I can't help but wonder if your mother's atypical GBS was actually CIDP or some other variant. A lot has probably been learned since then and, as you will see from the following, there is quite a bit of variation even within "classic" GBS:
Acute Immune Polyneuropathies
http://neuromuscular.wustl.edu/antibody ... .html#cidp
"Classic" Guillain-Barré Syndrome
Chronic Immune Demyelinating Polyneuropathy (CIDP)
Prognosis worse with
- Progressive course
Pathology: More Axonal loss
Here's a bit more information regarding prognosis, as well as a reference to Lyme disease. Keep in mind this 2004 article may not reflect the latest GBS/CIDP research:
DANA L. NEWSWANGER, LCDR, MC, USNR, National Naval Medical Center, Bethesda, Maryland
CHARLES R. WARREN, LCDR, MC, USNR, Naval Hospital Jacksonville, Jacksonville, Florida
Am Fam Physician. 2004 May 15;69(10):2405-2410d
Characteristic CSF findings consist of elevated protein (higher than 0.55 g per dL [5.5 g per L]) without pleocytosis (abnormal number of cells in the CSF). CSF is often normal when symptoms have been present for less than 48 hours, but by the end of one week the level of CSF protein is elevated. An increased white blood cell count in CSF (10 to 100 per mm3 [10 to 100 ×106 per L]) in a patient with typical GBS symptoms increases the possibility of Lyme disease, neoplasia, human immunodeficiency virus (HIV) infection, sarcoid meningitis, or other diseases.7,11
GBS has five distinct subtypes: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor sensory axonal neuropathy (AMSAN), Miller Fisher syndrome, and acute panautonomic neuropathy. The axonal forms are generally thought to have poorer prognoses, indicating a need for determining the specific subtype. These subtypes are distinguished electrodiagnostically and pathologically (Table 3).2,12–16
Prognosis and Recovery
Approximately 85 percent of patients with GBS achieve a full and functional recovery within six to 12 months. Recovery is maximal by 18 months past onset. However, some patients have persistent minor weakness, areflexia, and paresthesia. Approximately 7 to 15 percent of patients have permanent neurologic sequelae including bilateral footdrop, intrinsic hand muscle wasting, sensory ataxia, and dysesthesia.7 The mortality rate is less than 5 percent in tertiary care centers with a team of medical professionals who are familiar with GBS management.2 Causes of death include adult respiratory distress syndrome, sepsis, pulmonary emboli, and cardiac arrest.34
Several factors during the acute phase of illness predict subsequent poor recovery. These factors include age older than 60 years; severe, rapidly progressive disease; and low nerve conduction amplitudes on distal stimulation, which suggests axonal loss.6 In addition, prolonged mechanical ventilation for more than one month and preexisting pulmonary disease predict a poor outcome. In general, a poor long-term prognosis is directly related to the severity of the acute episode and delay in onset of specific treatment.
And last, but not least, I found the following snippets on a GBS/CIDP forum. As most of us have learned, there are almost always exceptions to the rules set out in medical textbooks and other reference material written and used by doctors.
https://forum.gbs-cidp.org/topic/has-an ... nal-fluid/
I had my total Protein tested and it was 21 mg/dl. Have the asymetrical sensory and motor decrement. I was probable diagnosed with Multifocal form of CIDP. With this form, a percentage of patients do not have elevated protein
It’s normal to have regular protein levels with CIDP
I have had 2 normal protein lps and 1 abnormally high lp result. 5% of all gbs/cidp have normal lp results.