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PBL Y2 S3 > Case 5 - Stroke > Flashcards

Case 5 - Stroke Flashcards

1
Q

What lobe does the sylvian fissure seperate?

A

Temporal lobe

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2
Q

What is the anterior circulation of the brain derived from and where do these arteries enter?

A

Left and right internal carotid arteries - enter via carotid canals

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3
Q

What do the internal carotid arteries give rise to? Give their functions

A
  • Ophthalmic artery: supplies all structures in orbit, as well as nose, face and meninges
  • Posterior communicating artery: connects ICA with posterior cerebral artery
  • Anterior cerebral artery: supplies blood to frontal and parietal lobes
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4
Q

What does the ICA continue as and where does this extend?

A

Continues as middle cerebral arteries
Extends to lateral cerebral cortex

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5
Q

Where does the posterior circulation supply?

A

Occipital lobes, cerebellum, brainstem

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6
Q

What is the posterior circulation of the brain derived from and where do these arteries enter?

A

Vertebral arteries - enter through foramen magnum

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7
Q

What are the branches of the vertebral arteries and where do they supply?

A
  • Posterior inferior cerebellar artery: largest, supplies the cerebellum
  • Anterior and posterior meningeal arteries: supply dura mater
  • Anterior and posterior spinal arteries: supplies spinal cord along its length
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8
Q

What does the vertebral artery continue as?

A

The L and R converge to form the basilar artery at the base of the pons

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9
Q

Where does the middle cerebral artery supply?

A

Enters sylvian fissure, supplies the lateral surface of cortex (lateral temporal, parietal and frontal lobes), including the basal ganglia and internal capsule

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10
Q

Where does the anterior cerebral artery supply?

A

Medial frontal and parietal lobes, including the corpus calosum and parts of the basal ganglia

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11
Q

Where does the posterior cerebral artery supply?

A

Occipital and temporal lobes, as well as the thalamus and midbrain

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12
Q

Name the nuclei for cranial nerves 1 and 2

A

CN I: olfactory bulb
CN II: lateral geniculate nucleus

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13
Q

List the 4 cranial nerve nuclei found in the midbrain

A

Edwinger- westphal nucleus
Oculomotor nucleus
Trochlear nucleus
Mesencephalic nucleus - extends from pons to midbrain

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14
Q

List the 4 nuclei found in the pons

A

Trigeminal motor nucleus
Abducens nucleus
Facial motor nucleus
Chief nucleus (trigeminal)

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15
Q

Name the nuclei found at the pons-medullary junction

A

Vestibular and cochlear nuclei

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16
Q

List the 5 nuclei found in the medulla

A

Spinal nucleus
Nucleus solitarius
Nucleus ambiguus
Dorsal motor nucleus of vagus
Hypoglossal nucleus

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17
Q

What cranial nerves synapse at the nucleus solitarius? What fibres does it contain?

A

9th, 7th, 10th cranial nerves (glossopharyngeal, facial, vagus)
- Think ‘Non Stop Training’
Contains sensory fibres

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18
Q

List the 3 areas involved in language and their location

A

Brocas area= frontal lobe
Wernickes area= temporal and inferior parietal lobe
Angular gyrus = parietal lobe

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19
Q

What connects Broca’s and Wernicke’s areas?

A

Arcuate fasciculus

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20
Q

What is the role of Broca’s area?

A

Speech production and articulation. Controls ability to articulate ideas, and use words accurately in spoken language

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21
Q

What would damage of Broca’s area lead to?

A

Words being poorly articulated = expressive (non-fluent) dysphasia, i.e. deficits in speech production although comprehension would be good

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22
Q

What is the role of Wernicke’s area?

A

Critical language area, primarily involved in comprehension and language processing

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23
Q

What would damage to Wernicke’s area lead to?

A

Speech devoid of meaning, i.e. receptive dysphasia (fluent) - language production is in tact but comprehension isn’t. Patients usually unaware of their difficulties

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24
Q

What is the role of the angular gyrus?

A

Allows us to associate multiple types of language-related information, i.e. visual, auditory and sensory. Allows us to associate perceived words with images and ideas

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25
Q

What would damage to the angular gyrus lead to?

A

Inability to read and copy written work (agraphia)

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26
Q

Other than dysphasia, what can damage to Broca’s area also lead to?

A

Dysphagia - difficulty swallowing, as it’s close to the swallowing centre

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27
Q

What would cause a UMN lesion?

A

Damage to either corticospinal or corticobulbar tracts; tracts that arise from the cortex and extend to the ventral grey horn or CN nuclei in pons/ medulla

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28
Q

Damage to which CN nuclei can cause a LMN lesion?

A

Trigeminal (V), facial (VI), nucleus ambiguus (IX, X, XI) and hypoglossal (XII)

Or if damage to the cranial nerve axons

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29
Q

Which nucleus controls speech?

A

Nucleus ambiguus - controls muscles of larynx etc.

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30
Q

What can cause a UMN lesion?

A

Stroke, MS, Fredrick’s ataxia, B12 deficiency, ALD

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31
Q

What can cause a LMN lesion?

A

Polio virus, ALS, cauda equina, diabetes mellitus neuropathy

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32
Q

How would a UMN lesion present in terms of muscle mass, strength, tone and deep tendon reflexes?

A

15-20% decrease in mass (disuse atrophy)
Spastic paralysis
Hypertonia
Hyperreflexia

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33
Q

How would a LMN lesion present in terms of muscle mass, strength, tone and deep tendon reflexes?

A

80% decrease in mass (denervation atrophy)
Flaccid paralysis
Hypotonia
Hyporeflexia

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34
Q

Why do UMN and LMN lesions lead to different responses in tone and reflexes?

A

UMN lesions lead to increased stimulation of alpha motor neurones (hypertonia) and increased stimulation of gamma motor neurones (hyperreflexia)
LMN lesions lead to decreased stimulation so the opposite

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35
Q

How does UMN and LMN lesions lead to a loss of muscle mass?

A

UMN - loses connection between brain and muscle so dont use it as much
LMN - lower ACh production so protein synthesis decreases

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36
Q

What is the difference between flaccid and spastic paralysis?

A

Spastic: velocity-dependent (resistance increases with increased velocity) and in 1 direction only (i.e. resistance when flexing) = accompanied by weakness
Flaccid: weakness with a loss of muscle tone

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37
Q

Are fasiculations/ fibrillatitons (EMG) present in UMN or LMN lesions? Why?

A

Present in LMN lesions and absent in UMN lesions.
LMN lesions = decreases ACh & in response the muscle increases ACh receptors - muscle is more sensitive to ion changes so leads to pathological contractions

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38
Q

Is Babinski’s reflex response present in UMN or LMN lesions? Why?

A

UMN lesions - as you lose the inhibition to dorsiflexors thus they are stimulated, therefore the toe dorsiflexes rather than plantarflexes

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39
Q

Is pronator drift present in UMN or LMN lesions?

A

UMN lesion - as this damages the supinators so pronators overcome the power of supinators

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40
Q

Is Hoffman’s sign present in UMN or LMN lesions?

A

UMN lesion - causes hyperreflexia of the thumb so moves towards the index finger

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41
Q

Compare alpha and gamma motor fibres

A

Alpha = extrafusal fibres, generate movement
Gamma= intrafusal fibres, stretch reflex

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42
Q

Why is the Babkinski reflex seen in children <1 year?

A

UMNs aren’t fully myelinated yet so theres decreased functioning

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43
Q

Define stroke

A

Acute neurological deficit lasting >24hr, or leading to death and caused by cerebrovascular aetiology (decreased blood to brain)

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44
Q

What are some general symptoms of a stroke?

A

Weakness/ paralysis
Paresthesia
Aphasia
Dysarthria
Visual defects
Imbalance
Impaired consciousness
Nausea
Headaches
Seizures

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45
Q

Which ethnicity is most at risk for a stroke?

A

Black Africans

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46
Q

What are the 2 main types of stroke and their epidemiology?

A

Ischaemic = 85% of strokes
Haemorrhagic = 15%

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47
Q

What is a thrombotic ischaemic stroke caused by?

A

Rupture of atherosclerotic plaque and exposure of subendothelial collagen - leads to formation of a thrombus

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48
Q

What is an embolic ischaemic stroke caused by?

A

Embolus from elsewhere in the body travelling to the brain, e.g. from heart (due to atrial fibrillation) or infection (i.e. bacterial endocarditis)

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49
Q

How can global cerebral ischaemia be caused?

A

Systemic hypotension - i.e. watershed infarct, hypoglycaemia, chronic hypoxia, cardiac arrest

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50
Q

What are the risk factors for ischaemic strokes?

A

Hypertension
Diabetes mellitus
Obesity
Previous TIA
Atrial fibrillation
Hypercoagulable states
Infections
Alcohol and drugs
Male
Older age
Ethnicity - African Americans and Hispanics

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51
Q

What are the clinical features of an ischaemic stoke?

A
  • Contralateral hemiplegia (paralysis) or hemiparesis (limb weakness/ tingling), develops over seconds to hours
  • Dysphasia / aphasia: if dominant hemisphere is affected
  • Sudden confusion and difficulty understanding speech
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52
Q

What is the pathophysiology of an ischaemic stroke?

A

1: low blood supply = hypoxic cells, cannot generate ATP
2: Na+/K+ ATP pump fails, Na+ accumulates which changes osmotic balance
3: oedema - cells in direct area of infarct swell and die
4: NA+ causes change in charge, which opens Ca2+ channels = Ca2+ influx
5: Excess glutamate release (excitotoxicity) - overstimulates NMDA receptors
6: Release of free radicals = necrosis
7: production of cytokines (i.e. IL-1) = inflammation, further adds to oedema
8: infarcted tissue

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53
Q

Describe the difference between the primary region of ischaemic damage and surrounding areas

A

Core = primary region of damage, blood flow is dramatically reduced (<20% of normal) = severe ischaemia = cells die in minutes- hours

Penumbra= surrounding area, around 20-50% of normal blood flow. Neurons are still functional but not at full capacity = at ‘threat’ of dying - hope for rescue with quick treatment

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54
Q

What are the 2 types of haemorrhagic strokes?

A

Intracerebral - 10-12%
Subarachnoid - 3%

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55
Q

What is an intracerebral stroke?

A

Bleeding within the brain itself, secondary to a ruptured vessel. This is a space-occupying lesion so it can push structures across the midline and lead to herniation

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56
Q

What are 2 types of intracerebral strokes?

A

Intraparenchymal (within brain parenchyma)
Intraventricular (within ventricles)

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57
Q

How can intracerebral strokes be caused?

A

Trauma - head injuries etc.
Non-traumatic causes - hypertension, coagulopathy, i.e. antiplatelet medications, neoplasms, aneurysm rupture

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58
Q

What is the most common cause of an intracerebral stroke?

A

Uncontrolled hypertension

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59
Q

What is the clinical presentation of an haemorrhagic stroke?

A

Sudden, severe headache (‘thunderclap’ headache)
Nausea and vomiting
Temporary or persistent loss of consciousness
Very high BP

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60
Q

What is the pathophysiology of haemorrhagic strokes?

A

1: ruptured blood vessel = blood leaks into tissues and displaces them
2: BBB breakdown and increased intracranial pressure
3: decreased blood flow leading to secondary ischaemia
4: extreme cases: midline shift and herniation

Secondary damage= thrombin, haemoglobin, heme and iron damage surrounding tissue - innate immune system phagocytoses the haematoma = glial scar formation

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61
Q

What is a subarachnoid haemorrhage?

A

Bleeding into sub-arachnoid space between arachnoid and pia mater (i.e. subdural haematoma)

62
Q

What disease is linked to a subarachnoid haemorrhage?

A

Polycystic kidney disease

63
Q

What symptoms may be present with a subarachnoid haemorrhage?

A

Similar to ICH, but can also cause visual defects
Patients may have an ‘occipital headache’ (piercing, throbbing pain in upper neck to back of head) and complain of neck stiffness

64
Q

What does think FAST stand for?

A

F= Face, sudden weakness of the face, i.e. has it fallen to one side, can they smile
A= Arms, sudden weakness of one or both arms
S= Speech, difficulty speaking, slurred speech
T= Time (sooner treatment is started the better)

65
Q

What scans may be performed for a suspected stroke?

A

Non-contrast CT: shows haemorrhage immediately but infarction isn’t detected (only subtle changes initially)

MRI: changes in early infarction, later scans can show the core and penumbra

Diffusion weighted MRI: cerebral infarction immediately but not as accurate as CT for haemorrhage

CT angiogram and perfusion: combines CT scan with IV injection of contrast dye to find an aneurysm or occluded blood vessels

66
Q

How might an ischaemic stroke appear on a CT scan?

A

Wedge-shaped hypodensity
Loss of grey/ white matter differentiation
Localised swelling
Recognisable arterial territory

67
Q

How might an intracerebral haemorrhage appear on a CT scan?

A

Bright white blood - seen pooling in 3rd ventricle and around the lateral ventricle
May see a shift in midline of some structures

68
Q

How might an subarachnoid haemorrhage appear on a CT scan?

A

White blood pools in subarachnoid spaces, surrounding the brain stem and extends through the sylvian fissure.
Usually crescent shape

69
Q

What is a transient ischaemic attack?

A

Disturbance in brain function from a temporary blockage in the brains blood supply. They can resemble ischaemic strokes, except there’s no permenant damage and symptoms usually resolve in 1 hour

70
Q

Whats the most common cause of a TIA?

A

80% caused by microemboli/ thromboembolus

71
Q

What are the symptoms of a TIA?

A

Same as ischaemic stroke, i.e. limb weakness, visual defects, but usually last for 2-30 mintues then resolve

72
Q

How are TIAs treated?

A

Aspirin 300mg daily unless contraindicated
Urgent assessment if suspected TIA in last 7d
Lifestyle changes - control BP, cholesterol, stop smoking etc.

73
Q

What are the symptoms of a stroke in the anterior circulation?

A
  • Contralateral weakness and sensory loss: MCA= more marked in face and upper limbs (lateral cortex), ACA= more marked in lower limbs (medial cortex)
  • Contralateral homonymous hemianopia: visual field loss on same side - if inferior MCA
  • Ipsilateral gaze deviation
  • Dysphasia - if affecting dominant hemisphere
74
Q

What occlusion in the anterior circulation can lead to dysphasia?

A

Left superior occlusion = expressive dysphasia (Broca’s)
Left inferior occlusion = receptive aphasia (Wernicke’s)

75
Q

What are symptoms of a stroke in the posterior cerebral artery?

A
  • Contralateral homonymous hemianopia
  • Contralateral III nerve palsy
  • Contralateral pain
76
Q

What are symptoms of a stroke in the basilar artery?

A

Affects mainly the cerebellum and pons, so cranial nerves 5-8
- VI nerve palsy
- Contralateral weakness and sensory loss (both S + M as infarct is higher than decussation)
- More severe bilateral symptoms, i.e. quadriplegia and ‘locked-in’ syndrome

77
Q

What are symptoms of a stroke in the vertebral artery?

A

Affects below the pons so nerves 9-12

78
Q

Where is the occlusion if a patient suffers from a lacunar stroke? What do these arteries supply?

A

In lenticulostriate arteries (deep branches of MCA)
Supply the internal capsule, basal ganglia, thalamus and pons

79
Q

What are symptoms of a lacunar stroke?

A

NO cortical signs, leads to either:
- Pure motor loss: contralateral of face, arms and leg
- Pure sensory loss: contralateral numbness and parasthesia of face, arm and leg
- Sensorimotor loss: contralateral hemiparesis and sensory impairment

80
Q

What are symptoms of a stroke in the posterior inferior cerebellar artery?

A
  • Nystagmus
  • Ataxia
  • Ipsilateral facial pain and temperature loss
  • Contralateral limb pain and temperature loss
81
Q

What are the symptoms if a stroke has affected the cerebellum?

A

Loss of coordination and balance
Ataxia - fall to same side of lesion
Hypotonia
Nystagmus

82
Q

How can watershed infarcts occur?

A

With severe drops in systemic BP because watershed zones require high BP to receive enough blood, can be caused by occlusion of ICA or carotid stenosis

83
Q

What symptoms can occur with a watershed infarct of MCA/ PCA territory?

A

Visual dysfunction - prosopagnosia (can visually see but can’t recognise, analyse or identify objects), balint syndrome, optic ataxia
Disturbed high order processing

84
Q

According to the Bamford circulation, how is an anterior stroke diagnosed?

A
  • Unilateral weakness of face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction, i.e. dysphasia

Total anterior stroke = all 3 symptoms
Partial anterior stroke= 2 of the symptoms

85
Q

According to the Bamford circulation, how is Lacunar syndrome diagnosed?

A

1 of:
- Pure sensory stroke
- pure motor stroke
- Sensorimotor stroke
- Ataxic hemiparesis

86
Q

According to the Bamford circulation, how is a posterior stroke diagnosed?

A

1 of:
- Cranial nerve palsy and contralateral motor or sensory deficit
- Bilateral motor/ sensory deficit
- Conjugate eye movement disorder, e.g. gaze palsy
- Cerebellar dysfunction
- Isolated homonymous hemianopia

87
Q

What does the ABCDE assessment acronym stand for?

A

A: Airway
B: Breathing (may need to provide O2)
C: Circulation
D: Disability
E: Exposure (and keep warm)

88
Q

How does the Glasgow Coma Scale assess disability?

A

Measures eyes, motor and verbal responses. Overall score is on a scale of 3 (unconscious) to 15 (fully conscious)

89
Q

How does the NIH stroke scale assess severity of strokes? What type strokes is this a better predictive of?

A

15-item neurological exam, scored from 0-42
- Very severe >25
- Severe 15-24
- Mild-moderate 5-14
- Mild 1-5

Best for L hemisphere strokes (as uses aspect of language)

90
Q

What investigations may be done to exclude differentials and identify the source of the stroke?

A

Carotid doppler ultrasound - look for stenosis, a level of >50-60% usually requires carotid endarectomy to reduce stroke risk
ECG - check for AF as a source of clots that may have traveled from heart to brain
Chest X-ray - checks size of heart

91
Q

List the 6 mechanisms behind ischaemic damage

A

Excitotoxicity
Reperfusion injury
Oxidative stress
Apoptosis
Inflammation
Peri-infarct depolarisation

92
Q

How can excitotoxicity lead to ischaemic damage?

A

1: Hypoxia can lead to a fall in ATP
2: Failure of pumps, i.e. Na+/ K+
3: Increases glutamate release into ECF
4: Glutamate leads to influx of Ca2+ and Na+
5: Calcium overload leads to mitochondrial injury, increased production of NO and protease activation

93
Q

How can reperfusion injury lead to ischaemic damage?

A

Restoring blood flow to an area previously ischaemic can lead to inflammation and oxidative stress, which can increase death of neurones

94
Q

How can oxidative stress lead to ischaemic damage?

A

1- Collapse of membrane potential
2- Generation of reactive oxygen species (i.e. hydrogen peroxide)
3- formation of NO and superoxide = DNA damage

95
Q

How can apoptosis lead to ischaemic damage?

A

Oxidative stress leads to release of cytochrome C, which activates caspases = DNA damage and apoptosis

96
Q

How can post-ischaemic inflammation lead to ischaemic damage?

A

Reperfusion leads to changes vasculature, activating inflammatory cells. Cytokines (i.e. IL-1) activate proteases = free radicals

Inflammation = oedema, activation of resident micoglia and damage

97
Q

How can thrombo-inflammation lead to ischaemic damage?

A

Degradation of ECM exposes underlying basement and release of vWF. This binds platelets, which then binds fibrin, RBCs and neutrophils -> clot formation

98
Q

How can peri-infarct depolarisation lead to ischaemic damage?

A

Release of glutamate spreads to nearby cells and leads to damage

99
Q

List the 5 mechanisms of repair following a cerebrovascular accident

A
  • Axonal sprouting - formation of new connections in cortex
  • Neurogenesis/ neuroplasticity - restoration of neuronal network
  • Angiogenesis - restoring blood supply via growth of new BVs
  • Neurorepair - by M2 microglia
  • Glial scarring - protective
100
Q

How does neurogenesis occur?

A

Brain sends signals to zones which proliferate and send cells (newborn neural precursors) to damaged areas. Regeneration occurs in 2 areas:
- Subgranular zone (SGZ): new cells migrate from outer SGZ to inner granular layer in hippocampal dentate gyrus = memory functions
- Subventricular zone (SVZ): alongside the lateral ventricle, cells migrate from SVZ to olfactory bulb via Rostral Migratory Stream, then migrate to damaged area

101
Q

What factor is responsible for angiogenesis?

A

Vascular endothelial growth factor (VEGF) - binds to VEGF receptor 2 during repair = angiotensin 1 release

102
Q

What are the 2 types of microglia and their roles?

A

M1= neurotoxic, produce inflammatory factors - tissue injury
M2= phagocytic, role in repair, immunosuppression to lower inflammation

103
Q

How is a glial scar formed?

A

Astrocytes proliferate to form the scar - protects the surrounding tissue from necrotic cavity (which has inflammatory mediators)

104
Q

What is DVLA advice for group 1 drivers post-stroke?

A

Group 1= normal cars
No driving for 1 month post stroke, if after 1 month no deficit then can drive, but if you have deficits then contact DVLA

105
Q

What is DVLA advice for group 2 drivers post-stroke?

A

Group 2= lorries, buses, etc.
Must not drive and immediately inform DVLA. Licenses revoked for 1 year, if no deficit after this time may be considered

106
Q

If a patient has had multiple TIAs in a short period, how long must they wait until they can drive again?

A

3 months with no TIAs

107
Q

When is thrombolysis used?

A

For ischaemic strokes only, if within 4.5 hours of presenting symptoms.

108
Q

How does thrombolysis work?

A

Give a tissue plasminogen activator, e.g. alteplase, of 1mg/ kg over 1 hour. This activates plasminogen -> plasmin, which then breaks down fibrin in the clot

109
Q

What are the contraindications to thrombolysis?

A

Previous ICH, pregnancy, uncontrolled hypertension, major surgery in last 2 weeks, or if the patient can’t remember when symptoms started

110
Q

What are the risks of thrombolysis/ tPA?

A
  • Intracerebral haemorrhage: 1/30 risk, can see on CT scans so patient is monitored regularly after
  • Angioedema: allergic reaction - swelling of the lips and tongue, 1/14 risk: if noticed give hydrocortisone and anti-histamines as the swelling can interefere with their airway
111
Q

How can ischaemic strokes be treated?

A

Thrombolysis
Thrombectomy
Antiplatelets - aspirin and clopidogrel
Carotid endarectomy

112
Q

What is thrombectomy and when would it be done?

A

Within 6 hours of the ischaemic stroke, physical removal of the clot. Catheter is inserted into an artery in the groin and guided to the brain where it pulls the clot out

113
Q

What medication may be given to a patient who suffered from an ischaemic stroke or as aftercare following a thrombectomy?

A

300mg aspirin for 2 weeks (anti-platelet)
then 75mg clopidogrel (secondary prophylaxis)

114
Q

If atrial fibrillation is the source of the ischaemic stroke, what medication may be given?

A

Direct oral anti-coagulants (DOACs) - i.e. apixaban, dabigatran

115
Q

What adjuvant may be given to a patient if they’re intolerant to aspirin and why?

A

Proton pump inhibitor, e.g. omeprazole
Reduce stomach symptoms

116
Q

What is aspirins mechanism of action?

A

Inhibits COX enzymes, suppresses prostaglandin and thromboxane production:
- Inhibiting PGs= anti-inflammatory
- Inhibiting thromboxane= stops activation of new platelets and platelet aggregation

117
Q

How are haemorrhagic strokes treated?

A

Think ABC:
Anti-coagulant reversal - i.e. vitamin K, platelete transfusions
Blood pressure lowering
Care pathway, i.e. referral for surgery

118
Q

What drugs are used for blood pressure lowering post- haemorrhagic stroke?

A

ABCD-ARB:
ACE inhibitor
Beta-blocker
Calcium channel blocker
Diuretic
Angiotensin-II Receptor Blocker

119
Q

How are diuretics blood pressure lowering?

A

Osmotic diuretics decrease intracranial pressure in subarachnoid space

120
Q

How does long-term management differ for haemorrhagic and ischaemic strokes?

A

Haemorrhagic: control BP (aim <130mmHg SBP) and lower cholesterol
Ischaemic: anticoagulants (heparin and warfarin, if AF) and aspirin (anti-platelet)

For both - treat modifiable risk factors such as hypertension and diabetes

121
Q

List the roles involved in a stroke rehabilitation team

A

Nurses - continence, oral hygiene (as associated with increased risk of pneumonia)
Speech and language therapy - assessment of dysarthria and swallowing
Physiotherapy - early mobilisation and balance
Occupational therapy - ADL and cognition

122
Q

What is generalised anxiety disorder?

A

State of inappropriate and sometimes severe anxiety, but without adequate cause, that lasts for at least 6 months

123
Q

What structures of the limbic system are affected by GAD?

A

Overactivity of amygdala
Underactivity of hippocampus

124
Q

How does chest pain in GAD differ from cardiac chest pain?

A

Stabbing chest pain which doesn’t radiate

125
Q

How can GAD be caused?

A

Genetics, personality type, major life events/ trauma, major stress, chronic illness

126
Q

What needs to be excluded before a diagnosis of GAD is made?

A

Alcohol/ drug misuse
Hyperthyroidism
Phaeochromocytoma

127
Q

How is an operational diagnoses of GAD made?

A

If have persistent fear and worry, with at least 3 of the following symptoms, which impairs everyday function:
- Poor concentration
- Restlessness
- Fatigue
- Muscle tension
- Initial insomnia
= Symptoms have to be present >6 months

128
Q

How much CBT does NICE recommend for treatment of GAD?

A

12-15 x 1 hour long sessions over 4 months

129
Q

How is GAD treated pharmacologically short- and long-term?

A

Short-term: benzodiazepines, e.g. diazepam
Long-term: beta-blockers, SSRIs (e.g. sertraline), pregabalin

130
Q

Why are benzodiazepines only used short-term?

A

1- Can cause tolerance and dependence, so patient may experience withdrawal symptoms
2- GABA receptor can become desensitised so can increase anxiety in the long run

131
Q

Which GABA receptor mediates IPSPs?

A

GABA-a

132
Q

Where does GABA bind to the GABA-a receptor and what is its effect?

A

Between alpha-1 and beta-2 subunits, causes chloride ions to enter the neurone = hyperpolarisation, less likely to lead to an action potential so is inhibitory

133
Q

Where do benzodiazepines bind and how does this reduce anxiety?

A

Between alpha and gamma subunits of GABA-a receptor, this potentiates GABA, i.e. enhances its action and increases Cl- influx

134
Q

When is diazepam used? How does this differ to other benzodiazepines?

A

In the short term, i.e. 2-4 weeks max, as it reduces symptoms within 30-60 minutes but is very addictive
Differs in its half life: 30 hours compared to 2 hours of triazolam

135
Q

What are the side effects of benzodiazepines?

A

Sedation, respiratory depression, tolerance, dependence

136
Q

How do SSRIs work to treat GAD? How long does it take to reach anxiolytic effects?

A

Blocks serotonin reuptake from the synapse, prolonging its action

Takes 1-2 weeks to start working as the effect is due to the nervous system adapting to chronically elevated brain serotonin

137
Q

Give examples of SSRIs used in GAD and how long they’re used for

A

Escitalopram, paroxetine, sertraline
Used for at least 6 months, otherwise increased chance of relapse if stopped before

138
Q

What are some side effects of SSRIs?

A

GI disturbance, sexual dysfunction, sweating, insomnia

139
Q

How do beta-blockers work to treat GAD? Give some examples

A

Antagonists at adrenergic B-receptors in heart muscle, smooth muscle and tissues of the sympathetic NS. This helps reduce adrenaline and noradrenaline

Examples - propanolol, atenolol

140
Q

How do anti-convulsants treat GAD? Give an example

A

Exact mechanism unknown but thought to bind to voltage-gated Ca2+ channels, stopping Ca2+ from causing NT release, i.e. reduces glutamate, noradrenaline and substance P

Example - pregabalin

141
Q

How do barbiturates work?

A

Enhance action of GABA by binding GABA-a receptors (between a and b subunits) to open the chloride channel
= CNS depressants - produce effects from mild sedation to general anaesthesia (less specific action)

142
Q

What drug might be used for patients with insomnia?

A

Zolpidem; a GABA-a receptor agonist of the imidazopyridine class

143
Q

What is sensory memory?

A

Unconscious process, includes iconic (visual) and echoic (auditory) sensory memory

144
Q

What is the difference between explicit and implicit memory?

A

Explicit = declarative, i.e. consciously recalled - memory you’re aware of learning

Implicit= non-declarative, i.e. unconscious - doesn’t rely on conscious awareness, incidentally learned

145
Q

What are the 2 types of explicit memory?

A

Episodic memory: autobiographical, i.e. record of life experiences
Semantic memory: conceptual; general knowledge, data, facts, information

146
Q

What is the multi-store memory model?

A

Information comes in as sensory stimuli and is initially held in the sensory memory store (lasts 0.1-0.5s), this is transferred to short-term memory if attention towards the stimuli, which then can transfer to long-term memory if the information is rehearsed

147
Q

According to the multi-store memory model, what is the capacity of STM?

A

Rule of 7 capacity, i.e. 7+/-2, but may be increased with chunking (i.e. remembering 2 and 5 as 25)

148
Q

According to the multi-store memory model, what is areas are involved with STM and LTM?

A

STM: frontal and parietal lobes
LTM: hippocampus essential, amygdala for emotional LTM

149
Q

What is the working memory model?

A

Central executive = supervisor, allocates resources, performs cognitive tasks.
3 subsidary areas:
- Phonological loop = inner ear/ voice, stores auditory information by speaking continuously to yourself
- Visuo-spatial sketchpad = inner eye, stores visual and spatial info
-Episodic buffer = links info across visual, spatial and verbal domains, puts memories in chronological order (links to LTM and semantic)

149
Q

What is the level of processing model?

A

Depth of processing leads to stronger memories, which is through elaborative rehearsal (i.e. active recall) = leads to more neuronal connections.
More meaning and understanding = longer info. will be remembered

150
Q

How does the level of processing model state verbal information is processed?

A

1: structural processing; appearing (what the word looks like) = superficial processing
2: phonemic processing: sounds = superficial
3: semantic processing: meaning, so stronger lasting memory = deep processing

PBL Y2 S3 (10 decks)

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