Profile of electrodiagnostic abnormalities in cats with GM1 gangliosidosis

J. E. Steiss From the Scott-Ritchey Research Center (Steiss, Baker, Braund, Cox) and the Department of Pathobiology (Wright), College of Veterinary Medicine, Auburn University, AL 36849.

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H. J. Baker From the Scott-Ritchey Research Center (Steiss, Baker, Braund, Cox) and the Department of Pathobiology (Wright), College of Veterinary Medicine, Auburn University, AL 36849.

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K. G. Braund From the Scott-Ritchey Research Center (Steiss, Baker, Braund, Cox) and the Department of Pathobiology (Wright), College of Veterinary Medicine, Auburn University, AL 36849.

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N. R. Cox From the Scott-Ritchey Research Center (Steiss, Baker, Braund, Cox) and the Department of Pathobiology (Wright), College of Veterinary Medicine, Auburn University, AL 36849.

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J. C. Wright From the Scott-Ritchey Research Center (Steiss, Baker, Braund, Cox) and the Department of Pathobiology (Wright), College of Veterinary Medicine, Auburn University, AL 36849.

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Abstract

Objective

To determine which electrodiagnostic tests yield abnormal findings in cats with GM1 gangliosidosis, and to determine the approximate age of onset of electrodiagnostic abnormalities.

Animals

Cats (28 to 335 days old) affected with GM1 gangliosidosis (n = 11) and unaffected controls (n = 14).

Procedure

Cats were grouped by age: group 1, ≤ 90 days; group 2, 91 to 200 days; and group 3, > 200 days. Electrodiagnostic tests were conducted, including needle electromyography, motor and sensory nerve conduction velocity, spinal evoked potentials, and brainstem auditory evoked potentials. Results for control and affected cats were compared, using the general linear model for ANOVA and Scheffe's test for multiple comparisons.

Results

Needle electromyography did not reveal abnormal spontaneous activity in skeletal muscles of any cat; furthermore, statistical analysis did not indicate significant difference between affected and control groups for nerve conduction velocity, confirming that degeneration of peripheral nerve fibers is not a feature of this disease. However, spinal evoked potentials were abnormal in group-3 cats; conduction velocity within sensory pathways in the cranial part of the spinal cord was significantly slower in GM1-affected cats (P = 0.0002). Brainstem auditory evoked responses also were abnormal: wave V (generated in the region of the pons) had prolonged latency in cats of groups 2 and 3 (P = 0.0003 and 0.0001, respectively, at 90 decibels sound pressure level). In the oldest cats, latencies for earlier waves within the auditory pathway also were prolonged; wave I (generated by the cochlear nerve) was prolonged in group-3 cats (P = 0.0423).

Conclusion

Motor and sensory nerve conduction velocities remained within normal limits in GM1-affected cats. However, spinal evoked potentials indicated slowing in conduction velocity along the cranial part of the spinal cord in group 3 cats. Brainstem auditory evoked responses indicated prolonged latencies in cats of groups 2 and 3. (Am J Vet Res 1997;58:706–709)

Abstract

Objective

To determine which electrodiagnostic tests yield abnormal findings in cats with GM1 gangliosidosis, and to determine the approximate age of onset of electrodiagnostic abnormalities.

Animals

Cats (28 to 335 days old) affected with GM1 gangliosidosis (n = 11) and unaffected controls (n = 14).

Procedure

Cats were grouped by age: group 1, ≤ 90 days; group 2, 91 to 200 days; and group 3, > 200 days. Electrodiagnostic tests were conducted, including needle electromyography, motor and sensory nerve conduction velocity, spinal evoked potentials, and brainstem auditory evoked potentials. Results for control and affected cats were compared, using the general linear model for ANOVA and Scheffe's test for multiple comparisons.

Results

Needle electromyography did not reveal abnormal spontaneous activity in skeletal muscles of any cat; furthermore, statistical analysis did not indicate significant difference between affected and control groups for nerve conduction velocity, confirming that degeneration of peripheral nerve fibers is not a feature of this disease. However, spinal evoked potentials were abnormal in group-3 cats; conduction velocity within sensory pathways in the cranial part of the spinal cord was significantly slower in GM1-affected cats (P = 0.0002). Brainstem auditory evoked responses also were abnormal: wave V (generated in the region of the pons) had prolonged latency in cats of groups 2 and 3 (P = 0.0003 and 0.0001, respectively, at 90 decibels sound pressure level). In the oldest cats, latencies for earlier waves within the auditory pathway also were prolonged; wave I (generated by the cochlear nerve) was prolonged in group-3 cats (P = 0.0423).

Conclusion

Motor and sensory nerve conduction velocities remained within normal limits in GM1-affected cats. However, spinal evoked potentials indicated slowing in conduction velocity along the cranial part of the spinal cord in group 3 cats. Brainstem auditory evoked responses indicated prolonged latencies in cats of groups 2 and 3. (Am J Vet Res 1997;58:706–709)

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