Inputs to nigra neurons from caudate nucleus and fundus striati.
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Biomedical subjects
Publications and source records attributed to A Wagner.
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We present a clinical and morphological study concerning a kindred with slowly progressive X-linked muscular dystrophy (Becker type). Five males were affected; one died of heart failure at age 16. Severe and early cardiac disorder is unusual in this type of muscular dystrophy, and death at such an early age had not been reported previously. In the other patients of the kindred, cardiac abnormalities, if present at all, were nonspecific. Another unusual feature in this kindred was severe muscle pain at an early stage of the disease, a feature that cannot yet be explained.
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The Leipzig Center for Wilson's Disease in the GDR is charged with the registration and diagnosis of all homozygous Wilson gene carriers, the clarification of all suspected cases, including the heterozygote test, and the co-ordination of long-term treatment. At present, there are 78 recorded Wilson gene carriers living. On the basis of our own comprehensive observations and investigations over prolonged periods of time, questions concerning pathogenesis, genetics, diagnosis and therapeutic measures, including their side-effects, are dealt with.
During a study tour of the Neurological Clinic in Warsaw, the automatic EMG analysis procedure by means of the Polish computer ANOPS was tested, standard values worked out and their diagnostic information value tested on patients with neuromuscular diseases. To obtain normal values, leads from four muscles of each of 21 healthy persons were made and the electromyograms of each muscle described by five different parameters. For a differentiated neuromuscular diagnosis it is significant that the computer not only calculates the mean values of each EMG parameter but provides histograms from which further statistical indices and diagnostic information can be obtained.
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The unusual occurrence of microcytic anemia with hypochromia, high iron blood levels and excess of sideroblasts in the bone marrow, observed during the treatment of tuberculosis with isoniazid and rifampicine is reported. Three particularities were noted. First, in our experience, the occurrence of this type of anemia has never been noted previously as a result of these two drugs. Secondly, the improvement of the blood abnormalities was obtained by the combined use of vitamin B6 and vitamin C. Thirdly, the anemia was associated with neuropathy, characterized by areflexia and dysesthesia, which improved with vitamin B6 therapy (but not with vitamin C). Some mechanisms are discussed as being possibly the origin of this kind of anemia, particularly a lack of vitamin B6 resulting from a massive urinary loss of pyridoxal induced by isoniazid as well as both a tissue depletion and an overconsumption of this vitamin. The anemia may be the consequence of a deficiency of hemoglobin synthesis involving probably the first step of the biosynthesis of heme.
It is reported on a 39-year-old patient who revealed pathological ECG-findings of the most different kind during several years. Since there were no clues to a myocarditis, later on, however, pareses of atrophical skeletal muscles developed and a distropia myotonica could be diagnosed, the cardiological disturbances are to be regarded as a symptom of this disease. When also a participation of the myocardium in the distrophia myotonica is not unknown, so even in our case the frequently changing disturbances of the nervous impulses of the heart, of the ventricular stimulus conduction and of the replolarisation of different expression as well as the pronounced hypersensitivity to heart glycosides are remarkable individual findings. The interpretation of these findings is problematic. Morphologic and dystrophic changes of the myocardium as well as functional myotonic disturbances on the membraneous system may influence the process of stimulation and may cause the clinical appearances.
In the cat caudate nucleus the same nine types of synapses are found as in putamen and fundus striati. The three parts of the striatum in the strict sense do not differ in the morphological differentiation of synapse types but only in their quantitative distribution. One-third of all synapses in the caudate nucleus are axo-spinous type IV synapses with a curved and divided asymmetric contact. This strongly suggests that the caudate nucleus interneuronal apparatus is dominated by centre-median input, in contrast to the putamen which is controlled by the cortico-striatal input to its internuncial cells and by its strong intrastriatal feedback mechanism. Extensive destruction of the convexity of the cortex and the medial cortex in one hemisphere results in dark degeneration of a large proportion of two of the nine types of caudate synapses: a) the axo-dendritic type VII synapses exciting the large spiny caudate neurons and b) the axo-spinous type III synapses making contact with the small spiny neurons of the interneuronal cell apparatus.
Evaluation of 500 arteriograms in children over a period of three years revealed a complication rate of 7.4% (37 cases). In these, thrombosis occurred which had to be treated conservatively. The factors increasing the complication rate were low age, weight below 5000 grammes, exposure of the vessel, excessively large instruments and long duration of the examination. For the early recognition of thrombosis the Doppler technique is most valuable. Prophylactic measures are discussed.
After columnar isolation of the cat's fundus striati with a survival time of 2 days or 2 or 4 weeks all axospinous boutons (type I, III And iv) and most axo-dendritic (or axo-somatic) boutons (type II, VI and VII) undergo dark degeneration. All specimens of axo-somatic (or axodendritic) type IX bouton (containing large, round vesicles in a clear axoplasm) and most specimens of type V bouton (with pleomorphic and some dense core vesicles) are unaltered. Many type VIII boutons (dindritic terminals containing scattered, small, sphrical vesicles suspended between the filaments of many microtubules in clear dendroplasm) are almost preserved, in the fundus more than in the caudate nucleus. After 2 or 4 weeks, some perikarya and many dendrites have undergone an electron-dense retrograde degeneration resulting from interuption of the efferent axons of the large striatal cells. The type IX synapses are interpreted as intrinsic between the small spiny and the large efferent striatal neurons; the type V as intrastriatal axon-collaterals of the large efferent neurons and the type VIII as dendritic terminals of intrastriatal Golgi type II nerve cells (possibly dwarf cells).
A study has been made to determine the usefulness of triggered correlation as a method of automatic quantitative analysis of graphic representations of the somatic electric currents associated with muscular action. Although an electromyogram is neither a normally distributed nor a stationary random process, the method has been found to be suitable for clinical electromyography. The method is easy to use, with measuring values that may be used for diagnostic purposes being obtained within a few seconds. In the case of normal subjects and patients with neuromuscular diseases, parameters of triggered correlograms are compared with those of visuamanually analyzed or digitally averaged potentials of individual motor units.
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The efficacy of a new low dosage trimethoprim-sulfamoxole combination (Supristol) was tested in a joint therapeutic study in 6 medical clinics or departments and in a general practice. A good therapeutic result (healing) was achieved in about 80% of the 143 patients included in the trial. The preparation was well tolerated. Symptoms of intolerance appeared in only 2% of the cases. It is assumed that the low dosage of the preparation influences the tolerance favorably without affecting the efficacy.
The cat putamen contains the identical nine types of synapses and the same proportion of axo-dendritic (or axo-somatic) synapses as described for the fundus striati. However, type III (cortico-striatal) (31:16%) and type V Caxon-callateral) (13:1%) occur much more frequently and type I (nigro-striatal) much less frequently (14:34%) in the putamen than in the fundus striati. Of the axo-spinous synapses only type IV, with densely arranged small round vesicles and interrrupted, asymmetric contact, shows a dark degeneration after center median lesions, mainly in the parvocellular part. Of the six axo-dendritic (or axo-somatic) synapses, only type VII, with densely packed small round vesicles and asymmmetric contact, is degenerated after the same lesion in the center median nucleus. However, after such lesions type VII synapses are much more frequently degenerated in the putamen than those of type IV.
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