G. Grimm

Wilson's disease Evidence of subgroups derived from clinical findings and brain lesions

Using exploratory factor analysis, we prospectively investigated neuropsychiatric symptoms and structural brain lesions of 47 patients with proven Wilsons disease and identified three subgroups. The first subgroup clinically exhibited bradykinesia, rigidity, cognitive impairment, and an organic mood syndrome and by MM showed a dilatation of the third ventricle. The second subgroup was characterized by ataxia, tremor, reduced functional capacity, and focal thalamic lesions. The third subgroup showed dyskinesia, dysarthria, an organic personality syndrome, and focal lesions in the putamen and in the pallidum.

Comparison of functional and structural brain disturbances in Wilson's disease

We assessed the functional and structural brain disturbances in Wilsons disease (WD) by evoked potentials (EPs) and magnetic resonance imaging (MRI). All the 25 neurologically symptomatic and 44% of the 16 asymptomatic patients, assessed by both EPs (n = 48) and imaging (n = 41), had at least 1 abnormality of either prolonged EP conduction times, imaging-outlined presence of cerebral lesions, or brain atrophy. Our findings indicate that EPs and MRI are sensitive techniques for the evaluation of brain involvement in WD.

Evoked potentials in severe herpes simplex encephalitis.

Diagnostic and prognostic value of evoked potentials (EP) were studied in 5 patients with severe herpes simplex encephalitis (HSE). Latency of the third negative cortical N70 peak, elicited by median nerve stimulation, was prolonged in 3 survivors with Glasgow coma score of ≤6 (115 vs 71 ms in controls,p<0.05), but normal after improvement of the acute disease, N70 right to left interhemisphere difference was increased initially in the 4 survivors (26 vs 3 ms in controls,p<0.05) indicating focal brain involvement, a crucial finding in HSE. The first cortical N 20 peak was preserved in all survivors even during deep coma where evaluation of brain function is difficult. Auditory brainstem EP were normal in all patients and useful to exclude brainstem death. In severe HSE, somatosensory long-latency EP are an effective monitor of the level of impaired consciousness and can detect brain focal signs. Short-latency N20 components may be predictive of the outcome.

Detection of subclinical brain dysfunction by sensory evoked potentials in patients with severe diabetic ketoacidosis

Objective: Subclinical brain dysfunction is a potentially deleterious complication of diabetic ketoacidosis but is rarely recognized. Thus, we investigated the diagnostic value of sensory evoked potentials for detecting subclinical brain dysfunction in patients with diabetic ketoacidosis. Design: Prospective trial. Setting: Intensive care unit in a university hospital. Patients: 5 neurologically asymptomatic patients (Glasgow Coma Scale score 15, slight drowsiness; aged 20 to 66 years) with an established diagnosis of severe diabetic ketoacidosis were studied. Measurements and results: Short- and long-latency sensory evoked potentials were recorded within 2 h of initiation of therapy for ketoacidosis and 7 days after normalization of ketoacidosis, respectively. Two hours after starting therapy, sensory evoked potential peak latencies were prolonged in all five patients compared to age-matched healthy subjects [cervical N 13 to cortical N 20 interpeak latency of short-latency evoked potentials (mean) 5.8 vs 5.3 ms, p < 0.05; N 35 peak latency 40 vs 34 ms, p < 0.05; N 70 peak latency of long-latency evoked potentials 102 vs 76 ms, p < 0.01]. In all five patients, cervical N 13 to cortical N 20 interpeak latency and N 35 and N 70 peak latency reverted to normal 7 days after recovery from diabetic ketoacidosis. Conclusions: Our study indicates that the recording of sensory evoked potentials is a sensitive method of detecting subclinical brain dysfunction in patients with severe diabetic ketoacidosis. Since sensory evoked potentials were significantly prolonged in all five patients, this strongly suggests that subclinical brain dysfunction occurs more frequently than is generally recognized.

Diagnosis of gallbladder perforation in acute acalculous cholecystitis in critically ill patients

In the presence of ascites ultrasound is not appropriate to distinguish between gallbladder perforation and acute acalculous cholecystitis. However, the correct and early diagnosis of gallbladder perforation is important for the treatment and prognosis. We report 4 critically ill patients with ascites. All patients had evidence of gallbladder perforation by ultrasound and underwent cholecystectomy: 2 patients had gallbladder perforation, but 2 had acalculous cholecystitis without perforation. markedly elevated serum alkaline phosphatase was the only discriminating finding indicating gallbladder perforation.

Multiple organ failure

Longterm prognosis of patients with cirrhosis depends on the occurence of ascltes, jaundice or GI-bleeding. Inhospital outcome depends on the occurence of additional complications. In a retrospective andlysis we studied the outcome of 78 patients with decompensated cirrhosis admitted to the medical ICU of our clinic because of the occurence of additional organ failure. Patients : n-7B (age 51±12years) male=57, female-21, ICU survival 19% (overall ICU survival Bt%). Studyperiod: 1.1.81 -31.12.90. On admission 51 patients showed renal failure (survival 191) 24 patients had a respiratory failure (survival 13%) and 14 patients were in circulatory shock (survival 21%). In 56 patients severe bleeding led to the admission (survival lit), in 53 patients Clinical symptoms of sepsis were found on admission (survival 19%). Most of the patients with bleeding or sepals showed addition[ complications (Table 1).

Das Multiorganversagen auf einer internistischen Intensivstation. Ursachen — Inzidenz — Prognose

Das Multiorganversagen (MOF) wurde initial als ein Versagen mehrerer Organe nach einem Polytrauma beschrieben [1]. In der Folge wurde jedoch das Auftreten des MOF auch nach Sepsis, Pankreatitis und Blutungsschock beschrieben [2, 3].

Brain death and organ donors

Results: The prognostic value of the KISS could be shown by the close correlation of the increasing scorepoints and mortality. For class I (age < 30) and class VI (age > 70) the distribution and the mortality rate was shown in Fig. 1. There were no signifikant differences in the mortality rate in both groups up to risk class 7. In the higher risk groups the mortality rate was significant lower in age class I compared to age class VI.

EDV-unterstützte Analyse bakteriologischer Daten zur Erfassung von Resistenzänderungen an einer internistischen Intensivstation

Seit dem Jahre 1982 wird an der Intensivstation der I. Medizinischen Universitatsklinik eine EDV-masige Verarbeitung bakteriologischer Befunde durchgefuhrt [1].

Verlauf und Therapie der viralen Meningoenzephalitis

Die akute, virale Meningoenzephalitis reprasentiert eine wichtige, wenn auch seltene Erkrankung des zentralen Nervensystems. Relevante Erreger sind Herpes-, Picorna-, Toga-, Paramyxo-, Retro- und Rhabdoviren. Epidemiologische Untersuchungen aus den USA berichten uber 20 000 Neuerkrankungen pro Jahr, ca. 1 000–2 000 (5–10%) davon werden durch Herpes simplex verursacht. Die Herpes simplex Enzephalitis (HSE) ist die haufigste Form der spontanen akuten Enzephalitis der westlichen Welt [1], sie befallt als hamorrhagischnekrotisierender Prozes bevorzugt die Temporallappen und hat unbehandelt eine Mortalitat von 70% (nur 10% werden voll rehabilitiert) [2]. Die fruhzeitige Therapie mit Acyclovir vermag Mortalitat (auf 20%) und Prognose (nach 6 Monaten 50% rehabilitiert) entscheidend zu verbessern [3]. Betreffend die Morbiditat der akuten viralen Meningoenzephalitis besteht keine gesicherte Pradilektion zu immunsupprimierten Patienten.