Page 1106 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Nervous system 1081

VetBooks.ir for bacterial colonisation of the CNS. Intracranial nerve(s). Swelling of the cerebral hemispheres may
cause herniation caudally against the midbrain (sub-
bleeding is more common in neonates.
It is thought that the shock of the skull trauma
initiates marked neuronal depolarisation and a tran- tentorial herniation) and lead to signs such as dilated
unresponsive pupils (Fig. 10.33) and tetraparesis.
sient coma, a characteristic of severe concussion. Non-neurological signs may include epistaxis
This depolarisation results in a huge rise in intracel- (from the sinuses, ethmoids or nasal turbinates). Via
lular calcium, which disrupts the usual axonoplasmic poorly understood mechanisms, there may also be
flow. This results in degeneration of the distal axon (1) neurogenic pulmonary oedema and consequent
and is referred to as diffuse axonal injury. Trauma respiratory distress and (2) sympathetic arterial
to the frontal or parietal bones is more concerning hypotension due to myocardial damage (possibly
when the object causing the trauma is narrow and mediated by sympathetic neurons).
irregular (a hoof, or narrow post) than when it has
a broader focus. In fact, when a horse stumbles and Diagnosis
hits a tree, a wall or the ground (the broadest of all A history of head trauma or clinical evidence of
structures to head-butt!) at speed, the impact forces trauma (abrasions, lacerations) is often present. If
tend to be carried through the occipital condyles to head trauma is known or highly suspected, the diag-
the cervical vertebrae, causing upper cervical verte- nostic plan should be to localise the lesion and estab-
bral fractures and spinal cord injury. lish a baseline neurological examination to monitor
progression of the disease. If a history of trauma is
Clinical presentation less clear, testing to rule out other conditions may be
In severe cases, an initial period of unconsciousness warranted. The possibility of an unobserved primary
of variable length may be encountered. Depending generalised seizure, with secondary head trauma,
on the degree of intracranial hypertension (associ- should be considered in horses found where there
ated with cerebral oedema and haemorrhage), vary- are signs of a struggle (broken fences, abrasions of
ing degrees of consciousness and central depression the trunk/bony prominences/head and depression).
may be observed over time. Horses may stay in lateral
recumbency for several hours with minimal reflexes, Management
and then may remain in sternal recumbency for a In most cases (i.e. those that do not require immedi-
significant period before attempting to rise. When ate surgical intervention because of depressed skull
horses remain standing, or do get up quickly after a fractures) early management is supportive and medi-
fall, they may be seen to wander towards the side of cal. Any other life-threatening conditions should
the lesion. If made to stand still, these horses tend to be attended to first, because the trauma associated
display a head and neck turn towards the direction with the cerebral injury may have caused other more
of their circling. Ataxia is not usually seen unless immediate problems such as cardiac arrhythmias.
there is progressive involvement of other parts of the Seizures or excessive, difficult to manage, thrash-
brain. ing may require sedation or short-term anaesthesia.
PLRs are usually brisk, but there may be Diazepam (5 mg [foal] or 50–100 mg [adult] i/v or
some asymmetry of the pupils and miosis. i/m) can be repeated as necessary to control seizures.
Characteristically there is central blindness and Phenobarbital (12 mg/kg i/v loading dose followed
depressed menace responses. However, in cases with by 6 mg/kg i/v q12 h) or pentobarbital (150–
optic nerve avulsion, PLRs are reduced or absent, 1,000 mg i/v for foals; for adults, slow increments
and the pupils are often dilated immediately after of 500–1,000 mg i/v to effect) may also be used to
the injury (Figs. 10.31, 10.32). As mentioned above, control seizures. Care should be taken with these
blindness from optic nerve injury is notorious for drugs, as they are highly protein bound and can be
appearing several hours, days or even weeks after the displaced by other drugs, leading to a larger amount
original traumatic incident, due to secondary inflam- of free or active drug. Repeated seizures may require
matory or ischaemic/reperfusion injury to the optic long-term therapy and more than one antiseizure