smoh/medical-transcriptions huggingface dataset:
MRI Cervical Spine - 1  ( Neurology)
Description:  MRI cervical spine.

EXAM:,MRI CERVICAL SPINE,CLINICAL:, A57-year-old male. Received for outside consultation is an MRI examination performed on 11/28/2005.,FINDINGS:,Normal brainstem-cervical cord junction. Normal cisterna magna with no tonsillar ectopia. Normal clivus with a normal craniovertebral junction. Normal anterior atlantoaxial articulation.,C2-3: Normal intervertebral disc with no spondylosis or uncovertebral joint arthrosis. Normal central canal and intervertebral neural foramina with no cord or radicular impingement.,C3-4: There is disc desiccation with minimal annular bulging. The residual AP diameter of the central canal measures approximately 10mm. CSF remains present surrounding the cord.,C4-5: There is disc desiccation with endplate spondylosis and mild uncovertebral joint arthrosis. The residual AP diameter of the central canal measures approximately 8mm with effacement of the circumferential CSF cleft producing a borderline central canal stenosis but no cord distortion or cord edema. There is minimal uncovertebral joint arthrosis.,C5-6: There is disc desiccation with minimal posterior annular bulging and a right posterolateral preforaminal disc protrusion measuring approximately 2 x 8mm (AP x transverse). The disc protrusion produces minimal rightward ventral thecal sac flattening but no cord impingement.,C6-7: There is disc desiccation with mild loss of disc space height and posterior endplate spondylosis and annular bulging producing central canal stenosis. The residual AP diameter of the central canal measures 8 mm with effacement of the circumferential CSF cleft. There is a left posterolateral disc-osteophyte complex encroaching upon the left intervertebral neural foramen with probable radicular impingement upon the exiting left C7 nerve root.,C7-T1, T1-2: Minimal disc desiccation with no disc displacement or endplate spondylosis.,IMPRESSION:,Multilevel degenerative disc disease as described above.,C4-5 borderline central canal stenosis with mild bilateral foraminal compromise.,C5-6 disc desiccation with a borderline central canal stenosis and a right posterolateral preforaminal disc protrusion producing thecal sac distortion.,C6-7 degenerative disc disease and endplate spondylosis with a left posterolateral disc-osteophyte complex producing probable neural impingement upon the exiting left C7 nerve root with a borderline central canal stenosis.,Normal cervical cord.
MRI Brain - Pontine Stroke  ( Neurology)
Description:  Right pontine pyramidal tract infarct.

CC:, Left sided weakness.,HX:, 74 y/o RHF awoke from a nap at 11:00 AM on 11/22/92 and felt weak on her left side. She required support on that side to ambulate. In addition, she felt spoke as though she "was drunk." Nevertheless, she was able to comprehend what was being spoken around her. Her difficulty with speech completely resolved by 12:00 noon. She was brought to UIHC ETC at 8:30AM on 11/23/92 for evaluation.,MEDS:, none. ,ALLERGIES:,  ASA/ PCN both cause rash.,PMH:, 1)?HTN. 2)COPD. 3)h/o hepatitis (unknown type). 4)Macular degeneration.,SHX:, Widowed; lives alone. Denied ETOH/Tobacco/illicit drug use.,FHX:, unremarkable.,EXAM: , BP191/89 HR68 RR16 37.2C,MS: A & O to person, place and time. Speech fluent; without dysarthria. Intact naming, comprehension, and repetition.,CN: Central scotoma, OS (old). Mild upper lid ptosis, OD (old per picture). Lower left facial weakness.,Motor: Mild Left hemiparesis (4+ to 5- strength throughout affected side). No mention of muscle tone in chart.,Sensory: unremarkable.,Coord: impaired FNF and HKS movement secondary to weakness.,Station: Left pronator drift. No Romberg sign seen.,Gait: Left hemiparetic gait with decreased LUE swing.,Reflexes: 3/3+ biceps and triceps. 3/3+ patellae. 2/3+ ankles with 3-4beats of non-sustained ankle clonus on left. Plantars: Left babinski sign; and flexor on right.,General Exam: 2/6 SEM at left sternal border.,COURSE:, GS, CBC, PT, PTT, CK, ESR were within normal limits. ABC 7.4/46/63 on room air. EKG showed a sinus rhythm with right bundle branch block. MRI brain, 11/23/95, revealed a right pontine pyramidal tract infarction. She was treated with Ticlopidine 250mg bid. On 11/26/92, her left hemiparesis worsened. A HCT, 11/27/92, was unremarkable. The patient was treated with IV Heparin. This was discontinued the following day when her strength returned to that noted on 11/23/95. On 11/27/92, she developed angina and was ruled out for MI by serial EKG and cardiac enzyme studies. Carotid duplex showed 0-15% bilateral ICA stenosis and antegrade vertebral artery flow bilaterally. Transthoracic echocardiogram revealed aortic insufficiency only. Transesophageal echocardiogram revealed trivial mitral and tricuspid regurgitation, aortic valvular fibrosis. There was calcification and possible thrombus seen in the descending aorta. Cardiology did not feel the later was an indication for anticoagulation. She was discharged home on Isordil 20 tid, Metoprolol 25mg q12hours, and Ticlid 250mg bid.
MRI Brain - Lyme Disease  ( Neurology)
Description:  A middle-aged male with increasing memory loss and history of Lyme disease.

FINDINGS:,There is a large intrasellar mass lesion producing diffuse expansion of the sella turcica. This mass lesions measures approximately 16 x 18 x 18mm (craniocaudal x AP x mediolateral) in size.
Meningioma  ( Neurology)
Description:  Progressive loss of color vision OD.

CC: ,Progressive loss of color vision OD,HX:, 58 y/o female presents with a one year history of progressive loss of color vision. In the past two months she has developed blurred vision and a central scotoma OD. There are no symptoms of photopsias, diplopia, headache, or eye pain. There are no other complaints. There have been mild fluctuations of her symptoms, but her vision has never returned to its baseline prior to symptom onset one year ago.,EXAM: ,Visual acuity with correction: 20/25+1 OD; 20/20-1 OS. Pupils were 3.5mm OU. There was a 0.8 log unit RAPD OD. Intraocular pressures were 25 and 24, OD and OS respectively; and there was an increase to 27 on upgaze OD, but no increase on upgaze OS. Optic disk pallor was evident OD, but not OS. Additionally, there was a small area of peripheral chorioretinal scarring in the inferotemporal area of the right eye. Foveal flicker fusion occurred at a frequency of 21.9 OD and 30.7 OS. Color plate testing scores: 6/14 OD and 10/14 OS. Goldman visual field examination showed an enlarged and deepened blind spot with an infero-temporal defect especially in the smaller diopters.,IMPRESSION ON 2/6/89: ,Optic neuropathy/atrophy OD, rule out mass lesion affecting optic nerve. Particular attention was paid to the area of the optic canal, cavernous sinus and sphenoid sinus.,BRAIN CT W/CONTRAST, 2/13/89:, Enhancing calcified lesion in the posterior aspect of the right optic nerve, probable meningioma.,MRI ORBITS W/ AND W/OUT GADOLINIUM CONTRAST, 4/26/89:, 7x3mm irregular soft tissue mass just inferior and lateral to the optic nerve OD. The mass is just proximal to the orbital apex. There is relatively homogeneous enhancement of the mass. The findings are most consistent with meningioma.,MRI 1995:, Mild enlargement of tumor with possible slight extension into the right cavernous sinus.,COURSE: ,Resection and biopsy were deferred due to risk of blindness, and suspicion that the tumor was a slow growing meningioma. 3 years after initial evaluation Hertel measurements indicated a 3mm proptosis OD. Visual field testing revealed gradual worsening of deficits seen on her initial Goldman visual field exam. There was greater red color desaturation of the temporal field OD. Visual acuity had decreased from 20/20 to 20/64, OD. All other deficits seen on her initial exam remained stable or slightly worsened. By 1996 she continued to be followed at 6 months intervals and had not undergone surgical resection.
MRI Brain - Memory Loss  ( Neurology)
Description:  A middle-aged female with memory loss.

FINDINGS:,There is moderate to severe generalized neuronal loss of the cerebral hemispheres with moderate to severe ventricular enlargement and prominent CSF within the subarachnoid spaces. There is confluent white matter hyperintensity in a bi-hemispherical centrum semiovale distribution extending to the lateral ventricles consistent with severe vasculopathic small vessel disease and extensive white matter ischemic changes. There is normal enhancement of the dural sinuses and cortical veins and there are no enhancing intra-axial or extraaxial mass lesions. There is a cavum velum interpositum (normal variant).,There is a linear area of T1 hypointensity becoming hyperintense on T2 images in a left para-atrial trigonal region representing either a remote lacunar infarction or prominent perivascular space.,Normal basal ganglia and thalami. Normal internal and external capsules. Normal midbrain.,There is amorphus hyperintensity of the basis pontis consistent with vasculopathic small vessel disease. There are areas of T2 hyperintensity involving the bilateral brachium pontis (left greater than right) with no enhancement following gadolinium augmentation most compatible with areas of chronic white matter ischemic changes. The area of white matter signal alteration in the left brachium pontis is of some concern in that is has a round morphology. Interval reassessment of this lesion is recommended.,There is a remote lacunar infarction of the right cerebellar hemisphere. Normal left cerebellar hemisphere and vermis.,There is increased CSF within the sella turcica and mild flattening of the pituitary gland but no sellar enlargement. There is elongation of the basilar artery elevating the mammary bodies but no dolichoectasia of the basilar artery.,Normal flow within the carotid arteries and circle of Willis.,Normal calvarium, central skull base and temporal bones.  There is no demonstrated calvarium metastases.,IMPRESSION:,Severe generalized cerebral atrophy.,Extensive chronic white matter ischemic changes in a bi-hemispheric centrum semiovale distribution with involvement of the basis pontis and probable bilateral brachium pontis. The area of white matter hyperintensity in the left brachium pontis is of some concern is that it has a round morphology but no enhancement following gadolinium augmentation. Interval reassessment of this lesion is recommended.,Remote lacunar infarction in the right cerebellar hemisphere.,Linear signal alteration of the left periatrial trigonal region representing either a prominent vascular space or,lacunar infarction.,No demonstrated calvarial metastases.
Malignant Meningioma - Consult  ( Neurology)
Description:  Problems with seizures, hemiparesis, has been to the hospital, developed C-diff, and is in the nursing home currently. 

REASON FOR VISIT: , This is a new patient evaluation for Mr. A. There is a malignant meningioma.  He is referred by Dr. X.,HISTORY OF PRESENT ILLNESS: , He said he has had two surgeries in 07/06 followed by radiation and then again in 08/07.  He then had a problem with seizures, hemiparesis, has been to the hospital, developed C-diff, and is in the nursing home currently.  He is unable to stand at the moment.  He is unable to care for himself. ,I reviewed the information that was sent down with him from the nursing home which includes his medical history.,MEDICATIONS:  ,Keppra 1500 twice a day and Decadron 6 mg four times a day.  His other medicines include oxycodone, an aspirin a day, Prilosec, Dilantin 300 a day, and Flagyl.,FINDINGS:,  On examination, he is lying on the stretcher.  He has oxygen on and has periods of spontaneous hyperventilation.  He is unable to lift his right arm or right leg.  He has an expressive dysphasia and confusion.,I reviewed the imaging studies from summer from the beginning of 10/07, end of 10/07 as well as the current MRI he had last week.  This shows that he has had progression of disease with recurrence along the surface of the brain and there is significant brain edema.  This is a malignant meningioma by diagnosis.,ASSESSMENT/PLAN: , In summary, Mr. A has significant disability and is not independent currently.  I believe that because of this that the likelihood of benefit from surgery is small and there is a very good chance that he would not be able to recover from surgery.  I do not think that surgery will help his quality of life and a need to control the tumor would be dependent on another therapy impacting the tumor.  Given that there are not good therapies and chemotherapy would be the option at the moment, and he certainly is not in a condition where chemotherapy would be given, I believe that surgery would not be in his best interest.  I discussed this both with him, although it is not clear to me how much he understood, as well as his family.
MRI Brain - Bilateral Thalamic Strokes  ( Neurology)
Description:  MRI Brain to evaluate sudden onset blindness - Basilar/bilateral thalamic strokes.

CC:, Sudden onset blindness.,HX:, This 58 y/o RHF was in her usual healthy state, until 4:00PM, 1/8/93, when she suddenly became blind. Tongue numbness and slurred speech occurred simultaneously with the loss of vision. The vision transiently improved to "severe blurring" enroute to a local ER, but worsened again once there. While being evaluated she became unresponsive, even to deep noxious stimuli. She was transferred to UIHC for further evaluation. Upon arrival at UIHC her signs and symptoms were present but markedly improved.,PMH:, 1) Hysterectomy many years previous. 2) Herniorrhaphy in past. 3) DJD, relieved with NSAIDs.,FHX/SHX:, Married x 27yrs. Husband denied Tobacco/ETOH/illicit drug use for her.,Unremarkable FHx.,MEDS:, none.,EXAM:, Vitals: 36.9C.  HR 93.  BP 151/93.  RR 22.  98% O2Sat.,MS: somnolent, but arousable to verbal stimulation. minimal speech. followed simple commands on occasion.,CN: Blinked to threat from all directions. EOM appeared full, Pupils 2/2 decreasing to 1/1. +/+Corneas. Winced to PP in all areas of Face. +/+Gag. Tongue midline. Oculocephalic reflex intact.,Motor: UE 4/5 proximally. Full strength in all other areas. Normal tone and muscle bulk.,Sensory: Withdrew to PP in all extremities.,Gait: ND.,Reflexes: 2+/2+ throughout UE, 3/3 patella, 2/2 ankles, Plantar responses were flexor bilaterally.,Gen exam: unremarkable.,COURSE: ,MRI Brain revealed bilateral thalamic strokes. Transthoracic echocardiogram (TTE) showed an intraatrial septal aneurysm with right to left shunt. Transesophageal echocardiogram (TEE) revealed the same. No intracardiac thrombus was found. Lower extremity dopplers were unremarkable. Carotid duplex revealed 0-15% bilateral ICA stenosis. Neuroophthalmologic evaluation revealed evidence of a supranuclear vertical gaze palsy OU (diminished up and down gaze). Neuropsychologic assessment 1/12-15/93 revealed severe impairment of anterograde verbal and visual memory, including acquisition and delayed recall and recognition. Speech was effortful and hypophonic with very defective verbal associative fluency. Reading comprehension was somewhat preserved, though she complained that despite the ability to see type clearly, she could not make sense of words. There was impairment of 2-D constructional praxis. A follow-up Neuropsychology evaluation in 7/93 revealed little improvement. Laboratory studies, TSH, FT4, CRP, ESR, GS, PT/PTT were unremarkable. Total serum cholesterol 195, Triglycerides 57, HDL 43, LDL 141. She was placed on ASA and discharged1/19/93.,She was last seen on 5/2/95 and was speaking fluently and lucidly. She continued to have mild decreased vertical eye movements. Coordination and strength testing were fairly unremarkable. She continues to take ASA 325 mg qd.
MRI Brain -  Meningioma (Olfactory)  ( Neurology)
Description:  MRI Brain - Olfactory groove meningioma.

CC:, Progressive visual loss.,HX:, 76 y/o male suddenly became anosmic following shoulder surgery 13 years prior to this presentation. He continues to be anosmic, but has also recently noted decreased vision OD. He denies any headaches, weakness, numbness, weight loss, or nasal discharge.,MEDS:, none.,PMH:, 1) Diabetes Mellitus dx 1 year ago. 2) Benign Prostatic Hypertrophy, s/p TURP. 3) Right shoulder surgery (?DJD).,FHX:, noncontributory.,SHX:, Denies history of Tobacco/ETOH/illicit drug use.,EXAM:, BP132/66 HR78 RR16 36.0C,MS: A&O to person, place, and time. No other specifics given in Neurosurgery/Otolaryngology/Neuro-ophthalmology notes.,CN: Visual acuity has declined from 20/40 to 20/400, OD; 20/30, OS. No RAPD. EOM was full and smooth and without nystagmus. Goldmann visual fields revealed a central scotoma and enlarged blind spot OD and OS (OD worse) with a normal periphery. Intraocular pressures were 15/14 (OD/OS). There was moderate pallor of the disc, OD. Facial sensation was decreased on the right side (V1 distribution).,Motor/Sensory/Coord/Station/Gait: were all unremarkable.,Reflexes: 2/2 and symmetric throughout. Plantars were flexor, bilaterally.,Gen Exam: unremarkable.,COURSE:, MRI Brain, 10/7/92, revealed: a large 6x5x6cm slightly heterogeneous, mostly isointense lesion on both T1 and T2 weighted images arising from the planum sphenoidale and olfactory groove. The mass extends approximately 3.6cm superior to the planum into both frontal regions with edema in both frontal lobes. The mass extends 2.5cm inferiorly involving the ethmoid sinuses with resultant obstruction of the sphenoid and frontal sinuses.,It also extends into the superomedial aspect of the right maxillary sinus. There is probable partial encasement of both internal carotid arteries just above the siphon. The optic nerves are difficult to visualize but there is also probable encasement of these structures as well. The mass enhances significantly with gadolinium contrast. These finds are consistent with Meningioma.,The patient underwent excision of this tumor by simultaneous bifrontal craniotomy and lateral rhinotomy following an intrasinus biopsy which confirmed the meningioma. Postoperatively, he lost visual acuity, OS, but this gradually returned to baseline. His 9/6/96 neuro-ophthalmology evaluation revealed visual acuity of 20/25-3 (OD) and 20/80-2 (OS). His visual fields continued to abnormal, but improved and stable when compared to 10/92. His anosmia never resolved.
MCA Aneurysm  ( Neurology)
Description:  Patient with sudden onset dizziness and RUE clumsiness.  Giant Left MCA Aneurysm.

HX: ,This 46y/o RHM with HTN was well until 2 weeks prior to exam when he experienced sudden onset dizziness and RUE clumsiness. The symptoms resolved within 10 min. He did well until the afternoon of admission when while moving the lawn he experienced lightheadedness, RUE dysfunction and expressive aphasia (could not get the words out). His wife took him to his local MD, and on the way there his symptoms resolved. His aphasia recurred at his physician's office and a CT scan of the brain revealed a left temporal mass. He was transferred to UIHC.,PMH:, HTN for many years,MEDS:, Vasotec and Dyazide,SHX/FHX:, ETOH abuse (quit '92), 30pk-yr Cigarettes (quit '92),EXAM:, BP158/92, HR91, RR16,MS: Speech fluent without dysarthria,CN: no deficits noted,Motor: no weakness or abnormal tone noted,Sensory: no deficits noted,Coord: normal,Station: no drift,Gait ND,Reflexes: 3+ throughout. Plantars down-going bilaterally.,Gen exam: unremarkable,STUDIES:, WBC14.3K, Na 132, Cl 94, CO2 22, Glucose 129.,CT Brain without contrast: Calcified 2.5 x 2.5cm mass arising from left sylvian fissure/temporal lobe.,MRI Brain, 8/31/92: right temporo-parietal mass with mixed signal on T1 and T2 images. It has a peripheral dark rim on T1 and T2 with surrounding edema. This suggests a component of methemoglobin and hemosiderin within it. Slight peripheral enhancement was identified. There are two smaller foci of enhancement in the posterior parietal lobe on the right. There is nonspecific white matter foci within the pons and right thalamus. Impression: right temporoparietal hemorrhage, suggesting aneurysm or mass. The two smaller foci may suggest metastasis. The white matter changes probably reflect microvascular disease.,3 Vessel cerebroangiogram, 8/31/92: Lobulated fusiform aneurysm off a peripheral branch of the left middle cerebral artery with slow flow into the vessel distal to the aneurysm.,COURSE:, The aneurysm was felt to be inoperable and he was discharged home on Dilantin, ASA, and Diltiazem.
Lobar Holoprosencephaly  ( Neurology)
Description:  A 21-month-old male presented for delayed motor development, "jaw quivering" and "lazy eye." 

CC: ,Delayed motor development.,HX:, This 21 month old male presented for delayed motor development, "jaw quivering" and "lazy eye." He was an 8 pound 10 ounce product of a full term, uncomplicated pregnancy-labor-spontaneous vaginal delivery to a G3P3 married white female mother. There had been no known toxic intrauterine exposures. He had no serious illnesses or hospitalizations since birth. He sat independently at 7 months, stood at 11 months, crawled at 16 months, but did not cruise until 18 months.,He currently cannot walk and easily falls. His gait is reportedly marked by left "intoeing." His upper extremity strength and coordination reportedly appear quite normal and he is able to feed himself, throw and transfer objects easily. He knows greater than 20 words and speaks two-word phrases.,No seizures or unusual behavior were reported except for "quivering" movement of his jaw. This has occurred since birth. In addition the parents have noted transient left exotropia.,PMH: ,As above.,FHX:, Many family members with "lazy eye." No other neurologic diseases declared.,9 and 5 year old sisters who are healthy.,SHX:, lives with parents and sisters.,EXAM:, BP83/67 HR122 36.4C Head circumference 48.0cm Weight 12.68kg (70%) Height 86.0cm (70%),MS: fairly cooperative.,CN: Minimal transient esotropia OS. Tremulous quivering of jaw--increased with crying. No obvious papilledema, though difficult to evaluate due to patient movement.,Motor: sat independently with normal posture and no truncal ataxia. symmetric and normal strength and muscle bulk throughout.,Sensory: withdrew to vibration.,Coordination: unremarkable in BUE.,Station: no truncal ataxia.,Gait: On attempting to walk, his right foot rotated laterally at almost 70degrees. Both lower extremities could rotate outward to 90degrees. There was marked passive eversion at the ankles as well.,Reflexes: 2+/2+ throughout.,Musculoskeletal: pes planovalgus bilaterally.,COURSE: ,CK normal. The parents decided to forego an MRI in 8/90. The patient returned 12/11/92 at age 4 years. He was ambulatory and able to run awkwardly. His general health had been good, but he showed signs developmental delay. Formal evaluation had tested his IQ at 87 at age 3.5 years. He was weakest on tasks requiring visual/motor integration and fine motor and visual discrimination skills. He was 6 months delayed in cognitive development at that time. On exam, age 4 years, he displayed mild right ankle laxity on eversion and inversion, but normal gait. The rest of the neurological exam was normal. Head circumference was 49.5cm (50%) and height and weight were in the 90th percentile. Fragile X analysis and karyotyping were unremarkable.