Instruction: Generate impression based on findings.

Input: Diagnosis: Other alteration of consciousnessClinical question: eval lumbar disc Five lumbar type vertebral bodies are presumed to be present. The patient is status post posterior fusion at L3-4, L4-5 and L5-S1 associated with bilateral pedicle screws at L3, L4, L5 and S1. Patient is status post laminectomies at L4 and L5. There is anterior wedging of the L3 vertebral body. The conus medullaris on sagittal imaging is grossly intact.At L5-S1 there is no significant compromise to spinal canal or neural foramina. There is loss of disc space height and a diffuse disc bulge at this level. There is partial effacement of the fat surrounding the exiting nerve roots within the neural foramina at this level.At L4-5 there is no significant compromise to spinal canal or neural foramina. There is loss of disc space height and a diffuse disc bulge at this level associated with effacement of the fat surrounding the exiting nerve roots within the neural foramina.At L3-4 there is no significant compromise to spinal canal or neural foramina.There is mild anterior subluxation of L3 and L4. There is ligamentum flavum hypertrophy present at this level as well as facet hypertrophy.At L2-3 there is a large left lateral recess disc extrusion present with disc material extending behind the L2 and L3 vertebral bodies and compressing the thecal sac and effacing spinal fluid surrounding the nerve roots of the cauda equina at this level. On sagittal imaging the disc extrusion measures approximately 26 x 11 mm sagittal dimensions. There is also a left far lateral disc protrusion at this level which displaces the left-sided exiting nerve root after it exits the neural foramen.At L1-2 there is no significant compromise to spinal canal or neural foramina.Examination is degraded by patient motion which may obscure more subtle abnormalities.There is atrophy of the left psoas muscle.

Output: 1.There is a large disc extrusion at L2-3 which create significant spinal stenosis.2.The patient is status post lower lumbar spine surgery as described above with posterior fusion and laminectomies3.The examination is degraded by patient motion which may obscure more subtle abnormalities. No T1 axial images were acquired because of patient's inability to tolerate further imaging


Instruction: Generate impression based on findings.

Input: 23-year-old male with preoperative planning for occipital lesion biopsy and questionable lymphoma. Redemonstrated is an intraparenchymal enhancing lesion in the left parietal lobe, measuring up to 28 x 24 x 26 mm in the anteroposterior, transverse, and craniocaudal dimensions, respectively. There is extensive surrounding vasogenic edema. There are no additional parenchymal lesions. There is local mass effect without midline shift or herniation. The ventricles are unchanged in appearance. The calvarium is intact. There is a retention cyst in the right maxillary sinus. There is also mild right mastoid air cell opacification. There are skin fiducial markers.

Output: Preoperative planning MRI demonstrates a left parietal mass that may represent lymphoma with surrounding vasogenic edema.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Syncope with nausea/vomiting and previous possible staring. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma, brainstem, and cerebellum appear unremarkable. The pituitary and pineal glands are not enlarged. 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 gross intracranial structural abnormality.


Instruction: Generate impression based on findings.

Input: Female 16 years old with knee pain and swelling, evaluate for ACL tear MENISCI: No significant abnormality noted.ARTICULAR CARTILAGE AND BONE: Increased T2 and decreased T1 signal along the posterior aspect of the lateral tibial plateau consistent with osseous contusion. No evidence of acute fracture.LIGAMENTS: Fiber discontinuity and increased signal on PD and T2 within the ACL compatible with a complete tear. The LCL complex, MCL, and PCL are intact.EXTENSOR MECHANISM: Increased signal on PD and T2 along the inferior patellar tendon at the insertion site of the tibial tuberosity compatible with a partial tear.ADDITIONAL

Output: 1. Complete ACL tear with a moderate joint effusion and osseous contusion of the posterolateral tibial plateau.2. Partial tear of inferior portion of the patellar tendon at the tibial tuberosity insertion site.


Instruction: Generate impression based on findings.

Input: New headache for 7 months There is no evidence of acute ischemic or hemorrhagic lesion on this scan.There is however about 10.5mmx9.8mmx15mm sized well circumscribed mass on the left parotid gland. The mass shows low signal intensity on T2, iso signal intensity with muscles on T1 with diffuse but more on peripheral enhancement on Gad infusion. On DWI and ADC map, the lesion shows restricted diffusion. These findings suggest possibility of benign neoplasm such as Warthin's tumor but a malignant lesion cannot be completely excluded thus, biopsy is recommended. The ventricles, sulci and cisterns are symmetric and unremarkable. There is no mass, mass effect, edema, midline shift, intra or extra-axial fluid collection/hemorrhage, restricted diffusion/acute ischemia, or abnormal contrast enhancement. The midline structures and cranial-cervical junction are normal. The paranasal sinuses and mastoid air cells are clear.3D time of flight MOTSA MRA brain images with maximum intensity projections of the anterior/posterior intracranial circulation demonstrate normal ICAs, MCAs and ACAs. Vertebrobasilar system appears to be normal. Bilateral Pcom arteries and Acom artery are patent.There is no intracranial arterial aneurysm or arterial luminal narrowing or irregularity.

Output: 1. 10.5mmx9.8mmx15mm sized left parotid gland mass. Diagnostic possibility includes Warthin's tumor but needs to exclude malignant lesion, thus consider biopsy.2. No evidence of acute ischemic or hemorrhagic lesion. No mass.3. Normal intracranial MRA.


Instruction: Generate impression based on findings.

Input: Clinical question: Evaluate for progression of atrophy and information weight NMO. Signs and symptoms: NMO with paraplegia, worsening weakness. Pre-and post-enhanced cervical MRI:Examination redemonstrates patchy foci of T2 and T2 stir hyperintensity throughout cervical cord and with resultant decreased cord caliber/atrophy (most noticeably at C2 level) without appreciable significant change since prior exam from 2013. Examination however is degraded due to motion artifact which precludes precise comparison. Post-enhanced images also fail to demonstrate any convincing evidence of an abnormal foci cord or leptomeningeal enhancement.There is normal signal intensity and the alignment of the vertebral column and without evidence of spinal canal or neural foraminal compromise or stenosis.Pre-and post-enhanced thoracic MRI:This examination is also mildly compromised due to motion artifact. Within this limitation examination redemonstrates previously known extensive atrophic changes of thoracic cord secondary to NMO. There is a new focus of T2 hyperintensity and with resultant decreased cord caliber anteriorly on the right at T9 -- T10 disk level (axial T2 series 1502 images 18 through 20. There is no convincing evidence of enhancement of this new however chronic lesion.Additionally a new focus of T2 hyperintensity in the posterior left lateral aspect of the cord at the level of T10 lower endplate (axial T2 series 1502 image 15) without detectable change in the caliber of the cord. There is enhancement or an artifact of this finding on sagittal T1 post enhanced series 1801 image 8. The enhancement however cannot be confirmed on axial post enhanced series.The signal intensity and alignment of the tubercle is within normal and without detectable spinal canal or neural foraminal compromise/stenosis.

Output: 1.Suboptimal pre-and post enhanced MRI of cervical spine demonstrate atrophic changes of cervical cord more noticeable at C2 level and without convincing evidence of any new lesion or detectable abnormal enhancement.2.Pre-and post enhanced MRI of thoracic spine demonstrate extensive atrophic changes of the thoracic cord secondary to patient's known NMO. New since prior exam is a small focus of T2 hyperintensity and decreased cord caliber at T9 -- T10 disk level without detectable abnormal enhancement. Additional focus of T2 hyperintensity in the posterior left lateral aspect of the cord at the level of inferior endplate of T10 without change in the caliber of the cord or definitive evidence of enhancement as detailed.


Instruction: Generate impression based on findings.

Input: 65-year-old male with pain and weakness. Evaluate for biceps tendon rupture versus brachialis rupture. LIGAMENTS: No significant abnormality noted.TENDONS: There is increased signal abnormality and thickening of the distal biceps brachii tendon just proximal to its insertion on the bicipital tuberosity consistent with tendinopathy. There is circumferential fluid signal abnormality about the distal biceps tendon and within the bicipitoradial bursa consistent with a bursitis.ARTICULAR SURFACES AND BONE: No bone marrow signal abnormality is identified. Mild degenerative changes affect the elbow. No articular cartilage defects are identified.SURROUNDING STRUCTURES: No significant abnormality noted.ADDITIONAL

Output: Findings consistent with biceps brachii tendinopathy and bicipitoradial bursitis without evidence of tendon rupture, as clinically questioned.


Instruction: Generate impression based on findings.

Input: Male, 68 years old, with history of CML in blast phase, now in remission, asymptomatic, with new dural thickening seen on sinus CT. A thin subdural collection is evident along nearly the entirety of the right cerebral hemisphere and to a lesser degree along the left frontal lobe demonstrating heterogeneous T1 hyperintensity, T2 hypointensity and susceptibility effect compatible with hemorrhage. The collection measures at most up to 5 mm in thickness and exerts mild regional mass effect with slight effacement of the adjacent sulci, and mild generalized mass effect with approximately 4 mm midline shift to the left.There may be minimal associated dural enhancement, likely reactive to the hemorrhage, but this is difficult to discern from the intrinsic T1 hyperintensity of the collection. No evidence to suggest an infiltrative dural process is seen.Minimal scattered ill-defined T2 hyperintense foci are seen within the bilateral cerebral hemispheres, a nonspecific finding. No evidence of restricted diffusion is seen. No pathologic parenchymal enhancement or parenchymal edema is suspected. The ventricles are within normal limits for size, though the right lateral ventricle is slightly smaller than the left at the level of the atria which could represent the mild generalized mass effect indicated above.Marrow signal of the calvarium is mildly heterogeneous which can be seen in anemia and chronic disease in general. No aggressive appearing or frankly destructive osseous lesions are demonstrated.

Output: A thin holohemispheric subdural hematoma is evident along the right cerebrum, with a small subdural hematoma also seen along the left frontal lobe. At most, the right-sided collection measures up to 5 mm in thickness, inducing mild regional and generalized mass effect.


Instruction: Generate impression based on findings.

Input: Female, 74 years old, with history of aneurysm of the anterior communicating artery status post clipping with worsening memory complaints. Artifact from the patient's ACOM region aneurysm clip is again seen. Mild signal abnormality and encephalomalacia affecting the left anterior temporal lobe, the orbital gyrus and gyrus rectus are unchanged. Scattered additional foci of nonspecific parenchymal FLAIR hyperintensity are unchanged. No edema or mass effect is seen. No diffusion restricting lesions are detected. There is no evidence to suggest acute intracranial hemorrhage or any abnormal extra-axial fluid collection. A focus of susceptibility in the inferior right frontal lobe is unchanged and likely represents chronic microhemorrhage. Ventricular size and morphology are within normal limits. The right central sulcus and postcentral sulcus are more prominent than the left, but this finding is stable. Elsewhere, brain parenchymal volume is preserved.

Output: 1.Sequelae of prior surgery for aneurysm clipping are redemonstrated.2.Scattered foci of signal abnormality are unchanged.3.No new or acute findings are seen which would account for the patient's symptoms.


Instruction: Generate impression based on findings.

Input: 25-year-old female with family history of breast cancer. There is extreme amount of fibroglandular tissue in both breasts.Marked parenchymal enhancement is noted bilaterally.No abnormal enhancement is seen in either breast. No abnormal axillary lymph nodes are identified in either axillary region.

Output: No MRI evidence for malignancy. BIRADS: 1 - Negative.RECOMMENDATION: NS - Routine Screening Mammogram.


Instruction: Generate impression based on findings.

Input: Clinical question: Status post lumbar decompression with fusion. Assess for spine stability and assess for postop bleeding. Signs and symptoms: Back pain. Nonenhanced CT of lumbar spine:Routine non-infused axial 3-mm CT images of the entire lumbar spine were obtained. Sagittal and coronal 2-D reformatted images were also acquired.Examination again demonstrates with no interval change extensive patchy sclerotic changes of the L5 vertebral body which extends into the bilateral pedicles.There is also evidence of mild compression fracture of L5 with slight bulge into the spinal canal similar to prior study.There is evidence of interval bilateral laminectomies at this level for spinal decompression. There is a drainage catheter extending from the canal at this level on the left (likely within the left epidural space) extending posteriorly and exiting the canal on the right side of the spinous process of L4.The alignment of vertebral column is similar to prior study an unremarkable.There is evidence of posterior fusion with placement of fixating rods extending from L4 to S1 and bilateral transpedicular screw placement in L4 and S1. There is no evidence of any detectable hardware abnormalities. There is extensive soft tissue thickening and and soft tissue emphysema posterior to the spinal canal in the soft tissues of lower back which appears to be within the expected range of. Findings. There is no detectable perispinal or prevertebral soft tissue abnormality or hemorrhage. Soft tissue densities there is thickening of the epidural space at the L4 level and suspected central spinal stenosis of approximately 6.5 mm. Follow-up with an MRI examination is recommended.

Output: 1.Stable patchy sclerotic changes of L4 vertebrae which extends into bilateral pedicles. There is also mild compression fracture of L4 similar to prior study. No appreciable interval change since prior study. Findings is suspected for a metastatic focus.2.Interval bilateral laminectomies at L4 vertebrae for decompression of the spinal canal. There is thickening of the lateral epidural spaces at L4 level contiguous with extensive increased soft tissue density posterior to the laminectomy site. This finding results in suspected central spinal stenosis at this level. Recommend further follow-up with an MRI to exclude hemorrhage.3.The alignment of vertebral column is unremarkable and stable since prior study.4.Postoperative changes of posterior fusion and bilateral transpedicular screw placement at L4 and S1 levels. No hardware abnormality.5.A drainage catheter extends from the right lateral epidural space at the L4 level posteriorly and exits the spinal canal as described above.


Instruction: Generate impression based on findings.

Input: Female 62 years old Reason: 62 yo female with hx of cystic mass in the head and body of pancreas; please evaluate for changed and or abnormalities History: pancreas mass ABDOMEN:LIVER, BILIARY TRACT: No intra or extrahepatic biliary ductal dilatation. No focal liver lesion.SPLEEN: No significant abnormality noted.PANCREAS: Unilocular cystic lesion is again seen in the pancreatic body which measures 1.2 x 0.9 cm (series 3, image 30), previously 1.1 x 0.9 cm. This appears to communicate with the main pancreatic duct. Additional subcentimeter cystic lesions are noted in the distal body and tail, best seen on series 3 which are unchanged. There is no abnormal enhancement within these lesions. There is no pancreatic duct dilatation. Patent hepatic vasculature.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Stable left upper pole renal cyst.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.

Output: 1.Stable cystic lesions in the pancreatic body and tail, likely IPMNs.


Instruction: Generate impression based on findings.

Input: Elevated PSA. Per an EPIC note the patient has newly diagnosed Gleason 6 cancer single core. TRUS-prostate biopsy pathology 2/9/16:L base: benignL mid: benignL apex Focal ASAPL lat base: No specimen presentL lat mid: benignL lat apex: prostate adenocarcinoma Gl 3+3=6, 20% of specimen, involving 2 of 3 core segments, with cores measuring 2, 5, and 9 mmR base: benignR mid: benignR apex: benignR lat base: benignR lat mid: benignR lat apex benign PELVIS:PROSTATE:Prostate Size: 3.3 x 4.4 x 3.1 cmPeripheral Zone: The peripheral zone is diffusely heterogeneously low on T2-weighted imaging with linear bands of low signal, likely representing diffuse prostatitis changes. This limits evaluation for underlying lesions.No dominant lesion is identified.Central Gland: The intra-prostatic proximal urethra is prominent without significant nodularity of the transition zone.Seminal Vesicles: No evidence of seminal vesicle invasion.Extracapsular Extension: No evidence of extracapsular extension.BLADDER: No significant abnormality noted.LYMPH NODES: Multiple prominent pelvic lymph nodes are nonspecific in the setting of sarcoidosis.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: 1.Evaluation is limited due to diffuse T2-weighted signal hypointensity in the peripheral zone which may be related to prostatitis. No superimposed dominant lesion is identified.2.Multiple prominent pelvic lymph nodes are nonspecific setting of sarcoidosis.


Instruction: Generate impression based on findings.

Input: 60 year-old female with pain and bloating. ABDOMEN:LUNG BASES: No significant abnormality notedLIVER, BILIARY TRACT: No significant abnormality notedSPLEEN: No significant abnormality notedPANCREAS: No significant abnormality notedADRENAL GLANDS: No significant abnormality notedKIDNEYS, URETERS: 11-mm lesion in the medial aspect of the right upper pole with peripheral, eccentric enhancement is suspicious for a small renal cell carcinoma. Further evaluation with a dedicated renal protocol CT or MRI is recommended.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality notedOTHER: No significant abnormality notedPELVIS:UTERUS, ADNEXA: Large pelvic mass with solid and cystic components measuring 17 x 11 cm on image number 105, series number 3. This lesion likely arises from the left ovary. Right ovary cannot be differentiated from the large mass but is likely seen on image number 122 of series number 3 and slightly enlarged. Ovarian torsion cannot the exclude by imaging.BLADDER: No significant abnormality notedLYMPH NODES: No significant abnormality notedBOWEL, MESENTERY: No significant abnormality notedBONES, SOFT TISSUES: No significant abnormality notedOTHER: No significant abnormality noted

Output: Large pelvic mass likely arising from the left ovary suspicious for a malignant ovarian neoplasm. Superimposed torsion cannot be excluded.Small right renal lesion with eccentric enhancement suspicious for renal cell carcinoma. Further evaluation with dedicated kidney protocol CT or MRI is recommended.


Instruction: Generate impression based on findings.

Input: Clinical question: PLEASE INCLUDE SI JOINTS., s/p Left hip arthroscopy, labral repair 8/26/14, continued low back SI joint pain, has had 2 SI joint injections without relief. Evaluate SI joints and evaluate for disc injury. Pain is on left sideSigns and Symptoms: Continued left side hip, SI joint pain. Nonenhanced lumbar MRI:There is normal anatomical alignment of vertebral column.The signal intensity of vertebral column is unremarkable changes secondary to discogenic disease.Unremarkable medial and most visualized thoracic spine and thoracic cord from T10 inferiorly.T12-L1 is unremarkable.L1-L2 demonstrates advanced disc disease and significant loss of disc height, there is shallow ventral disc osteophyte with resultant partial effacement of subarachnoid space however without central spinal stenosis. There is also no evidence of neural foraminal compromise.L2-L3 is unremarkable.L3-L4 is unremarkable.L4-L5 demonstrate mild degenerative changes without spinal stenosis or neural foraminal compromise.L4-L5 demonstrate mild disc disease and loss of disc height, mild bilateral ligamentum flavum and facet hypertrophic changes. No spinal stenosis or neural foraminal compromise. There is a linear T2 increased signal intensity within the annulus of the disc in the midline and consistent with an annular fissure.There is a shallow broad-based disc protrusion with resultant effacement of ventral subarachnoid space and without detectable mass effect on the thecal sac.L5-S1 demonstrate mild disc disease and loss of disc height, mild bilateral (L>R) facet and ligamentum flavum hypertrophy. No evidence of a spinal stenosis or neural foraminal compromise.Sacral spine demonstrate a left sided CSF signal intensity expansile lesion proximal left S2 neural foramina which a benign Tarlov cyst or perineural cyst. This finding demonstrate mass effect on the left S1 nerve root and its resultant flattening deformity which is best appreciated on axial T2 series 701 on images 2 through 4.Perispinal soft tissues demonstrate a smaller left psoas muscle compared to right and suspected of mild atrophy.Visualized SI joints demonstrate no appreciable degenerative changes or signal abnormality. On the left there is a well demarcated and primarily fatty signal intensity lesion measuring approximately 11 x 14 mm in transaxial dimensions. The finding is contiguous with the SI joint and medial well-demarcated cortical rim and is not associated with any adjacent marrow signal changes or soft tissue mass. Finding is consistent with benign fatty deposit and possibility of a benign hemangioma should also be considered. The clinical significance of this finding is questionable. This finding was also present on prior lumbar MRI exam without additional change.

Output: 1.Nonenhanced MRI of the lumbar spine demonstrate degenerative changes without evidence of central spinal stenosis or clinically significant neural foraminal compromise as detailed above. Small central disc protrusion at L5-S1 without mass effect on the thecal sac. Perineural cyst on the left at S2 neural foramina with resultant expansion of foramina and mass effect / flattening of left S2 nerve root. 2.Unremarkable SI joints. Fatty signal intensity lesion inseparable from the left SI joint space could represent benign fatty deposit or a benign hemangioma as detailed above..


Instruction: Generate impression based on findings.

Input: 33-year-old male status post right knee arthroscopy, chondroplasty of a patellar chondral lesion, as well as a DeNovo NT procedure in the right knee trochlea. Now presenting with persistent knee pain. MENISCI: There is mild intrasubstance degeneration of the menisci, but no discrete tears are identified.ARTICULAR CARTILAGE AND BONE: There is full thickness degeneration and marked fraying of the articular cartilage of the medial facet of the patella, which appears progressed from the prior study. There is a full-thickness cleft within the articular cartilage just lateral to the median eminence of the patella with additional fraying of the articular cartilage of the patella centrally.Full-thickness central trochlear defects seen on the prior study have been replaced with heterogeneous signal intensity, presumably the site of prior microfracture, likely reflecting new cartilage formation, which is either immature or degenerated, based on the signal characteristics. There is a near full-thickness cleft within the articular cartilage along the inferior margin of this heterogeneous signal, best seen on the sagittal images. There is a near full-thickness cleft traversing the articular cartilage of the lateral trochlear facet with what appears to be delamination of the articular cartilage from the underlying bone. There is mild increased signal within the underlying bone consistent with edema, which is likely degenerative in etiology.There is a new near full-thickness to full-thickness defect of the articular cartilage of the medial femoral condyle, measuring just under one cm in AP dimension, just above the posterior horn of medial meniscus with heterogeneous signal of the adjacent articular cartilage posteriorly, suggesting degeneration. There is also what appears to be thinning of the articular cartilage of the lateral femoral condyle above the anterior horn of the lateral meniscus, but this may be artifactual.LIGAMENTS: The anterior cruciate and posterior cruciate ligaments are intact, as are the medial collateral and lateral collateral ligament complexes.EXTENSOR MECHANISM: The extensor mechanism is intact.ADDITIONAL

Output: Findings of trochlear microfracture, but with overall progression of cartilage degeneration in the patellofemoral and medial tibiofemoral compartments as described above.


Instruction: Generate impression based on findings.

Input: Ms. Mitchell is a 48 year old female with a personal history of right breast mastectomy in 2008 for multifocal IDC and prophylactic left breast mastectomy in 2009. Patient now has bilateral gel implants with capsular irregularity. Bilateral silicone implants are identified. There is no evidence of intra- or extra-capsular rupture of these implants.No abnormal enhancement is seen in either reconstructed breast. No abnormal axillary lymph nodes are identified in either axillary region.

Output: No MRI evidence for malignancy. No MRI evidence of capsular rupture.BIRADS: 1 - Negative.RECOMMENDATION: T - Take Appropriate Action - No Letter.


Instruction: Generate impression based on findings.

Input: Patient status post patellar tendon repair and possible lateral meniscectomy versus repair. Pain MENISCI: Marked globular signal largely in the body extending into the posterior horn of the lateral meniscus with associated suspected surgical re-shaping of the inner edge. No discrete definite linear components. The medial meniscus is otherwise intact.ARTICULAR CARTILAGE AND BONE: Cartilaginous and associated marrow otherwise unremarkableLIGAMENTS: The ACL is torn with the proximal fibers extending and partially adherent to the PCL. PCL is grossly tacked although mildly redundant. The MCL and LCL are otherwise intactEXTENSOR MECHANISM: The extensor complex extending to the superior patella appears unremarkable, however the patellar tendon is markedly thickened and demonstrates abnormal internal signal with internal intrasubstance tearing of the more superficial fibers, however the deeper and less superficial aspect and fibers are otherwise intact.ADDITIONAL

Output: Complete ACL and partial patellar tendon tears with associated suspected globular degeneration in possibly surgically revised lateral meniscus; see detail provided.


Instruction: Generate impression based on findings.

Input: 42-year-old female with newly diagnosed triple negative left breast cancer There is heterogeneous amount of fibroglandular tissue in both breasts.Mild parenchymal enhancement is noted bilaterally.A heterogeneously enhancing mass with central nonenhancing component at 11:00 in the left far posterior corresponding to the patient's known cancer measures 20 x 18 x 21 mm (AP x transverse x CC). There is associated clip artifact within the mass and the enhancement kinetics demonstrate rapid uptake and washout. The mass is situated 5 mm from the prepectoral fascia without visualized extension of abnormal enhancement into the chest wall. No additional suspicious enhancing lesions are identified in either breast.There are multiple bilateral simple and proteinaceous cysts, left greater than right, some with rim enhancement.Normal morphology lymph nodes are identified in the left axillary region.

Output: Unifocal left breast cancer with measurements provided above.BIRADS: 6 - Known cancer.RECOMMENDATION: T - Take Appropriate Action - No Letter.


Instruction: Generate impression based on findings.

Input: Male, 20 years old, with low back pain, wrestler. Assess for disk injury or spondylolysis. Spinal alignment is within normal limits. Vertebral body heights are maintained. Bone marrow signal intensity is within normal limits. Small scattered Schmorl's nodes are seen without evidence of edema. No findings to suggest spondylolysis are evident.The visualized spinal cord, conus and cauda equina demonstrate normal signal intensity and morphology. A small central/right paracentral disk protrusion is present at L5-S1 with slight loss of disk height posteriorly. No significant spinal canal or neuroforaminal stenosis is seen at this level. There is no evidence of nerve root impingement.Elsewhere, no significant disk herniation, spinal canal or neuroforaminal stenosis is seen. Mild to moderate facet hypertrophy becomes evident at lower lumbar levels.

Output: Small disk herniation at L5-S1 without nerve impingement, spinal canal stenosis, or neuroforaminal narrowing.


Instruction: Generate impression based on findings.

Input: Reason: large uterine fibroids History: uterine fibroids PELVIS:UTERUS, ADNEXA: There is a large intramural fibroid along the posterior wall of the uterus measuring 11.6 x 12.8 cm in transverse dimension and 13.7 cm in craniocaudal dimension (1201/22, 801/19). There is significant mass effect with displacement of the uterus anteriorly and extension into the presacral space. There is significant enhancement on postcontrast images. The lesion is heterogeneously T2 hyperintense, suggesting degeneration.BLADDER: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: 1.2 x 0.7 cm Bartholin's gland cyst is present on the left. Diffuse disc bulges at L4-L5 and L5-S1. OTHER: No significant abnormality noted.

Output: Large avidly enhancing intramural fibroid measuring up to 13.7 cm.


Instruction: Generate impression based on findings.

Input: Again seen are remote postoperative findings related to prior laminectomies at T8 to T12. Again seen is displacement of the thoracic cord anteriorly at T8 to T11-T12 disk space. There are septations within the thecal sac with suggestion of posterior arachnoid cyst in this region. There is severely diminished caliber of the lower thoracic cord with linear low T2 signal abnormality at T9 and mid T11 where the cord caliber is markedly thinned (up to 3 mm) and abuts the ventral surface of the spinal canal. Conus is not clearly demarcated given the extent distal cord myelomalacia and clumping of the cauda equina nerve roots. Appearance is unchanged. No thoracic syrinx. There is normal alignment of the thoracic spine with a benign homogeneous osseous marrow signal. Small central disk protrusion at T9-T10 and mild disk bulges at T10-T11 and T11-T12 are noted. Findings are not significantly changed from prior study. Prone images demonstrate mild anterior motion of the mid thoracic cord. No significant change is seen in the anterior positioning of the lower thoracic cord at T9-T10 and T10-T11 as well as the proximal cauda equina nerve roots at T11-T12, which may be dorsally tethered.

Output: Again seen is evidence of intradural septations in the lower thoracic spinal canal and formation of arachnoid cysts. The severely myelomalacic lower thoracic cord appears plastered anteriorly to the ventral dural margin from T9-T10 to T10-T11 which may be related to the posterior arachnoid cyst or ventral scarring. Ventral transdural herniation not excluded. More inferiorly, the clumped upper cauda equina nerve roots at T11-T12 approximate the dorsal dural surface and do not demonstrate anterior motion on the prone sequence suggesting tethering. Overall no significant change since 12/20/2014.


Instruction: Generate impression based on findings.

Input: 67-year-old male with elevated PSA. PELVIS:PROSTATE:Prostate Size: 4 x 5.3 x 4.3 cm.Peripheral Zone: 6 mm focus of low T2 signal with restricted diffusion at the right apex posteriorly, suspicious for prostate cancer (series 801/12). 7 mm focus of low T2 signal with restricted diffusion at the right base posteriorly, suspicious for prostate cancer (series 801/20). Mild diffuse thinning of the left peripheral zone with patchy low T2 signal, suggestive of prior inflammation.Central Gland: Heterogeneous.Seminal Vesicles: No significant abnormality noted.Extracapsular Extension: None.BLADDER: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: Penile implant, partially visualized, with intrapelvic reservoir.

Output: Findings suspicious for multifocal right-sided prostate cancer without evidence of extracapsular extension.


Instruction: Generate impression based on findings.

Input: Headaches, worse over the past 4 months. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is a punctate focus of T2 hyperintensity in the right parietal lobe subcortical white matter. The brain and cerebellar parenchyma otherwise appear unremarkable. The ventricles and basal cisterns are normal in size and configuration. There is flattening of the pituitary gland. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: 1.Flattening of the pituitary is nonspecific, but could potentially be a manifestation of pseudotumor cerebri, although no other stigmata of this are evident.2.Nonspecific focus of T2 hyperintensity in the right parietal subcortical white matter, but no evidence of acute intracranial hemorrhage, mass, or acute infarct. I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Patient with lower tibial pain anteriorly. Check for stress fracture The left lower leg appears completely unremarkable and without abnormality. Particular attention was placed in the lower third adjacent to the placed markers. A normal-appearing vascular supply is identified in this area without abnormal underlying marrow signal or cortical bone findings. Superficial soft tissues and surrounding muscular compartments are all unremarkable.

Output: Normal exam


Instruction: Generate impression based on findings.

Input: Diagnosis: Migraine with aura, not intractable, without status migrainosusClinical question: vertiginous migrainesSigns and Symptoms: blurred visions, headache, dizziness 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.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.Incidental note is made of an arachnoid granulation in the right transverse sinus. The right transverse sinus and sigmoid sinus are dominant.

Output: MRI of the brain is within normal limits. There is no evidence for intracranial mass lesion or other explanation for the patient's headaches on the basis of this MRI exam..


Instruction: Generate impression based on findings.

Input: 65-year-old male, sore and thickened. Suspected partial complete left acute Achilles tendon. TENDONS: There is marked thickening of the Achilles tendon, most pronounced approximately 5 cm proximal to its insertion on the calcaneus tuberosity with associated intrasubstance intermediate signal intensity on T1, STIR and T2-weighted images coursing longitudinally along the tendinous fibers most compatible with a longitudinal split tear with internal fluid; there is no transverse component. There is mild edema within the peritendinous region. The remaining tendons of the ankle are intact.LIGAMENTS: No significant abnormality noted.ARTICULAR SURFACES AND BONE: Oval/round structure within the posterior process of the talus which demonstrates low signal intensity on T1 and right signal on T2-weighted images most compatible with a small cyst. Otherwise no significant abnormalities noted.ADDITIONAL

Output: Findings are most compatible with a longitudinal split tear of the Achilles tendon with internal fluid. There is associated mild peritendinous edema.


Instruction: Generate impression based on findings.

Input: 69 year old male patient with a pancreatic mass. Evaluate for changes and/or abnormalities. ABDOMEN:LIVER, BILIARY TRACT: No focal hepatic lesion is identified. The common bile duct is prominent in size. There is mild intrahepatic biliary ductal dilatation. SPLEEN: No significant abnormality noted.PANCREAS: The main pancreatic duct is dilated, measuring up to 6 mm in diameter. There is a lobulated cystic lesion within the pancreatic head measuring approximately 2.3 x 1.8 cm (image 31, series 9), previously 2.3 x 1.8 cm when measured similarly. This lesion appears to be contiguous with the main pancreatic duct. There is no appreciable internal enhancement. ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: Grossly stable appearance of a cystic lesion within the pancreatic head without appreciable enhancement and with communication with the main pancreatic duct; this may represent a combined type IPMN.


Instruction: Generate impression based on findings.

Input: Odynophagia, weight loss. History of neutropenia; evaluate for sinus infection. Sinus CT :Polypoid mucosal thickening is seen in left maxillary sinus. No air fluid level is seen.Neck CT:There is poor contrast opacification which may limit the sensitivity of the study.There are large CSF density lesions in bilateral middle cranial fossa, which may represent arachnoid cysts. There is compression of the adjacent brain parenchyma in the temporal lobes. Further correlation with MRI brain should be considered.No obvious mass or adenopathy based on size criteria is seen in the neck. There is subtle asymmetric thickening of the right aryepiglottic fold of uncertain clinical significance. No obvious mass is seen.There is mild thickening of the esophagus, but this can be secondary to lack of distention.Atherosclerotic changes are seen in the carotid arteries.The right submandibular gland is atrophic.There is severe degenerative disease of the cervical spine. There is anterolisthesis of C2 on C3 and C3 on C4. Disk osteophyte complexes and degenerative disease of the uncovertebral joints and facet joints are seen in multiple levels, resulting in spinal canal and neuroforaminal stenosis, with mild impingement of the spinal cord, and nerve roots.

Output: 1. Polypoid mucosal thickening in the left maxillary sinus.2. Subtle asymmetric thickening of the right aryepiglottic fold of uncertain clinical significance. No obvious mass is seen. Please also correlate with clinical examination.3. Mild thickening of the esophagus may be related to lack of distention. If patient's symptoms persist, barium swallowing study or endoscopic examination of the esophagus should be considered. 4. Large arachnoid cysts in bilateral middle cranial fossa, causing compression of the brain parenchyma. Further evaluation with MRI brain should be considered.5. Severe degenerative disease of cervical spine, with listhesis at multiple levels. There is spinal canal and neuroforaminal stenosis at multiple levels.


Instruction: Generate impression based on findings.

Input: Meningioma. There are postoperative findings related to right frontotemporal craniotomy. There is slight interval increase in size of the extra-axial avidly enhancing tumors along the right frontotemporal convexity, which now measures up to 17 mm in thickness, previously 15 mm. There is also increase in the extent of confluent white matter T2 hyperintensity in the brain parenchyma adjacent to the tumors. There are scattered punctate foci of cerebral white matter T2 hyperintensity, which are not specific. There is a punctate focus of encephalomalacia in the left caudate head. 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. There are bilateral lens implants. There is a right maxillary sinus retention cyst.

Output: Postoperative findings related to right frontotemporal craniotomy with slight interval increase in size of the meningiomas along the right frontotemporal convexity and associated vasogenic edema.


Instruction: Generate impression based on findings.

Input: Back pain, history of psoriasis BONE MARROW: Diffuse intermediate signal on T1 sequence is seen throughout the pelvis and lower lumbar spine.SOFT TISSUES: No significant abnormality noted. JOINTS: No significant abnormality noted.ADDITIONAL

Output: Normal appearance of the sacroiliac joints. Diffuse intermediate signal of the osseous pelvis and lumbar spine likely relate to hematopoetic marrow reconversion.


Instruction: Generate impression based on findings.

Input: 73-year-old male with history of bladder cancer status post cystectomy ABDOMEN:LIVER, BILIARY TRACT: Common bile duct is dilated to the level of the ampulla and may represent mild stricturing, likely benign. Status post cholecystectomy.SPLEEN: Unchanged accessory splenule is noted.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: T2 hyperintense cysts are noted bilaterally. No hydronephrosis or perinephric inflammation.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: Right lower quadrant ileal conduit. A parastomal hernia containing a loop of bowel is noted. Small bowel caliber is within normal limits without evidence of obstruction. BONES, SOFT TISSUES: No significant abnormality noted.

Output: 1.No evidence of tumor recurrence or metastatic disease in the abdomen or pelvis.


Instruction: Generate impression based on findings.

Input: The last well formed disk space is referred to as L5-S1. Marrow signal is benign. There is no spondylolisthesis. There is loss of T2 signal in the L5-S1 disk. The conus terminates at L2 and shows normal caliber and signal. There are tiny hepatic T2 hyperintensity foci likely representing cysts.T11-12: No spinal stenosis.T12-L1: Mild disk bulge with no spinal stenosis.L1-2: No disk herniation or spinal stenosis.L2-3: No disk herniation or spinal stenosis. Mild ligamenta flava thickening and facet arthropathy.L3-4: Mild disk bulge, ligamenta flava thickening and facet arthropathy with no spinal stenosis.L4-5: Mild disk bulge, ligamenta flava thickening and facet arthropathy with no spinal canal stenosis and minimal left neural foraminal stenosis.L5-S1: Mild disk bulge, moderate ligament flava thickening and facet arthropathy causing no significant spinal canal stenosis and mild bilateral neural foraminal stenosis. Mild edema in the bilateral L5-S1 pedicles and facets with a small right L5-S1 facet effusion.

Output: Bilateral L5-S1 facet arthrosis with small right facet effusion, and reactive mild edema in the bilateral L5, and S1 pedicles and facets. Mild bilateral L5-S1 neural foraminal stenosis.


Instruction: Generate impression based on findings.

Input: Neck pain, history of NF type I. Craniovertebral junction appears within normal limits. The cervical vertebral bodies are appropriate in height. Alignment is maintained. Bone marrow signal is within normal limits. The cervical spinal cord has normal signal characteristics and overall morphology. No discrete masses within the spinal canal or neural foramina are appreciated within the limits of noncontrast study. There is developmental narrowing of the cervical spinal canal, particularly from C2-C3 to the C4-C5 levels. There is otherwise no significant spinal canal and neural foraminal stenosis. No significant disc bulge or herniation. There is a mildly T2/STIR hyperintense fusiform lesion in the retropharyngeal space along the ventral aspect of the prevertebral muscles on the right measuring up to 6 x 21 mm in the AP and transverse dimension and 3 cm in the craniocaudal dimension.

Output: 1. No discrete masses within the spinal canal or neural foramina are appreciated within the limits of noncontrast imaging.2. Fusiform lesion in the retropharyngeal space on the right at the C2 level is suspected to represent a neurofibroma. Postcontrast imaging can be considered for confirmation.3. Development of narrowing of the cervical spinal canal.


Instruction: Generate impression based on findings.

Input: Neoplasm of uncertain behavior of pituitary gland [D44.3] / Neoplasm of uncertain behavior of craniopharyngeal duct [D44.4], Reason for Study: ^Reason: yearly follow up on pituitary tumor- eval change History: yearly follow up Redemonstration of diffusely enhancing pituitary gland mass which shows homogeneous low signal intensity on T2 and low signal intensity on T1. The maximum diameter of the lesion appears to be slightly increased since prior scan [on postcontrast coronal scan, at the level of pituitary stalk, 20,5mm (CC) x 21.5mm (RL), was 18.3mm (CC) x 20.9mm (RL); on sagittal post contrast scan, 16.6mm (CC) x 22.4mm (AP) was 15.7mm].The pituitary stalk shows slightly deviated toward left side, unchanged since prior scan.Enhancing mass abuts mesial aspects of bilateral ICAs' cavernous sinus segment which is unchanged.The orbits and contents are unremarkable.  The ventricles, sulci and cisterns are symmetric and unremarkable.

Output: Subtle interval increase in size of enhancing pituitary mass as described above. Otherwise no remarkable changes since prior scan.


Instruction: Generate impression based on findings.

Input: Reason: 71 yo M hx of recurrent acute pancreatitis, OSH imaging shows calcifications in the pancreatic tail, and pseudocyst near the head of the pancreas. MRI/MRCP to assess pancreatic parenchyma, rule out small tumor, also eval pancreatic duct and emptying History: recurrent acute pancreatitis ABDOMEN:LIVER, BILIARY TRACT: No significant abnormality noted.SPLEEN: No significant abnormality noted.PANCREAS: 9 mm cystic lesion within the pancreatic body with additional cystic lesions, most prominent in the pancreatic head and tail. These most likely represent dilated side branches from chronic pancreatitis. The main pancreatic duct within the head, neck and body is nondilated.There is abrupt dilatation of the main pancreatic duct involving the distal 5 cm of the tail suggesting a focal stricture or obstructing lesion. Within the associated pancreatic tail, there is atrophy with low T1 signal and diffusion restriction, which may be associated with chronic obstruction and pancreatitis.There is overall loss of lobulations throughout the pancreas with a bulbous appearing uncinate.An appropriate response is present following secretin administration.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Bilateral renal cysts.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: Right chest wall lipoma measuring 0.3 cm (8/4).OTHER: No significant abnormality noted.

Output: 1.Focal stricturing of the main pancreatic duct within the pancreatic tail with associated ductal dilatation and findings suggestive of chronic pancreatitis. An obstructing lesion or stone is not visualized, however a lesion cannot be excluded at the site of obstruction. Recommend three-month follow-up MRCP if an endoscopic ultrasound is not planned.2.Loss of pancreatic lobulations and a bulbous appearing uncinate may be related to resolving pancreatitis or an autoimmune pancreatitis.


Instruction: Generate impression based on findings.

Input: Multiple sclerosis [G35], Reason for Study: ^Reason: eval for new MS lesions History: fever, chest pain, abd pain, hx MS Multifocal patch T2 high signal intensity lesions of cervical and thoracic spinal cord are consistent with demyelinating disease involvement such as multiple sclerosis.Mild loss of normal cervical lordosis with central to left focal disc protrusion at the level of C6-C7 as well as mild disc bulging of C4-5 level. At the level of C6-C7, there is a mild/moderate left lateral recess stenosis due to disc bulging.There is normal thoracic kyphosis.There is diffuse disc bulging at at the level of T6-7.There is no evidence of spinal canal stenosis at thoracic levels.The conus medullaris terminates at the level of L1. The spine alignment is anatomic. The vertebral body height is preserved. The bone marrow and end plates demonstrate a normal MR appearance. The paraspinal soft tissues and musculature are unremarkable.

Output: 1. Multifocal patchy T2 high signal intensity lesions mainly on cervical cord as well as thoracic cord indicating spinal cord involvement of demyelinating disease such as multiple sclerosis.2. Degenerative changes of cervical and thoracic spine are seen including central to left disc protrusion at the level of C67 and diffuse bulging of discs at the level of C45 and T67.


Instruction: Generate impression based on findings.

Input: Malignant neoplasm of connective and soft tissue, unspecified [C49.9] / Secondary malignant neoplasm of brain [C79.31] / Secondary malignant neoplasm of other parts of nervous system [C79.49] / Secondary malignant neoplasm of liver and intrahepatic bile duct. Significant motion artifacts especially for the postcontrast images. Since the comparison of the post contrast scans are essential part of the exam, the exam can be repeated at 3T scanner without additional charge if clinically indicated.There are multifocal fusiform enhancement of bilateral distal intracranial arteries indicating possible intracranial vasculitis. In particular, comparing to prior scan, there are interval decrease in enhancing lesions including bilateral distal ACA, left MCA M2, M3 and M4 branches, and right PCA indicating decreased inflammatory infiltration of distal arterial wall.Right inferior frontal sulcus T1 high signal intensity lesions may indicate intravascular thrombus or arterial wall thickening which do not show any significant interval change. Adjacent brain parenchymal FLAIR high signal intensities are again seen, unchanged since prior scan.Considering above findings, previously seen right posterior inferior temporal lobe focal encephalomalacia could come from prior rupture of PCA branch fusiform aneurysm. Again the extent of the encephalomalacia is unchanged but less enhancement. There is no evidence of acute ischemic or hemorrhagic lesion on this scan. The ventricles, sulci and cisterns are symmetric and unremarkable. The midline structures and cranial-cervical junction are normal. The paranasal sinuses and mastoid air cells are clear.

Output: 1. Unchanged extent of the right posterior inferior temporal lobe lesion but less enhancement.2. Multifocal bilateral intracranial vascular wall enhancement suggesting the feature of intracranial vasculitis with interval improvement of some of previously seen lesions.


Instruction: Generate impression based on findings.

Input: Brain MRI:Cerebellar peduncles extend 3-4 mm below the level of the foramen magnum, maintaining a rounded morphology, most consistent with cerebellar ectopia and not Chiari malformation.The ventricles and sulci are normal in size. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. Note is again made of a partially empty sella. There is no evidence for intracranial hemorrhage or acute cerebral, brainstem or cerebellar infarction. No diffusion-weighted abnormalities are identified. There are no extraaxial fluid collections or subdural hematomas. The paranasal sinuses and mastoid air cells are clear. Brain MRA: There is antegrade flow within the distal bilateral vertebral arteries, within the basilar artery, distal bilateral internal carotid arteries and carotid siphons and bilateral anterior, middle and posterior cerebral arteries. No arterial stenoses, occlusions or aneurysms are identified. No arteriovenous malformations are identified and there is no evidence for cerebral vasculitis. Note is made of a tiny fenestration of the basilar artery just past the vertebral artery confluence, of no clinical significance.Neck MRA:There is conventional takeoff of the great vessels from the aortic arch without evidence for stenosis of the origin of the great vessels or of the bilateral vertebral arteries. There are no stenoses of the bilateral common, internal or external carotid arteries or of the bilateral carotid bifurcations. There is no evidence for vasculitis, fibromuscular dysplasia or dissection of the carotid or vertebral arterial systems within the neck. There are no vascular masses identified.

Output: 1.Cerebellar peduncles extend 3-4 mm below the level of the foramen magnum, maintaining a rounded morphology, most consistent with cerebellar ectopia and not Chiari malformation.2.Note is again made of a partially up the sella.3.Otherwise negative MRI of the brain including gadolinium enhancement.4.Negative MRA of the brain.5.Negative MRA of the neck.


Instruction: Generate impression based on findings.

Input: 44-year-old male with right upper quadrant pain, persistent. Assess for masses or other lesions. ABDOMEN:LUNG BASES: No significant abnormality notedLIVER, BILIARY TRACT: 15 cm diameter hypodensity at the hepatic dome on axial image 15 of series 3 is indeterminate. This may represent a hemangioma, but further characterization would require dedicated hepatic CT or MRI examination. SPLEEN: No significant abnormality notedPANCREAS: No significant abnormality noted ADRENAL GLANDS: No significant abnormality notedKIDNEYS, URETERS: No significant abnormality notedRETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality notedOTHER: No significant abnormality notedPELVIS:PROSTATE, SEMINAL VESICLES: No significant abnormality notedBLADDER: No significant abnormality notedLYMPH NODES: No significant abnormality notedBOWEL, MESENTERY: No significant abnormality notedBONES, SOFT TISSUES: No significant abnormality notedOTHER: Fat-containing inguinal hernias bilaterally. There are some inflammatory changes in the left inguinal canal involving fat within the hernia.

Output: Small amount of fat inflammatory change in left inguinal fat.1.5 cm diameter hepatic dome lesion is indeterminate.Otherwise negative.


Instruction: Generate impression based on findings.

Input: MRI Brain: Mild generalized parenchymal volume loss with prominence of the ventricles and sulci. There are multiple nonspecific foci of T2/FLAIR hyperintensity in the periventricular and subcortical white matter compatible with chronic small vessel ischemic disease. There is evidence of an old watershed ischemia between the right ACA and MCA with small rounded foci of encephalomalacia within gliosis. 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. Trace mucosal thickening of the ethmoid air cells. Status post right partial mastoidectomy. Right lens implant is noted.MRA Brain: Lack of flow is noted involving the distal internal carotid artery. Note is made of a complete circle of Willis with small AComm and PComm arteries present. There is an attempt to supply anterograde flow to the right ACA via the AComm, as well as an attempt to supply antegrade flow to the right MCA via the AComm and right PComm. However, flow related signal appears diminished within the right ACA and MCA compared to the left.The right vertebral artery demonstrates loss of flow with minimal retrograde flow from the basilar artery. There appears to be a right AICA-PICA variant supplying the right PICA territory. No arteriovenous malformations or aneurysms are identified.MRA Neck: The neck portion of the exam is motion degraded. No appreciable flow is visualized in the brachiocephalic artery, although the immediately adjacent right subclavian and common carotid arteries demonstrate normal flow signal, suggesting the the brachiocephalic artery origin lies outside the plane of acquisition. This could be confirmed with CTA or catheter directed angiography. There is severe stenosis of the right common carotid artery at the bifurcation with near complete loss of flow in the right internal carotid artery throughout its entirety. There is a least 50% focal stenosis at the origin of the left internal carotid artery, although convincing measurements are difficult given the motion degradation. The right vertebral artery demonstrates near-complete loss of flow from the origin to its intracranial portion with only minimal retrograde flow from the basilar artery and only minimal attempts at muscular branch reconstitution within the neck. The left vertebral artery is large with a patent origin and appearing normal throughout its entirety. There are no vascular masses identified.

Output: 1.No acute ischemic infarction. Chronic small vessel ischemic disease.2.Evidence of chronic watershed ischemia between the right ACA and MCA.3.Near complete loss of flow of the right vertebral artery and the right internal carotid artery with attempts at compensatory flow to both supratentorial and infratentorial structures via a complete circle of Willis and a right AICA-PICA variant.4.At least 50% focal stenosis at the origin of the left internal carotid artery, although convincing measurements are difficult given motion degradation.5.No appreciable flow is visualized in the brachiocephalic artery, although the immediately adjacent right subclavian and common carotid arteries demonstrate normal flow signal, suggesting the the brachiocephalic artery origin lies outside the plane of acquisition. This could be confirmed with CTA or catheter directed angiography.


Instruction: Generate impression based on findings.

Input: Benign neoplasm of cranial nerves [D33.3] / Unspecified sensorineural hearing loss [H90.5], Reason for Study: ^Reason: re-evaluate known acoustic neuroma History: Unilateral SNHL Previously shown right IAC homogeneously enhancing mass lesion appears to be slightly increase in size especially short axis (on axial scan the width was measured about 6.6mm at the level of IAC entrance which was about 4.5mm). The long axis measurement also shows interval increase (14.6mm on axial scan and was 12.4mm). In addition, the mesial aspect of the mass is now demonstrating bulbous appearance which was relatively flat on prior scan.The right 6th nerve was not clearly visualized due to overlapped tortuous basilar artery. Otherwise bilateral 5th, left 6th, left 7th, left 8th and bilateral 9th to 11th cranial nerve complexes appear to be normal. The brainstem, cerebellum, vermis and tonsils are normal. The ventricles, cerebral sulci and cisterns are symmetric and unremarkable. lear.

Output: Interval increase in size and change in shape especially mesial aspect of the known right IAC homogeneously enhancing mass as described above.


Instruction: Generate impression based on findings.

Input: History of cystic fibrosis and liver disease. Presenting for HCC screening. ABDOMEN:LIVER, BILIARY TRACT: Cirrhotic liver morphology. The portal vein, hepatic artery and hepatic veins appear patent.There is suboptimal timing of the late arterial phase. Given this limitation there is no suspicious liver lesion. No biliary ductal dilatation.Normally distended gallbladder with pericholecystic fluid/wall thickening which is not atypical in the setting of cirrhosis.SPLEEN: Marked splenomegaly measuring 19.1 cm in craniocaudal dimension compatible with portal hypertension. Perisplenic collateral vessels.PANCREAS: Marked fatty atrophy of the pancreas. Prominent peripancreatic and porta hepatic lymph nodes, not uncommon in the setting of cirrhosis.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: The right hemicolon wall appears thickened and edematous which may reflect portal hypertensive colopathy.BONES, SOFT TISSUES: Recannulation of the umbilical vein.OTHER: No significant abnormality noted.

Output: 1.Cirrhosis with findings of portal hypertension. Splenomegaly.2.No suspicious liver lesion.3.Right hemicolon wall thickening may reflect portal hypertensive colopathy in the absence of signs and symptoms of colitis.


Instruction: Generate impression based on findings.

Input: Occipital fibrous dysplasia with headaches. 13-year-old male. There is redemonstration of thickening of the left occipital bone with a ground glass appearance consistent with the patient's clinical history of fibrous dysplasia extending from the foramen magnum along its posterior and left lateral aspect and its left lateral aspect of a left occipital condyles and of the left clivus involving the left hypoglossal canal completely and the left the jugular foramen partially. The left condylar canal is also involved. The left hypoglossal canal is a little bit smaller than the right. The right hypoglossal canal measures 3.5 mm in diameter. The left and measures 2.9 mm in diameter. Along the midline the bidimensional measures of fibrous dysplasia of the occipital bone measures at 28 x 68 mm on sagittal imaging. There is an MRI from 9/4/09 which had sagittal imaging. It appears that dimensions at that time were 28 by 68 mm on sagittal imaging as well. It is not possible to make a fair comparison on the in between the prior CT and the current CT due to differences in slice thickness and angulation on imaging. Overall I get the impression that it is larger on the current versus the prior exam. On the scout image a lateral dimensions are 24 x 63 mm indicating interval growth.There is a 15 x 11 mm in sagittal dimension ground glass appearing lesion within the odontoid process. The rest of the cervical or vertebral bodies are probably normal alignment and height.

Output: 1.Large area of ground glass appearance of the occipital bone consistent with fibrous dysplasia as described above with diameters hypoglossal canals as described above. A fair comparison the prior CT scan cannot be made as indicated above I suspect it appears larger in the overall thickness. The left jugular foramen is only partially involved.2.Focus of ground glass appearance of bone at the odontoid process consistent with fibrous dysplasia.


Instruction: Generate impression based on findings.

Input: Female, 10 months old, with status epilepticus, refractory seizures, prior history of hypoglycemia, ex 26 week premature with history of volvulus and short-gut syndrome. Since the prior examination, substantial generalized parenchymal volume loss has occurred. All of the supratentorial lobes are affected to some degree, though the parietal regions do seem to be slightly more prominently affected. As a result of this volume loss, the lateral and third ventricles demonstrate a dilated morphology and the cerebral sulci are diffusely widened. The pattern of white matter myelination is delayed, compatible with prematurity, and with no convincing evidence of interval maturation.On diffusion weighted images, a very subtle bilateral and symmetric pattern of restricted diffusion is seen suggesting cytotoxic edema involving the parietal and occipital regions predominantly, but also the remaining lobes to a lesser degree. The basal ganglia are spared but there is some questionable subtle involvement of the posterior medial thalami as well.On postcontrast imaging, and particularly on the postcontrast FLAIR sequences, small gyriform areas of enhancement are evident indicating breakdown of the blood-brain barrier in the medial parietal lobes, right side more than left. No other definite pathologic intracranial enhancement is seen.Single voxel spectroscopy was performed on the discretely enhancing right parietal lesion showing a marked reduction in the quantity of NAA as well as above-normal levels of lipid and a discrete moderate lactate presence. Single voxel spectroscopy was also performed on an area of parietal white matter which was free of discrete signal abnormality, and this also shows significant reduction in NAA and the presence of both lipid and lactate. Single voxel spectroscopy of the left basal ganglia shows a modest reduction in NAA but no convincing evidence of lipid or lactate.Dedicated imaging of the pituitary gland is within normal limits. The gland itself is normal in size and morphology. No discrete lesions are seen. The posterior pituitary is identified in its normal position. The pituitary stalk is midline and both the stalk and the gland show homogeneous enhancement.

Output: Findings on this examination indicate significant brain parenchymal injury with generalized volume loss predominantly affecting the white matter, as well as evidence of neuronal injury and loss. These changes have developed in the time interval since the prior examination at which point the brain appeared normal accounting for prematurity. Dedicated imaging of the pituitary is within normal limits.Although the parenchymal abnormalities are generalized, there is a slight preference for the posterior regions of the brain. In these areas, in addition, there is evidence of an ongoing or very recent pathologic process in the form of mild vasogenic edema and mild localized breakdown of the blood-brain barrier.Spectroscopic assessment over multiple areas of the brain demonstrates significant reduction in the level of NAA which indicates neuronal injury and loss. Moderately abnormal levels of lipid, which indicates cell membrane breakdown, and lactate, which indicates failure of energy metabolism, are also seen both in areas of blood brain barrier breakdown and in white matter which is free of significant signal abnormality. The presence of lactate also supports the likelihood of an ongoing or recent pathologic process as it is typically a transient finding after a parenchymal insult. Of note, no convincing lipid or lactate is detected in the basal ganglia.Taking into account the complex clinical course of this patient, a single unifying diagnosis cannot be made on the basis of this examination. One possibility is that the marked parenchymal changes reflect evolving hypoglycemic injury, and indeed the pattern of parenchymal involvement is supportive of this. Seizures may therefore be secondary to this injury. Alternately, ongoing seizure activity can itself induce some of the observed imaging findings including cytotoxic edema, blood brain barrier breakdown, and elevations of lactate. Finally, the possibility of an underlying inherited metabolic disorder does remain, though on the basis of this single examination it is felt to be less likely.The presence of ongoing seizure activity does complicate the interpretation of the imaging findings. If seizures can be controlled, there may be some benefit to repeating the imaging including spectroscopy after 1-2 weeks seizure-free.


Instruction: Generate impression based on findings.

Input: 45 years Male (DOB:5/23/1971)Reason: assessment for cause of dysarthria; further evaluation of punctate hypodensity in R thalamus on CT wo History: dysarthria after induction chemotherapy for AML (high dose cytarabine and mitoxantrone)PROVIDER/ATTENDING NAME: OLATOYOSI M ODENIKE There are punctate foci of signal loss and susceptibility weighted imaging left orbital gyrus, in the left inferior frontal gyrus as well as in the left frontal centrum semiovale. Additional punctate foci of signal loss and susceptibility imaging are present within the left cerebellar hemisphere.No abnormal enhancing mass lesions are appreciated within the brain parenchyma.The cerebellar tonsils extend 4 mm below the level of foramen magnum.The punctate hypodensity in the right thalamus and the CT scan probably represents a tiny perivascular space. It is bright on T2 imaging and dark on FLAIRNormal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.The right parotid gland extends into the buccal region. The left parotid gland is not identified on this exam it the exception of an accessory component of the left buccal tissues. Deep lobes of the parotid glands are not identified.

Output: 1.There are several microhemorrhages present in the left frontal lobe and the left cerebellar hemisphere. These are nonspecific. One possibility is that this is related to prior trauma though it is nonspecific related to other pathology.2.The punctate hypodensity in the right thalamus and the CT scan probably represents a tiny perivascular space3.No evidence for acute ischemic cerebral infarction.4.Low-lying cerebellar tonsils are borderline for Chiari I malformation.5.The parotid glands appear to be small and hypoplastic.


Instruction: Generate impression based on findings.

Input: Cyst and hydrocephalus: possible shunt malfunction. There is a catheter that enters via a right occipital burr hole and terminates in the anterior right lateral ventricle. There are thin septations within the dilated portion of the posterior right lateral ventricle, which has not significantly changed in size. The rest of the ventricular system is not particularly enlarged. There is confluent high T2 signal in the right frontal, parietal, and occipital white matter surrounding dilated right lateral ventricle, along with volume loss. There are also other scattered areas of periventricular and subcortical white matter T2 hyperattenuation. There is no evidence of acute infarction or intracranial hemorrhage. There are postoperative findings related to posterior fossa decompression with diminished flow of cerebrospinal fluid across the craniocervical junction. The cerebellum is not low-lying, however. There is an extra-axial catheter in the right frontoparietal convexity. There are no midline shift. The pituitary gland is normal in size. There is no abnormal intracranial enhancement. The major cerebral flow voids are intact. The orbits and paranasal sinuses are grossly unremarkable.

Output: 1. Dilatation of posterior portion of the shunted right lateral ventricle with septations, which may represent adhesions and perhaps cyst formation with surrounding encephalomalacia and gliosis. The constellation of findings may be the result of remote insult, such as infection and perhaps ischemia. Other scattered areas of periventricular and subcortical white matter T2 hyperattenuation may represent chronic small vessel ischemic disease, but no evidence of acute infarct. 2. Postoperative findings related to posterior fossa decompression with diminished flow of cerebrospinal fluid across the craniocervical junction.


Instruction: Generate impression based on findings.

Input: 19 year-old female with history of astrocytoma of the posterior fossa, off therapy evaluation. Redemonstrated are postoperative findings within the posterior fossa. Surgical deformation of the fourth ventricle is unchanged as is the degree and extent of T2 hyperintensity along the roof of the fourth ventricle, extending into the vermis, also unchanged. This tissue also redemonstrates mild intrinsic T1 hyperintensity. As before, there is no abnormal enhancement.Elsewhere, parenchymal signal intensity and morphology are within normal limits. No edema or mass effect is seen. No pathologic enhancement is detected. No evidence of intracranial hemorrhage or any new fluid collections are seen. Ventricles are stable in size and morphology. A small left sphenoid sinus mucous retention cyst is unchanged. The remaining paranasal sinuses and mastoid air cells are clear. Expected vascular flow voids are demonstrated.

Output: Redemonstration of postoperative findings in the cerebellum with no evidence to suggest progressive or recurrent disease.


Instruction: Generate impression based on findings.

Input: Reason: Cuff, Labrum Tear History: Shoulder Pain ROTATOR CUFF: Subtle intermediate signal intensity in the distal aspect of the supraspinatus tendon and indicates tendinopathy. There is no full-thickness rotator cuff tear. The remainder of the musculature/tendons of the rotator cuff are unremarkable. There is no communication with the subacromial/subdeltoid bursa.SUPRASPINATUS OUTLET: No significant abnormality noted.GLENOHUMERAL JOINT AND GLENOID LABRUM: No significant abnormality noted.BICEPS TENDON: No significant abnormality noted. ADDITIONAL

Output: Tendinopathy of the distal supraspinatus tendon. Otherwise, unremarkable appearance of the right shoulder.


Instruction: Generate impression based on findings.

Input: 87-year-old male with elevated INR and history of falls. There is no evidence of intracranial hemorrhage, mass or edema. Hypodensities in both cerebellar hemispheres, left greater than right, as well as in the basal ganglia, are consistent with prior strokes. Confluent areas of hypodensity in periventricular and subcortical white matter are consistent with extensive small vessel ischemic disease of indeterminate age.There is prominence of the ventricles and sulci, consistent with parenchymal volume loss, appearing similar to prior MRI.The calvaria and skull base are radiographically normal. The visualized paranasal sinuses and mastoid air cells are normally pneumatized.

Output: 1.No evidence of intracranial hemorrhage or other acute abnormality. 2.Evidence of extensive small vessel ischemic disease and prior strokes in basal ganglia and cerebellum.


Instruction: Generate impression based on findings.

Input: Stage 4 neuroblastoma with recurrent disease to posterior fossa; assess for progression of disease. Brain: There are postoperative findings related to suboccipital craniotomy. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma and pituitary gland appear unremarkable. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits are grossly unremarkable.Internal Auditory Canals: The bilateral cranial nerve 7 and 8 complexes are intact. There is no evidence of mass lesions. The inner ear structures, including the cochlea, vestibule, endolymphatic duct, and semicircular canals, appear unremarkable. There is persistent left mastoid fluid signal.

Output: No evidence of intracranial neuroblastoma recurrence.


Instruction: Generate impression based on findings.

Input: Enhancing soft tissue thickening is again seen within the left pre-maxillary cheek which continues along the inferolateral edge of the maxilla. As seen previously, this tissue erodes the maxilla slightly invading the floor of the maxillary sinus. Lobular mucosal thickening is seen in the maxillary sinus, whicho is probably largely reactive to tumor invasion. Compared to the previous studies, all the above findings are progressed.From the left cheek the mass spreads posteriorly along the lateral border of the maxilla into the masticator space, where there is invasion of the muscles of mastication. Vague soft tissue thickening and enhancement is seen extending further posteriorly below the zygomatic arch, reaching into the left parotid space.Abnormal enhancing tissue tracks up along the posterior wall of the left maxillary sinus to enter the widened pterygopalatine fossa. From here, abnormal tissue tracks along the V2 through the foramen rotundum and V3 through the foramen ovale. The cisternal portion of the trigeminal nerve is not involved. The left vidian nerve is also infiltrated.Along the left maxillary gingival tissue, there is an oval focus of low signal, which could represent a bubble of air within fluid trapped between the gum and the lip, an osseous fragment, or surgical material.Given the field of view, no pathologic lymph nodes are seen by size criteria. A hypoenhancing lesion is again seen in the right pituitary gland.

Output: Progressive tumor is seen in the soft tissues of the left face. There is evidence of invasion of the left maxillary sinus, and perineural spread into the left pterygopalatine fossa with extension along V2, V3, and the vidian canal.


Instruction: Generate impression based on findings.

Input: 47-year-old female with right hip pain for one year. Evaluate for labral tear versus FAI. Limited examination secondary to patient's inability to complete the examination due to extreme claustrophobia.ACETABULAR LABRUM: Note is made of linear increased signal abnormality traversing the anterior superior acetabular labrum consistent with a tear (image 1; series 11).ARTICULAR CARTILAGE AND BONE: Heterogeneous bone marrow signal may represent residual islands of red marrow. Otherwise no bone marrow signal abnormality is identified.SOFT TISSUES: The imaged musculature is normal in appearance. ADDITIONAL

Output: Acetabular labral tear.


Instruction: Generate impression based on findings.

Input: History of ganglioglioma and subdural fluid collection, yearly follow up for changes. There are postoperative findings related to left temporal mass resection with interval decreased confluent T2 hyperintensity in the left temporal lobe, where there is parenchymal volume loss, but no evidence of abnormal intraparenchymal enhancement. The previously described exophytic cystic lesion in this region is no longer apparent. There is no significant interval change in the size of the left cerebral convexity subdural fluid collection, which measures up to 25 mm in width, with drainage catheter in position. Likewise, there is no significant interval change in the associated midline shift to the right, compression of the left cerebral hemisphere with focal tenting of the left frontal lobe to the overlying dura, and expansion of the overlying calvarium. However, the diffuse left hemisphere dural enhancement has subsided. The ventricles are unchanged in size and configuration, with partial effacement of the left lateral ventricle, but prominence of the right lateral ventricle. There is no evidence of acute infarction or intracranial hemorrhage. Fluid within the left mastoid air cells has resolved.

Output: 1. Post-treatment findings in the left temporal lobe region with decreased extent of the intraparenchymal signal abnormality.2. No significant interval change in the size of the left cerebral convexity subdural fluid collection, which measures up to 25 mm in width, and no significant interval change in the associated midline shift to the right and compression of the left cerebral hemisphere with focal tenting of the left frontal lobe to the overlying dura.


Instruction: Generate impression based on findings.

Input: Male, 15 years old, with history of ependymoma status post resection x2. Evaluate disease status. A small resection cavity in the left middle frontal gyrus is unchanged in size and morphology. Minimal surrounding gliosis is seen. Nonspecific enhancement within the cavity is likely related to surgery and is unchanged. No new pathologic enhancement is seen.Elsewhere brain parenchymal morphology and signal characteristics are within normal limits. No evidence of edema or mass effect is seen. No pathologic parenchymal or extra-axial enhancement is detected. The ventricular system is stable in size and morphology.

Output: Stable left frontal lobe resection cavity with no evidence to suggest recurrent tumor.


Instruction: Generate impression based on findings.

Input: Midbrain and thalamus neuroglial cyst with associated arachnoid cyst: surveillance. There is no significant interval change in the right thalmus and midbrain multilocular cystic lesion, which measures up to approximately 35 mm and protrudes into the otherwise collapsed third ventricle. There is an unchanged right transfrontal ventricular shunt catheter, with unchanged nearly-collapsed right lateral ventricle and generally small caliber left lateral ventricle. There is unchanged diffuse high T2 signal along the path of the catheter in the right frontal lobe, which may represent gliosis. There is no evidence of acute intracranial hemorrhage or acute infarct. The major cerebral flow voids are intact. The orbits are grossly unremarkable. There is moderate mucosal thickening in the right sphenoid sinus and bubbly secretions in the left maxillary sinus.

Output: 1. Unchanged right thalmus and midbrain neuroglial cyst with associated arachnoid cyst. 2. Unchanged shunted ventricular system.3. Bubbly secretions in the left maxillary sinus may represent acute sinusitis.


Instruction: Generate impression based on findings.

Input: There is stable mild grade 1 retrolisthesis of L4 on L5. The spine is in otherwise normal alignment. The vertebral body heights are well-maintained. There is mild scattered disc narrowing throughout the cervical spine, with redemonstration of moderate-severe disc narrowing at L4-L5 with vacuum phenomenon.Prominent endplate degenerative marrow changes are seen again at L4-L5. Multiple areas of abnormal marrow signal are again visualized, with increased size and conspicuity of rounded areas and punctate foci of T1 and T2 hypointensity consistent with sclerosis. The largest lesion in the lumbar spine is now located at L1 along its superior endplate, increased in size since the prior MRI. There is slight associated convexity of the superior endplate due to the metastasis. A prominent area of T1 and T2 hypointensity corresponding to a sclerotic lesion is seen in the T8 vertebral body, similar to prior CT. Some of the lesions demonstrate mild peripheral STIR hyperintensity. Heterogeneous STIR hyperintensity is noted in the T1 vertebral body.The spinal cord is grossly of normal caliber and signal. There is at most mild central spinal canal stenosis at C4-C5 and C5-C6 with a focal central disc protrusion at C5-C6. Along the thoracic spine, there is a minimal shallow central disc protrusion at T9-T10 which indents the sac and may abut the ventral cord. Along the lumbar spine, there is redemonstration of focal spondylotic changes from L2-L3 through L4-L5 resulting in moderate-severe central spinal canal stenosis at these levels as previously seen. Grossly on sagittal images, the degree of narrowing appears similar. Scattered moderate foraminal narrowing is again noted along the lumbar spine.Mild STIR hyperintensity is noted along the left paraspinal musculature at the lumbosacral junction which may relate to postprocedural changes following recent steroid injection. There is no focal fluid collection identified.

Output: 1.No evidence of overt cord compression or evidence of acute pathologic compression deformity. Grossly similar degree of high-grade central spinal canal stenosis at L3-L4 and L4-L5 as previously seen, with significant crowding of cauda equina nerve roots. This is in part relating to grade 1 retrolisthesis of L4 on L5, which is stable.2.Compared to prior remote MRI of the lumbar spine, progressed size and conspicuity of sclerotic appearing osseous metastatic lesions within the spine. Findings do appear slightly progressed since more recent prior CT.3.Minimal signal changes along left lumbosacral paraspinal musculature which may relate to recent procedure. Please correlate clinically.


Instruction: Generate impression based on findings.

Input: Female, 33 years old, with severe headache, status post Chiari decompression. Brain:Image quality is compromised due to motion artifact. Multiple repeat sequences were attempted.Findings are seen compatible with Chiari decompression including suboccipital craniectomy, resection of the posterior arch of C1, and probable cauterization of the cerebellar tonsils. Allowing for motion artifact, the appearance of the cerebellum is not significantly changed. Phase contrast flow imaging is technically inadequate for the assessment of CSF flow through the foramen magnum.The remainder of the brain parenchyma is within normal limits. No areas of pathologic signal abnormality are seen. No edema or mass effect is detected. There are no findings to suggest acute intracranial hemorrhage or any abnormal extra-axial fluid collection. The ventricular system is normal in size and morphology.C-spine:Findings related to posterior instrumented fusion and multilevel laminectomy are again seen appearing similar to prior. The spinal canal and thecal sac are expanded between C3 and C6.Again, allowing for motion artifact, the spinal cord demonstrates normal signal intensity and morphology. No epidural abnormalities are suspected.Spinal alignment is anatomic. Vertebral body height and morphology are within normal limits. No pathologic marrow replacement or marrow edema is observed. No spinal canal stenosis is observed. Most of the neural foramina are not well assessed due to metallic artifact.

Output: 1.Image quality is significantly compromised due to motion artifact. In particular, the phase imaging CSF flow sequence is technically inadequate.2.Findings related to Chiari decompression are seen showing no significant change from the prior examination.3.Evaluation of the brain is otherwise unremarkable with no evidence of any acute intracranial abnormality.4.Imaging of the cervical spine redemonstrates findings related to posterior decompression and instrumented posterior fusion. The spinal canal remains well decompressed from C3 through C6. No spinal cord abnormalities are observed within the limitations of significant artifact.


Instruction: Generate impression based on findings.

Input: History of Chiari malformation status post decompression. Interval follow-up exam. Evaluate CSF flow. Brain:Postoperative changes from suboccipital craniectomy. There is an unchanged pointed appearance of the cerebellar tonsils which extend down to the inferior margin of C1. CSF flow imaging through the foramen magnum shows biphasic flow ventrally. This is questionably decreased from prior, however this is suspected to be predominantly due to technical factors in the CSF flow scan as there is a stable appearance of the CSF spaces at the level of the foramen magnum. CSF flow dorsally through the foramen magnum remains decreased.Stable prominence of the supratentorial ventricular system. No abnormal T1, T2, or diffusion weighted signal in the brain. No extra-axial fluid collection. Myelination appears appropriate for age. The expected intracranial vascular flow voids are present. The paranasal sinuses are clear. The visualized mastoid air cells are clear. The orbits are unremarkable.Cervical spine:The vertebral body and intervertebral disc heights are maintained. There is straightening of the cervical lordosis likely related to positioning. Alignment is otherwise maintained. Stable partially visualized epidural lipomatosis in the thoracic spine. The cord signal and morphology is within normal limits.

Output: 1. Postoperative changes from suboccipital craniectomy. CSF flow sequences show questionably decreased flow ventrally through the foramen magnum when compared to prior, however this is suspected to be predominantly due to technical factors in the CSF flow scan as there is a stable appearance of the CSF spaces at the foramen magnum. CSF flow dorsally through the foramen magnum remains decreased.2. Stable prominence of the supratentorial ventricular system. I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: 40 years Male (DOB:4/8/1975)Reason: stroke? History: r weaknessPROVIDER/ATTENDING NAME: ROBERT A MULLIKEN HELENE G RUBEIZ MRI of the brainNo diffusion weighted abnormalities are appreciated.The CSF spaces are appropriate for the patient's stated age with no midline shift. No intracranial hemorrhage is identified. No edema is identified within the brain parenchyma.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.Cervical spine:The cervical vertebral bodies are appropriate in overall alignment and height. The cervical spinal cord has normal signal characteristics and overall morphology. There is mild multilevel disc desiccation present.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.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.Exam is mildly degraded due to patient motion.MRA brain:Antegrade flow is present in the distal internal carotid arteries, the distal vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries. The basilar artery is fenestrated.There is no evidence for intracranial aneurysm or cerebrovascular occlusion.The anterior communicating artery is identified and is medium size. The posterior communicating arteries are intact. The vertebral arteries are similar in size.MRA neck:There is opacification of the aortic arch, great vessels from the aortic arch and carotid arteries and vertebral arteries. There is no stenosis identified of the great vessels from the aortic arch. On the basis of NASCET criteria there is no significant stenosis at the carotid bifurcations. There is no significant stenosis along the course of the vertebral arteries. The left common carotid artery originates from the innominate artery. The left vertebral artery originates from the aortic arch.

Output: 1.There is no evidence for acute ischemic cerebral infarction.2.There are minor degenerative changes present in the cervical spine without significant compromise to spinal canal or neural foramina.3.No abnormal mass lesions are appreciated in the spinal cord or intracranially to explain the patient's right-sided weakness4.There is no evidence for intracranial or extracranial cerebrovascular occlusive disease.


Instruction: Generate impression based on findings.

Input: Left otalgia, left base of tongue tingling and tenderness, left jaw pain radiating to ear. History of colloid nodule in the thyroid gland. Although many of the sequences are degraded by patient motion, there is no evidence of mass lesions in the left mandibular angle region where there is an overlying skin marker. There is no evidence of significant cervical lymphadenopathy based on size criteria. There is a mylohyoid defect on the right with slight protrusion of the sublingual gland, which is an anatomic variant. The major salivary glands are otherwise unremarkable. The upper aerodigestive track, including the base of tongue, also appears unremarkable, aside from aside from a retention cyst within the left maxillary sinus. There is a T1 hyperintense nodule in the left lobe of the thyroid gland that measures up to 20 mm. The major cervical vascular flow voids appear to be grossly intact. The osseous structures are unremarkable. The airways are patent. The imaged intracranial structures are unremarkable. There is a retention cyst within the left maxillary sinus. There appear to be degenerative changes of the left temporomandibular joint with associated mild joint effusion and perhaps synovial cyst formation.

Output: 1. No evidence of mass lesions in the left mandibular angle region, where there is an overlying skin marker. 2. No evidence of significant cervical lymphadenopathy based on size criteria. 3. A left lobe of the thyroid gland that measures up to 20 mm corresponds to a known colloid cyst. 4. Apparent degenerative changes of the left temporomandibular joint with associated mild joint effusion and perhaps synovial cyst formation. Dedicated temporomandibular joint imaging via CT or MRI may be useful for further characterization if clinically warranted.


Instruction: Generate impression based on findings.

Input: Swelling, pain along the medial aspect for one month. Evaluate for injury. MENISCI: The medial and lateral menisci are intact.ARTICULAR CARTILAGE AND BONE: There is focal slight prominence and increased signal intensity of the articular cartilage of the medial facet of the patella which may represent a small "blister" (early degeneration), but this is equivocal. Otherwise, the articular cartilage is normal.LIGAMENTS: The collateral and cruciate ligaments are intact. EXTENSOR MECHANISM: No significant abnormality noted.ADDITIONAL

Output: Mild focal slight prominence and increased signal intensity of the articular cartilage of the patella may represent early degeneration, but this is equivocal.


Instruction: Generate impression based on findings.

Input: 83-year-old man with history of sarcoma and newly diagnosed lung cancer. There are moderate scattered foci of T2 hyperintensity in the cerebral white matter with associated global parenchymal volume loss. There are also punctate foci of T2 hyperintensity in the left cerebral peduncle. There are no abnormal enhancing lesions. There is a CSF signal arachnoid cyst medial to the left inferior cerebellar hemisphere. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. There are bilateral lens replacements. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: 1.No evidence of intracranial metastasis.2.Moderate small vessel white matter ischemia and volume loss, likely chronic.


Instruction: Generate impression based on findings.

Input: 41Yrs old female with HTN, breast cancer s/p mastectomy, chemotherapy, radiation therapy and presumed chemotherapy induced LV dysfunction. Referred for cardiac MRI to rule out infiltrative cardiac disorders. Left VentricleThe left ventricle is normal in size with mild-moderately reduced systolic function. The overall LV ejection fraction is 42%. The LVEDV is 119 ml (normal range 109+/-23), LV end diastolic volume index is 75 ml/m2 (normal range: 65+/-11), LVESV is 70 ml (normal range 31+/-10), and LV end systolic volume index is 44 ml/m2 (normal range 18+/-5). The LV mass is 62 g (normal range 114+/-24) and the LV mass index is 39 g/m2 (normal range 67+/-11). 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 myocardial iron overload. 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 56%, the RVEDV is 103 ml (normal range 110+/-24), the RV end diastolic volume index is 64 ml/m2 (normal range 69+/-14), the RVESV is 46 ml (normal range 35+/-13), and the RV end systolic volume index is 29 ml/m2 (normal range 22+/-8).Right AtriumThe right atrium is normal in size. Aortic ValveThe aortic valve is trileaflet, 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 no obvious pericardial disease.Extracardiac FindingsThis 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.Normal sized LV with mild-moderately reduced systolic function (LVEF 42%). There is global hypokinesis.2.No evidence of late gadolinium enhancement.3.Normal sized RV with normal systolic function (RVEF 56%).I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.