Neurology Module 2 Flashcards
What is the primary and secondary injury related to traumatic brain injury?
Primary injury: high impact and results in mechanical disruption to brain tissue - this can not be stopped
Secondary injury: caused by swelling, haemorrhage, Increased ICP, ischaemia that results - can try to prevent and manage
What scores are good at lending prognosis for brain injury?
Modified GCS, ATT
What is the treatment for raised ICP and what are the goals?
Goals: Maintain cerebral perufsion, control ICP and hypotension BP 100-120mmHg
1. Elevate head - 30
2. Avoid jugular compression - decreased cerebral drainage - sample from peripherals
3. turn q4-6hrs
4. Avoid anything that will further increase ICP - vomiting/sneezing/coughing/urinating /seizures
5. Fluid therapy - maintain normovolaemic to hypervolaemic state - hypertonic saline or colloids followed with isotonic
6. Pain relief
7. Temperature - avoid hypo and hyper (increased O2 demand)
8. Enteral nutrition
9. Oxygenation and ventilation
10. urination management
11. Osmotic diuretic - mannitol - better for deteriorating patients
12. Steroids - only if underlying inflam cause to ICP
13. Control seizures
How is acute brain disease categorised?
- Diffuse or symmetrical lesions: metabolic, anomolous conditions, inflammatory/infectious, degenerative
- Focal or lateralised intracranial lesions: unilateral, blindness/proprioceptive deficits, circling, vestibular - neoplastic, inflam/infectious, vascular (ishaemia/strokes)
- Multifocal : infectious/inflamm, vascular, trauma, neoplastic, degenerative
What are the two types of stroke?
Ischaemic - caused by arterial or venous obstruction
Haemorrhagic: caused by rupture of intracranial vessels
What is the onset of action of a ischaemic stroke v. haemorrhagic stroke?
Typically acute and are non-progressive after the intial 24 hours. If less than 24hours of clinical signs = transient ischaemic attack, haem is more variable
What are concurrent metabolic problems with strokes
Mostly cats
- CKD
- Hypertension
- Protein losing disease
- Cushings
- Neoplasia
- Angiostronglyus
- DM
- HypoT4
- Cardiac disease
What is the normal presentation of inflammatory disease?
Can be infectious or non-infectious in origin
Can be acute or subacute in onset with variable progression
Often multifocal and asymmetric
What are infectious causes of inflammatory disease?
Distemper
Toxo, neospora - progressie cerebellar ataxia over weeks, cerebellar atrophy on MRI - clindamycin/TMPS
FIP - 30% cats have CNS involvement, immune mediated vasculitis, uveitis, insidious signs - most commonly tetraparesis, ataxia, nystagmus, and occasionally spinal cord disease
What breeds are commonly affected with MUO
Young to middle aged, small and toy breed dogs - 3-8yrs
What are the three forms of granulomatous meningo-encephalitis?
Disseminated: multifocal
Focal
Ocular: dilated, non-responsive pupils with edematous optic discs
What breeds are affected by necrotising meningitis?
Pugs/maltese/chihuahua/yorkie/boston T
acute onset
rapidly progressive (often forebrain) - seizures
causes necrosis of tissue
What diagnostics would you use to diagnose MUO?
Bloods: metabolic causes
Serology for infectious disease + culture
CSF analysis
What is the treatment of inflammatory brain diseases?
Antimicrobials if secondary to protozoal or bacteria disease
Immunosuppressive meds if immune mediated
AEDs if seizuring - levitir/phenobarb - pheno better for necrotising
Idiopathic Tremor syndrome: CS, Dx, Tx
Mostly young dogs
CS: fine tremor - rapid, low amplitude and worse with stress/excitement +/- head tilt, ataxia, decreased menace
Dx: CSF/MRI - rule out other
Tx: corticosteroids 4-6mths +/- other immunosup
Eosinophilic ME: CS, Dx, Tx
CS: large breed dogs, obtundation, vision impairment, ataxia, seizures
Dx: MRI/CSF - cortical atrophy on MRI
Pachymeningitis: CS, Dx, Tx
Causes multiple CN deficits, abnormal mental status, visual deficits - sighthounds - thickened dura matter
What percentage of seizures are caused by toxins?
40%
Common cause of status epilepticus - tends to need infusions (propofol)
Toxins that can cause seizures
Metronidazole - diazepam outcompetes metro
Mycotoxin
Grapes
Cannibus
Metadehyde (blue GI content)
Metabolic causes of seizures?
-Toxins
- Hypoglycaemia
- Hepatic encephalopathy
- Sodium derangements
How does hypoglycaemia cause seizures?
Glucose is the major nutritive carbohydrate substrate of the brain. Can not store it effectively, needs to oxidise it and is brains primary source of E.
- Glucose less than 3mmol/L
- underlying diseases: juvenile hypogly, insulinoma, insulin overdose, liver disease, glycogen storage disease
Treatment of hepatic encephalopathy?
- Lactulose: traps ammonia as non-diffusible in intestinal lumen, and decreases uptake
- Abs: decreased ammonia producing baceria
- Diet: aim is to decrease gut derived blood ammoia, restricted protein content, aromatic aminoacids and short chain fatty acids
- AEDs for seizures control
How do sodium derrangements result in seizures?
Hypernatraemia: cell shrinkage - excess H2O loss - DM, D+, osmotic diuresis, cushings, salt poisoning
Hyponatraemia: cell swelling - hypovolaemia (renal, GI disease, cutaenous loss, 3rd space disease), hypervolaemia (CHf, liver failure, nephrotic syndrome)
Normovolaemia (primary polydipsia, waer intox, hypot4)
What is the management of neoplasia causing seizures?
- AEDs - levitiracetam
- Anti-inflam preds
- Analgesia - paracetamol
Optic Neuropathy: CS, Dx, Tx
CS: acute blindness, absent PLRs, uni or bilateral, swollen optic discs,
Dx: MRI inflam of nerve heads, CSF
Ddx: MUO, microbial infections, trauma, orbital inflam, toxins, neoplasia
Tx: ais
Trigeminal neuritis: CS, Dx, Tx
Most common cause of dropped jaw in dogs - idiopathic condition with benign course and resolution in 3-4 weeks
- Muscle to help eat, supportive care, feeding tube
Underlying neoplasia/inflam/infection
Facial nerve paralysis/paresis CS, Dx, Tx
Most commonly idiopathic - esp if bilateral
DDX: middle ear disease, polyneuropathies, brainstem lesions, Hypot4
Dx: Bloods, MRI/CT, CSF
- Most cases improve over 6-8 weeks some have permenant deficits
TX: avoid KCC
What are the structures passing through the middle ear?
CNV5, CNV8, Sympathetic supply to the eye
Clinical signs of otitis media?
Common in CKCS
mucus initially produced in TM and draining through the auditory tube to nasopharynx
Hearing loss, peripheral vestibular disease, facial paralysis
Dx: otoscopy, CT/MRI
