Diagnosing hydrocephalus in infants by ultrasound sector scanning through the open fontanelles. A study comparing ultrasound-sonography and CAT-scan.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Sauer.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Twenty-eight patients with peroneal muscular atrophy (PMA) have been investigated. Eighteen of them were affected by the Charcot-Marie-Tooth disease and three by Dejerine-Sottas disease. In these 21 cases the nerve conduction velocity (NCV) was decreased. Four patients presented the neuronal type of PMA, two cases showed sensory neuropathy of the neuronal type with ophthalmoplegia, and one case, PMA with ataxia, i.e., a myatrophic ataxia. In the neuronal type of PMA, including both cases with ophthalmophegia, the amplitudes of the sensory nerve action potentials were decreased, and the NCV was normal to slightly subnormal. In myatrophic ataxia NCV was decreased. In all cases with reduced NCV, the latencies of the spinal-evoked potentials (spinEP) and somatosensory-evoked potentials (ssEP) were prolonged. In the neuronal type of PMA, these latencies were normal. The central latencies (from thoracic and cervical level) were normal in all 28 patients with PMA of different types. Seventeen patients with Friedreich's heredoatazia have been investigated. In all except two cases, NCV was normal. The sensory nerve-action potentials markedly decreased or disappeared in all cases. The peripheral neurographic picture, accordingly, corresponds to that of patients with the neuronal type of PMA. The latencies of spinEP were normal. All patients with Friedreich's heredoatazia, however, showed prolonged latencies of ssEP. Calculating the central latencies as the difference between ssEP and spinEP latencies (cervical and thoracic) confirms that this is due to a slowing of the conduction velocity via the spinobulbar tracts.
The syndrome of septo-optic dysplasia with congenital hypopituitarism consists of optic nerve hypoplasia, midline malformations of the prosencephalon and hypothalamic hypopituitarism. There is great variability of these features and clinical manifestation is age-dependent: Newborns present with hypoglycemic seizures, apnea, cyanosis, hypotonia, prolonged jaundice (and micropenis in boys) because of growth hormone and/or ACTH-deficiencies. Wandering eye movements and more or less visual disturbance become evident during infancy and growth retardation even later in some cases. Early recognition is facilitated by the pathognomonic fundoscopic findings, together with normal electroretinogram, absent visually evoked potentials and computer tomography. Early hormone substitution is essential to prevent hypoglycemic damage.
The binding of estradiol (E2) and testosterone (T) to testosterone-estradiol-binding globulin (TeBG) was studied in vivo at 37 C by three independent methods: equilibrium dialysis, steady state polyacrylamide gel electrophoresis, and TeBG-ligand dissociation kinetics. Equilibrium dialysis was performed at 37 C with the dialysate containing human serum albumin in amounts equivalent to that of the plasma dialysand. Scatchard analysis indicated that under these conditions E2 does not measurably bind to TeBG, while T has a Kd of 3.7 X 10(-10) M. Similarly, Scatchard-type analysis of E2 binding to TeBG in steady state polyacryalmide gel electrophoresis at 37 C revealed no high affinity saturable binding, while dihydrotestosterone was bound with a Kd of 2.7 X 10(-10) M. Examination of the dissociation kinetics of T and E2 ffrom TeBG revealed that the mean (+/-SD) T1/2 of dissociation of T from plasma at 37 C (10.8 +/- 2.4 min) was significantly shortened to 3.5 +/- 0.4 min by saturation of plasma with dihydrotestosterone (P less than 0.01), whereas that of E2 (8.9 +/- 1.4 min) was not changed (9.6 +/- 3.0 min). These data suggest that TeBG is not an important binder of plasma E2 at physiological temperatures and explain the observation that in diseases characterized by high TeBG levels, such as hyperthyroidism and liver disease, the MCR and free E2 levels have generally been normal.
A method for continuous measurement of the anaesthetic Ethrane in blood and gas samples is described. Using the same GC-parameters for the analyses of gases and blood extracts, a short GC-column together with high oven temperature as well as shortening of preparation (extraction) time allows the analysis of two blood samples and one gas sample within 15 minutes' steps (the time for an additional gas sample analysis being max. 3 min). Thus a quasi simultaneous follow up of the course of anaesthesia in animals and in humans may be guaranteed.
Explore the source record for details and available documents.
A stystematic neurological and electroencephalographical follow-up study in 344 head injured adults gave the following results: 1. 52% of all the hospitalized (mostly primarily amnesic) patients had a cerebral contusion. A contusion was assumed in cases with focal neurological signs (13%), amnesias of more than 8 hours (16%) and/or EEG-abnormalities lasting for more than 24 hours (49%). 2. Traumatic EEG-abnormalities were general slowing (43%) and foci (32%). In 40% of the cases with general slowing the slowing (greater than or equal to 1.5/sec) was within the alpha-frequency band and could only retrospectively be assed. 3. The EEG was invariably abnormal in cases with an amnesia exceeding 8 hours. If the amnesia exceeded 1 hour abnormalities were found in 73%. 4. Among the patients with contusion 6.5% had no amnesia, 48% less than 30 minutes and only 30% an amnesia for more than 8 hours. In 75% of the patients with concussion amnesia lasted less than one hour. 5. Skull fractures were mostly combined with contusion (74%). 6. Impaired drive, reduced ability to concentrate, memory deficits, headache and dizziness were significantly more frequent 6 months after contusion than after concussion. 7. 21% of the patients with traumatic dizziness (44%) had a labyrinthine contusion. 8. Among the contusions diagnosed with the aid of EEG recordings 58% would have been missed after exclusive neurological examination and 82% after application of the classical criteria used by surgeons and general practitioners.
42 patients with ALL were treated according to the following protocol: induction with vincristine + prednisone (+/- L-asparaginase), CNS-prophylaxis with cranial irradiation (2400 rads) and intrathecal methotrexate, maintenance for 3 years with 6-MP 50 mg/m2/d p.o. + MTX 75-150 mg/m2/2 wk i.v. X 4, alternating in a cyclic fashion with 6-MP 50 mg/m2/d p.o. + cyclophophshamide 600 mg/m2/2 wk i.v. X 4. The observation time is 24-67 (median 49) months. The actuarial complete remission curve shows 40% continuous complete remissions at 36 months and 30% at 60 months.--The frequency and temporal distribution of typical infectious complications are presented. The incidence of varicella was comparable to that in a southgerman normal control group (5,7% per year). During treatment there were two zoster manifestations per one varicella case, the incidence of zoster being 1 case per 106 patient-months, viz 11,4% per year.
We report the case of a 56-years old patient with clinical symptoms of an unresolved neuromuscular disease. The light microscopic studies of a muscle biopsy from the m. triceps shows the picture of a diffuse muscular atrophy. By electron microscopy, myelin-like degeneration zones with tubular-filamentous inclusions can be shown in the cytoplasma of the atrophic muscle cells. These filamentous structures correspond morphologically to the nucleocapside of paramyxoviruses. These results lead, even without the proof of inflammatory cells, to the diagnosis of an "inclusion body" myositis also taking into account the clinical and electrophysiological findings.
Somatosensory spinal (spinEP) and primary cortical evoked responses (ssEP) to median and tibial nerve stimulation (at forefinger, wrist, and ankle respectively) were investigated by means of summation techniques in 23 normal children aged 6 to 14 years. Amplitude recovery functions of cervical spinEP were tested by paired stimuli and short tetanic stimulation at the wrist; spinEP amplitudes were unchanged for stimulus intervals down to 5 ms. The amplitudes of the cervical spinEP after strong stimuli to the finger were only a quarter as great as those obtained by stimulation of the wrist at motor threshold strength. In one patient with the Brown-Séquard syndrome cervical spinEP were absent for stimuli on the side of position sense impairment, but were unaffected for stimuli on the side of dissociated sensory loss. The normal latencies of spinEP (to the onset of the negative potential) and ssEP (to first negative peak) are presented as functions of body height. The difference between these two latencies yielded a central latency from the lower cervical spinal cord of about 9--10 ms. The spinal afferent conduction velocity, calculated from the difference between the lumbar and cervical latencies after tibial nerve stimulation at the ankle, was found to be 74m/s.
1. Selective deprivation of slow-wave and paradoxical sleep was performed in 10 children with pycnoleptic attacks (8 of them before anticonvulsive treatment, 2 of them while under medication). The frequency and duration of petit mal attacks were intraindividually compared during night sleep and after waking for a 5-h period. 2. After deprivation of slow-wave sleep with reduction of EEG stages 3 and 4 to about one-third of the baseline but normal duration of sleep, petit mal attacks are more frequent and long-lasting than after normal sleep or selective deprivation of REM sleep. 3. Although total sleep time is significantly diminished after selective deprivation of paradoxical sleep the frequency of attacks during the waking state was lower than after normal sleep and deprivation of slow wave sleep. This observation shows a clear i nfluence of the quality of sleep on the frequency of epileptic attacks. 4. During sleep petit mal seizures were mainly found during stages 2 and paradoxical sleep. Single spike and irregular spike were discharges, however, occurred more frequently during slow-wave sleep. Their frequency was not significantly different in the deprivation conditions. 5. In contrast to experimental data in animals, REM deprivation is less provoking to epileptic attacks outside sleep than deprivation of stages 3 and 4 sleep. Therefore a sufficient amount of slow-wave should be preserved for pycnoleptic children.
The roentgenological and clinical findings of a five year old girl suffering from cytomegalic inclusion body disease are reported. In this disease unusual circumscript and large calcareous deposits of the basal ganglia and scattered gyriform calcifications of the occipito-parietal cortex were shown on plain skull x-rays and their paraventricular localization demonstrated on pneumoencephalotomogram.
With the aid of our own method of gas chromatography we determined serum concentrations of anticonvulsants in a large number of children who were being treated with diphenylhydantoin, primidone and phenobarbitone. The drugs were being prescribed either as monotherapy, or in combination with each other, or with other substances which have anticonvulsive activity. Regression lines showed good correlations between the quantity of drugs administered (total daily dose) and serum concentrations. The regression lines for diphenylhydantoin and primidone, however, showed no differences, irrespective of whether they were being given alone or in combination. In view of the frequency of symptoms of intoxication and of non-responders, we established a therapeutic range for diphenylhydantoin and primidone (diphenylhydantoin: 5--16 mcg/ml; primidone: 4--14 mcg/ml). The required serum concentrations could be obtained by giving 8--12 mg/kg of diphenylhydantoin, and 15-22 mg/kg of primidone. In spite of the satisfactory correlation between total daily dose and serum concentrations, however, many patients showed departures from this normal behaviour, especially where combination treatments were being conducted. This demonstrates the necessity for routine controls of serum levels.
Although good correlation can be obtained between total daily dose and serum concentration in treatment with anticonvulsant drugs, many patients still show departures from this relation. The various factors which can influence serum concentrations of the administered drugs were to be domonstrated in a number of children who were receiving anticonvulsants at average dose levels and who developed evidence of overdose, or who failed to respond to therapy. The most important feature is that combined adminstration of several drugs may increase or inhibit metabolisation of the various substances, so that inadequate or excessively high serum concentrations result. Furthermore, irregular intake of the necessary medication must always be taken into account in the case of treatment on an out patient basis. Routine determinations of serum levels of anticonvulsant drugs in these patients are called for because of this.
The radiological appearance and localization of collateral cerebrovascular networks are described. The development and distribution of these arterial networks is due to the site of internal carotid artery stenoses. Including interposed arterial nets, the following types are classified: (1) basal arterial networks near the carotid siphon; (2) arterial networks in the region of the basal ganglia (Moyamoya syndrome); (3) ethmoid arterial networks; (4) arterial networks on the cerebral convexity representing transdural external-internal carotid anastomoses, and (5) circumscribed arterial networks interposed in the course of a major cerebral vessel. The differential diagnostic criteria and aetiological factors of these anastomotic intracranial networks are discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.