Page 1137 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1112 CHAPTER 10

VetBooks.ir Aetiology/pathophysiology those where the sole abnormal finding is hyperflex-
ion of a hindlimb when manually lifted.
Shivering occurs most commonly in draught and
warmblood breeds, but has been reported in light
breeds such as carriage horses and Thoroughbreds. Management
One recent study found that, compared with con- No effective treatment can be recommended for
trols without shivering signs, shiverers were taller shiverer cases.
horses. A genetic basis for shivering has been sug-
gested since recent epidemiological studies have Prognosis
demonstrated particular breed and physical predis- The long-term prognosis is guarded. This condi-
position. A revelatory study of the neuroanatomy tion is slowly progressive, although in some cases
and neurophysiology of a large group of shiverers the signs may plateau. Horses may stabilise or
demonstrated Purkinje cell axonal degeneration. improve with rest; however, signs may return when
More specifically, this study revealed end-terminal exercise is resumed.
neuroaxonal degeneration in the deep cerebellar
nuclei that results in the context-specific myoclo- HEPATIC/HYPERAMMONAEMIC
nus and hypermetria observed in affected shiverer ENCEPHALOPATHY
horses. A loss of inhibitory output from the cerebel-
lum as a result of this loss of neurons could result Definition/overview
in extreme excitatory stimulation of hindlimb mus- Hepatic encephalopathy is a neuropsychological
culature and, to support this hypothesis, abnormal syndrome that is characterised by biochemical dis-
locomotor muscle recruitment has been illustrated turbance of CNS function in patients with liver
in a recent EMG study of shiverers. disease. A similar encephalopathy is recognised in
horses suffering from hyperammonaemia associated
Clinical presentation with portosystemic shunts, portal vein thrombosis
A recent study of the hindlimb posture and movement and renal or GI disease.
characteristics of shiverers reported the following
characteristic findings in affected horses: Aetiology/pathophysiology
Liver failure of any origin may result in development
• Difficulty backing-up, including muscle of hepatic encephalopathy. Other causes of hyperam-
hypertonicity that results in hyperflexion or monaemia such as portosystemic shunts and throm-
hyperextension and rigidity of the hindlimb(s). bosis of portal vasculature are other potential causes
• Intermittent hyperflexion and abduction of the but are uncommon in horses. Persistent hyperam-
hindlimb at the onset of walking or turning. monaemia of Morgan foals could also be included in
• The sole sign of hyperflexion when manually this category, as the defect is believed to be at the
lifting a hindlimb is not sufficiently specific for level of the hepatic mitochondria.
shivering and should be considered insufficient The pathophysiology of hepatic encephalopathy is
for the detection of shiverers as a lone finding. not completely understood. It is thought that ammo-
nia has an important role, but the exact mechanism
Differential diagnosis by which ammonia inhibits normal brain function
Hindlimb laminitis, trauma, EHV-1 neuralgia and has yet to be established. Potential mechanisms
idiopathic neuralgia should be considered. include the presence of pseudo-neurotransmitters
and activation of the GABA inhibitory system,
Diagnosis which are thought to have a detrimental effect on the
Diagnosis is based on clinical findings and ruling out brain’s electrolyte concentrations. Blood ammonia
other neuromuscular or musculoskeletal abnormali- concentrations increase in patients with liver failure
ties, particularly in cases with only mild signs, or because of a lack of conversion of ammonia in the