Neurology Flashcards
what locations of the brain can a lesion be localised to?
forebrain
brainstem
cerebellum
vestibular system (central/peripheral)
what mnemonic can be used to generate a differential diagnosis list?
Vascular
Inflammatory/infectious
Trauma
Anomalous
Metabolic
Idiopathic
Neoplasia
Degenerative
what are the main four clinical signs that would localise the lesion to the forebrain?
seizure
disorientation
contralateral blindness (normal PLR)
circling
what clinical signs would suggest a forebrain lesion?
seizures
behavioural changes
disorientation, depression
contralateral blindness (normal PLR)
facial hypoasthesia
normal gait
circling (ipsilateral), head pressing, pacing
decreased postural response (contralateral limb)
what are the two main clinical signs that suggest a cerebellar lesion?
hypermetria
tremors (intention)
what clinical signs suggest a forebrain lesion?
normal mentation
abnormal menace (normal vision/PLR)
vestibular signs - head tilt…
ataxia, broad stance, hypermetria
intention tremors
decerebellate rigidity
hypermetric postural response
what are the main three clinical signs of a brainstem lesion?
cranial nerve deficits
vestibular signs
paresis (all four/ipsilateral limbs)
what are the clinical signs of brain stem lesions?
depression, stupor, coma
cranial nerve deficits
vestibular signs
paresis
decerebrate rigidity
decreased postural response
respiratory/cardiac abnormalities
what are the differentials for a focal/lateralised brain lesion?
neoplasia
vascular
what are the differentials for a multifocal brain lesion?
inflammatory
infectious
what are the differentials for a diffuse/symmetrical brain lesion?
metabolic
toxic
what contributes to intracranial pressure (ICP)?
brain
blood supply to brain
cerebrospinal fluid
what is compliance in relation to intracranial pressure?
can accommodate mild changes in ICP as when one factor contributing to it (eg. blood supply) increases the others with decrease
what happens when ICP gets too high?
herniation underneath the tentorium of through foramen magnum
what structure of the brain does formen magnum herniation effect?
cerebellum
what are the signs of raised ICP?
mental status (ARAS)
bushings reflex
pupil size and PLR
vestibular eye movement
posture - decerebrate/decerebellate
why does raised ICP effect the mental status of patients?
(ARAS - ascending reticular activation system)
awakeness centre in brainstem will decrease in activity with raised ICP causing depression, stupor and coma
what is bushings reflex?
very unwell patients with bradycardia and hypertension due to cerebral ischaemia (end stage sign)
how can pupil size change with raised ICP?
anisocoria
miosis
mydriasis
what is anisocoria?
pupils are different sizes
what is miosis?
excessive constriction (shrinkage) of pupil
what is mydriasis?
excessive dilation of pupils
how does physiological nystagmus change with raised ICP?
eyes don’t move due to a delay in connection between vestibular system and cranial nerves
what is a peracute presentation?
extremely sudden onset (change from one second to the next)
what are the differentials for peracute onset brain disease?
vascular (stroke)
trauma (RTA…)
toxic
what primary injuries are associated with head trauma?
concussion
contusion
laceration (physical disruption of parenchyma)
what secondary injuries are associated with head trauma?
inflammatory mediator release
haemorrhage
(raised ICP)
what is used to assess head trauma?
modified Glasgow coma scale
what is the modified Glasgow coma scale based on?
signs of raised ICP
how does the score of the modified Glasgow coma scale compare to the prognosis?
low the score the worse the prognosis
how can the modified Glasgow coma scale be used to monitor ICP?
do every couple of hours, if it is getting worse then ICP is increasing
what is done to treat head trauma patients?
fluid therapy
what is the aim of fluid therapy for head trauma cases?
restore intravascular volume to ensure adequate cranial perfusion pressure
what fluid should be avoided for fluid therapy of head trauma cases?
glucose containing fluid - hyperglycaemia is associated with poor outcome
what fluid should be given as an initial bolus in head trauma cases?
7.5% saline
what are the advantages of 7.5% saline boluses in head trauma cases?
treats shock
decreases intracranial pressure
increases blood flow and oxygen delivery to the brain
what fluids are indicated for head trauma with raised ICP?
mannitol or hypertonic saline
what needs to be monitored in head trauma cases?
blood pressure
oxygenation
pain
temperature
what pain management should be avoided in head trauma cases?
morphine - vomit resulting in raised ICP and herniation
why does temperature need monitoring in head trauma cases?
hyperthermia - affects metabolic rate
hypothermia - shivering/oxygen demand
in terms of general care, what are some good things to do to head trauma cases?
keep head elevated
catheterise bladder
nutritional support
should steroids be given to head trauma patients?
no - hyperglycaemia, increased infection risk, lactic acid production
what are the main differentials for acute/subacute onset brain disease?
inflammatory
infectious
metabolic (wax and wane)
what are the three main routes of infection of bacterial meningitis?
haematogenous
direct invasion (eyes, ear, nose, bone, trauma)
CSF
what is the prognosis for bacterial meningitis?
guarded
what are the main two infectious brain disease?
Neospora caninum
FIP
what are the two main metabolic diseases of the brain?
hepatic encephalopathy
hypoglycaemia
what is the main cause of hepatic encephalopathy?
portosystemic shunts
what causes the clinical signs of hepatic encephalopathy?
hyperammoneaemia
neuroinflammation
deranged neurotransmission
cerebral oedema
what are the ways of treating hepatic encephalopathy?
lactulose
antibiotics
diet
seizure control
why is lactulose used in hepatic encephalopathy cases?
traps ammonia as non-diffusible ammonium in intestines to decrease the absorption into blood
what is the aim of altering diet to treat hepatic encephalopathy?
restrict protein and amino acids to reduce ammonia in blood
what are the clinical signs of hypoglycaemia?
lethargy, ravenous appetite, anxiety
weakness/tremors
reduced vision and seizures
(all wax and wane)
why is hypoglycaemia seen in the brain?
has no storage for glucose
why does care need to be taken when correcting hypernatraemia?
do it too rapidly and the cells will burst - permanent brain damage
what are the differentials for chronic brain disease?
neoplasia
anomalous
degenerative
what primary neoplasms can be seen in the brain?
intra-axial - glioma
extra-axial - meningioma, chord plexus tumour
what is the median survival time of infratentorial and supratentorial tumours?
infratentorial - 28 days
supratentorial - 178 days
what should be done to treat brain neoplasia?
analgesia (paracetamol)
anti-inflammatory dose of prednisolone
what are the most common anomalous brain diseases?
hydrocephalus
hydranencephaly
what is storage disease of the brain due to?
lysosomal hydrolase enzyme defect
what are the functions of the vestibular system?
maintain balance
maintain normal orientation relative to gravitational field
maintain position of eyes, neck, trunk, limbs in relation to the head
what makes up the peripheral vestibular system?
3 ducts at right angles to each other with endolymph within
vestibulocochlear nerve (CN8)
what triggers nerve impulses in the vestibulocochlear nerve?
hair bending due to fluid
what makes up the central vestibular system?
brainstem - 4 nuclei
cerebellum (inhibits nuclei)
what are the clinical signs of vestibular disease?
ipsilateral head tilt
head sway (both sides of system effected)
ataxia and wide base stance
leaning/falling
nystagmus
tight circling (less common)
positional strabismus
what causes a paradoxical head tilt?
cerebellar disease causes head tilt contralateral to lesion (loss of inhibition)
how can the lesion of vestibular disease be localised using nystagmus?
lesion on the slower side
what does vertical nystagmus suggest about the location of the lesion?
central vestibular disease
what is positional strabismus?
when the head is lifted the eye will drop
can paresis be a clinical sign of peripheral or dental vestibular disease?
central - yes
peripheral - no
can proprioceptive deficits be a clinical sign of peripheral or dental vestibular disease?
central - yes
peripheral - no
how can mentation be affected by peripheral or central vestibular disease?
central - may be altered
peripheral - alert
can cranial nerve deficits be a clinical sign of peripheral or dental vestibular disease?
central - V-XII may be affected
peripheral - VII may be affected
can Horners be a clinical sign of peripheral or dental vestibular disease?
central - rare
peripheral - yes
how does nystagmus indicate central or peripheral vestibular disease?
vertical is always central
horizontal or rotary can be either
what are the most common differentials for central vestibular disease?
cerebrovascular disease
MUEs, FIP
brain tumour
what are the most common differentials for peripheral vestibular disease?
otitis media/interna
idiopathic
what are the two types of strokes?
ischaemic (obstruction)
haemorrhagic (rupture)
how does cerebrovascular disease present?
stroke or cerebrovascular accident
what are the most common underlying diseases causing cerebrovascular disease?
chronic kidney disease
hypertension
hyperadrenocorticism
what does MUO stand for?
meningoencephalomyelitis of unknown origin
what type of disease are MUOs?
auto-immune disease of the brain
what are the subtypes of MUOs?
granulomatous ME
necrotising ME
necrotising leukoencephalitis
what breeds are granulomatous MEs most common in?
toy/terrier breeds
how old are dogs with granulomatous ME?
3-8 years old
how are granulomatous MEs distributed?
multifocal distribution
what is the prognosis for MUOs?
very poor (progressive chronic disease)
how are MUOs treated?
corticosteroids (immunosuppression)
what causes CNS involvement of FIP?
immune-complex-mediated vasculitis
what are the most common neurological signs of FIP?
tetra paresis, ataxia, nystagmus, loss of balance (cerebellomedullary region)
why is FIP causing neurological signs difficult to diagnose?
usually wet form of disease
why does otitis media/interna cause peripheral vestibular disease?
CN VII and VIII pass through the middle ear
what are some clinical signs of otitis media/interna?
facial paralysis
peripheral vestibular signs
Horner syndrome
pain opening mouth
how is idiopathic vestibular disease treated?
spontaneous recovery without treatment
what are the clinical signs of idiopathic vestibular disease?
acute onset peripheral signs - rolling, falling, vomiting, ataxia, head tilt, nystagmus
what supportive treatment can be given to idiopathic vestibular disease patients?
maropitant (nauseous)
reduce stimulation but keep active
what are the clinical signs of facial nerve paralysis?
face drooping
widening of palpebral fissure
food dropping from mouth
reduced/absent palpebral relfex
what is the most common cause of deafness?
congenital sensorineural deafness
what can cause acquired deafness?
chronic otitis interna/media
ototoxicity
noise trauma
anaesthesia associated
