Page 808 - Clinical Small Animal Internal Medicine
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776  Section 8  Neurologic Disease

              Causes of obstruction may be either congenital (steno-  fourth ventricle and mesencephalic aqueduct may also
  VetBooks.ir  sis of the mesencephalic aqueduct, failure of opening of   be enlarged. MRI may reveal the presence of increased
                                                              fluid signal (on T2‐weighted or FLAIR scans) in the
            the lateral apertures of the fourth ventricle) or acquired
            (secondary to inflammatory disease or neoplasia or other
                                                              cephalus is acute. The septum pellucidum which
            cysts obstructing part of the system). Dilation of the ven-  periventricular tissue if the development of the hydro-
            tricular system upstream of the obstruction results in     normally separates the lateral ventricles on midline may
            clinical signs. In mature animals with acquired hydro-  be absent.
            cephalus, the cause may not be determinable and is often   Treatment is either medical or surgical; reasonable
            presumed to be the result of clinically inapparent inflam-  long‐term management is possible with corticosteroid
            mation or hemorrhage within the ventricular system.   therapy at antiinflammatory doses. Carbonic anhydrase
            Enlargement of the ventricular system can also occur   inhibitors have also been used in acute stages of disease
            with age – as the cerebral cortex tissue volume decreases,   but cause significant electrolyte disturbances in the long
            so ventricles get larger to take up the extra space availa-  term so are not recommended for chronic management.
            ble (this is also known as hydrocephalus ex vacuo).  Recently, some authors have described omeprazole in
              Clinical signs predominantly refer to the area affected,   some cases of acquired hydrocephalus based on experi-
            most commonly the forebrain but potentially also hind-  mental studies that suggest it may reduce CSF produc-
            brain  if  the  fourth  ventricle  is  affected.  Seizures,   tion by 26% but no evidence supports its use in dogs with
            behavioral changes, cortical blindness, dullness, head   hydrocephalus. Surgical treatment is also commonly
            pressing, and circling are all reported in association   performed which involves placement of a ventriculop-
            with  this condition. Occasionally vestibular signs are   eritoneal shunt via a small craniotomy which transfers
            also present. Diagnosis requires imaging – either MRI   fluid via a one‐way, pressure‐sensitive valve into the
            or CT, or ultrasound in dogs where an open fontanelle is   abdominal cavity for absorption by mesentery.
            present for placement of the ultrasound probe. This   Long‐term prognosis is generally good, with approxi-
            applies to congenital cases in particular, and often the   mately 75% of cases improving or resolving following
            skull is abnormally large and dome‐shaped with diver-  shunt placement. However, up to 22% may require sub-
            gent strabismus as a result of displacement of the orbits.   sequent revision to deal with blockage or infection which
            On all imaging modalities, the lateral ventricles appear   are common complications
            abnormally enlarged, and in congenital cases a very thin
            rim of cerebral cortex may surround these (Figure 71.2).
            Depending on the level of obstruction, the third and/or     Metabolic Causes


                                                              Hepatic and Uremic Encephalopathy
                                                              The pathogenesis of  hepatic  encephalopathy (HE)  is
                                                              poorly understood. Hepatic insufficiency from a number
                                                              of  causes,  including  acute  liver  failure,  chronic  liver
                                                              failure (including cirrhosis), congenital portosystemic
                                                              shunts and congenital urea cycle enzyme abnormalities,
                                                              can all result in secondary prosencephalic disease. As a
                                                              consequence, various substances pass from the portal
                                                              circulation directly into the systemic circulation without
                                                              undergoing detoxification. These include ammonia
                                                              (probably integral to the pathogenesis of dysfunction),
                                                              various amino acids (especially the aromatic amino acids
                                                              phenylalanine, tyrosine, and tryptophan), short‐chain fatty
                                                              acids, mercaptan and various biogenic amines, indoles
                                                              and skatoles, incriminated in causing HE. Increased intra-
                                                              cellular osmolality from too‐rapid glutamine accumula-
                                                              tion (ammonia is metabolized by astrocytes to glutamine)
                                                              may result in cerebral edema, which also may play a role
                                                              in development of cerebral hyperemia and increased
                                                              intracranial pressure. Glutamine, short‐chain fatty acids,
            Figure 71.2  Dorsal plane CT scan of the brain of a dog with
            obstructive hydrocephalus. Note the extreme paucity of cerebral   aromatic amino acids, and mercaptans are sodium/
            cortex.                                           potassium ATPase inhibitors.
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