Subakutně probíhající reverzibilní hypertenzní leukoencefalopatie - kazuistika

HALUZOVÁ, Adéla, René JURA, Josef BEDNAŘÍK, Světlana SKUTILOVÁ, Tereza ANDRAŠINOVÁ, Miloš KEŘKOVSKÝ a Andrea KŘIVANOVÁ. Subakutně probíhající reverzibilní hypertenzní leukoencefalopatie - kazuistika. Online. CESKA A SLOVENSKA NEUROLOGIE A NEUROCHIRURGIE. Praha: Česká lékařská společnost J.E.Purkyně, 2008, roč. 71, č. 6, s. 726-731. ISSN 1210-7859. [citováno 2024-04-23]

Základní údaje

• Originální název: Subakutně probíhající reverzibilní hypertenzní leukoencefalopatie - kazuistika
• Název anglicky: Subacute Hypertensive Reversible Leukoencephalopathy - a Case Report
• Autoři: HALUZOVÁ, Adéla (203 Česká republika, garant, domácí), René JURA (203 Česká republika, domácí), Josef BEDNAŘÍK (203 Česká republika, domácí), Světlana SKUTILOVÁ (203 Česká republika, domácí), Tereza ANDRAŠINOVÁ (203 Česká republika, domácí), Miloš KEŘKOVSKÝ (203 Česká republika, domácí) a Andrea KŘIVANOVÁ (203 Česká republika, domácí)
• Vydání: CESKA A SLOVENSKA NEUROLOGIE A NEUROCHIRURGIE, Praha, Česká lékařská společnost J.E.Purkyně, 2008, 1210-7859.

Další údaje

• Originální jazyk: čeština
• Typ výsledku: Článek v odborném periodiku
• Obor: 30103 Neurosciences
• Stát vydavatele: Česká republika
• Utajení: není předmětem státního či obchodního tajemství
• Impakt faktor: Impact factor: 0.319
• Kód RIV: RIV/00216224:14110/08:00107022
• Organizační jednotka: Lékařská fakulta
• UT WoS: 000261867200013
• Klíčová slova anglicky: hypertensive encephalopathy; leukoencephalopathy
• Příznaky: Recenzováno

Anotace

Hypertensive encephalopathy induced by essential or secondary arterial hypertension is characterised by a sudden onset of symptoms pointing to diffuse encephalopathy (headache, nausea, vomiting, vision problems, confusion or epileptic seizures) linked with an increase in blood pressure (BP, hypertensive crisis). in such case, the imaging methods applied, especially magnetic resonance (MR), show leukoencephalopathy. Both clinical symptoms and MR imaging findings are reversible after the blood pressure values have been normalised. We report a case of a 37-year old man who developed non-specific symptoms of encephalopathy over the period of one year (cephalea, vision disorders, behaviour changes, atactic walk). CT and MRI of the patient's brain showed diffuse affection of the white matter of the brain, cerebellum and of the cerebral trunk. Inflammatory, demyelinisating, ischaemic, oncologic, metabolic and toxic aetiologies of leukoencephalopathy were excluded. In spite of absence of anamnestic data on arterial hypertension, and of normotensive values at admission, a hypertension crisis developed and clinical symptoms progressed into a picture of delirium. Blood pressure compensation resulted in the regression of clinical symptoms and a significant attenuation of cardiologic signs of encephalopathy, which was a confirmation of hypertensive etiology of leukoencephalopathy. Subsequently, the presence of chronic idiopathic arterial hypertension was confirmed, and secondary causes of hypertension including phaeochromocytoma were excluded. Hypertensive encephalopathy should be considered also in the case of protracted and fluctuating symptoms of encephalopathy and normal results for current blood pressure measurements.

Anotace anglicky

Hypertensive encephalopathy induced by essential or secondary arterial hypertension is characterised by a sudden onset of symptoms pointing to diffuse encephalopathy (headache, nausea, vomiting, vision problems, confusion or epileptic seizures) linked with an increase in blood pressure (BP, hypertensive crisis). in such case, the imaging methods applied, especially magnetic resonance (MR), show leukoencephalopathy. Both clinical symptoms and MR imaging findings are reversible after the blood pressure values have been normalised. We report a case of a 37-year old man who developed non-specific symptoms of encephalopathy over the period of one year (cephalea, vision disorders, behaviour changes, atactic walk). CT and MRI of the patient's brain showed diffuse affection of the white matter of the brain, cerebellum and of the cerebral trunk. Inflammatory, demyelinisating, ischaemic, oncologic, metabolic and toxic aetiologies of leukoencephalopathy were excluded. In spite of absence of anamnestic data on arterial hypertension, and of normotensive values at admission, a hypertension crisis developed and clinical symptoms progressed into a picture of delirium. Blood pressure compensation resulted in the regression of clinical symptoms and a significant attenuation of cardiologic signs of encephalopathy, which was a confirmation of hypertensive etiology of leukoencephalopathy. Subsequently, the presence of chronic idiopathic arterial hypertension was confirmed, and secondary causes of hypertension including phaeochromocytoma were excluded. Hypertensive encephalopathy should be considered also in the case of protracted and fluctuating symptoms of encephalopathy and normal results for current blood pressure measurements.