Altered synaptic organization in facial nucleus following facial nerve regeneration: An electrophysiological study in man

Bratzlavsky, M; Eecken, H. vander

doi:10.1002/ana.410020114

Cited by 55 publications

(12 citation statements)

References 12 publications

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“…1,20 Such dysfunction consists not only of synkinetic activity, but also of muscle tightness or spasms that mostly occur during movement. 3,16,17,27 The most widely accepted pathogenetic mechanisms for such a postparalytic facial syndrome (PFS) are aberrant axonal regeneration and ephaptic transmission. 13,18,23 However, these mechanisms on their own cannot explain certain phenomena, such as the involvement of all hemifacial muscles after lesions of distal branches of the facial nerve, 16,17 or the occurrence of rhythmic myokymic discharges and the enhancement of reflex responses.…”

Section: Discussionmentioning

confidence: 99%

Reflex excitability of facial motoneurons at onset of muscle reinnervation after facial nerve palsy

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Reflex excitability of facial motoneurons at onset of muscle reinnervation after facial nerve palsy

et al. 1999

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“…Evidence of the increased responsiveness of orbicularis oculi motoneurons surviving facial nerve damage is the appearance of an R1 response evoked by contralateral SO stimulation (Bratzlavsky and vander Eecken, 1977;Nacimiento et al, 1992). In addition, Cossu et al (1999) present electrophysiological evidence of hyperexcitability of orbicularis oculi motoneurons recovering from facial palsy.…”

Section: Facial Nerve Palsy and Lid Restraint Produce The Same Blink mentioning

confidence: 97%

Lid Restraint Evokes Two Types of Motor Adaptation

Schicatano

Mantzouranis²,

Peshori³

et al. 2002

J. Neurosci.

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Unilateral reduction in eyelid motility produced two modes of blink adaptation in humans. The first adaptive modification affected both eyelids. Stimulation of the supraorbital branch of the trigeminal nerve (SO) ipsilateral to the upper eyelid with reduced motility evoked bilateral, hyperexcitable reflex blinks, whereas contralateral SO stimulation elicited normally excitable blinks bilaterally. The probability of blink oscillations evoked by stimulation of the ipsilateral SO also increased with a reduction in lid motility. The increased probability of blink oscillations correlated with the enhanced trigeminal reflex blink excitability. Thus, the trigeminal complex ipsilateral to the restrained eyelid coordinated an increase in excitability and blink oscillations independent of the eyelid experiencing reduced motility. The second type of modification appeared only in the eyelid experiencing reduced motility. When tested immediately after removing lid restraint, blink amplitude increased in this eyelid relative to the normal eyelid regardless of the stimulated SO. A patient with seventh nerve palsy exhibited the same two patterns of blink adaptation. These results were consistent with two forms of adaptation, presumably because unilateral lid restraint produced two error signals. The corneal irritation caused by reduced blink amplitude generated abnormal corneal inputs. The difference between proprioceptive feedback from the blink and expected blink magnitude signaled an error in blink amplitude. The corneal irritation appeared to drive an adaptive process organized through the trigeminal complex, whereas the proprioceptive error signal drove an adaptive process involving just the motoneurons controlling the restrained eyelid.

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“…A peripheral origin is suggested by cases of infection, tumour and vascular lesions at the root of the facial nerve, ' -5 and is supported by the favourable results obtained by intracranial facial neurolysis.68 This mechanism would depend on ephaptic interaction of nerve fibres at the level of the lesion.9-13 A central origin, causing facial neuron hyperexcitability, in both primary as well as postparalytic facial spasm, has been claimed for a long time ' 14 15 and also in recent publicatons. [16][17][18][19][20][21][22][23] The present study concerns blink reflexes obtained by trigeminal and facial stimulation in a group of 53 patients with primary hemifacial spasm. Blink reflexes were abnormal in 36 cases, in the form of either trigemino-facial hyperactivity (19 cases) or facial nerve impairment (17 cases).…”

mentioning

confidence: 99%