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Noon Conference Presentation Amanda C.

Ayala MD CC: I feel weak

4/24/12

HPI: 42 year old Hispanic male previously independent with ambulation and activities of daily loving was transferred to Temple from Frankford Hospital on 5/13. The patient fell at home the night prior to admission and was noted to be weak on the right side was helped to bed by his brother. On the day of admission he was found unresponsive the next morning by his brother. The patient was anemic, coagulopathic, and hyperammonemic on admission. He received vitamin K, multiple units of plts and FFP plus Potassium and magnesium riders both at Frankford and Temple. Past Medical History/ Past Surgical History: Hypertension, Cirrhosis, Multiple visits to CRC substance abuse treatment referrals. ? psychiatric history ( depression +/- schizophrenia). Cholecystectomy. Hernia repair. Appendectomy. Social history: Lives with brother in a 2 SH, 7 STE, no first floor setup. Longstanding history of ETOH abuse, reports stopped drinking 1 month ago. Labs: 5/13: NH3: 108. HGB: 8.6, HCT: 25.9, PLT; 112. PT: 18.6, INR: 1.5, Na: 140, K 3.1, Cl: 108, CO2: 26. BUN: 3, Cr: 0.5, Glu 85. Alk Phos: 120, AST: 67, ALT: 23. T. Bili: 6.0, Alb 1.7. 5/14: Homocysteine: 8.2. CRP: 1.72 ( 0-0.8). Folate 8.0. Vit B12: 1192. HDL: 18. Trig: 84. T chol: 110. Hepatitis profile: ALL negative. RPR: unreactive. Fecal occult blood: NEG 5/16: Fe: 90, TIBC: 135, Ferritin: 632. Tbili: 3.9. Transthoracic Echo: 55-60% LVEF, Mild atrial dilation. Moderate left ventricle dilation. Mild tricuspid regurgitation. The hepatologist recommended CT A/P to rule out HCC, paracentesis to evaluate for malignancy and diuretics to control ascites and to switch patient from lactulose to rifamixin.

Based on the findings on this MRI what kind of deficits/findings


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Noon Conference Presentation Amanda C. Ayala MD

4/24/12

would you expect on physical exam?

T2 weighed MRI

Noon Conference Presentation Amanda C. Ayala MD

4/24/12

Possible findings include:


MLF sensory disturbances ( pain/light touch/propriception), CN III ptosis, inability to adduct, Red Nucleus tremor/ movement abnormalities CT Head: left midbrain IC. Acute intraparenchymal hemorrhage in the left parasaggital midbrain extending to the left cerebral and superior cerebellar peduncle. Mild surrounding edema extending to the left thalamus and pons. MRI/MRA Brain: T1 and T2 hyperintensities. Moderate amount of surrounding edema with mild expansion of the left midbrain. No midline shift or masss effect. No IVH. MRA: P1 segment of left PCA is absent. No aneurysm or AVM identified

What other deficits would you expect?


Physical Exam: General: In NAD. Oriented to person not place or time. Dysarthric speech. Perseverative at times. Prolonged response times HEENT: NCAT. Mildly icteric sclera. R nasolabial fold somewhat flattened Heart: RRR S1-S1 Lungs: Clear to auscultation bilaterally Abdomen: Mildly distended. Slight Caput medusa. No spider angiomata. No hepatosplenomegaly. Fluid wave(+) Extremities: no swelling EYES: Mild ptosis L Mild exotropion R. Right pupil appears lower than the left. Anisocoria L pupil> R. Sluggish/non responsive to light or accomodation. No convergence with accommodation. Upward gaze paresis bilaterally. EOM LR MR SO (down and in) IO ( up and in) IR SR R WFL WFL WFL WFL WFL impaired L WFL Impaired Impaired Impaired Impaired Impaired

Tongue midline. Palate elevation symmetric. R pronator drift. CereAsterixis R. Increased tone R arm/ leg. Hyperreflexic on the right compared to the left side. Decreased Proprioception bilaterally. Difficulty with rapid alternating movements bilaterally R>L. Dysmetria (+) R. 1

Noon Conference Presentation Amanda C. Ayala MD Function of the midbrain

4/24/12

smallest and most rostral component of the brain stem, mediates eye movements and coordination of visual and auditory reflexes. contains the nuclei for cranial nerves III and IV. Also contains the red nuclei, substantia nigra and periaqueductal area Divided into tectum/ tegmentum and crus cerebri ( basis pedunculi)

Although hemorrhage within a specific vascular territory may give rise to many of the same effects (as some vascular syndromes), the total clinical picture is different because it usually involves regions supplied by more than one artery and, by its deep extension and pressure effects, causes secondary features of headache, vomiting, and hypertension, as well as a series of falsely localizing signs1
The common manifestations of nuclear third cranial nerve palsies are diplopia and eyelid ptosis. The signs present on the side of the lesion are weakness of the inferior and medial recti and the inferior oblique muscles. Upgaze limitation is present in both eyes because the superior rectus subnucleus is contralateral, and the axons cross within the nuclear complex. In addition, eyelid ptosis and dilated, unreactive pupils may be present on both sides because the levator subnucleus and Edinger-Westphal nuclei are bilaterally represented. To localize a lesion to the third cranial nerve nucleus, both eyes must have some involvement because of the bilateral representation. The superior rectus and levator of the eyelid, however, are bilaterally represented and thus cannot demonstrate single muscle involvement. In addition, because the medial rectus subnucleus is in the most ventral portion of the nucleus, and all of the dorsal subnuclei send axons through it, single muscle involvement of the medial rectus may not be possible. The eyelid levator subnucleus may be spared, because it is located at the dorsocaudal periphery of the nuclear complex. The main considerations in the differential diagnosis are stroke (either ischemic or hemorrhagic), metastatic tumor, and multiple sclerosis. Of these diagnoses, only ischemic stroke is common. Disorders that simulate nuclear third cranial nerve palsy are myasthenia gravis, CPEO, thyroid ophthalmopathy, and the Guillain-Barr? syndrome

Ropper AH, Samuels MA, "Chapter 34. Cerebrovascular Diseases" (Chapter). Ropper AH, Samuels MA: Adams and Victor's Principles of Neurology, 9e: http://www.accessmedicine.com.libproxy.temple.edu/content.aspx?aID=3635560. 1

Noon Conference Presentation Amanda C. Ayala MD

4/24/12

A. What is ventral midbrain syndrome?


Ventral midbrain (Weber's) syndrome is caused by occlusion of median and paramedian perforating branches and results in the following signs: 1. Ipsilateral oculomotor paresis, ptosis, and dilated pupil (damage to fascicle of cranial nerve III, including parasympathetic fibers) 2. Contralateral hemiplegia, including the lower face (damage to corticospinal and

B. What is paramedian midbrain syndrome?


Dorsal midbrain (Benedikt's) syndrome results from a lesion in the midbrain tegmentum caused by occlusion of paramedian branches of the basilar or posterior cerebral arteries or both. It results in the following signs: 1. Ipsilateral oculomotor paresis, ptosis, and dilated pupil (damage to fascicle of cranial nerve III, including parasympathetic fibers as in Weber's syndrome) 2. Contralateral involuntary movements, such as intention tremor, ataxia, and chorea (damage to red nucleus) 3. Contralateral hemiparesis may be present if the lesion extends ventrally.

C. Upgaze Paresis (Dorsal Midbrain or Parinaud's Syndrome)


1. often occurs without symptoms 2. When symptoms do occur, the patient has difficulty looking up and may have blurry distant vision caused by accommodative spasm. 3. Findings incluide: (1) loss of upgaze, which usually is supranuclear (loss of pursuit and saccades with preservation of the VOR); (2) normal to large pupils with light-near dissociation (loss of the light reaction with preservation of pupilloconstriction in response to a near target) or pupillary areflexia; (3) convergence-retraction nystagmus, in which the eyes make convergent and retracting oscillations after an

QuickTime and a TIFF (Uncompressed) decompressor are needed to see this picture.

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Noon Conference Presentation Amanda C. Ayala MD

4/24/12

From Neurology:
examination & board review Nizar Souayah, Sami Khella

Noon Conference Presentation Amanda C. Ayala MD

4/24/12

Noon Conference Presentation Amanda C. Ayala MD

4/24/12

Noon Conference Presentation Amanda C. Ayala MD

4/24/12

QuickTime and a TIFF (Uncompressed) decompressor are needed to see this picture.