Oppenheimer and Fischberg's vasoconstriction-hypothesis on the pathogenesis of hypertensive encephalopathy
was subsequently supported by animal experiments. Later on the role of decompensation
of the autoregulatory mechanism of the cerebral blood flow was revealed.
The transient symptomatology comprises headache, seizures, focal cerebral symptoms
(hemiplegia etc.), visual disturbances, mental disorders, papiledema etc. The age-dependency
of the influence of edema is probably expressed by the predominance of seizures in
childhood and the long duration of the symptoms in our third and fourth patient.
The differentiation between hypertensive encephalopathy and a local complication of
hypertension (hemorrhage) can be difficult, not at least because the first disturbance
may be followed by the second (patient 3). Hypertension is not always present as initial
symptom (patient 1 and 2). Hence a series of bloodpressure readings is required in
acute cerebral incidents in childhood. Steroid-treatment may lead, especially in patients
suffering from a hypocomplementemic form of membranoproliferative glomerulonephritis,
to a sudden rise of the bloodpressure and subsequently to hypertensive encephalopathy
(patients 2 and 3).
Hypertensive encephalopathy is a neuropediatric emergency. The urgent treatment with
dioxaside, fursemide and sodium nitroprusside is shortly reviewed.
Hypertension - encephalopathy - glomerulonephritis - intracerebral hematoma - steroid
treatment
