Non-infectious neurological disease Flashcards
Non-infectious causes of neurological disease in horses
Head trauma*
Headshaking* - common and important
Hyperammonaemia and hepatic encephalopathy*
EMND*
Cauda equina syndrome
Polyneuritis equi
THO
Horner’s syndrome
Shivers
Common mechanisms of head injury
Blunt trauma - run into something
Forward roll - flip over fence
Common injuries after a head on impact
Frontal/parietal fractures
Cerebral injury
- Coup/contrecoup injuries
- bruising/swelling
- may take time
Cervical trauma
- cranial C-spine injury
CN abnormalities
What is a coup injury?
when the contusions on the brain are directly below the point of trauma
What is a contrecoup injury>
when the contusions on the brain are directly opposite the point of trauma
Common injuries after a poll impact
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
Approach to head trauma
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
Management of seizures
Diazepam (?), phenobarbital, midazolam
KBr
Management of increased intracranial pressure
7.2% saline> mannitol
Steroid use after a head injury
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.
Clinical signs of head shaking
Shaking/flipping vertically
‘Insect up the nose’
Muzzle/face rubbing
Snorting
Shaking horizontally
Strikes at face with foot
Presentation of head shaking horses
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.
Less common signs of head shaking
Avoidance of airflow straight onto face whilst exercising
Muscle fasciculations and facial grimacing
Lip smacking
What can trigger head shaking?
Wind
Rain
Sunlight
Cause of head shaking
“Neurosis of the intra-orbital portion of the supermaxillary division of the trifacial nerve”
Trigeminal neuropathy
Gross pathological diseases causing direct trigeminal neuropathy
Pemphigous foliaceous
Temporohyoid osteopathy
Idiopathic headshakers - ? lower threshold of activation of trigeminal nerve
Pemphigus foliaceous in horses
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
Temporohyoid osteopathy
Unilateral signs
- ear sensitivity
- facial nerve paralysis
- corneal ulceration
Violent vertical headshaking
Idiopathic head shakers
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.
Roberts et al grading of head shaking
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
Infraorbital block for headshakers
More horses made worse than improved
Complications of maxillary nerve block for head shakers
Haematoma
Worsening of signs
Temporary blindness
Abscess/neuroma
Limitations of maxillary nerve block for headshakers
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
Treatment of idiopathic headshakers
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
Pharmaceutics for headshaking
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)
Percutaneous electrical nerve therapy for idiopathic headshakers
To treat trigeminal neuropathy
Sedate (ACP, detomidine drip, morphine)
Needle of probe just superficial to nerve
Safe, well tolerated, repeatable, short competition withdrawal time
Hyperammonia and hepatic encephalopathy (HE)
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
Clinical signs of Hyperammonia and hepatic encephalopathy (HE)
Yawning frequently, dull, aimless wandering, head pressing, aggression
Treatment of hyperammonia and hepatic encephalopathy
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
Equine motor neurone disease
EMND
Neurodegenerative disease causing LMN signs
Secondary to vitamin E deficiency
30% neurons affected before clinical signs
Clinial signs of equine motor neurone disease (EMND)
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)
Diangosis of equine motor neurone disease
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
Treatment of equine motor neurone disease
Vitamin E supplementation
20% deteriorate, 40% stabilise, 40% improve significantly – manage expectations
Cauda equina syndrome
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
Polyneuritis equi
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
Diseases relating to the guttural pouch that cause neuro signs
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
Cranial nerves in/adjacent to medial guttural pouch
pharyngeal X, IX, XI, XII, cranial sympathetic ganglia
Cranial nerves in/adjacent to lateral guttural pouch
Mandibular V, VII, VIII
Temporohyoid osteoarthropathy
‘THO’
Degenerative temporohyoid articulation change
○ Articulation between stylohyoid and temporal bones
○ -> fractures of petrous temporal/stylohyoid bones
Possible aetiologies of temporohyoid osteoarthropathy
Spread of infection from middle/inner ear
Non-septic degenerative joint disease
Traumatic
Clinical signs of temporohyoid osteoarthropathy
CN VII dysfunction
§ asymmetry, corneal ulcers from exposure keratopathy
CN VIII nerve dysfunction
§ Head tilt, nystagmus, ‘dizzy’, ataxia
Dysphagia
Diagnosis of temporohyoid oesteoarthropathy
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
Treatment of temporohyoid osteoarthropathy
Anti-inflammatories +/- antimicrobials
Surgical ceratohyoidectomy
Horner’s syndrome in horses
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.
Sympathetic innervation to the head - pathway
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
Cervical trauma leading to head sweating in horses
Loss of sympathetic innervation leaves hypersensitive to circulating adrenaline?
The line is perfectly smooth - only affects one side of the body
Shivers
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
Post anaesthetic facial nerve paralysis
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
Post anaesthetic radial nerve paralysis
Present with dropped elbow and unable to bear weight
Either trauma or a relatively common anaesthetic complication
Post anaesthetic spinal cord malacia
Dog sitting after general anaesthesia, flaccid paralysis caudal to lesion
Usually young heavy breed horses
Hopeless prognosis
Cervical vertebral stenotic myelopathy
-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
What are the two main types of Cervical vertebral stenotic myelopathy (CVSM)
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)
Pathogenesis of Cervical vertebral stenotic myelopathy
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
Diagnosis of Cervical vertebral stenotic myelopathy
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
Treatment of cervical vertebral stenosic myelopathy
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
