The neurological Latency is the time between a stimulus and the stimulus response. Its duration is therefore equal to the nerve conduction velocity. In medicine, the latency period can also mean the time between contact with a noxious substance and the first symptoms. The neurological latency period increases with demyelination.
The neurological latency is the time between a stimulus and the stimulus response. Its duration is therefore equal to the nerve conduction velocity.
The period of time between the perception of a stimulus and the stimulus response is called the latency period. The latency period depends on the one hand on the neurological structures involved in stimulus perception and on the other hand on the respective type of stimulus. In neurology, the latency period is the basic duration of a conduction velocity in the nervous system.
In clinical practice, however, the expression of the latency period is associated in particular with the exposure of an organism to harmful substances. These so-called noxae are absorbed by the body. Contact with the harmful substance is followed by a clinically asymptomatic interval. In this context, the latency period is the time between the effects of noxious substances such as radiation, mechanical stress or poison and the first manifestations of symptoms.
If the noxious agent is of a microbiological nature and thus corresponds to bacteria, fungi, parasites or viruses, for example, an incubation period is used instead of the latency period.
The neurological definition corresponds to the narrow definition. The damage-associated definition only corresponds in the broadest sense to an actual latency period.
Any type of latency is ultimately a delay or response time. In the case of noxious substances, the latency period consists, for example, of the time it takes for an organism to react to them. In the same sense, the neurological latency period corresponds to the reaction time that a nerve conduction needs to transmit stimuli.
The neurological latency period depends not only on the type of stimulus, but also on the type of conduction and transmission speed of all neuronal structures that are involved in the transmission of stimuli to the target organ. In most cases, the target organs are muscles.
The nervous system contains different types of conduction, the running times and structures of which are ideally matched to the desired stimulus reactions. Each nerve fiber consists of an insulating myelin sheath and the conductive content. A voltage is conducted in the line according to electrodynamic laws. As an insulator, the nerve membrane is only incomplete. The electrolyte of the nerve tract has a high resistance compared to copper veins, for example. For this reason, there is a rapid drop in voltage along the nerve fiber and nerve impulses can only be passed on over short distances.
Therefore, a change in ion permeability is also initiated by the voltage-dependent ion channels of the membranes. The run of stimuli along the nerve pathways to the response organ, such as a muscle, is the transit time or latency period.
The latency period is subject to a temperature dependency. The nerve conduction speed increases by up to 2 m / s per degree Celsius. In addition, the strength of the line has an impact on the latency. For example, thick axons transmit stimuli with higher nerve conduction speed than thin axons.
Other factors play a role in the latency period associated with noxious agents. In addition to the type of noxious agents acting, the immunological constitution of the individual can determine the latency period, for example.
The neurological latency period is measured by default in certain neurophysiological examinations. The measurement does not take place on a single nerve fiber, but relates to the sum of all responses from fibers of a particular nerve. A special case of the measurement is that of the motor transfer time. Measurable nerve tensions on the skin surface are extremely small and prone to errors. Therefore, motor nerves are stimulated to determine the latency period and the doctor derives the ability to run from the muscle response and the range between stimulation and muscle movement.
Strictly speaking, the time between the stimulus and the muscle response not only includes the latency time and with it the nerve conduction time, but also the transmission time to the respective muscle group via motor end plates. This time is around 0.8 ms. With the type of measurement described, the transmission times to the muscles must be subtracted from the determined motor transmission time in order to obtain the latency time.
If the latency period is pathological and thus slowed down, then the cause is usually demyelination of the transmitting nerves. Such demyelination is associated with either neurological diseases, mechanical nerve injuries, or poisoning. Demyelination is always referred to when the insulating myelin around individual nerve fibers has broken down or shows degenerative symptoms.
In the central nervous system, the cause of nerve demyelination can be, for example, the autoimmune disease multiple sclerosis. In this disease, the body's own immune system mistakenly sees the nerve tissue of the central nervous system as a danger and attacks central nerve tissue sections with autoantibodies that cause demyelinating inflammation. In contrast to the central nervous system, remyelination of demyelinated nerve fibers can definitely take place in the peripheral nervous system.
Demyelinations on peripheral nerves are summarized under the term neuropathy. In most cases such neuropathies are related to other diseases and are therefore only the secondary appearance of a specific primary disease. Neuropathies and the associated demyelination of peripheral nerves are sometimes observed most frequently in the context of diabetes or after exposure to neurotoxic substances. The latter connection explains, for example, why neuropathies are often observed in chronically alcohol-dependent people.