15 Neurological and Locomotory Conditions • Cases involving the brain will show abnormal behaviour, e.g. wandering and head-pressing. • There may be apparent blindness. • More advanced signs will include seizures, dementia and coma, which will lead to death. • The cerebellum regulates the rate and range of motion, and correlates proprioceptive information. Signs will include the lack of both menace response and blink reflex to light. There may be head tremors, a base-wide stance and ataxia. • The brainstem includes the cranial nerves. There may be ptosis and an altered eye position with damage to the 3rd, 4th or 6th cranial nerves. There will be a loss of facial sensation with damage to the 5th cranial nerve. Damage to the 7th cranial nerve will show facial paralysis. There will be a head tilt and nystagmus with damage to the 8th cranial nerve. Damage to the 9th and 10th cranial nerves will be manifest as dysphagia. The brainstem includes long tracts to the spinal cord, and damage to these may be seen as weakness, ataxia and spastic limbs, all with concurrent cranial nerve deficits. • There will be a loss of coordination and weakness caudal to the lesion, and possibly sensory deficits. Focal sweating due to sympathetic fibre damage or tectosegmental spinal tract damage may also be evident. • Tetanus is the classic upper motor neuron disease. The associated neurotoxins block inhibition of the spinal motor neurons, leading to an over-response from the lower motor neurons. • There will be a regional loss of motor function. • There will be muscle atrophy and profound weakness localized to specific areas. • With equine motor neuron disease (see Section 15.15) there is profound and progressive diffuse muscle atrophy and weakness. • The botulism toxin affects neuromuscular junctions, causing poor muscle tone (as evidenced by a flaccid anus), weakness, stumbling, dysphagia and eventual recumbency. The 12 cranial nerves and their respective functions are listed in Table 15.1. Is the horse ill and does it have neurological signs? Is there a neurological disorder? The following checklist is recommended: • mental attitude (cerebrum); • normal behaviour, e.g. nystagmus, eye position (cranial nerves III, VI); • check menace tests (cranial nerves II, VII); • pupillary light reflexes (cranial nerves II, III); • swinging light test (cranial nerve II); • funduscopic examination; • symmetry of the head; • inspection of the tongue; • nasal septum response; • gait at walk and trot, turning and faster gaits if not dangerous. Is the neurological disorder primary or secondary? The following checklist is recommended: • depression from systemic illness, e.g. endotoxaemia; • Horner’s syndrome with guttural pouch empyaema; • patchy sweating from excitement or distress; • abnormal limb placement due to dullness, lethargy, pyrexia from other systemic disease; • unusual lameness, e.g. equine granulocytic ehrlichiosis; • difficulty in rising, e.g. muscular weakness or arthritis; • collapse under excessive weight being carried. Neurological examination protocol is as follows: • Perform a full clinical examination first before concentrating on the neurological signs. • Initiate a chart to record findings and try to have a consistent order of examination. • One logical course of action is to start at the head and move caudally: ੦ head (brain and cranial nerves); ੦ neck; ੦ fore limbs; ੦ trunk; ੦ hind limbs; ੦ tail; ੦ anus; ੦ gait and posture. The aim of the examination is to localize the lesion(s): • brain cortex; • cerebellum; • vestibulum; • any other part of the brain stem; • spinal cord; • peripheral nerves; • neuromuscular junction; • muscles. Ancillary diagnostics can then be considered: • blood tests for bacterial infections, potassium and calcium concentrations and liver disease; • radiography for fracture lines in the head, which are often difficult to image; frontoparietal fractures are often visible externally; • cerebrospinal fluid (CSF) analysis, which may be unremarkable but will reveal EPM, EHV-1 (see Section 13.3) and bacterial meningitis in the foal. • Liver disease (hepatoencephalopathy). This clinical syndrome occurs in severe hepatic insufficiency from a variety of causes. Toxins, e.g. ammonia, fatty acids and indoles, which would normally be detoxified by the liver increase in the peripheral blood and cross the blood–brain barrier. There is marked cranial depression. The signs seen will include head-pressing, head-hanging, yawning, ataxia, inappetance, sham drinking and even compulsive walking and aggression. Unfortunately, the prognosis at this stage is hopeless and euthanasia is advocated.
15.1 Neurological Locations and Associated Signs
The brain
More specific areas of the brain
The spinal cord
Peripheral nervous system
Assessment of cranial nerve function
15.2 Approach to the Equine Neurological Case
Some common neurological conditions causing illness