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Equine II > Non-infectious neurological disease > Flashcards

Non-infectious neurological disease Flashcards

1
Q

Non-infectious causes of neurological disease in horses

A

Head trauma*

Headshaking* - common and important

Hyperammonaemia and hepatic encephalopathy*

EMND*

Cauda equina syndrome

Polyneuritis equi

THO

Horner’s syndrome

Shivers

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2
Q

Common mechanisms of head injury

A

Blunt trauma - run into something

Forward roll - flip over fence

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3
Q

Common injuries after a head on impact

A

Frontal/parietal fractures

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

Cervical trauma
- cranial C-spine injury

CN abnormalities

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4
Q

What is a coup injury?

A

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

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5
Q

What is a contrecoup injury>

A

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

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6
Q

Common injuries after a poll impact

A

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

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7
Q

Approach to head trauma

A

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

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8
Q

Management of seizures

A

Diazepam (?), phenobarbital, midazolam

KBr

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9
Q

Management of increased intracranial pressure

A

7.2% saline> mannitol

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10
Q

Steroid use after a head injury

A

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.

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11
Q

Clinical signs of head shaking

A

Shaking/flipping vertically

‘Insect up the nose’

Muzzle/face rubbing

Snorting

Shaking horizontally

Strikes at face with foot

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12
Q

Presentation of head shaking horses

A

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.

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13
Q

Less common signs of head shaking

A

Avoidance of airflow straight onto face whilst exercising

Muscle fasciculations and facial grimacing

Lip smacking

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14
Q

What can trigger head shaking?

A

Wind

Rain

Sunlight

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15
Q

Cause of head shaking

A

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

Trigeminal neuropathy

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16
Q

Gross pathological diseases causing direct trigeminal neuropathy

A

Pemphigous foliaceous

Temporohyoid osteopathy

Idiopathic headshakers - ? lower threshold of activation of trigeminal nerve

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17
Q

Pemphigus foliaceous in horses

A

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

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18
Q

Temporohyoid osteopathy

A

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

Violent vertical headshaking

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19
Q

Idiopathic head shakers

A

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.

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20
Q

Roberts et al grading of head shaking

A

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

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21
Q

Infraorbital block for headshakers

A

More horses made worse than improved

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22
Q

Complications of maxillary nerve block for head shakers

A

Haematoma

Worsening of signs

Temporary blindness

Abscess/neuroma

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23
Q

Limitations of maxillary nerve block for headshakers

A

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

24
Q

Treatment of idiopathic headshakers

A

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

25
Q

Pharmaceutics for headshaking

A

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)

26
Q

Percutaneous electrical nerve therapy for idiopathic headshakers

A

To treat trigeminal neuropathy

Sedate (ACP, detomidine drip, morphine)

Needle of probe just superficial to nerve

Safe, well tolerated, repeatable, short competition withdrawal time

27
Q

Hyperammonia and hepatic encephalopathy (HE)

A

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

28
Q

Clinical signs of Hyperammonia and hepatic encephalopathy (HE)

A

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

29
Q

Treatment of hyperammonia and hepatic encephalopathy

A

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

30
Q

Equine motor neurone disease

A

EMND

Neurodegenerative disease causing LMN signs

Secondary to vitamin E deficiency

30% neurons affected before clinical signs

31
Q

Clinial signs of equine motor neurone disease (EMND)

A

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)

32
Q

Diangosis of equine motor neurone disease

A

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

33
Q

Treatment of equine motor neurone disease

A

Vitamin E supplementation

20% deteriorate, 40% stabilise, 40% improve significantly – manage expectations

34
Q

Cauda equina syndrome

A

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

35
Q

Polyneuritis equi

A

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

36
Q

Diseases relating to the guttural pouch that cause neuro signs

A

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

37
Q

Cranial nerves in/adjacent to medial guttural pouch

A

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

38
Q

Cranial nerves in/adjacent to lateral guttural pouch

A

Mandibular V, VII, VIII

39
Q

Temporohyoid osteoarthropathy

A

‘THO’

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

40
Q

Possible aetiologies of temporohyoid osteoarthropathy

A

Spread of infection from middle/inner ear

Non-septic degenerative joint disease

Traumatic

41
Q

Clinical signs of temporohyoid osteoarthropathy

A

CN VII dysfunction
§ asymmetry, corneal ulcers from exposure keratopathy

CN VIII nerve dysfunction
§ Head tilt, nystagmus, ‘dizzy’, ataxia

Dysphagia

42
Q

Diagnosis of temporohyoid oesteoarthropathy

A

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

43
Q

Treatment of temporohyoid osteoarthropathy

A

Anti-inflammatories +/- antimicrobials

Surgical ceratohyoidectomy

44
Q

Horner’s syndrome in horses

A

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.

45
Q

Sympathetic innervation to the head - pathway

A

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

46
Q

Cervical trauma leading to head sweating in horses

A

Loss of sympathetic innervation leaves hypersensitive to circulating adrenaline?

The line is perfectly smooth - only affects one side of the body

47
Q

Shivers

A

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

48
Q

Post anaesthetic facial nerve paralysis

A

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

49
Q

Post anaesthetic radial nerve paralysis

A

Present with dropped elbow and unable to bear weight

Either trauma or a relatively common anaesthetic complication

50
Q

Post anaesthetic spinal cord malacia

A

Dog sitting after general anaesthesia, flaccid paralysis caudal to lesion

Usually young heavy breed horses

Hopeless prognosis

51
Q

Cervical vertebral stenotic myelopathy

A

-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

52
Q

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

A

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)

53
Q

Pathogenesis of Cervical vertebral stenotic myelopathy

A

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

54
Q

Diagnosis of Cervical vertebral stenotic myelopathy

A

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

55
Q

Treatment of cervical vertebral stenosic myelopathy

A

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

Equine II (28 decks)

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