Relapse one year later…anyone else?

Michael,
I just went back & read all of your old posts. It seems that your symptoms did not come on rapidly (such as in 48 hours), but they came on over the course of weeks. Also, you did not go completely paralyzed, nor did you have breathing problems. Assuming you had a “mild case” of GBS, you were still having symptoms long after you should have made a faster recovery.

All of this leads me to think you are probably dealing with CIDP & not GBS. I was just wondering how long has it been since you had any IVIG infusions? When you did, did you make a fairly rapid recovery? No one wants to have CIDP, but there are many treatment options out there that I think you may not have explored when the doctor changed your dx to GBS. Please keep us posted or feel free to email me.

Pam

michael,

ct in both hands is unlikely. chalk it up to gbs or hopefully not cidp. recurring gbs is also a possible Dx. your neuro does not want to mislabel recurring w chronic [cidp]. a tough call. if he ever Dxes you w cidp, the Rx should be ivig at intervals [usually 6 weeks]. this covers 2 bases. it keeps a cidper from getting those nasty other meds & if you are really recurring gbs, those nasty meds are counterproductive to gbs. 3% of gbsers get another gbs attack. these are not cidp cases. take care. be well.

gene gbs 8-99
in numbers there is strength

[B]RECURRENCE[/B]
[B]Recurrent Guillain Barre’ Syndrome: a clinical, electrophysiological and morphological study.[/B]
[B]Taly AB, Gupta SK, Anisya V, Shankar SK, Rao S, Das KB, Nagaraja D, Swamy HS.[/B]

J Assoc Physicians India 1995 Apr;43(4):249-52 Abstract quote Of the 220 patients of acute idiopathic demyelinating polyneuritis (AIDP/GBS) seen over a seven year period, 15 patients (M:F:11:4) had a relapsing course (6.8%).
Their ages ranged from 8 yrs to 70 yrs. They had 36 episodes at a variable interval of 3 months to 25 yrs. Relapse rate varied from one to four. Antecedent events were noted during 16 episodes in 9 patients but the triggering factors were varied. Clinical features of individual episodes were similar to the acute monophasic illness, although they differed inseverity from one episode to the other. Autonomic disturbances were rare. Albuminocytological dissociation was observed during 19 of the 24 episodes.
Electrophysiological abnormalities were observed during 19 of the 24 episodes. Electrophysiological abnormalities were present in all and were comparable with patients of non-recurrent illness. Sural nerve biopsy in 3 patients showed evidence of demyelination, remyelination, Wallerian degeneration and myelin breakdown but none had features of inflammation. With the exception of one death, functional recovery was complete in the majority of patients, irrespective of the type of therapeutic intervention.
Acute onset, frequent facial involvement, brief clinical course, near complete recovery and very long asymptomatic periods may distinguish these patients of acute relapsing demyelinating polyneuropathy (ARDP) from chronic relapsing demyelinating polyneuropathy.
Relapses in GBS are however unpredictable and recurrent GBS is indistinguishable clinically, electrophysiologically and morphologically from the more frequently seen non-recurrent form of monophasic GB Syndrome. A biochemical or immunological marker may help in this distinction.

[B]Recurrent Guillain-Barre syndrome. Clinical and laboratory features.[/B]
[B]Grand’Maison F, Feasby TE, Hahn AF, Koopman WJ.[/B]
[B]Department of Clinical Neurological Sciences, Victoria Hospital, University of Western Ontario, London, Canada.[/B]

Brain 1992 Aug;115 ( Pt 4):1093-106 Abstract quote The clinical and laboratory features of recurrent Guillain-Barre syndrome (RGBS) were reviewed in 12 patients in whom a total of 32 episodes fulfilled accepted criteria for Guillain-Barre syndrome (GBS). All patients were asymptomatic or only mildly symptomatic between attacks. In a given patient, the time to reach peak deficit from the onset of symptoms, the functional grade at peak deficit and the duration of the intervals between episodes varied considerably and unpredictably from one episode to the next. Analysis of these parameters across the entire group revealed no significant change as the number of attacks increased. The distribution of weakness varied between episodes with the possible exception of features of the Miller Fisher variant which were more constant. Tremor was noted in two patients and enlarged nerves in one patient. There was no evident response to immunosuppressive therapy. Results of cerebrospinal fluid (CSF) analysis and nerve conduction studies during recurrences were those expected in typical monophasic GBS. On nerve biopsy, onion bulb formations were sometimes observed after several recurrences. The following characteristics of RGBS may be sufficiently distinctive from those of chronic relapsing polyneuropathy to justify their nosological separation: rapid onset of symptoms with subsequent complete or near complete recovery, high incidence of an antecedent illness, lack of an apparent response to immunosuppressive therapy and normal CSF protein levels at the onset of a recurrence.

[B]Acute relapsing Guillain-Barre syndrome after long asymptomatic intervals.[/B]
[B]Wijdicks EF, Ropper AH.[/B]
[B]Neurological/Neurosurgical Intensive Care Unit, Massachusetts General Hospital, Boston 02114.[/B]

Arch Neurol 1990 Jan;47(1):82-4 Abstract quote Five patients who recovered from an initial episode of Guillain-Barre syndrome had acute relapses 4, 10, 15, 17, and 36 years later, respectively. Two patients had multiple subsequent relapses.
The antecedent illnesses, distribution of weakness, and clinical courses of each relapse were similar for each patient, except that relapses in three patients were briefer than the initial episode. One patient had asymptomatic sarcoidosis. Pharyngeal, oculomotor, and diaphragmatic weakness requiring a ventilator were common.
Complete recovery or mild residual deficits, return of reflexes, normal cerebrospinal fluid protein at the onset of recurrent episodes, and normal or virtually normal nerve conduction velocities at various times distinguished these patients from those with more typical chronic relapsing inflammatory polyneuropathy.