Electroacupuncture-induced cannabinoid receptor expression in repair of abducens nerve.

Objective: Through the development of beagle abducens nerve injury model, taking electroacupuncture as the core and microglia as the starting point, the author investigated whether electroacupuncture can promote the repair of injured abducens nerve by cannabinoid receptor-mediated regulation of microglia activation. Methods: Healthy beagle dogs were randomly divided into five groups: sham operation group (A), injury group (B), electroacupuncture pretreatment group (C), antagonist group (D) and solvent group (E). After stimulation with electroacupuncture, the expression of cannabinoid 1 receptor (CB1R) and cannabinoid 2 receptor (CB2R) in A, B and C microglia cells was detected by Western Bolt analysis, and further the expression of CB2R in five groups was further analyzed by immunofluorescence, thereby statistical differences were analyzed. Results: Among group A, group B and group C, Western Blot analysis showed that there were no significant changes in the expression of CB1R protein after electroacupuncture [F (2, 12)=1.75, p = 0.215]. After electroacupuncture preconditioning for 15 min for 2 weeks, group C was compared with group A and group B, which showed CB2 was affected. The expression of CB2R protein was significantly increased among groups A, B and C [F (2, 12)=5189.57, p < 0.001], but there was no significant difference in the expression of CB2R protein between group A and group B (p > 0.05). The results of immunofluorescence showed that Arginse/CD11b was significantly increased in group C comparing to group A (*p < 0.001), while there was a significant increase in group E comparing to group A about Arginse/CD11b [F (4, 20)=4345.44, p < 0.001]. Conclusions: The CB2R in the cannabinoid receptor is mainly involved in the electro-acupuncture-induced neuroprotection. Electroacupuncture can promote the repair of injured abducens nerve by CB2R-mediated activation of microglia.

Physiotherapy in Postinfection Injury to Cranial Nerves III, IV, and VI: A Case Study.

The patient with bacterial infection sequelae in the form of damage to cranial nerves III, IV, and VI was followed up. He had exhibited clinical and radiographic signs of paranasal sinusitis. Before his physiotherapy, the patient received standard treatment with natural and synthetic antibiotics and steroids. After acute signs of infection resolved without any functional improvement, the patient was referred to a rehabilitation unit to undergo neuromuscular re-education of the paralyzed extraocular muscles. Periorbital hydrocortisone iontophoresis and visuomotor exercises with intense ideomotor stimulation led to complete and rapid resolution of extraocular muscle paralysis and diplopia. Physiotherapy can be an effective treatment of choice after failed pharmacological treatment in patients with damage to cranial nerves III and VI. It has many theoretical advantages, including noninvasiveness and avoidance of first-pass metabolism of drugs administered systemically.

Abducens Nerve Avulsion and Facial Nerve Palsy After Temporal Bone Fracture: A Rare Concomitance of Injuries.

BACKGROUND: Avulsion of the abducens nerve in the setting of geniculate ganglion injury after temporal bone fracture is unreported previously. We discuss clinical assessment and management of a patient with traumatic avulsion of cranial nerve (CN) VI in the setting of an ipsilateral CN VII injury after temporal bone fracture and call attention to this unusual injury. CASE DESCRIPTION: A 26-year-old man suffered a temporal bone fracture after a motor vehicle accident and developed diplopia and right-sided facial droop. Six weeks after the accident, the patient was readmitted with worsening diplopia and ipsilateral facial weakness. He demonstrated absent lateral gaze on the right suggestive of either restrictive movement or right. CN VI DEFICIT: In addition, he had right-sided facial palsy graded as 6/6 House-Brackmann. High-resolution computed tomography demonstrated a right-sided longitudinal otic capsule-sparing temporal bone fracture that propagated into the facial nerve canal and geniculate fossa. Magnetic resonance imaging revealed discontinuity of the right CN VI between the pons and the Dorello canal, as well as injury to the ipsilateral geniculate ganglion. CN VII was intact proximally, from the pons through the internal auditory canal. Consensus was reached to proceed with conservative management. At 13 months after injury, the patient reported 1/6 House-Brackmann with no improvement in CN VI function. CONCLUSIONS: This case illustrates 2 subtle findings on imaging with potential therapeutic implications, notably the role of surgical intervention for facial nerve palsy.