Page 1150 - Small Animal Internal Medicine, 6th Edition
P. 1150

1122   PART IX   Nervous System and Neuromuscular Disorders


              No specific treatment has been shown to consistently alter   or doxycycline may be considered. Signs usually persist until
            the course of this disease, but long-term remission has been   prednisone therapy is initiated (1-2 mg/kg PO q12h for 14
  VetBooks.ir  achieved in a few dogs using treatment protocols as outlined   days). Tremors usually improve or resolve within the first
                                                                 week or two after initiating therapy. Once the tremors have
            for GME (see Box 64.3). Treatment with antiepileptic doses
            of phenobarbital may decrease the severity and frequency of
                                                                 3 to 6 months to the lowest effective dose (usually 0.25 mg/
            seizures. The prognosis for long-term improvement and sur-  resolved, the prednisone dose can be tapered gradually over
            vival must be considered poor.                       kg q48h) and then can usually be discontinued. If the tremors
                                                                 return, immunosuppressive prednisone therapy is reiniti-
            NECROTIZING LEUKOENCEPHALITIS                        ated, with more gradual tapering. Some dogs require addi-
            NLE  is a breed-specific  idiopathic  multifocal  necrotizing,   tional  immunosuppressive  treatment  with  cyclosporine  or
            nonsuppurative encephalitis affecting the brains of Yorkshire   azathioprine to taper the prednisone dose to acceptable
            Terriers, French Bulldogs, and occasionally Maltese Terriers.   levels and prevent relapses. The prognosis is good for recov-
            Dogs first show clinical signs between 1 and 10 years of age,   ery, but occasionally dogs will require lifelong continuous or
            with a mean age of onset around 4.5 years. Males and females   intermittent therapy. Histologically, some affected dogs have
            are affected equally.                                had a mild nonsuppurative meningoencephalitis with peri-
              Lesions predominate in the white matter (“leuko-”) of the   vascular cuffing that is most severe in the cerebellum.
            cerebrum, thalamus, and brainstem. Signs may include
            altered mentation, seizures, visual deficits, head tilt, nystag-  CANINE EOSINOPHILIC MENINGITIS/
            mus, cranial nerve abnormalities, and proprioceptive defi-  MENINGOENCEPHALITIS
            cits. Neurologic deterioration is rapid, and within 5 to 7 days   Eosinophilic meningitis and meningoencephalitis occur
            most dogs are recumbent or dead. A diagnosis of NLE should   uncommonly in dogs. Eosinophilic inflammation can be the
            be suspected on the basis of signalment and characteristic   response to migrating helminths, protozoal or fungal infec-
            rapidly progressive cortical and brainstem signs. MRI studies   tion, or rarely viral infection of the CNS. There is also a
            show multiple asymmetric hyperintense (T2W) lesions and   primary allergic or immune-mediated disorder of dogs char-
            cystic areas of necrosis restricted to the white matter of the   acterized by eosinophilic inflammation of the CNS and
            cerebrum, thalamus, and brainstem. CSF analysis reveals a   known as idiopathic eosinophilic meningoencephalitis (EME).
            mild to moderate increase in protein and a mixed inflamma-  This idiopathic disorder is most common in young (8-month
            tory  pleocytosis  consisting  of  macrophages,  monocytes,    to 3-year-old) large-breed dogs, particularly Golden Retriev-
            lymphocytes, and plasma cells. Treatment as for GME is   ers and Rottweilers. Neurologic signs of EME reflect cerebral
            recommended, but the prognosis for recovery is poor.  cortical involvement and include behavior change, circling,
                                                                 and pacing. Ataxia and proprioceptive deficits are uncom-
            CANINE STEROID-RESPONSIVE                            mon. Some dogs (10%-20%) also manifest systemic signs of
            TREMOR SYNDROME                                      diarrhea, vomiting, and abdominal pain. Peripheral eosino-
            An acute-onset whole-body tremor disorder is most com-  philia is uncommon. MRI can be normal or reveal focal or
            monly recognized in small white dogs such as Maltese and   multifocal patchy regions of T2 hyperintensity with variable
            West Highland White Terriers and Bichon Frise, leading to   contrast enhancement. CSF analysis reveals increased cel-
            the name “little white shaker syndrome.” Although this dis-  lularity, with 20% to 99% eosinophils (often  >80%). It is
            order  is  most  common  in  young  adult  dogs  of  the  small   important to rule out or treat parasitic and infectious disease
            white breeds, it can occur in any breed and in dogs of any   before initiating treatment for EME. If testing is negative for
            coat color. Cairn Terriers and Miniature Pinschers are also   heartworm disease, fungal and protozoal pathogens, and
            predisposed. Affected dogs are presented for evaluation of   Baylisascaris (serology), broad-spectrum deworming with
            tremors and incoordination. Tremors can range from mild   fenbendazole and ivermectin is recommended, followed by
            to incapacitating and tend to worsen with exercise, stress,   2 to 4 weeks of oral clindamycin and immunosuppressive
            and excitement. In most dogs, signs are restricted to tremor,   doses of prednisone. Some dogs recover without treatment.
            but occasionally vestibular or cerebellar ataxia, nystagmus,   Most dogs (75%) have a good response to treatment and can
            or loss of menace response can accompany the tremor.  be weaned off oral prednisone after 3 to 4 months.
              Diagnosis should be suspected based on signalment,
            history, and clinical signs. Lack of access to tremorgenic   FELINE POLIOENCEPHALITIS
            toxins and failure to progress to more severe signs like sei-  A nonsuppurative encephalomyelitis with no etiologic agent
            zures make intoxication unlikely. Normal metabolic testing   identified (viral non-FIP encephalitis) occasionally causes
            (glucose, liver function) and normal mentation are expected.   progressive seizures or brainstem and spinal cord signs in
            MR imaging is usually normal. CSF can be normal, but most   young adult cats. Affected cats range from 3 months to 6
            often there is a slight increase in protein and a lymphocytic   years of age, but most are younger than 2 years. Affected
            pleocytosis. Testing for infectious causes of CNS inflamma-  animals have a subacute to chronic course with neurologic
            tion, including neosporosis, canine distemper, West Nile   signs progressing over 3 to 5 weeks. Ataxia, paresis, and
            virus, and tick-borne pathogens, should be performed where   proprioceptive deficits affecting the pelvic limbs or the
            appropriate, and treatment for 1 to 2 weeks with clindamycin   pelvic and thoracic limbs are common. When inflammation
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