[Guillain-Barré syndrome of axonal type, Campylobacter jejuni infection and anti-ganglioside GM1 antibodies]. / Syndrome de Guillain-Barré de type axonal, infection à Campylobacter jejuni et anticorps anti-ganglioside GM1.

Infection by Campylobacter jejuni (C. jejuni) has been reported in 17 to 55 p. 100 of the GBS. The "axonal" GBS has been recently attributed to such an association. It is characterized by rapid progression to severe widespread paralysis, respiratory failure, poor and delayed recovery. The acute "axonal" form of Guillain-Barré syndrome has been and remains a matter of controversy. A typical case of GBS with serological evidence of recent C. jejuni infection and increased antibodies to GM1 is reported. An immune mechanism remains most likely. Recent studies have suggested the hypothesis of "shared epitope" between C. jejuni and peripheral nervous system cell (Gal beta 1-3 N Acetylgalactosamine epitope). Such a cross-reactivity could provoke a severe form of GBS with a poor recovery in some predisposed hosts (antiganglioside antibodies, HLA "immunogenic" groups such as B8, B35 or DR3).

Organization of the nervous control of urethral sphincter. A study in the anaesthetized cat with intact central nervous system.

The electromyographic response of the striated urethral sphincter has been evoked following stimulation of its motor nerve, the pudic nerve. Stimulation of the intact nerve fires the muscular fibres directly with a latency of approximately 1.2 msec and also in a reflex manner via the ipsilateral and contralateral pathways. The two paths transmit the reflex responses with a minimal latency of 8--10 msec (chloralose). During Halothane anaesthesia the reflex appears with a longer latency (up to 26 msec). The variability of this latency and the central delay of around 5 msec agree well with a polysynaptic central pathway. The reflex response is generally composed of an early wave of large amplitude followed by an afterdischarge lasting (between 30--60 msec) and of higher threshold. This response is triggered by the fastest afferents in the pudic nerve. The excitability of the motoneurones controlling the sphincter was tested by the double shock method and was shown to be analogous to other somatic motoneurones. The electrically evoked reflex response is slightly inhibited by bladder distension. A more powerful type of inhibition of the sphincter activity is associated with activation of the bladder motor centre.

Behaviour of the urethral striated sphincter and of the bladder in the chronic spinal cat. Implications at the Central Nervous System Level.

Nine cats were spinalized at the thoraco-lumbar junction (T12-L7) and the subsequent behaviour of the bladder and urethral striated sphincter was observed during periods of up to 27 days after spinalization by means of bladder manometry and of urethral electromyography. On the day following operation, the urethral sphincter responds to stimulation of its intact motor nerve, the pudic nerve by reflex (R) and direct (M) responses analogous to those of the intact animal anaesthetized with chloralose. The ratio R/M lies between 1 and 0.6 in the chronic spinal cat whereas it is generally less than 0.5 in the intact chloralose-anaesthetized cat. The tonic activity of the sphincter is weak or not present. The continence, however, is well maintained. The bladder activity appears only 4 to 8 days after spinalization. The bladder can thus void urine during brief contractions. These micturitions are always incomplete. The urethral reflex activity, either spontaneous or triggered by stimulation of the pudic nerve, may be inhibited, i: to a moderate degree by passive bladder distension; ii: almost completely by activation of vesicomotor neurones which provoke the bladder contraction. The first inhibition is seen the day after spinalization and is probably a protective reflex against vesical hypertension. The second inhibition develops progressively and in parallel to the functional recovery of vesical preganglionic neurones. It takes place on a background of antagnostic equilibrium of bladder and of urethral sphincter activities during micturition.