Brain diseases Flashcards
1
Q
What are the 4 main parts of the brain?
A
Forebrain
Brainstem
Cerebellum
Vestibular system - central vs peripheral
2
Q
The spinal cord is split into which 4 main locations?
A
C1-C5
C6-T2
T3-L3
L4-S3
3
Q
The central vestibular system is made up of?
A
The brainstem and cerebellum
4
Q
Why are blood tests done in brain disease?
A
To rule out metabolic disease
5
Q
Why is CSF analysis done in brain disease?
A
To rule out or confirm inflammatory disease
6
Q
Which features of a patient can give you clues to help their diagnosis?
A
- Age
- History
- Acute/peracute, subacute or chronic
- Progressive, static, improving or waxing and waning - Neuro exam
- Localisation
- Lateralised or symmetrical
- Focal, multifocal or diffuse
7
Q
List the signs of forebrain lesions that patients may present with
A
- Disorientation, depression
- Contralateral blindness, normal PLR, facial hypoasthesia
- Normal gait
- Circling (ipsilateral), head turn, head pressing, pacing
- Decreased postural responses in contralateral limbs
- SEIZURES. behavioural changes
8
Q
List the signs of cerebellar lesions that patients may present with
A
- Normal mentation
- Ipsilateral abnormal menace with normal vision and PLR
- Head tilt
- Ataxia, broad-based stance, hypermetria
- Intention tumours
- Decerebellate rigidity
9
Q
List the signs of brainstem lesions that patients may present with
A
- Depression, stupor, coma
- Cranial nerve deficits (III-XII)
- Vestibular signs
- Paresis of all or ipsilateral limbs
- Decerebrate rigidity
- Decreased postural responses in all limbs or just ipsilateral limbs
- Respiratory or cardiac abnormalities
10
Q
A focal and lateralised lesion has which DDx?
A
Neoplasia
Vascular
Inflammatory/infectious
Trauma
11
Q
A multifocal lesion has which DDx?
A
Inflammatory/infectious
Neoplasia
Vascular
Trauma
Degenerative
12
Q
A diffuse and symmetrical lesion has which DDx?
A
Metabolic
Toxic
Anomalous
Degenerative
Inflammatory/infectious
Trauma
13
Q
Why is tissue swelling in the brain particularly problematic?
A
Skull limits the extent of the expansion
Pressure within the skull (intracranial pressure –ICP) is related to the volume of the contents:
- Brain itself
- Blood supplying the brain
- Cerebrospinal fluid (CSF)
14
Q
Rate of blood flow through the brain is governed mainly by …?
A
Cerebral perfusion pressure
15
Q
Cerebral perfusion pressure is controlled by?
A
- Mean systemic arterial pressure
- Intracerebral pressure (effectively the resistance to blood flow)
CPP = MABP - ICP
16
Q
Describe the compensatory mechanisms within the brain when there are changes in cerebral perfusion pressure
A
- If one component (tissue, blood, CSF) increases, another has to decrease to maintain pressure
- Can happen to a certain extent - COMPLIANCE
- There is limit and once this is exceeded ICP can rise precipitously
17
Q
What are some causes of increased cranial pressure?
A
- Mass (neoplasia, haemorrhage, etc)
- Trauma (#, blood, oedema)
- Inflammatory dx (oedema)
- Metabolic, anomalous less commonly
18
Q
What is brain herniation?
A
Brain then starts to squeeze into places it doesn’t belong – forebrain herniates underneath the tentorium or cerebellum herniates through the foramen magnum
19
Q
What are the clinical signs of raised intracranial pressure?
A
- Mental status - ARAS
- Cushing’s reflex (happens when ischemia has reached the brain – end stage sign)
- Pupil size and PLR
- Vestibular eye movement - MLF
- Abnormal postures: Decerebrate, Decerebellate
20
Q
Describe the decerebrate prosture
A
All 4 limbs rigid
21
Q
Describe the decerebellate posture
A
Forelimbs rigid
Hindlimbs flexed under body
22
Q
Describe the features of the Cushings reflex
A
- Bradycardia and hypertension
- ICP increases resulting in cerebral ischaemia
- Systemic vasoconstriction -> hypertension
23
Q
Describe normal nystagmus and nystagmus when there is raised ICP
A
Move head from side to side slowly, eyes should follow the direction the head is moving
Swollen brain - eyes stay in a fixed position and don’t move
24
Q
What are some DDx of brain disease
A
- CVAs - ischaemic or hemorrhagic strokes
- Meningoencephaltis of unknown origin (MUOs), bacterial ME, protozoal MEs (Toxoplasma, Neospora), viral MEs (CDV, FIP, FIV), fungal MEs
- Head trauma, toxins
- hydrocephalus, lisencephaly, hydranencephaly and porencephaly, CCA
- hepatic encephalopathy, hypoglycaemia, electrolyte imbalances
- meningiomas, gliomas, pituitary tumours, lymphoma, metastases
- lysosomal storage diseases, cognitive dysfunction, many degenerative GM and WM disorders
25
What are the DDx for peracute onset presentations of brain disease?
Vascular – strokes
Trauma – big trauma!! - RTAs, falls, big dog bites
Toxic
26
What are some examples of brain primary traumatic injuries and how are they treated?
Physical disruption of parenchyma
- Concussion
- Contusion
- Laceration
No intervention possible
27
What happens when there is a secondary injury in the brain following head trauma?
Release of inflammatory mediators
Continued haemorrhage
Leads to ↑ ICP (oedema, haemorrhage)
28
Describe assessment of a patient following head trauma
Initial assessment
Serial neurological assessment
Imaging
+/- surgical intervention
29
Describe medical management of a patient following head trauma
Fluid therapy
ICP management
O2
Temperature
BP
Pain
General care
30
Which scale is used for assessing and monitoring a pateint after a head injury?
Modified Glasgow Coma Scale
Useful for serial monitoring
↑ score → better prognosis
31
When is surgery indicated following a head injury?
Fractures compressing brain parenchyma or contaminated fragments
Haematomas
Severe raised ICP…
32
What is the role in fluid therapy following head traumas?
Restore intravascular volume to ensure adequate cerebral perfusion pressure (CPP)
Hypotension significantly increases mortality
33
Which fluids should be avoided in head trauma patients?
Avoid glucose containing fluids as hyperglycaemia is associated with a poorer outcome
34
Why is mannitol given to patients following a head injury?
↓ blood viscosity, ↑ CBF and oxygen delivery, free radical scavenger, osmotic effect
- Follow with crystalloid therapy to prevent dehydration
- Contraindicated in hypovolemia
35
Blood pressure in head trauma patients should be maintained at what level?
Maintain SBP100-140 mmHg
36
Describe oxygenation in head trauma patients
Establish clear airway
Supplement O2 by face mask or mechanical ventilation
O2 essential for brain
↑CO2 → ↑CBF
37
Why must pain be managed in head trauma patients?
Pain increases blood pressure and therefore ICP
Caution as morphine may cause emesis and result in increased ICP
38
Why must temperature be managed in head trauma patients?
Avoid hyperthermia (affects metabolic rate)
Avoid hypothermia (shivering increases oxygen demands)
39
Describe the general care needed for head trauma patients
- Keep head elevated (~30°)
- Avoid jugular compression
- Turn q4-6h
- Catheterise bladder q6h (or maintain catheterised)
- Maintain nutritional support (oesophageal or nasogastric tube)
40
Describe the use of steroids in head trauma patients
Dont use!
Associated with hyperglycaemia and production of lactic acid – cell death!
Increased risk of infection
Other significant effects on metabolism
41
40% of reactive seizures are caused by?
Intoxications
42
Describe the main features of intoxication presentations
- Acute (<24h) onset
- Often GI, cardiovascular or respiratory signs before or at same time
- Muscle tremors and fasciculations often seen
- SE common – infusions usually needed to control seizures
43
List some DDx of brain disease that have acute-subacute presentations
1. Inflammatory/infectious
- MUO
- Bacterial, viral, fungal
2. Metabolic – often waxing and waning
- Hypoglycaemia
- Hepatic
- Electrolytes (Na, Ca…)
3. Neoplasia, anomalous…
44
What are the 3 main routes of infection for bacterial meningitis?
- Haematogenous
- Direct invasion (inner ear, eyes, nasal or bone infection, trauma)
- CSF
45
How does bacterial meningitis present?
- Usually acute CNS signs (obtundation and CN deficits most common), neck pain (~30%), pyrexia (~50%)
- CSF: neutrophilic; phagocytosed organisms in CSF rare
- CSF/blood culture (positive ~15-30%) – inside abscess or in small amounts
46
How is bacterial meningitis treated?
Antibiotics +/- surgical drainage, guarded prognosis
47
Which other infectious diseases cause brain lesions?
Neospora caninum
Toxoplasma gondii
FIP
FIV, Borna virus…
Canine Distemper virus
Cryptococcus
48
What is hepatic encephalopathy?
Reversible neurological manifestations secondary to any aetiology of acute or chronic liver failure - most commonly portosystemic shunt (PSS)
49
Describe the pathogenesis and signs of hepatic encephalopathy
Multifactorial and poorly understood
- Hyperammonemia + neuroinflammation + deranged neurotransmission + cerebral oedema
- Vague signs: failure to thrive; weight loss; PU/PD; GI signs
- Forebrain signs: behaviour changes; pacing; blindness; seizures
- Rare brainstem or cerebellar signs reported in older dogs
50
How is hepatic encephalopathy diagnosed?
Diagnosis relies on bile acid stimulation test, fasting ammonia, ultrasound or CT angiography
51
How is hepatic encephalopathy treated?
- Lactulose
- Antibiotics: reduce ammonia-producing bacteria in the gut
- Diet
- Seizure control (levetiracetam, KBr, PB, propofol)
52
How does lactulose help treat hepatic encephalopathy?
Traps ammonia as non-diffusible ammonium in intestinal lumen, decreases absorption of ammonia through cathartic effect and inhibits uptake of glutamine by intestinal wall
53
How does diet help treat hepatic encephalopathy?
- Aim to reduce gut derived blood ammonia
- Restricted protein content, aromatic amino acids and short chain fatty acids
54
What are the aims of treating hepatic encephalopathy?
Minimising contributing factors that:
- Increase ammonia production (constipation, GI bleeding, azotaemia, infection, hypokalem)
- Reduce clearance of toxins (dehydration, hypotension, anaemia)
- Affect neurotransmission (benzodiazepines)
55
What is the major carbohydrate substrate of the brain?
Glucose - no glycogen storage
- Glucose oxidation is primary source of energy
- Brain consumes ~25% of total blood glucose
- Brain has 3x metabolic rate of peripheral tissues
56
What are the clinical signs of hypoglycaemia?
- Lethargy, ravenous appetite and anxiety
- Weakness and tremors
- Reduced vision and seizures
57
How is hypoglycaemia diagnosed?
Low glucose levels (typically less than 3 mmol/l) – check insulin at same time
58
How does hypernatremia affect the brain?
Causes cell shrinkage - rapid correction dangerous
59
How does hyponatremia affect the brain?
Cell swelling
60
What are the neurological signs of sodium derangements?
Altered mentation, blindness, seizures, coma and death
61
List the DDx for chronic onset presentations of neurological disease
Neoplasia
Anomalous
Degenerative
Inflam/infectious, metabolic
62
List some primary neoplasia's of the CNS
Intra-axial – gliomas
Extra-axial – meningiomas, choroid plexus tumours
63
List some secondary neoplasia's of the CNS
- Metastases (e.g. haemangiosarcoma)
- Direct extension of neoplasia outside brain (e.g. nasal tumours, pituitary macroadenomas)
64
What are the most common signs of CNS in the brain?
Seizures in supratentorial tumours
Central vestibular dysfunction in infratentorial tumours
65
Name 2 anomalous conditions of the brain
Hydrocephalus
Hydranencephaly and porencephaly
66
Describe hydrocephalus and its clinical signs
- Abnormal dilation of ventricular system within cranium
- Toy breeds, young age
- Domed shaped head, persistent fontanelle, abnormal behaviour, cognitive dysfunction, obtundation, circling/pacing, seizures, vestibular signs
67
Describe Hydranencephaly and porencephaly
- Communicating with subarachnoid space and/or lateral ventricles
- Signs in 1st few months (circling, abnormal behaviour) or up to years few years (seizures)
68
Describe the signs of cognitive dysfunction
Pathological deterioration of the brain
Changes in behaviour, memory, and learning ability:
- Disturbances in sleeping, staring into space, getting stuck in corners, loss of housetraining ability, pacing or vocalizing at night, newly developed behaviour problems
