Dr. Bernd F. Reitter (1943 - 2021) was a pedriatric neurologist and
professor of pediatrics at the University of Mainz,
Germany. Born in the city of Halle and having grown up in
Augsburg, Bavaria, Dr. Reitter studied medicine in Erlangen, Vienna,
Freiburg, Paris, and spent two years in a visiting position at UCLA on invitation of
Richard J.
Schain. His 1981 habilitation thesis under Prof. Dieter Scheffner at the University of Heidelberg is available below.
Bernd Reitter worked as a doctor at the University of Heidelberg and, in 1984, took a
position as a professor of pediatrics at the University of Mainz, heading the department of neuropediatrics at the Center for Pediatric and Adolescent Medicine (Zentrum für Kinder- und Jugendmedizin).
Experimental neurophysiology has developed a series of investigative techniques that allow extensive insight into nerve and muscle function. Only some of these examination techniques have found their way into clinical electrodiagnosis. The use in children is even more limited. Thus, the previously described methods for detecting the refractory periods of the peripheral nerve in children are hardly applicable. Refractory periods represent the second essential criterion of neural function in addition to action potential speed. Therefore, a method for recording the neuromuscular resection was designed to clinical needs using pair stimulation (NMRPS). There, the response of a dependent muscle is examined after supramaximal double stimulation of the associated nerve. An electronic subtraction method allows to represent the conditioned action potential of the muscle derived from surface electrodes, isolated from the bond-forming response. Amplitude, time of the amplitude, baseline and inclination of the patent are evaluated in relation to a single potential. For various stimulus intervals, these parameters have been standardized for adults and children and checked for defined symptoms of the peripheral nerve and muscles.
In the polyradiculoneuropathy Guillain-Barre as an example of de-and remyelination, the values of the NMRPS remained barely influenced despite a significant reduction in the motor nerve conduction velocity.
As an example of primary axonal degeneration, vineristin neuropathy was chosen. Despite constancy of normal motor nerve conduction speed, measured values of the NMRPS deviated in a dose-dependent manner from the normal range and returned to normal after completion of the vitamin administration, depending on the time interval to the medication. Significant treatment effects (p = 0.0009, p = 0.0301, respectively) were found for the group of 13 children.
For the progressive muscle atrophy Charcot - Marie - Tooth (HMSN I) as an example of primary axonal damage with subsequent de- and remyelination, a deviation of the potentials from the normal range could also be detected.
Children with uremic neuropathy due to chronic renal insufficiency of various stages showed no regular changes for motor nerve conduction velocities or NMRPS. However, a smaller proportion of these 24 children had clinical signs of uremic polyneuropathy. Statistically significant deviations were only seen in the children under chronic hemodialysis dialysis when comparing the data before and after single dialysis. Significant correlations with the change in the serum creatinine level and residual diuresis were also detectable. As expected, the NMRPS values also deviated from the norm range in the selected example of myopathy, the progressive Duchenne muscular dystrophy.
Noticeable for this group is the abnormal deceleration of the conditioned muscle action potential, since abnormally short refractory periods have been reported for the muscle fibers themselves.
For clinical - electrophysiological diagnosis of myopathies, other methods are available. The NMRPS should be used especially for the assessment of peripheral neuropathies. The NMRPS proved to be sensitive to primary axonal nerve damage. Thus, in neuropathic differential diagnosis of polyneuropathies, this method could help differentiate between primary axonal and primary demyelinating polyneuropathies. A quantification of axonal lesions was also possible. In addition, the method can reflect short-term changes in the responsiveness of the peripheral nerve in improving the metabolic state as in hemodialysis.