Page 964 - Problem-Based Feline Medicine
P. 964

956   PART 11  CAT WITH AN ABNORMAL GAIT


          Muscle tremors are usually episodic and occur in mus-  organophosphate toxicity (decreased serum cholin-
          cles that are being used.                     esterase activity).
          A stiff, stilted gait is often noted prior to collapse.
                                                        Treatment
          Weakness of facial muscle may also be seen, and this is
          most evident as a decrease in the palpebral reflex and  A long-acting anticholinesterase product (pyridostig-
          narrowing of the palpebral fissure. This appears to be a  mine Mestinon, 0.5–3 mg/kg PO q 8–12 hours) can be
          more consistent finding in cats versus dogs.  given to enhance the effect of ACH at the neuromuscu-
                                                        lar junction. Start at the lower dose and increase as
          Megaesophagus is uncommon and may lead to aspira-  required.
          tion pneumonia.
                                                        Cats may be more sensitive to the effect of this drug,
          One cat has been reported with a jaw-drop and dyspha-  and therefore, slightly lower dosages than those used in
          gia as the only clinical signs.               dogs should be used initially.

          Diagnosis                                     Additionally, immunosuppressive therapy with corticos-
                                                        teroid (1–2 mg/kg PO q 12 hours) or plasmapheresis may
          Diagnosis is based upon clinical signs of exercise-  be needed to control clinical signs in acquired forms.
          induced weakness that is resolved with edrophonium.
          An edrophonium response test may suggest the  Prognosis
          disease if strongly positive. Edrophonium is an anti-
                                                        Prognosis for some animals is good, with occasional
          cholinesterase that potentiates acetylcholine (ACH) at
                                                        spontaneous cures or remission. Recurrences may occur.
          the neuromuscular junction. When given IV (0.1 mg/kg),
          this drug can reverse the clinical weakness seen with  Treatment responses may not be as dramatic in cats
          myasthenia gravis for a short period of time.  compared to dogs.
          Electromyography and nerve conduction studies will  Complicating factors include severe weakness with res-
          be normal. A decremental response may be seen during  piratory compromise and aspiration pneumonia sec-
          repeated stimulation of a peripheral nerve in some, but  ondary to megaesophagus.
          not all cats.
                                                        Prevention
          Single fiber EMG is a relatively new technique that
          may aid diagnosis of this disease in the future.  Avoiding breeding from sires and dams known to pro-
          Documentation of  antibodies to the acetylcholine  duce congenitally affected offspring. Advise pedigree
          receptor in serum appears to be the most definitive  analysis to remove carriers.
          diagnostic test. In congenital disease, however, these
          antibodies will not be present.
                                                        HYPOGLYCEMIA*
          Differential diagnosis                         Classical signs

          Rule out other inflammatory, toxic and degenerative  ● Trembling, weakness are most common.
          causes of muscle weakness and tremor.          ● Dilated pupils.
                                                         ● Reduced alertness or lethargy.
          Other causes of ventral neck flexion and generalized
                                                         ● If hypoglycemia is severe, seizures and
          weakness include thiamine deficiency (response to
                                                           progression to coma may result.
          therapy), polymyositis (increased CK, abnormal EMG
          and muscle biopsy), hypokalemic myopathy (low
          plasma potassium), hypernatremia (very rare, hype-
                                                        Pathogenesis
          rnatremia), polyneuropathy (abnormal EMG and de-
          creased nerve conduction velocities), hyperthyroidism  Hypoglycemia can also occur secondary to some
          (other clinical signs and elevated plasma thyroxine) and  endocrine disorders such as hypoadrenocorticism, lack
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