Guillain-barre and the vagus nerve

[nursingjudgment]

Hey everyone,

So I had a patient with Guillain-barre this week, and I have a few questions. First of all, it seems that this gentleman was not a typical case as he did not present with ascending paralysis. However, he did eventually go into ARF and so he was intubated and brought to the ICU for a run of IVIG. Eventually he was trached and pegged, despite an episode of pneumonia.

So here's my question: while I had him, he did not have a gag reflex. He also tended to run tachycardic (around the 120s). I mentally attributed this to loss of his vagus nerve and moved on with what were some very busy ICU days. But now that I'm at home, I'm wondering -- when you have GBS, do you lose some cranial nerves and not others? He didn't have full facial paralysis (although he did have notable weakness). Is there an 'ascension of paralysis' of the cranial nerves as well, up from the medulla to the midbrain?

Also, as I was leaving yesterday, he began to go bradycardic. Again, I assume he was hypertensive and tachycardic because his vagus nerve could not counteract his SNS responding to the natural fear/stress of being trached and pegged in an ICU. But what would be the reason for his bradycardia?

[KatieMI, BSN, MSN, RN]

Cardiac rhythm changes in GBS are usually not due to vagus nerve demielinization. They are due to injury of autonomic ganglia which are affected by demielinization like other peripheral nerves. These patients may have any arrhythmia you can think of, totally spontaneous and not related to anything. Arrhythmias is a common case of death in this population and often require pacing to for severe bradycardia and synus arrest. Abnormality of perspiration, "hot flashes", instability of body temperature and changes if pupil larynx reflexes (different and not related to injury of corresponding cranial nerves) are other symptoms of GBS autonomic dysfunction.

About 50% of GBS patients have cranial nerves involvement, of different degrees. As a rule, the "lower" the nerve, the more commonly it is involved (i.e. XII pair dysfunction is more common than V). Involvement of "uppermost" parts (IV - I) is very rare, the reason for that is unknown. The most common cranial nerves-related symptoms are weakness of neck muscles, bulb are symptoms (swallowing, gag reflex) and Bell palsy (VII pair).

[nursingjudgment]

Cardiac rhythm changes in GBS are usually not due to vagus nerve demielinization. They are due to injury of autonomic ganglia which are affected by demielinization like other peripheral nerves. These patients may have any arrhythmia you can think of, totally spontaneous and not related to anything. Arrhythmias is a common case of death in this population and often require pacing to for severe bradycardia and synus arrest. Abnormality of perspiration, "hot flashes", instability of body temperature and changes if pupil larynx reflexes (different and not related to injury of corresponding cranial nerves) are other symptoms of GBS autonomic dysfunction.

About 50% of GBS patients have cranial nerves involvement, of different degrees. As a rule, the "lower" the nerve, the more commonly it is involved (i.e. XII pair dysfunction is more common than V). Involvement of "uppermost" parts (IV - I) is very rare, the reason for that is unknown. The most common cranial nerves-related symptoms are weakness of neck muscles, bulb are symptoms (swallowing, gag reflex) and Bell palsy (VII pair).

Thanks for the response! I was still a little confused so I went and looked at some journal articles, and it looks like tachycardia is usually caused by autonomic nervous system dysfunction, while bradycardia can be caused by 1)over activity of the vagus nerve with corresponding ANS dysfunction or 2) autonomic nervous system dysfunction.

I think probably what was happening to my patient is what is described here: "Episodes of sinus arrest can happen during endotracheal suctioning in patients on ventilators, but can also happen spontaneously (as in our patient). It results from a malfunction of afferent baroreceptor reflex. Ropper et al [9] postulated that afferent baroreflex failure causes labile blood pressure and release of sympathetic efferents leading to catecholamine excess. This, in turn, sensitizes left ventricular stretch receptors and other nociceptors causing a compensatory reflex bradycardia. Manifestations of both sympathetic and parasympathetic excess may be seen in the same patient." (Journal of Medical Case Reports | Full text | Guillain Barre Syndrome with Asystole Requiring Permanent Pacemaker: A Case Report).

I hope he was alright overnight! The bradycardia was a new issue, and we don't see a lot of GBS on our floor.