Instruction: Generate impression based on findings.

Input: Female, 18 years old, with history of recent cavernoma bleed with seizures. A bubbly heterogeneous lesion with T1 and T2 hyperintensity and strong susceptibility effect is demonstrated involving the right inferior postcentral gyrus and parietal operculum. The lesion measures up to 3 cm in diameter. The lesion causes mild local mass effect but there is no detectable edema in the surrounding brain parenchyma.The lesion itself enhances minimally if at all and there is no clear evidence of an associated developmental venous anomaly. No additional susceptibility inducing or enhancing lesions are identified.The remainder of the brain is within normal limits. No evidence of acute ischemia is seen. No evidence of significant parenchymal edema is detected. The ventricles are normal in size and morphology.

Output: A 3 cm lesion is evident involving the right inferior postcentral gyrus and parietal operculum with imaging characteristics compatible with a cavernous malformation. No evidence of significant edema in the surrounding parenchyma is seen. No associated developmental venous anomaly is detected.


Instruction: Generate impression based on findings.

Input: There is no acute cord compression. Degenerative spondylitic change in the cervical spine causes central stenoses at C4/5 and C5/6. Multiple metastases are noted involving multiple osseous structures. A previously characterized right carotid space mass is partially imaged.

Output: There is no acute cord compression.


Instruction: Generate impression based on findings.

Input: 51-year-old female with pain, stiffness and swelling. MENISCI: There is globular increased signal abnormality within the anterior horn of the lateral meniscus consistent with intrasubstance degeneration. Some of this signal extends to the tibial articular surface consistent with degenerative tearing/fraying. There is focal fluid signal intensity within the body of the lateral meniscus consistent with meniscal cyst, indicating a tear. The posterior horn appears intact. There is globular increased signal abnormality within the posterior horn of the medial meniscus consistent with intrasubstance degeneration. Some signal extends to the tibial and femoral articular surfaces consistent with degenerative fraying. There is a full-thickness radial tear affecting the posterior horn of the medial meniscus (coronal series 8; image 20).ARTICULAR CARTILAGE AND BONE: No bone marrow signal abnormalities identified. No full-thickness or near full-thickness articular cartilage defects are identified.LIGAMENTS: The cruciate and collateral ligaments appear intact. EXTENSOR MECHANISM: The extensor mechanism appears intact.ADDITIONAL

Output: 1. Tearing of the medial and lateral meniscus, including a radial tear of the posterior horn of the medial meniscus as described above.2. Small joint effusion. Other findings as described above.


Instruction: Generate impression based on findings.

Input: Female, 42 years old, with headache and cranial 6 palsy. Assess for dural thickening/enhancement. Also history of lumbar spine epidural fluid collection, assess for resolution. Brain:Brain parenchymal morphology and signal characteristics are within normal limits. No evidence of parenchymal edema or mass effect is seen. No restricted diffusion is detected.On postcontrast imaging, diffuse pachymeningeal thickening and enhancement shown on outside imaging has resolved. There is no evidence of any pathologic parenchymal or extra-axial enhancement on the present examination.No evidence of intracranial hemorrhage or any abnormal extra-axial fluid collection is detected. The ventricles are normal in size and morphology.Lumber spine:Spinal alignment is anatomic. Vertebral height and morphology are normal. No pathologic marrow replacement or evidence of marrow edema is seen.The visualized spinal canal is patent and unremarkable. Ventral epidural collections seen previously at L2-3 and L5 have resolved. No new epidural collections are detected.Visualized spinal cord, conus and cauda equina are within normal limits.The paraspinal soft tissues are normal.Intervertebral disk height and morphology are unremarkable. No evidence of disk bulge or herniation is seen. Mild facet hypertrophy is demonstrated at lower lumbar levels. No evidence of any significant spinal canal or neuroforaminal stenosis is detected.

Output: 1.Interval resolution of previously seen diffuse pachymeningeal thickening and enhancement. Evaluation of the brain is unremarkable.2.Interval resolution of previously seen ventral epidural collections in the lumbar spine. No new or significant abnormalities are detected.


Instruction: Generate impression based on findings.

Input: Clinical question: History of grade 1 meningioma status post RT, surveillance MRI. Signs and symptoms: None Pre and post enhanced brain MRI:No diffusion-weighted abnormality.Examination demonstrates a dural base well-demarcated enhancing mass arising from the right leaf of tentorium with extension inferiorly into the posterior fossa and superiorly into right sub-temporal region consistent with patient's known meningioma. There is no detectable vasogenic edema of the right temporal or right cerebellum secondary to meningioma.The mass measures nearly identical to prior study. On sagittal reformatted images it measures 36 in AP and 28 mm in CC dimensions similar to prior exam. On axial post enhanced series measures approximately 36 x 27 mm in transaxial dimensions similar to prior exam.A second small left pterional meningioma is again identified measuring 12 mm in AP and 8 mm in transverse axis without significant change since prior study. This mass similar to prior exam is also seen minimal buckling of the adjacent cortex without FLAIR/T2 hyperintensity.Focus of FLAIR hyperintensity in the pons similar to prior exam and likely as result of treatment.Stable tiny focus of nonspecific FLAIR hyperintensity in the right frontal lobe. Unremarkable anatomical morphology and signal intensity of brain parenchyma otherwise on all MRI sequences and without detectable abnormal enhancement.

Output: 1.Stable size of a meningioma arising from the right leaf of tentorium with growth into the posterior fossa and right subtemporal region as detailed/measured above. Stable mass effect on the adjacent parenchyma without further hyperintensity/edema.2.Stable small left pterional meningioma since prior study as detail/measured.3.Stable focus of FLAIR hyperintensity in the pons likely treatment related since prior study.4.Stable and unremarkable exam otherwise.


Instruction: Generate impression based on findings.

Input: Dizziness and giddiness [780.4], Reason for Study: ^Reason: ischemic stroke? History: vertigo Exam is limited due to motion artifact.No evidence of acute ischemic or hemorrhagic lesion on the scan.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. Normal flow voids are identified in the major intracranial vessels. 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.3D MRA neck post-gadolinium images with maximum intensity projections of the cervical vasculature demonstrate normal flow through the bilateral common carotid, carotid bifurcations, internal/external carotid, and vertebral arteries.

Output: 1. Although limited due to patient motion artifact, there is no evidence of acute ischemic or hemorrhagic lesion on the scan.2. Brain MR angiogram and neck MRA angiography without contrast enhancement shows no evidence of significant (more than 50%) arterial luminal stenosis or arterial aneurysm.


Instruction: Generate impression based on findings.

Input: Male, 30 years old, history of Ewing's sarcoma, status post cryoablation in January of 2014, with findings concerning for progressive disease on a scan from July 2014, status post second cryoablation in August 2014, assess for progression of disease, recent cryoablation resulted in paralysis. Again seen is the sequelae of prior ablation and cement placement within the T10 vertebral body. This includes bilateral transpedicular access tracts and low signal centrally within the vertebral body likely related to the presence of cement. There is abnormal STIR signal and enhancement involving this vertebral body extending into the pedicles not significantly changed since 11/19/2014.Again seen is thinning of the spinal cord at the T10 level. The cord seems to be retracted anteriorly towards the vertebral body as seen before. There is slight decrease in enhancement along the anterior aspect of the cord at this level. Abnormal T2 signal involves the central cord bilaterally as well as ventrally slightly more inferiorly at T10.Interval increase in size of T12 vertebral body lesion, previously 6x6 mm, now 20 x 15 in the AP and craniocaudal dimensions in the sagittal plane. There is also a 9x11 mm lesion measured similarly which is new since 11/19/2014 MRI. These lesions are hypermetabolic on PET from same day.Elsewhere, there signal characteristics are unremarkable. There is minimal loss of height at T10 involving the superior endplate which is stable to minimally worse than prior. Vertebral body heights are otherwise preserved. Spinal alignment is anatomic. The remainder of the spinal cord shows normal signal intensity and morphology. No evidence of spinal canal stenosis or neuroforaminal narrowing is detected.

Output: 1. Compared to MRI 11/19/2014, there is progression of osseous metastatic disease in the thoracic spine with enlarging T12 lesion and new T3 lesion. These lesions are hypermetabolic on PET from same day.2. Previously treated enhancing T10 vertebral lesion is not significantly changed. There is minimal depression of the superior endplate which is slightly worse than prior. Otherwise no compression fractures. No epidural tumor. 3. Sequela of prior cryoablation related injury to the thoracic cord with mild cord atrophy and ventral cord enhancement at T10; enhancement is slightly decreased in the interval consistent with evolution of injury.


Instruction: Generate impression based on findings.

Input: Pain and swelling of the Achilles tendon insertion unresponsive to conservative treatment. TENDONS: There is perhaps slight thickening of the Achilles tendon distally with a prominent enthesophyte at the insertion on the calcaneus indicating insertional tendinosis. We see no discrete tear of the Achilles tendon. The anterior and medial tendons appear intact. There appears to be a longitudinal split tear of the peroneus brevis tendon as it courses posteriorly beneath the fibular tip of questionable significance. There is minimal if any associated peroneal tenosynovitis.LIGAMENTS: The study is not protocoled for optimal evaluation of ankle ligaments. The anterior talofibular ligament appears slightly thinned which may represent old injury, but this is equivocal. The calcaneofibular and posterior talofibular ligaments appear intact. The distal tibiofibular syndesmotic complex appears intact. The visualized components of the deltoid ligament appear intact.ARTICULAR SURFACES AND BONE: Mild osteoarthritis affects the ankle and midfoot. Bone marrow signal is unremarkable. We see no osteochondral defects.ADDITIONAL

Output: 1.Mild insertional Achilles tendinosis without tear.2.Mild nonspecific subcutaneous edema.3.Mild edema type signal in the flexor hallucis longus muscle which is nonspecific but may represent subacute atrophy or mild strain.4.Longitudinal split tear of the peroneus brevis of questionable significance.5.Other findings as described above.


Instruction: Generate impression based on findings.

Input: Medical question: Rule out intracranial hemorrhage. Signs and symptoms: Altered mental status, respiratory failure, anemia. Nonenhanced CT of brain:A there is revisualization of bilateral symmetrical ventriculomegaly of lateral ventricles as well as the third ventricle. This remains identical to prior examination from 6 -- 7 -- 2010.Very minimal periventricular low-attenuation is again identified. These may represent minimal small vessel disease of indeterminate age. The cortical sulci remain within normal size and disproportionately smaller than the ventricular system. All of the findings remain stable since prior exam. Prominence of ventricular system may be at the upper limits of normal for patient's stated stated age of 78. Possibility of hydrocephalus however cannot be entirely excluded. There are no additional older studies for comparison.Also stable since prior exam is expansion of the left cavernous sinus in size possible minimal associated bony remodeling this finding is best the patient or axial images 7 and 8. There is no evidence of calcification within the cavernous sinus to suggest this finding is secondary to atherosclerotic tortuosity and ectasia of the internal carotid. I recommend follow-up with an MRI to exclude possibility of a mass in this location and in particular a meningioma.

Output: 1.No evidence of any new acute finding since prior exam.2.Stable uniform bilateral enlargement of lateral ventricles and minimally of the third ventricle. Finding may represent central atrophy or hydrocephalus. Follow-up with an MRI is recommended.3.Prominent soft tissue density of left cavernous sinus with expansion remains stable since prior study. Recommend follow-up with an infused MRI for assessment of tumor.


Instruction: Generate impression based on findings.

Input: There has been interval expected evolution of previously seen immediate postoperative changes from right parietal craniotomy for biopsy of right posterior and medial temporal lobe multifocal mass. Since the prior preoperative MRI, there has been interval further progression of multiple sites of enhancing tumor. For example, there is an oval satellite lesion anterolateral to the dominant mass which measures 8 x 12 mm on 1201/82, compared to previous 5 x 6 mm. The dominant component of the solid and cystic mass measures 3.9 cm transverse x 4.1 cm AP, and 4.4 cm CC, compared to previous measurements of 3.8 x 3.8 cm axially. There is overall increased cystic component of the dominant portion of the mass. There is likely interval slight progression of tumor involvement of the splenium of the right corpus callosum, which is now increasingly thickened with T2/FLAIR hyperintensity which now minimally crosses midline on 701/18.There are small areas of lobulated intrinsic T1 hyperintensity peripherally in the right posterior temporal lobe underlying the craniotomy site with corresponding susceptibility, consistent with blood products. Of note, there are small blood-fluid levels in the area of the most peripheral biopsy site, with increased associated nodular enhancement. Additional lobulated areas of intrinsic T1 hyperintensity within the dominant portion of the lesion not present on the prior precontrast T1-weighted images may represent a combination of proteinaceous material and/or blood products. There is additional slightly more remote ill-defined enhancement along the peripheral right parietal lobe as seen on 1201/110 which appears perhaps slightly increased in conspicuity and extent. There is slight increased thickening of masslike FLAIR hyperintensity in the right parietal periventricular and deep white matter. Right optic tract is difficult to delineate and may be minimally thickened on coronal T2-weighted images.Midline shift is similar, measuring 7 mm to the left. There is also localized mass effect, predominantly on the right lateral ventricle, with again focal dilatation of the right temporal horn which appear similar in degree. The lateral ventricles are overall moderately dilated. There is again extension of the mass into the right midbrain with distortion of surrounding architecture, including anteromedial displacement of the red nucleus and substantia nigra. FLAIR hyperintensity continues to extend into the posterior aspect of the external capsule and the posterior limb of the right internal capsule. Allowing for differences in technique, there is overall similar extent of FLAIR abnormality in the right temporal lobe white matter. There are few nonspecific punctate foci of FLAIR hyperintensity in the left subcortical and periventricular white matter which appear mostly unchanged. There remains diffuse right cerebral sulcal effacement, as well as diffuse right temporal cortical FLAIR hyperintensity and gyral thickening.There is no diffusion abnormality to suggest recent ischemia. No extra-axial fluid collection is identified. Normal flow-voids are demonstrated in the major intracranial vascular structures. The midline structures and craniocervical junction are within normal limits. MR perfusion demonstrates elevated rCBV in the area of enhancing mass, especially in the area of more confluent enhancing soft tissue, cranial to the dominant cystic components, consistent with known high-grade glioma.

Output: 1.Interval expected evolution of previously seen postoperative changes following lesion biopsy, with overall progression of heterogeneously enhancing solid and cystic right temporal lobe mass extending to the midbrain with multiple adjacent satellite lesions which have also worsened. This is consistent with tumor progression. However, similar degree of midline shift and localized mass effect.2.Likely interval slight progression of presumed tumor involvement of the splenium of the right corpus callosum with increased thickening and minimal midline crossing of abnormal signal.3.Areas of interval increased T1 signal within components of the mass likely relating to areas of proteinaceous material and/or blood products.4.Similar degree of right temporal horn dilatation likely relating to trapping by the tumor, with otherwise more symmetric moderate prominence of the lateral ventricles.5.Similar degree of nonenhancing areas of FLAIR hyperintensity within predominantly the right temporal lobe white matter as well as extending minimally into the right internal/external capsules. These are nonspecific and may relate to a combination of nonenhancing tumor and/or vasogenic edema.


Instruction: Generate impression based on findings.

Input: This 37-year-old female with two days headache. Rule out subarachnoid hemorrhage. There is a hyperdense extra-axial mass in the left subarachnoid space of the high convexity. There is suspected communication between this mass and a hyperdense tubular structure that extends from the high left convexity into the brain parenchyma. Intraparenchymal hypodensity around this tubular structure may represent edema. An MRI is recommended for further evaluation of this mass.There is no evidence of intracranial hemorrhage or midline shift. The ventricles and basal cisterns are normal in size and configuration.The calvaria and skull base are radiographically normal. The visualized paranasal sinuses and mastoid air cells are normally pneumatized.These findings were discussed with Dr. Jeffrey Kuo at the time of interpretation.

Output: Hyperdense extra-axial mass and tubular structure extending into the brain parenchyma. An MRI is recommended for further evaluation.


Instruction: Generate impression based on findings.

Input: Reason: right CP angle enhancing masss History: compare to previous BRAINThe CSF spaces are appropriate for the patient's stated age with no midline shift. There is a small focus of encephalomalacia present along the inferior lateral aspect of the right cerebellar hemisphere. This is unchanged since the prior examThe patient is status post right suboccipital craniotomy.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.IACThere is a 19x 13 mm axial dimension mass at the right cerebellopontine angle cistern which previously measured 19x13 mm on 12/5/13. This mass abuts the right trigeminal nerve at its origin from the pons. The cochlea and semicircular canals appear intact. The cochlear nerve can be followed bilaterally tracking into the cochlea. The modiolus is well formed bilaterally.

Output: 1.Stable right cerebellopontine angle cistern mass.2.Encephalomalacia along the right cerebellar hemisphere


Instruction: Generate impression based on findings.

Input: Female, 69 years old, with spinal level at about T12, fecal incontinence. Evaluate for cord compression. Cervical:Straightening of the cervical lordosis is likely positional. Vertebral body heights are preserved. Marrow signal characteristics are within normal limits. The visualized spinal cord demonstrates normal signal intensity throughout. No epidural lesions are suspected.C2-3: Minimal posterior disc-osteophyte complex formation. No spinal canal or foraminal stenosis. No changes. C3-4: Minimal posterior disc-osteophyte complex formation. No spinal canal or foraminal stenosis. No changes. C4-5: Posterior disc-osteophyte complex formation with a small disc protrusion. Mild spinal canal stenosis. Mild right foraminal narrowing. No changes. C5-6: Posterior disc-osteophyte complex formation and ligamentum flavum thickening. Moderate spinal canal stenosis with slight flattening of the ventral cord. Moderate bilateral foraminal narrowing. No changes.C6-7: Posterior disc-osteophyte complex formation. Ligamentum flavum thickening. Mild spinal canal stenosis. Moderate left and mild right foraminal narrowing. No changes. C7-T1: Posterior disc-osteophyte complex formation. No spinal canal or foraminal stenosis. No changes. Thoracic:Apart from a minimal kyphotic angulation at T11-12, spinal alignment is anatomic. Vertebral body height and morphology are within normal limits. Marrow signal characteristics are unremarkable. The visualized spinal cord is normal in signal intensity. No epidural lesions are suspected. Minimal scattered disc degeneration is seen with no large herniations or areas of significant spinal canal stenosis. The neural foramina are patent as well. A large hepatic cystic lesion is partially visualized on this examination.Lumbar:Alignment is anatomic. Vertebral body height and morphology are within normal limits. Marrow signal characteristics are unremarkable. The visualized distal spinal cord, conus and nerve roots of the cauda equina are within normal limits. No epidural lesions are seen.L1-2 through L3-4: No significant spinal canal or foraminal stenosis.L4-5: Facet arthropathy and ligamentum flavum thickening. Minimal disc bulging. No significant spinal canal or foraminal stenosis.L5-S1: Facet arthropathy. Mild disc bulging with a small superimposed central protrusion. No spinal canal stenosis. Mild bilateral foraminal narrowing. Findings are slightly progressed from the prior examination.

Output: 1.Scattered disc and posterior element degeneration is again seen. These findings are most pronounced in the cervical spine where there are areas of spinal canal stenosis. However, there has been no significant interval change from the prior examination.2.Elsewhere, no significant compromise of the spinal canal or neural foramina is demonstrated. No cord compression is seen. No other specific findings are detected which would account for the patient's symptoms.


Instruction: Generate impression based on findings.

Input: Left knee pain MENISCI: Intermediate signal intensity is noted in the posterior horn of the medial meniscus indicating intrasubstance degeneration but there is no evidence of tear of the medial meniscus. There is no discrete lateral meniscal tear.ARTICULAR CARTILAGE AND BONE: Severe articular cartilage loss of the medial compartment is noted particularly of the femoral condyle anteriorly at the level of the anterior horn of the meniscus. There is associated underlying degenerative marrow signal. Additionally, there is abnormal contour of the femoral trochlea posteriorly with multiple ossific fragments identified in the intercondylar notch which may represent osteochondral fragments from prior trauma or loose bodies. There is thinning of the articular cartilage of the lateral compartment although no discrete full-thickness defects are appreciated. Moderate articular cartilage loss of the patellofemoral compartment is noted particularly of the medial facet where there is underlying degenerative marrow signal.Small foci of low signal intensity seen within the joint space may reflect ligamentous or meniscal fragments. LIGAMENTS: The ACL is ruptured. The PCL is intact. The collateral ligaments are intact.EXTENSOR MECHANISM: No significant abnormality noted.ADDITIONAL

Output: 1. Ruptured ACL.2. Osteoarthritis of varying degrees with articular cartilage loss that is most severe in the medial compartment with suspected loose bodies.3. No discrete meniscal tear.


Instruction: Generate impression based on findings.

Input: Clinical question: Rule out intracranial bleed. Signs and symptoms: multiple falls. Unenhanced head CT:Findings highly suspected for moderate to advanced small vessel disease of indeterminate age are noted. The large area of low-attenuation in high convexity right frontal lobe white matter with associated mass effect suspected for edema. Recommend further follow-up with an enhanced CT or an MRI with infusion to exclude possibility of malignancy. This is a new finding since prior examination from 2006.There is no evidence of hemorrhage, hydrocephalus or midline shift. Calvarium is intact. Extensive right maxillary sinus opacification and otherwise unremarkable visualized paranasal sinuses.There is also subtle low attenuation of the cortex of the right posterior high convexity frontal lobe suspected for subacute ischemic disease.

Output: 1.High convexity right frontal low attenuation of white matter has the appearance of vasogenic edema and recommend further follow-up with an enhanced study to exclude underlying malignancy.2.Small vessel disease of indeterminate age.3.Subtle low attenuation of the right posterior high convexity frontal cortex may represent a focal area of subacute stroke.4.Recommend follow-up with an enhanced MRI for further evaluation of the above findings.


Instruction: Generate impression based on findings.

Input: 83 year old female with right side neck mass. Again identified is a well-defined, heterogeneous soft tissue mass involving the superficial lobe of the right parotid gland. This lesion measures approximately 1.5 x 1.3 cm (image 43 series 3), unchanged. There is mild enhancement of the soft tissue component anteriorly. No definite additional masses are abnormal enhancement. The left parotid, sublingual, and submandibular glands are unremarkable. The oral cavity, oro/nasopharynx, hypopharynx, larynx and subglottic airways are unremarkable. The epiglottis, vallecula, piriform sinuses, and vocal cords are normal. No abnormal lymphadenopathy is noted. Calcified atherosclerosis affects both carotid arteries at the bifurcation, left greater than right. Small hypodense nodules are present within left thyroid gland. The jugular veins are patent. The osseous structures are unremarkable. The prevertebral and paraspinal soft tissues are unremarkable.  The visualized intracranial structures demonstrate ventriculomegaly, unchanged since prior brain MRI. The intraorbital structures are unremarkable. Degenerative changes affect the cervical spine. No suspicious focal osseous lesions are seen. Limited views of the chest are unremarkable.

Output: Stable partially-enhancing right parotid mass. Benign etiology, such as pleomorphic adenoma, is favored.


Instruction: Generate impression based on findings.

Input: Chiari malformation, pseudotumor cerebri, shunt, drainage from nose possibly CSF fluid, worsening symptoms: back/neck pain, headaches, and fatigue. Brain: There are postoperative findings related to Chiari decompression surgery with an unchanged appearance of the cerebellum. There is mildly constricted cerebrospinal fluid flow across the anterior neo-foramen magnum and paucity flow posteriorly. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is a linear T2 hyperintensity that traverses the right frontal lobe and anterior corpus callosum, related to a prior surgical tract. There is a shunt device in position at the posterior craniocervical junction, with susceptibility artifact associated with the reservoir. The ventricles are unchanged in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, paranasal sinuses, and nasal cavity are grossly unremarkable.Spine: There is no evidence of syringohydromyelia. There is an eccentric left posterior disc-osteophyte complex at T7-T8 that slightly impinges upon the spinal cord. There is mild thoracolumbar scoliosis. There is no evidence of vertebral subluxation, however. The vertebral body heights are intact. An endotracheal tube is in position, with fluid in the surrounding pharyngeal cavity, which may represent secretions.

Output: 1. Unchanged postoperative findings related to Chiari decompression, with mildly constricted cerebrospinal fluid flow across the anterior neo-foramen magnum and paucity of flow posteriorly.2. No evidence of syringohydromyelia. 3. An eccentric left posterior disc-osteophyte complex at T7-T8 slightly impinges upon the spinal cord.


Instruction: Generate impression based on findings.

Input: Female 62 years old Reason: 61 yo female with hx of pancreas lesion; please evaluate for changes and or abnormalities History: pancreas lesion ABDOMEN:LIVER, BILIARY TRACT: No focal hepatic lesions. Hepatic and portal veins are patent. No intra-or extrahepatic ductal dilatation.SPLEEN: No significant abnormality noted.PANCREAS: Pancreas is normal in morphology, and signal. The pancreatic duct is normal in caliber. There are two unchanged subcentimeter cystic foci in the body of the pancreas (series 2/26) and near the tail (series 2/25). They are located adjacent to the pancreatic duct and again likely represent small side branch type IPMNs. No new pancreatic mass is evident.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS:Left kidney cysts are unchanged. Stable prominence of the right proximal renal collecting system.RETROPERITONEUM, LYMPH NODES: No retroperitoneal lymphadenopathy.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: Stable small pancreatic cystic foci, which again likely represent small side branch type IPMNs.


Instruction: Generate impression based on findings.

Input: Male; 61 years old. Reason: cholelithiasis; choledocholithiasis; common bile duct dilation History: RUQ abdominal pain; fevers; elevated total bilirubin, ggt, elevated AST/ALT ABDOMEN:LUNG BASES: Trace right pleural effusion. Stable right lower lobe peripheral air space opacity suspicious for infarct with central increased T2 hyperintensity, suggesting necrosis (partially visualized); underlying infection cannot be excluded.LIVER, BILIARY TRACT: Unchanged diffuse hepatic metastatic disease.Cholelithiasis. No significant gallbladder wall thickening or enhancement. Mild pericholecystic free fluid is likely related to generalized ascites with mild perihepatic ascites seen. Normal caliber of the biliary tree. No choledochalithiasis.SPLEEN: No significant abnormality noted.PANCREAS: Unchanged pancreatic body mass, most compatible with pancreatic adenocarcinoma. Stable focal stenosis of the splenic vein posterior to the mass to compression by the mass.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: Stable gastrohepatic lymphadenopathy.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: Mild abdominal ascites.

Output: 1.No significant interval change in multiple findings since CT exam performed yesterday, including right lower lobe infarct, diffuse hepatic metastatic disease, pancreatic mass, and abdominal lymphadenopathy.2.Normal caliber of the biliary tree without evidence of choledocholithiasis or obstruction.3.Cholelithiasis without specific evidence of acute cholecystitis.


Instruction: Generate impression based on findings.

Input: Right knee pain and swelling MENISCI: No significant abnormality noted.ARTICULAR CARTILAGE AND BONE: No significant abnormality noted.LIGAMENTS: The ACL and PCL are intact. The lateral collateral complex is intact. There is some increased signal about the medial collateral ligament consistent with a sprain. No evidence of a tear.EXTENSOR MECHANISM: No significant abnormality noted.ADDITIONAL

Output: Large joint effusion and a sprain of the medial collateral ligament


Instruction: Generate impression based on findings.

Input: There is no acute intracranial hemorrhage or acute infarction. There is diffuse cerebral volume loss with prominent sulci and third and lateral the ventricles. There are jets of cerebrospinal fluid flow into the third and lateral ventricles. There is deep bilateral cerebellar hemisphere mineralization. There is midline shift, or mass effect. There is a chronic deformity of the left lateral wall of the maxillary sinus. The osseous structures are otherwise intact. The imaged contents of the paranasal sinuses and mastoid air cells are grossly unremarkable. There is deformity of the left zygomatic arch and posterior wall of the maxillary sinus.

Output: 1. No acute intracranial hemorrhage or acute infarction. 2. Diffuse cerebral volume loss. Superimposed normal pressure hydrocephalus is a potential consideration, nevertheless.3. Sequela of remote left zygomaticomaxillary complex fracture.


Instruction: Generate impression based on findings.

Input: 66-year-old female, evaluate rotator cuff ROTATOR CUFF: There is increased T2 signal within the distal supraspinatus tendon with extension of fluid in the subacromial subdeltoid bursa consistent with a full-thickness rotator cuff tear without significant retraction of the tendon. There is no significant muscular atrophy. The remaining rotator cuff tendons and muscles are intact. Small degenerative cyst is noted in the humeral head.SUPRASPINATUS OUTLET: Moderate AC joint osteoarthritisGLENOHUMERAL JOINT AND GLENOID LABRUM: The glenoid labrum is grossly normal.BICEPS TENDON: The biceps tendon is properly situated within the bicipital groove.ADDITIONAL

Output: 1. Full-thickness tear of the distal supraspinatus tendon without significant retraction.2. Findings suggestive of adhesive capsulitis.


Instruction: Generate impression based on findings.

Input: 78-year-old male. Left lateral knee pain. Evaluation of lateral fluctuant mass previously evaluated by ultrasound without conclusive characterization. MENISCI: The body and posterior horn of the medial meniscus are torn and flipped into the intercondylar notch in front of the PCL, consistent with a bucket handle tear. Complex branching signal abnormality in the body and lateral aspect of the posterior horn of the medial meniscus consistent with a complex tear; the medial aspect of the posterior horn is not visualized towards its insertion consistent with a component of complete radial tearing.LIGAMENTS: The ACL is not visualized consistent with a complete tear. The PCL, MCL, and LCL are intact.ARTICULAR CARTILAGE AND BONE: Marked diffuse articular cartilage thinning of the lateral femoral condyle with areas of full-thickness cartilage loss anteriorly. Large areas of full thickness cartilage loss of the weight bearing surfaces of the medial tibiofemoral compartment. Marked diffuse cartilage thinning of the patellofemoral compartment articular cartilage with full thickness cartilage loss of the lateral patellar facet.Underlying subchondral marrow edema and cysts in the tibia and femur are most likely degenerative in etiology. EXTENSOR MECHANISM: Intact.ADDITIONAL

Output: 1. Large bucket handle tear of the medial meniscus. Complex tear of the body and posterior horn of the lateral meniscus.2. Complete tear of the ACL.3. Palpable abnormality at the lateral joint line is likely due to a combination of ganglion cysts and a small hematoma.


Instruction: Generate impression based on findings.

Input: Clinical question: 64-year-old female with lumbar degenerative disease. Signs and symptoms: LLE radiculopathy. Nonenhanced lumbar MRI:T11-T12 is unremarkable.T12-L1 demonstrate moderate disc disease and loss of disc height, mild broadbase bulging disc and mild facet and ligamentum flavum degenerative changes. No spinal stenosis or neural foraminal compromise.L1-L2 demonstrate mild degenerative changes without spinal or neural foraminal compromise.L2-L3 demonstrate mild disc disease and loss of disc height, mild diffuse bulging disc, moderate left and mild right facet and ligamentum flavum hypertrophy. No spinal stenosis or neural foraminal compromise.L3-L4 demonstrate mild disc disease and loss of disc height, left lateral and far lateral shallow broad-based disc protrusion, mild bilateral ligamentum flavum hypertrophy, mild bilateral facet disease and with evidence of mild bilateral facet effusion. Constellation of changes results in mild central spinal stenosis without neural foraminal compromise. There is however moderate left lateral recess compromise.L4-L5 demonstrate advanced disc disease and loss of disc height, diffuse broad base bulging disc, mild to moderate bilateral facet and ligamentum flavum hypertrophy. Constellation of changes results in moderate central spinal stenosis without significant neural foraminal compromise.L5-S1 demonstrate advanced disc disease and loss of disc height, mild bilateral facet and ligamentum flavum hypertrophy (R>L). There is no spinal stenosis however moderate bilateral (L>R) neural foraminal and lateral recess compromise is detected.No detectable. Spinal soft tissue abnormalities.

Output: 1.Degenerative changes of lumbar spine as detailed above with resultant moderate central spinal stenosis at L4-L5 and mild stenosis at L3-L4 levels.2.Neural foraminal and lateral recess compromise as detail per level above.


Instruction: Generate impression based on findings.

Input: Diagnosis: LumbagoClinical question: rule out diskitis, likely herniated diskSigns and Symptoms: low back pain, elevated esr, crp Five lumbar type vertebral bodies are presumed to be present which are appropriate in overall alignment and height. The conus medullaris on sagittal imaging is grossly intact. No abnormal enhancing lesions are appreciated in the lumbar spine. There is multilevel disk dessication present. There is mild fatty replacement along the paraspinous musculature.At L5-S1 there is no significant compromise to spinal canal or neural foramina. There is loss of disk space height, disk dessication, diffuse disk bulge and mild to moderate facet hypertrophy. The fat surrounding the nerve root sleeves at the lateral recesses and the fat surrounding the nerve roots within the neural foramina are preserved. There is contrast enhancement and T2 signal hyperintensity along the facet joints at this level.At L4-5 there is no significant compromise to spinal canal or neural foramina. There is a 7mm focus of T2 hyperintensity associated with contrast enhancement at the posterior aspect of the L4 vertebral body at the inferior endplate adjacent to the disk annulus at the midline. There is loss of disk space height, disk dessication, diffuse disk bulge and a minor degree of facet hypertrophy. The fat surrounding the nerve root sleeves at the lateral recesses and the fat surrounding the nerve roots within the neural foramina are preserved.At L3-4 there is no significant compromise to spinal canal or neural foramina. There is loss of disk space height, disk dessication, a minor diffuse disk bulge and mild facet hypertrophy. The fat surrounding the nerve root sleeves at the lateral recesses and the fat surrounding the nerve roots within the neural foramina are preserved.At L2-3 there is no significant compromise to spinal canal or neural foramina. There is loss of disk space height, disk dessication and a minor diffuse disk bulge.At L1-2 there is no significant compromise to spinal canal or neural foramina. There is loss of disk space height, disk dessication and a minor diffuse disk bulge. There is some endplate reactive change present which is bright on T1 and dark of Fat sat imaging suggesting chronic stage.There is a 21x22mm right renal cystic lesion present most likely representing a simple cyst.

Output: 1.There is no evidence that is convincing for diskitis.2.There are multilevel degenerative changes present mostly in the chronic stage but in an acute/subacute stage at L4-5 (L4 endplate)and L5-S1 (facets) without compromise to spinal canal or neural foramina.


Instruction: Generate impression based on findings.

Input: Motion artifact mildly degrades the image quality. The alignment is normal. The vertebral bone marrow signal is unremarkable. The cervical spinal cord displays normal in signal without abnormal enhancement. The cerebellar tonsils are in normal position. The paraspinal contents are unremarkable. There are small disc-osteophyte complexes at C4-C5, C5-C6, C6-C7, and T1-T2 without significant spinal canal or neural foraminal narrowing. There is partially-imaged paranasal sinus mucosal thickening.

Output: Mild multilevel degenerative disc-osteophyte complexes spinal canal or neural foraminal narrowing.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: There is a rudimentary disk at S1-S2. The lumbar spine is in normal alignment, with a normal lumbar lordosis. Redemonstrated is multilevel disk narrowing and desiccation, most prominent at L5-S1 where there is moderate narrowing. The vertebral body heights are well-maintained. The distal spinal cord and conus are within normal limits with the conus terminating at the mid L2 level. No worrisome focal marrow signal abnormality is appreciated. There are endplate degenerative changes on the right at T10-T11. There is narrowing of the distal lumbar spinal canal predominantly due to shortened pedicles. There is thickening and slight redundancy of the cauda equina nerve root relating to spinal stenosis to be detailed below.New T2 signal is seen within the right paraspinal musculature at the level of S1 through S3 (best seen series 5, images 2/17 through 7/17).At T10-T11 and T11-T12, sagittal images suggest a mild diffuse disk bulge with right sided moderate foraminal narrowing. There may be mild central spinal canal stenosis. These findings are unchanged.At T12-L1, there is a mild diffuse disk bulge without stenosis, unchanged.At L1-L2, there is a mild diffuse disk bulge resulting in mild-moderate right and moderate left foraminal narrowing, unchanged.At L2-L3, there is a shallow right foraminal disk protrusion without stenosis, unchanged.At L3-L4, there is a trace diffuse disk bulge with mild left facet arthropathy. There is mild developmental narrowing of the lumbar spinal canal with overall moderate central spinal canal stenosis. There is also mild bilateral lateral recess stenosis as well as minimal right and moderate left foraminal narrowing. These findings are unchanged.At L4-L5, there is a mild diffuse disk bulge with left paracentral prominence. There is also prominent facet arthropathy and ligamentum flavum thickening. Superimposed upon the developmental narrowing, there is moderate-severe central spinal canal stenosis, moderate bilateral lateral recess stenosis as well as moderate left and mild-moderate right foraminal narrowing. These findings are unchanged.At L5-S1, there is a diffuse disk bulge with bilateral facet arthropathy and ligamentum flavum thickening. There is mild-moderate central spinal canal stenosis, although there is moderate-severe bilateral foraminal narrowing. These findings are unchanged.

Output: 1.New T2 signal is seen within the right paraspinal musculature at the level of S1 through S3. This appearance is most suggestive of muscle strain or other soft tissue injury.2.Multilevel degenerative disease with stenoses, stable in appearance, as described in detail above on a level by level basis.


Instruction: Generate impression based on findings.

Input: Clinical question: Evaluate for facet hypertrophy and spinal stenosis. Signs and symptoms: Significantly decreased are ROM. Nonenhanced cervical MRI:Foramen magnum is unremarkable other than mild ligamentous hypertrophy. Incidental note is made of a small foci of T2 hyperintensity within the pons consistent with patient's history of small vessel ischemic strokes.C2-C3 demonstrate degenerative changes without spinal stenosis or neural foraminal compromise.C3-C4 demonstrate moderate disc disease and loss of disc height, and minimal degenerative changes of posterior elements. There is result in moderate left neural foraminal compromise and no central spinal stenosis. There are anteriorly projecting hypertrophic spur.C4-C5 demonstrate moderate disease and loss of disc height, moderate left and mild right facet hypertrophic changes, mild bilateral ligamentum flavum hypertrophy. Constellation of changes results in mild left neural foraminal compromise and mild central spinal stenosis. Incidental note is made of a tortuous right vertebral artery that partially traverses the right neural foramina.C5-C6 demonstrate advanced loss of disc height, mild facet and ligamentum flavum hypertrophy. Mild central spinal stenosis and mild to moderate left neural foraminal compromise.C6-C7 demonstrate advanced disc disease and loss of disc height, moderate bilateral ligamentum flavum hypertrophy and mild facet disease and prominent (L>R) disc-osteophyte complex which results in mild flattening of the cord and complete effacement of subarachnoid with moderate central spinal stenosis. There is no detectable cord signal abnormality. There is also significant right and moderate left neural foraminal compromise at this level.C7-T1 demonstrate mild degenerative disc disease, moderate bilateral ligamentum flavum hypertrophy and moderate asymmetric right-sided facet hypertrophy. Constellation of changes result in mild central spinal stenosis and mild right neural foraminal compromise.Upper most visualized thoracic spine and cord is unremarkable other than degenerative changes.

Output: 1.At C6-C7 extensive degenerative changes results in moderate central spinal stenosis, significant right and moderate left neural foraminal compromise as detailed.2.Degenerative changes at other levels with resultant multilevel mild central spinal stenosis as detailed.3.Multilevel neural foraminal compromise as detailed per level above.4.No detectable signal abnormality of the cord.


Instruction: Generate impression based on findings.

Input: Male 15 years old Reason: s/p Knee dislocation MENISCI: Increased linear signal in the posterior horn of the medial meniscus could represent longitudinal tear. The lateral meniscus is intact.ARTICULAR CARTILAGE AND BONE: Stellate configuration of T2 hyperintensity and T1 hypointensity in the lateral tibial plateau raises question of microtrabecular fracturing. Bone contusion in the lateral femoral condyle.LIGAMENTS: Complete PCL rupture. ACL is intact. MCL and LCL are intact. T2 hyperintense signal in the medial retinaculum could represent injury.EXTENSOR MECHANISM: Patellar ligament is wavy which could be due to laxity. The quadriceps tendon is intact.ADDITIONAL

Output: 1.Complete PCL rupture.2.Bone contusion lateral femoral condyle. Possible microtrabecular fracturing of the lateral tibial plateau.3.Marked diffuse soft tissue swelling, most prominent posteriorly.4.Popliteal artery thrombosis.5.Possible longitudinal tear of the posterior horn medial meniscus.


Instruction: Generate impression based on findings.

Input: 32-year-old female with pain and left hip FAI. There is metallic susceptibility artifact along the anterior acetabulum with 2 low signal intensity tunnels within the anterior acetabular dome presumably reflecting prior labral repair. There is amorphous globular increased signal intensity within the adjacent base and substance of the anterior superior labrum at approximately the 1 o'clock position suggesting intrasubstance degeneration. There is also mild irregularity of the surface of the labrum from 1-3 o'clock suggesting fraying. The margins of the anterosuperior labrum are difficult to define due to the adjacent scarring. There is also linear increased signal intensity within the posterior superior labrum at the 10 to 11 o'clock position that appears to involve both the superficial and undersurface fibers of the labrum, suggestive of a nondisplaced tear that was not clearly evident on the outside study from 2/11/2011. These findings are best seen on the radial images as well as on series 1801. There is articular cartilage loss along the anterior superior aspect of the femoral head. The ligamentum teres appears intact. The bone marrow signal intensity is normal. There is scalloping of the anterior aspect of the femoral head/neck junction likely reflecting prior osteotomy. There is atrophy of the left iliopsoas muscle presumably related to prior surgical release. The remaining musculature is unremarkable. On the large field-of-view images, the sacroiliac joints and pubic symphysis appear normal.

Output: 1. Surgical changes of prior anterior superior labral repair with increased signal intensity within the labrum suggesting degeneration as well as mild undersurface fraying with adjacent scarring. There is also thinning of the articular cartilage of the adjacent femoral head.2. New linear signal abnormality within the posterior superior labrum likely representing a tear that was not evident on the prior examination.


Instruction: Generate impression based on findings.

Input: Smoldering myeloma There is a diffusely heterogeneous appearance of the bone marrow throughout the pelvis and lower spine which is thought to reflect red marrow reconversion as opposed to true myeloma. No definite myelomatous lesions are identified. Following gadolinium administration, there is no abnormal soft tissue or marrow enhancement.The soft tissues are normal in signal intensity. The muscles of the pelvis are normal in signal and caliber.

Output: Diffusely heterogeneous marrow signal intensity likely the result of red marrow reconversion and this appears similar to the prior exam. There is no discrete myelomatous lesion.


Instruction: Generate impression based on findings.

Input: Headache and presyncope. Evaluate for vascular malformation. MRI BRAIN: There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is a right frontal lobe developmental venous anomaly. There is also prominence of the caliber of the superificial cerebral veins in the right anterior temporal and left parietal regions which is of uncertain significance but favored to be a developmental variation. The brain parenchyma otherwise appears unremarkable. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. There are mucus retention cysts in the bilateral maxillary sinuses. The skull and extracranial soft tissues are unremarkable. MRA HEAD: The intracranial internal carotid arteries are normal in course and caliber. The middle and anterior cerebral arteries are unremarkable. The vertebral arteries, basilar artery, and posterior cerebral arteries are normal in course and caliber. There is no evidence of flow-limiting stenosis or aneurysm.

Output: 1. MRI of the brain is essentially within normal limits. No evidence of intracranial hemorrhage, infarct, or mass. There is a prominent right frontal lobe developmental venous anomaly which is an incidental finding. There is also prominence of the caliber of the superificial cerebral veins (particularly left vein of Trolard and the right superficial middle cerebral vein) which is of uncertain significance but favored to be a developmental variation. Please note entities such as dural arteriovenous fistula cannot be excluded by MRI and further evaluation could be considered if there is specific clinical suspicion.2. Unremarkable MRA without flow-limiting stenosis or aneurysm.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Diagnosis: Other forms of epilepsy and recurrent seizures with intractable epilepsyClinical question: epilepsy presurgical evaluation. Epilepsy protocol 2. 1 mm thin cut. Please include 3 D T1 contrast and DTI is requested. Please contact Dr. Carina Yang for questions.Signs and Symptoms: Medically intractable right frontal epilepsyComments: Please include 3 D T1 contrast and DTI is requested. Please contact Dr. Carina Yang for questions. Thanks. | 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. The hippocampi are symmetric.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 left sigmoid sinus and left transverse sinus and in left jugular fossa are larger than their right counterparts.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.

Output: MRI of the brain is within normal limits. No etiology for the patient's known seizures is appreciated.


Instruction: Generate impression based on findings.

Input: 58-year-old male with a left hand lesion. Evaluate for abscess. Limited examination due to patient motion, wrap around artifact, inability to use a dedicated wrist coil, and inability to optimally position the patient. Evaluation for abscess formation is further limited due to lack of intravenous contrast.The patient is status post amputation of the first and second rays as well as the third, fourth, and fifth fingers at the level of the PIP joints. There is a soft tissue defect along the radial aspect of the palm of the hand. There is diffuse edema type signal within the underlying volar soft tissues of the hand and wrist. There is a small amount of fluid noted within the carpal tunnel, which extends distal to the tunnel for a few centimeters along the flexor tendons of the ring finger. There is also fluid signal intensity within the soft tissues of the hand dorsal to the remaining metacarpals, which is nonspecific but could represent abscess formation with fluid extending along the extensor tendons of the middle and ring fingers to the level of the MCP joint. The bone marrow signal intensity appears normal given the aforementioned limitations.

Output: 1. Postoperative changes and radial sided soft tissue defect with diffuse soft tissue edema as described above.2. Fluid signal intensity within the dorsal soft tissues of the hand could represent abscess formation. Additional fluid signal intensity arising within the carpal tunnel is nonspecific but the possibility of infection cannot be excluded.


Instruction: Generate impression based on findings.

Input: 34 years, Female, Reason: assess for crohns dz, bowel wall thickening History: hx abd pain/diarrhea. endo shows apthous ulcers in distal stomach \T\ ileum. family hx Crohn's dz. ABDOMEN:LIVER, BILIARY TRACT: Subcentimeter T2 hyperintense focus with enhancement (2001/65) is too small to accurately characterize, but most likely represents a hemangioma.SPLEEN: No significant abnormality notedPANCREAS: No significant abnormality notedADRENAL GLANDS: No significant abnormality notedKIDNEYS, URETERS: No significant abnormality notedRETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No bowel wall thickening or abnormal enhancement. The terminal ileum appears normal. No abscesses or fistulas. No findings suggesting chronic inflammation.BONES, SOFT TISSUES: No significant abnormality notedOTHER: No significant abnormality notedPELVIS: FemaleUTERUS, ADNEXA: No significant abnormality noted.BLADDER: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: No evidence of inflammatory bowel disease.


Instruction: Generate impression based on findings.

Input: 19-year-old female patient with history of progressive pelvic desmoid tumor, currently being treated with tamoxifen. PELVIS: The ill-defined infiltrating mass in the left hemipelvis is mildly increased in size and currently measures 9.5 x 6.6 cm (series 8 image 43), previously 9.5 x 5.7 cm when measured similarly. The mass encases the left external iliac artery. The mass invades and occludes the left external iliac vein, with numerous collateral vessels identified. Anteriorly, the mass further invades and enlarges the left rectus muscle and adductor brevis. Laterally, the mass invades the left pelvic side wall, iliacus muscle, psoas muscle, and abuts the left acetabular cortex, similar to prior. Posteriorly, the mass extends into obturator internus muscle. Medially, the mass abuts left lateral bladder wall and adjacent loops of small intestine. The rectum appears uninvolved. UTERUS, ADNEXA: T1 and T2 hypointense probable pessary device in place in the vagina.BLADDER: The urinary bladder is displaced to the right.LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: Mildly increased left thigh soft tissue edema, reflecting venous congestion of the aforementioned left external iliac vein occlusion.

Output: 1.Approximately 1 cm increase in size in the mediolateral plane with other dimensions and degree of invasion of pelvic musculature remaining stable.2.Persistent occlusion of the left iliac vein with venous collateral formation.


Instruction: Generate impression based on findings.

Input: 61-year-old female with abdominal nodularity seen on CT. ABDOMEN:LIVER, BILIARY TRACT: The liver measures up to 21 cm in craniocaudal length. Diffuse loss of signal intensity on the out of phase sequence is compatible with hepatic steatosis. There is a persistent gallbladder wall thickening with intraluminal stones versus sludge. Findings could represent chronic cholecystitis. Diffuse heterogenous enhancement of the hepatic parenchyma particularly in the arterial phase is likely due to the fatty infiltration. No suspicious enhancing parenchymal lesions. No intra or extrahepatic biliary ductal dilatation. The portal and hepatic veins are patent.SPLEEN: No significant abnormality noted.PANCREAS: Normal T1 hyperintense signal on precontrast series. No pancreatic ductal dilatation. No suspicious pancreatic lesions.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: Mild periportal and mesenteric lymphadenopathy is noted on the diffusion weighted series. For reference, a periportal lymph node measures 2.4 x 1.3 cm (axial series 406 image 184). BOWEL, MESENTERY: Moderate upper abdominal ascites, and mild fluid motion artifacts limit the exam. No nodular enhancement or focal restricted diffusion is visualized. Uniform peritoneal enhancement is nonspecific.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: 1.Moderate upper abdominal ascites without nodular enhancement or focal restricted diffusion. 2.Hepatic steatosis. No suspicious hepatic lesions.3. Mild periportal and mesenteric lymphadenopathy.4. Persistent gallbladder wall thickening with intraluminal stones versus sludge, which could represent chronic cholecystitis. Clinical correlation suggested.


Instruction: Generate impression based on findings.

Input: Brain lesion and cyst, abnormal MRI in the past, 3 month post surgical follow up. There has been interval evolution of postoperative findings related to left frontal convexity cyst fenestration, with a small amount of high T1 and low T2 signal extra-axial blood products along the anteromedial left frontal convexity and collapse of the cyst cavity. There is minimal residual T2 hyperintensity in the underwing brain parenchyma and no significant mass effect upon the underlying brain parenchyma. There is no evidence of acute territorial cerebral infarct. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact.

Output: Interval evolution of postoperative findings related to left frontal convexity cyst fenestration, with a small amount of late subacute extra-axial blood products along the anteromedial left frontal convexity and collapse of the cyst cavity.


Instruction: Generate impression based on findings.

Input: Hereditary hemorrhagic telangiectasia, evaluate for brain AVM There is no evidence of acute ischemic or hemorrhagic lesion.Bilateral basal ganglia especially globus pallidus shows high signal intensity on T1-weighted imaging but reasonably normal signal intensity on T2 and FLAIR imaging indicate differential diagnosis of chronic liver disease, non ketotic hyperglycemia, chronic exposure to Manganese and long term treatment with total parenteral nutrition.There is no definitive evidence of abnormal enhancement.On FLAIR images, there are scattered punctate high signal intensity lesions on bilateral periventricular white matter indicate non specific small vessel disease.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. Normal flow voids are identified in the major intracranial vessels. 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.However, the source image shows vascular enhancement of the anterior aspect of the Superior Sagittal Sinus as well as a cortical vein on the right frontal lobe (series #401, image . There is also slightly increased vascularity on the superior posterior aspect of the vermis (series #401, image 103/192). Since this is a TOF MRA, unless there is technical errors, visualization of venous structure may indicate arteriovenous shunting. Therefore, diagnostic catheter angiography may be considered for further imaging investigations.

Output: 1. No evidence of acute ischemic or hemorrhagic lesion.2. Bilateral globus pallidi high signal intensities on T1 weighted image indicate possibilities of chronic liver disease,non ketotic hyperglycemia, chronic exposure to Manganese and long term treatment with total parenteral nutrition as discussed above.3. Visualization of cortical vein of the right frontal lobe and anterior aspect of the superior sagittal sinus may indicate possible arteriovenous shunting. Catheter angiography can be considered for further evaluation.


Instruction: Generate impression based on findings.

Input: Female, 72 years old. Reason: thyroid nodule RIGHT LOBE MEASUREMENTS: 2.5 x 2.3 x 5.6 cmLEFT LOBE MEASUREMENTS: 1.9 x 1.8 x 4.5 cmISTHMUS MEASUREMENTS: 0.5 cmRIGHT LOBE: A heterogeneous nodule in the posterior aspect of the right thyroid lobe measures 1.4 x 1.4 x 1.9 centimeters, with small cystic components, without calcification or significant blood flow. No other significant abnormality noted.LEFT LOBE: No significant abnormality noted.ISTHMUS: No significant abnormality noted.PARATHYROID GLANDS: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.OTHER: Carotid artery atherosclerosis.

Output: A dominant 1 - 2 cm complex right thyroid nodule is identified.


Instruction: Generate impression based on findings.

Input: Postsurgical changes of laminoplasty from C3 to C6. There is minimal retrolisthesis at C4-C5 and C5-C6 and anterolisthesis at C7-T1. Vertebral body heights are intact. There is multilevel disc desiccation with mild multilevel disc space loss. Moderate disc space loss at C6-C7. Endplate degenerative changes at C4-C5 and C7-T1. Mild increased signal within the cord at C4-C5 where there is thinning, suggesting myelomalacia. No abnormal enhancement.C2-C3: Uncovertebral joint hypertrophy. Mild left neural foraminal stenosis. No right neural foraminal stenosis. No spinal canal stenosis.C3-C4: Minimal uncovertebral joint hypertrophy. Moderate left and mild right neural foraminal stenosis. Mild effacement of the ventral and dorsal thecal sac.C4-C5: Uncovertebral joint hypertrophy. Mild effacement of the ventral and dorsal thecal sac. Severe right neuroforaminal stenosis. Moderate to severe left neural foraminal stenosis. C5-C6: Posterior disc osteophyte complex, asymmetric to the right, and uncovertebral joint hypertrophy. Moderate spinal canal stenosis with effacement of the ventral thecal sac and mild indentation of the ventral cord. Severe right neural foraminal stenosis. Moderate to severe left neural foraminal stenosis.C6-C7: Mild uncovertebral joint hypertrophy. No spinal canal stenosis. Mild to moderate right and mild left neural foraminal stenosis.C7-T1: Posterior disc osteophyte complex and uncovertebral joint hypertrophy. Mild effacement of the ventral thecal sac. Moderate bilateral neural foraminal stenosis, left greater than right.There is subtle increased T2 signal within the proximal C7 and C8 nerves on the right, presumably related to proximal impingement. Otherwise, no avulsions or abnormal enhancement is noted throughout the brachial plexus. No masses are seen within the course of the brachial plexus.

Output: 1.Evidence of prior laminoplasty with myelomalacia within the cord at C4-C5, presumably related to prior compressive myelopathy.2.Up to moderate spinal canal stenosis at C5-C6 and multiple levels of neural foraminal narrowing, including severe right neural foraminal stenosis at C4-C5 and C5-C6 which may be impinging on the exiting right C5 and C6 nerve roots. There is foraminal stenosis to a lesser degree at C6-C7 and C7-T1 as well.3.Subtle increased T2 signal within the C7 and C8 nerve roots on the right, presumably related to proximal impingement at the neural foramina. Brachial plexus exam is otherwise unremarkable.


Instruction: Generate impression based on findings.

Input: Brain MRI:The ventricles and sulci are normal in size. Incidental note is made of a cava septum pellucidum. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. The pituitary gland is normal in size. There is no evidence for intracranial hemorrhage or acute cerebral, brainstem or cerebellar infarction. No diffusion-weighted abnormalities are identified. There are no extraaxial fluid collections or subdural hematomas. Flow voids are present within the major vessels indicating patency. The paranasal sinuses and mastoid air cells are clear. There is no abnormal enhancement within the brain. Incidental note is made of a subcentimeter cutaneous focus overlying the anterior right parietal bone, most likely representing a sebaceous cyst.Cervical spine MRI:Alignment is normal. The marrow signal is benign. The cervical and upper thoracic cord is normal in signal without abnormal enhancement. The cervicomedullary junction is normal. The cerebellar tonsils are in normal position. The visualized paraspinal contents are unremarkable. There are no stenoses.

Output: Negative MRI of the brain and cervical spine including gadolinium enhancement. Specifically, there are no findings to explain the patient's left hand weakness.


Instruction: Generate impression based on findings.

Input: Reason: concern for CVA, unable to further assess chronicity on CT History: ams, contracted MRI of the brainThere is encephalomalacia present along the left parietal lobe as well as in the watershed zone between left anterior and middle cerebral artery territories. There is associated susceptibility effect along the left parietal lobe.There is flair and T2 signal change along the medial aspect of the left parietal lobe as well as the adjacent left and right gyrus along the posterior aspects . There are punctate foci of susceptibility present along the cortex of these structures . Associated increase in diffusion weighted imaging signal along these territories is not accompanied by loss of signal on ADC maps.There are several punctate foci of increased signal on diffusion weighted imaging in the subcortical white matter of the right frontal lobe medially that are associated with flair signal hyperintensity. One of these appears to be associated with diffusion restriction on the ADC map.No abnormal 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.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.There is no evidence for intracranial aneurysm or cerebrovascular occlusion.The anterior communicating artery is identified and is medium-sized there. The posterior communicating arteries are identified and are very small. The vertebral arteries are similar in size. The left posterior inferior cerebellar artery is extracranial origin.The exam is mildly compromised by patient motion.

Output: 1.Findings suggest late subacute infarction along the medial aspect of the left parietal lobe and in the posterior aspects of the cingulate gyrus bilaterally.2.Encephalomalacia is present along the left parietal lobe and watershed zone between the left middle and anterior cerebral artery territories.3.Punctate lesions in the subcortical white matter of the right medial frontal lobe are present which are suspected to be vascular related. One of these may represent a more acute punctate focus of infarction.4.No evidence for intracranial aneurysm.


Instruction: Generate impression based on findings.

Input: Secondary or tertiary adrenal insufficiency, evaluate pituitary and hypothalamus. BRAIN: The ventricles and sulci are within normal limits. The basal cisterns remain patent. There is no midline shift or mass effect. There are no areas of abnormal signal or pathologic enhancement. There is no diffusion abnormality. No extra-axial fluid collection is identified. Normal flow-voids are demonstrated in the major intracranial vascular structures. The midline structures and craniocervical junction are within normal limits. A mucous retention cyst is present within the right maxillary sinus. The orbits, skull, paranasal sinuses, and scalp soft tissues are otherwise grossly unremarkable.PITUITARY: Dedicated images through the sella demonstrate that the pituitary appears slightly small, however, this could reflect normal variation. No focal abnormal signal intensity or mass is seen within the pituitary gland. The pituitary stalk lies in the midline. Suprasellar cistern, optic chiasm, cavernous sinuses and intracranial portions of the optic nerves appear unremarkable.

Output: 1.No evidence of acute intracranial hemorrhage, mass, or acute infarct.2.No pituitary lesions identified. The pituitary appears slightly small, however, this could simply reflect normal variation.


Instruction: Generate impression based on findings.

Input: Clinical question:? Intracranial hemorrhage. Signs and symptoms: Status post blunt head trauma and loss of consciousness. CT of brain without infusion:Diffuse periventricular and subcortical foci of decreased attenuation in bilateral cerebral hemispheres are not specific however more likely diagnosis of small vessel disease and multiple sclerosis should be considered. Please correlate with history. There are no old studies available. There is no associated mass effect with the above findings. The cortical sulci and ventricular system remain within normal. There are no old studies for comparison and please correlate with clinical findings and history and if clinically desired follow-up with an MRI is recommended. No evidence of any post traumatic finding is detected.Calvarium is intact. Mastoid air cells, middle ear cavities and limited view of paranasal sinuses are unremarkable. No abnormality of the scalp is detected.CT of the maxillofacial region:Paranasal sinuses are well pneumatized and with no evidence of acute or chronic sinus disease. The ostiomeatal units of maxillary sinuses are patent bilaterally. Images through the nasal cavity demonstrate minimal nasal septum deviation to the left and a very small approximately 3 mm bony septal spur projecting to the left.Images through the orbits demonstrate no evidence of adenopathy.The minimal soft tissue thickening of the right cheek is present.

Output: 1.No evidence of post traumatic finding on CT of brain.2.Findings highly suspect that of advanced small vessel disease or demyelinating disease as described. Follow-up with an MRI is recommended.3.With the exception of minimal soft tissue thickening/edema of the right cheek the CT of maxillofacial region remains within normal.


Instruction: Generate impression based on findings.

Input: Chronic paroxysmal hemicrania, not intractable [G44.049], Reason for Study: ^Reason: headache etiology History: change HA frequency No evidence of acute ischemic or hemorrhagic lesion on the scan.There is about 5mm downward displacement of cerebellar tonsil through the foramen magnum.The ventricles, sulci and cisterns are symmetric and unremarkable. The gray-white matter differentiation is normal. There is no mass, mass effect, edema, midline shift, intra or extra-axial fluid collection/hemorrhage, or restricted diffusion/acute ischemia. The midline structures and cranial-cervical junction are normal. Normal flow voids are identified in the major intracranial vessels. The paranasal sinuses and mastoid air cells are clear.

Output: No evidence of acute ischemic or hemorrhagic lesion.About 5mm cerebellar tonsilar herniation through the foramen magnum.


Instruction: Generate impression based on findings.

Input: 76-year-old woman with soft tissue disorder. Evaluate for osteomyelitis. Left leg:There is diffuse skin thickening and subcutaneous edema with enhancement of the subcutaneous fat, as well as widespread muscle atrophy. Bone marrow signal intensity is within normal limits, with no evidence of osteomyelitis.Right leg:There is diffuse skin thickening and subcutaneous edema with enhancement of the subcutaneous fat, as well as widespread muscle atrophy. Bone marrow signal intensity is within normal limits, with no evidence of osteomyelitis.

Output: Diffuse skin thickening and subcutaneous edema without osteomyelitis.


Instruction: Generate impression based on findings.

Input: Pathological fracture, other site, subsequent encounter for fracture with delayed healing [M84.48XG], Reason for Study: ^Reason: T8 compression fracture, please obtain STIR images to evaluate acuity of fracture There are multifocal abnormal bone marrow signal on thoracic vertebral bodies including T7, T8, T9, T10, and T11 suggesting metastatic lesions.At the level of T7, T8 and T9, the STIR images show high signal intensity indicate possible acute/subacute bone marrow edema.Comparing to prior scan, the T8 vertebral body height has been decreased implying progressive compression fracture. There is moderate to severe degree spinal stenosis at the level of T8, however, the spinal cord signal intensity appears to be normal.The T9 vertebral body shows about 10% of compression fracture, T10 and T11 vertebral bodies show abnormal signal intensity lesions with bone marrow edema without losing the vertebral body height suggesting metastatic lesions.Multifocal degenerative changes of intervertebral discs which abuts thecal sac on lower thoracic and upper lumbar region.

Output: 1. Progressed compression fracture of T8 vertebral body with sustained bone marrow edema indicating chronic compression fracture with acute component. Mild retropulsion of the compression fracture narrowed spinal canal at this level but the spinal cord signal intensity appears to be normal.2. About 10% of acute compression fracture at the level of T9 without retropulsion.3. Multiple vertebral body metastasis with bone marrow edema at the level of T7, T10 and T11.


Instruction: Generate impression based on findings.

Input: Please evaluate for seizure focus such as old stroke, dysplasia, or tumor: Tonic seizure with left parietal/occipital interictals. There are a few prominent perivascular spaces in the bilateral parietal lobes. The brain parenchyma otherwise appears unremarkable, without evidence of prior infarction, hemorrhage, mass, medial temporal sclerosis, hamartomas, or heterotopias. 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 seizure foci.


Instruction: Generate impression based on findings.

Input: Craniopharyngioma status post resection in July 2014 and radiation therapy in September 2014: surveillance. There are postoperative findings related to right frontal craniotomy. There is unchanged curvilinear enhancement in region of the hypothalamus, perhaps associated with a subcentimeter cystic component. There is unchanged encephalomalacia and intrinsic T1 hyperintensity in the right basal ganglia and subcallosal region, as well as volume loss along the right aspect of the optic apparatus. There is no evidence of mass lesions of abnormal enhancement in the sellar and parasellar regions. There is scattered nonspecific T2 hyperintensity in the cerebral white matter, but no evidence of acute infarction or intracranial hemorrhage. The orbits, skull, and scalp appear unchanged.

Output: Post-treatment findings without evidence of tumor progression.


Instruction: Generate impression based on findings.

Input: 17-year-old female with evidence of residual Crohn's disease. Evaluate signs of partial obstruction.Additional history obtained from DR. Mak's EPIC note 1/13/2016: Patient with history of laparoscopic assisted ileal resection on 12/10/2015 with approximately 55 cm of ileum which was resected with primary anastomosis. ABDOMEN:LIVER, BILIARY TRACT: No significant abnormality noted.SPLEEN: No significant abnormality noted.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: No significant abnormality noted.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: Postoperative changes of ileal resection. No evidence of a small bowel obstruction. No evidence of small bowel wall thickening or inflammatory changes. The colon is normal in caliber.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.PELVIS:UTERUS, ADNEXA: No significant abnormality noted.BLADDER: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: Postoperative changes of ileal resection. No evidence of a small bowel obstruction. No evidence of small bowel wall thickening or inflammatory changes. The colon is normal in caliber.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: Postoperative changes of ileal resection without evidence of residual inflammatory changes or partial small bowel obstruction as clinically questioned.


Instruction: Generate impression based on findings.

Input: MRI Brain:Small areas of T2 hyperintensity and questionable diffusion restriction are seen involving scattered areas of the cortex, including involving the left precentral gyrus and the hand area of the pre and postcentral gyri on the right without significant mass effect. Some of the lesions demonstrate volume loss potentially indicating chronicity. In addition, there are numerous scattered foci of periventricular and subcortical white matter signal abnormalities, some of which very likely represent chronic small vessel ischemic disease and chronic lacunar infarcts. However some of these lesions have a morphology suggestive of a demyelinating process, including lesions involving the corpus callosum. Abnormal increased T2 signal is present in the right mesial temporal lobe, specifically affecting the right parahippocampal gyrus, which is an atypical location for small vessel ischemic disease. In addition, there are small foci of mild restricted diffusion in the bilateral middle cerebellar peduncles without a clear T2 FLAIR correlate. There are scattered areas of susceptibility punctate foci of susceptibility included within the right thalamus. 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. MRA Brain: The intracranial internal carotid arteries demonstrate no significant stenosis. The middle and anterior cerebral arteries are also patent. The vertebral arteries, basilar artery, and posterior cerebral arteries also are patent with no significant stenosis. No evidence of aneurysms or vascular malformations. The right globe has abnormal signal which may be related to prior hemorrhage or ophthalmologic treatment.MRA Neck: There is a separate origin of the left subclavian artery, left common carotid artery, and brachiocephalic artery from the arch. The common carotid arteries and cervical internal carotid arteries are normal in course and caliber. Both vertebral artery origins are patent. There is no evidence of stenosis or occlusion. The origins of the vertebral arteries are not well assessed given artifact in this region.

Output: Multiple periventricular lesions are seen, some likely representing small vessel ischemic disease and/or old lacunar infarcts. However, some of the periventricular lesions show a morphology more suggestive of demyelination. In addition, signal abnormality present within the right mesial temporal lobe structures is atypical for small vessel ischemic disease. More superficially, there are scattered lesions involving the cortex, some of which may demonstrate mild diffusion restriction, while others are likely chronic. This is nonspecific and could reflect an ischemic, vasculitic or demyelinating etiology. The possibility of metastases is considered unlikely, but definitive assessment require postcontrast imaging. In addition, there may be some benefit to dedicated spine imaging as the presence of additional lesions may narrow the differential.No significant flow limiting stenosis involving the intracranial and neck vasculature.As seen on the previous head CT, the right globe demonstrates abnormal signal which may represent prior hemorrhage or ophthalmologic treatment.


Instruction: Generate impression based on findings.

Input: 31-year-old female with biopsy proven right breast fibroadenoma (4/21/15), underwent a research MRI that demonstrated 15-mm mass in the right breast 8 o'clock position and 9-mm mass in the left breast 10 o'clock position for which a second look ultrasound is recommended. A targeted bilateral breast ultrasound was performed. Right breast 8 o'clock position and there is an oval parallel oriented hypoechoic mass with lobulations, very similar in morphology to the previously biopsied fibroadenoma in the right breast 12 o'clock position. This mass measures 1.4 x 0.7 x 1.3 cm and most likely corresponds to the finding seen on MRI.In the left breast 10 o'clock position, there is an oval parallel oriented hypoechoic mass measuring 7 x 4 x 8 mm, most likely corresponding to the finding seen on MRI. Both these lesions most likely represent benign fibroadenomas.

Output: Two benign morphology masses, in the right breast 8 o'clock position, and left breast 10 o'clock position, corresponding to the finding seen on MRI. Both these lesions most likely represent benign fibroadenomas. Follow-up right breast ultrasound and bilateral breast research MRI is recommended in 6 months to confirm stability.BIRADS: 3 - Probably benign finding.RECOMMENDATION: 3B - Followup at Short Interval (1-11 Months).


Instruction: Generate impression based on findings.

Input: New diagnosis of multiple myeloma: saddle anesthesia, right hip and buttock pain, and acute renal failure. There is degenerative spondylosis in the cervical spine, particularly at C3-4 and C4-5, with mild indentation of the spinal cord. Patchy high T2 signal projecting over the spinal cord in this region may be artifactual or may represent myelomalacia. There is a T2 hyperintense mass within the posterior aspect of the T12 vertebral body with epidural extension associated with compression of the spinal cord. There is also mild deformity of the superior endplate of T12. There may be trace edema in the spinal cord at this level versus artifact. There is focal fat in the inferior T7 vertebral body. There appears to be a predominantly T2 hyperintense lesion in the superior portion of the L2 vertebral body with mild irregularity of the superior endplate. The vertebral column alignment is grossly intact. There is a partially-imaged mass arising from the right sacrum and iliac bone. The cerebellar tonsils are mildly low-lying.

Output: 1. Degenerative spondylosis in the cervical spine, most pronounced at C3-4 and C4-5 with mild indentation of the spinal cord. 2. A myelomatous deposit in the T12 vertebra with pathological fracture and epidural extension results in spinal cord compression.3. A lesion in the superior portion of the L2 vertebral body with mild irregularity of the superior endplate may represent an additional myelomatous deposit versus an intravertebral disc herniation, although characterization is limited without intravenous contrast. 4. Partially-imaged mass arising from the right sacrum and iliac bone. Please refer to the separate pelvis MRI report for additional details.5. Diffuse enlargement of the bilateral kidneys likely represents myelomatous infiltration.6. The cerebellar tonsils are mildly low-lying.


Instruction: Generate impression based on findings.

Input: Right lumpectomy followed by radiation and chemotherapy and hormonal therapy in 2004 for IDC. There is scattered fibroglandular tissue in both breasts.Mild parenchymal enhancement is noted bilaterally. Postsurgical changes are present within the right breast, compatible with patient's history of lumpectomy. No abnormal enhancement is seen in either breast. No abnormal lymph nodes are identified in either axillary region.

Output: No MRI evidence for malignancy. BIRADS: 1 - Negative.RECOMMENDATION: ND - Routine Diagnostic Mammogram.


Instruction: Generate impression based on findings.

Input: There is minimal scattered areas of subcortical white matter T2 hyperintensity. There is no evidence of acute infarct or intracranial hemorrhage. There are no abnormal intracranial enhancement. There is no intracranial mass or mass effect. Specifically, the cerebellum and the cerebellopontine angle appear normal. The major intracranial vascular structures enhance normally. The ventricles and sulci appear normal in size and configuration.There are scattered paranasal sinus secretions and mucosal thickening.

Output: 1. No evidence of cerebellar lesions.2. Minimal nonspecific cerebral white matter T2 hyperintensity.3. Mild inflammatory paranasal sinus disease. I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Clinical question: 21-year-old female with AIDS. Right frontal headaches and vomiting. Nonenhanced head CT: New since prior examination is a focus of vasogenic edema in height comment CT right paramedian frontal lobe. This finding measures approximately 16 x 33 mm in transaxial dimensions. There is minimal high density material within this area of edema along its medial aspect. Recommend further follow-up with an MRI examination. Finding is concerning for an infection, neoplasm considering provided clinical history of AIDS.This examination is otherwise unremarkable and within normal limits for patient's stated age.

Output: Focus of vasogenic edema in high convexity right frontal lobe measuring 16 times 33-mm in size. Recommend follow-up with an enhanced MRI examination.


Instruction: Generate impression based on findings.

Input: RUE and RLE weakness Anterior cervical diskectomy device is noted from C3 to C5. There is also anatomic fusion of C5-6. No evidence for fracture or dislocation. Degenerative changes are noted in the lower cervical spine. Refer to the same day MRI for evaluation for cervical spinal canal stenosis.Mild to moderate degenerative changes of the lumbar spine with anterior bony disc osteophyte complex from L3-4. There is preservation of the vertebral body heights and intervertebral disk spaces. No fracture or subluxation.

Output: Degenerative changes but no fracture or dislocation. Refer to the same day MRI for evaluation for spinal canal stenosis.


Instruction: Generate impression based on findings.

Input: History of vaginal cancer undergoing evaluation prior to brachytherapy administration. PELVIS:UTERUS, ADNEXA: Status post hysterectomy.BLADDER: A Foley catheter is in place. There is air within the bladder presumably related to placement.LYMPH NODES: No pelvic lymphadenopathy. Scattered normally sized inguinal lymph nodes appearing similar to prior.BOWEL, MESENTERY: There is persistent tethering of the sigmoid colon and small bowel to the vaginal cuff.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: There is an intracavitary device within the vagina. Associated susceptibility artifact limits evaluation of the patient's known vaginal cuff mass. Overall the mass appears slightly smaller when compared to prior with less extension into the adjacent bladder and sigmoid colon. There has been interval increase in ill-defined surrounding the vaginal cuff and extending into the adjacent tissues, parametrium, and the posterior aspect of the bladder. However this enhancement is poorly defined as opposed to masslike and particularly in light of the short interval change this is presumed to reflect inflammatory changes related to treatment as opposed to tumor growth.

Output: 1.Intracavitary device in the vagina. Associated susceptibility artifact limits evaluation of the patient's known vaginal cuff mass. Compared to prior, the mass appears slightly smaller with less extension into the adjacent sigmoid colon and bladder. Interval increase in ill-defined enhancement surrounding the mass and extending into the adjacent soft tissues is felt to most likely reflect treatment-related inflammatory change rather than neoplastic spread.


Instruction: Generate impression based on findings.

Input: 45 years, Female, paresthesias. Multiple sclerosis, follow-up progression. There is extensive confluent T2/FLAIR hyperintensity throughout the bilateral supratentorial subcortical and periventricular white matter compatible advanced chronic demyelinating disease. There is advanced global parenchymal volume loss including diffuse thinning of the corpus callosum. Compared to prior study from 3/15/2011, no significant change is appreciated. Minimal signal abnormality is evident in the brainstem and cerebellum and more evident on remote MRI study from 6/19/2008.No evidence of intracranial mass effect, midline shift, or herniation. No hydrocephalus. No extra-axial collections. Calvarium and extra cranial soft tissues are grossly unremarkable.

Output: Extensive white matter signal abnormality throughout the bilateral cerebral hemispheres compatible with advanced chronic demyelinating disease. Extensive parenchymal volume loss is also evident. These findings are not appreciably changed since 3/15/2011.


Instruction: Generate impression based on findings.

Input: 37-year-old female with history of shunt, now with difficult to control seizures and altered mental status. Evaluate ventricles. Evaluate shunt. CT at outside hospital two weeks ago said there was subarachnoid hemorrhage. Possible PRES. There is diffuse cerebral edema with increased density surrounding the basal cisterns and cerebellar tentorium compatible with pseudo-subarachnoid hemorrhage. Low attenuation is seen throughout the cerebral convexities bilaterally involving the bilateral frontal and occipital lobes. There is crowding at the level of the foramen magnum suggestive of ectopia versus artifact. All the cisterns are effaced.There is a focus of high attenuation within the right posterior occipital lobe compatible with hemorrhage this may be secondary to hypertensive hemorrhage.The ventricles are mildly enlarged however not significantly different compared to the previous MRI brain dated 3/11/2005.Again noted is a shunt catheter which traverses the right lateral neck soft tissues the catheter tip terminates within the foramen magnum and upper cervical spine. Within the limits of CT examination there is no evidence of shunt discontinuity or kinking.The calvaria and skull base are radiographically normal. The visualized paranasal sinuses and mastoid air cells are normally pneumatized.

Output: 1. Diffuse cerebral edema with multifocal patchy white matter hypoattenuation with focus of parenchymal hemorrhage in the right occipital lobe compatible with hypertensive hemorrhage. Further evaluation with MRI may be considered as clinically indicated2. No evidence of subarachnoid hemorrhage as clinically questioned.3. Shunt catheter at the level of the foramen magnum and upper cervical spine without evidence of discontinuity or kinking.


Instruction: Generate impression based on findings.

Input: Malignant neoplasm of unspecified site of unspecified female breast [C50.919], Reason for Study: ^Reason: Hx: metastatic breast cancer on letrozole and Denosumab now with worsening upper arm pain, not reproducible on exam. History: RUE pain that radiates C-Spine:The cranial-cervical junction is normal. There multilevel degenerative changes including disc dessication.The C7 vertebral body shows loss of normal bone marrow signal intensity indicating possible metastatic lesion which do not show any significant interval change since prior scan.C2 and C4 vertebral body show focal enhancement which again can represent focal metastatic lesion, no change since prior scan.There is no evidence of spinal cord signal abnormality.At the level of C34, there is broad based disc protrusion central to left which abuts thecal sac with minimal spinal canal stenosis.At the level of C45, broad based central disc bulging with ligamentum flavum thickening especially on the left side create mild to moderate spinal canal stenosis.At the level of C56, diffuse bulging of disc with ligamentum flavum thickening create mild to moderate spinal canal stenosis. In addition, there is moderate to severe neuroforaminal stenosis on the left side and mild neuroforaminal stenosis on the right.At the level of C67, there is broad based disc protrusion toward right side lateral recess creating right side lateral recess narrowing with possible compression of the right side nerve root. There is left side neuroforaminal narrowing due to uncovertebral joint hypertrophy.Thoracic spine:The pattern of metastatic lesions on thoracic vertebral bodies appear to be changed significantly.In particular, previously seen diffuse vertebral body involving lesions are now more likely confined appearance. There also interval development of compression fractures on T4 (about 10%), T6 (about 10%), T9 (about 15%) and T11 (about 5%). The large extruded disc at the level of T67 which abuts thecal sac and spinal cord do not show any significant interval change since piror scan. There is left side ligamentum flavum thickening at the level of T9-T10 which creates minimal spinal canal narrowing. Except the level of T67 and T9-T10, there is no evidence of spinal canal narrowing.There is no evidence of abnormal signal intensity of the spinal cord.Lumbar spine Again multiple vertebral body metastatic lesions were seen which demonstrate interval change.The patterns of interval changes are similar to those of thoracic spine. Specifically, those seen as diffuse vertebral body involvement is now showing more confined lesion with development of interval compression fracture of L2 (about 30%) as well as L3 and L4 endplate fractures.However, the S1 vertebral body shows a bit more progressed vertebral body involvement comparing to prior study.Disc dessication was seen in all lumbar spine with ligamentum flavum thickening indicating degenerative changes. In particular, at the level of L34 and L45, there is mild to minimal spinal canal narrowing. Diffuse involvement of bilateral ilium and remained sacrum.Spinal cord signal intensity appears to be normal without evidence of abnormal enhancement.The conus medullaris terminates at the L1 level.

Output: 1. Interval change of pattern of vertebral body metastasis on both thoracic and lumbar spine, specifically the lesions appear to be more confined and developed various degree of compression fractures as described above.2. Multi-level various degree degenerative changes especially cervical spine including spinal canal stenosis and neuroforaminal stenosis.3. No change of T67 intervertebral disc extrusion since prior scan.4. Interval progression of S1 vertebral metastatic lesion comparing to prior scan.