Timothy C. Hain, MD • Page last modified: January 1, 2017
Bulbar palsies (BPs) are syndromes in which there is weakness in the brainstem innervated (bulbar; in the head) muscles. The type of weakness is peripheral (as opposed to central), due to damage to either the muscles or the nerves to the muscles in the head. BPs can be caused by motor neuron disease (Karam et al, 2010), stroke, myasthenia gravis, botulism, multiple sclerosis (rarely), and some variants of Guillain-Barre syndrome. The most famous variant reported of bulbar palsy was called the "Miller Fisher" syndrome, named after C. Miller Fisher, and was a GB variant with ataxia and opthalmoparesis. Bulbar palsy may be congenital.The Brown-Violetto-Van Laere syndrome, is a rare variant associated with deafness (Green et al, 2010). There are various sporadic reports of patients with bulbar palsy, and various viruses. Radiation to the head has been reported to cause a delayed progressive bulbar palsy in some. (Shapiro et al, 1996)
Pseudo-bulbar palsy means that the muscles in the face are weak, but the problem is not in the nerve or muscle, but rather in the parts of the brain that control these nerves and muscles. Patients with pseudo-bulbar palsy, generally can move their face to a much greater extent, but sometimes have a peculiar "emotional incontinence", where they laugh or cry very easily.
Typical symptoms of bulbar palsy include slowed or paralyzed eye movements, facial weakness, slurred speech (dysarthria or nasal), gait disturbance and dizziness. The recent literature seems to be "splitting" up patients, with the idea that certain presentations are associated with particular antibodies. If this follows the usually pathway for autoimmune brain disease -- one can get a paper published by claiming that an antibody has some meaning -- this idea will provoke many papers, that will eventually turn out to be much ado about nothing.
There have been numerous reports of bulbar palsy with antibodies to various gangliosides.
- Kim et al (2016) discussed a particular form of Guillain Barre that they termed "ABP-plus", for acute bulbar palsy, often associated with IGG anti-GT1a, or anti GQ1b.
- Barone et al (2016) discussed another variant without ophthalmoplegia, associated with anti-GD3 IGM antibodies.
- Onodera et al, 2002; Yoshino et al, 2000 and Koda et al (1999) reported variants of guillain barre with antigangliosides.
- Mehta reported another case with anti-GM2 antibodies.
- Koga (1999) reported that anti-GT1a was NOT associated with bulbar palsy. They suggested that other antibodies were more important (e.g. anti GQ1b).
- Hashiguchi et al (1997) reported Guillain-Barre with anti-GT1a.
Lametery et al (2016) reported PCB -- pharyngeal-cervical brachial syndrome, a bulbar palsy, without ataxia. Basically Miller Fisher without ataxia.
Patients with autoimmune variants of bulbar palsy may be treated with IVIG infusions. The other types of bulbar palsy may or may not have a specific treatment, depending on their cause.