Reversible posterior leukoencephalopathy Int 林君賢

Brief case present 49y/o female with L’t breast cancer in 93/9 s/p C/T Taxotere + Epirubicin Underlying HTN,no DM C.C: Incoherent speech then convulsion of right limb with consciousness change on 8/10 night

Brief history speak incoherently on 8/10 night. Later in this early morning(about 1AM) convulsion of right limbs was noted accompanied by eye deviation to right side. Mild fever at ER. AED was given brain CT, CSF were done for survey the etiology. No evidence of ICH was impressed. Emperic A/B was given for suspected CNS infection.

CT on 8/11 Leukoencephalopathies involving the bilateral occipital lobes. Leukoencephalopathies involving the bilateral occipital lobes.

8/21 MRI

DWI

Hypertensive encephalopathy

Many names Hypertensive encephalopathy, reversible occipitoparietal encephalopathy reversible posterior leukoencephalopathy Hypertensive encephalopathy, reversible occipitoparietal encephalopathy, or reversible posterior leukoencephalopathy: three names for an old syndrome J Child Neurol. 1999 May;14(5):277-81

History 1928, Oppenheimer and Fishberg s/s: headaches, confusion, drowsiness, blurring of vision, occasional seizures, and infrequent focal signs DBP: > 140mmHg D/D: stroke, systemic dz(ex: uremia,e- imbalance )

Cause Postgrad. Med. J. 2001;77;24- Some suggest RPLS a predicator of eclampsia even if there is no other HELLP Malignant hypertension is not necessary for the RPLS Postgrad. Med. J. 2001;77;24-

Immunosuppresive agent Postgrad. Med. J. 2001;77;24-

Symptom and sign H/A,N/V Visual disturbance, cortical blindness(Anton’s syndrome) Altered mental status(less coma and stupor) Seziure: most seen GTC, preciptated by V/H,usually multiple attack

NE findings CN II; intact, but maybe with hemianopia, neglect,anton’s syndrome,papilledema DTR: increased and babinski sign may positive May have muscle weakness and nild incoordination

Lab CSF: protein > 100mg/dl and pressure elevated BUN mild elevation except in renal failure

Radiologic finding Reduced density on CT Increased intensity bilateral white matter on T2WI, usually in occipital-parietal lobe,May not involved calcarine fissure asymmetrical not unusal Advanced in brainstem, basal ganglion, frontal lobe,cerebellum Often misinterpretated as large area infarction or demyelination But reversible within weeks

Radiologic finding unlike the edema in trauma, neoplasm, or stroke—there is little or no mass effect and the water does not tend to course along white matter tracts such as the corpus callosum scattered cortical lesions occur in a watershed distribution and probably correspond to small infarctions

DWI & ADC maps

Typical image finding

TOB image

attack remission

Image D/D Top of basilar syndrome Cerebral venous thrombosis

Pathophysiology Vasospasm? Angio proved but not correlated with treatment improved image Vasodilatation ? Image proved Why post involved most? Carotid system innerved by sympathetic sysmtem better than vertebro-basilar system

Treatment Nitroprusside: 0.5-0.8ug/kg/min Lebetalol :20-40mg IV then 2mg/min Then f/u with long acting ACEI or CCB Only 15-20% MBP decreased but above 125 mmHg must be controlled, otherwise watershed infarction would be complicated.

Reference Adam 6th edition Merrit 8th edition Postgrad. Med. J. 2001;77;24- Magnetic resonance imaging in Posterior Reversible EncephalopathySyndrome: report of three cases and review of literature Arch Gynecol Obstet (2005) 271: 79–85