[Traumatic brain injury]. / Schädel-Hirn-Trauma.

Since traumatic brain injury is the most common cause of long-term disability and death among young adults, it represents an enormous socio-economic and healthcare burden. As a consequence of the primary lesion, a perifocal brain edema develops causing an elevation of the intracranial pressure due to the limited intracranial space. This entails a reduction of the cerebral perfusion pressure and the cerebral blood flow. A cerebral perfusion deficit below the threshold for ischemia leads to further ischemic lesions and to a progression of the contusion. As the irreversible primary lesion can only be inhibited by primary prevention, the therapy of traumatic brain injury focuses on the secondary injuries. The treatment consists of surgical therapy evacuating the space-occupying intracranial lesion and conservative intensive medical care. Due to the complex pathophysiology the therapy of traumatic brain injury should be rapidly performed in a neurosurgical unit.

Pseudohypoparathyroidism and Graves'disease: a rare combination of two endocrinological diseases.

We report a 26-year-old woman presented at the day of admission in the I.C.U. with increased perspiration, plethora and distinct tetany of both legs. Particularly unusual was an exophthalmus on both sides, a rectal temperature of 38.3 degrees Celsius and a blood pressure of high level (180/110 mmHg). Laboratory findings were a low serum calcium concentration of 2.86 mval/l, a hyperphosphataemia (5.0 mg/dl), free thyroxine of 31.7 pmol/l, TSH basal of < 0.01 U/ml and positive MAK and TRAK. Serum parathormone concentration was excessively high: 766 ng/l (12-72). Ultrasound of the thyroid gland revealed a normal size with a volume of 10.4 ml; the echosonic state was not typical for Graves' disease. The initial treatment consisted of high dose thiamazole and hydrocortisone intravenous, calciumcarbonate and propranolol per os. After acute situation the treatment continued with thyreostatics, calcitriol and calciumcarbonate. The symptoms at the day of admission (tetany) disappeared within 2 days; only local paraesthesia of fingers persisted longer. Normalization of thyroid parameters was reached after 11 days; the serum calcium concentration persisted on an increasing but still lower level than standard (3.8 mval/l). During substitution parathormone decreased to 443 ng/l. What is unusual about this case is the combined appearance of autoimmunethyreoiditis (Graves' disease) and pseudohypoparathyroidism.

Carbamazepine monotherapy in the treatment of alcohol withdrawal.

More than 135 different strategies for medical treatment have been described for the treatment of alcohol withdrawal syndromes. The substances used most frequently (benzodiazepines, barbiturates, or clomethiazol) themselves pose some risk for abuse or addiction. Anticonvulsants, especially carbamazepine (CBZ), have been discussed for the treatment of alcohol withdrawal since the early seventies. Various studies report favourable results with CBZ, usually combined with sedative agents. Nineteen out-patients and 19 in-patients took part in an open study of CBZ in alcohol withdrawal. The dose of CBZ was adjusted individually and ranged from a mean dose of 761 mg on day 1 to 616 mg on day 3 and to 388 mg on day 7 in the group of out-patients, and from 789 mg on day 1, 694 mg on day 3 to 562 mg on day 7 in the sample of in-patients. The "Objective Clinical Scale in Assessment and Measurement of Alcohol Withdrawal" (OCSAMAW) was used for treatment evaluation. Statistical analysis showed a significant improvement on the 5%-level in both groups; four in-patients needed concomitant treatment with oxazepam. Nausea and pruritus were the most common side-effects of CBZ treatment.

RTIME: a program for time-series measurements and evaluation in electrophysiology with the AT-PC.

This work describes a program which uses a standard RS232-serial interface of an IBM-AT-compatible microcomputer to receive via four data lines input from any laboratory equipment (spike discriminators, stimulus equipment, etc.) generating pulses between 0 to -15 V (low) and +5 to +15 V (high). Therefore, program operation is independent from any hardware extensions of the computer. The time of occurrence of input pulses is recorded with a resolution of 10 microseconds. Depending on processor speed and optional on-line display of interval histograms, a maximum sampling rate of 1.3-6 kHz is attained. Designed primarily for electrophysiological applications, the program comprises an extensive set of functions for off-line analysis of data either in the time- or in the phase-domain. The program is controlled by menu-selectable commands with detailed on-line explanation and is therefore suited for use even by operators without computer experience, e.g., students on courses in experimental physiology. Elaborate schemes of evaluation can be defined as macro commands to speed up and simplify complex data analysis in actual research.

Glibenclamide reduces secondary brain damage after experimental traumatic brain injury.

Following traumatic brain injury (TBI) SUR1-regulated NCCa-ATP (SUR1/TRPM4) channels are transcriptionally up-regulated in ischemic astrocytes, neurons, and capillaries. ATP depletion results in depolarization and opening of the channel leading to cytotoxic edema. Glibenclamide is an inhibitor of SUR-1 and, thus, might prevent cytotoxic edema and secondary brain damage following TBI. Anesthetized adult Sprague-Dawley rats underwent parietal craniotomy and were subjected to controlled cortical impact injury (CCI). Glibenclamide was administered as a bolus injection 15min after CCI injury and continuously via osmotic pumps throughout 7days. In an acute trial (180min) mean arterial blood pressure, heart rate, intracranial pressure, encephalographic activity, and cerebral metabolism were monitored. Brain water content was assessed gravimetrically 24h after CCI injury and contusion volumes were measured by MRI scanning technique at 8h, 24h, 72h, and 7d post injury. Throughout the entire time of observation neurological function was quantified using the "beam-walking" test. Glibenclamide-treated animals showed a significant reduction in the development of brain tissue water content(80.47%±0.37% (glibenclamide) vs. 80.83%±0.44% (control); p<0.05; n=14). Contusion sizes increased continuously within 72h following CCI injury, but glibenclamide-treated animals had significantly smaller volumes at any time-points, like 172.53±38.74mm(3) (glibenclamide) vs. 299.20±64.02mm(3) (control) (p<0.01; n=10; 24h) or 211.10±41.03mm(3) (glibenclamide) vs. 309.76±19.45mm(3) (control) (p<0.05; n=10; 72h), respectively. An effect on acute parameters, however, could not be detected, most likely because of the up-regulation of the channel within 3-6h after injury. Furthermore, there was no significant effect on motor function assessed by the beam-walking test throughout 7days. In accordance to these results and the available literature, glibenclamide seems to have promising potency in the treatment of TBI.

[Unusually high iodine excretion in hyperthyroidism in an iodine-poor area]. / Ungewöhnlich hohe Jodausscheidung bei Hyperthyroesen aus einem Jodmangelgebiet

In 27 thyrotoxic patients and in 177 healthy controls from the area of Essen we studied the total urinary iodine excretion. Whereas the iodine excretion was only 43.7 +/- 27.3 mug iodine per g creatine in the controls, the corresponding average value was significantly higher in thyrotoxic patients. It amounted to 193.3 +/- 201.7 mug iodine per g creatinine. This finding can not be explained by selection of patients with autonomous adenomas and contamination with iodine. Possible causes are an increased daily iodine uptake by increased dietary intake or iodine containing drugs that might not be remembered by the patients and increased renal clearance of iodine. Strong evidence for a contamination with iodine is the finding of increased differences between measured and calculated PBI, the latter being derived from T4 (D). The differences averaged in both groups 5.3 and 3.2 mug/100 ml. Our data can not exclude a basedowification of preexisting goiters. This unexpected finding gives rise to corresponding investigations in other thyroid centers.

[T-cells in thyroid disease (author's transl)]. / T-Lymphocyten bei Schilddrüsenerkrankungen

Thymus-derived peripheral blood lymphocytes were studied in untreated (n = 18), methimazole-treated (n = 28) thyrotoxicosis, after radioiodine (n = 14), in Hashimoto thyroiditis (n = 7) and in euthyroid goiter (n = 7). The results were compared with normal persons (n = 40) without thyroid disease. There was no significant difference in the total and relative counts of T-cells either between the different groups nor compared with the controls. These findings confirm that T-cells in peripheral blood cannot give any information about activity or prognosis of the various thyroid diseases. Thus T-cells give no further suggestion concerning the possible pathogenetic role of cell-mediated-immunity.

[Acute liver necrosis caused by valproate]. / Akute Lebernekrose durch Valproinat.

After treatment with valproic acid a 19-year-old female patient with Friedreich's ataxia and generalised epilepsy died following acute hepatic failure with massive lactacidosis. The clinical symptoms were characterised by hyperventilation, increasing loss of consciousness and shock, leading to treatment-resistant hepatic coma. Morbid anatomy showed extensive confluent lytic necroses of liver acini with accentuation of centrolobular and intermediary structures as well as small and medium-sized fatty degeneration increasing from the periphery towards the centre. The disease picture is quite characteristic for being caused by valproic acid. As a safety measure liver function tests should be done should prodromal symptoms such as anorexia, weakness and apathy arise. If necessary the dosage has to be reduced or medication stopped. Serum valproic acid levels should remain in the lower half of the therapeutic range.