Primary and Secondary Hypothalamus and Brain Stem Lesions

Pia, H. W.

doi:10.1007/978-3-642-70603-5_37

Cited by 5 publications

(1 citation statement)

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“…Beim zentralen Salzverlust-Syndrom (48,51) wird bei intakter Nierenfunktion eine große Menge Na + ausgeschieden; dies ist möglicherweise zentral oder durch eine Änderung der Nierenperfusion bedingt (48). Das extrazelluläre Volumen nimmt ab, worauf verstärkt antidiuretisches Hormon ausgeschieden und nachfolgend Flüssigkeit retiniert wird: inappropriates ADH-Sekretions-Syndrom.…”

Section: Zu Den Hilfsuntersuchungenunclassified

Zur Klinik und Pathophysiologie der intrakraniellen Drucksteigerung

Jacobi¹,

Klinter²,

Weiermann³

1988

Klin Padiatr

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In 48 children who had raised intracranial pressure (icp) this was monitored continuously by an epidural route. Icp-values were correlated with other important parameters like the mean arterial pressure (map) and the early components of brainstem acoustic evoked responses (BAER). The results were as follows: 1. focal and multifocal brain lesions resulting in vasogenic brain edema have better prognosis than those morbid conditions causing cytotoxic edema. In the letter group the whole brain's metabolism is impaired, brainstem, cerebellum and spinal cord included. 2. by monitoring map and icp we are enabled to assess the cerebral perfusion pressure. If this value falls short of 20 Torr the duration of unconsciousness and the frequency of brainstem related symptoms increases as well as impairment of cranial nerves and cerebellar-extrapyramidal symptoms and mental handicaps in the long term course. 3. cerebral dysfunction and organic brain syndromes in general are not related to icp-increase. They resemble local brain damage, e.g. after contusions. 4. serial registration of BAER is a good aid in iatrogenic induced deep phenobarbital coma. If there are critical values of the perfusion pressure mainly the waves III and V of BAER have increased peak latencies and go flattened. This trend takes place slowly within hours or even days. Loss of the components III and V is prompted by an irreversible damage of the caudal brainstem. This finding after cytotoxic brain edema is even more relevant than after vasogenic edema. If the component loss III-V is bilateral dissociated brain death has to be anticipated. Some important issues of icp-pathophysiology are discussed according to the literature.

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Section: Zu Den Hilfsuntersuchungenunclassified