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Canine cognitive dysfunction (CCD) is the canine analog of human Alzheimer disease (AD). The pathophysiology of CCD/AD is multifaceted. CCD is common in aged (>8 years) dogs, affecting between 14% and 35% of the pet dog population. Apparent confusion, anxiety, disturbance of the sleep/wake cycle, and decreased interaction with owners are all common clinical signs of CCD. Although there is no cure for CCD, several proven effective therapeutic approaches are available for improving cognitive ability and maintaining a good quality of life; instituting such therapies early in the disease course is likely to have the greatest positive clinical effect.

Congenital malformations of the thoracic vertebral bodies are commonly encountered in veterinary practice. These anomalies are prevalent in juvenile and adult small-breed dogs. These anomalous vertebrae typically result in various degrees of kyphosis and scoliosis in the region of the abnormality. They are thought to occur following developmental errors during embryonic or fetal vertebral segmentation and ossification; most are incidental. This article focuses on those anomalies of the thoracic vertebral bodies that lead to clinical signs of neurologic dysfunction. Based on a limited number of reported cases, the prognosis for surgically managed dogs with thoracic vertebral body abnormalities is favorable.

Craniocervical junction disorders are most frequently seen in toy and small-breed dogs. They can present a diagnostic challenge, as multiple anomalies can be present concurrently and share similar clinical manifestations. Some, such as Chiari-like malformations, may be present in asymptomatic dogs. A thorough evaluation of the entire craniocervical junction, frequently using more than 1 imaging modality, is necessary before making treatment decisions.

Background: Granulomatous meningoencephalomyelitis (GME) is an idiopathic inflammatory disease of the central nervous system. Remission often is short‐lived in dogs treated with glucocorticoids. Procarbazine is T cell‐specific and crosses the blood‐brain barrier.

Management of the severely brain-injured dog or cat can be frustrating, especially considering the lack of proven effective therapies for head trauma patients. A working knowledge of the basic pathophysiology of head trauma and intracranial pressure (ICP) dynamics is essential to the logical treatment of head traumatized patients. Prevention and correction of hypotension and hypoxemia are necessary for preventing progressive increases in ICP. Mannitol is recommended in most cases of severe head trauma, but there is little evidence to support the use of glucocorticoids in acutely brain-injured dogs and cats. The role of surgical intervention for head-traumatized dogs and cats is still uncertain, but may be beneficial in some cases. Aggressive, expedient treatment and attentive patient monitoring are key aspects of successfully managing canine and feline head trauma patients.

The accuracy of an inexpensive, easily implantable, epidural intracranial pressure (ICP) monitoring system was assessed in six normal cats by comparing measurements from this system to those obtained with a fiberoptic intraparenchymal monitoring system. The epidural monitoring system consisted of a three‐way stopcock and saline‐filled extension tubing, connected to a standard blood pressure transducer. Each cat was placed under halothane anesthesia and mechanically ventilated. Both an epidural and a fiberoptic intraparenchymal monitoring device were placed in the left cranium of each cat; correct placement was verified by computed tomography. Mean ICP values were simultaneously recorded from both monitoring devices. After obtaining baseline ICP measurements, the ICP was manipulated via ventilation, jugular compression, and pharmacologic agents. Arterial blood pressure levels, arterial blood gas values, end‐tidal carbon dioxide levels, and end‐tidal halothane levels were recorded throughout the study. Cerebral perfusion pressure was calculated for each level of ICP. Repeated measures analysis of variance method was used to compare mean ICP values between the two monitoring systems. No significant differences in ICP values obtained from the two systems were found (p>0.05) at any level of ICP. The results of this study show that the epidural monitoring system is a reliable alternative to the fiberoptic intraparenchymal ICP monitoring system in normal cats. The accuracy of the epidural monitoring system in pathologic states needs to be investigated.

The purpose of this project was to investigate the clinical forms of acquired myasthenia gravis in dogs. The medical records from 25 dogs with seropositive acquired myasthenia gravis were reviewed, and the following data were recorded for each patient: signalment, history, clinical findings; results of IV edrophonium chloride administration, repetitive nerve stimulation, and presence or absence of muscle membrane staining by immunocytochemical methods; serum acetyl‐choline receptor antibody concentration; treatment; and outcome. Several clinical forms of acquired myasthenia gravis were identified. Nine of the 25 patients (36%) had no historical or clinical evidence of appendicular muscle weakness, and were designated as focal myasthenics. These dogs exhibited focal weakness in one or more of the following muscle groups: facial {3 of 9), pharyngeal (3 of 9), and laryn‐geal (3 of 9). The remaining 16 dogs (64%) exhibited appendicular muscle weakness. Four of these 16 dogs had acute onset and rapid development of clinical signs, and were designated as acute fulminating myasthenics. The remaining 12 dogs were classified as generalized myasthenics. All 4 dogs with acute fulminating myasthenia gravis had megaesophagus, 2 had facial muscle weakness, and 1 had pharyngeal muscle weakness. Ten of the 12 dogs with generalized myasthenia gravis had megaesophagus, 4 had facial muscle weakness, 4 had pharyngeal muscle weakness, and 3 had laryngeal muscle weakness. Historical or clinical evidence of exercise‐associated appendicular weakness was found in only 6 of the 12 (50%) dogs with generalized myasthenia gravis, and in none of the dogs with acute fulminating myasthenia gravis. Seven of the 12 dogs with generalized myasthenia gravis had weakness primarily (n = 1) or exclusively (n = 6) of the pelvic limbs. Two of the 4 dogs with acute fulminating myasthenia gravis had primarily pelvic limb weakness. Twelve of the 25 dogs (48%) died or were euthanized shortly after admission to the hospital due to aspiration pneumonia. The dogs with acute fulminating myasthenia gravis had a markedly higher 1‐year mortality rate in comparison with the other 2 groups. The use of immunosuppressive therapy had a significant positive effect on patient survival, regardless of the type of myasthenia gravis. This investigation demonstrates that acquired myasthenia gravis in dogs is a disorder with a wide spectrum of clinical forms, similar to the analagous disorder in people.

Application of external fixators requires a thorough understanding of fixator biomechanics, fracture healing, and regional anatomy. Techniques of applying fixators utilize predrilling pilot holes followed by hand or slow-speed pin insertion. A combination of smooth and threaded pins can be used to improve stability of the fixator and reduce patient morbidity. Postoperative care of fixators consists of bulky wraps to reduce soft-tissue motion and cleansing of drainage from pin tracts. Staged disassembly of the fixator permits bone loading to stimulate osteogenesis.

A 1 year old female Aurstralian Heeler dog was presented for fever and paraplegia of recent onset. Radiography and myelography revealed osteolysis of the first lumber (L1) vertebra and extensive epidural spinal cord compression from the level of the thirteenth thoracic (T13) to the fourth lumbar (L4) vertebra. A decompressive hemilaminectomy was performed; purulent‐appearing fluid and inflamed epidural fat were present in the vertebral canal. The neurologic recovery of the dog was satisfactory 6 months following surgery.