Instruction: Generate impression based on findings.

Input: Frontal and retro-orbital pressure bilaterally after fall while snowboarding 6 wks ago, with symptoms worsening over past 3 weeks, but the neurological exam is non-focal. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is a small area of mild patchy posterior right frontal lobe periventricular white matter T2 hyperintensity. The brain parenchyma otherwise appear unremarkable. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: Nonspecific mild patchy posterior right frontal lobe periventricular white matter T2 hyperintensity, which may possibly be related to remote ischemia, but no evidence of intracranial hemorrhage, mass, or acute infarct.


Instruction: Generate impression based on findings.

Input: There is a 59 x 54 mm sagittal dimension homogeneously CSF signal intensity posterior fossa cyst without enhancement. There is associated adjacent bone remodeling and minimal mass effect on the cerebellum. Lesion extends from the cisterna magna into the superior cerebellar cistern. There is no diffusion abnormality associated with this lesion.The pituitary gland is normal in size. However, there is a 7 x 9 mm focus of intrinsic T1 hyperintense signal in the posterior and inferior aspect of the pituitary gland (series 401 image 12) which is larger than what is expected for a normal neurohypophysis. This may represent a proteinaceous Rathke's cleft cyst. There is no focus of susceptibility effect to suggest prior hemorrhage. There is no deviation of the pituitary stalk, effacement of the suprasellar cistern or mass effect on the optic chiasm.There is no suspicious intracranial enhancement, acute infarct, or cerebral edema. The ventricles and basal cisterns are normal in size and configuration. There is no hydrocephalus. There is no midline shift or herniation.

Output: 1.Findings consistent with an arachnoid cyst in the posterior fossa with minimal local mass effect.2.Normal sized pituitary gland with a prominent 7 x 9 mm focus of intrinsic T1 hyperintensity in its posterior and inferior aspect which is favored to represent a Rathke's cleft cyst with proteinaceous material. No associated mass effect.3.No evidence of intracranial traumatic injury.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Pre-and post enhanced brain MRI: Evaluate for seizure etiology. Signs and symptoms: GTC seizures. Pre-and post enhanced brain MRI:No acute intracranial process.There is a large focus of mildly hemorrhagic encephalomalacia involving the right posterior parietal and extending inferiorly into the right posterior temporal lobe, posterior aspect of the right insular cortex and right basal ganglia and right thalamus. The finding results in expansion of adjacent cortical sulci and right lateral ventricle. Finding is highly suggestive of a chronic right MCA hemorrhagic ischemic stroke. There is no evidence of enhancement at the site.Additionally there are small patchy foci of periventricular and subcortical flair/T2 hyperintensity in bilateral cerebral hemispheres without hemorrhagic changes or enhancement and highly suggestive of mild to moderate degree of chronic small vessel ischemic stroke.There is also suggestion of slight generalized prominence of cortical sulci for stated age which may represent mild underlying volume loss. Images through posterior fossa are unremarkable.Post enhanced images are negative or any detectable abnormal parenchymal, leptomeningeal, calvarial or retropatellar enhancement.Barium demonstrate a tiny bony defect in the right parietal representing a burr hole as was seen on head CT.

Output: 1.No acute intracranial findings.2.Large right hemispheric focus of mildly hemorrhagic encephalomalacia suggestive of a large chronic ischemic stroke as detailed above.3.Findings of mild to moderate chronic nonhemorrhagic small vessel ischemic strokes in the supratentorial parenchyma.4.No detectable abnormal enhancement.


Instruction: Generate impression based on findings.

Input: 62-year-old woman with history of approximately 6 mm right flank lipoma felt on clinical examination. ABDOMEN:LIVER, BILIARY TRACT: The liver is normal in signal and morphology. The gallbladder is normal. There is no intra or extrahepatic biliary duct dilatation.SPLEEN: The spleen is normal.PANCREAS: The pancreas is normal. There is no significant pancreatic duct dilatation.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: The kidneys are normal.RETROPERITONEUM, LYMPH NODES: No significant lymphadenopathy noted.BOWEL, MESENTERY: The partially visualized small bowel and colon are normal.BONES, SOFT TISSUES: There is an incompletely circumscribed area of homogenous high T1 and T2 signal seen immediately superficial to the right abdominal oblique musculature (series 901, image 39). This area measures 45 x 27 mm and appears slightly asymmetric compared to the contralateral side.OTHER: No significant abnormality noted.

Output: Thinly encapsulated lipoma versus focal lobulation of the patient's subcutaneous fat seen in the right flank. No suspicious imaging features.


Instruction: Generate impression based on findings.

Input: History of Crohn's disease presenting with rectal pain and bleeding. Evaluate for fistula or abscess. PELVIS:UTERUS, ADNEXA: No significant abnormality noted.BLADDER: No significant abnormality noted.LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: Note is made of mild bowel wall thickening, enhancement and restricted diffusion of the distal small bowel in the right lower quadrant.BONES, SOFT TISSUES: There is a very thin T2-hyperintense linear focus adjacent to the very distal left lateral anal canal which does not appear to extend through the external sphincter complex and is not associated with a discrete fluid collection. It is at approximately the 4:00 position. It extends 1.4 cm in AP dimension and 1.0 cm in craniocaudal dimension. There is mild associated postcontrast enhancement.OTHER: No significant abnormality noted.

Output: 1. Suspected 1.4 cm intersphincteric left (approximately 4:00) lateral peri-anal fistula. No discrete fluid collection. 2. Acute inflammation of the partially imaged distal small bowel in the right lower quadrant.


Instruction: Generate impression based on findings.

Input: There is an abnormal iron accumulation pattern, specifically demonstrating asymmetric putamen greater than globus pallidus iron. Associated with this is extensive bilateral caudate iron accumulation. There is also T2 hyperintensity just inferior to the tectum and involving the bilateral superior cerebellar peduncles. There are also scattered foci of T2 hyperintensity in the periventricular and subcortical white matter, as well as pons, confluent in some locations, without associated mass effect, restricted diffusion, or susceptibility abnormality. The ventricles and sulci are normal in size, and there is no evidence of preferential cerebellar/pontine atrophy. There is no MRI evident "hot cross bun sign". 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. 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. Note is made of degenerative changes of the upper cervical spine including anterolisthesis C3 on C4 with probable central stenoses at C3/4 and C4/5.

Output: 1.There is an abnormal iron accumulation pattern, specifically demonstrating asymmetric putamen greater than globus pallidus iron. Associated with this is extensive bilateral caudate iron accumulation. There is also T2 hyperintensity just inferior to the tectum and involving the bilateral superior cerebellar peduncles. There is no evidence of preferential cerebellar/pontine atrophy. The constellation of these features are suggestive of an iron accumulating neurodegenerative disorder.2.Moderate chronic small vessel ischemic disease.3.Note is made of degenerative changes of the upper cervical spine including anterolisthesis C3 on C4 with probable central stenoses at C3/4 and C4/5.


Instruction: Generate impression based on findings.

Input: 62 year-old female with altered mental status and history of multiple sclerosis. Evaluate for intracranial hemorrhage. There is no evidence of intracranial hemorrhage, mass or edema. Extensive white matter changes are stable when compared to previous examination. No evidence of cortical stroke. If there is clinical concern for acute ischemia an MRI may be considered. 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.

Output: Stable, extensive white matter changes. If there is clinical concern for acute ischemia an MRI may be considered.


Instruction: Generate impression based on findings.

Input: Reason: eval sp occlusion of the R PCOMM, R anterior choroidal, and Lt ICA aneurysm History: cerebral aneurysm MRA: There is nodular enhancement of the aneurysmal wall with irregular shape compared to round appearance on prior exam, suggestive of shrinkage of left cavernous sinus segment giant aneurysm. Unchanged MR characteristics of local enhancement of adjacent dura. There is no brain parenchymal enhancement. The intra aneurysmal non thrombotic luminal enhancement of the left cavernous sinus segment aneurysm seen on prior scan is no longer seen, compatible with left ICA aneurysmal progressive thrombosis. Left anterior cerebral circulation is reconstituted by the right ICA via circle of Willis especially through the Acom artery. Right posterior communicating artery aneurysm was coiled without residual arterial flow and shows patent right PCom artery. Right anterior choroidal artery aneurysm has expected small residual lumen. Distal right ICA stent is patent without evidence of intimal hyperplasia. Stable ectatic and tortuous appearance of the vertebrobasilar system.MRI brain: No abnormal diffusion restriction. No acute intracranial hemorrhage. No ventriculomegaly. Cisterns are patent. No midline shift. There is stable right gyriform susceptibility artifact in the superior frontal sulcus, consistent with prior hemorrhage, unchanged. Scattered periventricular and subcortical white matter T2/FLAIR hyperintensities compatible with chronic small vessel ischemic disease. Scattered ethmoid air cell opacification. Partial opacification of the left mastoid air cells. Small left maxillary mucous retention cyst. Orbits are intact.

Output: 1.Thrombosing left cavernous sinus aneurysm status post left ICA endovascular occlusion. Stable adjacent dura and aneurysmal wall enhancement without parenchymal enhancement.2.Status post coiling of the right posterior communicating artery aneurysm without recannulization.3.Status post coiling of the right anterior choroidal artery aneurysm with expected residual arterial flow.4.Stented right distal ICA is patent without restenosis.5.No acute intracranial hemorrhage, no new acute ischemic lesion.


Instruction: Generate impression based on findings.

Input: MRI PELVIS WWO; 11/11/2015 12:50 PM PELVIS:UTERUS, ADNEXA: There are multiple T1 and T2 hypointense lesions within the myometrium. The largest of these lesions is intramural in the uterine fundus (series 9, image 34), measures 61 x 56 mm, and demonstrates minimal enhancement. There are additional intramural lesions with similar signal characteristics. There is a intramural 21 x 21 mm T1 and T2 hypointense, avidly enhancing lesion in the posterior uterine body (series 11, image 18).The junctional zone of the uterus is thickened measuring up to 18 mm and there are small internal foci of T2 hyperintense signal.The endometrial stripe is normal.BLADDER: No significant abnormality noted.LYMPH NODES: No significant lymphadenopathy noted.BOWEL, MESENTERY: The rectosigmoid colon is normal.BONES, SOFT TISSUES: Anterior subcutaneous scarring likely related to prior C-section.OTHER: No significant abnormality noted.

Output: 1.Multiple, minimally enhancing intramural fibroids.2.Additional, single avidly enhancing intramural fibroid in the uterine body.3.Findings compatible with adenomyomatosis.


Instruction: Generate impression based on findings.

Input: 19-year-old male with a history of sickle cell disease status post allogenic stem cell transplant one year ago. Assess for abnormality. MRI brain:No significant parenchymal signal abnormality is seen. There is no evidence of edema or mass effect. Diffusion-weighted images are within normal limits. No intracranial hemorrhage or abnormal extra-axial fluid is detected. The ventricular system is normal in size and morphology. A normal variant subcentimeter hippocampal sulcus remnant cyst is seen along the left medial temporal lobe. A subcentimeter focus of T1 hyperintensity again seen within the left parietal calvarium likely represents a benign hemangioma.MRA brain:On MR angiographic imaging, there is a 2 x 3 mm superiorly projecting aneurysm at the junction between the left PCA and left P-comm artery, which in retrospect was present previously and is unchanged. No significant intracranial vascular stenosis or occlusion is seen. The vessels of the anterior and posterior circulation demonstrate normal flow related signal. Patent anterior and bilateral posterior communicating arteries.

Output: 1.No significant brain parenchymal abnormalities are seen.2.2 x 3 mm superiorly projecting left posterior cerebral artery aneurysm at the P1/P2 junction which is unchanged since 9/9/2015. Otherwise the evaluation of the intracranial vasculature is unremarkable with no significant stenosis.


Instruction: Generate impression based on findings.

Input: 33-year-old male with perilunate disassociation. Foci of air may represent post-traumatic vacuum phenomena and mildly limits examination. There has been reduction of the previously described peri-lunate dislocation.LIGAMENTS: Signal abnormality within the ulnar collateral ligament with findings compatible with tear. Further, increased scapholunate interval indicates a tear of the scapholunate ligament.TRIANGULAR FIBROCARTILAGE COMPLEX: There is complete disruption of the TFCC with increased fluid visualized within the DRUJ, indicating tear. TENDONS: The flexor tendons appear intact, without significant abnormality of the carpal tunnel. Guyon's canal appears within normal limits. The extensor tendons also appear intact, but there is increased signal within adjacent soft tissues and within some compartments (specifically the third and fourth), likely indicative of reactive edema from recent injury and reduction.BONES: Fractures of the carpus are better described on same-day CT. However, there is no significant bony edema of the carpus. There is signal abnormality of the ulnar styloid, likely secondary to fracture. ADDITIONAL

Output: 1. Findings compatible with TFCC tear as outlined above.2. Increased radiolunate interval, indicative of tear of the the radiolunate ligament.3. Ulnar collateral ligament tear.4. Ulnar styloid fracture. For further fracture findings, please same day CT.5. Diffuse soft tissue infiltration along the dorsum of the wrist, likely reactive edema from recent procedure.


Instruction: Generate impression based on findings.

Input: Clinical question: Rule out underlying structural lesion. Signs and symptoms: Headache awakening from sleep. Pre and post enhanced brain MRI:No acute intracranial process and negative diffusion weighted images.There is normal anatomical morphology and development of brain parenchymal. There is normal signal intensity of brain parenchyma on all MRI sequences.Unremarkable cerebral cortex, cortical sulci, ventricular system, CSF spaces and brain myelination.No detectable abnormal parenchymal or leptomeningeal enhancement.Unremarkable images through the calvarium and orbits without abnormal enhancement.All paranasal sinuses and bilateral mastoid air cells and middle ear cavities demonstrate normal pneumatization signal patterns.

Output: Unremarkable pre and post enhanced brain MRI as detailed above.


Instruction: Generate impression based on findings.

Input: Male, 59 years old, status-post spinal fusion with removal of C3 nerve root tumor. Assess for residual disease. Please note that a dedicated preoperative cervical spine MRI is not available for comparison. An enhancing lesion is partially visualized within the right C2-3 neural foramen on a prior brain MRI.Postoperative findings are seen compatible with a right C3 laminectomy. Instrumented spinal fusion has also been performed from C2 through C4 with bilateral lateral mass screws except on the right at C3. A fluid collection is present with blood fluid levels occupying the right C3 laminectomy bed tracking posteriorly. Another fluid collection is seen in the superficial subcutaneous tissues of the operative region.The right C2-3 neural foramen remains chronically widened. Nonspecific enhancing soft tissue is present within the foramen and extending into the right lateral aspect of the spinal canal where it seems to contact the lateral edge of the cord. The cervical lordosis is mildly straightened. Alignment is otherwise unremarkable. Marrow signal characteristics are mildly heterogeneous but with no evidence of concerning marrow replacement or marrow edema.The right lateral aspect of the spinal cord is slightly deformed at the level of the right C2-3 foramen which may indicate the effect of prior tumor or surgery. Elsewhere, the spinal cord is unremarkable. Extensive T2 hyperintensity is partially visualized in the pons.C2-3: Postoperative changes. No significant spinal canal stenosis. The left neural foramen is unremarkable. C3-4: Unremarkable. C4-5: Left uncovertebral hypertrophy. No significant spinal canal stenosis. The left neural foramen is mildly narrowed. C5-6: Posterior disk osteophyte formation. Facet hypertrophy. No significant spinal canal stenosis. Mild to moderate foraminal narrowing. C6-7: Posterior disk osteophyte formation asymmetric to the right. No significant spinal canal stenosis. Severe right and mild left foraminal narrowing. C7-T1: Posterior disk osteophyte formation asymmetric to the right. No significant spinal canal stenosis. Mild right foraminal narrowing. At T1-2 as visualized on the sagittal images, there is a bulging disk or disk protrusion with a left neural foramen causing moderate foraminal narrowing.

Output: Postoperative findings are seen consistent with tumor resection from the right C2-3 neural foramen. There remains ill-defined enhancing soft tissue within the neural foramen which projects slightly into the adjacent right lateral spinal canal. The nature of this tissue is uncertain, particularly given the lack of dedicated comparison study, and could represent postoperative granulation, though the possibility of some residual tumor cannot be excluded. A fluid collection is present within the right C3 laminectomy bed as well as another within the more superficial subcutaneous tissues of the operative bed. These findings can be normal in the immediate postoperative state, but clinical and/or imaging follow-up is suggested to ensure resolution.


Instruction: Generate impression based on findings.

Input: The ventricles and sulci are normal in size. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. The pituitary gland is normal in size. There is no evidence for intracranial hemorrhage or acute cerebral, brainstem or cerebellar infarction. No diffusion-weighted abnormalities are identified. Myelination is appropriate for age. 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.Coronal images of the temporal lobes demonstrate the temporal horns, hippocampal formations and parahippocampal gyri to be normal in size and symmetric bilaterally without signal abnormalities or masses identified within the medial temporal lobes on either side. There is no evidence of mesial temporal sclerosis and there are no foci of heterotopic gray matter.

Output: Negative MRI of the brain without contrast. Specifically, there are no MRI images to explain the patient's symptoms.


Instruction: Generate impression based on findings.

Input: 57-year-old male with pain in wrist. LIGAMENTS: The scapholunate ligament appears abnormally thickened which may reflect prior injury but no contrast extends through the ligament to indicate a tear. The lunotriquetral ligament appears intact. There is a small amount of contrast entering the midcarpal joint via what we believe to be communication with the radiocarpal joint along the lateral supporting structures of the wrist; the clinical significance of this is uncertain. TRIANGULAR FIBROCARTILAGE COMPLEX: Contrast extends from the radiocarpal joint into the distal radioulnar joint via a tear of the articular disc of the triangular fibrocartilage complex near its radial attachment.TENDONS: The tendons appear intact.BONES: There is mild cartilage degeneration affecting the wrist, particularly at the capitolunate and lunohamate articulations. Bone marrow signal intensity is otherwise unremarkable.

Output: Tear of the articular disc of the triangular fibrocartilage complex and other findings as described above.


Instruction: Generate impression based on findings.

Input: There is mild to moderate motion degradation limiting evaluation. There is no acute infarct, mass effect, or cerebral edema. There is mild periventricular and subcortical white matter T2 signal abnormality, likely representing chronic microvascular ischemic changes. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. There is mild bilateral maxillary, sphenoid and ethmoid sinus mucosal thickening. The skull and extracranial soft tissues are unremarkable.

Output: Motion degraded exam with no acute infarct. Mild chronic microvascular ischemic changes.


Instruction: Generate impression based on findings.

Input: MRI BRAIN: The lateral ventricles are slightly small with a subjective "pinched" appearance of the lateral ventricular frontal horns. There is a partially empty sella for the patient's age and there is slight optic nerve cupping as well optic nerve sheath dilatation. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There are no areas of abnormal parenchymal signal. There is no abnormal intracranial enhancement. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull and scalp soft tissues are unremarkable. There is mucosal thickening within the right maxillary sinus.MRV HEAD: There is no evidence of venous sinus thrombosis. Note is made of a hypoplastic right transverse sinus.

Output: 1.Findings which would be consistent with a clinical diagnosis of idiopathic intracranial hypertension (pseudotumor cerebri). 2.No evidence of intracranial mass or venous sinus thrombosis. 3.Nonspecific maxillary sinus mucosal thickening.


Instruction: Generate impression based on findings.

Input: History of Guillain Barre with unilateral right-sided retroorbital headache (sharp pain without radiation). Follow-up of abnormal left hippocampal signal abnormality. Mildly elevated T2 hyperintensity and minimal thickening of the left hippocampus head and body are unchanged. This is not associated with abnormal contrast enhancement or diffusion restriction. The remainder of the brain, including the right hippocampus, is normal. There is no evidence of intracranial hemorrhage or acute infarct. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, and scalp soft tissues are grossly unremarkable. There is mild mucosal thickening in the paranasal sinuses without fluid.

Output: Mild thickening and increased T2 signal involving the left hippocampus remain unchanged. The followup interval is probably to short to confidently discriminate between noninfectious/autoimmune encephalitis and a neoplastic process (such as low-grade glioma) though infectious encephalitis is unlikely at this point. A follow-up examination in 2-3 months is suggested.


Instruction: Generate impression based on findings.

Input: Male, 60 years old, breast cancer with bony lesions in the thoracic spine. Assess for cord compression. Diffuse marrow signal heterogeneity is seen compatible with widespread osseous prostatic disease. There is a partial compression of the L4 vertebral body with only trace retropulsion. No epidural disease spread is seen. No acute cord compression is evident. The lower lumbar spinal canal is narrowed due to a combination of a congenitally slender canal and posterior element hypertrophy.

Output: 1.Evidence of widespread osseous metastatic disease.2.Partial compression of the L4 vertebral body without significant retropulsion or associated canal impingement.3.No acute cord compression.4.Narrowing of the lower lumbar spinal canal due to a combination of a congenitally slender canal and posterior element hypertrophy. If clinically warranted, this can be assessed with dedicated lumbar spine imaging.


Instruction: Generate impression based on findings.

Input: Cervical radiculopathy, and pain. Patient motion artifact limits evaluation. The cranial-cervical junction is normal. The cervical spine alignment is anatomic. Mild loss of height of C4-C7 vertebral bodies is likely degenerative in nature, and appears similar to the prior examination. The signal of the visualized cord is normal. The paraspinal soft tissues are unremarkable. Intervertebral disc spaces are preserved, with the exception of mild loss of disc height at C6-7. Bulky anterior osteophyte complexes are again present from C4-5 through C6-7.Degenerative changes are specified by the intervertebral level as follows: C2-C3: Right uncovertebral and facet hypertrophy with mild right foraminal narrowing, similar to prior exam. No significant spinal canal stenosis.C3-C4: Right facet hypertrophy. No significant spinal canal stenosis or foraminal narrowing.C4-C5: Mild posterior disc osteophyte complex. Left facet hypertrophy with moderate left foraminal narrowing, mildly progressed compared to prior exam. No spinal canal stenosis.C5-C6: No significant spinal canal stenosis or foraminal narrowing.C6-C7: Posterior disc osteophyte complex with bilateral foraminal protrusions. Mild bilateral foraminal narrowing. No significant spinal canal stenosis.C7-T1: Mild facet hypertrophy. No significant foraminal narrowing or spinal canal stenosis.

Output: Multilevel degenerative disc disease with scattered foraminal narrowing as described above, with moderate left foraminal narrowing at C4-5, mildly progressed compared to prior exam, otherwise overall not significantly changed since prior exam.


Instruction: Generate impression based on findings.

Input: Severe neck muscle spasm requiring necrotic. Sickle cell disease. Rule out subluxation on right. No evidence of cervical spine subluxation. The cervical spine is in normal alignment aside from dextrocurvature. Craniocervical junction is unremarkable. Ligaments are intact. The vertebral body and disk heights are well-maintained. No worrisome focal marrow signal abnormality is appreciated. The spinal cord is of normal caliber and signal. There is no significant disk bulge, herniation, spinal canal or foraminal stenosis within the cervical spine.

Output: Convex rightward curvature of the cervical spine, which may be positional or related to known spasm. Cervical spine MRI is otherwise unremarkable.


Instruction: Generate impression based on findings.

Input: Female 58 years old Reason: 58 yo with h/o HCC please screen for recurrence ABDOMEN:LIVER, BILIARY TRACT: Nodular hepatic contour with widening of the fissures consistent with hepatic cirrhosis.The reference lesion in the right hepatic lobe measures 1.6 x 1.1 cm (series 11, image 28), remeasured on prior 1.6 x 1.1 cm. There is an incomplete halo of arterial enhancement on the caudal aspect of this lesion with subtle T2 hyperintense signal but without washout. The second subcapsular ablation defect measures 0.8 x 0.8 cm (series 11, image 27) previously remeasured at 0.8 x 0.9 cm stable/mildly decreased in size.Patent hepatic vasculature.SPLEEN: Massive splenomegaly of 18.7 cm. Stable T2 hyperintense lesion within the posterior spleen which may represent a small hemangioma.PANCREAS: There is a 1.0 x 0.7 cm T2 hyperintense lesion within the pancreatic body, compatible with IPMN and not significantly changed compared to prior.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Bilateral renal cysts.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.

Output: 1.Posttreatment changes relating to prior TACE RFA. Suspicious area of arterial enhancement and T2 hyperintense signal surrounding the reference lesion. While this does not meet criteria for HCC it remains suspicious for recurrence and short interval surveillance recommended.2.Hepatic cirrhosis with portal hypertension.3.Stable pancreatic body IPMN.


Instruction: Generate impression based on findings.

Input: Male 81 years old with metastatic renal cell carcinoma. Evaluate for progression. ABDOMEN:LIVER, BILIARY TRACT: Normal morphology liver. Bilobar T2 hyperintense hepatic lesions are redemonstrated with reference measurements provided below. The segment 6 lesion has more nodular contrast enhancement than on the previous exam. A nonreference segment 5 lesion is demonstrates progressive peripheral, nodular discontinuous enhancement compatible with hemangioma. No new lesions are identified. Reference measurements are provided below.The hepatic vasculature is patent. No intra or extrahepatic biliary ductal dilatation. The gallbladder is normally distended.SPLEEN: No significant abnormality noted.PANCREAS: No significant abnormality noted.ADRENAL GLANDS: Status post right adrenalectomy.KIDNEYS, URETERS: Status post right nephrectomy. The left upper pole complex cystic lesion has dense calcification (as seen on same day CT) and is unchanged. Several other simple cysts in the left kidney are stable. No suspicious left renal lesion.RETROPERITONEUM, LYMPH NODES: No retroperitoneal lymphadenopathy.BOWEL, MESENTERY: No significant abnormality noted.BONES, SOFT TISSUES: Levoscoliosis and degenerative changes affect the lumbar spine.OTHER: No significant abnormality noted.INDEX LESION MEASUREMENTS (Current exam date/time: 12/13/2016 10:30:00)SEGMENT 8 LESION: 3.5 x 2.6 cm (Image 204, Series 10); 3.7 x 3.0 cm on prior (8/30/2016) (Image 28, Series 1200).SEGMENT 2 LESION: 1.6 x 1.6 cm (Image 192, Series 10); 2.2 x 2.0 cm on prior (8/30/2016) (Image 28, Series 1200).SEGMENT 6 LESION: 3.5 x 3.4 cm (Image 179, Series 10); 2.7 x 3.2 cm on prior (8/30/2016) (Image 46, Series 1200).

Output: 1.Interval decrease in the size of reference segment 2 and 8 hepatic lesions. The reference lesion in segment 6 has increased in size and demonstrates increased nodular enhancement.2.No new sites of disease.


Instruction: Generate impression based on findings.

Input: 65-year-old female patient with history of metastatic colon cancer to liver. Patient received several cycles of chemotherapy. ABDOMEN:LIVER, BILIARY TRACT: There is a 3.2 x 2.5 cm region of signal abnormality within segment 4A which demonstrates mild T2 hyperintensity, no appreciable enhancement, and loss of signal on out of phase imaging compatible with focal fat deposition. No suspicious hepatic lesion is identified. No intra or extrahepatic biliary ductal dilatation.SPLEEN: There is an accessory splenule.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: A cystic structure adjacent to the distal esophagus immediately proximal to the diaphragm may represent epiphrenic diverticulum.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: No significant abnormality noted.

Output: 1. Region of signal abnormality within segment 4A of the liver is compatible with focal fat deposition. No suspicious hepatic lesion is identified.2. Probable small epiphrenic esophageal diverticulum.


Instruction: Generate impression based on findings.

Input: Status post depth electrode placement for seizure monitoring. There are several transoccipital and transtemporal depth electrodes positioned in the various portions of the medial right temporal lobe region. There is no evidence of any substantial intracranial hemorrhage. The ventricles are unchanged in size and configuration, with a small amount of pneumoventricle. There is no midline shift or herniation.

Output: Several transoccipital and transtemporal depth electrodes positioned in the various portions of the medial right temporal lobe region.


Instruction: Generate impression based on findings.

Input: There is no evidence of intracranial hemorrhage, mass or edema. The ventricles and basal cisterns are normal in size and configuration. No abnormal extra-axial fluid collection is identified. There is no midline shift. The midline structures and craniocervical junction are within normal limits. Note is made of a cavum septum pellucidum, a normal variant. There are a few punctate foci of T2 hyperintensity within the periventricular and subcortical white matter bilaterally which are nonspecific. There is no diffusion abnormality or susceptibility artifact. Normal flow-voids are demonstrated in the major intracranial vascular structures.A mucosal retention cyst is present within the right maxillary sinus. There is mucosal thickening within the bilateral ethmoid air cells. The visualized mastoid air cells are clear. The orbits are unremarkable.

Output: 1.No evidence of intracranial mass, hemorrhage or acute.2.Mild paranasal sinus disease.


Instruction: Generate impression based on findings.

Input: Chest pain, unspecified [786.50] / Cervicalgia [723.1], Reason for Study: ^Reason: please r/o ischemia, vs mass, vs structural abnormality History: left sided weakness. Brain MRI:There is no evidence of acute ischemic or hemorrhagic lesion.There is a focal susceptibility artifact on the right temporal lobe on gradient echo images indicating small blood product. The possibility of cavernous malformation of this lesion cannot be completely excluded, however, the chance appear to be low considering the configuration of the lesion.Multifocal scattered high signal intensity lesions on bilateral deep white matter and periventricular white matter on FLAIR images indicate nonspecific small vessel disease.There is a large developmental venous malformation on the right cerebellar hemisphere.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 mastoid air cells are clear.Small retention cyst on the left side sphenoid sinus.Thornwaldt cyst was also seen.Brain MRA: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.C-Spine:There is about 6mm sized T1 low and T2 high signal intensity well marginated lesion within the odontoid process of C2 indicating benign nature cystic lesion such as osteochondral cyst.There is evidence of atlanto-occipital assimilation, right greater than left.Severe neural foraminal stenosis on the right side of C23, C34, and mild neural foraminal stenosis on the C45 right side, C67 left side.There is no evidence of spinal canal stenosis.Spinal cord signal intensity appears to be normal.

Output: 1. No evidence of acute ischemic or hemorrhagic lesion.2. A small susceptibility artifact on the right temporal lobe anterior aspect, possible prior hemorrhagic focus or small cavernous malformation.3. Non specific white matter lesions on FLAIR and T2 weighted images.4. Developmental venous anomaly on the right cerebellar hemisphere 5. Normal MRA of brain.6. Degenerative disease of C-spine, multilevel various degree neural foraminal stenosis as described above.


Instruction: Generate impression based on findings.

Input: Neurofibromatosis, arm mass Within the medial soft tissues of the arm is a well-circumscribed mass measuring 4.3 x 4.6 x 7.3 cm in the greatest transverse, AP, and craniocaudal dimensions. The mass is predominantly hyperintense to skeletal muscle on T2-weighted sequences (although contains some areas of heterogeneous low signal intensity) and isointense to skeletal muscle on T1 sequences. The mass does not appear to invade the surrounding fat planes and is and otherwise does not demonstrate aggressive features. Following contrast administration, there is solid but heterogeneous enhancement. This mass was evident on the comparison examination from 2011 and has increased from that exam when it measured approximately 3.9 x 4.3 x 6.5 cm.A second similar appearing mass is identified just posterior to the humerus at the same level. This mass measures approximately 1.7 x 1.6 x 3.2 cm in the greatest transverse, AP, and craniocaudal dimensions. Following contrast administration, there is solid central enhancement. This mass was evident on the comparison examination from 2011 and has increased from that exam when it measured 1.3 x 1.2 x 2.5 cm.A third smaller mass is seen within the anterior soft tissues and is further detailed on the dedicated MRI of the left elbow.The underlying marrow signal of the humerus is normal.

Output: Multiple soft tissue masses consistent with peripheral nerve sheath tumors. These have increased in size from a comparison exam of the left humerus dated 4/20/2011.


Instruction: Generate impression based on findings.

Input: 41-year-old female with a family history of ovarian cancer and BRCA2 mutation. High risk breast cancer screening. Retropectoral saline implant appears intact bilaterally. There is heterogeneous amount of fibroglandular tissue in both breasts.Mild parenchymal enhancement is noted bilaterally.New linear non-mass enhancing lesion at 12:00 position in the left breast, measuring 6 x 9 x 21 mm (AP x LR x CC).No abnormal enhancement is seen in right breast. No abnormal lymph nodes are identified in either axillary region.

Output: 1. Suspicious linear non-mass enhancement in the left breast. In view of the small amount of breast tissue and presence of saline implant, MR guided biopsy is not feasible. We recommend targeted ultrasound study, and if any sonographic correlate is found, ultrasound guided biopsy can be performed. If no sonographic correlate is detected, surgical consultation is recommended.2. No MRI evidence of malignancy in the right breast.BIRADS: 4 - Suspicious Abnormality.RECOMMENDATION: T - Take Appropriate Action - No Letter.


Instruction: Generate impression based on findings.

Input: Left arm pain concerning for cervical radiculopathy, please evaluate. Craniovertebral junction appears within normal limits. The cervical vertebral bodies are appropriate in height. Alignment is maintained. Bone marrow signal is within normal limits. The cervical spinal cord has normal signal characteristics and overall morphology.Degenerative changes are seen in the cervical spine as described below:C2-3: No significant compromise to the spinal canal or neural foramina.C3-4: A small disc bulge is visualized but there is no significant compromise to the spinal canal or neural foramina.C4-5: A small disc bulge is visualized but there is no significant compromise to the spinal canal or neural foramina.C5-6: A mild disc bulge and mild uncovertebral and facet degenerative changes cause encroachment of the right greater than left neural foramen. No significant central canal stenosis.C6-7: A mild disc bulge and mild uncovertebral and facet degenerative changes are visualized which cause left greater than right neural foraminal encroachment. No significant central canal stenosis.C7-T1: No significant compromise to the spinal canal or neural foramina.The vertebral artery flow voids appear to be intact. Paraspinous soft tissue structures appear within normal limits.

Output: Degenerative changes about the cervical spine with right greater than left neural foraminal encroachment at the C5-6 level and left greater than right neural foraminal encroachment at the C6-7 level due to uncovertebral osteophytes and disc disease. There is no central canal stenosis within cervical spine.


Instruction: Generate impression based on findings.

Input: Male, 14 years old, with history of incidentally detected pineal lesion, yearly follow-up exam. Again seen is a partially cystic lesion within the pineal region. As on prior exams, a rind of enhancing tissue is evident predominantly posteriorly. On postcontrast images, the lesion measures 12 x 11 x 8 mm with no significant interval change from the prior exam.Remainder of the brain is within normal limits. No evidence of concerning parenchymal signal abnormality, mass effect or edema is detected. No pathologic parenchymal enhancement is seen. No abnormal extra-axial collections are detected. The ventricular system is patent and within normal limits for size.Mucosal thickening and accumulated secretions within the right sphenoid sinus are seen, similar to prior.

Output: Stable partially cystic pineal lesion.


Instruction: Generate impression based on findings.

Input: Grade 2 endometrial cancer. Evaluate for myometrial and cervical involvement. PELVIS:UTERUS, ADNEXA: Small amount of fluid within the endometrial cavity. There are T2-weighted hypointense multilobular endometrial thickening predominantly in the body and fundus of the uterus compatible with patient's stated history of endometrial carcinoma. This region is hypoenhancing relative to the myometrium on postcontrast images. There is suspected myometrial invasion in the fundus, most significantly in the right aspect of the fundus (series 601/20; series 502/66) where it involves at least 50% of the myometrium. No serosal/extramural invasion is evident.There is no evidence of cervical stromal invasion.Borderline thickening of the junctional zone, measuring 12 mm. BLADDER: Partially contracted without significant abnormality.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: Endometrial carcinoma with suspected at least 50% myometrial invasion at the right fundus. No cervical stomal invasion.


Instruction: Generate impression based on findings.

Input: Lumbago with sciatica, unspecified side [M54.40] / Pain in right hip [M25.551] / Muscle weakness (generalized) [M62.81], Reason for Study: ^Reason: evaluate for compression, hx of sever DDD with RLE weakness History: low back pain with radiation down RLE For the purpose of this dictation, the lowest visualized intervertebral disc space is labeled L5-S1. There is large soft tissue mass replacing normal fatty marrow of L5 and sacrum with extension toward spinal canal. The mass lesion shows inhomogenous enhancement with evidence of extension toward neuroforamen and spinal canal. The bladder appears to be significantly enlarged, thus considering the mass location and its extent, cauda equina syndrome needs to be considered and excluded.There is normal lumbar lordosis. The spine alignment is anatomic. The vertebral body height is preserved. The signal of the visualized cord is normal.The conus medullaris terminates at the T12-L1 level. Degenerative changes are specified by the intervertebral level as follows: T12-L1: disc dessication, no neuroforaminal narrowing or spinal stenosis. L1-L2: disc dessication, no neuroforaminal narrowing or spinal stenosis. L2-L3: disc dessication, diffuse bulging of disc, no neuroforaminal narrowing. Minimal spinal canal stenosis. L3-L4: disc dessication, diffuse bulging of disc, mild to moderate spinal stenosis. L4-L5: disc dessication, diffuse bulging of disc, moderate to severe spinal stenosis. L5-S1: inferior aspect of the L5 vertebral body shows tumor involvement with spinal canal at the level of L5S1 appears to be filled with soft tissue mass indicating spinal canal involvement by the mass.

Output: 1. Inhomogeneously enhancing soft tissue mass replacing normal fatty marrow signal intensity of the L5 and sacral vertebral body with evidence of spinal canal and bilateral sacral neuroforamen. Most likely etiology of the soft tissue mass is metastatic lesion.2. Multilevel various degree degenerative changes of lumbar spine. Especially at the level of L45, there is moderate to severe spinal stenosis.Comment: Due to obliteration of the spinal canal and bilateral sacral neuroforamen associated with enlarged bladder, Joan Bigane ANP was contacted at the time of this dictation.I have informed her that the patient has large soft tissue mass at the sacrum and possible development of cauda equina syndrome due to the mass.


Instruction: Generate impression based on findings.

Input: Metastatic tonsillar squamous cell carcinoma. Evaluate for progression of brain metastasis.Additional clinical history from electronic medical records: 60 y/o female with a history of stage IV tonsil SCCa (HPV-) s/p CRT completed in 2/2012, salvage R neck dissection in 7/2012, with biopsy-proven lung oligometastasis in 6/2014, s/p RT to a LUL nodule (40 Gy/10 fxs) and two left perihilar lesions (50 Gy/10 fxs) completed in 8/2014. She was found to have brain metastases in 2015 and underwent resection followed by post-op SRS for a L temporal lesion in 3/2015. She recently presented with progressive intracranial and extracranial disease. She also received palliative whole brain radiotherapy in April 2016. Multiple cortically-based and intra-sulcal, contrast-enhancing lesions involving both cerebral hemispheres have become more prominent and slightly larger. The largest lesion which involves the left occipital lobe measures maximally in the axial plane 16 mm, compared to 13 mm previously. The lesion seems to involve the adjacent leptomeningeal disease and is associated with mild but increased perilesional edema. The second largest lesion, which is located more superiorly at the junction between the left parietal and occipital lobes, measures maximally 8 mm compared to 7 mm previously and is also now associated with mild surrounding edema. A third lesion involving the right precentral gyrus measures up to 8 mm in the axial plane, compared to 7 mm previously. There are also a few tiny new contrast-enhancing lesions with associated focal diffusion restriction in the left frontal and anterior left parietal lobes. There is slightly increased contrast enhancement at the site of previous metastectomy from the lateral left temporal lobe but this area is partially obscured and affected by susceptibility artefact from the overlying craniotomy. There is no significant mass-effect. The ventricles and other CSF-containing spaces are slightly larger than before, reflecting mild underlying volume loss. There is no acute territorial infarct or intracranial hemorrhage. Foci of diffusion restriction involving the left supramarginal gyrus and left cerebellar hemisphere are resolved/evolved. There is no midline shift or herniation. The major vascular flow voids are preserved.There are multiple contrast-enhancing skull lesions, the largest of which involves the left occipitotemporal region and measures up to 9 mm in the axial plane, compared to 5 mm previously. Minimal fluid intensity in the left mastoid air cells is unchanged. The orbits are grossly unremarkable.

Output: 1.Since March 2016, there has been an increase in the number and, to a lesser extent, the size of multiple small cortical and intra-sulcal contrast-enhancing lesions, concerning for progression of metastatic disease. The larger lesions are now associated with mild surrounding edema. There is no significant mass-effect or brain herniation. There is no acute intracranial hemorrhage.2.Increased contrast enhancement at the site of previous surgery in the left temporal lobe is less specific and may reflect progression of residual/recurrent metastasis but may also reflect posttreatment change.3.New/enlarging skull lesions are compatible with osseous metastasis.


Instruction: Generate impression based on findings.

Input: 15-year-old female patient with transaminitis with elevated GGT. Evaluate for PSC.EXAMINATION: MRI/MRCP of the abdomen without and with IV contrast 5/1/2015 ABDOMEN:LIVER, BILIARY TRACT: No focal hepatic lesion is identified. No intra- or extrahepatic biliary ductal dilatation. No filling defect is identified in the common bile duct. No gallstones are seen.SPLEEN: The spleen is normal in appearance.PANCREAS: The pancreas is normal in appearance.ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Normal enhancement of the kidneys without evidence of hydronephrosis.RETROPERITONEUM, LYMPH NODES: No significant abnormality noted.BOWEL, MESENTERY:No significant abnormality noted.BONES, SOFT TISSUES: No significant abnormality noted.OTHER: A one centimeter high T2 signal lesion is noted in the right breast.

Output: 1. No evidence of intra- or extrahepatic biliary ductal dilatation.2. Small high T2 signal lesion in the right breast may represent a cyst or lymph node; further evaluation with ultrasound may be considered if clinically warranted.


Instruction: Generate impression based on findings.

Input: 3-year-old male with seizure disorder and history of grade 4 IVH. Evaluate for acute changes Low attenuation of left cerebellar hemisphere consistent with encephalomalacia. Regions of encephalomalacia are also seen in the periventricular areas consistent with findings on prior MRIThere is no evidence of intracranial hemorrhage, mass or edema. 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.

Output: 1. No acute intracranial abnormality. 2. Left cerebellar and periventricular encephalomalacia as described in prior MRI.


Instruction: Generate impression based on findings.

Input: Clinical question: History of craniopharyngioma. Signs and symptoms: Surveillance scan. Pre-and post enhanced brain MRI:Negative diffusion weighted series.The examination redemonstrates stable extensive bilateral frontal cystic encephalomalacia with resultant mild ex vacuo dilatation of frontal horns.There is an irregular T2 hypointensity and T1 isointensity with mild enhancement within the basal cistern consistent with known residual calcific craniopharyngioma. This finding remains stable since prior exam in its size, morphology and pattern of enhancement.Similar to prior exam there is a metallic hardware artifact overlapping the basal cistern. There is no detectable new finding since prior study. Stable postoperative changes of bilateral frontal craniotomy and unremarkable pre-and post enhanced exam otherwise..

Output: 1.Stable MRI exam since prior study re-demonstrating an approximately 11 mm mildly enhancing lesion in the basal cistern consistent with residual lymphangioma.2.Stable extensive bilateral frontal encephalomalacia.3.Unremarkable and stable pre-and post enhanced brain MRI otherwise.4.Chronic sinus disease most noticeable within the left maxillary with no significant change.


Instruction: Generate impression based on findings.

Input: Check for AVN. Patient on chronic steroids for lupus. Pain specifically for glenohumeral rotational movement ROTATOR CUFF: No significant abnormality noted. Rotator cuff is well visualized and intact throughoutSUPRASPINATUS OUTLET: No significant abnormality noted.GLENOHUMERAL JOINT AND GLENOID LABRUM: No marrow changes are abnormalities within the humeral head to suggest AVN. The labrum is grossly intact given nonaugmented exam technique. Please also note that the anterior superior aspect of the labrum is not well visualized and likely secondary to a Buford's normal variant.BICEPS TENDON: No significant abnormality noted. ADDITIONAL

Output: Normal shoulder without specific findings to support or suggest AVN


Instruction: Generate impression based on findings.

Input: Ms. Clark is a 40 year old female with a personal history of benign left breast biopsy in April 2016, with pathology revealing UDH. She also has a personal history of prior benign right and left breast biopsy. She has a family history of breast cancer in her mother, breast cancer in aunt and ovarian cancer in an aunt. Three standard views of both breasts were performed digitally and reviewed with the aid of R2 CAD 9.3. The breast parenchyma is heterogeneously dense, which may obscure small masses (BiRads Density Category C), unchanged in pattern and distribution. An X shaped clip in the upper outer quadrant of the left breast indicates the site of stereotactic biopsy performed on 4/12/2016. A second X shaped clip within the middle outer quadrant of the left breast is unchanged in position. A circumscribed oval mass at the right 6:00 position containing a wing-shaped biopsy marker clip is stable. Multiple small masses are present in both breasts, and appear unchanged when compared to prior mammograms, but were better evaluated by MRI. There are no new masses, suspicious microcalcifications or areas of architectural distortion identified in either breast.

Output: No mammographic evidence of malignancy. As long as the patient's physical examination remains normal, bilateral diagnostic mammogram is recommended annually. Results and recommendation were discussed with the patient. If the patient has greater than 20% lifetime risk, annual MRI should be performed. BIRADS: 2 - Benign finding.RECOMMENDATION: ND - Diagnostic Mammogram.


Instruction: Generate impression based on findings.

Input: 70 years, Male, Reason: 1 week jaundice - bili 7.6; no evident stone or mass on RUQ U/S 3/2 History: painless jaundice. ABDOMEN:LUNG BASES: No significant abnormality notedLIVER, BILIARY TRACT: Mild diffuse single loss on opposed phase imaging suggests steatosis.Common bile duct is dilated to 1.8 cm to just above the ampulla. There is concentric narrowing at this point with associated surrounding low T2 signal (9/17). Diffusion and postcontrast images are somewhat limited in this region due to patient motion. There is also moderate to marked intrahepatic biliary ductal dilatation.SPLEEN: No significant abnormality noted.PANCREAS: Pancreatic duct is normal in caliber. Small punctate cystic lesions in the neck and tail of the pancreas (8/10, 8/16, 8/15) likely represent small side branch intraductal papillary mucinous neoplasms (IPMNs).ADRENAL GLANDS: No significant abnormality noted.KIDNEYS, URETERS: Bilateral simple renal cysts.RETROPERITONEUM, LYMPH NODES: Enlarged peripancreatic lymph nodes, measuring up to 2.1 x 1.4 cm (4/23).BONES, SOFT TISSUES: No significant abnormality noted.

Output: 1.Moderate to marked intrahepatic and extrahepatic biliary ductal dilatation to just above the level of the ampulla where there is a region of T2 hypointense concentric narrowing. ERCP is recommended to exclude a periampullary lesion (or stricture) in this region.2.Punctate cystic lesions within the pancreas likely represent sidebranch IPMNs.3.Mildly enlarged peripancreatic lymph node.


Instruction: Generate impression based on findings.

Input: 61-year-old male with acute mental status changes. Now with change in pupil sizes, right pupil pinpoint. Neither pupil reactive to light. Concern for herniation. There is significant beam hardening artifact affecting the posterior fossa which limits the evaluation. Since the prior study, there is suggestion of decreased density in the left cerebellar hemisphere which may be due to ischemia. The basilar cisterns are less well visualized. An MRI is recommended for further characterization of this region.Other findings appear similar to the prior CT from earlier the same day.These findings were discussed with Dr. Harshal Sheth at the time of interpretation.

Output: Limited examination, but new decreased density in the left cerebellar hemisphere which may be due to ischemia. An MRI is recommended for further characterization of this region.


Instruction: Generate impression based on findings.

Input: There are no diffusion-weighted abnormalities to suggest acute ischemia. There is a subtle, small focus of increased T1 signal and enhancement within the cortex of the left postcentral gyrus (image 12, series 301 and image 137, series 12 one) with associated minimal increased FLAIR signal. This region appears to correlate to an area of hypoattenuation seen on a prior outside hospital CT. There is no other identifiable area of abnormal T2 signal or enhancement within the brain. The ventricles and sulci are normal in size. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. The pituitary gland is normal in size. There is no evidence for intracranial hemorrhage. 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.

Output: Small focus of abnormal T1 & T2 signal with subtle enhancement within the cortex of the left postcentral gyrus may represent laminar necrosis secondary to a resolving subacute infarct. A follow up MRI of the brain with contrast is recommended in 6 months to evaluate for resolution.


Instruction: Generate impression based on findings.

Input: 51 year old female patient with lung cancer with history of brain metastases status post SRS 7/2015. Evaluate disease. There is interval decrease in size of the ring-enhancing lesion within the left superior frontal gyrus, now measuring 6 mm in diameter, previously 14 mm, with a significant decrease in surrounding vasogenic edema. Several punctate enhancing lesions in the bilateral cerebral hemisphere are otherwise not significantly changes. Some of the lesions demonstrate mild surrounding vasogenic edema. There is no evidence of acute ischemia. The ventricles and basal cisterns are stable in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. There is scattered minimal paranasal sinus mucosal thickening. The orbits, skull, and scalp soft tissues are grossly unremarkable.

Output: Interval decrease in size of a left superior frontal gyrus lesion with significant decrease in surrounding vasogenic edema, but no significant change in size of several other punctate metastases otherwise.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: Left hip pain ACETABULAR LABRUM: There is degeneration of the acetabular labrum with a focal degenerative tear in the anterosuperior labrum.ARTICULAR CARTILAGE AND BONE: There is full thickness cartilage loss involving the acetabulum and femoral head focally. There is abnormal offset of the femoral head-neck junction representing a cam type deformity.SOFT TISSUES: No significant abnormality noted. ADDITIONAL

Output: 1. Degenerative tear of the anterosuperior labrum.2. Cam type deformity of the femoral head-neck junction.3. Mild full-thickness cartilage loss involving the acetabulum and femoral head focally.


Instruction: Generate impression based on findings.

Input: Evaluate for structural abnormality, especially in occipital lobe: flashing lights/spots. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma and pituitary gland appear unremarkable. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, and scalp soft tissues are grossly unremarkable. There is mucosal thickening in the bilateral maxillary sinuses.

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


Instruction: Generate impression based on findings.

Input: Metastatic cancer. There is an enhancing mass that measures up to 15 mm in the right temporal bone squamosal portion. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is nonspecific mild scattered cerebral white matter T2 hyperintensity. There are small chronic lacunar infarcts in the bilateral cerebellar hemispheres. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: Right temporal bone metastasis, but no evidence of brain metastases.


Instruction: Generate impression based on findings.

Input: Male, 42 years old, with history of right anterior skull base encephalocele, preoperative imaging. Correlating with findings on the same day CT, a lobular lesion is present centered on the left paramedian clivus with extension into the sphenoid sinus and minimally into the prepontine cistern. The lesion is T1 hypointense and markedly T2 hyperintense with some signal heterogeneity. The lesion does not enhance on postcontrast images.Although osseous structures are better assessed on prior CT, again no definite defect in the anterior skull base is seen. There are no areas of suspected meningeal or parenchymal herniation. Scattered mucosal thickening and/or secretions are redemonstrated in the paranasal sinuses.The signal characteristics and morphology of the brain are otherwise unremarkable. No evidence of restricted diffusion, edema or focal signal abnormality is seen. There are no findings to suggest acute intracranial hemorrhage or any abnormal extra-axial fluid collections. No pathologic intracranial enhancement is observed. A small right frontal developmental venous anomaly is noted incidentally. The ventricles are normal in size and morphology. A right suboccipital subcutaneous lipoma is redemonstrated.

Output: 1.A lobular, non-enhancing lesion is evident centered on the left paramedian clivus with extension into the sphenoid sinus and minimally into the prepontine cistern. Given the CT and MRI findings of this lesion, the differential diagnosis would include a notochordal remnant (ecchordosis physaliphora), as well as a neurenteric or developmental cyst. Lack of enhancement and absence of specific symptoms related to this lesion argue against chordoma or some other aggressive lesion, though this possibility is not entirely excluded.2.No evidence of any defect in the anterior skull base is seen. There are no findings to indicate herniation of meninges or brain parenchyma.3.Evaluation the brain is otherwise within normal limits.


Instruction: Generate impression based on findings.

Input: A 63 year old male with known severe left ventricular dysfunction and no coronary artery disease, referred to cardiac MRI for evaluation of etiology and degree of fibrosis. Left VentricleThe left ventricle is severely dilated with severe systolic dysfunction. The overall LV ejection fraction is 18%, the LV end diastolic volume index is 135 ml/m2 (normal range: 74+/-15), the LVEDV is 229 ml (normal range 142+/-34), the LV end systolic volume index is 111 ml/m2 (normal range 25+/-9), the LVESV is 187 ml (normal range 47+/-19), the LV mass index is 88 g/m2 (normal range 85+/-15), and the LV mass is 149 g (normal range 164+/-36). There is global hypokinesis with regional variation. There is mid-myocardial late gadolinium enhancement of the basal interventricular septum. The finding is atypical for prior myocardial infarction and likely represents myocardial fibrosis. This pattern of late gadolinium enhancement is most commonly seen in dilated cardiomyopathy. No evidence of myocardial iron overload. Findings unlikely to represent amyloidosis. Left AtriumThe left atrium is severely dilated. Right VentricleThe right ventricle is severely dilated with severe systolic dysfunction. The overall RV ejection fraction is 14%, the RV end diastolic volume index is 170 ml/m2 (normal range 82+/-16), the RVEDV is 188 ml (normal range 142+/-31), the RV end systolic volume index is 146 ml/m2 (normal range 31+/-9), and the RVESV is 246 ml (normal range 54+/-17).Right AtriumThe right atrium is severely dilated.Aortic ValveThe aortic valve opens widely and there is no significant aortic regurgitation. The aortic valve is trileaflet.Mitral ValveThe mitral valve opens widely and there is moderate to severe mitral regurgitation.Pulmonic ValveThe pulmonic valve opens widely. There is no significant pulmonic regurgitation.Tricuspid ValveThe tricuspid valve opens widely. There is no significant tricuspid regurgitation.AortaThere is a left sided aortic arch with a normal brachiocephalic branching pattern. The aortic root is normal in size. There is mild atherosclerosis of the aortic arch and descending aorta.Pulmonary VeinsAll four pulmonary veins drain normally into the left atrium.Pulmonary ArteryThe main pulmonary artery is moderately dilated.Venous AnatomyThe SVC and IVC are normal in size and drain normally into the right atrium.PericardiumThere is mild pericardial effusion.Extracardiac FindingsThere is mild bilateral pleural effusion. This study is not designed for the specific evaluation of extra-cardiac findings; therefore, the differentiation between artifacts and real extracardiac pathology may be difficult. If clinically indicated, a separate dedicated evaluation should be considered.

Output: 1. Severe LV dilation with severely reduced systolic function (LVEF 18%). 2. There is mid-myocardial late gadolinium enhancement of the basal interventricular septum. The finding is atypical for prior myocardial infarction and likely represents myocardial fibrosis. This pattern of late gadolinium enhancement is most commonly seen in dilated cardiomyopathy. 3. Severe RV dilation with severely reduced systolic function (RVEF 14%).4. Severe biatrial dilation.5 Moderate to severe mitral regurgitation.6. Mild atherosclerosis of thoracic aorta.7. Mild pericardial and pleural effusions.


Instruction: Generate impression based on findings.

Input: 64-year-old female with right arm weakness Hypodense area is seen in the high left frontoparietal area that is consistent with vasogenic edema. MRI with contrast is recommended for further characterization ischemic change versus mass. No hemorrhage or mass-effect is seen.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.

Output: Hypodense area consistent with vasogenic edema identified in the left high frontoparietal area. An MRI with contrast is recommended for further characterization. Discussed with ER staff at time of dictation.


Instruction: Generate impression based on findings.

Input: Episodic dizziness and vertigo. No restricted diffusion to suggest acute ischemia. No intracranial hemorrhage. No intracranial mass or mass-effect. The ventricles are within normal limits in size and configuration. Few scattered foci of T2/FLAIR hyperintensity are seen in the bilateral subcortical and periventricular white matter, which are nonspecific, but compatible with mild age-related white matter changes. Brain parenchyma is otherwise unremarkable for age. Major flow-voids are preserved.Sella and orbits are grossly within normal limits. Minimal mucosal thickening is seen involving the anterior ethmoid sinuses. Paranasal sinuses and mastoid cells are otherwise clear. Bone marrow signal and extracranial soft tissues are within normal limits.

Output: MRI of the brain is within normal limits for age. No evidence of acute infarct, intracranial mass, or mass effect.


Instruction: Generate impression based on findings.

Input: Reason: ? abnl, tendon History: elbow pain with pitching LIGAMENTS: The ulnar collateral ligament, radial collateral ligament, and lateral ulnar collateral ligament appear grossly intact within the limitations of this non arthrogram study.TENDONS: The biceps and brachialis tendons appear intact. The triceps tendon appears intact. There is increased signal abnormality on fluid sensitive sequences within the flexor digitorum superficialis just proximal to the level of its insertion, which is nonspecific, but may represent the sequela of medial epicondylitis or perhaps a strain injury.ARTICULAR SURFACES AND BONE: No osteochondral defects are identified. No full-thickness or near full-thickness articular cartilage defects are seen. No bone marrow signal abnormality is identified. SURROUNDING STRUCTURES: There is thickening and increased signal abnormality within the ulnar nerve as it courses within the cubital tunnel beneath the ligament of Osbourne, indicating a neuritis.ADDITIONAL

Output: 1. Increased signal abnormality within the flexor digitorum superficialis which is nonspecific, but likely represents medial epicondylitis or perhaps a strain injury in the correct clinical context.2. Mild thickening and increased signal abnormality within the ulnar nerve as it courses through the cubital tunnel, which may represent a very mild neuritis. Other findings as described.


Instruction: Generate impression based on findings.

Input: pre eclampsia with severe headache No evidence of acute ischemic or hemorrhagic lesion.Diffuse pachymeningeal enhancement was demonstrated on post Gad enhancement images.Differential diagnosis include; post lumbar puncture status, pachymeningitis, pachymeningeal metastasis and intracranial hypotension.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, restricted diffusion/acute ischemia. The midline structures and cranial-cervical junction are normal. Normal flow voids are identified in the major intracranial vessels. The mastoid air cells are clear.Left maxillary sinus opacification with atrophic changes.

Output: 1. Diffuse pachymeningeal enhancement as described above; possible underlying diagnosis include post LP status, pahcymeningitis, granulomatous disease, carcinomatosis or intracranial hypotension.2. No evidence of acute ischemic or hemorrhagic lesion.


Instruction: Generate impression based on findings.

Input: 77-year-old male with left-sided weakness, poor balance and dysarthria Multiple areas of vasogenic edema and some with internal areas of high density are believed to represent multiple metastatic lesions some with hemorrhagic component. Further correlation with an MRI or a postinfusion CT is recommended. There appears to be a large mass within the corpus callosum with bilateral extension. Images through posterior fossa are unremarkable.

Output: 1.Findings findings concerning for multiple metastatic lesions some with hemorrhagic components.2.Follow-up with an MRI with infusion is recommended.


Instruction: Generate impression based on findings.

Input: Altered mental status, evaluate for infarct. There is no evidence of diffusion restriction. There are scattered and confluent areas of increased signal on T2/FLAIR images in the periventricular and subcortical white matter consistent with mild to moderate chronic small vessel ischemic changes. There is a more focal area of increased signal on T2/FLAIR images with volume loss in the left frontal lobe posteriorly involving the middle and superior gyri. There is also moderate degree of global parenchymal volume loss. There is dilatation of the ventricular system which is likely on an ex vacuo basis. The flow voids of the internal carotid arteries are not seen with occlusion and high-grade stenosis involving the right and left internal carotid arteries, respectively, demonstrated on the recent CTA. There is no evidence of an intracranial mass. Calvarium and extra cranial soft tissues are grossly unremarkable.

Output: 1. No evidence of acute infarct.2. Chronic infarct in the left posterior frontal lobe.3. Mild to moderate chronic small vessel ischemic disease.4. Absence of bilateral internal carotid artery flow voids compatible with occlusion/stenosis demonstrated on recent CTA.5. Moderate degree of global parenchymal volume loss.


Instruction: Generate impression based on findings.

Input: Reason: eval mass in webspace of 4/5 History: mass, pain Note is made of a lobulated mass measuring 1.8 x 1.5 x 1.2 cm situated along the plantar aspect of the PIP joint of the fifth digit of the right foot which demonstrates decreased signal abnormality on T1-weighted images, heterogeneous but predominantly increased signal abnormality on T2-weighted images and heterogeneous enhancement on postcontrast sequences corresponding to the patient's palpable area of concern. There is a skin marker in the overlying area. There is no erosion of the underlying bone. No bone marrow signal abnormalities are identified in the surrounding area. Severe osteoarthritis affects the first MTP joint with an associated hallux valgus deformity. Osteoarthritis affects scattered interphalangeal joints.

Output: Nonspecific enhancing mass along the plantar aspect of the PIP joint of the fifth digit of the right foot. Differential considerations include giant cell tumor of tendon sheath or perhaps a peculiar Morton's neuroma. A bursitis or synovitis could also be considered. Other findings as described above.


Instruction: Generate impression based on findings.

Input: 61 year old male with a history of Hypertension, Hyperlipidemia, obstructive sleep apnea, pulmonary embolism (2013) and Diabetes. Referred for vasodilator stress cardiovascular MRI due to SOB with exertion and new T-wave inversion on EKG.MEDICATIONS: Warfarin, Simvastatin, HCTZ/aliskiren, Amlodipine, Irbesartan, Maxair, Flonase, Omeprazole. First Pass PerfusionDuring hyperemia, no perfusion defects were present.Viability/ Myocardial ScarThere is no evidence of prior myocardial infarction and the entire myocardium is viable. However, there is a small amount of late gadolinium enhancement in an atypical pattern which involves the basal inferior and inferolateral wall suggesting the presence of myocardial fibrosis, inflammation, or infiltration, such as might be seen with old myocarditis.Left VentricleThe left ventricle is normal in size and systolic function. The overall LV ejection fraction is 72%, the LV end diastolic volume index is 71ml/m2 (normal range: 74+/-15), the LVEDV is 189 ml (normal range 142+/-34), the LV end systolic volume index is 19 ml/m2 (normal range 25+/-9), the LVESV is 52 ml (normal range 47+/-19), the LV mass index is 52 g/m2, and the LV mass is 140 gm. There are no regional wall motion abnormalities present.Left AtriumThe left atrium is mildly enlarged. Right VentricleThe right ventricle is normal in size and systolic function. The overall RV ejection fraction is 56%, the RV end diastolic volume index is 91 ml/m2 (normal range 82+/-16), the RVEDV is 244 ml (normal range 142+/-31), the RV end systolic volume index is 40 ml/m2 (normal range 31+/-9), and the RVESV is 107 ml (normal range 54+/-17).Right AtriumThe right atrium is mildly enlarged.Aortic ValveThe aortic valve opens widely and there is no significant aortic regurgitation.Mitral ValveThe mitral valve opens widely and there is no significant mitral regurgitation.Pulmonic ValveThe pulmonic valve opens widely. There is no significant pulmonic regurgitation.Tricuspid ValveThe tricuspid valve opens widely. There is no significant tricuspid regurgitation.AortaThe aortic root is mildly dilated (42 x 43mm). There is a left sided aortic arch with a normal brachiocephalic branching pattern.Pulmonary VeinsAll four pulmonary veins drain normally into the left atrium.Pulmonary ArteryThe main pulmonary artery is mildly dilated (32mm).Venous AnatomyThe SVC and IVC are normal in size and drain normally into the right atrium.PericardiumThere is no obvious pericardial disease.Extracardiac FindingsThis study is not designed for the specific evaluation of extra-cardiac findings; therefore, the differentiation between artifacts and real extracardiac pathology may be difficult. If clinically indicated, a separate dedicated evaluation should be considered.

Output: 1. No perfusion defects/ "ischemia" present during hyperemia.2. No prior myocardial infarction. The entire myocardium is viable.3. Normal LV size and systolic function (LVEF 72%) with evidence of a small amount of late gadolinium enhancement in a pattern atypical for prior myocardial infarction and suggestive of myocardial fibrosis, inflammation, or infiltration. The abnormality most likely represents old myocarditis; however, other possibilities remain on the differential diagnosis.4. Normal RV size and systolic function (RVEF 56%).5. Mildly dilated ascending aorta.6. Mildly dilated main pulmonary artery.


Instruction: Generate impression based on findings.

Input: History of congenital cavernous malformation, yearly surveillance. There is redemonstration of multiple areas of susceptibility artifact compatible with cavernous malformations. The lesion in the medulla appears minimally larger, now measuring up to 10 mm, previously 9 mm and demonstrates a slightly changed internal composition with increased T1 signal. There is no associated perilesional edema. Several other lesions including the dominant 12 mm lesion in the left frontal lobe appear unchanged.The ventricles and sulci are within normal limits. The basal cisterns remain patent. There is no midline shift or mass effect. There is redemonstration of scattered punctate T2 hyperintensities in the bilateral supratentorial white matter, unchanged in appearance. There is no evidence of acute infarct. No abnormal pathological enhancement is identified. Normal flow-voids are demonstrated in the major intracranial vascular structures. There is a persistent right fetal origin PCA.The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.

Output: Minimal increase in size and change in composition of medullary cavernous malformation without evidence of perilesional edema. Additional cavernous malformations not significantly changed.


Instruction: Generate impression based on findings.

Input: CVA No evidence of hemorrhage, edema, mass-effect, midline shift or hydrocephalus is detected. No definitive evidence of an acute cortical stroke is detected. A very small punctate low density in the right external capsule is again demonstrated with no interval change. Third of admission with a dedicated MRI examination is recommended to exclude acute small strokes. This examination remains stable since prior study.

Output: Essentially unremarkable CT of brain without infusion and no interval change since prior study. If clinical concern for stroke persists an MRI is highly recommended.


Instruction: Generate impression based on findings.

Input: Male, 48 years old, with left shoulder arthritis. Evaluate the glenoid. No fracture is evident. Severe osteoarthritis affects the glenohumeral joint with bone on bone apposition. Multiple subcentimeter subchondral lucencies penetrate the articular surface of the humeral head and glenoid, representing erosions. A large joint effusion is also noted (better seen on the patient's prior MRI). These findings raise the possibility of an underlying chronic inflammatory arthritis. Fluid is also seen distending the biceps tendon sheath.Please note that rotator cuff tearing and tendinosis seen on the prior MRI are not well visualized on the current CT study.A large, normal variant os acromiale is again noted. Moderate osteoarthritis affects the acromioclavicular joint.Note is made of a patulous esophagus with a dependent fluid level. If there is clinical concern for a motility disorder, further evaluation with an esophagram may be considered.The remaining bony and soft tissue structures are within normal limits.

Output: Severe arthritic changes at the shoulder joint as described above with multiple small erosions and a large joint effusion suggesting osteoarthritis with an underlying chronic inflammatory arthritis.


Instruction: Generate impression based on findings.

Input: Brain: There is a punctate focus of diffusion restriction, susceptibility effect, and T1 hyperintensity within the right superior frontal gyrus anteriorly and an additional similar punctate focus within the left frontal operculum. There is extensive confluent T2 hyperintensity throughout the supratentorial white matter compatible with chronic small vessel ischemic disease as well as numerous chronic lacunar infarcts both supratentorially and infratentorially similar to prior allowing for differences in technique with the current scan obtained on the 3 Tesla and prior on 1.5 Tesla magnet. There is severe global volume loss. Focal areas of encephalomalacia are again noted in the right cerebellar hemisphere. There are also numerable punctate foci of susceptibility effect supratentorial and infratentorially, both within the subcortical and deep white matter as well as the deep gray nuclei. These have also progressed since the 2012 MRI. The ventricles and basal cisterns are unchanged in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull, paranasal sinuses, and scalp soft tissues are unremarkable. Cervical Spine:Vertebral body heights in the cervical spine are normal. There is reversal of cervical lordosis centered at the C3-C4 level. Alignment is otherwise maintained. Craniocervical junction is within normal limits.The cervical spinal cord has normal signal characteristics and overall morphology.Mild degenerative changes are seen in the cervical spine with multilevel loss of intervertebral disc space particularly at C3-C4, C4-C5, and C5-C6. Small disc osteophyte complexes. Mild thickening of the posterior longitudinal ligament from C3-C4 to C4-C5. Individual levels as below:C2-C3: No significant disc disease. No spinal canal or neural foraminal stenosis.C3-4: Small disc osteophyte complex and effacement of the ventral thecal sac. No significant spinal canal stenosis. Uncovertebral hypertrophy with minimal right greater than left neural foraminal stenosis.C4-5: Small disc osteophyte complex and uncovertebral hypertrophy. There is mild left neural foraminal stenosis. No significant spinal canal or right neural foraminal stenosis.C5-6: No significant spinal canal stenosis. There is uncovertebral hypertrophy with mild bilateral neural foraminal narrowing.C6-7: There is uncovertebral hypertrophy with mild bilateral neural foraminal stenosis. No significant spinal canal stenosis.C7-T1: There is bilateral uncovertebral hypertrophy and small foraminal disc protrusion on the left. There is mild bilateral neural foraminal stenosis.Visualized extraspinal soft tissue structures are unremarkable.

Output: 1.Two punctate foci of subacute hemorrhage within the right superior frontal gyrus and within the left frontal operculum superimposed upon interval progression of innumerable chronic microhemorrhages. Majority of these chronic microhemorrhages involve the bilateral thalami, basal ganglia, brainstem and cerebellum, favoring a chronic hypertensive etiology. 2.Extensive global volume loss including the brain stem, advanced chronic small vessel ischemic disease, and numerous supratentorial and infratentorial chronic lacunar infarcts appear similar since to 2012 MRI.3.Mild degenerative changes in the cervical spine without significant spinal canal stenosis at any level. No abnormal cord signal. Mild multilevel neural foraminal narrowing, as detailed above.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.


Instruction: Generate impression based on findings.

Input: 62 year-old female with strong family history of breast carcinoma in her mother at age 55, as well as a maternal cousin and great aunt. There is heterogeneous amount of fibroglandular tissue in both breasts.Minimal parenchymal enhancement is noted bilaterally.No abnormal enhancement is seen in either breast. No abnormal lymph nodes are identified in either axillary region.Focal skin enhancement is seen in the right medial upper chest wall. Clinical correlation is advised.

Output: No MRI evidence for malignancy. BIRADS: 1 - Negative.RECOMMENDATION: X - No Letter.


Instruction: Generate impression based on findings.

Input: Clinical question: Evaluate for new metastases. Signs and symptoms: New neurological findings with history of lymphoma. Pre-and post-enhanced brain MRI:Diffusion-weighted images are unremarkable.Examination fails to demonstrate any parenchymal, leptomeningeal or calvarial metastatic lesions.Small focus of T2 hyperintensity along the superior aspect of the left cerebellum is a nonspecific finding and demonstrate no interval change since prior study. Possibility of a tiny chronic ischemic stroke should be considered. Few additional tiny foci of T2 hyperintensity in the subcortical and periventricular white matter similar to prior exam from 2013 and suspicious for mild chronic small vessel ischemic strokes.Unremarkable cerebral cortex and cortical sulci as well as the ventricular system of the CSF spaces and brain myelination otherwise. No abnormal enhancement. Signal voids of major intracranial arterial branches are identified. Signal intensity of intracranial venous sinuses are within normal and normal pattern of enhancement.

Output: 1.No evidence of metastatic disease.2.Negative diffusion weighted images and stable findings suggestive of mild chronic small vessel ischemic strokes.


Instruction: Generate impression based on findings.

Input: 39-year-old female with diffuse ankle pain x2 months following injury TENDONS: No significant abnormality noted.LIGAMENTS: Increased signal within anterior talofibular ligament with surrounding soft tissue edema. The posterior talofibular ligament is intact. Calcaneofibular ligament is intact. The deltoid ligament is intact.ARTICULAR SURFACES AND BONE: Nonspecific edema type signal within the anterolateral aspect of the talus. ADDITIONAL

Output: Anterior talofibular ligament tear with surrounding edema and small joint effusion.


Instruction: Generate impression based on findings.

Input: Male, 72 years old, with mild cognitive impairment and recent impulsive behavior, concern for frontotemporal dementia. Extensive, almost confluent periventricular white matter T2 hyperintensity is seen. Some areas appear very cystic or cavitated compatible with chronic lacunar infarctions. No restricted diffusion is seen to suggest acute ischemia.No evidence of parenchymal edema or mass effect is seen. No abnormal extra-axial fluid collections are detected. No acute intracranial hemorrhage is suspected, though there are scattered foci of susceptibility which likely reflect chronic microscopic blood product.The sulci of the cerebral hemispheres and the ventricular system are moderately and symmetrically prominent compatible with underlying volume loss. There is, however, no specific distribution to this volume loss. In particular, features associated with frontotemporal dementia such as "knife edge" sulci in the frontal and temporal lobes are not seen.

Output: 1.No acute intracranial abnormality.2.No specific findings to suggest frontotemporal dementia.3.Moderate generalized parenchymal volume loss is noted, in the context of fairly extensive chronic microvascular and lacunar ischemic disease. Constellation of findings along with the clinical history would suggest multi-infarct dementia.


Instruction: Generate impression based on findings.

Input: Female, 44 years old, with neck pain, history of fusion at C4-5. Evidence of anterior instrumented fusion is seen at C5-6. The cervical lordosis is straightened. Otherwise, sagittal alignment is within normal limits. Vertebral body height and morphology are unremarkable. No evidence of marrow replacement or marrow edema is seen. The left aspect of the spinal cord appears slightly reduced in volume relative to the right at the C5-6 level. In addition, there is a small area of ill-defined T2 signal abnormality within the left cord at this level. Elsewhere, the spinal cord demonstrates normal signal intensity and morphology. No epidural abnormalities are suspected.Mild edema is demonstrated along the supraspinous ligament and soft tissues surrounding the C7 spinous process.C2-3: Mild facet arthropathy. No significant spinal canal or foraminal stenosis. C3-4: Mild facet arthropathy. No significant spinal canal or foraminal stenosis. C4-5: Facet arthropathy, left more than right. Posterior disc-osteophyte complex formation with a superimposed superiorly directed central extrusion and right paracentral protrusion. Effacement of the thecal sac with mild flattening of the ventral cord. No significant foraminal narrowing. C5-6: Mild facet arthropathy. Obliteration of the intervertebral disc. No significant spinal canal or foraminal stenosis.C6-7: Facet arthropathy. Minimal posterior disc-osteophyte complex formation. No significant spinal canal or foraminal stenosis. C7-T1: No spinal canal stenosis or neuroforaminal narrowing.

Output: 1.Evidence of prior anterior instrumented fusion is seen at the C5-6 level. Mild degree of left spinal cord myelomalacia and may represent the effect of a prior stenosis at this level. However, on the present examination, no significant spinal canal or foraminal stenosis is seen at this level.2.Relatively mild disc and facet degeneration are seen at additional levels as above. Most notably, a disc extrusion and protrusion are evident at the C4-5 level with resultant effacement of the ventral thecal sac. There are no additional areas of significant spinal canal or foraminal stenosis.3.Mild edema is seen along the supraspinous ligament and the soft tissue surrounding the C7 spinous process. Correlation with point tenderness is suggested. This could represent a mild strain injury or a mild traumatic injury.


Instruction: Generate impression based on findings.

Input: TIA with left hand numbness Noncontrast CT scan brain demonstrates periventricular hypodensity which given the patient's age and history most likely are present small vessel ischemic disease. There is no evidence of acute cortical infarct. If ischemia remains of clinical concern MRI would allow more sensitive evaluation of possible acute ischemic changes.Bone windows demonstrate opacification of a single posterior right ethmoid air cell. No other bony abnormality is identified.

Output: Small vessel ischemic disease with no evidence of acute ischemic change. If there is clinical concern MRI would allow more sensitive evaluation.


Instruction: Generate impression based on findings.

Input: 30-year-old male with history of lymphoma and known AVN with increasing hip pain Right hip: There is serpentine, bandlike signal abnormality within the femoral head indicating osteonecrosis involving the entire weightbearing surface of the femoral head. Osteonecrosis appears to have progressed slightly with new cysts in the femoral head. Edema within the femoral head and neck is also slightly more pronounced than the prior exam. Curvilinear subchondral T2 hyperintensity on fat suppressed images likely represents a subchondral fracture, however we see no frank surface collapse at this time. Mild right hip synovitis as well as a small joint effusion appears similar to the prior exam. The musculature of the right hip appears normal.Left hip: There is serpentine, bandlike signal abnormality within the femoral head indicating osteonecrosis involving the entire weightbearing surface of the femoral head. Edema within the femoral head and neck appears similar to the prior exam. Curvilinear subchondral increased T2 signal likely represents a subchondral fracture, however we see no frank articular surface collapse. Mild synovitis and a small joint effusion is unchanged. The musculature of the left hip appears normal.

Output: Findings indicating slight progression of bilateral femoral head AVN and other findings as described above.


Instruction: Generate impression based on findings.

Input: Neurosarcoid: new onset tremors and ataxia. There is extensive cerebral and pontine white matter T2 hyperintensity. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable. There are bilateral lens implants.

Output: Extensive cerebral and pontine white matter T2 hyperintensity is nonspecific, but may represent a manifestation of hypertensive encephalopathy. Otherwise, assessment for neurosarcoidosis is limited without intravenous contrast.


Instruction: Generate impression based on findings.

Input: Female, 13 years old, with seizures and mesial temporal abnormalities on prior imaging. Evaluate by spectroscopy, in particular for lactate expression. Atrophy of the right temporal lobe gyri is again seen. In addition, the right mesial temporal lobe and hippocampal formation are also atrophic and there is abnormal T2 signal corresponding to the amygdala and hippocampal head. The left temporal lobe may also be affected but to a much lesser degree than the right. The gyri recti also seem to be somewhat thinned. The right temporal horn demonstrates mild ex vacuo dilatation. These findings show no significant change from prior exams.Short TE single voxel spectroscopy was performed over the rightamygdala and hippocampal head, at the site of the most conspicuous atrophy and signal abnormality. Artifact compromises the far left end of the spectrum, likely due to poor water suppression. However, the majority of the spectrum is of acceptable quality and shows a uniform reduction in all metabolite peaks. In particular, the NAA peak is not detectable above background noise suggesting significant neuronal loss. No evidence of any lactate is seen. Single voxel spectroscopy of the left mesial temporal lobe shows a reduction in metabolite peaks, but less severe than that seen on the right, and with detectable NAA indicating viable neuronal tissue. A small negative doublet between 1.1 and 1.0 ppm is seen, which does not clearly correspond to any typical metabolite and which may be artifactual.Single voxel spectroscopy was also performed over areas of predominantly gray matter and predominantly white matter in the cerebral cortex. The spectra from these regions are within normal limits. Again, no significant lactate is detected.No evidence of restricted diffusion is seen. No pathologic parenchymal or extra-axial enhancement is observed. The atrophic right mesial temporal lobe shows some intrinsic T1 hyperintensity which may reflect cellular loss and laminar necrosis. No evidence of intracranial hemorrhage is seen. Except as above, the ventricular system is normal in size and morphology.

Output: Again seen is atrophy affecting a large portion of the right temporal lobe with particular volume loss and associated signal abnormality within the mesial temporal structures including the amygdala and hippocampal head. The left temporal lobe and inferior frontal lobes may also be involved, but to a much lesser degree. There has been no significant interval change in these findings.Single voxel spectroscopy performed over the right mesial temporal lobe shows a significant reduction in all major metabolites, particularly NAA which is not detectable above the level of background noise. This pattern is compatible with severe neuronal loss. No evidence of any significant lactate is seen. Spectroscopy of the left mesial temporal lobe shows some reduction in metabolite peaks, but much less severe than on the right, and again no evidence of lactate. Spectroscopy of normal-appearing gray matter and white matter is within normal limits.The above findings are again suggestive of sequelae of a prior encephalitis which could have been infectious/viral or autoimmune/para-neoplastic. Absence of detectable lactate would tend to argue against an ongoing failure of energy metabolism. However, it does not exclude metabolic disease in general as not all metabolic deficiencies are associated with detectable brain lactate.


Instruction: Generate impression based on findings.

Input: Incidentally discovered unruptured cerebral aneurysm. Orbit MRI: The images are degraded by patient motion. The optic nerve are grossly unremarkable. The globes and ocular adnexa appear to be intact. There is no abnormal intraorbital enhancement or mass lesions. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The brain parenchyma and pituitary gland appear unremarkable. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.Brain MRA: There is a tortuous right cavernous carotid artery. Otherwise, there is no evidence of aneurysms within the limits of MRA. In particular, the ACOM complex is unremarkable. The proximal right opthalmic artery is partially inapparent, likely due to susceptibility artifacts. Otherwise, there is no evidence of significant steno-occlusive lesions.

Output: 1. Unremarkable orbits.2. No evidence of cerebral aneurysms within the limits of MRA.3. No evidence of acute intracranial hemorrhage, mass, or acute infarction.