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Y4 SA - Neurology > Brain diseases > Flashcards

Brain diseases Flashcards

1
Q

What are the 4 main parts of the brain?

A

Forebrain
Brainstem
Cerebellum
Vestibular system - central vs peripheral

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2
Q

The spinal cord is split into which 4 main locations?

A

C1-C5
C6-T2
T3-L3
L4-S3

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3
Q

The central vestibular system is made up of?

A

The brainstem and cerebellum

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4
Q

Why are blood tests done in brain disease?

A

To rule out metabolic disease

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5
Q

Why is CSF analysis done in brain disease?

A

To rule out or confirm inflammatory disease

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6
Q

Which features of a patient can give you clues to help their diagnosis?

A
  1. Age
  2. History
    - Acute/peracute, subacute or chronic
    - Progressive, static, improving or waxing and waning
  3. Neuro exam
    - Localisation
    - Lateralised or symmetrical
    - Focal, multifocal or diffuse
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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
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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
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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
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10
Q

A focal and lateralised lesion has which DDx?

A

Neoplasia
Vascular
Inflammatory/infectious
Trauma

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11
Q

A multifocal lesion has which DDx?

A

Inflammatory/infectious
Neoplasia
Vascular
Trauma
Degenerative

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12
Q

A diffuse and symmetrical lesion has which DDx?

A

Metabolic
Toxic
Anomalous
Degenerative
Inflammatory/infectious
Trauma

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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)

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14
Q

Rate of blood flow through the brain is governed mainly by …?

A

Cerebral perfusion pressure

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15
Q

Cerebral perfusion pressure is controlled by?

A
  • Mean systemic arterial pressure
  • Intracerebral pressure (effectively the resistance to blood flow)
    CPP = MABP - ICP
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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
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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
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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

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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
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20
Q

Describe the decerebrate prosture

A

All 4 limbs rigid

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21
Q

Describe the decerebellate posture

A

Forelimbs rigid
Hindlimbs flexed under body

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22
Q

Describe the features of the Cushings reflex

A
  • Bradycardia and hypertension
  • ICP increases resulting in cerebral ischaemia
  • Systemic vasoconstriction -> hypertension
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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

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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
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25
Q

What are the DDx for peracute onset presentations of brain disease?

A

Vascular – strokes
Trauma – big trauma!! - RTAs, falls, big dog bites
Toxic

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26
Q

What are some examples of brain primary traumatic injuries and how are they treated?

A

Physical disruption of parenchyma
- Concussion
- Contusion
- Laceration
No intervention possible

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27
Q

What happens when there is a secondary injury in the brain following head trauma?

A

Release of inflammatory mediators
Continued haemorrhage
Leads to ↑ ICP (oedema, haemorrhage)

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28
Q

Describe assessment of a patient following head trauma

A

Initial assessment
Serial neurological assessment
Imaging
+/- surgical intervention

29
Q

Describe medical management of a patient following head trauma

A

Fluid therapy
ICP management
O2
Temperature
BP
Pain
General care

30
Q

Which scale is used for assessing and monitoring a pateint after a head injury?

A

Modified Glasgow Coma Scale
Useful for serial monitoring
↑ score → better prognosis

31
Q

When is surgery indicated following a head injury?

A

Fractures compressing brain parenchyma or contaminated fragments
Haematomas
Severe raised ICP…

32
Q

What is the role in fluid therapy following head traumas?

A

Restore intravascular volume to ensure adequate cerebral perfusion pressure (CPP)
Hypotension significantly increases mortality

33
Q

Which fluids should be avoided in head trauma patients?

A

Avoid glucose containing fluids as hyperglycaemia is associated with a poorer outcome

34
Q

Why is mannitol given to patients following a head injury?

A

↓ blood viscosity, ↑ CBF and oxygen delivery, free radical scavenger, osmotic effect
- Follow with crystalloid therapy to prevent dehydration
- Contraindicated in hypovolemia

35
Q

Blood pressure in head trauma patients should be maintained at what level?

A

Maintain SBP100-140 mmHg

36
Q

Describe oxygenation in head trauma patients

A

Establish clear airway
Supplement O2 by face mask or mechanical ventilation
O2 essential for brain
↑CO2 → ↑CBF

37
Q

Why must pain be managed in head trauma patients?

A

Pain increases blood pressure and therefore ICP
Caution as morphine may cause emesis and result in increased ICP

38
Q

Why must temperature be managed in head trauma patients?

A

Avoid hyperthermia (affects metabolic rate)
Avoid hypothermia (shivering increases oxygen demands)

39
Q

Describe the general care needed for head trauma patients

A
  • Keep head elevated (~30°)
  • Avoid jugular compression
  • Turn q4-6h
  • Catheterise bladder q6h (or maintain catheterised)
  • Maintain nutritional support (oesophageal or nasogastric tube)
40
Q

Describe the use of steroids in head trauma patients

A

Dont use!
Associated with hyperglycaemia and production of lactic acid – cell death!
Increased risk of infection
Other significant effects on metabolism

41
Q

40% of reactive seizures are caused by?

A

Intoxications

42
Q

Describe the main features of intoxication presentations

A
  • 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
Q

List some DDx of brain disease that have acute-subacute presentations

A
  1. Inflammatory/infectious
    - MUO
    - Bacterial, viral, fungal
  2. Metabolic – often waxing and waning
    - Hypoglycaemia
    - Hepatic
    - Electrolytes (Na, Ca…)
  3. Neoplasia, anomalous…
44
Q

What are the 3 main routes of infection for bacterial meningitis?

A
  • Haematogenous
  • Direct invasion (inner ear, eyes, nasal or bone infection, trauma)
  • CSF
45
Q

How does bacterial meningitis present?

A
  • 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
Q

How is bacterial meningitis treated?

A

Antibiotics +/- surgical drainage, guarded prognosis

47
Q

Which other infectious diseases cause brain lesions?

A

Neospora caninum
Toxoplasma gondii
FIP
FIV, Borna virus…
Canine Distemper virus
Cryptococcus

48
Q

What is hepatic encephalopathy?

A

Reversible neurological manifestations secondary to any aetiology of acute or chronic liver failure - most commonly portosystemic shunt (PSS)

49
Q

Describe the pathogenesis and signs of hepatic encephalopathy

A

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
Q

How is hepatic encephalopathy diagnosed?

A

Diagnosis relies on bile acid stimulation test, fasting ammonia, ultrasound or CT angiography

51
Q

How is hepatic encephalopathy treated?

A
  • Lactulose
  • Antibiotics: reduce ammonia-producing bacteria in the gut
  • Diet
  • Seizure control (levetiracetam, KBr, PB, propofol)
52
Q

How does lactulose help treat hepatic encephalopathy?

A

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
Q

How does diet help treat hepatic encephalopathy?

A
  • Aim to reduce gut derived blood ammonia
  • Restricted protein content, aromatic amino acids and short chain fatty acids
54
Q

What are the aims of treating hepatic encephalopathy?

A

Minimising contributing factors that:
- Increase ammonia production (constipation, GI bleeding, azotaemia, infection, hypokalem)
- Reduce clearance of toxins (dehydration, hypotension, anaemia)
- Affect neurotransmission (benzodiazepines)

55
Q

What is the major carbohydrate substrate of the brain?

A

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
Q

What are the clinical signs of hypoglycaemia?

A
  • Lethargy, ravenous appetite and anxiety
  • Weakness and tremors
  • Reduced vision and seizures
57
Q

How is hypoglycaemia diagnosed?

A

Low glucose levels (typically less than 3 mmol/l) – check insulin at same time

58
Q

How does hypernatremia affect the brain?

A

Causes cell shrinkage - rapid correction dangerous

59
Q

How does hyponatremia affect the brain?

A

Cell swelling

60
Q

What are the neurological signs of sodium derangements?

A

Altered mentation, blindness, seizures, coma and death

61
Q

List the DDx for chronic onset presentations of neurological disease

A

Neoplasia
Anomalous
Degenerative
Inflam/infectious, metabolic

62
Q

List some primary neoplasia’s of the CNS

A

Intra-axial – gliomas
Extra-axial – meningiomas, choroid plexus tumours

63
Q

List some secondary neoplasia’s of the CNS

A
  • Metastases (e.g. haemangiosarcoma)
  • Direct extension of neoplasia outside brain (e.g. nasal tumours, pituitary macroadenomas)
64
Q

What are the most common signs of CNS in the brain?

A

Seizures in supratentorial tumours
Central vestibular dysfunction in infratentorial tumours

65
Q

Name 2 anomalous conditions of the brain

A

Hydrocephalus
Hydranencephaly and porencephaly

66
Q

Describe hydrocephalus and its clinical signs

A
  • 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
Q

Describe Hydranencephaly and porencephaly

A
  • Communicating with subarachnoid space and/or lateral ventricles
  • Signs in 1st few months (circling, abnormal behaviour) or up to years few years (seizures)
68
Q

Describe the signs of cognitive dysfunction

A

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

Y4 SA - Neurology (7 decks)

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