Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Posterior reversible encephalopathy syndrome (PRES) is a central nervous system pathology characterized by headaches, altered mental status, seizures, and visual loss. The syndrome is a clincoradiologic diagnosis, which mandates neuroimaging. The aim of this study is to describe a case of asymptomatic PRES in which the only sign was incidental papilledema found on ophthalmologic examination. A thin 19-year-old female G1P1 s/p natural spontaneous vaginal delivery was referred to our emergency department (ED) by the ophthalmology clinic after finding bilateral papilledema on fundoscopic examination. She denied any fevers, chills, nausea, vomiting, as well as headache, lightheadedness, visual changes, or blurriness. Lumbar puncture was performed, and opening pressure was found to be greater than 55 cmH2O. After collecting Cerebrospinal fluid (CSF) for routine analysis, approximately 15 to 20 mL of CSF was drained. After several revisits to the ED, the neurology clinic was consulted. The magnetic resonance imaging ordered by the neurology clinic, as read by the radiologist, showed a focal lesion in splenium of the corpus callosum and diffusion restriction suggestive of acute infarction (although the anatomical location and age would be unusual). This is an atypical manifestation of PRES. The myriad of clinical symptoms and presentations of PRES has become more identifiable as more case reports of the syndrome are published. This case demonstrates that this atypical syndrome may present in an atypical way. The patient may be asymptomatic, and although imaging defines the diagnosis, a complete physical examination must not be ignored because the only sign may be papilledema.
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PMID:Posterior reversible encephalopathy syndrome presenting as papilledema. 2164 Nov 46

A 29-year-old right-handed G1P1 Caucasian woman presented with acute bifrontal headache (which resolved within 1 day), confusion, and difficulty using her right hand on postpartum day 10. She did not report nausea, vomiting, or visual complaints. The patient was previously healthy except for her recent preeclampsia, which required emergent cesarean section. On examination, the patient was afebrile, awake, alert, and apathetic. She was able to follow few one-step midline commands (e.g., eye opening and closing) inconsistently but not appendicular commands. Her neurologic deficits were remarkable for expressive aphasia, intermittent receptive aphasia, and hyperreflexia with bilateral extensor plantar responses. No meningismus or other focal neurologic deficits were present. Routine laboratory testing including urine toxicology screen was normal. C-reactive protein was 23 mg/L (reference range: <5 mg/L), and erythrocyte sedimentation rate (ESR) was 38 mm/h (reference range: 0-20 mm/h). Rheumatologic panel was negative. Brain MRI showed extensive non-contrast-enhancing T2/fluid-attenuated inversion recovery hyperintensities involving periventricular and deep white matter, especially the centrum semiovale, corpus callosum, bilateral anterior temporal lobes, bilateral caudate nucleus, and globus pallidus (figure, A-C). No evidence of acute or previous stroke was found. CT angiogram and venogram revealed no cerebral sinus thrombosis or large vessel vasculitis. Lumbar puncture opening pressure was 18.5 cm H2O. CSF showed normal cell counts, protein, and glucose levels without oligoclonal bands. EEG recorded in awake, drowsy, and sleep state was normal. Dilated ophthalmic examination showed no microangiopathy or retinal branch arterial occlusion. Audiologic examination was normal.
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PMID:Acute encephalopathy as the initial manifestation of CADASIL. 2363 79