Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 3 - Neurology > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What are some of the clinical features of transient global amnesia?

What can it be triggered by?

A

Abrupt onset antegrade > retrograde amnesia

Knowledge of self is preserved

Transient, lasting 4-6 hours (always less than 24 hours)

Generally once off

Typically seen in 70s, but can be seen +50s

Can be triggered by emotions, or (weirdly) changes in temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In Alzheimer’s Disease, there is a disruption of cholinergic pathways in the brain and synaptic loss due to accumulation of plaques. What plaques are seen extracellularly and what is seen intracellularly?

A

Extracellular amyloid plaques

Intracellular neurofibrillary tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the initial symptom that appears in Alzheimer’s Disease?

What areas of the brain are affected?

A

Initial symptom is forgetfulness

Degeneration of the hippocampus + (later) the parietal lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the age cut-off for Alzheimer’s being “early onset”?

A

If AD appears <65 years it is classed as early onset

May be an atypical presentation with genetic influences

If occurring >65 years, environmental factors have a greater influence than genetic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What investigations can be done if Alzheimer’s Disease is suspected?

A

MRI - shows atrophy of temporal/parietal lobes

MMSE

SPECT scan - shows reduced tempoparietal metabolism

CSF sample - shows reduced amyloid:increased tau ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What treatments can be given to slow the progression of Alzheimer’s Disease/manage the symptoms?

A

ACh-boosting treatments - cholinesterase inhibitors (e.g. Rivastigmine, Galantamine), NMDA-receptor blockers (e.g. Memantine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The majority of patients with frontotemporal dementia develop initial symptoms under 65 years/over 65 years of age

A

Frontotemporal dementia tends to develop under 65 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which proteins are associated with the following dementias?

  • Alzheimer’s disease and vascular dementia
  • Parkinson’s Disease dementia and Lewy Body dementia
  • CJD
  • Frontotemporal dementia
A

AD and VaD = amyloid

PD dementia and LB dementia = alpha-synuclein

CJD = prion disease

FTD = tau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What changes in the brain may be seen via CT/MRI in someone with Huntington’s Disease?

A

Caudate atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What % of people with Parkinson’s have developed dementia (PDD) after 20 years?

A

80%

(remember - PDD if Parkinson’s for at least 1 year before dementia, DLB if dementia precedes Parkinsonism, or if occurring less than 1 year after Parkinson’s diagnosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the criteria for diagnosing DLB?

A

1) fluctuating cognition
2) recurrent, well-formed visual hallucinations

+/- 3) presence of extrapyramidal features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the main differentiator for Frontotemporal dementia, when compared to other forms of dementia?

A

Other forms of dementia usually present >65 years of age

FTD usually presents <65 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the main symptoms seen in Frontotemporal dementia?

What would you see in the following investigations?

  • CT/MRI
  • SPECT
  • CSF
A

Main symptoms - early frontal features (disinhibition, change in behaviour, apathy, loss of empathy, stereotyped/compulsive behaviours). Also early loss of insight

MRI/CT - atrophy of frontotemporal lobes

SPECT - reduced frontotemporal metabolism

CSF - increased tau/normal amyloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Aggregation of what protein is associated with the development of Frontotemporal dementia?

How can this condition be managed?

A

Aggregation of Tau

Trial of Trazadone (antidepressant, SARI) or antipsychotics to manage behavioural symptoms

Safety management - control access to food, money, internet etc.

Structured activities

Power of attorney…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Presence of this cell type indicates what type of dementia?

A

Frontotemporal dementia

These are Pick bodies (a.k.a. Pick’s Disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the difference between allodynia and hyperalgesia?

A

Allodynia - pain from a stimulus that usually wouldn’t be painful

Hyperalgesia - excessive pain from a minorly painful stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the mode of action of NSAIDs (aspirin, ibuprofen)?

What are some of the possible side effects?

A

Mode of action - inhibition of cyclooxygenase 1, resulting in decreased synthesis of prostaglandins

Side effects - GI irritation/bleeding, renal toxicity, drug interactions, cardiovascular side effects (COX-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does paracetamol work?

A

Has analgesic and antipyretic effects, but no anti-inflammatory action

Inhibits central prostaglandin synthesis but ultimately no one really knows how it works…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do opioid analgesics work e.g. tramadol, codeine (weak), morphine, oxycodone (strong)?

A

Activate the body’s endogenous analgesic system

Does so by stimulating receptors in the limbic system to eliminate the ‘subjective feeling of pain’

Affects descending pathways and ascending pathways (reduces pain signals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do TCAs work?

A

Inhibit neuronal reuptake of serotonin and noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do SSRIs/SNRIs work?

Which is the better analgesic?

A

Selectively inhibit reuptake of serotonin, or noradrenaline, or both

Provide analgesia by intensifying the descending inhibition

SNRIs are better analgesics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do anticonvulsants work (gabapentin, pregabalin and carbamazepine)?

A

Gabapentin - binds presynaptic voltage-gated calcium channels

Pregabalin - interacts with special N-type calcium channels

Carbamazepine - blocks Na+ (mainly) and Ca2+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the usual cause of a subarachnoid haemorrhage?

A

Underlying arteriomalformation - Berry aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What’s the diagnosis?

  • sudden onset +++ headache (“worst I’ve ever had, like a thunderclap”)
  • takes less than 5 minutes for headache to peak
  • vomiting
  • collapse
  • neck pain and photophobia
  • reduced consciousness level
  • focal neurological deficits
A

Subarachnoid haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the gold standard investigation for suspected subarachnoid haemorrhage? What would it show? Why might a CT scan not be useful?
Gold standard is **lumbar puncture** - positive if CSF appears **blood-stained** or **xanthochromatic**. NB - need to determine that this is not the result of a traumatic tap, and so 3 separate samples are taken CT scans may indicate SAH, however **may be negative if \>3 days post event**. CT will also be negative in 15% of patients that have bled! (Fresh blood on CT appears white, but because the haemorrhage occurs into the CSF it may appear darker)
26
What is the gold standard investigation for identifying a Berry aneurysm? Why might it sometimes miss the diagnosis?
Gold standard for Berry aneurysm is **cerebral angiography** May occasionally miss pathology due to vasospasm
27
What are some of the major concerns/complications associated with subarachnoid haemorrhages (be sure to get the most important one!)?
**1. Re-bleeding** - 20% risk in first 14 days, 50% over the next 6 months 2. Delayed ischaemic neurological deficit - 3-12 days post SAH, presents with altered consciousness/focal deficit 3. Hydrocephalus 4. Hyponatraemia (probably due to hypothalamic ischaemia) - SIADH 5. Seizures
28
How are the symptoms of Delayed Ischaemic Neurological Deficit (DIND) following SAH managed pharmacologically?
**Nimodipine** (calcium channel blocker) - stabilises smooth muscle, preventing the vasospasms that cause symptoms Can also use '**Triple H** **therapy**' - hypervolaemia, hypertension and haemodilution
29
What % of people that develop Hydrocephalus following SAH are symptomatic? How does it present? How is it managed?
Only **6% are symptomatic** May present with increasing headache/altered consciousness level which is oftern transient Treatment is with **CSF drainage** via LP, an extraventricular drain or a shunt
30
What are Charcot-Bouchard microaneurysms? What type of bleed are they associated with?
Microaneurysms arising from the small perforating arteries in the brain, resulting in basal ganglia haematoma formation 50% are are secondary to hypertension Associated with **intracerebral haemorrhage** - bleeding into the brain parenchyma
31
What is the main distinction in symptoms between a subarachnoid haemorrhage and an intracerebral haemorrhage?
Intracerebral **don't present with secondary meningeal symptoms** (e.g. vomiting, photophobia) These symptoms are caused by blood products irritating the meninges, but in an intracerebral haemorrhage the bleed is contained within the parenchyma
32
What is the name of the condition that can occur if an intracerebral or subarachnoid haemorrhage bleeds into a ventricle?
Intraventricular haemorrhage
33
What is Steal Syndrome?
Presence of an areriovenous malformation results in blood being stolen away from normal brain tissue - shunts between the arterial and venous systems create a 'nidus'
34
Describe the location within the spinal cord of - The DCML - The corticospinal tracts - The spinothalamic tracts
DCML - posterior, divided into fasciculus cuneatus (lateral) and fasiculus gracilis (medial) Corticospinal tracts - lateral tract is in the middle of the lateral white matter column, anterior tract is next to the medial fissure Spinothalamic tracts - lateral tract is anterolateral, anterior tract is more medial, but they are both right next to each other
35
The corticospinal tract is a __ neurone tract
**2 neurone** Upper motor neurone is from the motor cortex to anterior grey horn, decussates at medullary level Lower motor neurone is from the anterior horn Tract runs **ipsilaterally**
36
The DCML pathway decussates at \_\_\_\_ The spinothalamic pathway decussates at \_\_\_\_
DMCL - decussates at medullary level Spinothalamic - decussates at spinal level
37
How does cord transection present?
Complete lesion affecting all motor and sensory modalities Initially a flaccid, areflexic paralysis - **spinal shock** UMN signs appear later
38
What sensory loss does Brown Sequard present wtih?
Loss of ipsilateral fine touch, fibration and conscious proprioception (DCML runs ipsilaterally) Loss of contralateral temperature and pain (spinothalamic crosses over @ spinal level)
39
What's the condition? - Hyperflexion/extension injury to a neck that is already stenotic - Predominantly distal upper limb weakness - Gives a "cape-like" spinothalamic sensory loss - Lower limbs and dorsal columns are preserved
**Central cord syndrome**
40
What is the most common cause of spinal cord compression?
**Tumours** Extradural - usually metastasis from elsewhere (lung, breast, kidney, prostate) Intradural - extramedullary (meningioma, Schwannoma), intramedullary (astrocytoma, ependymoma)
41
What condition would you suspect if you saw the following on MRI... - osteophyte formation - bulging of intervertebral discs - facet joint hypertrophy - subluxation
Spinal stenosis
42
Name some presynaptic neuromuscular disorders
**Botulism** (botulinum toxin) - present in food. Can infect food and wounds, associated with IV drug users (black tar heroine). Botulinum toxin cleaves presynaptic proteins involved in ACh vesicle formation and blocks the vesicle docking with the presynaptic membrane, causing **rapid onset weakness without sensory loss** **Lambert-Eaton Syndrome** - antiboides to presynaptic **calcium channels** lead to less vesicle release. Strong association with **small cell lung cancer**
43
80-90% of people with Myasthenia Gravis have anti-ACh receptor antibodies. What do approx. 5% have antibodies to?
**Anti-muscarinic antibodies** NB - Anti-AChR antibodies block ACh, but also cause an inflammatory response that damages the folds on postsynaptic membranes
44
What immune organ is seen to be hyperplastic in 75% of people with Myasthenia Gravis?
The **thymus** - thymectomy seems to improve symptoms for some reason
45
If you suspected a patient had Myasthenia Gravis, what quick test could you perform to test this theory?
Ask the patient to blink 20 times and see if they fatigue
46
A patient comes in complaining of peculiar sensory symptoms, and you suspect MS. What questions might you ask them?
Any changes in bathroom habits? Any eye pain/colour changes? Any cramping or fatigue? Noticed any balance/coordination problems? Family history of this, or any other autoimmune diseases? Diet okay? Thinking about vitamin D
47
Other than thymectomy, what treatments can be given for Myasthenia Gravis?
**Acetylcholinesterase inhibitors - pyridostigmine, neostigmine** IV immunoglobulins Immunomodulators Steroids, steroid-sparing agents (azathioprine, mycophenolate)
48
What's the diagnosis? - Symmetrical progressive proximal muscle weakness developing over weeks to months. Serum shows raised CK What's the diagnosis? - Same as above, but also has skin lesions and a "heliotrope" rash on the face
1. **Polymyositis** 2. **Dermatomyositis**
49
What's the diagnosis? - Suspected degenerative muscle disorder, slowly progressive weakness seen in the 6th decade of life. Characteristic thumb sparing
**Inclusion body myositis**
50
What's the diagnosis? - most common form of muscular dystrophy, inherited in an autosomal dominant manner - multisystem involvement, with symptoms including myotonia, weakness, cataracts, ptosis, frontal balding and cardiac defects
**Myotonic dystrophy** - trinucleotide repeat disorder (chromosome 19) that exhibits anticipation (like Huntington's)
51
What is the most common type of motor neurone disease?
**Amyotrophic lateral sclerosis** (ALS)
52
What are some of the features of a motor neurone disease?
- Untreatable, rapidly progressive, average survival time is 3 years - Muscle weakness and potentially problems with speech, swallowing and breathing - UMN and LMN signs **without sensory problems** - Focal onset and continuous spread, then finally generalised paresis
53
Sporadic mutations account for 90% of MNDs At what age do sporadic cases of MNDs peak?
Peak is seen betwen **50-75 years old**, then declines again after 80
54
MND has a very varied presentation. What % presents with symptoms affecting the extremities? What % presents with LMN symptoms?
**70%** present with symptoms affecting the extremities (upper moreso than lower), compared to 25% with bulbar symptoms and 5% with thoracic symptoms **90%** present with LMN symptoms, compared with 10% presenting with UMN symptoms
55
What are bulbar symptoms? Examples?
Bulbar symptoms = anything affecting the function of **CN 9, 10, 11 or 12** (due to LMN lesion affecting the **medulla**) Examples - dysphagia, difficulty chewing and swallowing, nasal regurgitation, slurring of speech, dysphonia, dysarthria
56
How do the following compare regarding appearance of UMN and LMN symptoms? - Amyotrophic lateral sclerosis - Primary lateral sclerosis - Progressive muscular atrophy
ALS - UMN yes, LMN yes PLS - UMN yes, LMN no PMA - UMN usually subclinical, LMN yes
57
What type of dementia is ALS associated with? Why?
ALS is associated with **frontotemporal dementia** (Pick's Disease) - due to **C9ORF hexanucleotide repeat expansion**
58
What group of muscles is typically preferentially wasted in ALS?
Muscles of the **thenar eminence**
59
Corticospinal tract - where is it's origin? This tract is made up of two tracts (lateral and anterior), what does each provide voluntary control over?
Origin - **primary motor cortex** (precentral gyrus) **Lateral** tract provides **voluntary control of limbs and digits** **Anterior** tract provides **voluntary control of trunk and maintains posture**
60
Which tract controls the muscles of the face, head and neck, and contains the upper motor neurones of cranial nerves? This tract provides bilateral innervation to the cranial nerve nuclei, except...?
The **corticobulbar tract** Exception - CN XII and lower part of CN VII (hence why Bell's palsy (LMN) affects the whole side of the face, while a stroke (UMN) only affects the lower half of one side of the face)
61
The descending pathways can be broken down into pyramidal tracts (corticospinal and corticobulbar) and extrapyramidal tracts - what are the 2 extrapyramidal tracts? What are their functions?
**Rubrospinal tract** - excites flexor muscles and inhibits extensor muscles of the upper limbs (abnormal flexion to pain if not functioning) **Reticulospinal tract** - excites extensors
62
State whether the following are arterial or venous bleeds - extra(epi)dural haemorrhage - subdural haemorrhage - subarachnoid haemorrhage
Extradural - arterial (middle meningeal a) Subdural - venous (bridging veins) SAH - arterial (Berry aneurysm)
63
What type of intracranial bleed presents with an initial period of lucidity followed by unconsciousness?
Extradural haematoma
64
What is Cushing's Triad?
Raised ICP causing brainstem herniation Results in **hypertension, irregular breathing and bradycardia**
65
What type of herniation might cause an unreactive pupil?
An **uncal herniation**
66
What kind of stroke would the following presentation make you suspect? - higher cerebral dysfunction e.g. dysphasia - homonymous visual field defect - ipsilateral motor and/or sensory deficit of at least two areas (face, arm, leg)
**Anterior circulation stroke**
67
What kind of stroke would the following presentation make you suspect? - cerebellar dysfunction - isolated homonymous visual field defect - cranial nerve dysfunction
**Posterior circulation stroke**
68
What kind of stroke would the following presentation make you suspect? - pure motor OR pure sensory loss
**Lacunar stroke**
69
Describe the WHO's Analgesic Ladder
1st - **paracetamol** 2nd - **NSAID** (aspirin, diclofenac, ibuprofen, indomethacin, naproxen) 3rd - **weak opioid** (codeine, tramadol, dextropropoxyphene) 4th - **strong opioid** (morphine, oxycodone, hydromorphone, heroin...)
70
Which nerve fibre types are involved in nociception?
**C** and **A delta**
71
What does the Gate Control Theory suggest?
Nociception involves both large diameter (Aß) sensory axons and unmyelinated (C/ð) nociceptive axons Inputs to the projection neurone (P) are inhibited by an interneurone (I), which is **excited by the Aß​ axon and inhibited by the C/ð axon**
72
What is the main **inhiBitory** neurotransmitter in the CNS? How about outside of the CNS? What is the main **exciTaTory** neurotransmitter in the CNS?
Inhibitory = **GABA** (**Glycine** outside of the CNS) Excitatory = **Glutamate**
73
Which part of the brain do opioids work on? How does this produce analgesia?
Affect the **Periaqueductal Grey (PAG)** Endogenous opioids and morphine/related compounds "inhibit the inhibitory GABAergic interneurones..." Basically they cause disinhibition, meaning more GABA to act on receptors Also act on the **Nucleus Raphe Magnus** (NRM) and the **Locus coeruleus** (LC)
74
Name some endogenous peptides that act as opioids
Endorphins Dymorphins Enkephalins
75
What are the 3 main cellular actions of opioids?
**Inhibition of opening of voltage-gated Ca2+ channels** (has a pre-synaptic effect, stopping the release of excitatory neurotransmitters from nocicpetor terminals) **Opening of K+ channels** (has a post-synaptic effect, suppresses excitation of projection neurones) **Inhibition of adenylate cyclase**
76
What are the 3 classes of opioid receptor?
**Mu - responsible for most of the analgesic actions of opioids** **Delta** - contributes to analgesia but some of the activation can cause convulsions **Kappa** - contributes to analgesia at the spinal and peripheral level, activation is associated with sedation, dysphoria and hallucinations
77
What are some of the potential side effects of opioid use?
Apnoea (blunting of respiratory centres to CO2) Orthostatic hypotension (reduced sympathetic tone and bradycardia) Nausea and vomiting, constipation (increased smooth muscle tone, decreased motility) Confusion, euphoria, dysphoria, hallucinations, dizziness, myoclonus, hyperalgesia
78
Is morphine safe to use in people with poor renal function?
Need to be careful - morphine is metabolised in the liver into **M3G** (inactive) and **M6G** (retains analgesic activity and is **excreted by the** **kidney**)
79
Diamorphine is more/less lipophilic than morphine When would you use diamorphine?
Diamorphine is **more lipophilic** Provides rapid onset of action when administered IV Used for **severe post-op pain**
80
How are oxycodone and hydrocodone related to codeine?
Codeine is naturally occurring and a weaker opioid for mild/moderate pain Oxycodone and hydrocodone are **semi-synthetic derivatives with higher potency**
81
Which opioid is given IV to provide maintenance analgesia?
**Fentanyl** (75-100 fold more potent than morphine)
82
Which opioid is used in acute pain and is especially useful in labour? Which medication should it NOT be used in conjunction with?
**Pethidine** - rapid onset but short duration Shouldn't be used in conjuction with **MAO inhibitors**
83
Which opioid medication is useful in chronic pain via patient-controlled injection systems/sublingual administration?
**Buprenophine** Slow onset but long duration of action
84
Which opioid, a weak mu-receptor agonist, should be avoided in people with epilepsy?
**Tramadol**
85
Which drug, which is a competitive antagonist at opioid mu-receptors, is used to reverse opioid toxicity What must be done when giving this drug? When else can this drug be given?
**Naloxone, given IV usually** Has a short half-life, so must be **clinically monitored very closely** Can also be given to **newborns with opioid toxicity** if their mother has been given pethidine during labour
86
How does Naltrexone differ to Naloxone?
Similar, but Naltrexone has oral availability and a much longer half-life
87
What is the mode of action of NSAIDs? Which drugs are similar to NSAIDs but selectively inhibit only one molecule?
Inhibition of **COX-1 and COX-2**, which prevents prostaglandin synthesis **COX-2 selective inhibitors** ('coxibs') - etoricoxib, celecoxib, lumiracoxib (COX-2 is induced locally at the sites of inflammation while COX-1 is constitutively active)
88
Why is paracetamol not classed as an NSAID?
Because is **lacks anti inflammatory activity** and acts only centrally (NSAIDs act both centrally and peripherally)
89
Which medication is useful in migraine prophylaxis?
Gabapentin
90
Which drug is first line in controlling pain intensity and frequency of attacks in trigeminal neuralgia?
**Carbamazepine** (anticonvulsant, blocks voltage-activated Na+ channels that are upregulated in damaged cells)
91
What is a useful diagnostic clue to determine whether or not someone is suffering from a neuromuscular condition?
If neuromuscular, there will be **no sensory symptoms**
92
Amitriptyline - mode of action and adverse effects
Mode of action - inhibits neuronal uptake of noradrenaline and serotonin Adverse effects - constipation, weight gain, dry mouth, mydriasis, sedation, hypotension. **Cardiotoxic in overdose**
93
Gabapentin/Pregabalin - mode of action and adverse effects
Mode of action - **inhibits voltage-activated presynaptic Ca2+ channels**. Designed as a GABA analogue Adverse effects - somnolence, dizziness, peripheral oedema, weight gain, ataxia
94
CSF analysis demonstrating 14-3-3 protein would suggest what pathology?
Creutzfeld-Jakob Disease
95
What is Uhthoff's phenomenon?
Exacerbation of sensory symptoms after being in a hot environemnt e.g. a bath or shower. Seen in **MS**
96
The acronym DANISH can be used to remember some of the associated symptoms that may be seen in someone with MS. What does DANISH stand for?
Dysdiadochokinesis Ataxia Nystagmus Intention tremor Slurred speech Hypotonia
97
Regarding symptom management in someone with MS, what medications would you give in the following circumstances? - spasticity - sensory symptoms - fatigue - bladder dysfunction
Spasticity - physio + **oral Baclofen or gabapentin** Sensory symptoms - **gabapentin** for neuropathic pain Fatigue - **amantidine** Bladder dysfunction - physio, catheterisation if retaining, **oxybutinin** (anticholinergic) in case of urge incontinence

Year 3 - Neurology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions