SA Neuro Flashcards
Limitations of MRI?
Many diseases have normal MRI
Anatomical imaging often lacks specificity - e.g. infiltrative neoplasia and lymphoma may look identical to inflammatory disease
High cost
Limited availability
Indications for aural radiography? View used? Limitations?
Chronic otitis
Peripheral vestibular disease
Facial nerve paralysis
Horner’s syndrome
Rostral-caudal (open mouth)
GA required
Often limited value in large dogs
CT preferred in available
Principles of CT?
X ray Contrast based on physical density Cross sectional No superimposition Better ST contrast (not as good as MRI) Excellent for bone For brain CT need to give iodinated contrast in most cases (potentially nephrotoxic)
MRI principles?
Imaging net magnetic vectors of spins of hydrogen protons
Strong magnetic field with varying gradients
Apply RF pulses at Lamour frequency
Turn off RF pulse
Spins rephrase and lose energy emitting RF signal
MRI safety?
Magnet extremely strong - need to be careful when taking objects into room, act as projectiles (can be fatal)
Acoustic damage - ear plugs and defenders for patients
Patient temperature:
- SAR effects: patient heating
- prolonged GA: patient cooling
What are the MRI contrasts?
T2W: fluid and fat are hyperintense (bright)
T1W: fluid is hypointense (dark, depends on protein content), fat is hyperintense
T2 FLAIR: fluid is hypointense, fat is hyperintense
STIR: fluid is hyperintense, fat is hypointense
Which MRI sequence to use?
T2W sequences most sensitive
If T2W normal consider additional sequences
STIR screening for pathology
T2* GRE bone lesions and haemorrhage
What to assess on MRI of the brain (T2W sequence)?
Look for abnormal signal intensity Symmetry on transverse and dorsal plane images Mass effect or atrophy Grey/white matter contrast Ventricles - size, shape Enhancement pattern Assess extracranial soft tissues
What is myelography? When is it used? Contraindications?
Injection of non-ionic low osmolar iodinated positive contrast (iohexol) into subarachnoid space
Outline surface of spinal cord on radiographs or CT - highlights extradural or bony lesions
Always take CSF first
Used to:
- localise spinal lesions
- surgical planning
- rule out surgical disease
- assessment of dynamic spinal cord lesions
Contraindications:
- coagulopathy
- spinal instability
- cloudy/turbid CCSF (suggests inflammatory process)
Complications of myelography?
Exacerbation of neurological signs Seizures Brainstem injection Central canalogram Spinal cord haematoma Epidurogram Rapid movement of contrast Subdural injection Infection Dysrhythmias Death
What to assess on spinal images?
Roentgen signs - shape, size etc Alignment Disk spaces Endplates Foraminal changes Facets Soft tissues
What incidental findings could there be with spinal images?
Spondylosis deformans (very rarely clinically significant)
Facet OA
Congenital anomalies common
What are the main alignment problems of the spine seen by imaging?
Atlanto-axial subluxation
Congenital malformations (e.g. hemivertebra causing kyphosis or compressive myelopathy)
Trauma
“Wobbler” - Dobermans and larger breeds
What is the most common cause of extradural compression? Other causes?
(Extradural is most common form of compression)
Disk herniation
Others:
- vertebral tumour
- superiosteal haemorrhage
- extradural cysts
- vertebral stenosis
- disk extrusion
- disk protrusion
How does intervertebral disk disease (IVDD) appear on imaging? Pitfall with radiography?
Narrowed disk space
Reduced size of foramina
Endplate changes (chronic)
Mineralised material in vertebral canal
Pitfall with radiography = artifactual narrowing further away from centre of beam
Differentials for destructive changes of spine seen on imaging?
Diskospondylitis - centred on disk space
Neoplasia - may see changes if involve bone
Which imaging is needed for intramedullary disease?
Not visible on radiographs and poorly seen on CT
MRI required in most cases
History and CSF often important for diagnosis
Causes of intramedullary disease?
Neoplasia Myelitis Ischaemic myelopathy Syrinx Contusion Haemorrhage
Causes of intradural-extramedullary disease?
Subarachnoid diverticulae/cyst
Masses - meningioma, peripheral nerve sheath tumour
What are the 3 localisations of spinal disease?
Intramedullary
Intradural-extramedullary
Extradural
Tests to rule out non neurological diseases causing neurological signs?
Haematology and biochemistry
Electrolytes
Liver function testing - e.g. for PSS (BAST, ammonia)
Endocrine function tests (hypothyroidism, addison’s, cushings, diabetes)
Clotting function - stroke
Anti-gluten antibodies (anti-gladin IgG, anti-transglutaminase 2 IgA)
Immune mediated disease - acute phase proteins, specific autoantibodies
Infectious diseases (quite uncommon with neurological signs in UK) - Toxoplasma, Neospora
Urinalysis - renal disease, electrolyte abnormalities, hypertension (PLN), UTI
Bacteriology
Why is urinalysis important for patients with paraparesis/urine dysfunction?
Increased risk of UTIs
What infectious CNS conditions could be find by bacteriology?
Encephalitis - penetrating cranial injuries (cats), extension from otitis media/interna Bacterial meningitis (CSF degenerative neutrophils) Empyema, paraspinal abscessation
Significance of bridging spondylosis below vertebrae?
Often doesn’t cause neurological signs as not affecting vertebral canal
May cause pain due to impingement on nerves
How do extradural, intradural-extramedullary and intramedullary lesions appear with myelography?
Extradural:
- axial displacement of 1 or more contrast columns
- columns often thin or partially disrupted at the site of the
lesion
- most common
Intradural- extramedullary
- filling defect within the contrast column
- ‘Golf tee’ sign or widening of subarachnoid space due to a arachnoid diverticulum
Intramedullary
- divergence of contrast columns
What is CSF analysis useful for? Limitations? Contraindications?
Most useful for infectious/inflammatory conditions
Can be abnormal in neoplastic or traumatic conditions
Limitations:
- may not be abnormal due to location (if parenchymal) or nature of the lesion (non exfoliating)
- can have non specific changes
- cell counts correlate with exfoliation into CSF not severity of disease
Contraindications:
- increased intracranial pressure (mental status, pupil size and PLR, abnormal postures, vestibular eye movement)
- coagulopathy
- cervical collection contraindicated in some conditions (Chiara-Like malformation, AA instability, cervical trauma)
How to take a CSF sample? Needle? Site? Volume? Analysis?
Spinal needle
Site caudal to lesion:
- cerebellomedullary cistern: easier, blood contamination less likely, greater risk
- lumbar cistern: L6-L7 (L5-L6 in larger dogs if none obtained), can be more challenging to obtain
Do not aspirate
Max volume 1ml/5kg
Analyse within 1 hour - differential count, cytology, protein, infectious disease testing
Normal analysis of CSF?
Clear
No RBCs, WBCs <6
Cervical protein <30
Lumbar protein <45
How does blood contamination affect CSF analysis?
Falsely increases WBC count by 1 per 500 RBC
Falsely increases protein by 1 per 1000 RBC
What is albuminocytological dissociation of CSF? What does it indicate?
= increased protein without increased WBC
Non specific
Extradural compression (disc disease), neoplasia, infection, vasculitis, trauma, springomyelia, degenerative myelopathy
What is pleocytosis of CSF? What could cause neutrophilic and mononuclear pleocytosis? Mixed? Eusinophilic?
Increased WBCs Neutrophilic pleocytosis: - SRMA - bacterial (intracellular) - GME/NE - fungal - FIP - post myelography, haemorrhage, trauma, neoplasia Mononuclear pleocytosis: - GME/NE - CNS lymphoma - viral (CDV) - bacterial and SRMA (chronic) Mixed pleocytosis: - GME - bacterial and SRMA (chronic) - fungal - protozoal - non inflammatory disease (infarct) Eosinophilic: - eosinophilic ME - fungal - protozoal - parasitic
What can Pilocarpine be used to test?
Functional test of autonomic NS 0.1% topical administration to the cornea -> miosis Rapid constriction (<30mins) suggestive of denervation hypersensitivty Supportive finding of dysautonomia (definitive diagnosis requires PME)
What is the Edrophonium response test?
Functional test
“Tension test”
For junctionopathies - acquired and some congenital myasthenia gravis
IV administration of edrophonium chloride (fast acting cholinesterase inhibitor)
Care for cholinergic crisis:
- bradycardia
- salivation
- miosis
- dyspnoea
- tremors
(Have incubation kit on stand by and atropine drawn up)
What are electrodiagnostics useful for?
Identifying denervated muscles
Extent and severity
Treatment monitoring
What can be seen with electromyography?
Normal muscle silent except in end-plate region
Spontaneous activity is abnormal
10-14 days to be apparent
What is motor nerve conduction velocity used for? How is it done?
Investigate suspected peripheral neuropathies
Stimulate a motor nerve at a minimum of 2 sites and record the
evoked electrical activity (CMAP)
Patient age and limb temperature should be taken into account
What are F-waves used for?
Assess the nerve roots
F wave latency or F ratio (polyradiculoneuritis)
What is repetitive nerve stimulation used for?
Assess neuromuscular junction
High repetition rate (3-5 per second)
Myasthenia gravis - consistent 10% decrease or more in the CMAP
What is electroencephalography (EEG) used for?
Assess forebrain activity
Identification of seizure activity (when used at the time of the
seizure)
Can be useful in status epilepticus
What does the brainstem auditory evoked response (BAER) screen for?
Congenital sensorineural deafness
Localise acquired deafness
Access hearing threshold
What type of problems are most likely with focal and lateralised, multifocal and diffuse and symmetrical brain lesions?
Focal and lateralised - neoplasia, vascular
Multifocal - inflammatory/infectious
Diffuse and symmetrical - metabolic, toxic
What controls the rate of blood flow through the brain? What is this controlled by?
Rate of blood flow is controlled mainly by CPP (cerebral perfusion pressure)
CPP is controlled by MABP and ICP
CPP = MABP - ICP
Compensatory mechanism of the ICP of the brain? What happens if exceeded?
If one component of the brain (tissue, blood, CSF) increases, another has to decreases
= Compliance
Once limit exceeded, ICP can rise precipitously -> brain herniation:
- forebrain herniates underneath tentorium
- or cerebellum herniates through foramen magnum
Signs of raised ICP?
Mental status - depression, stupor, coma
Cushing’s reflex:
- bradycardia and hypertension
- ICP increases above MAP resulting in cerebral ischaemia
- a1 adrenergic sympathetic activation -> systemic vasoconstriction -> hypertension
- carotid artery baroreceptors detect hypertension -> vagal activation -> bradycardia
Pupils:
- PLR
- aniscoria
- miosis
- mydriasis (worst sign)
Reduced physiological nystagmus (early sign of raised ICP)
Abnormal postures - decerebrate (seen with cerebrum herniation), decerebellate (seen with cerebellar herniation)
Differentials for raised ICP?
V: CVA - ischaemic or haemorrhagic strokes
I: MUOs, bacterial ME, protozoal MEs, viral MEs (CDV, FIP, FIV)
T: head trauma, toxins
A: hydrocephalus, lisencephaly, hydranencephaly and porencephaly, CCA
M: hepatic encephalopathy, hypoglycaemia, electrolyte imbalances
I
N: meningiomas, gliomas, pituitary tumours, lymphoma, metastases, MPNS T
D: lysosomal storage diseases, cognitive dysfunction, many degenerative GM and WM disorders
What types of meningoencephalitis are there? How do they present? Diagnosis?
GME (granulomatous
NME (necrotising)
NLE (necrotising leukoencephalitis
Usually acute and progressive, often multifocal
Diagnosis - advanced imaging, CSF analysis, sometimes biopsy
What is idiopathic tremor syndrome? Signs? Diagnosis? Treatment? Prognosis?
Mostly small breed dogs Fine tremor - rapid, low amplitude, worse with stress/excitement \+/- head tilt, reduced menace, ataxia Diagnosis: - CSF: very mildly inflammatory - +/- MRI to rule out other problems - no other condition causes this type of tremor Treatment: - corticosteroids for 4-6m - +/- other immunosuppressive drugs - diazepam initially Fair-good prognosis but possibility of relapse
What are the 3 main routes of infection for Bacterial ME? Signs? Diagnosis? Treatment? Prognosis?
3 main routes = haematogenous, direct invasion (inner ear, eyes, nasal sinuses or bone infection, trauma), CSF
Signs:
- usually acute CNS signs
- obtundation and CN deficits most common signs
- pyrexia
- neck pain
Diagnosis:
- CSF: increased protein concentration and pleocytosis (rare phagocytksed organisms)
- CSF/blood culture (positive 30%): inside abscess or in small amounts
Treatment = antibiotics +/- surgical drainage
Guarded prognosis
Clinical signs of CNS intoxications? Possible causes?
Acute (<24h) onset
Seizures (approx 40% of all reactive seizures)
Often GI, CV or resp signs before or at same time
Muscle tremors and fasciculations often seen
Status epilepticus (SE) common - infusions usually needed to control seizures
Toxins:
- organophosphates
- pyrethrin
- lead
- avermectins
- medications
- etc
Difference between primary and secondary head trauma?
Primary injury: - physical disruption of parenchyma: concussion, contusion, laceration - no intervention possible Secondary injury: - release of inflammatory mediators - continued haemorrhage - leads to increased ICP - can intervene
Assessment of head trauma? When is surgery needed?
Modified Glascow Coma Scale (useful for serial monitoring, high score is better prognosis)
Imaging: MRI or CT (need for decompressive surgery)
Surgery if fractures compressing brain parenchyma or contaminated fragments, haematomas or severe raised ICP
Medical management of head trauma?
Fluids
- restore IV volume to ensure adequate CPP
- hypotension significantly increases mortality
- resuscitation then maintenance
- isotonic or hypertonic crystalloids, colloids and blood products
- avoid glucose as hyperglycaemia associated with poorer outcome
ICP management
- Mannitol: reduces blood viscosity, increases CBF an oxygen delivery, free radical scavenger, osmotic effect, contraindicated in hypovolaemia, can become refractory
- hypertonic saline: contraindicated if hyponatraemia or cardiac/respiratory disease
Oxygen
- establish clear airway
- essential for brain (high CO2 increases CBF)
Temperature
- avoid hyperthermia (affects metabolic rate) and hypothermia (shivering oxygen demands)
BP:
- maintain between 90-140mmHg
- cerebral blood flow is affected outside this range
- avoid hypotension to maintain CPP
Pain
- pain increases BP and therefore ICP
- caution as morphine may cause emesis and result in increased ICP
General care
- keep head elevated
- avoid jugular compression
- turn every 4-6h
- catheterise bladder every 6h
- nutritional support
Are steroids good for head trauma?
No
Associated with hyperglycaemia and production of lactic acid -> cell death
Increased risk of infection
Affects metabolism
What is hydrocephalus? Which breeds and age usually? Signs?
= Abnormal dilation of ventricular system within cranium Toy breeds, young age Signs: - domed shaped head - persistent fontanelle - abnormal behaviour - cognitive dysfunction - obtundation - circling/pacing - seizures(?) - vestibular signs
What are corpus callus anomalies? Signs? Which breeds?
Corpus callous = white matter that connects cortex of one hemisphere with the other Anomalies = hypogenesis, agenesis Signs: - adipsia associated with hypernatremia - seizures - abnormal behaviour - tremors - circling Min Schnauzer, SBT
What are arachnoid diverticulae?
Prevalence of supracollicular fluid accumulations
What are hydranencephaly and porencephaly? Signs?
= presence of cerebral cavities, usually communicating with subarachnoid space and/or lateral ventricles
Signs in first few months (circling, abnormal behaviour) or up to years (seizures_
Most common cause of hepatic encephalopathy? Pathogenesis?
Most common cause = secondary to PSS Pathogenesis: - hyperammonaemia - neuroinflammation - deranged neurotransmission - cerebral oedema
Signs of hepatic encephalopathy?
Vague signs - failure to thrive, weight loss, PUPD, GI signs
Forebrain signs - behaviour changes, pacing, blindness, seizures
Rare brainstem or cerebellar signs in older dogs
Neuro signs may develop after surgery
Diagnosis and treatment of hepatic encephalopathy?
Diagnosis - BAST, fasting ammonia, US, CT angiography
Treatment:
- lactulose: traps ammonia in intestine, decreases absorption, inhibits uptake of glutamine by intestinal wall
- antibiotics: reduce ammonia producing bacteria in gut
- diet: reduce gut derived ammonia, low protein, aromatic amino acids and short chain fatty acids
- minimise factors causing increased ammonia (constipation, GI bleeding, azotaemia, infection, hypokalaemia)
- minimise factors causing reduced toxin clearance (dehydration, hypotension, anaemia)
- reduce factors affecting neurotransmission (benzodiazepines)
- seizure control: levetiracetam first choice
What is the primary source of energy for the brain?
Glucose oxidation
Brain consumes 25% of total blood glucose
Brain has 3x metabolic rate of peripheral tissues but 10-30% less extracellular glucose
Lack of glycogen ctores
Underlying causes of hypoglycaemia?
Insulinoma Liver disease Insulin overdose Glycogen storage diseases Juvenile hypoglycaemia
Clinical signs and diagnosis of hypoglycaemia?
Clinical signs: - lethargy, ravenous appetite, anxiety - depression - weakness and tremors - reduced vision - seizures Diagnosis: - low glucose levels (typically <3mmol/l) - clinical signs
Causes of hypernatraemia?
Excess water loss (e.g. diabetes insipidus, osmotic diuresis, diarrhoea)
Excess salt intake (e.g. salt poisoning, administration of IV hypertonic solutions, hyperadrenocorticism)
Insufficient water intake (e.g., lack of access, inability to drink or CNS disease resulting in primary adipsia)
Causes of hyponatraemia?
Hypovolemic (e.g., renal and GI disease, third space or cutaneous losses)
Hypervolemic (e.g. congestive heart failure, liver failure, nephrotic syndrome, hypoalbuminemic states)
Normovolemic (e.g., primary polydipsia, water intoxication, hypothyroidism, adrenal insufficiency or renal failure
Signs of sodium derangements?
Altered mentation Blindness Seizures Coma Death
What happens with chronic Na abnormalities? What happens with rapid correction?
In chronic Na abnormalities, there is active movement of electrolytes (Na, K and Cl) followed by “idiogenic osmoles”
With rapid correction, the compensatory influx of electrolytes is not matched by the slower moving organic osmolytes
Signs of hypocalcaemia?
Excitability due to increased neuronal permeability to Na -> nerve fibre discharges spontaneously -> muscle contraction and tetany
Muscle spasm, cramping, muscle twitching, trembling, stiffness, tonic-clonic spasms, episodic rigidity, tetraparesis, seizures
Types of brain neoplasia?
Primary:
- intra-axial: gliomas
- extra-axial: meningiomas, choroid plexus tumours
Secondary:
- metastases e.g. haemangiosarcoma
- direct extension of neoplasia outside brain e.g. nasal tumours, pituitary macro adenoma
Most common clinical signs of brain neoplasia? Which animals? Treatment?
More common in older and larger breed dogs
Most common signs:
- seizures in suratentorial tumours
- central vestibular dysfunction in infratentorial tumours
Treatment:
- less sedative AEDs
- anti-inflammatory doses of prednisolone
- analgesia: paracetamol, gabapentin
What degenerative disorders of the brain are there?
Storage diseases - defect of a lysosomal hydrolase enzyme
Accumulation and storage of substrate(s) within the cytoplasm of neurons - early onset, diffuse neurological dysfunction, progessive course leading to death
Cognitive dysfunction
Signs of cognitive dysfunction? Why does it happen? Treatment?
Changes in behaviour, memory and learning ability: - disturbances in sleeping - staring into space - getting stuck in corners - loss of house training - pacing or vocalising at night - newly developed behaviour problems Due to: - accumulation of beta-amyloid with senile plaque formation and neurofibrillary tangles Treatment: - selegiline - nutritional supplementation with antioxidants and other brain protective compounds - behaviour modification
What makes up the vestibular system?
Peripheral:
- 3 semicircular ducts at right angles to each other, rotation of head makes endolymph flow
- vestibulocochlear nerve (CN8) in connection with hair cells of each receptor, movement of endolymph causes bending of hair cells
Central:
- brainstem: 4 nuclei receive information from nerve and pass to brain and spinal cord
- cerebellum: inhibits vestibular nuclei
Clinical signs of vestibular disease?
Ispilateral head tilt Head sway if affecting both sides Ataxia and wide based stance Leaning and falling Less commonly tight circling Nystagmus - horizontal, rotatory or vertical - lesion on side of slower phase - vertical suggests central - may be positional Positional strabismus
When is a paradoxical head tilt seen?
= contralateral head tilt
Lesion of flocculonodular lobe or caudal cerebellar peduncle
Have other cerebellar signs
Cerebllum inhibits ipsilateral vestibular nuclei -> disinhibition:
- inhibition of ipsilateral extensors
- facilitation of contralateral extensors
What is convergence-related nystagmus?
Seen with small dorsal midbrain lesions - mostly infarcts
Irregular, jerky nystagmus in which both eyeballs rhythmically converge and retract into orbit
Which is opsoclonus nystagmus?
Seen with cerebellar disease
Bursts of rapid multidirectional eye movements without an interval between saccades
How to differentiate between central and peripheral vestibular disease?
Central - paresis possible, proprioceptive deficits possible, mentation may be affected, may be CNV-XII deficits, Horner’s rare, nystagmus can be vertical, horizontal or rotatory and may change direction
Peripheral - no paresis, no proprioceptive deficits, alert mentation, may be VII CN deficit, Horner’s possible, nystagmus is horizontal or rotatory, fast phase away from lesion
Causes of central vestibular disease?
V: cerebrovascular disease I: MUEs, FIP T: head trauma, metronidazole A: brain malformation M: hypothyroidism I N: brain tumours, thiamine deficiency D: lysosomal storage diseases, degenerative diseases
