Non-infectious neurological disease

Question 1

Non-infectious causes of neurological disease in horses

Answer 1

Head trauma*

Headshaking* - common and important

Hyperammonaemia and hepatic encephalopathy*

EMND*

Cauda equina syndrome

Polyneuritis equi

THO

Horner’s syndrome

Shivers

Question 2

Common mechanisms of head injury

Answer 2

Blunt trauma - run into something

Forward roll - flip over fence

Question 3

Common injuries after a head on impact

Answer 3

Frontal/parietal fractures

Cerebral injury
- Coup/contrecoup injuries
- bruising/swelling
- may take time

Cervical trauma
- cranial C-spine injury

CN abnormalities

Question 4

What is a coup injury?

Answer 4

when the contusions on the brain are directly below the point of trauma

Question 5

What is a contrecoup injury>

Answer 5

when the contusions on the brain are directly opposite the point of trauma

Question 6

Common injuries after a poll impact

Answer 6

commonly younger horses that rear up and go over backwards

Basilar/occipital/temporal bone fractures

Cerebral/brainstem injury

CN abnormalities

Rectus capitus muscle avulsion fractures

Question 7

Approach to head trauma

Answer 7

Managed symptomatically in the majority of cases

Head CT > radiographs

If you need to collect CSF then it is safer to collect from the lumbosacral space after a head injury

Question 8

Management of seizures

Answer 8

Diazepam (?), phenobarbital, midazolam

KBr

Question 9

Management of increased intracranial pressure

Answer 9

7.2% saline> mannitol

Question 10

Steroid use after a head injury

Answer 10

Remains controversial – some sources say they are harmful (extrapolated from human data) at high doses but are happy to give traditional anti-inflammatory doses of dexamethasone or prednisolone.

Question 11

Clinical signs of head shaking

Answer 11

Shaking/flipping vertically

‘Insect up the nose’

Muzzle/face rubbing

Snorting

Shaking horizontally

Strikes at face with foot

Question 12

Presentation of head shaking horses

Answer 12

Usually present with uncontrollable (spontaneous), repeatable, persistent or intermittent repeatable vertical or horizontal movements of the head and neck.

In most cases, when examined carefully at rest, there is some evidence of subtle signs.

It is the exception that horses show signs at rest only, the majority of cases have signs at rest that are worse at exercise.

Question 13

Less common signs of head shaking

Answer 13

Avoidance of airflow straight onto face whilst exercising

Muscle fasciculations and facial grimacing

Lip smacking

Question 14

What can trigger head shaking?

Answer 14

Wind

Rain

Sunlight

Question 15

Cause of head shaking

Answer 15

“Neurosis of the intra-orbital portion of the supermaxillary division of the trifacial nerve”

Trigeminal neuropathy

Question 16

Gross pathological diseases causing direct trigeminal neuropathy

Answer 16

Pemphigous foliaceous

Temporohyoid osteopathy

Idiopathic headshakers - ? lower threshold of activation of trigeminal nerve

Question 17

Pemphigus foliaceous in horses

Answer 17

Autoimmune disease affecting the cell to cell attachment

Dermatopathy with excessive crusting

Most likely painful, can turn face away from flow of air as that can make it more uncomfortable

Question 18

Temporohyoid osteopathy

Answer 18

Unilateral signs
- ear sensitivity
- facial nerve paralysis
- corneal ulceration

Violent vertical headshaking

Question 19

Idiopathic head shakers

Answer 19

may have lower threshold of activation of trigeminal nerve

Affected horses had a much lower threshold (< 5 mA) compared to control horses (> 10 mA). In remission, one horses tested like a control horse suggesting that the condition could be a reversible functional problem.

Question 20

Roberts et al grading of head shaking

Answer 20

Grade 1 - signs only whilst exercising and can still be ridden

Grade 2 - signs at exercise but cannot be ridden (unsafe/impossible)

Grade 3 - signs at rest and exercise

Question 21

Infraorbital block for headshakers

Answer 21

More horses made worse than improved

Question 22

Complications of maxillary nerve block for head shakers

Answer 22

Haematoma

Worsening of signs

Temporary blindness

Abscess/neuroma

Question 23

Limitations of maxillary nerve block for headshakers

Answer 23

Not a specific diagnosis of idiopathic headshaking

Anything causing pain in the desensitised region (e.g. dental pain) could be blocked out

maxillary nerve block does not reduce conduction velocity of the nerve

Question 24

Treatment of idiopathic headshakers

Answer 24

Current treatments are not specific

None have been shown to be entirely curative

Surgical treatment is a last resort
- compression of the infraorbital nerve by titanium coils

Nose nets/facemasks

Medication

Percutaneous electrical nerve therapy

Question 25

Pharmaceutics for headshaking

Answer 25

Cyprohepadine - antihistamine - antiseratogenic drug - can cause lethery, inappetance, and drowsiness Carbamazepine - GABA agonist and voltage gated Na channel blocker - reduced excitability of neurones Gabapentin - GABA agonist - NMDA R (analgesia)

Question 26

Percutaneous electrical nerve therapy for idiopathic headshakers

Answer 26

To treat trigeminal neuropathy Sedate (ACP, detomidine drip, morphine) Needle of probe just superficial to nerve Safe, well tolerated, repeatable, short competition withdrawal time

Question 27

Hyperammonia and hepatic encephalopathy (HE)

Answer 27

Mechanism not fully understood Increased ammonia concentration from either liver disease, or secondary to gastrointestinal pathology Cerebral oedema, ?astrocyte swelling May have other signs of liver disease

Question 28

Clinical signs of Hyperammonia and hepatic encephalopathy (HE)

Answer 28

Yawning frequently, dull, aimless wandering, head pressing, aggression

Question 29

Treatment of hyperammonia and hepatic encephalopathy

Answer 29

May not attempt if severe liver disease Hypertonic saline to reduce cerebral oedema Lactulose - to decrease ammonia in circulation Antimicrobials? DMSO? Liver biopsy Fix primary intestinal dysbiosis

Question 30

Equine motor neurone disease

Answer 30

EMND Neurodegenerative disease causing LMN signs Secondary to vitamin E deficiency 30% neurons affected before clinical signs

Question 31

Clinial signs of equine motor neurone disease (EMND)

Answer 31

Lose muscle mass, narrow based stance, weakness rather than ataxia Oxidative neuronal damage and neurogenic muscle atrophy - Type I muscle worst affected as higher oxidative requirement Pigment retinopathy - Lipofuscin deposits (brown)

Question 32

Diangosis of equine motor neurone disease

Answer 32

Serum vitamin E concentration SCMD muscle biopsy ○ Usually diagnostic EMG? ○ Nice if you have access but most do not Ventral branch of spinal accessory nerve biopsy ○ More sensitive than muscle biopsy but not widely available

Question 33

Treatment of equine motor neurone disease

Answer 33

Vitamin E supplementation 20% deteriorate, 40% stabilise, 40% improve significantly – manage expectations

Question 34

Cauda equina syndrome

Answer 34

Syndrome, not single disease entity – different potential causes Varying degrees of urinary and faecal incontinence May have hindlimb ataxia/weakness Cauda equina neuritis (can cause the syndrome but is own disease entity) immune mediated inflammatory often also causes cranial nerve signs - CNs asymmetric

Question 35

Polyneuritis equi

Answer 35

Granulomatous infiltration of extradural cauda equina Also includes cranial nerves relatively commonly ○ Esp. VII, V, and vestibular signs common Paralysis of tail/anus/perineum/rectum/bladder etc as per cauda equina syndrome Prognosis is poor Supportive short term

Question 36

Diseases relating to the guttural pouch that cause neuro signs

Answer 36

A lot of important structures in the guttural pouches, including major vessels as well as cranial nerves Guttural pouch disease is commonly implicated in neurological equine cases, especially those showing cranial nerve deficits. Therefore endoscopic evaluation is commonly performed in neurological cases coming through medicine Clinical signs of guttural pouch disease can be very variable Wide ranging clinical signs possible with GP disease

Question 37

Cranial nerves in/adjacent to medial guttural pouch

Answer 37

pharyngeal X, IX, XI, XII, cranial sympathetic ganglia

Question 38

Cranial nerves in/adjacent to lateral guttural pouch

Answer 38

Mandibular V, VII, VIII

Question 39

Temporohyoid osteoarthropathy

Answer 39

‘THO’ Degenerative temporohyoid articulation change ○ Articulation between stylohyoid and temporal bones ○ -> fractures of petrous temporal/stylohyoid bones

Question 40

Possible aetiologies of temporohyoid osteoarthropathy

Answer 40

Spread of infection from middle/inner ear Non-septic degenerative joint disease Traumatic

Question 41

Clinical signs of temporohyoid osteoarthropathy

Answer 41

CN VII dysfunction § asymmetry, corneal ulcers from exposure keratopathy CN VIII nerve dysfunction § Head tilt, nystagmus, ‘dizzy’, ataxia Dysphagia

Question 42

Diagnosis of temporohyoid oesteoarthropathy

Answer 42

Endoscopy § Look for thickening of the articulation of the stylohyoid bone in the dorsal GP § Stylohyoid bone divides the GP into medial and lateral compartments Advanced imaging § E.g. CT, radiography may be helpful but is less sensitive

Question 43

Treatment of temporohyoid osteoarthropathy

Answer 43

Anti-inflammatories +/- antimicrobials Surgical ceratohyoidectomy

Question 44

Horner's syndrome in horses

Answer 44

Interruption to sympathetic innervation Lesions can be anywhere (neck, guttural pouch, cranial thorax) Guttural pouch disease and neck lesions (e.g. secondary to injection complications) are more common than thoracic lesions Sweating, miosis, ptosis etc.

Question 45

Sympathetic innervation to the head - pathway

Answer 45

starts in midbrain -> down spinal cord -> T1-T3 -> exit in ventral spinal nerve roots -> cervicothoracic and middle cervical ganglia -> ascend in cervical vagosympathetic trunk -> cranial cervical ganglia (next to GPs) -> postganglionic sympathetic nerve

Question 46

Cervical trauma leading to head sweating in horses

Answer 46

Loss of sympathetic innervation leaves hypersensitive to circulating adrenaline? The line is perfectly smooth - only affects one side of the body

Question 47

Shivers

Answer 47

Flexed, shivering hindlimb posture Worse when backing up, may progress to affect forward movement too Limb held in hyperflexion away from body, rigidly for prolonged time, hip extended Unilateral or bilateral Chronic, progressive condition Neuromuscular condition of unknown aetiology No treatment

Question 48

Post anaesthetic facial nerve paralysis

Answer 48

Deviated muzzle away from lesion Facial nerve is superficial and easily damaged – check table padding, take headcollar off etc. May also see corneal ulcers with facial nerve paralysis due to exposure keratopathy

Question 49

Post anaesthetic radial nerve paralysis

Answer 49

Present with dropped elbow and unable to bear weight Either trauma or a relatively common anaesthetic complication

Question 50

Post anaesthetic spinal cord malacia

Answer 50

Dog sitting after general anaesthesia, flaccid paralysis caudal to lesion Usually young heavy breed horses Hopeless prognosis

Question 51

Cervical vertebral stenotic myelopathy

Answer 51

-CVSM, also called CVM, CVCM (compressive myelopathy), wobblers syndrome… The most common non-infectious cause of spinal cord ataxia in horses in the UK Two main types

Question 52

What are the two main types of Cervical vertebral stenotic myelopathy (CVSM)

Answer 52

Young horses (usually rapid growing) - malformation of the vertebral canal, cervical vertebrae, or ligamentous attachments - mid C-spine most common Older horses with osteoarthritic change of articular processes - caudal C-spine (C5-T1)

Question 53

Pathogenesis of Cervical vertebral stenotic myelopathy

Answer 53

Stenosis of canal causes compression of spinal cord at one or more sites in the spine Static – compression in neutral position Dynamic – compression when neck flexed/extended First sign is reduced proprioception (ataxia) Progressing to paresis and/or spasticity as the compression worsens Hindlimbs > forelimbs ○ Hindlimbs – spinocerebellar tracts are more peripheral and therefore compressed first Bilateral, but degree of change in each limb can vary depending on area of compression

Question 54

Diagnosis of Cervical vertebral stenotic myelopathy

Answer 54

History Clinical exam Image C1-T1 if possible - narrowing of vertebral canal Plain radiography - standing lateral - hard to interpret as only one plane Myelography - more definitive

Question 55

Treatment of cervical vertebral stenosic myelopathy

Answer 55

Conservative - anti-infalmmatories - restrict diet - restrict exercise - can inject facet joint with steroid in older horses Surgery - aim to fuse ventral vertebral bodies - success variable - can have fatal complications - recovery can take >1yr