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ArtikelPontine Warning Syndrome: A Chameleon of Ischemic Stroke  
Oleh: Enriquez-Marulanda, Alejandro ; Amaya-Gonzalez, Pablo ; Orozco, Jorge L.
Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Neurologist vol. 21 no. 06 (Nov. 2016), page 93-96.
Topik: Stroke; Warning Syndromes
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  • Perpustakaan FK
    • Nomor Panggil: N06.K
    • Non-tandon: 1 (dapat dipinjam: 0)
    • Tandon: tidak ada
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Isi artikelIntroduction: Crescendo transient ischemic attacks or “Stroke Warning Syndromes” consist of stereotyped frequent short-lasting episodes of focal neurological deficits. This is explained by intermittent hypoperfusion of the vascular territory of terminal arteries with insufficient collateral flow, presenting a high risk for subsequent infarction. Pontine warning syndrome (PWS) is a subtype of this atypical presentation of stroke/transient ischemic attack and is considered a challenge for diagnosis. Case Report: We describe 2 cases of patients with PWS who were admitted to our institution. They presented acute neurological deficits that fluctuated during the course of their hospitalization; interestingly, this neurological worsening and improvement was associated with blood pressure fluctuations. In both cases, brain magnetic resonance imaging revealed an ischemic lesion in the paramedian pons due to basilar artery branch disease. No outstanding infectious or metabolic factors contributed to neurological worsening/fluctuations. These patients received standard medical care without IV-thrombolysis because of the presence of contraindications for IV tissue plasminogen activator. Permissive hypertension was promoted to achieve adequate perfusion during hospitalization. At discharge and follow-up, the patients showed partial resolution from their stroke symptoms. Conclusions: PWS is a diagnostic and management challenge for the clinician. Because of its low incidence, this syndrome has been underestimated and understudied. There is, currently, no standard treatment for this condition; however, it is paramount, during treatment, that hypotension/hypoperfusion be avoided, with the goal being asymptomatic normotension to permissive hypertension. The probable mechanism of disease is hypoperfusion due to basilar artery branch disease and perhaps cerebral vascular dysregulation in the affected area.
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