Neurology: Brain Disease Flashcards
What is the purpose of blood work, MRI/Imaging and CSF for diagnostic invesigation of neurology?
- Blood work- rule out metabolic disease
- MRI- vitamin D
- CSF- inflammatory disease
What are the signs of forebrain lesions?
- Disorientation, depression
- Contralateral blindness
- Normal gait
- Circling- head pressing
- Reduced postural responses in contralateral limbs
- Seizures- behavioural changes, hemi-neglect
What are the signs of cerebellar lesion?
- Normal mentation
- Ipsilateral abnormal menace with normal vision
- Vestibular signs (head tilt)
- Ataxia, broad-based stance, hypermetria
- Intention tremors
- Delayed initiation and then often hypermetric postural responses
What are the signs of brainstem lesions?
- Depression, stupor, coma
- Cranial nerve defectics
- Vestiublar signs
- Paresis
- Decerebrate rigidity
- Decreased postural responses in all limbs
- Respiratory or cardiac abnomalities
What are the main differentials for:
1. focal and lateralised
2. Multifocal
3. Diffuse and symmetrical
- Neoplasia, vascular
- Inflammatory/infectious
- Metabolic/ toxic
What affects intracranial pressure?
Why does it show signs quickly?
Brain itselt, blood, CSF
Skull limits expansion
What are compensatory mechanisms to reduce intracranial pressure?
- If one one component increases another decreases
- Tissue/CSF/Blood decreases
What happens with sustained increase in intra-cranial pressure?
Brain herniation
* Forebrain herniates underneath the tentorium or cerebellum herniates through the foramen magnum
What are signs of raised ICP?
- Mental status- ARAS
depression, stupor, coma - Cushing’s reflex
bradycardia and hypertension- only with ischaemia - Pupil size and PLR
- Vestiublar eye movement- pysiological nystagmus
- Abnormal postures- decerebrate, decerebellate
What is the most likely cause with quick onset of disease?
Vascular- strokes
What is the difference between primary and secondary injury causing head trauma?
Primary
* Primary disruption of parenchyma
* Concussion, contusion, laceration
Secondary
* Release of inflammatory mediators
* Continues haemorrhage
* Leads to ICP
* Aim of our intervention
How is head trauma assessed and medically managed?
Assessment
* Initial assessment
* Serial neurological assessment
* Imaging
* ± surgical intervention
Medical managment
* Fluid therapy
* ICP managment
* O2
* BP
* Pain
* General care
How is head trauma assessed?
Modified glasgow coma scale
* Useful for serial monitoring
* Increased score is a better prognosis
How can decisions for head trauma be made?
MRI or CT
* Severity and prognosis of lesions
* Need for decompressive surgery or not
Surgery
* Fractures compression brain parenchyma or contaminated fragments
* Haematomas
What fluid therapy is indicated for head trauma?
- Restore intravascular volume to ensure adequate CPP
- Hypotension significantly increases mortality
- Resuscitation then maintenance
- 7.5% saline- reverses shock, decreases ICP, increases CBF and oxygen delivery
Avoid glucose containing fluids- hyperglycaemia associated with poorer outcome
With raised ICP what treatment is indicated?
Mannitol
* Reduces blood viscosity
* Increased CBF and oxygen delivery, free radical scavenger
* Follow with crystalloid therapy
* Contraindicated in hypovolaemia
Hypertonic saline
* hyperosmotic, free radical scavenger
* Contraindicated- hyponatraemia, cardiac or resp diease
Why does blood pressure need to be maintained between 100-140?
Head trauma
Cerebral blood flow is affected outside this range
Head trauma
- Why does pain of head trauma need to be managed?
- Why does temperature need to be managed?
- Increases blood pressure and therefore ICP- not morphine (emesis)
- Avoid hyperthermia/hypothermia- increases oxygen demands
What is the general care for head trauma?
- Keep head elevated- 30 degrees
- Avoid jugular compression
- turn q4-6h
- Catheterise bladder
- Maintain nutritional support- tube
NO STEROIDS
How do intoxications commonly present?
- Acute
- Often GI, CV, resp signs
- Muscle tremors and fasiculations often seen
Organophosphates, pyrethrin, lead etc
What is likely to cause acute and acute onset brain disease?
- Inflammatory
- Metabolic
- MUO, bacterial, viral, fungal
- Hypoglycaemia, hepatic, electrolytes
- What are the 3 main routed of bacterial ME?
- What are the acute signs?
- What does CSF show?
- How is it treated?
- Haematogenous, direct invasion, CSF
- CNS- obtundation, CN defecits
- Neutrophilic, phagoscyosed organisms possible
- ABs ± surgical drainage
Guarded prognosis
Other then bacteria what infectious diseases can cause ME?
- Neospora caninum
- Toxoplasma
- FIP
- FIV
- Canine distemper virus
- Cryptococcus
How is hepatic encephalopathy diagnosed?
- Bile acid stimulation test
- Fasting ammonia
- US
- CT
How is hepatic encephalopathy treated?
Lactulose
* traps ammonia as non-diffusable ammonium in intestinal lumen
* Decreases absorption
Antibiotics
* reduce of ammonia-prodcuing bacteria in gut
Diet
* aim to reduce gut derived blood ammonia
Minimise
* Increased ammonia production- constipation, GI bleed
* Reduced clearance- dehydration, hypotension
* Affect neurotransmission
Seizure control
- Why does hypoglycaemia cause brain disease?
- What are the clinical signs?
- Glucose oxidation primary energy source
- Lethargy, ravenous appetite, anxiet, weakness and tremors, reduced vision and seizures
Insulinoma, liver disease, insulin overdose, juvenile hypoglycaemia
Why does sodium derangments cause brain disease?
Blood levels reflect ratio of sodium to water in extracellular fluid
Hypernatraemia- cell shrinkage
Hyponatraemia- cell swelling
Rapid correction dangeous
What can cause chronic onset presentations?
Neoplasia
Anomalous
Degenerative
What primary and secondary neoplasia can affect the brain?
Primary
* Intra-axial- gliomas
* Extra-axial- meningiomas, choroid plexus tumours
Secondary
* Metastases
* Extension- nasal tumours
Tx
* less sedative AEDs
* Pred
* Analgesia
What are the 2 anomalous chronic causes of brain disease?
Hydrocephalus
* Abnormal dilaiton of ventricular system within cranium
* Domed shaped head, obtundation, seizures, vestiublar signs
* Toy breeds, young age
Hydrancephaly and porencephaly
* Communicating with subarachnoid space and/or lateral ventricles
* Signs within 1st few months
