How is the central auditory system involved in the acoustic startle reflex?
That is a great question because answering it requires addressing several perspectives about the acoustic startle. As always, there is the anatomy and physiology, about which our understanding has changed over the years. Then there is the professional perspective, that is, who is investigating this auditory phenomenon. Finally, there's the perspective of possible clinical applications.
The acoustic startle reflex (ASR) is best known to audiologists as a cursory test for hearing sensitivity. In audiologic testing of infants, children, or adults, a loud, abrupt sound will result in a quick, usually observable movement by the patient. Most audiologists take this response to mean that hearing sensitivity is somewhat intact. However, the ASR may mean that more than the hearing is intact. Also, hearing may be intact with an absent ASR. Therefore, it seems there is more to the ASR than audiologists may suspect.
Psychologists have long led the way in investigating and understanding this reflex. Their investigations have covered a wide range of factors that influence the ASR, only a few of which can be briefly addressed here.
One of the most critical factors is the anatomy of the startle neural circuitry. In the 1930s, the ASR circuit included the obligatory auditory periphery [external ear → middle ear → cochlea → auditory nerve] and then the central auditory system: the cochlear nucleus to the inferior colliculus to the mid-brain reticular formation to the motor neurons of the spinal cord via the medial longitudinal faciculus (MLF). It was thought that these connections provided acoustic processing in the central auditory system, attention, and muscle contraction for subsequent movement.
This anatomy was accepted until the 1980s when Mike Davis's work began to reveal a shorter circuit. This new pathway included the cochlear nucleus, to the ventral nucleus of the lateral lemniscus (VNLL), to the pontine reticular formation, to the MLF, and so on. Because the latency of the ASR in small animals was around 8 msec, this shorter circuit better fit the temporal aspects of the ASR. More recent work by Davis et al. has shortened the reflex pathway even more. This ASR circuit is as follows:
cochlear nucleus → ventral lateral pons → reticular formation (pons) → spinal motor neurons.
This circuitry allows an even quicker response in animals. Interestingly, the acoustic startle has a great range of latencies in humans, from as little as 10 msec up to 150 msec. The type of stimulus, recording techniques, and state of the organism all affect the magnitude and latency of the ASR. While most of these factors are beyond the scope of this discussion, knowing this anatomy causes the clinician to realize that multiple neural circuits are working in a certain locus and that the absence of an ASR does not necessarily mean a problem with hearing.
THE PRE-PULSE INHIBITION
Another aspect of the ASR that seems to have great clinical potential is the pre-pulse inhibition (PPI). The PPI centers around a signal (visual, tactile, or acoustic) that is at a sub-startle level that decreases the magnitude of the ASR. The PPI works when the pre-startle signal occurs approximately 30 to 500 msec before the startle signal.
The best interstimulus interval for the pre-pulse signal and the startle signal is about 100 to 120 msec. It appears that the stronger the pre-pulse signal the greater the reduction in magnitude of the ASR. For example, it has been shown that a pre-pulse signal at 70 dB creates a greater attenuation of the ASR than a 60-dB pre-pulse signal. It is noteworthy that the first pre-pulse results in a decreased ASR magnitude in animals, which indicates that learning is not necessary for this phenomenon to occur.
Humans show good test retest reliability—a favorable trait for potential clinical use. Of additional clinical interest is that pre-pulse signals close to the detection threshold can affect the ASR magnitude. Therefore, the PPI technique could possibly be used to approximate audiometric threshold by systematically decreasing the pre-pulse signal intensity until there is no effect on the magnitude of the ASR. Another consideration would be development of a device to measure the ASR in humans (this has already been done in regard to infant screening).
There is also some interesting research on the PPI of the ASR that may have potential clinical use other than approximating hearing threshold. There is some evidence that the PPI of the ASR is reduced in persons with schizophrenia, Huntington's disease, Tourette's syndrome, and ADHD. It is believed that a reduced PPI may be related to reduced attention.
It seems likely that auditory system dysfunction would affect the PPI in some manner since both the peripheral and central systems are involved in the PPI process. I feel the ASR awaits some interesting audiologic research.
1. Koch M: The neurobiology of startle. Progress Neurobiol 1999;59:107–128.
2. Yeomens J, Frankland P: The acoustic startle reflex: Neurons and connections. Brain Res Rev 1996;21:301–314.