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During 1986 and 1987, electroencephalographic examinations were done on 8 dogs with intracranial mass lesions confirmed by computerized tomography, biopsy, necropsy, or a combination of these techniques. Tumor types included 1 astrocytoma, 1 undifferentiated glioma, 2 mixed gliomas, 2 meningiomas, 1 choroid plexus papilloma, and 1 cholesterol granuloma. It was found that no EEG pattern was pathognomonic for tumor type or location. Slow-wave activity was observed in the EEG of most of the dogs; asymmetry in amplitude or frequency was observed in approximately half the cases.

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Spinal evoked potentials (SpEP) were recorded on an electromyograph from electrodes placed percutaneously in the ligamentum flava at the lumbosacral junction and between the 10th and 11th thoracic vertebrae following tibial nerve stimulation in 31 anesthetized dogs with acute compressive spinal cord injuries. The neurologic status of each dog was determined by clinical examination before SpEP recordings, and the neurologic status was monitored for 2 months in dogs that had surgical or conservative treatment. Two months after spinal injury, the response to treatment (outcome) of each dog was evaluated and graded as favorable (ambulatory and urinary continent) or unfavorable (nonambulatory, urinary incontinent, or euthanatized with confirmation of myelomalacia). Onset latencies, conduction velocities, amplitudes and durations of the wave forms, and the ratio of conduction velocity to combined durations of the first positive (P1) and first negative (N1) waves (CV/DPN index) were determined and were compared with reference data from clinically normal (control) dogs. Single SpEP recordings were of value in determining the prognosis for recovery. Significant differences were not found in the L7-S1 recordings between the reference (control) and spinal injury groups. Analysis of data from the T10-11 recordings indicated significant differences between the reference and spinal injury groups and between the favorable and unfavorable outcome groups within the spinal injury group. A CV/DPN index was less than 30 in dogs with unfavorable outcomes and greater than 30 in dogs with favorable outcomes. Stepwise discriminant analysis of data from the spinal injury group predicted outcome correctly in all dogs.

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Electroencephalograms were recorded from 10 dogs before, immediately after, and every 10 minutes (for 60 minutes) after IV injection of 0.005 ml of a fentanyl citrate and droperidol combination/kg of body weight. Narcosis was adequate for recording. At 30 to 40 minutes after injection, tail wagging was the only adverse reaction (EEG artifact) observed. The only changes in EEG activity observed were a slight increase in amplitude of the dominant activity and an increase in spindle-like activity. Daily repetition for 5 days did not alter the EEG pattern or the behavior of the dogs.

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The latencies and latency rates of H and F waves were determined by percutaneous stimulation of the ulnar and the tibial nerves of healthy cats. In the ulnar and tibial nerves, the latency rates of H wave evoked compound action potentials were 49.1 +/- 7.3 and 44.1 +/- 2.7 m/s, respectively, and of F waves were 68.1 +/- 9.6 and 57.1 +/- 6.2 m/s, respectively. The H wave response of cats was more variable in latency and amplitude than that reported in the dog.

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The voltage and duration of electrical rectangular pulsed stimuli needed to produce an F wave and a monosynaptic reflex (H wave) and the characteristics of these responses were recorded in clinically normal dogs. Optimal stimulus to produce H waves was 0.1 to 0.2 ms and less than 80 volts. F waves were variable in appearance and were most evident following 0.5 ms and 125 to 150 volt stimulation. F waves had shorter latency than comparable H waves.

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Electroencephalograms of 20 dogs given succinylcholine and concurrent artificial respiration were recorded. The amplitudes of the fast activity of the electroencephalograms were approximately one-fifth that observed in awake dogs. In addition, the occurrence of slow waves (6 to 8 Hz) was more marked in those dogs treated with succinylcholine. Succinylcholine caused a low amplitude dominant activity with increased moderate amplitude low frequency waves.

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Eleven dogs with signs of lead poisoning were examined. The principal clinical signs were neurologic and included ataxia, tremors, clonic-tonic seizures, amaurosis, and deafness. Basophilic stippling and circulating nucleated red cells were not common findings in blood films. Blood lead values varied from 0.22 ppm to 0.63 ppm before treatment. Electroencephalographic changes in nonsedated dogs were marked by intermittent high-amplitude slow wave activity.

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Signs of a central nervous system disorder were observed following 2 instances of accidental ingestion of glucocorticoid in a young female Doberman Pinscher. The signs included transient aggressive and paranoid behavior, amaurosis, disorientation, ataxia with circling backward, and depression. Vomiting, weight loss, and abnormal drinking behavior persisted for several weeks following recovery from the acute illness.

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A new fascial technique was used to repair artificially induced rupture of the cranial cruciate ligament in 20 dogs. Although technically simple to perform, the procedure resulted in only 12 animals free of lameness. In addition, a drawer sign was present in the stifle of 14 animals 31 days after surgery. Arthritis changes typical of cruciate ligament instability were observed in 16 joints; changes were slight to moderate in 10 joints.

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