Spontaneous dissection of the popliteal artery in a young man. A rare cause of the blue toe syndrome.

Spontaneous arterial dissection in peripheral arteries of the extremities is an extremely rare event. We report a case of a spontaneous dissection of a nonaneurysmal popliteal artery in an otherwise healthy 36-year-old man that came to clinical attention as an acute blue toe syndrome. The diagnosis was primarily made by high-resolution duplex ultrasound that revealed a dissection flap (length: 15.5 mm; thickness: 0.4 mm) together with the partially thrombosed false lumen at the dorsal wall of the left popliteal artery (degree of local diameter reduction: 56%). Further work-up by means of contrast-enhanced MR-A and conventional DSA confirmed a moderate stenosis of the popliteal artery compatible with focal dissection and excluded other causes such as popliteal artery entrapment syndrome. Under full-dose intravenous anticoagulation with unfractionated heparin that was switched to oral anticoagulation with vitamin K antagonists (target INR: 2-3) and conservative management of the blue toe the patient made a gradual, but eventually complete clinical recovery over 8 weeks.

Interrelations of age, sensory functions, and human brain signal processing.

Disturbances of sensory functions may additionally impair cognitive functions in elderly persons. To delineate the impact of visual sensory functions on brain signal processing during normal aging from an electrophysiological perspective, we investigated 289 fit community-dwelling subjects (162 men [56%] and 127 women [44%]; age range, 18-98 years) by means of visual event-related P300 potentials. By taking age, visual acuity, and stimulus-dependent components of visual-evoked potentials (PVEPs) into account, we found age to be the single most important factor for P300 variability (partial F > 10.0, p < .0001 for all P300 parameters; stepwise regression analysis). Furthermore, both the N75 (partial F = 12.415) and P100 latencies (partial F = 4.850) of the PVEPs were independently correlated with the P300 latencies, whereas the P300 amplitudes revealed additional correlations with the P100 amplitudes (partial F = 8.576; p < .0001, for all). Sex, however, did not influence these age-related P300 changes. Aging itself accounts for the largest proportion of variability in human brain signal processing as reflected by P300 potentials. Visual sensory functions, however, also provide an independent, but minor, contribution to P300 variability. Therefore, it seems prudent to take parameters of sensory functions into account especially for clinical P300 applications in the elderly population.

The impact of age-related changes in event-related P300 potentials on detecting early cognitive dysfunction.

Event-related P300 potentials that closely reflect cognitive brain functions show significant age-related latency prolongations. This aging-P300 interaction can best be approximated by third-order polynomial regressions. To delineate the clinical impact this special kind of regression function may have on detecting early cognitive dysfunction, we applied visual P300 potential data of healthy subjects (n = 344; age range, 18-98 years) to nondemented patients with either (i) chronic liver disease (n = 104; age range, 19-74 years) or (ii) cerebral arteriosclerosis (n = 80; age range, 38-80 years). As compared with linear regressions, third-order polynomial regressions for the age-related changes in P300 potential latencies showed a smaller latency increase during middle age, with an accelerating latency prolongation from age 60 onward. In patients with liver cirrhosis, third-order polynomial regressions yielded a rate of abnormal P300 potential latencies exceeding that of linear regressions absolutely by 17-21%, and relatively by 67-71%. Although the rate of P300 abnormalities was much lower in the CAD patients with either regression model, the relative increase in P300 abnormalities due to third-order polynomial regressions was 40-112.5%. In conclusion, normal data for the latencies of P300 potentials based on third-order polynomial regressions result in a higher sensitivity of P300 potentials for detecting early cognitive dysfunction. This gain in diagnostically important information is not offset by a loss in specificity, and may depend on the kind as well as stage of the disease, the age distribution of the patients and the degree of the P300 potential abnormalities.

The relationship between endothelin-1, event-related P300 potentials, and prognosis in cerebral arteriosclerosis.

OBJECTIVES: To search for a potential role of endothelin-1 (ET-1), a potent vasoconstrictor and presumably neurotoxic 21-amino acid peptide, for dysfunction of brain signal processing and cerebrovascular morbidity in nondemented patients with cerebral arteriosclerosis. DESIGN: Cross-sectional study with longitudinal follow-up. SETTING: University-affiliated teaching hospital. PARTICIPANTS: A total of 106 nondemented patients with significant stenosis of either the internal carotid (cAD, cases; n = 63, mean age +/- SD, 62 +/- 7 years) or peripheral arteries (pAD, disease controls; n = 43, 60 +/- 11 years) were investigated before carotid endarterectomy and bypass surgery, respectively. After a mean follow-up of about 19 months, cerebrovascular morbidity of the cAD and pAD patients was evaluated by phone. MEASUREMENTS: Brain signal processing functions by event-related visual P300 potentials; cerebrovascular events by a structured telephone interview; the extent of arteriosclerosis by venous ET-1 concentration. RESULTS: Venous ET-1 levels were elevated in both cAD and pAD patient groups, but to the same degree. In these patients, ET-1 concentration was correlated slightly with diastolic blood pressure (r = .334, P = .0326, stepwise regression). Only in cAD patients with ET-1 levels above the 75th percentile were P300 latencies markedly prolonged compared with their lower ET-1 level counterparts. Furthermore, the P300 latencies of the cAD patients, but not of the pAD patients, correlated positively with venous ET-1 concentration and inversely with pack years of smoking (r = .728, P = .0002; stepwise regression). In contrast to base-line P300 abnormalities and classical risk factors (e.g., hypertension), high ET-1 levels predicted an increased cerebrovascular morbidity of cAD, but not of pAD, patients (P = .0044; Mantel Cox test). CONCLUSIONS: In nondemented patients with cerebral arteriosclerosis, endothelin-1 is associated with P300 abnormalities reflecting subclinical dysfunction of brain signal processing. In the long-term, high venous ET-1 levels also appear to predict a higher cerebrovascular morbidity of cAD patients even after carotid endarterectomy.

Age-related dynamics of cognitive brain functions in humans: an electrophysiological approach.

Event-related P300 potentials closely reflect cognitive functions such as stimulus discrimination (N250) and processing time (P300 latencies) as well as attention capabilities (P300 amplitudes). To delineate the age-related dynamics of P300 potentials, we investigated 250 healthy subjects between 18 and 98 years of age in a cross-sectional study. A total of 330 visual P300 tests was performed in two different paradigms (PI, passive condition, n = 80; PII, active condition, n = 250). In both P300 paradigms, the N250 and P300 latencies were markedly prolonged (p < .0001) in older age, whereas the N250 and P300 latency differences between PII and PI did not change (p > .05). The P300 amplitudes in paradigm I and II revealed only a slight age-related reduction. In fact, the P300 amplitude ratios between PII and PI remained constant. Third-order polynomial regressions provided the best fit of the aging-P300 interactions in paradigms I and II for both males and females. Interestingly, females showed a greater and possibly earlier P300 latency increase during aging than males. These age-related changes of P300 potentials indicate a rather mild cognitive decline that does not accelerate before old age and may be different between both sexes.

The event-related P300 potential approach to cognitive functions of nondemented patients with cerebral and peripheral arteriosclerosis.

OBJECTIVES: To detect subtle cognitive dysfunction in non-demented patients with either cerebral (cAD) or peripheral (pAD) arteriosclerotic disease, and to evaluate in these patients the effects on cognitive functions of carotid endarterectomy and bypass surgery, respectively. DESIGN: Case-control study. SETTING: Tertiary care referral center. PARTICIPANTS: Eighty consecutive patients with moderate to high-grade stenosis of the internal carotid artery (ICA) (mean age +/- SD, 62 +/- 8 years), 53 patients with stenoses of the peripheral arteries (60 +/- 10 years), and 80 healthy volunteers (58 +/- 15 years) enrolled in a study on healthy aging. Cerebral and peripheral arteriosclerotic disease was verified by digital subtraction angiography, and all patients were screened for confounding effects of concomitant diseases. MAIN OUTCOME MEASURES: Cognitive functions by event-related visual P300 potentials. RESULTS: Patients with cAD showed prolonged P300 latencies and reduced P300 amplitudes, whereas pAD patients had reduced P300 amplitudes only. On an individual scale, 25% of cAD patients, but only 6% of pAD patients, revealed P300 abnormalities. In the cAD, but not in the pAD patients, the P300 latencies were especially prolonged in the older patients, but other factors such as sex, cerebral symptoms, degree of ICA stenosis, and premorbid intelligence did not play any role in either group. Within 1 to 2 weeks of surgery, the P300 latencies shortened in both cAD and pAD patients with high initial values. CONCLUSIONS: As demonstrated by P300 potentials, even nondemented arteriosclerotic patients reveal signs of subtle cognitive dysfunction affecting especially the older cAD patient. In the short-term, carotid endarterectomy presumably improves cognitive functions unspecifically in nondemented patients with a higher initial degree of P300 abnormality.

Relationship of the aminopyrine breath test and the Child-Pugh score to urinary sodium retention in patients with liver cirrhosis.

This study investigated the relationship between urinary sodium excretion and liver function, as assessed by the aminopyrine breath test (ABT) and conventional parameters, in 62 patients with cirrhosis kept on a constant salt diet. Urinary sodium excretion was related non-linearly to the ABT (r = 0.76). Less significant correlations were observed to the Child-Pugh score (r = -0.65), cholinesterase (r = 0.58), bilirubin (r = -0.56), albumin (r = 0.51) and prothrombin time (r = 0.49). When patients were arbitrarily divided into 6 groups according to the ABT, sodium excretion balanced the sodium intake up to a 50% reduction in ABT. In groups with more than a 50% reduction sodium retention occurred. When patients were grouped according to the Child-Pugh score, urinary salt output was balanced in patients with scores of 5 and 6 and decreased in patients with scores greater six. However, the change in sodium output from normal salt excretion to sodium retention was less pronounced in patients grouped according to the Child-Pugh score than in patients grouped according to the ABT. The results suggest a non-linear relationship between the impairment in hepatic and renal function in cirrhosis. They are compatible with the concept of a threshold of hepatic function necessary to maintain normal renal function.

Dynamics of cognitive brain dysfunction in patients with cirrhotic liver disease: an event-related P300 potential perspective.

The dynamics of cognitive brain functions of 104 patients with both chronic non-cirrhotic (NC) and cirrhotic liver disease (C: C1, non-encephalopathic; 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 muV, mean +/- 1 S.D.) were significantly (P < 0.01) smaller than in the non-cirrhotics (+ 7.5 +/- 5.2 muV) reflecting 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.

The event-related P300 potential analysis of cognitive human brain aging: a review.

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.

Visual event-related P300 potentials in early portosystemic encephalopathy.

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.

[Visual P300 in acute hepatic encephalopathy resulting from non-A-non-B fulminant hepatitis: analysis of the course before and after orthotopic liver transplantation]. / Das visuelle P300 bei einer akuten hepatischen Enzephalopathie in Folge einer fulminanten Hepatitis Non-A-Non-B: Verlaufsanalyse vor und nach orthotoper Lebertransplantation.

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.

[Dose-response relationships between blood alcohol concentrations and cognitive potentials (visual P300) in man]. / Dosiswirkungsbeziehungen zwischen Blutalkoholkonzentrationen und kognitiven Potentialen (visuelles P300) beim Menschen.

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.

Colour-black pattern reversal visual evoked potentials (colour-black-PVEPs): neurobiological aspects and clinical applicability of a new method.

The new method of Colour-Black-PVEPs was applied to 67 healthy subjects with normal colour vision who were subdivided into age groups (= AG) I (N = 40: 18-30 years) and AG II (N = 27: 31-60 years): 1. For the N80-, P100- latencies and the N80P100-amplitudes of all Colour-Black-PVEPs we obtained age-, sex- and eye-matched normative data. 2. The female subjects of AG I showed shorter (p less than or equal to 0.05 resp. 0.002) P100-latencies and higher (p less than or equal to 0.02 resp. 0.0001) N80P100-amplitudes in the Colour-Black-PVEPs than the male subjects. In AG II, however, the Colour-Black-PVEPs did not show any more sex-differences for the P100-latencies, whereas the N80P100-amplitudes remained significantly higher for the females. 3. In the Colour-Black-PVEPs the N80- and P100-latencies did not reveal age-dependent changes. The N80P100-amplitudes, however, decreased with increasing age, but this was significant for the females only. 4. The head sizes, although decreasing with age, were in both age groups significant smaller for the females only. 4. The head sizes, although decreasing with age, were in both age groups significant smaller for the females. Therefore, head size alone could not fully explain the sex-differences in the Colour-Black-PVEPs and their age-dependent changes. 5. In both age groups, the N80--and P100-latencies increased significantly for both sexes from the Green-Black- and Red-Black-PVEPs to the Blue-Black-PVEPs. The N80P100-amplitudes decreased in the same sequence. This method may become a valuable tool in the investigation of neurophysiological and ophthalmoneurological aspects of human colour vision.

The pattern flash elicited P300-complex (PF-P300): dynamics of its topographic scalp distribution in different states of visual attention.

PF-P300 has been recorded from 13 healthy male subjects (21-35 years) in two different conditions of visual attention (transient versus sustained attention) at 16 electrode locations (10/20-system) against linked mastoids. The PFP300 complexes were measured and mapped. Thus, we obtained the following: (1) N250 did not show any significant differences between both conditions. (2) PF-P300, however, showed significantly different (p less than or equal to .05) maps between both conditions, especially bilateral frontal and left occipital with the measured PFP300a-amplitudes being higher (p less than or equal to .01) under sustained attention. The PFP300a-latencies did not show such differences. (3) N400 showed similar (p less than or equal to .001) differences in its mean peak distribution, but its latencies were shorter (p less than or equal to .01 resp. .0001) at all recording sites (except Fz, Pz) in condition (2). (4) Further evaluation of the PFP300-complex under sustained attention by means of increment mapping and multichannel potential measurements showed that PFP300 first rises at Fz, Pz, then spreads over the left occipital region and culminates bilateral frontal and parieto-occipital. Interestingly, the latencies of N250 and PFP300a were shorter at O1 (p less than or equal to .01) than at O2. With the help of electrical brain mapping it is possible to study the dynamics of both the PFP300 scalp distribution between two distinct mental states and within one mental state.

[The visual P300 (pattern flash P300) in the physiologic aging process]. / Das visuelle P300 (PFP300) im physiologischen Alterungsprozess.

For studying the relationship between the PFP300 (Pattern Flash elicited P300) and age we investigated 73 healthy subjects - 34 males, 39 females - between 18 and 60 years of age by presenting randomly two different checkerboards A (16 X 16 caskets visual angle = 50') and B (64 X 64 caskets visual angle = 12.5') to them (A:B = 80:20). The subjects' task was to keep a running count in their heads of the infrequent B-stimuli only. The resulting A- and B-responses were derived from Oz to Fz (Cz was ground). The results were as follows: 1. Comparing the PFP300-parameters between age group I (N = 46, 18-30 years) and age group II (N = 27, 31-60 years) we found that in the elder group both the N250-latencies (in B-potentials) and the PFP300a-latencies (in A-potentials) are significantly prolonged (p less than or equal to 0.01). The ascending PFP300a-amplitudes, however, remain (still?) unchanged. 2. Regression analyses between the PFP300-parameters and age for the total group revealed significant relationships for both the N250- (r = 0.35, P less than or equal to 0.01) and PFP300a-latencies (r = 0.78, P less than or equal to 0.01) and PFP300a-latencies (r = 0.78, P less than or equal to 0.01). In contrast to this, we could only find a zero correlation for the ascending PFP300a-amplitudes. 3. The coefficient of the regression line was 0.71 ms/year for the N250-latency and 1.09 ms/year for the PFP300a-latency. These findings indicate that one has to build age-matched control groups for applying PFP300 to pathophysiological processes.

The pattern flash elicited P300-complex (PF-P300): a new method for studying cognitive processes of the brain.

For neurological purposes we developed a new method for eliciting P300-waves: Using two different kinds of checkerboard stimuli that were randomly flashed on a TV screen we obtained, besides the well-known usable primary complex, prominent PF-P300-complexes consisting of a marked negative potential (= N250), the PFP300a and the N400 peaks. These components could be related to different cognitive processes such as floating versus selective sustained attention and stimulus evaluation. N250 especially was shown to be closely related to different degrees of difficulty in visual discrimination. Further, the PFP300 components are test-retest reliable and sex-independent. Since they have relative small interindividual variabilities, we consider the N250- and PFP300a-latencies especially as well as the ascending PFP300a-amplitudes to be appropriate parameters for investigating diseases with cognitive disorders objectively.

Pattern reversal visual evoked potentials (white-black- and colour-black-PVEPs) in the study of eye dominance.

We investigated the influence of eye dominance scaled by 6 tests on the parameters (N80, P100 latency and N80-P100 amplitude) of the white-black-, green-black-, red-black- and blue-black-pattern visual evoked potentials (PVEPs) of 40 healthy subjects (20 males and 20 females) with normal visual acuity. The P100 latency of the white-black PVEPs was, for both sexes, shorter (P less than or equal to 0.001) in the PVEPs of the dominant eyes. This P100 latency shortening could also be verified for both right dominant and left dominant eyes with no significant difference between them. A consistent relationship, however, between the different degrees of eye dominance and the P100 latency shortening could not be established. In contrast to the P100 latency findings the N80 latencies of the white-black-PVEPs and the N80-P100 amplitudes did not show any significant differences with respect to eye dominance. Furthermore, the colour-black PVEPs did not present any differences of latency and amplitude depending on eye dominance. Thus our results give further electrophysiological evidence for eye dominance as a lateralized CNS phenomenon that is not influenced by colour.