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Biomedical subjects

A Siegel

Publications and source records attributed to A Siegel.

At least 19 recordsLinked to original sources
PubMed1995

[Total hip endoprosthesis following resection arthroplasty].

From 1976 to December 1994, a total of 347 patients underwent implantation of a hip prosthesis at the ENDO-Klinik for treatment of an unsatisfactory condition following resection arthroplasty. From 1976 to 1987, 143 patients were treated and in 1989 the results obtained in these patients were analysed: 99 of them were available for a follow-up examination in 1989, and 64 for a further examination in 1995. In 130 cases infection had been the reason for joint resection. At the time of the prosthesis operation (1-20 years later) intraoperative biopsy revealed that infection was still present in 41 cases (31.5%). Only 15 of these infections had been detected preoperatively by joint aspiration. This shows that the value of resection arthroplasty as a method of treating periprosthetic infection is limited and lends support to the one-stage exchange operation, which is the method we prefer in cases of infected hip prostheses. The operative technique and preparation for implantation of the prosthesis are described, as are septic and aseptic complications and the measures that can be taken to treat them. In spite of the patients' generally poor initial condition and with due consideration for the further revision operations, the medium-term results finally obtained are poor in only 9%.

Adult↗
PubMed1995

[Epidemiology of spinal diseases in nurses].

Epidemiology of spinal pathology among nurses. A cross-sectional study of 3300 German nurses was carried out in the course of an investigation of the prevention of occupation--related back problems. A much higher incidence of lumbar-spinal problems was observed than in a control group of office staff, not required to lift or carry. Evidence of much greater risk, especially of severe sciatic symptoms, was supported by a case-controlled study of patients with the diagnosis of disc-prolapse or disc-protrusion, carried out in two neuroradiology units. Nurses were significantly over represented. A lack of preventive measures for carrying and lifting patients was clearly demonstrated (availability and use of mechanical aids). To what extent the perception of spinal problems is influenced by psychological factors and not only by physical factors will be demonstrated by the recording of stress factors.

Humans↗
PubMed1995

Clinical efficacy of SPECT bone imaging for low back pain.

METHODS: We conducted a comprehensive structured review of the literature, analyzing 940 citations from 1966 through September 1993 and completed a narrative review. We also attempted quantitative synthesis of the accuracy of SPECT evaluation of low back pain. RESULTS: We found thirteen reports on accuracy. Only three provided a reasonable gold standard reference test and allowed the calculation of sensitivity and specificity. There is weak evidence that SPECT is useful in: (a) detecting pseudarthroses after failed spinal fusion, (b) evaluating young patients with back pain and (c) distinguishing benign from malignant lesions in cancer patients. SPECT has not been sufficiently studied in any other setting. We found no reports on the clinical outcome of SPECT or its cost-effectiveness. CONCLUSION: The decision to use SPECT in most patients with low back pain cannot be supported by clinical trials. Its effect on clinical management and cost-effectiveness are unknown. The medical community should mount a large-scale, prospective evaluation of SPECT in low back pain.

Cost-Benefit Analysis↗
PubMed1994

Basal amygdaloid facilitation of midbrain periaqueductal gray elicited defensive rage behavior in the cat is mediated through NMDA receptors.

The present study tested the hypotheses that: (1) defensive rage behavior elicited from the midbrain periaqueductal gray (PAG) in the cat is facilitated from the basal complex of amygdala; and (2) such facilitation from this region of amygdala is mediated via a pathway in which excitatory amino acids acting upon NMDA receptors within the PAG are utilized as a neurotransmitter. In the first phase of this study, cannula electrodes were implanted into PAG sites for the elicitation of defensive rage behavior as well as for drug delivery. Then, a second monopolar electrode was implanted into the basal nucleus of amygdala from which facilitation of defensive rage could be obtained. As a result of dual stimulation of the basal amygdala and PAG, response latencies for defensive rage were significantly lowered relative to PAG stimulation alone (P < 0.01). In the second phase of this experiment, 3 doses of a selective NMDA receptor antagonist, AP-7 (0.1, 0.5, 1.0 mg/kg), were peripherally (i.p.) administered in 5 animals. The results indicated a significant decrease in the facilitatory effects of amygdaloid stimulation in a dose and time dependent manner (P < 0.001). In the third phase, AP-7 was administered intracerebrally into PAG defensive rage sites in doses of 0.2 and 2.0 nmol. It was noted that intracerebral microinjections of AP-7 at the higher dose (2.0 nmol) also significantly suppressed the facilitatory effects of amygdaloid stimulation (P < 0.01); however, these effects were somewhat less potent then those observed following peripheral drug administration. A fourth phase of the study was conducted at the completion of the pharmacological experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1994

Electrical stimulation of the dorsal midbrain periaqueductal gray suppresses peripheral blood natural killer cell activity.

This study examined the effects of dorsal midbrain periaqueductal gray (PAG) stimulation on both splenic and peripheral blood natural killer (NK) cell function as well as the proliferative response of lymphocytes to phytohemagglutinin mitogen. Male Sprague-Dawley rats were implanted with bipolar electrodes in the dorsal PAG. Following recovery, bipolar electrical stimulation eliciting a flight response was delivered at the rate of one/min for 30 min to freely moving rats. While dorsal PAG stimulation did not alter mitogen response or splenic NK activity, stimulation of this region of the PAG produced a marked decrease in peripheral blood NK response. In order to begin to explore a possible mechanism regulating suppression of peripheral blood NK activity, naltrexone (10 mg/kg) was administered prior to dorsal PAG stimulation. The results of this experiment replicated the findings that demonstrated suppression of peripheral blood NK following dorsal PAG stimulation. Naltrexone did not effect PAG induced suppression of peripheral blood NK. These findings point to the importance of the dorsal aspect of the PAG in the regulation of peripheral blood NK activity and further suggest that this phenomenon may not be opioid mediated.

Animals↗
PubMed1994

Neuroanatomical and neurochemical mechanisms underlying amygdaloid control of defensive rage behavior in the cat.

1. It is well established that the hypothalamus and midbrain periaqueductal gray (PAG) play important roles in the expression of defensive rage behavior. While defensive rage is not elicited from the amygdala, this region of the limbic system nevertheless serves an important role in the modulation of defensive rage behavior. The present paper attempts to address the question of how the amygdala modulates defensive rage behavior in the cat. The studies were conducted using brain stimulation, pharmacological, neuroanatomical and immunocytochemical methods to identify the likely neural pathways and their associated neurotransmitters by which different regions of the amygdala modulate defensive rage behavior in the cat. 2. The experimental evidence provided thus far establishes that three regions of the amygdala have been identified as powerful modulators of defensive rage behavior. These include the medial nucleus, basal complex and central nucleus of the amygdala. Experiments involving dual stimulation of an amygdaloid nucleus and sites within the medial hypothalamus or PAG from which defensive rage behavior was elicited demonstrated that two of the regions facilitated defensive rage --the medial nucleus and basal complex--and a third region--the central nucleus--suppressed defensive rage. The mechanisms and substrates underlying modulation for each of these regions are different. Medial amygdaloid facilitation of defensive rage involves a pathway (i.e., the stria terminalis) that projects directly to the medial hypothalamus and utilizes substance P as a neurotransmitter. Basal amygdaloid facilitation of defensive rage behavior makes use of a pathway to the PAG in which excitatory amino acids acting on NMDA receptors are utilized as a neurotransmitter. The central nucleus also projects to the PAG. However, it is strongly inhibitory and utilizes enkephalins that act upon mu receptors within the PAG.

Aggression↗
PubMed1993

Evidence that substance P is utilized in medial amygdaloid facilitation of defensive rage behavior in the cat.

The present study was designed to test the hypothesis that a major excitatory mechanism for the expression of feline defensive rage behavior involves the medial nucleus of the amygdala which utilizes substance P as a neurotransmitter in a direct output pathway that supplies the medial hypothalamus. In phase I of the experiment, stimulating electrodes were implanted into the medial amygdala and cannula electrodes were implanted into the medial and lateral hypothalamus from which defensive rage and predatory attack behavior could be elicited by electrical stimulation, respectively. Response latencies for defensive rage were significantly lowered after dual stimulation of the medial amygdala and medial hypothalamus relative to single stimulation of the medial hypothalamus alone. In phase II, dose- and time-dependent decreases in medial amygdaloid-induced facilitation of defensive rage were observed after the i.p. administration of the NK1 antagonist, CP-96,345 (0.05, 2 and 4 mg/kg). In phase III of the study, the effects of microinjections of CP-96,345 placed directly into defensive rage sites within the medial hypothalamus (0.05, 0.5 and 2.5 nmol) upon medial amygdaloid modulation of this response were assessed. Again, intracerebral administration of this antagonist blocked the facilitatory effects of medial amygdaloid-induced facilitation of defensive rage in a manner parallel to that observed with peripheral administration of the NK1 antagonist. The results suggest that the medial amygdala facilitates defensive rage by acting through a substance P mechanism at the level of the medial hypothalamus. Other experiments revealed that peripheral administration of the NK1 antagonist: (1) had little upon the latency or threshold for elicitation of defensive rage, suggesting that the medial amygdaloid-substance P facilitatory mechanism acts in a phasic rather than tonic manner; and (2) also blocks the suppressive effects of medial amygdaloid stimulation upon predatory attack behavior elicited from the lateral hypothalamus. The latter finding suggest that similar neurochemical mechanisms regulate medial amygdaloid modulation of both forms of hypothalamically elicited aggression. The final aspect of this study utilized the combination of retrograde-tracing of amygdaloid neurons into the medial hypothalamus after microinjections of Fluoro-Gold into defensive rage sites, and the immunocytochemical analysis of substance P neurons within the amygdala. The data indicated that large numbers of retrogradely and immunocytochemically positive labeled cells were identified in the medial nucleus, including many that were double-labeled.(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗
PubMed1992

Role of NMDA receptors in hypothalamic facilitation of feline defensive rage elicited from the midbrain periaqueductal gray.

The present study tested the hypothesis that the pathway from the medial hypothalamus to the midbrain periaqueductal gray (PAG) subserving defensive rage behavior in the cat facilitates the occurrence of this response when elicited from the PAG by utilizing excitatory amino acids as a neurotransmitter or neuromodulator. Cannula electrodes were implanted into the PAG for the elicitation of defensive rage behavior as well as for microinjections of excitatory amino acid antagonists and N-methyl-D-aspartic acid (NMDA). Monopolar stimulating electrodes were also implanted into the medial hypothalamus from which this response could also be elicited and, when stimulated at subthreshold levels for elicitation of behavior, could also facilitate the occurrence of PAG elicited defensive rage. Initially, dual stimulation of the PAG and medial hypothalamus facilitated the occurrence of defensive rage elicited from the PAG. Then, the identical dual stimulation paradigm was repeated with the same current parameters following the infusion of various antagonists for different receptors into the PAG defensive rage sites. The results indicate that infusion of either kynurenic acid [(0.1-2.0 nmol), a non-selective excitatory amino acid receptor antagonist] or D-2-amino-7-phosphonoheptanoic acid (AP7) [(0.1-2.0 nmol), a specific NMDA receptor antagonist], produced a dose and time dependent blockade of the facilitatory effects of medial hypothalamic stimulation. In contrast, microinjections of relatively larger doses of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) [(4 nmol), a non-NMDA receptor (quisqualate and kainate) antagonist] or atropine [(4.4 nmol), a muscarinic receptor antagonist] had little effect upon medial hypothalamically elicited facilitation of the PAG response. In a second experiment, NMDA [0.1-1.0 nmol] was microinjected directly into PAG defensive rage sites in the absence of medial hypothalamic stimulation. In these animals, drug infusion mimicked the effects of dual stimulation by producing a dose and time dependent decrease in response latencies. A third experiment was designed to further test the hypothesis by neuroanatomical methods. Here, the retrograde label, Fluoro-Gold, was microinjected into defensive rage sites within the PAG and following a survival time of 5-6 days, the animals were sacrificed. The brains were then processed for immunocytochemical analysis of cells that immunoreact positively for aspartate and glutamate. The results indicated the presence of many retrogradely labelled and immunocytochemically positive cells within the rostro-caudal extent of the medial hypothalamus as well as others that were double labelled.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1992

Renal scintigraphy in a patient with pelvic lipomatosis.

A patient with a history of benign prostatic hypertrophy and pelvic lipomatosis was evaluated for pain and swelling of the abdomen and left leg. As part of his workup, renal imaging was performed and revealed medial deviation of the ureters, incomplete emptying of the collecting systems, and a pear-shaped bladder. Although these findings have been reported with other imaging modalities in patients with pelvic lipomatosis, they have not been described in renal scintigraphy. This constellation of findings should lead to the consideration of the diagnosis of pelvic lipomatosis.

Humans↗
PubMed1992

[Total hip joint endoprosthesis in osteopetrosis].

Albers-Schönberg disease (osteopetrosis) is a rare condition, and it very seldom occurs that a patient requiring a hip endoprosthesis is also suffering from this disease. The report describes the difficulties which may confront a surgeon unprepared for such a case and the author illustrates the problem taking the case history of a 46-year-old patient with X-rays and histological tests as an example. The reasons for implantation of either a cemented or cementless endoprosthesis are discussed.

Femur Head↗
PubMed1992

Acute retinal necrosis after chickenpox in a healthy adult.

A healthy man had acute retinal necrosis (ARN) two weeks after diffuse varicella eruption. Treatment with acyclovir and corticosteroids was associated with a favorable clinical outcome. To our knowledge, there are no reported occurrences of permanent visual loss or retinal detachment in healthy patients with postvaricella ARN.

Acyclovir↗
PubMed1991

An enkephalinergic mechanism involved in amygdaloid suppression of affective defence behavior elicited from the midbrain periaqueductal gray in the cat.

A series of recent studies in our laboratory have provided evidence that opioid peptides powerfully suppress feline affective defense behavior at the level of the midbrain periaqueductal gray (PAG). In the present study, we tested the hypothesis that the central (CE) nucleus of the amygdala constitutes a significant inhibitory input to the PAG which utilizes enkephalins as its neurotransmitter or neuromodulator. Cannula-electrodes were implanted into the PAG for the elicitation of affective defense behavior as well as for infusion of opioid antagonists. Monopolar stimulating electrodes were also implanted into the central, lateral and medial amygdaloid nuclei from which suppression or facilitation of affective defense behavior could be obtained. Initially, 4 trials of concurrent, subseizure stimulation of the CE or lateral amygdala at very low (100 microA, 60 Hz) currents and PAG resulted in an immediate suppression of this response which displayed a time dependent decline after 30 min. In the next stage of the experiment, naloxone (2.7, 18.9 and 27.5 nM) was microinjected through the cannula-electrode into the PAG affective defense site and the experimental procedures noted above were repeated. Naloxone treatment (at 27.5 and 18.9 nM) blocked the suppressive effects of CE and lateral amygdaloid stimulation in a dose and time dependent manner. Further analysis revealed that this effect is likely mediated via the mu receptor since the suppressive effects of amygdaloid stimulation were blocked by the selective mu antagonist, beta-Funaltrexamine (0.05 and 0.2 nM) but not by the selective delta-antagonist, ICI 174,864 (0.7 nM).(ABSTRACT TRUNCATED AT 250 WORDS)

Affect↗
PubMed1991

Affective defense behavior elicited from the feline midbrain periqueductal gray is regulated by mu and delta opioid receptors.

The present study sought to identify specific opioid receptor subtypes involved in the modulation of affective defense behavior (AD) at the level of the midbrain periaqueductal gray (PAG). Cannula electrodes were utilized for eliciting AD from the PAG as well as for microinjecting mu, delta and kappa agonists and antagonists into these sites. Following microinjections of morphiceptin, D-Pen2,D-Pen5 enkephalin (DPDPE), or U-488H into sites from which AD was elicited, threshold values were determined. The results indicated that morphiceptin and DPDPE significantly suppressed AD in a dose- and time-dependent manner. Pretreatment with mu and delta opioid antagonists, B-FNA and ICI 174,864, completely blocked the suppressive effects of morphiceptin and DPDPE, respectively. Microinjections of morphiceptin and DPDPE failed to alter response thresholds for circling behavior also elicited from electrical stimulation of dorsal PAG. Administration of the selective kappa agonist, U-488H, or vehicle alone, did not alter the threshold for AD. The results of this study indicate that opioid peptides interact with mu and delta receptors within the midbrain PAG to powerfully suppress AD.

Affect↗
PubMed1991

D2 dopamine receptor-mediated mechanisms in the medial preoptic-anterior hypothalamus regulate effective defense behavior in the cat.

The role of the dopaminergic innervation of the medial preoptic-anterior hypothalamus (mPO-AH) in regulating the expression of affective defense behavior in the cat has been investigated in the present study. Feline affective defense behavior, characterized mainly by autonomic arousal, ear retraction, growling, hissing and paw striking, was elicited by electrical stimulation of the ventromedial hypothalamic nucleus (VMH). Following the establishment of a stable threshold current for eliciting the hissing response of the behavior, the effect of injecting various DAergic agonists and antagonists into the mPO-AH on the hissing threshold was determined. The microinjection of the non-selective DA agonist apomorphine (0.03, 0.16, 0.33, 0.66, 1.56 and 3.3 nmol) into the mPO-AH facilitated hissing in a time- and dose-dependent manner. This effect was mimicked by the D2-selective agonist LY 171555 (0.2 and 1.0 nmol) but not by the D1-selective agonist SKF 38393 (1.7 and 17 nmol), and was blocked by the non-selective and the D2-selective antagonists haloperidol (1.3 nmol) and sulpiride (14.5 nmol), respectively. The injection of the D1-selective antagonist SCH 23390 (0.3 nmol), however, did not inhibit apomorphine-induced facilitation of hissing. In addition, the injection of haloperidol (1.3 nmol) and sulpiride (14.5 nmol), but not SCH 23390 (0.3 nmol), alone inhibited the behavior. It was therefore concluded that dopaminergic stimulation of the mPO-AH may facilitate the expression of affective defense behavior in the cat via a D2 receptor-mediated mechanism. The physiological significance of this effect and the interaction between dopaminergic, noradrenergic and serotonergic innervation of the mPO-AH in modulating the expression of affective defense behavior in response to threatening stimuli are discussed.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗