Vagus Nerve Stimulator Placement in Dogs: Surgical Implantation Technique, Complications, Long-Term Follow-Up, and Practical Considerations.

OBJECTIVE: To describe a modified implantation procedure of a vagus nerve stimulation (VNS) device in dogs and to report short- and long-term complications. STUDY DESIGN: Descriptive, experimental study. ANIMALS: Healthy, adult Beagle dogs (n = 10). METHODS: A VNS Therapy(®) System was implanted in the left cervical region of anesthetized dogs. During and within 48 hours after surgery, electrocardiography (ECG) and impedance testing of the system were performed. Dogs were monitored daily and the impedance of the system was determined regularly until VNS devices were surgically removed 3 years after implantation. RESULTS: The implantation procedure was successful in all dogs without intraoperative complications. ECG monitoring and impedance tests were within normal limits during and within 48 hours after surgery. Postoperative seroma formation was common (70%). One dog developed an irreversible Horner's syndrome leading to removal of the device 5 months after implantation. Another dog developed trauma-induced damage of the lead requiring surgical revision. The device could be safely removed in all dogs; however, electrodes were left in place to avoid nerve damage. At removal, the anchor tether was dislodged in 40% of dogs and the lead was twisted in 50% of dogs. CONCLUSION: Implantation of a VNS Therapy(®) System is safe and feasible in dogs; however, seroma formation, twisting of the lead, and dislodgement of the anchor tether were common. Practical improvements in the technique include stable device placement, use of a compression bandage, and exercise restriction. Regular evaluation of lead impedance is important, as altered values can indicate serious complications.

Regional brain perfusion changes during standard and microburst vagus nerve stimulation in dogs.

PURPOSE: Vagus nerve stimulation (VNS) is an effective adjunctive treatment for refractory epilepsy in humans, but its mechanism of action (MOA) and optimal stimulation parameters are still unknown. Functional neuroimaging studies could provide better insight into the brain structures involved in the activity of VNS, but have not yet been described in dogs. The aim of this study was to investigate the effect of acute VNS on the regional cerebral blood flow (rCBF) in dogs using micro-SPECT (µ-SPECT). Additionally, a novel stimulation paradigm (microburst VNS) was used and compared with standard VNS. METHODS: A VNS Therapy System was implanted in ten Beagle dogs. µ-SPECT was performed after sham, standard and microburst VNS in a randomized, cross-over study. Nineteen volumes of interest (VOIs) were semi-quantitatively analysed and perfusion indices (PIs) were calculated. Furthermore, a rostro-caudal gradient (R-C), an asymmetry index (AI) and a cortical-subcortical index (Co-SCo) were determined. The SPECT results after standard and microburst VNS were compared pairwise with sham stimulation. RESULTS: Acute standard VNS did not cause significant rCBF alterations. Acute microburst VNS caused a significant hypoperfusion in the left frontal lobe (P=0.023) and in the right parietal lobe (P=0.035). Both stimulation paradigms did not cause changes in R-C, AI nor Co-SCo. CONCLUSIONS: Microburst VNS is more potent than standard VNS to modulate the rCBF in the dog. Our results promote further research towards the antiepileptic effect of microburst VNS in dogs and humans.

Surgical treatment of disk-associated wobbler syndrome by a distractable vertebral titanium cage in seven dogs.

OBJECTIVE: To evaluate a distractable titanium cage for the treatment of disk-associated wobbler syndrome (DAWS). STUDY DESIGN: Prospective study. ANIMALS: Dogs (n = 7) with DAWS. METHODS: After total discectomy of C5-C6 and C6-C7, the median part of the vertebral body of C6 was removed with preservation of the lateral walls and dorsal cortex. The removed cancellous bone was collected. The implant was placed in the bony defect of C6. After placement, the titanium cage was distracted and affixed by 4 screws. Finally, the implant was filled and covered with cancellous bone. Dogs had follow-up examinations at 1, 3, 6, 12, and 24 months. Six months after surgery, cervical radiographs and computed tomography (CT) were performed. RESULTS: Although no intraoperative complications occurred, correct placement of the cage was technically challenging. Revision surgery was necessary in 2 dogs because of implant loosening and aggravation of vertebral tilting. All dogs improved after discharge from the hospital. In 1 dog, recurrence of clinical signs caused by articular facet proliferation at an adjacent intervertebral disk space occurred. Radiographs at 6 months demonstrated cage subsidence in 4 dogs. In all dogs, CT was suggestive for fusion of the bone graft with the vertebral body. CONCLUSIONS: Although results are promising, technical adaptations will be necessary to make this specific surgical technique, designed for humans, suitable for routine use in dogs.

Surgical treatment of a canine intranasal meningoencephalocele.

OBJECTIVE: To report the clinical signs, diagnosis, and surgical treatment of an intranasal meningoencephalocele in a dog. STUDY DESIGN: Case report. ANIMAL: Female Border collie, 5 months old. METHODS: A right intranasal meningoencephalocele was identified by computed tomography and magnetic resonance imaging. RESULTS: The lesion was approached by a modified transfrontal craniotomy. Surgical closure of the defect at the level of the cribriform plate and removal of extruded brain tissue resulted in regression of lacrimation and coincided with absence of seizuring. Treatment with phenobarbital was gradually reduced and stopped at 7 months after surgery. At 28 months the dog remained free of seizures. CONCLUSION: Meningoencephalocele, although rare, can cause seizures in dogs and can be treated surgically. CLINICAL RELEVANCE: A transfrontal craniotomy with excision of the meningoencephalocele and closure of the defect can be an effective treatment for an intranasal meningoencephalocele in dogs.

Magnetic stimulation of the radial nerve in dogs and cats with brachial plexus trauma: a report of 53 cases.

Brachial plexus trauma is a common clinical entity in small animal practice and prognostic indicators are essential early in the course of the disease. Magnetic stimulation of the radial nerve and consequent recording of the magnetic motor evoked potential (MMEP) was examined in 36 dogs and 17 cats with unilateral brachial plexus trauma. Absence of deep pain perception (DPP), ipsilateral loss of panniculus reflex, partial Horner's syndrome and a poor response to MMEP were related to the clinical outcome in 29 of the dogs and 13 of the cats. For all animals, a significant difference was found in MMEP between the normal and the affected limb. Absence of DPP and unilateral loss of the panniculus reflex were indicative of an unsuccessful outcome in dogs. Additionally, the inability to evoke a MMEP was associated with an unsuccessful outcome in all animals. It was concluded that magnetic stimulation of the radial nerve in dogs and cats with brachial plexus trauma may provide an additional diagnostic and prognostic tool.

Effects of sedative and hypnotic drug combinations on transcranial magnetic motor evoked potential, bispectral index and ARX-derived auditory evoked potential index in dogs.

Relationships between onset latency and peak-to-peak amplitude of magnetic motor evoked potentials (MMEP) after transcranial magnetic stimulation (TMS), together with the electroencephalographic parameters bispectral analysis index (BIS) and the autoregressive model with exogenous input (ARX)-derived auditory evoked potential index (AAI) were explored during different sedative and hypnotic drug combinations in six dogs. TMS was performed under sedation with acepromazine/methadone or medetomidine and after a single bolus injection of propofol or etomidate. Data for BIS and AAI were continuously collected during the periods of treatment with the hypnotic drugs. Changes in BIS and AAI during both periods were not statistically correlated with changes in onset latencies and peak-to-peak amplitudes of MMEP after TMS. Therefore, both electroencephalographic techniques are of limited use in titrating sedation and anaesthesia during TMS in the dog.

Role of progestin-induced mammary-derived growth hormone in the pathogenesis of cystic endometrial hyperplasia in the bitch.

Endogenous progesterone and synthetic progestins may induce hypersecretion of growth hormone (GH) of mammary origin, hyperplastic ductular changes in the mammary gland, and the development of cystic endometrial hyperplasia (CEH) in dogs. It was investigated whether progestin-induced mammary GH plays a role in the pathogenesis of CEH in the bitch. During 1 year, bitches with surgically excised mammary glands and healthy control bitches received medroxyprogesterone acetate (MPA). Before and after MPA treatment, uterine and mammary tissues were collected for histological, immunohistochemical, and RT-PCR examination. After MPA administration, the mammary tissue in the control dogs had differentiated into lobulo-alveolar structures and CEH was present in all uteri of both dog groups. In the MPA-exposed mammary tissue of the control dogs, GH could only be demonstrated immunohistochemically in proliferating epithelium. After treatment with MPA the dogs of both groups had immunohistochemically demonstrable GH in the cytoplasm of hyperplastic glandular uterine epithelial cells. RT-PCR analysis of the mammary gland tissue after MPA administration demonstrated a significant higher GH gene, and lower GHR gene expression than before treatment. In the uterus, the expression of the gene encoding for GH was significantly increased in the mastectomized dogs, whereas in the control dogs the expression of the gene encoding for insulin-like growth factor-I had significantly increased with MPA administration. MPA treatment significantly down regulated PR gene expression in the uterus in both dog groups. These results indicate that progestin-induced GH of mammary origin is not an essential component in the development of CEH in the bitch.

Cardiopulmonary effects of sufentanil long acting on sevoflurane anaesthesia in dogs.

OBJECTIVE: To evaluate the cardiopulmonary effects of sufentanil long acting (SLA) in sevoflurane-anaesthetized dogs. STUDY DESIGN: Randomized prospective study. Animals Forty female dogs (beagles) aged 1-2 years, weighing 11.97 +/- 1.40 kg. MATERIALS AND METHODS: The dogs were divided into five groups of eight. Two control groups were used: group A received intramuscular (IM), SLA (50 microg kg(-1)) alone, while group B received the SLA vehicle followed by sevoflurane anaesthesia for 90 minutes. In the other groups, SLA (50 microg kg(-1) IM) was given immediately before (group C(0)), 15 minutes before (group D(15)) or 30 minutes (group E(30)) before induction [with intravenous (IV) thiopental] of sevoflurane anaesthesia lasting for 90 minutes. Heart rate, arterial blood pressure, respiratory rate (f(r)), arterial oxygen haemoglobin saturation and end-tidal sevoflurane concentration (Fe'SEVO) were measured every 10 minutes during anaesthesia and at 2, 4 and 24 hours after induction (not Fe'SEVO). Acid-base and blood gas analyses were performed. RESULTS: Sufentanil LA reduced heart rate and increased arterial CO(2) tensions during anaesthesia. Respiratory depression was least in group E(30) compared with groups C(0) and D(15). Bradycardia was present for at least 24 hours. Respiratory rate was least in group B although arterial O(2) and CO(2) tension values were acceptable up to 24 hours after anaesthesia. CONCLUSIONS: Pre-anaesthetic medication with SLA moderately aggravated the cardiopulmonary effects of sevoflurane. CLINICAL RELEVANCE: In spite of a moderate depressant effect on cardiorespiratory parameters, SLA may be of use as pre-anaesthetic medication before sevoflurane anaesthesia in dogs. Intermittent positive pressure ventilation may occasionally be necessary.

Suboccipital craniectomy, dorsal laminectomy of C1, durotomy and dural graft placement as a treatment for syringohydromyelia with cerebellar tonsil herniation in Cavalier King Charles spaniels.

OBJECTIVE: To evaluate retrospectively the efficacy of the suboccipital craniectomy and dorsal laminectomy of C1 with durotomy and placement of a dural graft for treatment of syringohydromyelia (SHM) because of cerebellar tonsil herniation in Cavalier King Charles spaniels (CKCS). This technique is used with great success in human medicine. STUDY DESIGN: Four CKCS diagnosed by Magnetic resonance imaging (MRI) of SHM because of cerebellar tonsil herniation and not responsive to medical therapy underwent a suboccipital craniectomy and dorsal laminectomy of C1 (2 dogs) and of C1 and partial C2 (2 dogs) with durotomy and placement of a dural graft. Three dogs were evaluated neurologically 24 hours, 1 month, and 3 months postoperatively and evaluations were compared with preoperative neurological examination. Repeat MRI took place 3 months postoperatively. RESULTS: Neurological examinations showed neither improvement nor progression of clinical signs 3 months postoperatively. MRI showed no regression of syrinx size 3 months postoperatively. CONCLUSION: Improvement was not seen. Given the progressive nature of the disorder, evaluation over a longer period of time is necessary to detect if progression has stopped. Some modification to the surgical technique is needed to accomplish the same results as in human medicine. A study of a larger population is needed to attain more reliable information. CLINICAL RELEVANCE: Suboccipital craniectomy and dorsal laminectomy of C1 with durotomy and placement of a dural graft is a feasible technique in CKCS, but needs some modification to accomplish the same results as in human medicine.