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Nervenheilkunde 2003; 22(01): 11-14
DOI: 10.1055/s-0038-1624363
Original- und Übersichtsarbeiten/Original and Review Articles
Schattauer GmbH

Hypoglykämische Enzephalopathie

Hypoglycemic encephalopathy
J. G. Heckmann
1   Neurologische Klinik und Poliklinik der Universität Erlangen-Nürnberg
,
C. J. G. Lang
1   Neurologische Klinik und Poliklinik der Universität Erlangen-Nürnberg
,
B. Neundörfer
1   Neurologische Klinik und Poliklinik der Universität Erlangen-Nürnberg
› Author Affiliations
Further Information

Publication History

Publication Date:
15 January 2018 (online)

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Zusammenfassung

Eine Hypoglykämie liegt bei einem Blutzuckerspiegel <40 mg/100 ml vor und kann durch zahlreiche Ursachen hervorgerufen werden, meist im Zusammenhang mit inadäquater Insulingabe und/oder unzureichender Nahrungsaufnahme beim Patienten mit insulinpflichtigem Diabetes mellitus. Als weitere Faktoren sind der endogene Insulinüberschuss (Insulinom), die Hormondefizienz (GH, Kortisol), der Alkoholmissbrauch, die Medikamenteneinnahme (Amphetamine u.a.), Leber-, Nieren-und Stoffwechselerkrankungen zu berücksichtigen.

Bei anhaltender Hypoglykämie kommt es neurophysiologisch zu einer verminderten und schließlich fehlenden hirnelektrischen EEG-und evozierten Potenzial-Aktivität sowie zu epileptischen Entladungen. Pathomorphologisch finden sich Mikrovakuolationen, Schrumpfungen und Zellnekrosen sowohl an Neuronen als auch an Gliazellen. Biochemisch tritt bei Hypoglykämie eine eskalierende Schädigungskaskade mit Anstieg des intrazellulären Kalziums und Freisetzung freier Radikale sowie destruktiver Enzyme auf. Die Oxygenation und der zerebrale Blutfluss bleiben jedoch erhalten. Klinisch werden bei Hypoglykämie delirante Syndrome, epileptische Anfälle, transiente neurologische Symptome, anhaltende fokal-neurologische Zeichen und in schweren Fällen Stupor und Koma beobachtet, die z.T. in schwere neurologische Defektsyndrome (akinetischer Mutismus, apallisches Syndrom) einmünden. Aufgrund der erheblichen Schädigungspotenz von Hypoglykämien kommt der Prophylaxe große Bedeutung zu. Bei Risikopatienten ist ein intensives Hypoglykämiewahrnehmungstraining sinnvoll.

Summary

Hypoglycemia is defined as a glucose level of <40 mg/100 ml and is caused by a number of clinical conditions. Mostly it is associated with inadequate insuline treatment and/or insufficient caloric intake in diabetics. Occasionally there are other causes such as insulin overdose (insulinoma), hormone deficiency (cortisole, GH), alcohol abuse, drugs (amphetamine, etc.), hepatic and renal diseases, genetic metabolic disorders etc.

Neurophysiologically prolonged and severe hypoglycemia leads to a diminished and finally flat electroencephalographic and evoked potential activity as well as epileptic discharges. Neuropathological studies revealed neuronal and glial microvacuolations, shrinkage and cell necrosis. In biochemical studies hypoglycemia induced a cascade of damage including a dramatic increase in intracellular calcium, release of free radicals and autodestructive enzymes. In contrast, the cerebral oxygenation and blood flow were preserved. In clinical practice hypoglycemia manifests itself as delirium, epileptic seizures, transient neurological signs and symptoms, persistent focal disorders and in extreme cases as stupor or coma. If the patients survive, marked neurological defect syndromes such as akinetic mutism or even persistent vegetative state may occur.

Hypoglycemia should be quickly diagnosed and treated accordingly. In patients with risk of hypoglycemia hypoglycemia awareness education is advisable.

Schlüsselwörter

Glukose - Diabetes mellitus - Hypoglykämie - Enzephalopathie

Keywords

Glucose - diabetes mellitus - hypoglycemia - encephalopathy
 

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