Neurosarcoidosis

Case #88: MRI Brain, 3/26/93: Neurosarcoidosis

CC: Blurred vision OD.

 

Hx: 29 y/o RHF experienced a sore throat, rhinorrhea and 2-3 "red round" lesions on her legs 3 weeks prior to presentation. The lesions tended to migrate outward, but completely resolved in 2-3 days. On 10/24/90, she began feeling "strain" in her right eye, but denied any pain or visual change. On 10/27/90, she developed blurred vision, OD. Since then there has been no change in her visual symptoms; and no symptoms have developed in the left eye. She was seen in the Student Health Clinic at W. Illinois University today, and was found to have a temperature of 100.0F and started on ampicillin. She was then referred to Neuro-ophthalmology at UIHC and then to Neurology (UIHC).

She denied any dysarthria, dysphagia, diplopia, night blindness, transient visual obscuration--except blurred vision OD, or weakness/numbness.

She has a 10 year history of mixed migraine/tension type headaches

which were described bifrontal, and rarely unilateral, dull headaches associated with photophobia but no nausea/vomiting. Once a year the headaches are associated with LUE numbness. The headaches typically occur during periods of academic/social stress and are completely relieved with Excedrin. HCT done at Mayo Clinic 9 years ago was reportedly negative.

 

MEDS: Actifed prn. Ampicillin (started 11/7/90). Excedrin prn.

PMH: 1)Headaches, 2)Infrequent UTI, 3)"Postnasal drip" and No history of allergy or pregnancy.

FHx: 1st cousin with polymyositis. GGF died of ALS. One GF(smoker) died of Lung CA. Twin brother who is alive and well.

SHx: College Student. Denies tobacco/ETOH/illicit drug use.

ROS: No productive cough or purulent nasal drainage. No recent weight loss, CP, SOB or lymphadenopathy.

EXAM: BP145/91 HR78 RR16 37.3C Moderately obese.

MS: A & O to person, place, time. Cooperative and anxious. Speech: fluent and without dysarthria. Thought processes were lucid and logical. Intact concentration/calculation and recall.

CN: Goldman Visual fields testing revealed a central scotoma and superior altitudinal defect OD. Markedly swollen disc OD with hemorrhages. Mildly swollen disc OS without hemorrhages. 2.4 RAPD OD. 20/200 visual acuity OD and normal acuity OS. (all per neuro-ophthamology exam 11/7/90). EOM intact and without nystagmus. Face: symmetrical appearance and movement and intact sensation. Gag-corneal-SCM responses were intact bilaterally. Tongue midline.

MOTOR: 5/5 strength throughout. Normal muscle tone and bulk.

Sensory: intact PP/VIB/PROP/LT/T throughout all extremities.

Coord: unremarkable.

Station and Gait were unremarkable.

Reflexes: 3/3 throughout. Plantar responses were flexor, bilaterally.

Gen Exam: unremarkable.

 

COURSE: ESR, CBC, GS were unremarkable. CBC was notable for a WBC 11.0 (no differential done). HCT: revealed a 1.5cm enhancing suprasellar cistern mass which appeared to lift the optic chiasm slightly in the cephalad direction. It did not appear to invade the pituitary, but was adjacent to the posterior aspect of the left hypothalamus. There was no dural tail seen. CSF: opening pressure not noted, total protein 20mg/dl, IgG 1.9mg/dl(normal), IgG index 0.6(normal), no oligoclonal banding was found, glucose 77mg/dl (serum 177gm/dl), 3RBC, 6WBC(5 lymphocytes, 1 histiocyte). CSF: AFB, Cryptococcal Ag, and cultures were negative.. CSF ACE, serum ACE, SPEP, Aldolase and Prolactin levels/titers were normal. MRI Brain revealed a heterogeneous gadolinium enhancement of tissue in areas around optic chiasm, the anterior recesses of the 3rd ventricle, hypothalamus and meninges about the sella. Conjunctival biopsies (OU) and bronchoscopic biopsies were inconclusive of sarcoidosis or granulomatous infections.

The patient was presumed to have sarcoidosis and was empirically placed on a trial of prednisone 60mg qd. She had documented exacerbations of her presenting symptoms at doses less than 5 mg qd. Serial MRI studies during the first 6 months following the initial MRI scan revealed worsening of the brain lesion, but no clinical worsening was noted. She was treated with Cytoxan and IV Solu-Medrol following worsening of vision in 2/93. She remained on Cytoxan and prednisone until 5/94 when she was changed to Imuran and prednisone. She was last seen on 1/6/96 in the Neurology clinic. Her ophthalmologic exam and pulmonary function testing had been stable for 2 years: she was taking Imuran 50mg bid and was placed on a prednisone taper starting at 11mg qod down to 5mg qod. 3/26/93 MRI brain revealed substantial improvement in the large area of inhomogeneous enhancement, now limited primarily to the hypothalamus and left basal ganglia.

 

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