Hochgradige asymptomatische Stenosen der arteria carotis interna (> 70 %) werden oft als Zufallsbefund bei peripherer arterieller Verschlußkrankheit oder koronarer Herzkrankheit gefunden. Auf der anderen Seite führt eine Carotis-Stenose oft zu transitorischen ischämischen Attacken (TIAs).

Unilateral internal carotid artery (ICA) stenosis may be accompanied by widespread atherosclerosis of extra- and intracranial vessels leading to subtle cognitive disorders. We applied multichannel recording of P300 in 28 patients (68.3 +/- 8.1 years; 15 asymptomatic, 13 with a history of transient ischemic attack (TIA)) and compared them with an age- and sex-matched control group. All underwent a visual "odd-ball paradigm" as well as a psychometric test, the Cognitive Performance Test (CPT), testing mainly visual attention and memory. The potentials were derived from 16 electrodes according to the 10/20 system against linked mastoids. The latencies and amplitudes of N250 and P300 were measured and their amplitudes additionally mapped. Furthermore, the early sensory exogenous potentials, P1 and N1, within the P300 potentials as well as conventional pattern reversal visual evoked potentials (PVEPs) were evaluated. (1) Both the early exogenous potentials and the conventional PVEPs showed no significant differences among all groups. (2) There were no significant differences between asymptomatic patients and those with a TIA history in all parameters of the P300 complex so that one total patient group was constructed and compared to the controls. (3) Patients' P300 amplitudes showed significant reductions over hemispheres ipsilateral (P < or = 0.014) and contralateral (P < or = 0.044) to the stenosis. (4) The N250 amplitudes were reduced only in the central leads (P < or = 0.05). (5) The latencies of N250 potentials were significantly prolonged at many electrodes, not only ipsi-(P < or = 0.0007) but also contralateral (P < or = 0.022) to the stenosis. (6) The patients' P300 latencies showed significant lengthening only at occipital sites (P < or = 0.05) compared to controls. (7) In all measured parameters, within the patient group, the differences between hemispheres ipsilateral versus contralateral to the ICA stenoses did not reach statistical significance. (8) The CPT values detected slight cognitive disorders for both patient groups and they correlated significantly with the latencies in many leads. (9) The highest test sensitivity to classify patients versus controls (z score > 2) was reached in P300 maps of TIA patients (77%). An altered P300 indicates electrophysiologically, and CPT behaviorally, subclinical cognitive deficits even in asymptomatic patients with unilateral tight ICA stenoses. Interestingly, no differences between asymptomatic and TIA patients with a high-grade unilateral ICA stenosis could be found.

UNLABELLED:We investigated 11 patients (63.1 +/- 10.9 y) after recovery (median: 3 days) from amaurosis fugax of 12.1 +/- 12.0 min duration with the method of pattern reversal visual evoked potentials (PVEPs) derived from Oz to Fz (Cz ground) after randomized monocular stimulation. SELECTION CRITERIA:clear-cut cases with no hemispheric symptomatology, normal vision and normal cranial CT. The parameters were measured without knowing the affected eye and compared with age matched controls (n = 32). N80 latencies of the affected eyes were significantly prolonged (3.2 +/- 1.9 ms; p < .025) in comparison with the not affected eyes. The controls did not show such interocular difference. P100 latency behaved similarly but less prominently so (2.0 +/- 2.3 ms; p < .05; controls: p > .05). N80/P100 amplitude was reduced in 82% after stimulation of the affected side without reaching statistical significance. The 5 patients showing angiographically ipsilateral very tight stenosis of carotid artery (> 95%) behaved more prominently so in all 3 parameters. The findings indicate a damage of nerval tissue responsible for visual perception or a hemodynamic insufficiency under stimulus condition in affected eyes outlasting the clinical symptomatology for a certain period of time.

The dynamics of cognitive brain functions of 104 patients with both chronic non-cirrhotic (NC) and cirrhotic liver disease (C: C1, non-encephalophatic; C2, encephalopathic) were investigated by means of visual P300 potentials elicited in both the paradigms of transient (PI) and selective attention (PII). Conventional PVEPs, psychometric tests and quantitative liver function tests were also performed. As compared to both an age-matched control group (N) and the non-cirrhotic patients (NC), the N250 and P300 latencies of the cirrhotics (C) were equally prolonged in both P300 paradigms (P = 0.0001). By contrast, the P300 amplitudes were not different between the patient groups in either P300 paradigm. In the cirrhotics, however, the P300 amplitude differences between PII and PI (+ 3.7 ± 2.8 μV, mean ± 1 S.D.) were significantly (P < 0.01) smaller than in the non-cirrhotics (+ 7.5 ± 5.2 μV) lecting disturbances in the dynamics of visual attention. Interestingly, these P300 amplitude differences between both paradigms were positively correlated (r = 0.35; P = 0.005) with hepatic metabolic capacity, but not with liver blood flow (r = 0.23; P > 0.05). The diagnostic efficacy of the visual P300 in PI (sensitivity, 48%; specificity, 100%) was lower than that of the visual P300 in PII (79%; 100%) and that of the psychometric tests (63%; 94%), but it remained superior to that of the PVEPs (29%; 97%). It is concluded that in patients with cirrhotic liver disease visual P300 potentials can even reveal the dynamics of minor cognitive brain dysfunction and may also provide interesting pathophysiological information.

A brain stem infarction in the area of the nerve fascicle of the oculomotor nerve could be demonstrated by NMR to be the cause of a complete oculomotor nerve palsy in a patient with neurosyphilis. A second case presented the very rare finding of an isolated bilateral incomplete oculomotor nerve paresis with external paresis on the right and internal paresis on the left side.

Psychische Störungen in Folge zerebraler Erkrankungen sind nur hinsichtlich ihrer Ätiologie unspezifisch, nicht aber hinsichtlich ihrer zerebralen Lokalisation. 1983 haben z. B. Robinson et al. [3] gezeigt, daß depressive Verstimmungen signifikant häufiger bei Infarktpatienten im linken Anterior-Bereich vorkamen im Vergleich zu anderen Lokalisationen. Auf der anderen Seite findet man bei den sogenannten „zerebro-vaskulären Demenzen“überhäufig Infarkte im Bereich des Thalamus im Unterschied zu „nicht-dementen“Infarktpatienten [2].

Event-related P300 potentials are closely reflecting cognitive functions such as stimulus evaluation time (P300 latency) and task relevance (P300 amplitude). Hence, both their potential clinical application for detecting slight cognitive disturbances and an increasing interest in the aging of cognitive human brain functions resulted in a growing number of studies on age-related P300 changes. Although there are converging lines of evidence that aging results in prolongations of P300 latencies, reductions of P300 amplitudes and a more equipotential P300 scalp distribution, the amount of these changes and the best fit for the P300-age interactions, respectively, remain still controversial. In general, these P300 alterations obviously reflect only minor cognitive changes during normal aging. For their clinical application, however, it is necessary to obtain an age-matched normative database. Furthermore, the increased P300 variability in the elderly has to be reduced--as far as possible--by appropriate simple P300 paradigms which should be preferentially applied in longitudinal analyses to differentiate normal from pathological aging of cognitive functions. Finally, additional cross-correlational analyses between the P300 and morphological as well as neurobiochemical data are needed. By these means, our knowledge about age-related changes of cognitive brain functions should be considerably enlarged.

A brain stem infarction in the area of the nerve fascicle of the oculomotor nerve could be demonstrated by NMR to be the cause of a complete oculomotor nerve palsy in a patient with neurosyphilis. A second case presented the very rare finding of an isolated bilateral incomplete oculomotor nerve paresis with external paresis on the right and internal paresis on the left side.

Visual event-related P300 potentials, conventional visual evoked potentials, and psychometric tests were applied to patients with noncirrhotic chronic liver disease and to clinically nonencephalopathic and encephalopathic cirrhotics to compare their diagnostic efficacy in detecting early portosystemic encephalopathy (PSE). Sixty-four investigations were performed in 58 patients. The latencies of the P~OO parameters were significantly longer in both the encephalopathic and nonencephalopathic cirrhotics than in the noncirrhotics, indicating distinctly abnormal cortical processing of visual stimuli in cirrhotic patients. The visual P3OO potentials showed the highest sensitivity and specificity for grade I PSE. Abnormal P300 test results were also found in 78% of the clinically nonencephalopathic cirrhotics, while psychometric tests showed abnormalities in only 41%. The P300 latencies were similar in alcoholic and nonalcoholic cirrhotics. Significant inverse correlations were found between the P300 latencies and measures of quantitative liver function such as galactose-elimination capacity and aminopyrine breath test. It is concluded that visual event-related P~OO potentials are a sensitive index of subclinical and grade I PSE. Furthermore, the degree of cognitive dysfunction detected by this method in patients with liver cirrhosis appears to be related to the reduction in hepatic metabolic capacity.

Visual event-related P300 potentials, conventional visual evoked potentials, and psychometric tests were applied to patients with noncirrhotic chronic liver disease and to clinically nonencephalopathic and encephalopathic cirrhotics to compare their diagnostic efficacy in detecting early portosystemic encephalopathy (PSE). Sixty-four investigations were performed in 58 patients. The latencies of the P300 parameters were significantly longer in both the encephalopathic and nonencephalopathic cirrhotics than in the noncirrhotics, indicating distinctly abnormal cortical processing of visual stimuli in cirrhotic patients. The visual P300 potentials showed the highest sensitivity and specificity for grade I PSE. Abnormal P300 test results were also found in 78% of the clinically nonencephalopathic cirrhotics, while psychometric tests showed abnormalities in only 41%. The P300 latencies were similar in alcoholic and nonalcoholic cirrhotics. Significant inverse correlations were found between the P300 latencies and measures of quantitative liver function such as galactose-elimination capacity and aminopyrine breath test. It is concluded that visual event-related P300 potentials are a sensitive index of subclinical and grade I PSE. Furthermore, the degree of cognitive dysfunction detected by this method in patients with liver cirrhosis appears to be related to the reduction in hepatic metabolic capacity.

Over a period of 6 years (1985-1990) we reviewed records of patients with one or more TIAs or PRINDs (196 TIAs, 63 PRINDs). 111 patients (42.9%) suffered from TIAs/PRINDs of the anterior circulation. In all cranial CT scanning (CCT) was performed, whereas only in 79 EEG was recorded after recovery from the symptoms. 25 patients (22.5%) out of the 111 showed low density areas of recent onset in CCT made responsible for the attack. Among the EEGs of the 79 patients 35 (44.3%) revealed corresponding electrical abnormalities. Out of the 79 patients investigated by both methods in 14 (17.7%) a lesion was demonstrated in CCT and focal abnormality in EEG. In 11 (13.9%) EEG was normal despite a lesion manifested in CCT. Vice versa 21 patients (26.6%) showed normal CCTs but focal abnormalities in EEG. By far most cases (43%) had normal CCTs and EEGs. These results may contribute to a redefinition of TIA and PRIND as clinically defined syndromes in prae-CT-area.

Out of 75 patients with TIA or PRIND we selected 9 TIAs and 6 PRINDs with normal EEGs and CCTs, full recovery of neurological function, no history of amaurosis fugax and no findings of visual impairments. PVEPs were derived from 01-02 to Fz and Cz as ground following binocular pattern reversal visual stimuli of 1.9 Hz. Interhemispheric differences of the latencies of P60, N80, P100 and of the amplitudes N80/P100 and P100/N140 were compared with the corresponding parameters of 22 age matched controls. In contrary to the latency differences the interhemispheric difference of the amplitude N80/P100 was highly significantly larger (33.5 +/- 16.0%) in patients than in the control group (12.8 +/- 9.8%) (p < or = .0005). The amplitude P100/N140 behaved the same way (p < or = .025); the amplitude of the affected side being smaller. There were no statistical differences between TIAs and PRINDs and a tendency was seen for normalization of the differences with increasing time distances between the onset of the ischemic attack and the point of time of the recordings.

20 healthy male subjects with a mean age of 24 +/- 2.7 years were intravenously administered a mean total dose of ethanol of 1.33 +/- 0.04 g ethanol/kg body weight using a perfusor device. The ethanol kinetic resulted in a "rising phase" of 90.2 +/- 0.9 min. in average. The PFP300 parameter in this phase of acute alcohol intoxication showed the following changes: Along with the increasing blood alcohol level the N250- and PFP300a-latencies of both the A- and B-potentials are progressively prolonged and the ascending PFP300-amplitudes are progressively reduced. The N250-latency of the B-potentials is shown to be the most sensitive parameter of the PFP300-complex already changing at a blood alcohol concentration (= b.a.c.) of 0.59 +/- 0.11% with a mean linear prolongation of 2.5 ms per 0.1 g ethanol/kg body weight. This prolongation reflects the increasing disability of the subjects to discriminate between task-relevant and task-irrelevant stimuli at b.c.a.-levels much below that being presently permitted for driving in the Federal Republic of Germany.

Symptome seitens des N. vestibulocochlearis stehen bei der Encephalomyelitis disseminata (E.D.) in der Literatur eher im Hintergrund (5,9,10). Neben der Hörbahn gehört jedoch auch das gleichgewichtserhaltende System mit zu den Prädilektionsorten der disseminierten Entmarkungen. Deshalb möchten wir auf die Bedeutung der Vestibularisprüfung (3, 4) zur Diagnostik der E. D. hinweisen und wichtige Befunde herausstellen.

The method of Pattern Flash elicited P300 (PFP300) has been applied to evaluate the dynamic alterations in cognitive function of a 58 year old woman (H. C.) presenting with hepatic failure due to fulminant hepatitis Non-A-Non-B. At the time of the first investigation she complained about slight memory deficits and revealed signs of hepatic encephalopathy grade I according to Parson-Smith et al. (bilirubin 26.0 mg/dl, NH3 102 micrograms/dl, electrolytes and blood sugar normal). Psychometric tests: Number connection test (NCT): 54 s (28-53 s, greater than 2sd); Syndrom-Kurz-Test (SKT): total score = 9 (0-4), compatible with a slight "organic brain syndrome". PFP300: N250 latency 343.5 ms (276.4 +/- 14.7 ms, greater than 4sd); PFP300-latency: 442.5 ms (326.9 +/- 14.7, greater than 7sd); PFP300 amplitudes: 16.0 microV (14.4 +/- 8.4, +/- 1sd), indicating severe disturbance in visual discrimination without visual attention deficits. Due to progressive deterioration of liver function the patient had to undergo orthotopic liver transplantation. The patient was reinvestigated four weeks later. The clinical and laboratory status were normal and no signs of hepatic encephalopathy could be detected clinically or by means of the psychometric tests. The parameters of the PFP300 complex had also completely returned to normal: N250-latency: 273.0 ms (less than 1sd); PFP300-latency: 348.0 ms (less than 1sd). This observation suggests that the analysis of P300 can help to detect and follow minor cognitive deficits in cases of acute hepatic encephalopathy. It further underscores the hepatic etiology as well as the potential reversibility of this type of encephalopathy.