly reduced systolic function (EF 46%). There is global hypokinesis.2. There is no late gadolinium enhancement to suggest the presence of an underlying fibrosing, infiltrative, or inflammatory process. 3. Normal sized right ventricle with normal systolic function (EF 50%).4. Trivial pericardial effusion.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on medical findings.

Input: Thoracic spine: There are multiple osseous lesions compatible with metastatic disease with associated epidural extension. There is enhancing soft tissue epidural extension at T1, T4, and T6. There is greater than 50% loss of vertebral body height with retropulsion of approximately 4 mm at T4, which abuts the spinal cord, but there is no actual spinal cord compression. There is exaggerated kyphosis centered at the T4 level. The disc heights are well maintained. The spinal cord is of normal signal. Numerous lesions are also present in several ribs bilaterally, which are compatible with metastatic disease. There is a partially imaged left pleural effusion.Lumbar spine: There are numerous foci of abnormal bone marrow signal and enhancement throughout the lumbar spine compatible with metastatic disease. There has been further height loss of the L4 vertebral body to approximately 75% loss, which also demonstrates abnormal bone marrow signal. There is worsening of retropulsion/soft tissue extension. Combined with degenerative ligamentum flavum thickening, there is resultant severe spinal canal stenosis at this level. Vertebroplasty changes are present in the L1 vertebra. The distal spinal cord and conus medullaris are within normal limits. There is diffuse disc desiccation signal and loss of intervertebral disc height throughout the lumbar spine. There are disc bulges at T12-L1, L2-L3, L3-L4, L4-5, and multilevel bilateral ligamentum flavum thickening causing multilevel spinal canal stenosis up to a moderate degree at L4-L5. Multiple lesions are present in the sacrum and bilateral iliac bones, which are also compatible with metastatic disease.

Output: 1. Diffuse metastases to the axial skeleton, including a pathologic T4 compression fracture without spinal cord compression and interval progression of a pathologic L4 compression fracture with persistent severe spinal canal stenosis at this level. 2. Multilevel degenerative spondylosis in the lumbar spine.3. Partially imaged left pleural effusion.


Instruction: Generate impression based on medical findings.

Input: Clinical question: Rule out brain aneurysm. Signs and symptoms: Headaches CTA of intracranial circulation:Vertebrobasilar system.There is normal appearing bilateral intracranial vertebral arteries, bilateral pica branches and basilar artery. No abnormality in particular no aneurysm is detected.Carotid system there are normal bilateral internal carotid arteries, bilateral anterior and middle cerebral arteries and their branches.There are no posterior communicating arteries identified.A very large mass within the sella with expansion of the sella and extension superiorly into the basal cistern is identified. There is no evidence of contrast within this mass. Further evaluation with dedicated MRI examination of pituitary is recommended. This mass results in significant bony remodeling/thinning and posterior displacement of dorsum sella. There is also extension of mass anteriorly and inferiorly into the sphenoid sinus and posterior right ethmoid air cells. On the right side the mass supplies mass effect and displaces the right supraclinoid internal carotid artery to the right.65 cc of Omnipaque 350 is administered for above study.

Output: 1.No evidence of vascular abnormality and in particular no aneurysm of intracranial vasculature. 2.Large expansile mass within the sella with extension into the sphenoid sinus and right posterior ethmoid air cells and with associated mass-effect and lateral displacement of supraclinoid right internal carotid artery. There is no evidence of contrast within this mass on the CTA examination.


Instruction: Generate impression based on medical findings.

Input: A patient submitted outside study for review. Submitted for review are bilateral screening/diagnostic mammography 3/4/2015, bilateral breast MRI and MRI guided biopsy 3/14/2015, and right diagnostic mammography 3/25/2015 performed at Northwestern Memorial Hospital. For comparison, bilateral screening mammography 4/14/2011 are available. 46 year old female per report referred to outside diagnostic mammography for left breast symptoms. Patient was reportedly breast feeding and suddenly stopped from the left breast. Family history of ovarian cancer in aunts and cousins. Patient believes she underwent genetic testing in the past with negative results. 3/4/2015 SCREENING/BILATERAL DIAGNOSTIC MAMMOGRAPHY AND POSTPROCEDURAL MAMMOGRAM Two standard views of both breasts, additional right ML and four spot magnification views were provided. The breast parenchyma is heterogeneously dense, unchanged in pattern and distribution. Cluster of calcifications in the right upper outer breast, posterior depth, have developed. On spot magnification, they are pleomorphic and measure 0.5 cm. Additional scattered benign calcifications are stable.These calcifications were biopsied reportedly under stereotactic guidance (no images available). Post-procedural orthogonal mammogram of the right breast demonstrate post biopsy change including foci of gas and X shaped clip in the previous location of the cluster of calcifications in the 9 o'clock position. No residual calcifications are visualized.3/14/2015 DIAGNOSTIC BILATERAL BREAST MRI AND 3/25/2015 MRI GUIDED BIOPSY:Exam is limited by motion artifact, more so on the right. A vitamin E marker was placed along the right upper outer breast. Postbiopsy hematoma is noted in the 9 o'clock position with only thin peripheral enhancement around the cavity. In the 11 o'clock position, there is non-mass enhancement measuring 2.3 x 1.4 x 1.8 cm, which was subsequently biopsied under MRI guidance. MRI images from the biopsy were not submitted, however the MRI biopsy clip placement on 3/24/2015 mammogram is accurate for the findings on MRI.3/24/2015 DIAGNOSTIC RIGHT MAMMOGRAM:Two standard views of the right breast were provided. X shaped biopsy clip from stereotactic guided biopsy of cluster of calcifications with reported pathology of DCIS is located in the 9 o'clock position posterior depth. Previously seen post biopsy change have resolved. No residual calcifications are noted. Trimark clip from MRI guided biopsy is located in the 11 o'clock position with reported benign results. Postbiopsy change including foci of gas and small hematoma are noted.

Output: 1.Right 9 o'clock 5 mm cluster of calcifications with reported biopsy results of DCIS after stereotactic guided biopsy. X-shaped clip with no residual calcifications are visualized on subsequent mammogram. 2.Right 11 o'clock non-mass enhancement with reported benign biopsy results after MRI guided biopsy. Trimark clip is visualized on subsequent mammogram. Benign pathology is concordant. 3.No mammographic or MRI abnormality in the left breast.4.No abnormal lymph nodes.5.Recommend submission of outside pathology materials and surgical consultation.BIRADS: 6 - Known cancer.RECOMMENDATION: T - Take Appropriate Action - No Letter.


Instruction: Generate impression based on medical findings.

Input: Low back pain for 3 years. Hyperextension. Evaluate for spondylolysis. There is no spondylolisthesis. The vertebral bone marrow signal is unremarkable, without discernible edema or sclerosis involving the pars interarticularis at any of the lumbar spine levels. There are unchanged mild disc bulges in the lumbar spine at L3-4, L4-5, and L5-S1 with slight encroachment upon the bilateral neural foramina, but no significant spinal canal stenosis. There is no fatty filum or dysraphism. The spinal cord displays normal signal and morphology. The paravertebral soft tissues are unremarkable.

Output: 1. No definite evidence of spondylolysis, within the limits of MRI.2. Unchanged mild disc bulges at L3-4, L4-5, and L5-S1, with mild bilateral L5-S1 neural foramen stenosis, but no significant spinal canal stenosis. I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on medical findings.

Input: Headache with associated diplopia, evaluating for evidence of increased intracranial pressure. 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, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

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


Instruction: Generate impression based on medical findings.

Input: Diagnosis: Unspecified disorder of vestibular function, unspecified earClinical question: enhancing lesions in the brainSigns and Symptoms: severe vertigo and unusual looking 2 spots in the brain. History of autoimmune disease MRI brain:The CSF spaces are appropriate for the patient's stated age with no midline shift. No abnormal enhancing mass lesions are appreciated intracranially. No intracranial hemorrhage is identified. No edema is identified 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. These are asymmetric towards the right hemisphere versus the left. Compared to the prior exam these have not changed.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.Cervical Spine:The cervical vertebral bodies are appropriate in overall alignment and height. The cervical spinal cord has normal signal characteristics and overall morphology. No abnormal enhancing lesions are identified in the cervical spine. The exam is mildly degraded by patient motion which may obscure more subtle abnormalities.At C2-3 there is no significant compromise to the spinal canal or neural foramina.At C3-4 there is no significant compromise to the spinal canal or neural foramina.At C4-5 there is no significant compromise to the spinal canal or neural foramina. At C5-6 there is no significant compromise to the spinal canal or neural foramina. There is mild disc desiccation and a minor disc bulge at this level.At C6-7 there is no significant compromise to the spinal canal or neural foramina.At C7-T1 there is no significant compromise to the spinal canal or neural foramina.The vertebral artery flow voids appear to be intact.

Output: 1.There are several periventricular and subcortical white matter lesions present which are stable since the prior exam. These are nonspecific.2.The cervical spine exam is mildly degraded by patient motion which may obscure more subtle abnormalities. No cervical spinal cord lesions are appreciated.3.There are minimal degenerative changes present in the cervical spine.


Instruction: Generate impression based on medical findings.

Input: Ms. Hibbs is a 61 year old female with a personal history of left breast lumpectomy for breast cancer in 1997 followed by chemoradiation therapy. BRCA1 positive. Family history of breast cancer in sister and niece. There is scattered fibroglandular tissue in both breasts. Minimal parenchymal enhancement is noted bilaterally.Stable postsurgical changes are identified in the left lower breast, at site of prior lumpectomy. There is no abnormal enhancement seen in either breast. No abnormal axillary lymph nodes are identified in either axillary region.

Output: Stable postsurgical changes of the left breast. No MRI evidence for malignancy. BIRADS: 2 - Benign finding.RECOMMENDATION: ND - Routine Diagnostic Mammogram.


Instruction: Generate impression based on medical findings.

Input: Alteration of mental status. Evaluate for acute stroke. . Study is degraded by motion.There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma and pituitary gland appear unremarkable. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. There are very subtle nonspecific T2 hyperintensities, many in the posterior periventricular white matter, most likely related to chronic small vessel ischemic findings. There is prominence of the extra-axial space around the right cerebellum as compared to the contralateral side, with possible trace chronic subdural hygroma,The major cerebral flow voids are intact. The orbits, skull, and scalp soft tissues are grossly unremarkable. There is partial opacification of the right posterior ethmoid sinus.There is partially visualized degenerative changes in the cervical spine with probable spinal stenosis; however, not well evaluated.

Output: 1. Motion limited exam. No evidence of acute infarct.2. Mild chronic small vessel ischemic changes.3. Minimal asymmetric prominence of the extra-axial space around the right cerebellum, possibly representing a trace chronic subdural hygroma.4. Partially visualized degenerative changes in the cervical spine with possible spinal stenosis; however this is not well evaluated. Dedicated MRI of the cervical spine may be obtained as clinically indicated.


Instruction: Generate impression based on medical findings.

Input: Clinical question: 62-year-old female with SLL, history of subdural bleed with midline shift, now with hypertension and bradycardia, concern for elevated intracranial pressure. Signs and symptoms: Bradycardia, hypertension Non-infused CT of brain:Redemonstration of periventricular low attenuation in bifrontal lobes. In comparison to the prior examination there is suggestion of interval increase of this finding.Also new since prior examination is large area of low attenuation involving the left occipital lobe surrounding the occipital horn of left lateral ventricle. Also note is made of interval increase in the size of the supratentorial ventricles. There is no evidence of hemorrhage. I believe the above findings may represent transependymal exudate secondary to gradually increasing hydrocephalus. Further evaluation with an MRI is recommended to exclude other possibilities. There is no evidence of residual subdural. Small calcified meningioma along the left petroclinoid ligament is again identified.Images through posterior fossa suggests interval increase in the size of fourth ventricle as well.

Output: 1.Increased in size of all ventricular system since prior exam. 2.Increased in periventricular low attenuation is concerning for hydrocephalus and periventricular exudate of CSF.3.correlate with clinical history and if concerned an MRI is recommended.


Instruction: Generate impression based on medical findings.

Input: Male 60 years old Reason: eval for lesions, assess hepatic vessel patency History: cirrhosis, s/p OLT 10/94 ABDOMEN:LIVER, BILIARY TRACT: Liver has mildly widened fissures and and hypertrophy of the left hepatic lobe compatible with chronic liver disease.Hepatic artery and portal veins are patent. Hepatic veins are narrowed probably due to central fibrosis but remain patent. No suspicious hepatic lesions identified. Metallic artifact is noted in the right hepatic lobe that partially obscures the right hepatic lobe.Probable cyst in the left hepatic lobe near the dome.No significant intrahepatic biliary ductal dilatation. Common bile duct is normal in caliber.SPLEEN: Spleen is enlarged.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Bilateral renal cysts. No hydronephrosis.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: Small amount upper abdominal ascites.

Output: 1.Findings of chronic liver disease without suspicious hepatic lesion; patent hepatic vasculature.2.Biliary tree is normal in caliber.3.Findings suggestive of elevated portal pressures with mild upper abdominal ascites and splenomegaly.


Instruction: Generate impression based on medical findings.

Input: Male, 46 years old, ischemic stroke workup. Patient has aphasia, right arm hemiplegia and left-sided neglect. Status post embolectomy and recanalization of the left middle cerebral artery. There is diffusion restriction compatible with acute stroke in the left middle cerebral artery territory prominently affecting the left temporal lobe, basal ganglia, and minimally the insula. There are also small areas of acute infarct in the posterior left frontal and anterior parietal lobes, including the lateral post central gyrus. There is no evidence of hemorrhagic conversion. T2/FLAIR signal abnormality is associated with these regions. There is evidence of remote infarcts with small areas of encephalomalacia redemonstrated in the right frontal and occipital lobes. No significant mass effect or midline shift is present. There are no abnormal extra-axial fluid collections. Paranasal sinuses and mastoid air cells grossly clear.

Output: 1. Findings compatible with acute infarct in the left middle cerebral artery territory correlating with CTA findings of left middle cerebral artery occlusion. No evidence of hemorrhagic conversion.2. Small areas of encephalomalacia in the right frontal and occipital lobes likely related to remote ischemic events.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on medical findings.

Input: Clinical question: Pituitary adenoma. Signs and symptoms: Headache. Nonenhanced brain MRI:Negative diffusion weighted series.Examination demonstrate diffuse punctate foci of flair hyperintensity primarily in the subcortical and periventricular white matter of cerebral hemispheres consistent with chronic small vessel ischemic strokes of mild degree. Minimal similar signal changes are noted in basal ganglia and more extensively in the pons as well concerning for chronic microvascular ischemic changes.Tiny foci of flair hyperintensity in the cerebellar hemispheres consistent with prior ischemic strokes.There is a slight prominence of cortical sulci and cerebellar -- vermian folia.The signal void of major intracranial arterial branches are identified.The signal intensity of intracranial venous sinuses is within normal.Thin coronal T1 and T2-weighted images through the sella demonstrate a slight thickening along the left lateral aspect of pituitary gland with T2 hyperintensity suggestive of an adenoma. This finding results in subtle deviation of pituitary stalk to the right. There is no convincing evidence of extension of tumor into the cavernous sinus or basal cistern on this nonenhanced dedicated imaging. The finding measures approximately at 8.5 x 5.5-mm and coronal T2 weighted series 1301. Compared to prior exam from 2014 there is no convincing evidence of any appreciable interval change..

Output: 1.No acute intracranial process and negative diffusion weighted series.2.Findings of chronic small vessel ischemic strokes as detailed.3.Pituitary microadenoma on the left measuring approximately at 8.5 x 5.5-mm on this nonenhanced exam and without convincing evidence of interval change.


Instruction: Generate impression based on medical findings.

Input: Acute onset vertigo. Reduced visual acuity in the left eye after a motorcycle accident in 1999. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma and pituitary gland appear unremarkable. 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, paranasal sinuses, and scalp soft tissues are grossly unremarkable. The left globe is small and contains a deformed lens and possible retinal detachment.

Output: 1. No evidence of acute intracranial hemorrhage, mass, or acute infarct.2. Chronic post-traumatic changes in the left globe.