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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.
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T2 weighed MRI
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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
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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
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QuickTime and a TIFF (Uncompressed) decompressor are needed to see this picture.
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From Neurology:
examination & board review Nizar Souayah, Sami Khella
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QuickTime and a TIFF (Uncompressed) decompressor are needed to see this picture.