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Background: Optical neuronavigation systems using infrared light to create a virtual reality image of the brain allow the surgeon to track instruments in real time. Due to the high vulnerability of the brain, neurosurgical interventions must be performed with a high precision. The aim of the experimental cadaveric study was to determine the application accuracy of a frameless optical neuronavigation system as guide for craniotomies by determining the target point deviation of predefined target points at the skull surface in the area of access to the cerebrum, cerebellum and the pituitary fossa. On each of the five canine cadaver heads ten target points were marked in a preoperative computed tomography (CT) scan. These target points were found on the cadaver skulls using the optical neuronavigation system. Then a small drill hole (1.5 mm) was drilled at these points. Subsequently, another CT scan was made. Both CT data sets were fused into the neuronavigation software, and the actual target point coordinates were identified. The target point deviation was determined as the difference between the planned and drilled target point coordinates. The calculated deviation was compared between two observers. Results: The analysis of the target point accuracies of all dogs in both observers taken together showed a median target point deviation of 1.57 mm (range: 0.42 to 5.14 mm). No significant differences were found between the observers or the different areas of target regions. Conclusion: The application accuracy of the described system is similar to the accuracy of other optical neuronavigation systems previously described in veterinary medicine, in which mean values of 1.79 to 4.3 mm and median target point deviations of 0.79 to 3.53 mm were determined.

The most common form of muscular dystrophy in dogs and humans is caused by mutations in the dystrophin gene. The dystrophin gene is located on the X chromosome, and, therefore, disease‐causing mutations in dystrophin occur most often in males. Therefore, females with dystrophin deficiency or other forms of muscular dystrophy may be undiagnosed or misdiagnosed. Immunohisto‐chemistry was used to analyze dystrophin and a number of other muscle proteins associated with muscular dystrophy in humans, including sarcoglycans and laminin α2, in muscle biopsy specimens from 5 female dogs with pathologic changes consistent with muscular dystrophy. The female dogs were presented with a variety of clinical signs including generalized weakness, muscle wasting, tremors, exercise intolerance, gait abnormalities, and limb deformity. Serum creatine kinase activity was variably high. One dog had no detectable dystrophin in the muscle; another was mosaic, with some fibers normal and others partly dystrophin‐deficient. A 3rd dog had normal dystrophin but no detectable laminin α2. Two dogs could not be classified. This study demonstrates the occurrence of dystrophin‐ and laminin α2‐associated muscular dystrophy and the difficulty in clinical diagnosis of these disorders in female dogs.