Biomedical subjects
Publications and source records attributed to E Kraus.
The somnolence syndrome is a postirradiation syndrome in children. It is to be found after cranial irradiation of chemotherapeutically treated children with ALL (acute lymphocytic leukaemia). Rarely, however, it is a radiation sequela of operated cerebral tumors. We report on such a case of somnolence syndrome, review the literature and discuss the diagnostic and therapeutic problems.
Rheumatoid arthritis as a cause of medullary compression due to subluxation of rheumatically diseased joints is very common. However, spinal cord compression by rheumatoid nodules is seen rarely, usually by extradural lesions. We describe two cases of intradural rheumatoid nodules causing spinal cord compression.
We report on diagnosis, treatment and clinical course of a solitary schwannoma of the trigeminal nerve with consecutive metastatic spread in a 45-year-old woman. The patient presented a temporal lobe syndrome with psychomotor seizures. Trigeminal nerve function was intact apart from a transient hypaesthesia in the mandibular branch. Assuming a meningioma the tumor was removed via a temporal approach. Secondary to the definitive histological diagnosis radiation therapy was performed. After that the patient was symptom-free. 4 months later a large recurrent tumor was found involving the cavernous sinus and the pterygopalatine fossa. In a second operation the tumor was resected intra- and extradurally through an infratemporal preauricular approach in cooperation with an oral and maxillo-facial surgeon. At this time multiple pulmonary metastases developed showing no response to polychemotherapy (EVI). The patient died 13 months after onset of the disease. Hitherto, only 5 cases of a primary malignant schwannoma of the trigeminal nerve have been published in the world literature.
Urinary calcium excretion (UCa) is normal several weeks following subtotal nephrectomy (Nx) in the rat, despite factors such as magnified solute load per nephron which should promote hypercalciuria. To define the levels of UCa during the first few weeks after Nx and to determine if the development of compensatory mechanisms governing renal conservation of calcium are detectable, we measured UCa in Nx and sham Nx rats with matched food intake (10 g/day) from 10 days before through 20 days following Nx. In the sham Nx animals, UCa rose during the first 5 days following surgery from 27 +/- 8 to 66 +/- 5 microM/day and then plateaued for the remaining time. In Nx rats, UCa also rose during the first 5 postoperative days from 23 +/- 5 to 110 +/- 10 microM/day (Nx vs. sham Nx, p less than 0.05), but then fell over the next 3 days to levels observed simultaneously in sham Nx animals. The rise in UCa after Nx, but not after sham Nx, was associated with a doubling of urine flow rate and increased urinary titratable acid excretion. In parathyroidectomized rats, UCa also rose following Nx; however, maximum UCa was then sustained for at least 4 days. In an additional sham Nx group fed 20 g/day, no increase in UCa occurred following surgery. Thus, hypercalciuria is present following Nx in the rat, in part possibly attributable to increased acid excretion. The transient nature of calciuria reflects an adaptive phenomenon, most likely hyperparathyroidism. Diminished food intake following surgery independently contributes to hypercalciuria, regardless of the status of renal mass.
In 158 inpatients (61 m., 97 f.) with obesity-associated diseases were performed a diet-training-programme for about four weeks. We used a PSMF (protein sparing modified fasting) as a 350 kcal diabetic mixed diet, adequate to 4 carbohydrate units (40g carbohydrate, 30g protein, 5g fat) with weekly tea-vegetable-days, additionally wheat brain. The training programme was adapted individually. Reexamination were made by questionnaires and diabetic control cards concerning the body weight. The favourable influence of blood pressure and metabolism was registered. The diet schedule consist natural foodstuffs, fibers, minerals and vitamins. It can be varied, is very effective especially in combination with exercise. The middle term results are rather good more for women than men. Our diet-training-programme can be recommended for outpatients as well as for cures.
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A 20-year-old man developed myopia immediately after blunt trauma to the eye. The main finding was a shallow anterior chamber. Ultrasonography revealed anterior displacement of the iris lens diaphragm without change in lens thickness or axial length of the eye. After 1 week intraocular pressure decreased to a very low level, and edema of the optic disc and macula developed. Since hypotony and shallowness of the anterior chamber persisted for many months, we assume the cause to be detachment of the ciliary body. This is an uncommon mechanism for traumatic myopia, spasm of the ciliary body being more common.
Twenty-seven patients with vernal conjunctivitis who remained symptomatic following treatment with corticosteroid drops and/or Opticrom drops (sodium cromoglycate 2%, benzalkonium chloride 0.01%) were treated with aspirin. Aspirin produced marked improvement in all patients apart from three. The possible mechanism of the efficacy of aspirin in vernal conjunctivitis is discussed.
In this case report the authors present a patient in whom loss of vision developed in the left eye in the early stage of herpes zoster ophthalmicus. He suffered from optic neuropathy followed by central retinal artery occlusion. Ophthalmologists should be aware of this rare and early complication of herpes zoster.
The interaction between morphine analgesia and the heterotopic hypoalgesic effects induced by visceral pain was investigated using a behavioral approach in the rat. Both systemic morphine and a dull pain of peritoneal-visceral origin (induced by i.p. phenylbenzoquinone, PBQ) increase the threshold for vocalization to tail-shock. The question of the interaction between these two factors was assessed by administering morphine during the period of increase in threshold induced by PBQ. Not only did we find that morphine did not increase the threshold further, but, indeed, very significantly decreased it, with the more obvious effect being observed for a moderate dose (0.33 mg/kg, i.v.). It is concluded that morphine antagonizes the heterotopic hypoalgesic effects of visceral pain. These results do not support the hypothesis that morphine increases inhibitory controls of pain triggered by noxious inputs.
The results of operation in 851 intracranial aneurysms were statistically analysed. The influence of 22 factors on operative outcome is shown. The importance of the time of intervention for the prognosis of patients is of special interest. It is striking that the outcome of an operation within 48 hours only depends on the neurological status, whereas at operation in the stage of recovery further factors such as vasospasm, arteriosclerosis, brain oedema, ischaemia and blood in the subarachnoid space are of great importance. They lead to a more unfavourable outcome.
Infusion of phosphate into thyroparathyroidectomized rats on a normal phosphorus diet caused a decrease in net phosphate reabsorption, even though the plasma concentration of phosphate continued to rise. This response was expressed at the level of the proximal tubule brush-border membrane and was coincident with a decrease in sodium-dependent phosphate uptake in membrane vesicles. Kinetic experiments indicated that the increased phosphate load caused a decrease in the Vmax of the membrane uptake system with no change in the apparent Km for phosphate. The infusion of phosphate resulted in a lowered plasma calcium concentration, and it was previously hypothesized that the inhibition of maximal phosphate reabsorption was mediated by the hypocalcemia. When the fall in plasma calcium was prevented by the simultaneous infusions of calcium and phosphate, the reduction in maximal phosphate reabsorption was blunted; however, the phosphate infusion-induced inhibition of brush-border membrane vesicle phosphate uptake was still evident. Thus a major discrepancy was found to the general concept that renal phosphate reabsorption in vivo correlated positively with sodium-dependent phosphate uptake activity in proximal tubule brush-border membrane vesicles. Several possible explanations to account for this anomaly were discussed. It was also found that calcium infusion into saline-infused thyroparathyroidectomized rats slightly increased maximal phosphate reabsorption but did not affect phosphate uptake in the membrane vesicles.
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Infarction of the occipital cortex usually causes loss of the contralateral half of the visual field in both eyes. Although cases with complete transient loss of vision have been described, this is due to involvement of the second half of the cortex in the pathologic process. We report a case of a one-eyed patient with almost complete loss of vision in her only eye because of an infarction of the ipsilateral occipital cortex. During the patient's hospitalization, the temporal half of the visual field recovered. The case is of interest because of the difficulties in diagnosing cortical blindness in a one-eyed patient.
As progressive renal failure develops, phosphate excretion per functioning nephron increases, thus preserving homeostasis. To test whether dietary phosphate supply might contribute to the regulation of renal phosphate excretion in the uremic setting, groups of male Sprague-Dawley rats that were either parathyroidectomized (PTX) or sham PTX (S-PTX) and either five-sixths nephrectomized (Nx) or sham Nx (S-Nx) were studied following a 4-wk dietary regimen consisting of 0.1 or 0.7% phosphate. For Nx rats fed the 0.7% phosphate diet the fractional excretion of phosphate (FEPi) was enhanced (47 +/- 6 vs. 21 +/- 3%) and the maximum tubular reabsorption of phosphate per milliliter GFR (TmPi/GFR) was suppressed (1.65 +/- 0.19 vs. 2.33 +/- 0.19 mumol/ml). FEPi was unchanged by PTX in these Nx animals (42 +/- 6 vs. 47 +/- 6%). TmPi/GFR remained suppressed in PTX, NX animals when compared with S-Nx, PTX controls (3.38 +/- 0.33 vs. 5.07 +/- 0.41 mumol/ml). For rats fed the 0.1% phosphate diet Nx did not affect TmPi/GFR in either S-PTX (5.40 +/- 0.43 vs. 4.97 +/- 0.34 mumol/ml) or PTX (7.03 +/- 0.23 vs. 6.98 +/- 0.21 mumol/ml) animals. For both S-Nx and Nx animals the effects of PTX and dietary phosphate restriction on TmPi/GFR were independent and additive. In all groups of animals, tubular reabsorption of phosphate per milliliter GFR (TRPi/GFR) dropped acutely with continued infusion of phosphate once TmPi/GFR was achieved. Thus, a resetting of TRPi/GFR occurs among Nx rats in response to both chronic dietary phosphate deprivation and acute intravenous phosphate loading.(ABSTRACT TRUNCATED AT 250 WORDS)
Pseudo-Kaposi's sarcoma has been associated, in most cases, with an underlying congenital arteriovenous (AV) fistula. A patient with chronic renal failure and an acquired, iatrogenic AV fistula in his left wrist for hemodialysis developed pseudo-Kaposi's sarcoma on his left hand three years after placement of the AV fistula. Histologic findings included a proliferation of superficial dermal vessels and fibroblasts, extravasated red blood cells, and occasional fibrin thrombi in vessels. To our knowledge, this is the third case of an association between pseudo-Kaposi's sarcoma and an acquired, iatrogenic AV fistula, and the first to involve the hand. Pseudo-Kaposi's sarcoma occurs in association with underlying congenital and acquired AV fistulas.
The sustained in vivo infusion of phosphate into thyroparathyroidectomized rats resulted, after 1 h, in a marked decrease in net phosphate reabsorption, even though the plasma concentration of phosphate continued to rise. This response to phosphate infusion was expressed at the level of the proximal tubule brush border membrane. Within 40 min of the initiation of the infusion the Na+-dependent phosphate uptake system in isolated membrane vesicles was decreased. Phosphate uptake in the absence of Na+, Na+-dependent D-glucose uptake, and 22Na+ uptake were not affected. These findings demonstrate the locus of this parathyroid hormone-independent adaptation and indicate the rapidity with which the membrane transport system is regulated.
The effects of the serotonin precursor 5-HTP, were determined in a behavioral DNIC paradigm (increase in vocalization threshold after intraperitoneal injection of the algogenic agent, phenylbenzoquinone). This counter-irritation phenomenon was strongly potentiated by 5-HTP, such potentiation being blocked by the 5-HT receptor blocker, cinanserin. These results are in keeping with those of our recent single unit work in dorsal horn convergent neurons.