Facial Palsy and albumine – cellular dissociation in CSF – Forme fruste of Guillain-Barré-Syndrome?

The aetiology of facial palsy is protean. Also in acute peripheral neuropathy, Guillain-Barré-Syndrome (GBS), facial palsy may occur as well as in Miller – Fisher – Syndrome, a variant of GBS, characterized by ophthalmoplegia, ataxia and areflexia.

We report on a patient with unilateral facial palsy as the only abnormal neurological symptom and findings in CSF typical for GBS.

The 12 year old boy presented with right facial palsy that occurred one day before, the further neurological examination being normal. The patient himself reported about painful legs and impairment of ocular movements some days before.

IgM and IgG antibodies against B. burgdorferi were negative in serum and CSF in all 3 samples. Oligoclonal IgG was negative. GQ1b – IgG was slightly elevated in serum (13,7 Antibody-ratio, normal range <10), whereas GQ1b – IgG in CSF, GQ1b – IgM in serum and CSF were normal. The cranial MRI was normal. The EMG of the right facial nerve was consistent with a recent neurogenic damage, MEP demonstrated a conduction – impairment.

The facial palsy showed nearly complete spontaneous remission after 6 weeks without anti-inflammatory or antibiotic treatment.

The facial palsy in addition to the CSF – findings with „dissociation albumino – cytologique“ is consistent with a GBS. The painful legs may have been symptoms of a neuropathy that had resolved at the time of admission.

The case report illustrates the variability of GBS with possible monosymptomatic course facial palsy being the only neurological sign. In this case, immediate treatment does not seem to be necessary.

	protein	cell-count	CSF protein-analysis
On admission	1753mg/l	3/3	severe impairment of barrier- function
After 10 days	1303mg/l	11/3
After 1 month	595mg/l	10/3	mild impairment of barrier – function