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MRS211 > Central nervous system > Flashcards

Central nervous system Flashcards

1
Q

What is a traumatic brain injury?

A
  • External force causes brain dysfunction
  • Caused by violent blow or penetrating injury
  • Varies in severity
  • Mild: temporary dysfunction
  • Concussion
  • More serious: permanent brain damage or death
  • Cerebral oedema / haemorrhage
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2
Q

List 3 TBI causes

A
  • Motor vehicle, bike or skateboarding accident
  • Playing sports: contact sport
  • Recreation activities
  • Falls
  • Assault: shaking, hitting, or throwing
  • Exposure to blasts
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3
Q

Who are at greater risk of getting a TBI?

A
  • Young males
  • Elderly
  • Children
  • ATSI
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4
Q

What is a concussion?

A

Most common form of traumatic brain injury

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5
Q

What are the 3 types of concussions?

A
  • Mild: no loss of consciousness, symptoms last less than 15 min
  • Moderate: no loss of consciousness, symptoms last longer than 15 min
  • Severe: Loss of consciousness
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6
Q

List 5 symptoms of a concussion

A
  • Confusion or feeling dazed
  • Clumsiness
  • Slurred speech
  • Nausea or vomiting
  • Headache
  • Balance problems or dizziness
  • Blurred vision
  • Sensitivity to light
  • Sensitivity to noise
  • Sluggishness
  • Ringing in ears
  • Behaviour or personality changes
  • Concentration difficulties
  • Memory loss
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7
Q

How do they diagnose TBIs?

A
  • Physical examination
  • CT: primary imaging modality, moderate to severe head injuries, highly accurate and sensitive
  • MRI: Further investigation subtle injury, moderate injuries
  • NM: Brain death studies, severe injuries
  • Electroencephalogram: EEG
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8
Q

What are the 4 types of serious TBI?

A
  • Cerebral oedema
  • Cerebral contusion
  • Cerebral haemorrhage: epidural, subdural, subarachnoid, intracerebral, diffuse axonal injury
  • Skull fracture
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9
Q

What is cerebral oedema?

A
  • Decreasing level of consciousness – unconscious
  • Swelling of brain cells causing increase brain water content
  • CT initial imaging modality
  • Scans can initially be normal
  • Loss of grey – white matter differentiation
  • Hypodense brain parenchyma
  • Effaced sulci
  • Supra-sellar cistern obliteration (uncal herniation)
  • Cerebellar tonsil herniation
  • Reduced brain activity
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10
Q

What is a cerebral contusion?

A
  • Caused by movement of brain within the skull
  • Brain injury occurs when brain hits rough surfaces e.g. frontal, anterior temporal regions
  • CT usually modality of 1st contact
  • Areas of low density oedema
  • Multiple small high density areas: haemorrhage
  • MRI often used to further evaluate
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11
Q

What is a diffuse axonal injury?

A
  • Shearing of brains nerve fibres
  • Caused by rotational acceleration and deceleration
  • Commonly associated with high speed MVA
  • Loss of consciousness
  • Pt in vegetative state but death uncommon
  • Swelling of brain greatest risk
  • Difficult to diagnose on imaging alone
  • CT & MRI can be utilised
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12
Q

What is an epidural haematoma?

A
  • Caused by structural disruption of the dura and blood vessels
  • Trauma is the typical cause of EDH. The trauma frequently is a blunt impact to the head from an assault, fall, or other accident
  • Most commonly a blow to the temporal bone rupturing middle meningeal artery
  • Commonly associated with fractures of the calvarium
  • Causes mass effect and acute neurological symptoms
  • Biconvex or lens shaped
  • Acute stage hyper dense on CT
  • Rarely has non traumatic origin
  • Requires emergency decompression surgery
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13
Q

What is a subdural haematoma?

A
  • Haemorrhage between Dura and Arachnoid membrane
  • Most common form of traumatic intracranial mass lesion
  • Can be caused by major and minor head trauma
  • Caused by high speed acceleration and deceleration of the brain
  • Causes tears in blood vessels
  • Elderly on anticoagulants susceptible
  • 2-3x more common in men
  • Minor haemorrhage treated conservatively as blood naturally reabsorbed
  • Major haemorrhage surgical decompression
  • Categorised as acute, sub-acute and chronic
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14
Q

What is a subarachnoid haematoma?

A
  • Pt presents with severe headache, vomiting, blurred vision, stiff neck
  • Haemorrhage between arachnoid and pia mater spaces
  • Most commonly caused by trauma but can be spontaneous
  • Usually associated with aneurysm rupture
  • Can be pre-existing or created by trauma
  • Traumatic aneurysm associated with base of skull fractures
  • Aneurysm risk: Atherosclerosis, Hypertension, Advancing age, Smokers
  • More common in females 3:2
  • Can lead to increased ICP requiring surgical intervention
  • Primary diagnosis CT and lumbar puncture
  • Cerebral angiography can be used to find location of haemorrhage
  • Surgical repair of vessel may be necessary
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15
Q

What is an intercranial haemorrhage?

A
  • Haemorrhage into brain parenchyma
  • Caused by shearing forces to intraparenchymal arteries
  • Traumatic and non-traumatic origin
  • Traumatic causes can be penetrating or non-penetrating
  • Symptoms include headache, weakness, confusion, and paralysis
  • Serious condition, causes rapid increase in ICP
  • Major haemorrhage surgical decompression
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16
Q

What is an intraventricular haemorrhage?

A
  • Haemorrhage into the ventricles of the brain
  • Associated with subarachnoid and intracerebral haemorrhage
  • Increases morbidity and mortality rates of patients
  • Usually associated with dangerously raised ICP
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17
Q

What are some treatment options for TBI?

A
  • Treatment will vary with severity of injury
  • Usually conservative in nature
  • Monitor neurological signs
  • Monitor intracranial pressure (ICP)
  • Follow up imaging
  • Medical treatment to lower ICP (e.g. osmotherapy, diuretics, corticosteroids)
  • Surgical decompression if ICP becomes unmanageable
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18
Q

What is cerebrovascular disease?

A

Stroke

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19
Q

list three epidemiological facts regarding stroke

A
  • Second most common cause of death in the World
  • Kills more women than breast cancer and more men than prostate cancer
  • Leading cause of adult disability
  • In Australia 56,000 new and recurrent strokes this year– that is one stroke every nine minutes
  • 30% stroke survivors under 65
  • 65% of stroke survivors suffer a disability which impedes their ability to carry out daily living activities unassisted
  • The financial cost of stroke in Australia is estimated to be $5 billion each year
  • More than 80% of strokes can be prevented
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20
Q

What is a transient ischemic attack?

A
  • partial occlusion
  • ‘angina of the brain’
  • Focal neurological event lasting <24 hours
  • Focal loss of central nervous function due to decreased blood flow to part of the brain
  • precursor for CVA
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21
Q

Define cerebrovascular accident

A

Sudden and severe focal loss of Central Nervous System function due to decreased blood flow to focal region of the brain

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22
Q

Name 5 signs/symptoms of CVA

A
  • Abrupt onset of hemiparesis, monoparesis, or (rarely) quadriparesis
  • Hemisensory deficits
  • Monocular or binocular visual loss
  • Visual field deficits
  • Diplopia
  • Dysarthria (unable to articulate speech)
  • Facial droop
  • Ataxia (lack of muscle control)
  • Vertigo (rarely in isolation)
  • Nystagmus (involuntary eye movement)
  • Aphasia (unable to understand or produce speech)
  • Sudden decrease in level of consciousness
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23
Q

How do they diagnose CVA?

A
  • medical history/ risk factors check
  • physical examination: airway and breathing, reflexes, muscle strength etc., BP, listen to heart
  • Blood tests
  • ECG
  • imaging
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24
Q

What are the non-modifiable risk factors for CVA

A 
age
race
sex (F)
history of migraines
fibromuscular dysplasia
fam history of stroke or TIA
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25
Q

what are 5 modifiable risk factors for CVA

A 
hypertension
diabetes
cardiac disease
TIA
carotid stenosis
hypercholesterolemia
alcohol and drug use
obesity
oral contraceptive
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26
Q

What is the pathophysiology for ischaemic stroke

A
  • acute occlusion intracranial vessel
  • focal reduction in cerebral blood flow (collaterals)
  • ischaemic core or ischaemic penumbra
  • cell death and infarction of tissues
  • haemorrhagic transformation or cerebral oedema
  • patient death
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27
Q

what are the 3 stages/phases of an ischaemic stroke?

A

acute phase/stage (0-24/48 hours)
subacute phase/stage (24/48 + hours)
chronic phase/stage (4 to 6+ weeks)

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28
Q

what are the types of ischaemic stroke

A

large vessel
small vessel

thrombotic
embolic

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29
Q

what happens in a small vessel ischaemic attack?

A
  • Occlusion of small sub-cortical non-branching arteries (<15-20mm)
  • Occur most frequently in the basal ganglia and in the internal capsule, thalamus, corona radiata, and pons
  • Accounts for around 20% of ischaemic strokes
  • Symptomatic or non-symptomatic
  • Higher risk of more serious large vessel stroke
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30
Q

what happens in a large vessel ischaemic attack

A

Occlusion of large artery in the brain
Thrombotic origin most common
MCA most commonly occluded major artery
Clinical emergency

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31
Q

what imaging modalities are utilised for a CVA

A 
CT
MRI
US
catheter angio (DSA)
PET/SPECT
xray
32
Q

what is the purpose of imaging for CVA

A
  1. Confirm clinical diagnosis
  2. Distinguish between haemorrhagic & thromboembolic ischaemia
  3. Identify underlying cause of disease e.g. stenosis/occlusion in CVA
  4. Direct management/intervention e.g. thrombolytic therapy in CVA
33
Q

benefits of non con CTB

A

Nearly 100% sensitivity for acute haemorrhage
Identify skull fractures
Reported sensitivity for ischaemia varies greatly
CT is increasingly valuable in identifying occlusive disease in cerebrovascular circulation

34
Q

what does non con CTB aid in the diagnosis of

A

New ischaemia or infarction
Old areas of ischaemia
Intracranial mass
Intracranial haemorrhage

35
Q

what is the problem with non con CTB

A

Time since thromboembolic event
Size of infarct
Location of infarct
Reader variability

36
Q

changes to brain with ischaemia in CT

A
  • Changes to expected normal anatomy
  • Must understand normal and normal varients
  • Abnormalities can be Hyper, Iso or Hypo dense
  • Hyperdense indicates increased blood
  • Hypodense indicates high level of increase oedema / fluid
  • Isodense abnormalities indicate lower increase in oedema / fluid
37
Q

hyperdense abnormalities on CT non con brain

A

haemorrhage
- blood pooling outside of vascular system
- increased density
hyperdense artery
- thrombus within the occluded vessel
- increased haematocrit levels within thrombus

38
Q

hypodense abnormalities on CT non con brain

A

hypodense vascular territory

  • thrombus within the occluded vessel
  • causes increased oedema in cells due to the lack of blood supply
  • large area affected; hours after event
39
Q

isodense abnormalities of CT non con brain

A

loss of grey-white matter differentiation

  • loss of normal grey white matter interface
  • cytotoxic oedema within grey matter
  • occurs within region of vascular territory affected
40
Q

what does a CT contrast brain scan do?

A 
preceded by non con CTB
CTA arch COW
location of haemorrhage or aneurysm
CT perfusion
blood flow to brain tissue
41
Q

what does CTA do?

A

identifies occluded vessel
identifies location of aneurysm
identifies site of ruptured vessel

42
Q

what is a CT perfusion scan?

A

Used to differentiate between ischaemic core and penumbra

Available now on many CT scanners but not all

Increased use in stroke work up due to availability

Allows for more accurate patient management

43
Q

MRI is more sensitive than CT for?

A

acute ischemia
infarction
previous intracranial bleeding
underlying lesions

44
Q

What is Magnetic resonance angio (MRA) used for in regards to CVA?

A

can be performed with or without contrast

shows intracranial vessels +/- neck

45
Q

What is SPECT/CT in NM used for in regards to CVA

A

PET: most accurate test for identifying penumbra (time consuming test, can’t get access to the penumbra quick enough)
Ischemia: Changes in regional cerebral blood flow & metabolism
SPECT: cerebral blood volume, cerebral perfusion
PET: Ischaemic penumbra & infarction
- not usually used due to time involved

46
Q

What is US used for in a CVA

A

Post CVA; follow-up
Carotid Doppler: carotid stenosis (overestimation), plaque texture & volume, common F/U in TIA / minor CVA
Cardiac Echo

47
Q

What is DSA

A

Insertion of catheter into peripheral artery, then advanced and positioned to artery of choice using II guidance (at origin or further up)
Inject iodine contrast directly into vessel
Further investigate vessel abnormalities
Perform minor procedures, angioplasty, stenting, coiling

48
Q

What are some treatment options for a haemorrhagic stroke

A

Stop bleeding through medication (cause coagulation) and surgery (coiling, clip it)

49
Q

What are some treatment options for an ischaemic stroke?

A

Thrombolysis : Administration of strong clot dissolving drug (alteplase)
Endovascular Clot aspiration suck clot out through catheter
Needs to occur within 4.5 hrs of event

50
Q

List 3 types of stroke rehabilitation methods

A

Hospital stay in dedicated unit
Allied health (Physio, Speech Pathologist, Occupational therapist)  get back to some sort of normalcy
Permanent medication to reduce risk of recurrence
Lifestyle changes (diet, exercise, etc)
Potential for long term nursing care can occur in young people

51
Q

what is dementia

A

the broad term for a group of diseases causing a progressive decline of neurological function

52
Q

symptoms of dementia

A

memory loss, confusion, and personality and behavioural changes

53
Q

what are 5 epidemiological statistics on dementia

A

Presently over 400,000 people living with diagnosed dementia
55% female, 45% male
2nd leading cause of death in Australia (10.6% female, 5.4% male)
Estimated $5-15 billion spent on dementia care and treatment per year
>25,000 people diagnosed with younger onset dementia (<65 years old)

54
Q

what are the 10 early signs of dementia

A
  1. Subtle short-term memory changes
  2. Difficulty finding the right words
  3. Changes in mood
  4. Apathy
  5. Difficulty completing normal tasks
  6. Confusion
  7. Difficulty following storylines
  8. A failing sense of direction
  9. Being repetitive
  10. Struggling to adapt to change
55
Q

what is alzheimers disease

A

Most common progressive, neurodegenerative disease
Most common form of dementia in the elderly
Complex aetiology > genetics, environment & lifestyle
Classification based on heritability & age of onset:
-Late-onset AD; >65 YOA onset, classical disease
-Early-onset AD; <65 YOA onset, often inherited, rare, faster progression
High socioeconomic burden

56
Q

what are some risk factors for alzheimers disease

A
  • Age
  • Sex
  • Family history and genetics
  • Down syndrome
  • Mild cognitive impairment (MCI)
  • Head trauma
  • Chronic stress
  • Depression
  • Diabetes
  • Hypertension
  • Vascular disease
  • Oxidative stress
  • Vitamin D deficiency
  • Obesity & inflammation
  • Smoking or exposure to second-hand smoke
57
Q

what is the pathophysiology for alzheimer’s

A

Neuropathology:
- Formation of extracellular, neuritic plaques (amyloid-𝛽 peptide or A𝛽)
- Intraneuronal accumulation of neurofibrillary tangles (hyper-phosphorylated tau protein)
• Resultant neuronal loss & loss of synapses with marked cerebral atrophy
• Disruption of neurotransmitters (to include acetylcholine, norepinephrine, serotonin and somatostatin)
• Therapy development has predominantly focused on A𝛽-induced neurotoxicity
• Amyloid-𝛽 & tau pathology considered as sensitive biomarkers

58
Q

cognitive symptoms of Alzheimer’s

A
  • Attention deficit
  • Language impairment
  • Short term memory loss
  • Impaired activities of daily living (apraxia)
  • Loss of orientation (time, space)
59
Q

behavioural symptoms of Alzheimer’s

A
  • Apathy
  • Depression
  • Anxiety
  • Aggressive behaviour
  • Hallucinations
  • Social withdrawal
60
Q

appearance of alzheimers brain on CT

A
  • Similar appearance to normal aging brain in early stages
  • Atrophy
  • Enlarged ventricles
  • Prominent sulci
  • Correlate with clinical symptoms
  • Rule out other brain causes for symptoms
  • Impacts allocation for care funding
61
Q

appearance of alzheimers brain on MRI

A
  • Similar appearance to normal aging brain in early stages
  • Atrophy
  • Enlarged ventricles
  • Prominent sulci
  • High intensity periventricular region T2 / FLAIR
  • Correlate with clinical symptoms
62
Q

What are some treatment options for alzheimer’s

A

No cure, however can slow progression;
-Diet
-Exercise
-Education
-Memory aids
-Medication
• Acetylcholinesterase inhibitors (Prevent destruction of neurotransmitter acetylcholine)
• Memantine (Prevents calcium moving into brain cells causing damage
• Other drugs that treat symptoms (Sleep and psychological issues)

63
Q

What is Parkinson’s disease?

A

a complex and chronic, progressive, neurological degenerative movement disorder

64
Q

What are 3 epidemiological facts regarding Parkinson’s disease

A
  • Over 80,000 people living with Parkinson’s Disease
  • Most common major movement disorder and second highest prevalence
  • 37 new cases are diagnosed every day
  • 18% are of working age (65 and younger)
  • Prevalence of Parkinson’s was higher than many cancers including breast cancer, colorectal, stomach, liver and pancreatic cancer, lymphoma and leukaemia, kidney and bladder, uterine, cervical, and ovarian, and lung cancer
65
Q

What are some clinical presentations of Parkinson’s disease?

A

Bradykinesia; slowness of movement
Muscular rigidity; inability of the muscles to relax normally
Rest tremor; involuntary rhythmic tremor when limbs are relaxed
Postural and gait impairment; small shuffling steps

66
Q

What are some motor features of Parkisons

A

Tremor
Bradykinesia
Muscle rigidity
postural instability

67
Q

name 5 non-motor features of Parkinsons

A
  • Sensory dysfunction • Mood disorders including anxiety, apathy and depression
  • Constipation and gastrointestinal issues
  • Fatigue, pain and cramping
  • Speech problems
  • Sexual issues
  • Changes in hand writing
  • Postural hypotension
  • Excessive salivation
  • Sleep disorders
  • Swallowing difficulties
  • Sweating and increased sensitivity to temperatures
  • Cognitive changes
  • Urinary urgency, frequency and incontinence
  • Mental health issues
68
Q

what are 5 risk factors of parkinsons

A 
Pesticides 
Toxins  
Chemicals 
Genetic factors 
Head trauma
69
Q

what is pathophysiology of Parkinsons

A

2 major neuropathological findings:

  • Loss of pigmented dopaminergic neurons of the substantia nigra pars compacta
  • The presence of Lewy bodies and Lewy neurites
70
Q

how do they diagnose Parkinson’s

A

currently no lab test or radiological procedure, diagnosis checklist consists of:
Bradykinesia, muscle rigidity, tremor and postural instability

71
Q

what imaging modalities are utilised for Parkinson’s disease

A

CT to rule out structural abnormalities
MRI to rule out other neurological conditions
PET/SPECT
PET/CT

72
Q

what is CT used for in PD imaging

A

Similar appearance to normal aging brain
• Performed routinely to rule out other causes
• Many brain pathologies exhibit similar symptoms
• Rule out tumours, infective/inflammatory process, other degenerative disorder

73
Q

what is SPECT/PET used for in PD imaging

A
  • Functional imaging of dopamine transporter
  • Both SPECT and PET tracers have a high sensitivity for assessment of presynaptic dopaminergic deficits
  • SPECT (123 I) ioflupane (DaTscan) established
  • Demonstrates binding of 123I-fluoropropyl to DaT protein in the nigrostriatal nerve endings of the striatum
  • DaTscan can differentiate from essential tremor only
  • PET imaging using 6-fluorodopa (FDOPA) demonstrates decreased uptake in posterior striatum, particularly in the putamen
  • 18F Fluorodeoxyglucose (FDG) demonstrates diffuse cortical hypometabolism (marked in parietotemporal cortex)
  • Novel PET tracers β-amyloid, tau protein, or α-synuclein aggregates
74
Q

what is PET/CT used for in PD imaging

A
  • Gives exact anatomical reference for increased activity

* Important for PD diagnosis as it effects particular areas of the brain

75
Q

what is MRI used for in PD imaging

A
  • Recommended by NICE for PD differential & patients with atypical features
  • Structural & functional
  • 3-7T MR scanning can detect structural nigral abnormalities
  • Ultra high field MRI with diffusion-tensor (tractography) & diffusion-weighted imaging are being explored for early disease diagnosis
  • Other areas of research:
    * Spectroscopy
    * resting-state fMRI
    * arterial spin labeling
76
Q

what are 3 treatment options for PD

A

Exercise
Oral medications (to improve mobility)
Advanced therapy medications given by injection or by a tube directly into the small intestine
Surgical treatments
-Advice and support from a Parkinson’s Specialist Nurse
-Physical and Supportive therapies

MRS211 (10 decks)

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