| Transcript |
So, today, I'm going to tell you a little bit about peduncular hallucinosis which is a very strange sounding term. However, it does help us understand where the lesion is. It's a cerebral peduncle, even though it's really not the peduncle that's involved. And it's a hallucination, but it's a weird kind of hallucination, so it's a hallucinosis. And basically, these types of hallucinations, in these patients, are very vivid. They're extremely realistic and detailed. And often, they are familiar to the patient, so whatever they're seeing-an animal, a favorite pet, a dog, a person-they know the individuals or they know the animal. So, it's vivid, realistic, familiar, and formed, and so, it's usually like animals or people. And the thing that's weird about peduncular hallucinosis is, that word, "peduncular," (the cerebral peduncle) tells us that really it's one of these very strange localizations. And, in this case, the midbrain, and so, the lesions are often at the thalamic mesencephalic junction or the midbrain and that's the peduncle part, so it's a brainstem lesion. And that's a very strange concept because, as you know, the afferent visual pathway does not go to the brainstem, but I'm gonna show you how it does go there and how this could potentially be related to a patient who has a pontine or a midbrain lesion or a thalamic lesion might have a visual hallucination. So, as you know, the input to the eye-retina, optic nerve, chiasm, the usual thing, geniculate body radiations, and the cortex. So, all of that is a fairly straightforward pathway that's axially oriented. However, there's this longitudinal pathway, as well, which is an accessory pathway. And you might know about the reticular activating system which is our arousal mechanism and keeps us awake. And so, disruption of the reticular activating system can disrupt arousal and can make you go unconscious-like get knocked out in a boxing ring, for example. This accessory pathway is not really talked about a lot, but it's basically there as a filter of some kind and it probably also is involved in maintaining sleep-wake cycles and getting input from melanopsin ganglion cells and light reflexes and a whole bunch of other reasons why you wouldn't want to devote any kind of cortex, like your occipital cortex, to maintaining this type of visual information. And the reason it's important is that ascending pathway is an inhibitory pathway so...so when we inhibit the pathway, we are suppressing this excess noise. So it's a signal to noise suppression system because you're constantly bombarded by excess signals. That happens a lot, for example, when you're first waking up in the morning or when you're going to bed, so these we call hypnagogic and hypnopompic. So, the hallucinations can occur right when you're trying to turn off the reticular activating system and go to sleep. And that's why you have to close your eyes, probably, and turn off the lights right before you go to sleep because you want to you want to turn everything down, so that kind of signal turn off the light, turn off the consciousness, these are kind of linked together in the process of deactivating and going to the REM sleep. And so, when we inhibit that process these release hallucinations might come out, so this, to me, is a form of release hallucination because of loss of the inhibition and that lets this vivid, realistic, familiar form hallucination come out even though your lesion is in the midbrain or the pons. And that, we call, peduncular hallucinosis. It's very similar to a different kind of release hallucination called the Charles Bonnet syndrome. The Charles Bonnet syndrome is similar to the release hallucination of the peduncular hallucinosis in that it's often vivid, realistic, and formed. In contrast, the Charles Bonnet, usually the patient is not familiar with the person or the object and there's some overlap between the two types of release hallucinations. Both of them require that you have insight into the phenomenon, so you have to know that it's not real. The second thing is there can't be any auditory component, so we really can't have it speak to us, it can't really talk to us. There can't be any DSM-5 diagnosis which is delusional constructs, psychiatric illnesses, and you really can't have any kind of drugs on board that are hallucinogens or any other things that could cause this. They have to be awake, alert, and oriented. And in the Charles Bonnet syndrome, it's because you have decreased vision or decreased visual field. So that is the key and differentiating feature between the two release phenomena. They're both release. One is from decreased vision releasing the hallucination. The other is releasing the inhibitory signal releases it. And then, peduncular hallucinosis, there's no loss of acuity, there's no loss of field, but you still have to have good insight, no auditory component, no DSM-5 diagnosis, no drugs that could cause it, be awake, alert, and oriented. So you need to know about a brainstem cause of hallucinations. Peduncular hallucinosis. |
