Neurology

Grey matter vs. white matter

Grey matter = Cell-rich part of the CNS consisting of a neuron’s cell body, dendrite and synapse

White matter = Axons supporting neurons which link neurons to their targets within the brain, spinal cord or receptor/target organ

• Myelin = Fatty substance produced by oligodendrocytes (CNS) and Schwann cells (PNS) that coats axons in concentric layers

  • Different sections of myelin formed by different oligodendrocytes/Schwann cells

• Nodes of Ranvier = Unmyelinated gaps between the myelin

Sensory vs. motor neurons

Sensory Neuron = Cell body partway along axon → 2 axon terminals

• Proximal terminal synapses with neurons

• Distal terminal associated with receptor

• Neuronal cell bodies in CNS (nucleus) OR PNS (ganglion)

Motor Neuron = Cell body at one end → 1 axon terminal synapsing onto effector organ

Myelinated vs. unmyelinated axons

Larger and myelinated axons transmit information faster than smaller and unmyelinated axons

1. Large/Myelinated Axons = Convey reflexes → Sharp pain to avoid further damage

   • eg. High temperature, withdrawal reflex, gag reflex, palpebral reflex

   • Shorter pathway → Reduced reaction time

2. Small/Unmyelinated Axons = Convey dull throbbing pain

   • Caused by existing tissue damage and inflammation

   • eg. C-fibres and A-delta fibres

What is the difference between a response vs. reflex

Response = Conscious reaction to stimulus (processed by forebrain)

• Must be learned and can be suppressed with anxiety/stress

Reflex = Unconscious reaction to stimulus (processed by local brainstem/spinal cord)

• NOT learned, but protective mechanisms

List the common DDx using VITAMIN D:

• Forebrain (22)

• Cerebellum (7)

• Vestibular C/P (7)

Forebrain:

Inflammatory

1. Meningoencephalomyelitis of unknown origin (MUO)

Infectious

2. Bacterial

3. Viral

4. Fungal

5. Parasitic

Traumatic

6. Penetrating injury

7. Blunt trauma

Anomalous

8. Hydrocephalus

9. Porencephaly and hydranencephaly

10. Meningoencephalocele

Metabolic

11. Electrolyte imbalances

12. Mitochondrial encephalopathy

13. Hypoglycaemic encephalopathy

14. Acid-base related

15. Hepatic/renal encephalopathy

16. Endocrine-associated

Idiopathic

17. Epilepsy

18. Dyskinesia

Neoplasia

19. Meningioma, glioma, lymphoma, pituitary tumour, metastasis

Nutritional

20. Paroxysmal gluten-sensitive dyskinesia

21. Vitamin deficiency

Degenerative

22. Lafora disease

Cerebellum:

Vascular

1. Ischaemic infarction

2. Haemorrhage

3. Hypertension

Inflammatory

4. Idiopathic generalised tremour syndrome

Infectious

5. Protozoal (neosporosis)

Degenerative

6. Spinocerebellar ataxia

7. Cerebellar cortical degeneration

Vestibular:

Inflammatory

1. Nasopharyngeal polyp (primary secretory OM) (P)

2. Central (as for forebrain)

Infectious

3. Otitis media-interna (P)

4. Feline infectious peritonitis (C)

Toxin

5. Metronidazole (C)

Idiopathic

6. Idiopathic vestibular disease (P)

Nutritional

7. Thiamine deficiency (C)

Describe the structure of the forebrain

• Forebrain aka. prosencephalon =

  1. Telencephalon = Cerebral hemispheres

  2. Diencephalon =

     1. Epithalamus

     2. Hypothalamus

     3. Subthalamus

     4. Thalamus

• Consists of:

  • Grey matter located in the superficial cortex AND deeper structures (eg. hippocampi, basal and septal nuclei)

  • White matter located deeper within the forebrain to link different parts of the brain together (+ brain to spinal cord)

List 7 functions of the forebrain

1. Responsible for thought, behaviour and cognition

2. Processes sensory input to provide conscious recognition (eg. vision, hearing, tactile sensation, proprioception)

3. Includes the limbic system responsible for emotions, behaviour and long-term memory

4. Includes the thalamus = Gateway for information between brainstem and cerebrum, sorting into correct location

5. Includes the hypothalamus responsible for homeostasis (eg. thirst, sleep and body temperature) and synthesis of hormones to trigger trophic hormone release from the pituitary gland

6. Includes the subthalamus responsible for management of body movement

7. Includes the epithalamus associated with the limbic system and contributes to the maintenance of circadian rhythm

Describe 9 clinical manifestations of forebrain dysfunction (+ normal)

1. Abnormal Mentation

   • Abnormal level

     • Obtunded = Drowsy but rousable with reduced responsiveness (aka. depressed)

     • Stuporous = Sleeping but can be roused with painful stimulus

     • Comatose = Unconscious and cannot be roused with painful stimulus BUT still retains withdrawal reflex

   • Abnormal quality

     • Disoriented = Alert but inappropriate responses to stimuli

     • Delirium = Confusion and disrupted attention often accompanied by hallucinations

2. Abnormal Behaviour

   • eg. Wandering, lethargy, vocalisation, loss of learned behaviour, lack of recognition, aggression, loss of circadian rhythm

   • Hemi-neglect = Animal ignores all information from one side of the body (eg. only eating food from one half of the food bowl)

3. Abnormal Gait

   • Proprioceptive ataxia

   • Aimless wandering or compulsive pacing

   • WIDE circling towards side of brain with lesion: Cerebral hemisphere receives/sends instructions to CONTRALATERAL side

     • eg. L forebrain pathology → Information on R body is not being sent to forebrain → Animal circles to L as R does not exist in their brain

4. Abnormal Posture

   • Head turn OR pleurothotonus (head AND body turn) towards side of lesion

   • Head-pressing

   • Horizontal/low head carriage due to “headache” ± neck pain 2˚ to increased ICP

5. Contralateral Postural Reaction Deficits

   • Requires conscious realisation of need to correct posture

   • eg. Contralateral hemiparesis and delayed paw positioning response

6. Abnormal Movements = Epileptic seizure and dyskinesia

7. Hyperaesthesia = Excessive sensitivity and pain over calvarium on palpation (also cranial cervical spine with increased ICP)

   • Headache → Photophobia or head-pressing

8. Inappropriate Micturition = Loss of house-training or involuntary urination during seizure

9. Homeostatic Disorders = Endocrine dysfunction, loss of regulating water/food intake, loss of thermoregulation, abnormal growth

Normal:

1. Cranial nerve reflexes (processed in brainstem)

2. Spinal nerve reflexes (processed in spinal cord)

3. Nociception

Neurolocalisation: Where is the lesion?

1. Mild proprioceptive ataxia

2. Reluctance to turn left

3. Head turn to right when standing still

4. Absent paw positing responses in left limbs (does not correct knuckling)

5. Absent vision/menace response on left

6. No response when touched on left side of face BUT good palpebral reflex on left

7. Only ate from right side of bowl

Abnormal processing of information that requires a CONSCIOUS response → Suggests problem with RIGHT forebrain

NOT brainstem because:

1. Left eye can blink (facial nerve/nucleus normal)

2. Good palpebral reflex on left (trigeminal nerve → brainstem → facial nerve normal)

3. Does not track cotton ball on left side which only evaluates visual pathway with several forebrain structures

Meningoencephalomyelitis of Unknown Origin (MUO)

• 2 Types (+ severity)

• 4 Diagnostic tools

• Clinical signs

• Signalment (species, age and breed)

• Treatment

• Prognosis

Types:

1. Granulomatous meningoencephalitis (GME) = Swelling of brain on MRI → Less severe

2. Necrotising meningoencephalitis (NME) = Soft tissue loss → More severe

Diagnosis: Presumptive diagnosis based on signalment, history and neurolocalisation →

1. CSF result (± mononuclear pleocytosis and high protein)

2. MRI appearance

3. Response to treatment

4. Definitive diagnosis requires histopathology to differentiate GME from NME/NLE

Clinical Signs: Multifocal CNS signs with predominant forebrain involvement

• ± Cranial nerve dysfunction (i.e. brainstem involvement)

  1. Ocular GME form → Involves optic nerve

  2. Idiopathic hypertrophic pachymeningitis (form) → Cranial nerve compression

Signalment: Young to middle-aged dogs (4 - 8yr)

• GME: Small breeds (eg. terriers and poodles)

• NME: Pugs, Chihuahuas, Maltese, Pekingese, Shih Tze, West Highland White Terriers, Papillons, Coton du Tulear, Griffon Bruxellois

• NLE: Yorkshire Terriers, French Bulldogs

• Eosinophilic ME: Medium to large breeds

• Idiopathic hypertrophic pachymeningitis: Greyhounds/lurchers, labradors

Treatment: Multimodal immunosuppression

• eg. Prednisone ± cytarabine, cyclosporine, azathioprine, mycophenolate mofetil

• Duration: MONTHS to YEARS with very slow tapering (potentially lifelong)

  • Cessation of treatment is fatal

Prognosis: Up to 30% mortality BEFORE treatment (survival of 1 - 2 months from diagnosis → May survive years)

• Survival depends on MUO severity (worse outcome for NME/NLE)

  • Better outcomes for treatments than what is published (can only publish with definitive diagnoses of disease which requires PM biopsy and histology)

• Potential for permanent deficits

Infectious Disorders of the Forebrain

• 2 Bacterial infections

• 3 Viral infections

• 2 Fungal infections

• 2 Parasitic infections

Bacteria:

1. Abscess = Inflammatory pus walled off (superior drainage)

2. Empyema = Pus everywhere within cavity with no walling off

Virus:

1. Canine distemper virus (vaccine-induced in NZ)

2. Rabies*

3. Feline coronavirus (FIP)

Fungus: Local extension from nose OR haematogenous spread

1. Aspergillosis

2. Cryptococcosis

Parasite:

1. Protozoal (neosporosis OR toxoplasmosis)

2. Migrating parasites (eg. Cuterebra*)

Traumatic Disorders of the Forebrain

• 2 Types of traumatic brain injury

• 2 Reasons why clinical signs may be multifocal

Types:

1. Penetrating injury (eg. cat bite)

2. Blunt trauma (eg. HBC)

Multifocal: Various clinical signs

1. Haemorrhage

2. Coup and contrecoup injury

   • Coup = Brain trauma immediately below site of impact

   • Contrecoup = brain trauma directly opposite side of impact as brain collides into the back of the skull

6 Example toxins causing forebrain dysfunction

1. Plant and algal toxins

2. Anticoagulant rodenticides

3. Anti-parasitics (eg. flea and worm products)

   • Care with avermectins in collies (mdr1 mutation)

4. Recreational drugs (eg. CBD oil and THC)

5. Human medications (ask owner about human medications eg. anti-depressants)

6. Iatrogenic/overdose

List and define 5 examples of anomalies affecting forebrain function

1. Porencephaly (small chunks of brain replaced with CSF) or anencephaly (large chunk of brain missing)

   • Porencephaly more common and often clinically insignificant (vs. anencephaly → Clinical signs)

2. Meningocele and meningoencephalocele (CSF-filled meninges ± brain protrude through defect in skull)

   • Post-op OR anomalous

   • Do NOT poke lump on the head of a young animal (may be meningocele)

3. Skull malformation

   • eg. absent cribriform plate → Brain herniates through nasal cavity → Predisposes to dural tearing → Air enters ventricular system

4. Congenital hydrocephalus and cyst development (eg. quadrigeminal cyst)

5. Abnormal neuronal migration/neural tract pathways (eg. neurons in abnormal locations or absent neural tract pathways)

List 3 causes of acquired hydrocephalus

1. Obstruction/slowing of CSF flow (eg. tumours of arachnoid cell infection)

2. Increased CSF production

3. Impaired CSF absorption

Congenital Hydrocephalus

• Pathogenesis

• Clinical signs

• Diagnosis

• Signalment (species, breed and age)

• 3 Treatment options

Pathogenesis: Due to mesencephalic aqueduct stenosis (between 3rd and 4th ventricle → Lateral ventricles become enlarged with CSF) #1

• 3rd ventricle = CSF space encircling the interthalamic adhesion

• OR due to impaired reabsorption

Clinical Signs:

1. Domed head (skull bones not yet fused)

2. Difficulty training

3. Abnormal behaviour

Diagnosis: Signalment, history and clinical signs → U/S through fontanelle to visualise excessive CSF (compare with other litter mates)

• Do NOT need advanced imaging for definitive diagnosis

Signalment: Small dog breeds (eg. chihuahua, maltese, English bulldog, pug) with clinical signs observed in the first months of life

• Uncommon in cats

Treatments:

1. Medical = Decrease CSF production with prednisolone

2. Surgical = Shunt CSF into abdomen with drain placed in the ventricle → burrow under skin to exit in the abdomen

   • -ve:

     1. Infection, blockage, migration, inflammation → Replace regularly

     2. Overdraining CSF → Brain collapse

     3. Similar outcome to medical management

3. Treat seizures

Electrolyte Imbalances causing Forebrain Dysfunction

• Effects of calcium imbalance

• Effects of sodium imbalance (+ treatment when chronic)

Calcium:

• Hypercalcaemia = Intracellular toxicity → Cell death

• Hypocalcaemia = Increased cell membrane excitation → Seizures (eg. lactation)

Sodium:

• Hypernatraemia = Cell dehydration → Shrinkage → Shrunken RBCs tear blood vessels → Haemorrhage

• Hyponatraemia = Cells swell → Oedema

• Chronic sodium imbalance:

  1. Na+ extremes persist for > 2 - 3 days

  2. Brain cells actively produce osmolar substances (osmoles) to compensate for sodium imbalance

  3. RAPID correction of chronic sodium imbalance → Switch to other end of the spectrum

  4. → Severe oedema OR cell shrinkage + haemorrhage and demyelination

List 4 endocrine diseases causing forebrain dysfunction

1. Hyperthyroidism (→ flighty cat)

2. Hypothyroidism (→ slow/sluggish cat)

3. Diabetes mellitus (→ hypoglycaemic encephalopathy)

4. Hyperadrenocorticism

Paroxysmal Gluten-Sensitive Dyskinesia

• Signalment (breed)

• 2 Clinical signs

• Diagnosis

• Treatment

Signalment: Border terrier

Clinical Signs:

1. Paroxysmal cramping (responsive) lasting 2 - 30 minutes ± abnormal behaviour before/after

2. ± GI signs

Diagnosis: History of GI signs → Serology = Measure anti-gliadin and anti-transglutaminase-2 Ab (NOT in NZ)

Treatment: STRICT gluten-free diet (treatment trial for diagnosis)

List 2 vitamin deficiencies causing forebrain dysfunction

1. Cobalamin (vitB12)

2. Thiamine (vitB1) → Vestibular signs with cervical ventroflexion

List 5 primary and 3 secondary nervous system tumours

Primary:

1. Meningioma

2. Glioma (eg. oligodendroglioma and astrocytoma)

   • Oligodendrocyte = CNS myelination

   • Astrocyte = Structure, homeostasis and BBB

   • Microglia = CNS macrophages

3. Ependymoma

4. Choroid plexus tumour (papilloma and carcinoma)

5. Schwannoma/nerve sheath tumours

Secondary:

1. Sarcoma (dog = HSA #1)

2. Lymphoma (cat #1)

3. Carcinoma

Meningioma vs. glioma

Meningioma

• Extra-axial (OUTSIDE brain)

• Slow-growing

• Compression > invasion

  • “Benign”

Glioma

• Intra-axial (INSIDE brain)

• Relatively fast-growing

• Invasion > compression

Canine vs. feline intracranial neoplasia

• Prevalence of 1˚ vs. 2˚

• Signalment (breed and age) OR common types

Canine

Prevalence: EQUAL 1˚ and 2˚

Signalment: Boxer, Boston terrier, golden retriever, French bulldog

• Meningioma → Dolicocephalics and breeds >15kg

• Glioma → Brachycephalics

• 8yr 10m

  • Meningiomas present when significantly older than other 1˚ tumour types

Feline

Prevalence: 71% of intracranial tumours are 1˚

Most common:

1. Meningioma

2. Lymphoma

3. Pituitary

Neoplastic Disorders of the Forebrain

• Clinical sign

• 4 Treatment options

• Prognosis

Clinical Sign: Seizure activity = #1 abnormality noted (generalised seizure with cluster > single > SE)

Treatments:

1. Surgical resection ± radiotherapy

2. Radiotherapy

3. Palliative (corticosteroids, AEDs and analgesia)

4. Chemotherapy if 2˚ (NOT successful when 1˚)

Prognosis: Depends on tumour type, location, treatment and species

• Cats = Tumours shell out → Easy to resect → Long MST before meningioma grows back

• Dogs = Tumour removed in pieces → Radiotherapy preferred due to recurrence

Lafora Disease

• Pathogenesis

• Signalment (breed and age)

• 5 Clinical signs

• Treatment

Pathogenesis: Genetic mutation → Intracellular accumulation of polyglucosan (neurotoxin)

Signalment: Miniature wire-haired dachshund, beagle, basset hound

• Middle-aged and progressive

Clinical Signs:

1. Myoclonic seizure = Single contraction of muscle triggered by visual/audio cues →

2. Visual impairment

3. Dementia

4. Deafness

5. Aggression

Treatment: Levetiracetam → Myoclonus becomes refractory → Euthanasia

Describe the location and structure of the cerebellum

Location: Within the caudal fossa of the skull, dorsal to the medulla oblongata

Structure:

1. Vermis = Midline region (vermis = worm)

2. 2 bilateral hemispheres

Paired Peduncles: Stalks made of white matter tracts connecting the cerebellum to the brainstem

1. Rostral cerebellar peduncle = Connects cerebellum and midbrain (primarily efferent)

   • Afferent: Spinal cord and midbrain tracts

   • Efferent: Midbrain (esp. red nucleus), pallidum, thalamus

2. Middle cerebellar peduncle = Connects forebrain to cerebellum (completely afferent)

3. Caudal cerebellar peduncle = Connects spinal cord and medulla oblongata to cerebellum (primarily afferent)

   • Afferent: Spinal cord and vestibular system

   • Efferent: Vestibular nuclei and reticular formation (inhibition of vestibular nuclei)

Regions:

1. Cerebrocerebellum (pantocerebellum/nocerebellum) = Regulates skilled movement, planned movements and motor learning

2. Spinocerebellum (paleocerebellum) = Regulates truncal and limb movements through feedback loops

3. Vestibulocerebellum (archicerebellum) = Regulates balance, posture and coordination of eye movements

   • Clinical signs associated with ONE region more likely (vs. vestibular system AND cerebellum)

   • Receives proprioceptive information but does NOT determine if the animal will correct an abnormal posture

     • Animal with cerebellar disease SHOULD correct knuckled paw, but exaggerated way

3 Functions of the cerebellum

1. Coordination (controls rate, range and force of movement)

2. Equilibrium (regulate muscle tone at rest or during motion through close association with vestibular system)

3. Inhibit urination

Does NOT initiate movement: Cerebellum involved in multiple feedback loops to regulate movements

Describe 5 clinical manifestations of cerebellar dysfunction (+ normal)

3 Regions + Absent menace and pollakiuria

1. Cerebrocerebellum dysfunction = Movements not synchronised → Overshooting intended movements

   • Dysmetria = Loss of control of range, rate and force of movement → Cerebellar ataxia

   • Intention Tremours = Manifestation of loss of control over range and force of planned movements which worsen with concentration

     • Alternating over-reaching and under-reaching movements → Oscillation

     • Cerebellum required for planned movements, therefore, more planning → More difficulty accomplishing task

     • Refractory to diazepam

2. Spinocerebellum dysfunction = Exaggerated truncal and limb movements

   • Hypermetria = Excessive lifting of lower limbs when ambulating (“marching” or “prancing” gait)

   • Increased limb tone = Spasticity → Stumbling/falling

3. Vestibulocerebellum dysfunction = Loss of equilibrium/balance

   • Truncal sway, wide-based stance, falling to one side, head tilt ± strabismus and nystagmus

4. No menace response

5. Pollakiuria

Normal:

1. Mentation (no forebrain involvement)

2. Paw positioning (exaggerated)

Transient Ischaemic Attack on the Rostral Cerebellar Artery

• Clinical signs and duration

• Diagnosis

• 3 Causes

Clinical Signs: Vestibulocerebellar OR purely cerebellar signs which typically self-resolve after <24hr

• Small clots → Short signs (minutes to hours)

• Large clots → Lasting signs (days to weeks)

Diagnosis: Markedly elevated D-dimers → Presumptive diagnosis (must be run on 1st sample)

Causes:

1. Infarction

2. Brain tissue compression

3. Cardiac arrest/vessel compression

List 6 causes of haemorrhage into the nervous system

1. Coagulation disorder

2. Trauma

3. Haemangiosarcoma metastasis

4. Parasitic (migration tract of Angiostrongylus vasorum*)

5. Cerebral microbleeds

6. 2˚ to another lesion (eg. tumour or inflammation)

Corticosteroid-Responsive Generalised Tremour Syndrome (aka. Idiopathic Tremour Syndrome)

• Aetiology

• Signalment (species, breed, age)

• 3 Diagnostic tools

• 2 Treatments

Aetiology: Immune-mediated inflammation of the cerebellum

Signalment: Small/medium dogs (<15kg) @ 1 - 5yr (often <2yr)

Diagnosis: Signalment, history and neurolocalisation →

1. Normal brain on imaging

2. Response to treatment

3. ± Mild to moderate lymphocytic pleocytosis on CSF analysis

Treatments:

1. Immunosuppressive doses of corticosteroids and diazepam → Improvement within 3d

   • Max 5 days diazepam

   • Taper prednisolone over 6 months → Discontinuation

2. Spontaneous remission possible after several months

Neosporosis

• Prevalence

• 2 Modes of transmission

• Pathogenesis in puppies vs. adults (+ clinical signs)

• 2 Treatment options (+ duration)

Prevalence: 76% seroprevalence in urban dogs (22 - 100% in farm dogs)

• VERY common in NZ

Transmission:

1. Vertical (transplacental)

2. Horizontal (ingestion of infected tissues eg. raw meat)

Pathogenesis:

• Puppies = Protozoal myositis-polyradiculoneuritis → Ascending HL paresis and rigid hyperextension

• Adults = Protozoal encephalomyelitis → Necrotising cerebellitis

Treatments: FOUR weeks of

1. Clindamycin and/or

2. TMS

List 2 degenerative diseases targeting the cerebellum

1. Spinocerebellar ataxia (JRTs, Parson Russel Terriers)

2. Cerebellar cortical degeneration (abiotrophy)

Many other degenerative neurological diseases have a cerebellar component

• Genetic tests may be available

Non-Cerebellar Head Tremours (aka. Idiopathic Head Tremours)

• Signalment (breed, age)

• Clinical signs

• Prognosis

Signalment: Bulldog, boxer and dobermans <4yr

Clinical Signs: <5 minute episodes (may be up to several hours) which typically occur at REST and improve with distraction, supporting head or turning head in opposite direction

Prognosis: Episode resolves over time in most dogs

Describe the structure and location of the vestibular system

Structure:

1. Peripheral vestibular system = Vestibular receptors within the inner ear + vestibular component of the vestibulocochlear nerve (CN VIII)

2. Central vestibular system = Vestibular nuclei within the brain stem + vestibulocerebellum

   • Some axons leave CN VIII → Caudal cerebellar peduncle → Fastigial nucleus in cerebellum

   • Function of vestibulocerebellum: Feedback loop for regulation of balance and posture

     • Some cerebellar neurons travelling through the caudal cerebellar peduncle INHIBIT vestibular nuclei (interruption of this inhibitory pathway → PARADOXICAL vestibular syndrome)

Location: Inner ear located in the petrous temporal bone

• Cochlear nerve + vestibular nerve → Vestibulocochlear nerve (CN VIII)

  • 2 axons of the vestibulocochlear nerve separate at the brainstem to travel to their respective nuclei

5 Outputs of the vestibular system

1. Upper motor neuron spinal cord tracts to correct changes in body position

   • Turning heads to the RIGHT:

     1. Increased vestibular activity on the right side → Increased stimulation of RIGHT vestibular receptor

     2. → Vestibular system causes the following to prevent falling over: Extension of ipsilateral limb and flexion of contralateral limb

        • Stimulation of ipsilateral (RIGHT) extensor muscles

        • Inhibition of ipsilateral (RIGHT) flexor muscles

        • Inhibition of contralateral (LEFT) extensor muscles

          

2. Nuclei of CN III (oculomotor), IV (trochlear) and VI (abducens) to control eye movements

3. Cerebellum to coordinate movement of eyes, neck, trunk and limbs with respect to movement of the head

4. Cerebrum (via the thalamus) for conscious perception of balance

   • Occasional vestibular dysfunction due to thalamic pathology (forebrain dysfunction)

5. Vomiting centre of the brainstem

What is nystagmus? What is its purpose?

Nystagmus = Normal physiological reflex whereby eyes tend to flick towards the direct the head is turning and then move slowly in the opposite direction (left/right/dorsal)

• ONLY when head is changing position (no nystagmus when still → Pathological nystagmus)

• aka. vestibulo-ocular reflex

Purpose of physiological nystagmus: Allows line of sight to remain still as the head turns for as long as possible → Time for retinas to capture clear image before eyes flick again → Prevents vision blurring while moving head

Describe 3 clinical manifestations of vestibular system dysfunction (+ pathogenesis)

PEN

1. Postural and Gait Abnormalities = Head tilt, rolling/falling/tight circling, vestibular ataxia, wide-based stance with lowered centre of gravity

2. Abnormal Eye Movements

   1. Spontaneous/resting nystagmus = Brain triggers nystagmus as it thinks the head is turning (pathological)

      • Horizontal OR vertical with fast phase in one direction and slow phase in the opposite

      • Pendular nystagmus = Spontaneous nystagmus in normal, blue-eyed cats due to abnormal proportion of optic nerve axons crossing the optic chiasm (no lateralisation)

   2. Positional nystagmus = Head position must be changed to trigger pathological nystagmus

   3. Positional strabismus = Abnormal position of eye within orbit due to change in head position

      • NORMAL: Gaze remains central when head and neck extend dorsally (vs. horses)

      • Loss of vestibular function: Extraocular muscles on affected side fail to maintain central gaze → Ventral positional strabismus of affected side

      • Static strabismus = Abnormal eye position at ALL times (due to orbit conformation or mechanical dysfunction of the extraocular muscles)

3. Nausea

Pathogenesis:

1. Pathological lesion → Loss of input from vestibular receptors/loss of vestibular nuclei function on ONE side

2. → Less vestibular activity on that side

3. → Comparatively more vestibular activity on the CONTRALATERAL side

4. Brain cannot differentiate between an imbalanced vestibular system due to turning OR pathology → Normal vestibular stimulation results in ABNORMAL posture and movements

5. → Increased extensor muscle tone on side of greater activity

6. BUT because the animal is NOT turning, it causes them to lean/fall/circle/roll towards side of lesser vestibular activity

   • Tight circling to due stumbling and falling off balance

7. Increased extensor tone of neck on side of greater activity pushes the head to the other side causing head tilt TOWARDS the side of less vestibular activity

List and describe 3 types of ataxia

1. Vestibular ataxia = Usually unilateral

   • Bilateral = Crouching, reluctance to move, side-to-side head movements, wide-based stance, alterating rotation of head

2. Cerebellar ataxia = Dysmetria and hypermetria (over-reaching/high-stepping)

3. Proprioceptive ataxia = Scuffing paws, swaying gait, wide-based stance, long-limbed strides

Describe how you could neurolocalise for a dog with no menace response

Menace Response Pathway:

• Afferent = Retina, optic nerve, cerebellum, brainstem

• Site of processing = Forebrain

• Efferent = Facial nerve and muscles of the eyelids

Other Tests that Overlap with the Pathway:

1. Retina/Optic Nerve = PLR (bypasses forebrain) and electroretinography (ERG)

2. Visual Pathway = Maze testing or visual tracking

3. Forebrain = Nasal sensation, proprioception test

4. Cerebellum = Hypermetria/tremours?

5. Facial nerve and Eyelid Muscles = Palpebral reflex

Where do ascending nerves decussate?

AFTER the thalamus: In the forebrain, information is processed on the CONTRALATERAL side to the stimulus (brainstem, cerebellum and spinal cord → IPSILATERAL deficits)

Provide definitions for the following terms

Term	Definition
Ataxia
Paresis
Paralysis
-plegia
-paretic
Tetra-
Para-
Hemi-
Mono-

Term	Definition
Ataxia	Incoordinated movement, wobbliness and poor control of ambulation due to sensory dysfunction
Paresis	Motor weakness of limbs → Partial loss of motor function
Paralysis	Complete loss of voluntary motor function → Inability to move (BUT reflexes may be present)
-plegia	Paralysis
-paretic	Paresis (muscle weakness)
Tetra-	Affecting all FOUR limbs
Para-	Affecting hindlimbs
Hemi-	Affecting limbs on ONE side
Mono-	Affecting only ONE limb

5 Grades of spinal injury

Grade:

• 0 = Normal animal

• 1 = Pain from lesion ONLY (no neurological signs)

• 2 = Ataxia OR ambulatory paresis → Muscle weakness

• 3 = Non-ambulatory paresis → Partial loss of motor function (residual movement eg. wants to walk if supported off ground)

• 4 (IVa) = Plegia and motor paralysis → Complete loss of motor function

• 5 = Loss of pain sensation

  • Cutaneous (IVb) = Superficial pain (eg. pinching skin or webbing)

  • Periosteal (IVc) = Deep pain (eg. pinch P3 within base of claw OR long bone with crushing clamp over tibia)

• Deep pain fibres are last to be damaged → Loss of deep pain sensation = Most severe spinal injury

• Superficial pain fibres slightly easier to be damaged as larger and myelinated

• Motor nerves very easy to be damaged → Conscious movement (eg. walking) requires function of the UMN and LMN → 2nd thing to disappear (after ataxia and conscious perception)

List 5 types of spinal cord injuries requiring surgery (+ 3 example DDx)

1. Intervertebral disc disease (IVDD Type I/II)

2. Spinal fracture/luxation (eg. HBC)

3. Spinal tumour

4. Spinal abscess

5. Spinal cyst

Examples:

1. Lumbosacral disease (aka. Cauda Equina Syndrome)

2. Caudal Cervical Spondylomyelopathy (aka. Wobbler’s Syndrome)

3. Atlantoaxial instability

Describe the anatomy of a vertebra and intervertebral disc

Vertebra:

• Vertebral lamina = Roof of the vertebral canal

• Intervertebral foramen = Hole between two adjacent vertebrae to allow nerves to pass from the spinal cord

• Pedicles = Help encase the spinal cord and acts as a bridge between the vertebral body and the rest of the vertebra

Intervertebral Disc: Fibrocartilaginous disc between bodies of each pair of vertebrae to act as shock absorber and prevent damage to the spinal cord during movement

• Annulus fibrosus = Outer area of tough fibrous connective tissue (concentric rings of collagen)

• Nucleus pulposus = Inner core of gelatinous material

List 5 surgeries to treat neurological disease

1. Decompression = Remove pressure on spinal cord via removal of disc, clots, bone, cyst fluid or tumour mass

2. Stabilisation of spine = Required due to movement from disc degeneration or luxation from trauma

3. Stabilisation and decompression of fractures

4. Drainage and curettage of discospondylitis

5. Biopsy or removal of spinal cord/brain tumours

3 Surgical approaches to the spinal cord

• Definition

• Indication

1. Dorsal laminectomy = Removal of vertebral lamina (vertebral bone dorsal to spinal cord)

   • Indication: Dorsal lesions → NOT discs as too ventral

2. Hemilaminectomy = Removal of vertebral lamina on ONE side and lateral to the spinal cord

   • Indication: Disc disease

3. Ventral slot = Removal of rectangular portion of bone and intervertebral disc ventral to spinal cord → Push everything out of the way first

   • Indication: Access cervical vertebrae

List and describe 4 diagnostic methods for spinal cord injury

1. Plain radiographs: Assess for

   1. Narrow intervertebral disc space → IVDD

   2. Calcified disc → IVDD (usually cannot see disc if not calcified)

   3. Fractures and luxations

2. Myelography = Injection of water-soluble iodine contrast into the subarachnoid space

   • -ve: NOT common now due to high risk of seizures and spinal cord injury → Superseded by advanced imaging modalities

   • Sites:

     1. Lumbar puncture

     2. Cisterna magna

3. CT → Fracture diagnosis

4. MRI → Tumour diagnosis

Spinal Patient Care

• 5 Steps of pre-operative TRANSPORT care of spinal patients

• 2 Features of pre-operative IN-HOSPITAL care of spinal patients

• 7 Features of conservative management and post-op care

• 3 Features to monitor for (+ treatments)

Transport:

1. Handle with EXTREME care (poor handling → increases injury severity AND causes struggling if hurt)

2. Advise owner to gently slide onto sheet/coat/towel

3. On arrival, if dog is non-ambulatory, strap down with tape onto board to carry

4. Small dogs and cats can be carried by supporting backs in neutral position

5. Keep animal taped down to board until radiographs have been taken to rule out spinal injury

Pre-Op Care:

1. Total cage rest for 2 - 4w (analgesia and no cage rest → further herniation)

2. Analgesia (opioids OR NSAIDs)

Post-Op Care:

1. Intensive nursing care to avoid bed sores, decubital ulcers and muscle atrophy

2. Padded bedding (eg. water bed or air mattress)

3. Regular turning and periods in sternal recumbency if plegic

4. Passive flexion and extension physiotherapy

5. Active supported standing physiotherapy

6. Hydrotherapy (combine with bathing)

7. Access to feed and water → Monitor intake and assess weight changes + hydration status

Monitor:

1. Urination → Expression needed if UMN bladder

   1. Repeated catheterisation (males)

   2. Indwelling closed system (females)

   3. Diazepam → Decreased external skeletal muscle sphincter tone

   4. Phenoxybenzamine → Decreased internal smooth muscle sphincter tone

2. UTI → Common with spinal patients due to catheterisation and/or retained urination

   • Longer hospitalisation → Higher risk of UTI

   • Therapeutic antibiotics (empirical → culture and sensitivity of catheter)

3. Defaecation → Usually voluntary (otherwise microenemas)

Which drug should NEVER be given to spinal patients? Why?

NEVER give dexadreson = Most dangerous corticosteroid

-ve: Fatal colonic perforation in dogs with thoracolumbar disease → Septic shock

• Can give low dose prednisolone for inflammatory aetiologies

Intervertebral Disc Disease (IVDD)

• Definition

• 3 Types

  • Definition

  • Clinical features

  • Signalment

Definition: ANY type of cord compression due to intervertebral disc herniation (dorsal annulus fibrosus thinnest)

Types:

1. Hansen’s Type I IVDD (extrusion) = NP pushes through AF into vertebral canal

   • → Compression AND contusion

   • Acute ± progressive (grade 1 - 5 presentation)

   • Signalment: Chondrodystrophic breeds which deteriorate discs earlier in life (eg. Beagle, spaniel, dachshund) @ ~3 - 6yr

2. Acute Non-Compressive Nucleus Pulposus Extrusion (ANNPE) aka. Type III = Low volume, high velocity (bullet-like) NP shoots through the AF and hits the spinal cord → Disperses around spinal cord (no space occupying lesion and nothing to remove)

   • → Contusion

   • Peracute and non-/mild progressive

3. Hansen’s Type II IVDD (protrusion) = Hypertrophic AF bulges into the vertebral canal

   • → Compression

   • Insidious, static OR progressive (earlier grade presentation due to slow progression)

   • Signalment: Non-chondrodystrophic breeds (ANY old dog due to normal disc degeneration throughout life = Water loss of NP → Bulging of AF

5 GP vet roles in IVDD

1. Rapid recognition of clinical signs

2. Localise lesion site

3. Assess severity and relate to prognosis for owner

4. ID cases requiring surgery vs. those that can be managed conservatively

5. Rapid referral to neurosurgeon

Taking radiographs is NOT necessary

Cervical IVDD

• Typical grade of severity

• 2 Indications of surgical treatment

• 2 Disadvantages of conservative management of cervical IVDD

• 2 Methods of surgical treatment

  • Advantage

  • Disadvantage

Grade: Lower neurological grade as those more severe cannot move respiratory muscles → Euthanasia due to respiratory arrest

Indications for Surgery:

1. Lack of response to conservative treatment (still painful) after 1 - 2w

2. ALL dogs with neurological deficits (grade 2 - 5)

-ve of Conservative Management:

1. Significant pain due to mobile neck (faster recovery from pain post-op)

2. 30% recurrence with conservative treatment

Surgical Methods:

1. Ventral Fenestration = Remove window of annulus to free nucleus

   • +ve: Easy to perform

   • -ve: NOT recommended in all cases with neurological disease

2. Ventral Slot Decompression = Remove disc material from spinal canal via removal of central 1/3rd of body via ventral approach

   • +ve: Faster recover

   • -ve: Stabilisation NOT performed in most cases

Thoracolumbar IVDD

• Most common segments affected

• Diagnosis

• Indication for conservative management

• 3 Advantages of surgical treatment of thoracolumbar IVDD

• 3 Surgical methods

Segment: >50% at T12 - T13 OR T13 - L1

• 85% between T11 - T112 and L2 - L3

• → Lever arm at junction of thoracic and lumbar vertebrae

Diagnosis: Localisation of lesion from neurological exam → Radiographic and myelogram to determine site (lack of horse head intervertebral foramen shape)

Conservative Management: Indicated for lower grades of spinal injury and financial/equipment constraints

+ve of Surgical Treatment:

1. Faster recovery and better outcome for grade II - IV

2. Grade V must be operated ASAP (7% success with conservative management)

3. Less risk of residual neurological deficits

Surgical Methods:

• Dorsal or dorsolateral approach for:

  1. Hemi-laminectomy #1

  2. Mini-hemilaminectomy (minimal approach)

  3. Pediculectomy minimal approach

• → Retrieval of disc material and blood clots which is decompressive AND reduces inflammation

• Remove overlying lamina to allow cord to bulge with no compression

Prognosis for Type I IVDD (grade I - V)

• Conservative % recovery (wks)

• Decompression % recovery (wks)

Grade	Conservative	Surgical
I	100% (3w)	97% (<2w)
II	84% (6w)	95% (<2w)
III	93% (6w)	95% (<2w)
IV	81% (9 - 12w)	95% (1 - 4w)
V	7%	64% (5 - 10w)

• Grade I = Good response to conservative management BUT common relapse (investigate recurrent pain)

  • Grade I - II is good with conservative management

• Good recovery for dogs with grade I to III

• Recurrent after conservative therapy → More severe deficits later

• Higher grade = Better surgical prognosis and worse conservative prognosis

Describe the anatomy of the cauda equina

Bundle of spinal nerve roots at the end of the spinal cord derived from L5 - S2

• Dog spinal cord proper ends BEFORE vertebral column → Continues as the cauda equina to supply the caudal segments of the body

• 20% of dogs have the conus medullaris ending BEFORE the lumbosacral space

Overview of Cauda Equine Syndrome

• Definition

• 5 Clinical signs

• 5 Imaging modalities

• Most common DDx

Definition: Presentation of lumbosacral disease with MULTIPLE different causes → Compression of spinal nerve roots (NOT spinal cord) of the cauda equina

• eg. empyema due to grass seed

Clinical Signs:

1. Lumbosacral pain

   1. Tail Jack (-ve: Many normal dogs do not tolerate → False positives)

   2. Pelvic Tilt = Cradle pelvis with one hand and place other hand over back to act as fulcrum → Extension of back and NOT back legs (+ve: Best test with highest DSp)

   3. Lordosis Test = Concurrent hip AND back extension (-ve: Must test hip pain first to rule out possible cause of possible lordosis test)

   4. Nervous Dog = Place in lateral recumbency with knee in back while attempting to bring dog’s knees caudally to extend back

2. Difficulty jumping or climbing stairs (may walk normally, but hold hindlimb up after jumping into car/upstairs = Dynamic impingement of nerve)

3. Rare incontinence (severe signs)

4. Hindlimb ataxia but NOT paralysis

   • Femoral nerve (L4 - L6) has already passed out intervertebral foramen innervate hindlimb motor function before cauda equina is compressed

   • Sciatic nerve (L7 - S1) has yet to pass out of the intervertebral foramen → Dragging hindlimbs but not paralysis

5. LMN hindlimb signs and normal forelimbs = Decreased reflexes, poor muscle tone and neurogenic muscle atrophy in hindlimbs

Imaging: Dynamic views with flexion AND extension of back (differentiate between static vs. dynamic)

1. Plain radiographs

2. Myelogram (conus medullaris ends before lumbosacral space in 20% of dogs)

3. Epidurogram (difficult to interpret)

4. Discogram (inability to inject is diagnostic)

5. MRI #1 for lateralised disc material

   • BUT 20% normal dogs have false positive → Interpret with clinical signs

Most Common DDx: Degenerative Lumbosacral Stenosis (DLSS)

Degenerative Lumbosacral Stenosis (DLSS)

• Signalment

• Pathogenesis (4 causes of pain)

• 3 DDx

• 2 Treatment options

Signalment: Large working dogs (eg. GSD) required to jump into cars often

Pathogenesis: Extension/overuse of back → Pain due to

1. Nerve impingement

2. Type II IVDD → Compression of cauda equina

   • All dogs have a lumbosacral disc bulge, but not all cause pain → Over diagnosis of DLSS with radiography

3. Articular facet DJD

4. Instability/subluxation of lumbosacral joint

DDx:

1. Sore muscles (eg. torn semitendinosus or iliopsoas muscle)

2. Strains

3. Hip displasia

→ Get dog to jump into car or walk upstairs to place stress on lumbosacral region

Treatment:

1. Conservative Management (as for DJD + lifestyle modification eg. purchase ramp for car and stop running up stairs)

   • NOT for working dogs

2. Surgical = Decompression ± stabilisation

   • Decompression and removal of impinging soft tissue ± stabilisation by facet screws

     • Laminectomy or foraminotomy

     • ± 3D printed jack for screw placement of internal fixation between L6 and S1

Caudal Cervical Spondylomyelopathy (Wobbler’s Syndrome)

• 2 Signalments (+ type of disease)

• 3 Clinical signs

• 2 Imaging modalities (+ features)

• 3 Treatment options

  • Indication

• Prognosis with surgical treatment

• 2 Post-op risks

Signalment:

1. Middle-aged (~5yr) Doberman = Disc-associated wobblers (type II IVDD)

2. Young Great Danes = Osseous-associated wobblers (cervical vertebral malformation → improvement OR waxing/waning)

Clinical Signs: Progressive but waxing/waning

1. Ataxia of HL → FL (chronic)

   • Despite cervical lesion, absent forelimb ataxia is common in early disease

2. Neck pain

3. Rare tetraplegia

Imaging:

1. Plain radiographs

   1. Narrowed IVD space between C4 - T1 (usually C6/7 or C5/6)

   2. Plowshare-shaped vertebrae → Abnormal force of disc

   3. Spondylosis

   4. Stenosis of canal at disc space

2. Cervical myelography with CT → Referral but required due to high risk of seizures

   • Shows ventral and/or dorsal extra-dural sign which can be dynamic

     • Take multiple images in dorsal extension, ventral flexion and linear traction on neck to assess for dynamic change

Treatment:

1. Conservative Management = Harness (no neck collars), do not exercise where they will trip easily, dietary management with OA Wobbler’s in great dane

   • Indication: Minor signs, stable disease without severe neck pain

2. Ventral Slot Decompression = Remove annulus

   • Indication: Severe signs, deteriorating disease or severe neck pain and STATIC lesions

3. Distraction Fusion ± Ventral Slot = Make disc space wider with traction on neck then fuse this position to prevent disc bulging

   • Indication: Severe signs, deteriorating disease or severe neck pain and DYNAMIC lesions

Prognosis: 7/10 dogs (surgery often not recommended before conservative management attempted due to high risk of no response OR making pain worse)

Post-Op Risks:

1. Risk of dominos = Fusion of C5/6 with surgery → Transfer load to C6/7 and Wobblers in next cervical vertebra

2. Risk of haemorrhage

Atlantoaxial Instability

• Aetiology

• Signalment

• Pathology

• Clinical signs

• Diagnosis

• 2 Treatment options

  • Indication

  • Disadvantage

  • Methods

• Prognosis with surgical treatment (+ risk)

Aetiology: Congenital or developmental → Dens of axis too small + ligaments bad + stretching with trauma (eg. hitting head against wall)

Signalment: Toy dog breeds (esp. Yorkies and Chihuahuas) → Pathology of the atlantoaxial junction

Pathogenesis:

• Skull → C1 (atlas) and C1 → C2 (axis) are proper synovial joints (diarthrodial) with no discs

• Hence, ligaments between C1 and C2 + dens of axis are very important and AA instability results from failure of these supporting structures → Dens compresses spinal cord esp. in ventroflexion of neck

• Causes of Atlantoaxial Instability:

  1. Fracture/absence/malformation or hypoplasia of dens → Non-functional attachment of alar, apical and transverse ligaments

  2. Improper formation, laxity or rupture of alar, apical, transverse or dorsal atlantoaxial ligaments (required to hold dens against the floor of the spinal canal)

• → Instability, ventral subluxation and compression of cervical spinal cord (C1 - C5) by dens

Clinical Signs: Neck pain and tetraplegia with UMN forelimbs and hindlimbs

Diagnosis:

1. Radiographs in lateral and VD to assess for neck fractures and luxations

2. Normal → Progressively more flexed lateral views taken a step at a time to avoid pithing patient by dens hitting cord

   • As soon as you see distance between C2 and C1 changing → STOP flexing (will cause death in patient due to compression of spinal cord by dens)

3. Compare distance between dorsal process of C2 and lamina of C1

   • Arrows in image should NOT change

Treatments:

1. Conservative Management = Healing of minor ligamentous lesions with neck brace for few weeks to prevent neck movement

   • Indications:

     1. May help some dogs improve after traumatic exacerbation of signs

     2. Useful for stabilisation during transport

   • -ve: Poor tolerance and sedation in crate often required

2. Surgery

   • Indication: Unstable cases with bony abnormalities and those that recur with conservative management

   • Methods:

     1. Dorsal wiring (higher risk of cord injury or vertebral artery rupture)

        • → 3D print patient-specific jack for wire placement

     2. Ventral stabilisation with cross pins or screws

Prognosis: More successful in dogs <2yr and those with clinical signs <10 months

• Risk = Implant failure

• Excellent results assuming no implant failure (no recurrence vs. conservative management → Common relapse)