If the neurographic findings of the distal nerve segments show normal values (short distances in each case), but the minimum F-latency is prolonged, is this an indication of a slowing of only the proximal nerve segment? Or does this indicate a general reduction in nerve conduction velocity over the entire nerve, as in polyneuropathy?
The simple answer is that prolonged F-latency and slow velocity in distal segments (forearm, leg) indicates proximal slowing. This pattern is seen in e.g. GBS. Stålberg
Unfortunately not. Technical errors, anomaly give H-reflex at sligtly different muscle. Asbcense not absolute signs of pathology. Latency difference is more reliable
Thank you for sharing your knowledge and experience. I have a few questions and ambiguities about F-waves. Since F waves usually originate from only a few percent of motor neurons, their latency practically never reflects the fastest fibres, but the majority of fibres with medium speed (corresponding to the middle of the Gaussian distribution). Does this explain why the minimum F latency remains very stable in several successive examinations? Or is there a preference for thickly myelinated fast fibres in the F waves? Another question relates to the significance of the amplitude and duration of the F waves, possibly also in the bilateral comparison. Do both parameters only have something to do with the excitability of the motoneurons? On the other hand, I had understood that axonal reinnervation processes with enlargement of the motor unit also increase both parameters (amplitude and duration). Is this correct? Occasionally, when registering F-waves, despite a stable and artefact-free baseline, one sees individual potentials between M-response and F-waves, but these are clearly separated from the F-waves and also do not correspond to A-waves. Are these phenomena of hyperexcitability such as fasciculations? Thank you for your support.
Alexander I try my best to reply I agree, that there is a distributions of arrival times. Shortest latency is not necessarily fastest, since responses my come from different roots, i.e. different distance, may have different central delay. People have not agree that shortest latency represent fastest axons. I do not think that ampl or dur is related to excitability. The parameters increase after reinnervation. Each F wave is a surface recorded motor unit potential, and so parameters follow the rule. Signals between CMAPP and F. There are 2 possibilities. But first of all, an explanation. If suprastimulation is used (all axons to that muscle are stimulated), then they cannot be voluntary signals, because of proximal blocking of antidromic stim impulse and ortodromic F-wav es. Now, one possibility is that you have not been able to stimulate all axons (weak stimulation of very inexcitable axons in disease). The other possibility is that they represent fasciculations starting peripherally (like in ALS).
Does the physiological chronodispersion of F-latencies reflect the range of motor nerve conduction velocities? Or is the range of F-latencies smaller than the different nerve conduction velocities would suggest? I did not understand why chronodispersion increases in the case of spasticity. I previously thought that spasticity was a central phenomenon and therefore increased the amplitude and duration of F waves. What is the cause of the increase in chronodispersion of the F-waves?
Alexander In spasticity, more neurons are active. Without my own studies, I suggest that since the number of F waves with their distribution of latencies, it will be a large chance of increasing both latency and duration and chrono dispersion.@@alexanderrose189
This is awesome Dr. Stalberg! I'm going to link up your channel for other technologists :) Thank you!
That is amazing. We are trying to len EMG ourselves. Your videos are very helpful.
Glad to har
Erik Stålberg
Good luck
Erik S
❤❤❤❤
If the neurographic findings of the distal nerve segments show normal values (short distances in each case), but the minimum F-latency is prolonged, is this an indication of a slowing of only the proximal nerve segment?
Or does this indicate a general reduction in nerve conduction velocity over the entire nerve, as in polyneuropathy?
The simple answer is that prolonged F-latency and slow velocity in distal segments (forearm, leg) indicates proximal slowing. This pattern is seen in e.g. GBS.
Stålberg
Thanks, can I rely on on only absent H-reflex for diagnosing S1 radiculopathy?
Unfortunately not. Technical errors, anomaly give H-reflex at sligtly different muscle. Asbcense not absolute signs of pathology. Latency difference is more reliable
Thank you for sharing your knowledge and experience.
I have a few questions and ambiguities about F-waves. Since F waves usually originate from only a few percent of motor neurons, their latency practically never reflects the fastest fibres, but the majority of fibres with medium speed (corresponding to the middle of the Gaussian distribution). Does this explain why the minimum F latency remains very stable in several successive examinations? Or is there a preference for thickly myelinated fast fibres in the F waves?
Another question relates to the significance of the amplitude and duration of the F waves, possibly also in the bilateral comparison. Do both parameters only have something to do with the excitability of the motoneurons? On the other hand, I had understood that axonal reinnervation processes with enlargement of the motor unit also increase both parameters (amplitude and duration). Is this correct?
Occasionally, when registering F-waves, despite a stable and artefact-free baseline, one sees individual potentials between M-response and F-waves, but these are clearly separated from the F-waves and also do not correspond to A-waves. Are these phenomena of hyperexcitability such as fasciculations?
Thank you for your support.
Alexander
I try my best to reply
I agree, that there is a distributions of arrival times. Shortest latency is not necessarily fastest, since responses my come from different roots, i.e. different distance, may have different central delay. People have not agree that shortest latency represent fastest axons.
I do not think that ampl or dur is related to excitability.
The parameters increase after reinnervation. Each F wave is a surface recorded motor unit potential, and so parameters follow the rule.
Signals between CMAPP and F. There are 2 possibilities. But first of all, an explanation. If suprastimulation is used (all axons to that muscle are stimulated), then they cannot be voluntary signals, because of proximal blocking of antidromic stim impulse and ortodromic F-wav es. Now, one possibility is that you have not been able to stimulate all axons (weak stimulation of very inexcitable axons in disease). The other possibility is that they represent fasciculations starting peripherally (like in ALS).
Does the physiological chronodispersion of F-latencies reflect the range of motor nerve conduction velocities? Or is the range of F-latencies smaller than the different nerve conduction velocities would suggest?
I did not understand why chronodispersion increases in the case of spasticity. I previously thought that spasticity was a central phenomenon and therefore increased the amplitude and duration of F waves. What is the cause of the increase in chronodispersion of the F-waves?
Alexander
In spasticity, more neurons are active. Without my own studies, I suggest that since the number of F waves with their distribution of latencies, it will be a large chance of increasing both latency and duration and chrono dispersion.@@alexanderrose189
Favor traducir a español
Puedes activarla traduccion simultanea , si no lo sabes hacer lo puedes hacer con tu movil con el traductor de googel