Horner Syndrome in 2 Pigs (Sus scrofa) after Vascular Grafting of the Carotid Artery and Jugular Vein.

The term Horner syndrome refers to the clinical presentation of oculosympathoparesis, comprising miosis, ptosis, and facial anhydrosis. To date, there are 2 reports of postoperative Horner syndrome in pigs. In this species the cervical sympathetic chain and cranial cervical sympathetic ganglion are consistently within the carotid artery sheath. This case study describes the sudden onset of Horner syndrome in 2 pigs, from a study cohort of 8, after the placement of a vascular graft between the carotid artery and external jugular vein. Anesthesia and surgery was uneventful in all the pigs in the study, but 2 pigs demonstrated clinical signs including ptosis, enophthalmos and prolapse of the nictitating membrane immediately after recovery from anesthesia. Horner syndrome was diagnosed in light of the clinical signs. These clinical signs persisted throughout the 2-mo study period and did not appear to improve or deteriorate in that time. Gross examination of the surgery site at the end of the study did not reveal an obvious lesion in the carotid artery sheath. The risk of Horner syndrome after surgery involving the carotid artery in pigs had not been reported prior to this study. Without specific measures to protect the cervical sympathetic ganglion during surgery, the incidence of postoperative Horner syndrome was 25% in our population of pigs. Although the welfare implications of this syndrome are minimal, concerted effort to avoid intraoperative damage to the cervical ganglion is essential for future work.

Aberrant facial flushing following monobloc fronto-facial distraction.

BACKGROUND: Patients with syndromic forms of craniosynostosis may experience functional problems such as raised intracranial pressure, proptosis, obstructive sleep apnoea and failure to thrive. The monobloc fronto-facial advancement with osteogenic distraction is increasingly used to correct these functional problems in one procedure as well as improve appearance. The authors report the phenomenon of post operative aberrant facial flushing - an unusual and previously unreported complication of the procedure. METHODS: The case notes of 80 consecutive patients undergoing fronto-facial advancement by distraction using the rigid external distraction device (RED) were reviewed for features of aberrant facial flushing. RESULTS: Four out of eighty individuals developed facial flushing after monobloc fronto-facial distraction using the rigid external distractor (RED) frame. All were female with Crouzon or Pfeiffer syndromes causing the severe functional problems for which they underwent the surgery. They were aged 6-8 years. Following removal of the frame, they developed intermittent but severe facial flushing. The flushing spontaneously settled in three patients after up to four years but persists in the other child seven years after her surgery. CONCLUSION: Aberrant facial flushing is a rare but significant complication of monobloc fronto-facial surgery. It occurred in 4 of our 80 (5%) patients. The skull base osteotomies essential for the procedure are made anterior to the pterygopalatine ganglion and it is our contention that damage from these was responsible for a neuropraxia of its efferent nerve branches. A review of the autonomic control of the facial vascular system suggests that the phenomenon is due to an unequal process of recovery that leaves the cutaneous vasodilating parasympathetic or beta-adrenergic innervation relatively unopposed - a situation that persists until with time a normal balance of autonomic input is achieved.

Transient internal ophthalmoplegia after inferior oblique myectomy.

Internal ophthalmoplegia causing pupillary dilatation and loss of accommodation following damage to the ciliary ganglion is a rare complication of strabismus surgery. Here we report a case of parasympathetic neuropraxia resulting in transient internal ophthalmoplegia after inferior oblique myectomy in a 12-year-old girl. Short-term symptomatic relief was achieved with 1% pilocarpine. Normal visual function returned over several months.

Persistent inappropriate sinus tachycardia after radiofrequency ablation of left lateral accessory pathway.

A patient with palpitations and narrow QRS tachycardia was evaluated. In the EP study an atrioventricular reentrant tachycardia mediated by a left lateral accessory pathway was identified and catheter ablation was performed with success. A week later she returned with palpitations and pre-syncope. The resting ECG showed a sinus tachycardia with 110 bpm. After unsuccessful clinical treatment with beta-blockers, diltiazem and digoxin she underwent sinus node modification using radiofrequency catheter ablation with success. We postulated that RF application to ablate the lateral accessory pathway damaged the parasympathetic innervation in the left atrioventricular groove, causing inappropriate sinus tachycardia.

Polysialylated neural cell adhesion molecule is involved in the neuroplasticity induced by axonal injury in the avian ciliary ganglion.

We demonstrated previously in the quail ciliary ganglion, that the immunoreactivity for the neural cell adhesion molecule labeling the postsynaptic specializations of intraganglionic synapses decreases when synaptic remodeling is induced by crushing the postganglionic ciliary nerves. Here we show, in the same experimental conditions, that the immunolabeling for its polysialylated non-stabilizing isoform, which promotes cell plasticity, increases at these subcellular compartments. In control ganglia, poor immunolabeling for the polysialylated neural cell adhesion molecule was occasionally observed surrounding the soma of the ciliary neurons, in correspondence with the calyciform presynaptic ending and the perineuronal satellite cells sheath. At the electron microscope, several neuronal compartments, including some postsynaptic specializations, somatic spines and multivesicular bodies, were immunopositive. Three to six days after ciliary nerve crush, both the number of ciliary neurons labeled for the polysialylated neural cell adhesion molecule and the intensity of their immunolabeling increased markedly. Electron microscopy revealed that, in parallel to the injury-induced detachment of the preganglionic boutons, numerous postsynaptic specializations were found to be immunopositive. Twenty days later, when intraganglionic connections were re-established, polysialylated neural cell adhesion molecule immunoreactivity was comparable to that observed in control ganglia. The increase in immunolabeling also involved the other neuronal compartments mentioned above, the perineuronal satellite cells and the intercellular space between these and the ciliary neurons. From these results we suggest that the switch, at the postsynaptic specializations, between the neural cell adhesion molecule and its polysialylated form may be among the molecular changes occurring in axotomized neurons leading to injury-induced synaptic remodeling. Moreover, from the increase in polysialylated neural cell adhesion molecule immunolabeling, observed at the somatic spines and at the interface between neurons and perineuronal satellite cells, we suggest that this molecule may be involved not only in synaptic remodeling, but also in other more general aspects of injury-induced neuronal plasticity.

The rise in cytoplasmic ubiquitin levels is an early step in the response of parasympathetic ganglionic neurons to axonal injury followed by regeneration.

We investigated the involvement of ubiquitin in the neuronal response to axonal injury in the quail parasympathetic ciliary ganglion by immuno-light and electron microscopy. Image analysis of immunoreacted cryosections shows that ubiquitin-immunoreactivity in the ciliary neurons increases significantly 6 hours after postganglionic nerve crush. The immunolabeling reaches a peak 1 day after injury and begins to decrease between days 3 and 6 when, in contrast to the cytoplasm, numerous highly eccentric nuclei are strongly immunolabeled. Electron microscopy shows ubiquitin-immunoreactivity associated with cytoplasmic organelles and with several postsynaptic densities of the numerous synapses established by the preganglionic boutons on the soma of the ciliary neurons. The number of immunopositive postsynaptic densities increases significantly 1 day after axonal damage, followed by temporary detachment of the preganglionic boutons from the injured neurons between days 3 and 6. The early increase in cytoplasmic ubiquitin-immunoreactivity suggests a prompt ubiquitination of damaged proteins addressed to degradation, while the nuclear immunolabeling may reflect high histone ubiquitination, a process involved in keeping chromatin transcriptionally active. The possible ubiquitin-mediated removal of postsynaptic apparatus constituents such as ACh receptors, proteins involved in their clustering and stabilization, and/or adhesion molecules may be a crucial step for the detachment of the preganglionic boutons, thus favoring injury-induced synaptic plasticity.