Objective—To determine prevalence of initial clinical
signs and risk factors for acquired myasthenia gravis
(MG) in cats.
Design—Retrospective case-control study.
Animals—105 cats from the United States, Canada,
and the United Kingdom with a confirmed diagnosis
of acquired MG and 510 cats with other neuromuscular
disorders, including generalized weakness,
megaesophagus, and dysphagia (control group).
Procedures—Records were retrieved from a database
containing results of serum samples tested for
acetylcholine receptor antibodies. Signalment, including
breed, age, and state or country of origin, month
of onset, and initial clinical signs were obtained. An
acetylcholine receptor antibody titer > 0.3 nmol/L was
diagnostic for acquired MG. Unconditional logistic
regression was used for statistical analysis.
Results—Compared with mixed-breed cats, the
breed with the highest relative risk of acquired MG
was the Abyssinian (including Somali). Significant differences
between sexes were not detected. There
was no compelling evidence for a difference in risk of
developing MG between states or countries. Relative
risk increased after 3 years of age. The most common
clinical signs were generalized weakness without
megaesophagus and weakness associated with a cranial
mediastinal mass. Focal signs, including megaesophagus
and dysphagia without signs of generalized
weakness, were also evident.
Conclusions and Clinical Relevance—A breed predisposition
for acquired MG in Abyssinians (and related
Somalis) was observed. Clinical signs were variable
and included generalized weakness, megaesophagus,
and dysphagia. A cranial mediastinal
mass was commonly associated with MG in cats. ( J
Am Vet Med Assoc 2000;216:55–57)
Case Description—A 7-month-old neutered male ferret was evaluated for episodic pelvic limb weakness of 2 weeks' duration.
Clinical Findings—Neurologic examination revealed flaccid tetraparesis with decreased spinal reflexes suggestive of a neuromuscular disease. Results of hematologic and CSF analyses, thoracic radiography, and abdominal ultrasonography were unremarkable. Electrodiagnostic testing revealed subtle spontaneous activity localized to pelvic limb interosseous muscles, unremarkable motor nerve conduction velocities, and lower than typical compound muscle action potential (CMAP) amplitude for tibial nerve stimulation only. A severe decremental response of the CMAP was detected with repetitive nerve stimulation (45.5% at the third ulnar nerve). An esophagogram revealed mild megaesophagus. Intravenous neostigmine methylsulfate administration resulted in immediate resolution of muscle weakness. Cross-reacting anti-acetylcholine receptor (AChR) antibodies were detected in serum (0.35 nmol/L) by use of a canine- and feline-specific muscle extract. Clinical signs and ancillary test results were diagnostic of acquired myasthenia gravis.
Treatment and Outcome—Pyridostigmine bromide was administered (1 mg/kg [0.45 mg/lb], PO, q 8 h), resulting in complete remission of clinical signs. However, 1 month after the diagnosis, the ferret was euthanized because of recurrence of weakness despite anticholinesterase treatment.
Clinical Relevance—To the authors' knowledge, this is the first report of acquired myasthenia gravis in a ferret and the first identification of anti-AChR antibodies in this species. Autoimmune myasthenia gravis should be considered in ferrets when weakness and flaccid paresis suggest a neuromuscular disease. Electrodiagnostic testing, anticholinesterase challenge, and AChR antibody titer determination were helpful for diagnosis of this condition.
Case Description—A 4-year-old domestic shorthair cat was evaluated for a 1-week history of shifting limb lameness that progressed to tetraparesis.
Clinical Findings—Physical examination revealed generalized muscle atrophy and signs of discomfort when the muscles of the appendicular skeleton were palpated. Neurologic examination revealed diminished myotatic and withdrawal reflexes in all 4 limbs. Results of a CBC indicated mild neutrophilia, and serum biochemical analysis revealed mild hyperalbuminemia and high creatine kinase activity. The cat was anesthetized, and an electromyogram (EMG), CSF sample, and nerve and muscle biopsy specimens were obtained. The EMG revealed positive sharp waves and fibrillation potentials, CSF analysis revealed albuminocytologic dissociation, and histologic examination of muscle and nerve specimens revealed severe myositis and neuritis. Immune-mediated polymyositis and neuritis were suspected.
Treatment and Outcome—With physical therapy and long-term corticosteroid drug treatment, the cat recovered complete motor nerve function.
Clinical Relevance—The severity and rapid progression of clinical signs, combined with the EMG abnormalities and histologic findings, could have led to inappropriate euthanasia for this cat. Veterinarians should be aware that immune-mediated polymyositis and neuritis in cats can have an excellent prognosis with appropriate, long-term treatment.
A 4.5-year-old neutered male domestic ferret (Mustela putorius furo) was examined because of clinical signs compatible with neuromuscular disease.
Results of electrophysiologic assessment, including measurement of compound muscle action potentials following repetitive nerve stimulation, and measurement of the anti–acetylcholine receptor antibody titer were consistent with a diagnosis of acquired myasthenia gravis.
TREATMENT AND OUTCOME
Medical treatment with pyridostigmine and prednisolone was instituted. The first signs of clinical improvement were observed 2 months later, followed by a slow but steady improvement over the next months. Anti–acetylcholine receptor antibody titer was measured 10 months after initiation of treatment and was markedly decreased, compared with the initial titer. Pyridostigmine and prednisolone dosages were tapered over the following 4 months without any evidence of recurrence of clinical signs. Thirty months after initial examination, the ferret was clinically normal and not receiving any treatment. A follow-up anti–acetylcholine receptor antibody titer was similar to previously published values for healthy ferrets.
Findings indicated that clinical and serologic remission can be achieved in ferrets with myasthenia gravis. However, owner willingness to provide extensive supportive care was vital to the outcome for this patient, as was the owner's decision to not euthanize the ferret despite an initial lack of response to treatment.
Objective—To determine the neurologic effects of
reduced intake of phenylalanine and tyrosine in black-haired
Animals—53 specific pathogen-free black domestic
Procedure—Cats were fed purified diets containing
various concentrations of phenylalanine and tyrosine
for ≤ 9 months. Blood samples were obtained every 2
months for evaluation of serum aromatic amino acid
concentrations. Cats were monitored for changes in
hair color and neurologic or behavioral abnormalities.
Three cats with neurologic deficits underwent clinical
and electrophysiologic investigation; muscle and
nerve biopsy specimens were also obtained from
Results—After 6 months, neurologic and behavioral
abnormalities including vocalization and abnormal
posture and gait were observed in cats that had
received diets containing < 16 g of total aromatic
amino acid/kg of diet. Electrophysiologic data and
results of microscopic examination of muscle and
nerve biopsy specimens from 3 cats with neurologic
signs were consistent with sensory neuropathy with
primary axonal degeneration. Changes in hair color
were detected in cats from all groups receiving < 16
g of phenylalanine plus tyrosine/kg of diet.
Conclusions and Clinical Relevance—Findings suggested
that chronic dietary restriction of phenylalanine
and tyrosine in cats may result in a predominantly
sensory neuropathy. In cats, the long-term
nutritional requirement for phenylalanine and tyrosine
appears to be greater for normal neurologic function
than that required in short-term growth experiments.
Official present-day recommendations for dietary
phenylalanine and tyrosine in cats may be insufficient
to support normal long-term neurologic function. ( Am J Vet Res 2004;65:671–680)
Case Description—A 6-year-old castrated male Llewelyn Setter was evaluated because of an acute onset of myalgia and respiratory distress.
Clinical Findings—Physical examination revealed a stiff stilted gait, swollen muscles that appeared to cause signs of pain, panting, and ptyalism. The dog had a decrease in palpebral reflexes bilaterally and a decrease in myotatic reflexes in all 4 limbs. The panniculus reflex was considered normal, and all other cranial nerve reflexes were intact. Serum biochemical analysis revealed markedly high cardiac troponin-I concentration and creatine kinase and aspartate aminotransferase activities. Urinalysis revealed myoglobinuria. Results for thoracic and abdominal radiography, blood pressure measurement, and an ECG were within anticipated limits. Echocardiographic findings were consistent with secondary systolic myocardial failure. Arterial blood gas analysis confirmed hypoxemia and hypoventilation. The dog had negative results when tested for infectious diseases. Examination of skeletal muscle biopsy specimens identified necrotizing myopathy.
Treatment and Outcome—Treatment included ventilatory support; IV administration of an electrolyte solution supplemented with potassium chloride; administration of dantrolene; vasopressor administration; parenteral administration of nutrients; use of multimodal analgesics; administration of clindamycin, furosemide, mannitol, and enrofloxacin; and dietary supplementation with L-carnitine and coenzyme Q10. Other medical interventions were not required, and the dog made a rapid and complete recovery.
Clinical Relevance—Necrotizing myopathy resulting in rhabdomyolysis and myoglobinuria can lead to life-threatening physical and biochemical abnormalities. Making a correct diagnosis is essential, and patients require intensive supportive care. The prognosis can be excellent for recovery, provided there is no secondary organ dysfunction.
Objective—To study the effects of experimentally induced hypothyroidism on skeletal muscle and characterize any observed myopathic abnormalities in dogs.
Animals—9 female, adult mixed-breed dogs; 6 with hypothyroidism induced with irradiation with 131 iodine and 3 untreated control dogs.
Procedures—Clinical examinations were performed monthly. Electromyographic examinations; measurement of plasma creatine kinase, alanine aminotransferase, aspartate aminotransferase, lactate, and lactate dehydrogenase isoenzyme activities; and skeletal muscle morphologic-morphometric examinations were performed prior to and every 6 months for 18 months after induction of hypothyroidism. Baseline, 6-month, and 18-month assessments of plasma, urine, and skeletal muscle carnitine concentrations were also performed.
Results—Hypothyroid dogs developed electromyographic and morphologic evidence of myopathy by 6 months after treatment, which persisted throughout the study, although these changes were subclinical at all times. Hypothyroid myopathy was associated with significant increases in plasma creatine kinase, aspartate aminotransferase, and lactate dehydrogenase 5 isoenzyme activities and was characterized by nemaline rod inclusions, substantial and progressive predominance of type I myofibers, decrease in mean type II fiber area, subsarcolemmal accumulations of abnormal mitochondria, and myofiber degeneration. Chronic hypothyroidism was associated with substantial depletion in skeletal muscle free carnitine.
Conclusions and Clinical Relevance—Chronic, experimentally induced hypothyroidism resulted in substantial but subclinical phenotypic myopathic changes indicative of altered muscle energy metabolism and depletion of skeletal muscle carnitine. These abnormalities may contribute to nonspecific clinical signs, such as lethargy and exercise intolerance, often reported in hypothyroid dogs.