Neurology: Cattle Neurology Flashcards
What should be inspected of surroundings for neurological disease?
- Lead
- Ration- proprotion of conc, silage quality
- Poisonous plants
- Cadavers
What are the following observations signs of?
1. Circling
2. Falling over
3. Head-pressing
- Asymmetrical cortex lesion
- Cerebellum lesion
- ICP/encephalitis
What can be observed about stance and locomotion at a distance?
Stance
* Tremors- rapid contractions
* Spasms- sudden, contractoins of muscles- tetanus
* Spasticity- increased muscle tone- brain stem, spinal cord lesion
Locomotion
* Decreased coordination
* Weakness- paresis or paralysis
What can be inspected on hands on clinical exam of skull and vertebrae?
- Inspection- symmetry, muscle atrophy
- Palpation- pain, crepitus
- Percussion- finger (head), fist (neck)
- Passive movement- bend head/neck in all directions
Reflexes- cerebellum, brain stem, spinal reflex
What is the normal function of the brain stem/cranial nerves
Cerebellum
Spinal cord/peripheral nerves
Brain stem/CN
* cranial nerve functions
Cerebellum
* unconscious control of proprioceptive functions- coordination and smoothing of movements
Spinal cord/peripheral nerve
* Limb strength and movement
What are the 6 steps to neurological exam?
- Mental status
- Cranial nerves
- Gait and posture
- Postural reactions
- Spinal reflexes
- Response to pain
What does mental status tell us?
- Helps differentiate between intracranial and extracranial lesions
- Brainstem- arousal, appear sedated but aware of surrondings
- Thalamocortex- cognititive function, fail to react to environmental stimuli, seperates from herd- head pressing, tilt, circling, blindness
Check for menace response, nasal septum stim (absent if cortical involvement)
What does nasal septum stimulation test?
Tests CN V and thalamocortex
What are the 12 cranial nerves?
Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducent
Facial
Vestibulo-cochlear
Glossopharyngeal
Vagal
Accessory
Hypoglossal
What does the menace response test?
What does the PLR test?
Menace- CN II, VII, cortex, cerebellum
PLR- CN II and III
What is responsible for eye position and movement?
What is responsible for physiological nystagmus?
What is responsible for palpebral reflexes and facial symmetry?
Eye position and movement
* CN III, IV, VI
Physiological nystagmus
* CN III, IV, VI, VII
Palpebral reflex
* CN V, VII
Facial symmetry
* CN VII
What would caus head tilt and pathological nystagmus?
CN VII
- Assess animal facing you- eye should be horizontal
- Check for pathological nystamus- fast phase away from side of lesion
What CN are responsible for food prehension and chewing?
What CN dyfunctions can cause dysphagia and laryngeal problems?
Food prehension and chewing
* XII and V
* Unilateral XII- tongue falls from side of mouth toward lesion
Dysphagia and laryngeal- CN IX and X
What are the three types of ataxia?
- Vestibular
- Cerebellar
- Proprioceptive
How can vestibular ataxia be identified?
- Always head tilt
- Hypermetra
- Hypertonia
- Unilateral cerbellar- animal will lean towards head tilted side
- Bilateral vestibular dysfunction is more subtle
How can cerebeller ataxia be identified?
When is proprioceptive ataxua usually observed?
No proprioceptive defecits or weakness as pathways to and from the limbs to cerebrum are ok
Proprioceptive
Spinal cord disease
Look at foot placements
What spinal reflexes can be used?
Extensor reflex of front limb
* radial nerve dysfunction- dropped elbow
Patellar reflex
* tap patellar tendon and observe extension of stifle
Flexor
* front limbs axillary, median, ulnar,
Musce tone- passively flex and look for symmetry
How is the perineal reflex tested and what does it test?
Gently touch under the tail- downward contraction of the tail and anal sphincter contraction
Pudenal and caudal nerves
How can CSF fluid be taken and analysed?
- Lumbosacral space
- 4 inch spinal needle
- Protein and cytology
- Clear and colourless
What are common clinical signs localisable to cerebrum?
- Opisthotonos- stargazing
- Apparent blindness- intact PLR
- Abnormal mentation
- Change in behaviour
- Aimless wandering
- Seizures
- Abnormal vocalisation
- Ataxia without weakness
- Absent menace
- Hypermetria
What are clinical signs localisable to the vestibular system?
Peripheral and Central:
* Head tilt to lesion side
* Falling/circling/leaning
Just central:
* Nystagmus
* Proprioception defecits on side of lesion
* Depresion/Anorexia
How are the following CN assessed?
1. II
2. V
3. VI
4. VII
5. VIII
6. IX and X
7. XII
- Optic- blindness and abscence of PLR, dilated pupils
- Trigeminal- loss of sensation to head and cornea
- Abducens- ventromedial strabismus, inability to retract globe
- Facial- motor muscles to face- droopy ears/eyelids/lips, unable to blink
- Vestibulo-cochlear- head tilt, circling, leaning/falling
- Glossopharyngeal and vagal- can’t swallow
- Hypoglossal- cannot retract tongue
What clinical signs show reticular activation system, thalamus lesions?
- Depression, altered mentation
- Difficulty regulating body temp
- Depressed respiration
How can clinical signs be localised to spinal cord:
1. C1-C5
2. C6-T2
3. T3-L3
4. L4-L6
5. S1-S3
- Altered head and neck movements- no CN defectits- FL and HL reflexes exaggerated
- Depressed or absent reflexes with reduced muscle tone in the FLs and exaggerated HL reflexes with normal muscle tone in the HLs
- Reflexes in FL normal- HL exaggerated, proprioceptigve defectits in the HLs with ataxia
- Absence of HL reflexes and decreased muscle tone
- Decreased anal tone, loss of sensation to perineal region
What are the signs of cerebrum diseases?
- Circling
- Blindness
- Mania
- Aggressive behaviour
- Head pressing
What could cause acute cerebral cortex signs?
Acute:
* CCN
* Lead poisoning- contact APHA
* Nervous ketosis
* Hypocalcaemia
* Hypomag
* Salt poisoning
* IBR
* Pseudorabies- contact APHA
* Rabies- contact APHA
What could cause chronic cortical signs?
- Brain abscess
- BSE
- Hypovitaminosis A
- Brain tumour
What cattle most commonly are affected by meningitis?
Calves 1 week of age without enough colosturm
May present like staggers
* lack of suck reflex
* Head pressing
How is meninigitis diagnosed and treated?
Diagnosis
* CSF- increase in protein and WBC
Treatment
* Poor
* Consider euthanasia
* Can give IV ABs
What ABs penetrate the brain?
- B-lactams- do not diffuse well into the CSF but have high safety margin so can achieve therapeutic conc
- Potentiated sulphonamides
- Aminoglysides- high conc
- Fluoroquionolones- protected
- Pot Sulphonamides
What normally causes a brain abscess?
What are the initial signs and later signs?
Truperella pyogenes often extension of sinus infection
Initial: vision loss/mydriasis in contralateral eye, compulsive walking, head pressing, circling, head tilt, depression, mania
Later: hypertonicity, hyperflexia, opisthotonus, coma, convulsions
ABs- prognosis poor
What is hydrocephalus
- Failure of drainage of CSF therefore increased intracranial pressure
- Domed cranium
- Diffuse cerebral signs-mania, head pressing, muscle tremors
What is hydrocephalus
- Failure of drainage of CSF therefore increased intracranial pressure
- Domed cranium
- Diffuse cerebral signs-mania, head pressing, muscle tremors
What causes cerebrocortical necrosis?
When is it most common?
What are the clinical signs?
Thiamine- vit B1 deficiency
Necrosis of greay matter
Most common in cattle 6-18 months old
CS
* dead
* early- head in air, appear blind, PLR present, disorientates
* late- opisthotonos, head pressing, strabismus, miosis, exitement, recumbent
Blindness and stargazing
PM- brain pale and swollen
How is CCN treated and controlled?
- 10-15 mg/kg thiamine repeated every 4 hours for 24 hours
Identify and rectify underlying cause
What are the clinical signs of lead poisoning?
First
* stand alone and depressed
* hyperaesthesia, muscular fasiculations
Progress
* ataxia
* blindness
* head pressing
* episodic manic behaviour
* convulsions
* abdominal pain, rumen atony
* diarrhoea
How is lead poisoning treated?
- Controls fits- IV pento
- Chelate lead CaEDTA
- Thiamine
- Oral MgSO4
- What are the clinical signs of nervous ketosis?
- How is it treated?
- Obsessive licking, circling, staggering, head pressing, pica, aggression
- 40% dextrose IV, propylene glycol BID, corticosteroids
When is staggers most common?
Especially in pastured lactating beef cows in first months after calving
What are the clinical signs of staggers?
- Hyperexitable, may charge
- Erect ears, ears twitching, hyperaesthesia
- Muscle fasiculations/tremors
- Lateral recumbency with violent episodes of ophistotonus and convulsions
- Dead within hour of seizure
What can cause salt poisoning?
Why does it cause p
- Too much salty water or water deprivatoin
- Sodium deposition in the brain blocks anaerobic glycolytic pathways- increased intracranial presure may also occur
Poor prognosis- rehydrate first then hypertonic saline
How can pseudo and pseudorabies be distinguished?
Pseudo- pruritis- mad itch
Rabies- depression
What are the clinical signs of BSE?
3-6 years
* Weight loss
* Hyperaesthesia, fine fasiculations of head and neck, shoulder flank, teeth grinding
* Apprehensive when approached
* Ataxia
* Aggression
What is the action of BSE case?
- Inform APHA
- Visit to inspect animal to decide to PTS as suspect
- Farmer compensated and trace put on the offspring
When is hypovitaminosis A most commonly seen?
What causes the clinical signs?
Straw/cereal based diet in housed animals
Signs from thickening dura mater/abnormal bony growth in the brain cavity- increase CSF
Retina degeneration- absent PLR
Plenty of vitamin A in green forages and feeds
What are the signs of hypovitaminosis in calves to deficient dams and older cattle?
Calves to deficient dam- blindness, weakness, domed forehead, thickened carpal joints
Deficient calves- blindness, anorexia, diarrhoea, pneumonia
Older cattle- blindness, start gazing, nystagmus, ataxia, convulsions, diarrhoea, thickening and whitening of cornea
How is hypovitaminosis treated?
- Vitamin A daily
- Older cattle with ocular form often do not respond
What are the signs of cerebellar hypoplasia?
What can cause it?
Balance- ataxia, falling, unable to stand, tremor, hypermetria, nystagmus
Acquired BVD- 90-170d of gestation
Inherited
What diseases present principally with brain and cranial nerve dysfunction?
- Listeriosis
- Environmental pathogen- infectious sporadic and usually associated with feeding poor quality forage
- Infection travels upto brain stem from conjunctiva via trigeminal
- Forms microabscesses in brain stem/cerebellum/spinal cord
How is lepto treated?
- Stop disease worsening and hope defecits resolve
- High dose penicillin 7-14d or oxytet
What can cause spinal cord or peripheral nerve signs?
- Spinal fractures
- Spinal abscess
- Spastic paresis
- Tetanus
- Botulism
- Peripheral neuropathies
- When are spinal fracutures common?
- What are spinal abscesses normally secondary to?
- 3-6mo investigate underlying cause- VitD, calcium or copper deficiency
- Oestomyelitis- T. pyogenea, staph aureus, P. haemolytica, F. necrophorum
What are the signs of spastic paresis?
Asymmetric spasticity and hypertonia of extensor muscles of rear limbs
* Continuous when stand, not when it lays down
* Excessive tone of gastrocnemius
* Hyperextended hock
* Unilateral or Bilateral
How is spastic paresis treated?
Neurectomy of tibial nerve rootlets innervating the gastrocnemius
What are the clinical signs of tetanus?
- Incubation period variable
- Normally 2-4 weeks
- Progression of 4-5 days
- Stiffness, reluctance to move, muscle tremors
- Prolapsed 3rd eyelid
- RUMEN TYMPANY
- Recumbancy, convulsions, death
What can cause botulism?
Clostridium botulinum
* Ensiled poultry waste as food
* Poultry litter to pasture
* Carcasses in pasture or feed
What are the signs of botulism?
- Muscle weakness
- Progresses to ataxia and paralysis
- Excessive drooling
- Droopy expression, tonggue hanging out of mouth
- Decreased rumen motility, bloat, constipatoin
- Resp failure leading to death
How is botulisim diagnosed?
- History
- Clinical signs
- Toxin serum ELISA
- Samples of feed
When does obturator neuropathies occur?
- Following dystocia- especially heifers
- Obturator nerve damaged by foetal pressure
- Unable to adduct limb
- Treatment- chain between hindlimbs, soft bedding, steroids
What are the signs of peroneal neuropathy?
Hyperextension of hock, fetlock, digits flexed
Loss of skin sensation below fetlock
Self cure- bandage over fetlock to prevent damage
When does sciatic damage occur?
What is the signs?
When recumbent and struggling to rise
Non-weight bearing, no sensation distal to stilfe
DDX- femoral fracture
