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H Hampel

Publications and source records attributed to H Hampel.

At least 109 records · Page 6Linked to original sources
PubMed1997

Frequency variation of a pattern-flash visual stimulus during PET differentially activates brain from striate through frontal cortex.

We evaluate regional cerebral blood flow (rCBF) in 19 healthy elderly subjects, mean age 64 +/- 11 (SD, years), during a passive visual stimulus in which pattern-flash frequency was parametrically manipulated. Using goggles with a grid of red lights imbedded into each lens, we performed five positron emission tomography (PET) H2(15)O water scans on each subject at alternating (left to right eye) flash frequencies of 0, 1, 4, 7, and 14 Hz. We found a biphasic rising and falling rCBF response in the striate cortex (7 Hz peak) and left anterior cingulate (4 Hz peak), 1 Hz activation in left middle temporal gyrus (V5), monotonically increasing rCBF in posterior areas (lateral and inferior visual association areas, Brodmann 18 and 19), and monotonically decreasing rCBF in anterior areas (frontal, cingulate, and superior temporal) predominantly in right hemisphere. We suggest the striate rCBF changes at all frequencies primarily reflect lateral geniculate input, the middle temporal activation at 1 Hz reflects perception of apparent motion, and the posterior extrastriate rCBF monotonic increase represents a neural response to increasing luminance intensity and form and color complexity that occur as pattern-flash frequency increases. The anterior monotonic rCBF decrease may represent active cross-modal functional suppression of brain areas irrelevant for processing the passive visual stimulus. Pattern-flash rCBF responses were highly reproducible (no series effect), more so in posterior than in anterior brain regions. The reproducibility and systematically changing rCBF responses to this passive stimulus suggest that it could be successfully used as a disease probe to evaluate neural function and drug effects in cognitively impaired patients.

Aged↗
PubMed1997

[Structural magnetic resonance tomography in diagnosis and research of Alzheimer type dementia].

One of the most widely used neuroimaging procedures in Psychiatry and Neurology is magnetic resonance imaging (MRI). MRI has gained the position of a standard investigation in the differential diagnosis of dementia syndromes. In the clinical diagnosis of Alzheimer's disease (AD) MRI helps to improve the diagnostical accuracy. Recently new MRI-based techniques for performing volumetric measurement of cortical and subcortical structures have been developed. First reports indicate that MRI-based volumetric measurements can be accurate in differentiating AD patients from cognitively normal elderly individuals. These new techniques may be useful adjunct in assessing the clinical diagnosis of AD. Results could also yield insight in the fundamental pathology of the degenerative disease. It is the objective of this chapter to summarize and comment on the significance of MRI in the diagnosis and research of AD. Future directions are outlined, including the use of microscopic MRI, the differentiation of white matter signal hyperintensities and the combined evaluation of structural MRI and functional imaging techniques.

Adult↗
PubMed1997

Familial colorectal cancer in Ashkenazim due to a hypermutable tract in APC.

Approximately 130,000 cases of colorectal cancer (CRC) are diagnosed in the United States each year, and about 15% of these have a hereditary component. Two well-defined syndromes, familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC), account for up to 5% of the total new cases of CRC. Truncating APC mutations are responsible for FAP, and defective mismatch repair genes cause HNPCC. However, the genes responsible for most of the familial cases are unknown. Here we report a mutation (T to A at APC nucleotide 3920) found in 6% of Ashkenazi Jews and about 28% of Ashkenazim with a family history of CRC. Rather than altering the function of the encoded protein, this mutation creates a small hypermutable region of the gene, indirectly causing cancer predisposition.

Adenomatous Polyposis Coli↗
PubMed1997

Blood-cerebrospinal fluid barrier dysfunction for high molecular weight proteins in Alzheimer disease and major depression: indication for disease subsets.

There is a diversity of opinions concerning the function of the blood-brain barrier and the blood-cerebrospinal fluid barrier (BCB) in Alzheimer disease and other neuropsychiatric disorders. In this paper we investigate and review the evidence for BCB dysfunction in Alzheimer disease and major depression. The hypothetical roles of immunologically mediated mechanisms in the central nervous system (CNS) are discussed. Special consideration is given to methodological factors influencing BCB function and analysis. Serum and cerebrospinal fluid (CSF) of 29 patients with major depression (MD) and 51 patients with "probable Alzheimer disease" (AD) were investigated. The AD patients were subdivided in two groups of 21 early-onset (EO) and 30 late-onset (LO) cases and assayed for concentrations of albumin and IgG. The results were compared with those for 11 age-matched healthy controls. The severity of dementia was assessed with the Mini-Mental State Examination (MMSE). AD and MD patients showed significantly lower serum albumin [AD: p < 0.05 (LO: p < 0.038); MD p < 0.01] and IgG (AD: p < 0.01; MD: p < 0.013) concentrations compared with controls. MD (p < 0.001) and LO-AD (p < 0.07) patients displayed significantly lower absolute serum albumin levels than did EO-AD patients. The CSF/serum ratio for albumin and IgG was used to evaluate BCB function. There were no significant group differences; however, subsets of MD (29%) and AD (16%) patients showed a higher frequency of a pathological albumin ratio than did control subjects. Furthermore, a subset of 24% of MD and18% of AD patients and none of the controls showed an elevated IgG ratio. Different mechanisms of alteration of IgG distribution are presented. The degree of cognitive impairment in AD did not correlate positively with protein and ratio parameters. The BCB is critical to the maintenance of homeostasis within nervous system tissue. We suggest that the altered function can result from immune-mediated events such as altered levels of circulating inflammatory mediators. Furthermore, we assume that in the AD and MD subgroups, the BCB dysfunction for high molecular weight proteins permits access of components of the immune system to the CNS, which may contribute to disease pathology.

Age Factors↗
PubMed1996

Germline BRCA1 185delAG mutations in Jewish women with breast cancer.

BACKGROUND: We aimed to find out the proportion of breast cancers in Ashkenazi Jewish women attributable to the frameshift mutation at position 185 involving the deletion of adenine and guanine (185delAG) in the breast cancer gene BRCA1. METHODS: We studied 107 Ashkenazi Jewish women with breast cancer seen at medical oncology and genetic counseling clinics in New York over a three and a half year period beginning in 1992. 80 of the women were diagnosed before age 42 years; the other 27 were diagnosed between 42 and 50 years and had a positive family history. Genomic DNA testing by PCR amplification was done to identify any 185delAG mutations of the BRCA1 gene. FINDINGS: Of the 80 women diagnosed before the age of 42 years, 16 (20%, 95% CI 11.2-28.8) were heterozygous for the mutation. All 16 women had at least one first-degree or second-degree relative with breast or ovarian cancer. Of 27 probands diagnosed with breast cancer between the ages of 42 and 50 years who had at least one first-degree relative affected with breast or ovarian cancer, 8 (30%, 95% CI 12-47) had 185delAG mutations. INTERPRETATION: These data suggest that screening for the 185delAG mutation may be useful in genetic counselling of these women where options for detection and prevention of possible cancers can be discussed.

Adult↗
PubMed1996

Recurrent BRCA2 6174delT mutations in Ashkenazi Jewish women affected by breast cancer.

The lifetime risk of breast cancer may approach 80-90% in women who have germline mutations of either of two genes, BRCA1 or BRCA2. A single BRCA1 mutation, 185delAG, has been noted in approximately 20% of Ashkenazi Jewish women with early onset breast cancer and in 0.9% of the Ashkenazi population. We recently detected a 6174delT frameshift mutation in BRCA2 in an hereditary breast cancer kindred of Ashkenazi Jewish ancestry. Here, we investigated the frequency of this mutation in 200 women with early-onset breast cancer. Six of 80 Ashkenazi Jewish women (8%) diagnosed with breast cancer before the age of 42, wer heterozygous for the 6174delT mutation, compared to none of 93 non-Jewish women diagnosed with breast cancer at the same age (P = .005). These cases were ascertained without regard to family history. Two of 27 (7%) additional Jewish families in which the proband was diagnosed with breast cancer at age 42 to 50 and had a family history of breast or ovarian cancer had germline 6174delT mutations. The results of this report suggest that a recurrent mutation of BRCA1 and a recurrent mutation BRCA2 together may account for over a quarter of all early-onset breast cancer in the setting of a personal or family history of ovarian cancer in Ashkenazi Jewish women.

Adult↗
PubMed1996

Unstable anticoagulation in the course of amitriptyline treatment.

A potential drug-drug interaction between the tricyclic antidepressant amitriptyline and the oral anticoagulant phenprocoumon, causing intensified hypo- and/or hyperprothrombinemic effects, was investigated. In seven patients simultaneously receiving amitriptyline and phenprocoumon the course of the Quick values and the amitriptyline and phenprocoumon dosages were registered. The resulting data represented graphically was additionally compared with data and diagrams gained from a control group of seven phenprocoumon patients not receiving amitriptyline. Whereas in the control group the average Quick values (or the target International Normalized Ratio) lay within the required therapeutic range, massive fluctuations were seen in the amitriptyline-treated patients. These fluctuations did not disappear until the amitriptyline medication was discontinued. Whether our findings are actually due to a clinically relevant drug-drug interaction needs to be investigated in further controlled studies based on a larger number of patients, the more so as no comparable investigations and only few references to this subject are to be found in the literature. Should an amitriptyline influence on the frequently prescribed coumarin derivative be proven, an increased risk of rethrombosis or bleeding complications in patients receiving both amitriptyline and phenprocoumon would appear to be indicated.

Adult↗
PubMed1996

Modified oral anticoagulant potency in an amitriptyline-treated patient?

We report the case of a 74-year-old female patient who received the antide-pressant amitriptyline because of a major depression. Incidence of acute lower extremity venous thrombosis required an additional oral anticoagulant therapy with phenprocoumon. During the simultaneous adjustment of both substances, the Quick value displayed great fluctuations which only disappeared after discontinuation of the amitriptyline medication. This finding is discussed as an aspect of a possible drug-drug interaction between amitriptyline and phenprocoumon.

Aged↗
PubMed1996

A case of Ganser's state presenting as a dementia syndrome.

We report an atypical case of Ganser's syndrome in a 54-year-old male patient. The following symptoms which include approximate answers perceptual disturbances and dissociative mechanisms were observed over 7 years, improved during hospitalization, but reappeared just before the patient's discharge. The extremely long presence and bizarre manifestation of symptoms, the course of the disorder and the patient's premorbid high intelligence level point to an unusual presentation of this case. Following the concept of hysteria and dissociation, we discuss its diagnosis within the scope of the DSM-III-R, DSM-IV and ICD-10 classification of Dissociative Disorders. Problems in the differential diagnosis which result from an increasing awareness of Dissociative Disorders are outlined.

Factitious Disorders↗
PubMed1994

Expression of human heat-shock protein 70 antigens and gamma/delta T-cell receptor antigens in human central nervous tissue.

The human gamma delta T cell receptor is normally expressed on lymphoid tissue. Because expression of different molecules of the T-cell system has been described on human brain cells, we examined the expression of T-cell receptor gamma delta antigens with a panel of various anti-gamma/delta TCR mAbs using immunohistochemistry on different regions of frozen human postmortem tissue of five different brains. We found expression of gamma/delta TCR antigens on brain tissue in different regions of the brain, probably on neurons. Using mAbs against the 70-kd human heat-shock-protein (hsp 70), immunohistochemistry showed staining of microglia. A polymerase chain reaction analysis using a highly sensitive primer sequence against the constant region delta sequence supports the notion that the gamma/delta TCR is expressed in human brain; however, the sequence cannot be assigned to a specific tissue with this method. Both heat shock proteins and the gamma/delta TCR seem to be involved in autoimmune processes, and their expression on colocalizing structures in human CNS may play a role in triggering neuropsychiatric autoimmune disorders.

Base Sequence↗
PubMed1985

[Greater oral activity of etilefrine pivalate compared to etilefrine in the cat and dog].

Etilefrine pivalate (K 30 052, Ep) and etilefrine (E) were compared in regard to their effects on the circulation of cats and dogs and in regard to their effects on isolated organs (papillary muscles, atria, vena cava caudalis) of guinea pigs and rabbits. The effects of Ep and E were qualitatively equal. Ep was less effective than E on isolated organs and after intravenous injection, it was however more effective after oral or intraduodenal application. This result is in line with the hypothesis that Ep is inactivated during the first-pass to a smaller extent than E and is split after absorption to E and pivalinic acid.

Animals↗