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ESA 4 Rev > Neuro revision > Flashcards

Neuro revision Flashcards

1
Q

What is the role of hippocampus in memory?

A

Consolidation of declarative memories.

Strengthen synapses with cortex.

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2
Q

What are complications of meningitis?

A

Cerebral infarction
Subdural empyema
Cerebral abscess
Epilepsy

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3
Q

Outline how prions cause disease?

A

Abnormal prion proteins aggregate - spongiform encephalopathies.

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4
Q

Embolus within the brain can originate from where?

A

Atria - AF
Carotid atheroma debris
Aneurysm

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5
Q

What structure initiates REM sleep?

A

Pons

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6
Q

What happens in stages 2+3 of sleep on EEG?

A

Theta waves with sleep spindles and K complexes

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7
Q

What happens in stage 1 of sleep in EEG?

A

alpha waves and theta waves

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8
Q

What happens to muscle tone in REM sleep?

A

Loss of muscle tone - inhibitory of LMNS by descending glycernergic fibres from RF.

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9
Q

What are some reversible causes of dementia?

A 
Depression, delirium
Trauma
Vitamin deficiency
Alcohol
Thyroid disorder
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10
Q

How is the CAM score used to differentiate between delirium + dementia?

A

If 2 or more then delirium likely:

  • Acute
  • Altered consciousness
  • Inattention
  • Disorganised thinking
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11
Q

What symptoms are typical of lewy body dementia?

A

Fluctuations in cognitive impairment
Parkinson symptoms
Visual hallucinations
Frequent falls

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12
Q

What are features of fronto-temporal dementia?

A

Altered social behaviour + personality
Impaired judgement + insight
Speech - mutism/aphasia eventually

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13
Q

What are 2 types of partial seizures?

A

Temporal - auras, memory rush

Frontal - abnormal movements on contralateral side.

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14
Q

What investigations would you do if you suspected epilepsy?

A

History - pre, during and after
Collateral history
EEG
MRI and ECG to to rule out other causes.

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15
Q

Differential diagnosis for epilepsy.

A 
Vascular - stroke, TIA
Infection - abscess
Trauma - intracerebral haemorrhage
Autoimmune - SLE
Metabolic - hypoglycaemia, hypoxia, thyroid
Iatrogenic - alcohol withdrawal
Neoplasia - mass
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16
Q

What 3 things are tested on GCS.

A

Eye opening
Verbal response
Motor response

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17
Q

What are the 6 stages of motor response in GCS.

A 
Obeys commands
Localise to pain
Normal flexion
Abnormal flexion
Extension
None
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18
Q

What are the 4 stages of eye opening in GCS.

A

Spontaneous
To sound
To pressure
None

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19
Q

What is the name given to the pathophysiology of a raised ICP.

A

Cytotoxic cellular oedema

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20
Q

What are the signs and symptoms of raised ICP?

A 
Headache
Vomiting
Visual disturbances
CNVI palsy - abducens
Decreased conscious level - RF ischaemia 
Infants - increasing head size
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21
Q

Which CN is vulnerable with raised ICP and why?

A

Abducens - emerges from posterior pons and courses close to skull.

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22
Q

What are 3 effects of tentorial/uncal herniation?

A

Pressure on MIDBRAIN:
CNII palsy
Cerebral peduncle - contralateral leg weakness
CVS and rest centres - decreased consciousness

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23
Q

What is the consequence of tonsillar herniation?

A

Decreased consciousness - compress CVS and resp centres

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24
Q

Explain why the Cushing’s reflex might occur.

A

Hypertension - ischeamia at medulla, increased sympathetic activation
Baroreceptor response - bradycardia
Ischaemia at resp centres - low RR

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25
Q

What 4 things can cause a raised ICP?

A

SoL
Increased cerebral blood volume
Increased CSF
Cerebral oedema

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26
Q

What might cause increased cerebral blood volume?

A

Venous outflow obstruction

Venous sinus thrombosis

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27
Q

What might cause cerebral oedema?

A

Meningitis
Encaphalitis
Infarction
Diffuse head injury

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28
Q

What might cause increased CSF?

A

Excess secretion - choroid plexus papilloma

Impaired absorption - hydrocephalus, benign intracranial hypertension

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29
Q

Give 3 examples of SoL.

A

Abscess
Haemorrhage
Tumour

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30
Q

What does normal CSF look like and contain?

A

Clear
Little protein + cells
Hyperosmotic to plasma - Na+, Cl-

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31
Q

What is the difference between non-communicating and communicating hydrocephalus?

A

Non-communicating = obstruction in ventricles. Dilation of ventricles superior to obstruction.
Communicating - outside ventricles - decrease absorption or increased production. Dilation of all ventricles.

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32
Q

What might cause non-communicating hydrocephalus?

A

Tumours- meningioma

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33
Q

What is idiopathic intracranial hypertension and who is it most common in?

A

Raised ICP without hydrocephalus or mass lesion.
Normal imaging but signs of raised ICP.
Obese young women after weight gain.

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34
Q

What is contusion.

A

Microhaemorrhages and small blood vessel leaks - blood mixes with cortical tissue.
Oedema - raised ICP - coma

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35
Q

What is concussion and its effects?

A

Concussion - temporary loss of brain function following head injury.
Stretching and injury to axons - impaired NT and blood flow - temp dysfunction

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36
Q

What is diffuse axonal injury?

A

Shearing of interface between grey and white matter - axonal death - cerebral oedema - raised ICP - coma

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37
Q

Describe the trend in consciousness associated with extradural haemorrhage.

A
  1. LOC from initial concussion- Reticular activating system damaged
  2. Lucid interval of recovery with ongoing headache
  3. Decline as haematoma grows and ICP increases
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38
Q

What complications are associated with extradural haemorrhage?

A 
Permanent brain damage
Coma
Seizures
Weakness
Psuedoaneurysm
Ateriovenous fistula = vasc malformations increase risk of future bleeds.
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39
Q

Which intracranial haemorrhage can be chronic and present like dementia?

A

Subdural in elderly as tension on bridging veins- confusion and cognitive decline

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40
Q

What are the CT changes as haemorrhage gets older?

A

Acute - hyper dense = brighter

Chronic - hypo dense = darker

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41
Q

What age group usually suffer from subarachnoid haemorrhage?

A

< 60

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42
Q

Which brain haemorrhage is associated with a sudden thunderclap headache?

A

Subarachnoid

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43
Q

Which type of brain haemorrhage can present with meningism despite no infection?

A

Subarachnoid

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44
Q

What investigation can aid diagnosis of subarachnoid haemorrhage?

A

Lumbar puncture -rbc present or xanthochromia = yellow from RBC breakdown

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45
Q

What are RF for subarachnoid haemorrhage?

A

FH
CT problems
Smoking
Alcohol

46
Q

Why can ACA stroke cause a loss of control of micturition?

A
  1. Genitals is medial on motor homunculus

2. Supplies paracentral lobules - role in voluntary control of micturition.

47
Q

Damage to which lobe can cause spatial neglect?

A

Right parietal lobe - neglect left side

48
Q

An occlusion in which artery could result in contralateral homonymous hemianopia?

A

MCA, proximal - both superior and inferior optic radiations

49
Q

An occlusion in which artery may cause issues in laying down new declarative memories?

A

PCA - supplies inferior temporal lobe where hippocampus is

50
Q

What sensory changes might you see with PCA stroke?

A

Sensory loss on contralateral side - thalamus

51
Q

What would be the effects of a distal basilar artery occlusion?

A

PCA also affected - bilateral occipital infarct - blindness
Bilateral thalamic infarct - anaesthatised
Bilateral midbrain infarction

52
Q

What would be the effect of proximal occlusion of basilar artery?

A

Pontine vessels

Quadriplegia - corticospinal tract infarction.

53
Q

Occlusion of which artery could cause a purely motor stroke?

A

Lenticulostriate artery - contralateral face, upper and lower limb

54
Q

Occlusion of which artery could cause a purely sensory stroke?

A

Thalamoperforator artery - contralateral face, upper and lower limb

55
Q

Other than stroke, name 4 other causes of ‘stroke mimics’?

A

Hypoglycaemia
Epilepsy
Migraine
Intracranial tumours, Infection

56
Q

What deficits might be present if there is occlusion of ICA?

A

Contralateral paralysis of both upper and lower limbs, trunk and speech deficit.

57
Q

What are 2 theories for anxiety?

A

Low GABA - BZD reduce anxiety

Low serotonin - SSRI’s reduce anxiety

58
Q

What is the treatment for anxiety?

A
  1. SSRI
  2. CBT
  3. Pregabalin - GABA analogue
59
Q

What are 3 theories for OCD?

A
  • Re-entry circuit in basal ganglia
  • Reduced serotonin
  • PANDAS
60
Q

What is PANDAS?

A

Sudden onset OCD symptoms after group A strep infection

Cross-reaction of antibodies with basal ganglia neurones.

61
Q

What is the recommended treatment for OCD?

A
  1. CBT
  2. Exposure response prevention
  3. High dose SSRI - higher doses than depression
62
Q

What is the pathophysiology of PTSD?

A

Hyperactivity of amygdala

Low cortisol - cortisol inhibits traumatic memory retrieval

63
Q

What 3 things contribute to cause of depression?

A

Predisposing factors
Precipitating factors - triggers
Perpetuating factors - maintain

64
Q

Give examples of perpetuating factors.

A

Social stressers - job, studies, unemployment, financial strain, housing, substance misuse

65
Q

Give examples of precipitating factors.

A

Life events - losses, health, relationship break up

66
Q

What are 5 positive symptoms of schizophrenia?

A 
Auditory hallucinations
Passivity experiences
Thought withdrawal, broadcast + insertion
Delusional perception
Somatic hallucinations
67
Q

What are negative symptoms of schizophrenia?

A

Underactivity
Low motivation
Social withdrawal
Self neglect

68
Q

What are the 5 types of schizophrenia?

A 
Paranoid
Simple
Hebephrenic
Catatonic
Undifferentiated
69
Q

What is the pathophysiology of schizophrenia?

A

Underactive mesolimbic pathway

Overactive mesocortical pathway

70
Q

What is the autoimmune hypothesis for schizophrenia?

A

Anti-NMDA encaphalitis

  • ovarian teratoma antibodies bind to NMDA receptor in brain.
  • Acute psychosis
71
Q

What type of receptor is D2?

A

GPCR - Gi

72
Q

What is the pathophysiology of catatonic schizophrenia?

A

Decreased movement although dopamine excess..

increased GABA inhibition.

73
Q

What are organic causes of psychosis?

A

Delirium - infection
Hypercalcaemia
Hyperthyroidism
Drug/alcohol intoxication

74
Q

What are the clinical features of a complete cord transection at C5?

A
  • Loss of all sensory modalities at and below C5
  • Loss of all motor modalities at and and below C5
  • LMN signs at C5
  • UMN signs below C5
  • Priapism + hypotension - increased PS
75
Q

What are common causes of complete cord transection?

A 
Trauma
Infarction
Abscess
Tumour
Transverse myelitis
76
Q

What are causes of brown-sequard syndrome?

A 
Penetrating trauma
Fractured vertebrae
Abscess 
Tumour
MS
77
Q

What are causes of anterior cord syndrome?

A

Flexion injuries - dislocation/fractured vertebrae, herniated discs
Anterior spinal artery - atherosclerosis in elderly

78
Q

Which tracts are affected in anterior cord syndrome?

A

Spinothalamic

Corticospinal

79
Q

What type of trauma can cause central cord syndrome in elderly and younger patients?

A

Elderly - hyperextension

Young - hyperflexion

80
Q

Other than trauma, what can cause central cord syndrome?

A

Syringomyelia
Cervical spine stenosis
Degenerative spinal disease- spondylosis

81
Q

What are the clinical features of central cord syndrome?

A

Cape-like distribution - upper limbs > lower limbs (medial in tracts)
Motor function > Sensory
Distal > proximal
Bladder dysfunction and urinary retention

82
Q

What is often responsible for the initial symptoms of central cord syndrome?

A

Obliteration of spinothalamic fibres decussating in ventral white commissure.

83
Q

What are causes for posterior cord syndrome?

A 
Spondylosis
Spinal stenosis
Infections
Vit B12 deficiency
Occlusion of posterior spinal arteries
84
Q

Before removing the collar, what must the patient be?

A 
Alert and orientated
No language barrier
Not intoxicated
No midline posterior tenderness - palpate spine
No focal neurological deficit
No painful distracting injuries
85
Q

Which grey matter horn do UMN synapse onto?

A

Ventral

86
Q

What synapses in dorsal horn?

A

Spinothalamic onto secondary neurone.

87
Q

Which part of the brain is affected in huntington’s disease?

A

Striatum - putamen

88
Q

What are arteriovenous malformations?

A

Connections between arteries and veins.

Congenital.

89
Q

What is the effect of arteriovenous malformations?

A

Blood flows artery to vein before supplying tissues.
Ischaemia
Heart has to work harder.

90
Q

What is the pathophysiology of MS?

A

Sclerosis forms along neurones, slow transmission impairs movement and sensation.

91
Q

How does MS usually present?

A

Visual symptoms due to demyelination of optic nerve.

92
Q

A tumour at the cerebellopontine angle might affect which nerve?

A

CNVIII - ispilateral hearing loss

93
Q

A patient presents with right sided facial droop, forehead and eyebrows are unaffected. Where is the lesion likely to be?

A

Left genu - corticonuclear fibres run in the genu of the internal capsule

94
Q

What type of injury can cause anterior cord syndrome?

A

Flexion

95
Q

What spinal cord syndrome is usually caused by chronic pathology, give examples?

A

Posterior cord syndrome

  • spondylosis
  • spinal stenosis
  • infections
  • B12 deficiency
96
Q

Which spinal cord syndromes lead to bladder dysfunction and urinary retention?

A

Anterior and central

97
Q

What is an example of evidence that 5-HT has a role in depression?

A

SSRIs increase synaptic levels of 5-HT and treat depression
Tryptophan (precursor) depletion induces depression
Lower 5-HT metabolites in depressed patients

98
Q

What is an example of evidence that NA has a role in depression?

A

AMPT inhibits tyrosine conversion to L-dopa - causes depressive symptoms
TCAs and SNRIs treat depression

99
Q

What is sleep apnoea?

A

Soft tissue in the neck transiently obstructed the airway during sleep. Hypoxia wakes people up.

100
Q

The thalamoperforator arteries are a branch of which main artery?

A

PCA

101
Q

What structural changes have been recorded in patients with Schizophrenia?

A

Enlarged ventricles

Reduced hippocampal formation, amygdala, prefrontal cortex

102
Q

Where are D2 receptors highest in concentration?

A

Midbrain and striatum

103
Q

How would damage to thalamus affect movement?

A

Decreased - theoretical decreased activation of motor cortex.

104
Q

Why do UMN lesions lead to spasticity?

A

Loss of descending inhibition of LMNs - flexors more powerful resulting in spastic posture.

105
Q

Why would a stroke affecting lateral motor cortex compromise swallowing?

A

lesion of UMNs which distribute LMN to the vagus nerve.

106
Q

What is the mechanism explaining why somebody can experience no pain despite a significant injury?

A

Increased activity of enkaphalinergic neurones in the spinal cord. Activation of descending analgesic systems.

107
Q

Which CN emerges ventrally from the ponto-medullary junction?

A

Abducens

108
Q

Which CN emerges laterally from the ponto-medullary junction?

A

Facial n.

109
Q

Rapid onset dementia in a young person might be suggestive of what condition?

A

Prion disease

110
Q

How would a lesion in the arcuate fasciculus present?

A

Articulate words clearly
Unable to repeat the name of an object
Can point to the object the word refers to

ESA 4 Rev (16 decks)

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