Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2 Quick > Neuro > Flashcards

Neuro Flashcards

1
Q

What is status epilepticus?

A

When seizures last > 5 mins without stopping in between
MEDICAL EMERGENCY

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

Tx Status Epilepticus

A

IV Lorazepam

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

What is a Transient Ischaemic Attack (TIA)?

A

Acute loss of cerebral/ocular function
Lasting < 24 hours
COMPLETE CLINICAL RECOVERY
Ischaemia without infarction

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

RF TIA

Other than atherosclerotic RFs

A

Male
AF
VSD
COCP

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

How many of 1st strokes are preceded by TIA?

A

15%

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

Causes TIA

A

Atherothromboembolism! from Carotid artery - MC!!

Small vessel occlusion

Cardioembolism - emboli from MI, AF etc or valve disease or prosthetic valve

Hyperviscosity - polycythaemia, sickle cell anaemia

Hypoperfusion (important to look at in younger people) - cardiac dysrhythmia, postural hypotension

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

Where do the majority of TIAs affect?
How do these type of TIAs present?

A

90% affect CAROTID ARTERY

Weak, numb contralateral leg (+/- similar but less intense in arm)
Hemiparesis
Dysphasia
Hemi-sensory disturbances
AMOUROSIS FUGAX

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

What is amourosis fugax?

A

Sudden painless transient loss of vision in one eye
Described as “curtain descending over field of vision”

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

Pathophysiology Amourosis Fugax

A

Emboli passes into retinal, opthalmic or ciliary artery

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

Ix TIA

A

Until recovery, NO WAY TO DIFFERENTIATE FROM A STROKE

So i assume urgent CT? because you would act like it’s a stroke

But i guess once recovered,
GS = Diffusion weighted MRI

Carotid dopple
CT angiography
ECG - AF

Also, ABCD^2 score but NICE don’t recommend this anymore

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

Where do the lesser proportion of TIAs affect?
How do they present?

A

Posterior circulation (Vertebrobasilar artery)

Diplopia
Vertigo
Vomiting
Ataxia
Choking
Dysarthria
Hemisensory loss
Transient global amnesia
Tetraparesis

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

Tx TIA

A

Urgent 300mg aspirin
Refer to specialist within 7 days

Then will be put on statin or clopidogrel

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

What are the different classes in the Bamford Stroke Classification?

A

TACI - total anterior circulation infarct
PACI - partial anterior circulation infarct
LACI - lacunar infart
POCI - posterior circular infarct

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

How does a TACI present?

A

MUST have all 3 of the following :

  1. Unilateral weakness +/- sensory deficit of face, arms and legs
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction (dysphasia, visuospatial disorder)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does a PACI present?

A

MUST have 2 of the following :

  1. Unilateral weakness +/- sensory deficit of face, arms and legs
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction (dysphasia, visuospatial disorder)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does a LACI present?

A

MUST have 1 of the following :

Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis

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

What is Charcot’s neurological triad?

A
  1. Dysarthria
  2. Nystagmus
  3. Intention tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Uhthoff’s phenomenon?

A

Sx exacerbated by heat

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

What type of HS R is MS?

A

Type 4

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

Define MS

A

Chronic, autoimmune T-cell mediated inflammation disorder of CNS
Multiple plaques of demyelination

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

RF MS

A

More common the further from equator (link to Vit D?)
FHx
Exposure to EBV in childhood
Female!
Some genetic link (HLA-DR2) but def environment affects

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

Typical MS Patient

A

F 20-40yrs

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

Types of MS Progression

A

Relapsing/Remitting MC!!
Clear relapses w partial/full recovery, no progression in between

1º Progressive
Linear progression, no relapse

2º Progressive
Starts at RR then 1º

Progressive/Relapsing
Same as RR but progression in between relapses

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

Signs / Symptoms MS

A

LOSS NB
Lhermitte’s sign - tingling when neck flexion
Optic neuritis - also struggle to see red
Sensory Sx + Sx
Spasticity

Nystagmus
Bladder/sexual dysfunction
–
UHTHOFF’S PHENOMENON!!!
–
Charcot’s neuro triad
UMN signs (not LMN)
Paraesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Ix MS

A

MACDONALD’S CRITERIA!!
At least 2 events disseminated by time and space
–
GS!! (w above) - MRI W CONTRAST
Lesions appear white

Lumbar puncture w CSF electrophoresis
(inflam proteins only in CSF bc nervous system disease)

Evoked potentials - how long impulses travel
the more demyelination, the slower the conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Tx MS
Acute

A

Acute attacks = IV methylprednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tx MS
CHRONIC

A

NO CURE!

1st Line - beta interferon and glatiramer acetate

Sx Tx :
Tremor - BB

Muscle spasticity -
Mild-Mod : Oral diazeam, baclofen
Focal disabling : periph nerve blocks e.g. botulinum, alcohol, phenol

SEVERE :
Reversible invasive procedures e.g. intrathecal baclofen
Irreversible e.g. functional neurosurgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

S/E beta interferon

A

Injection site reactions
Flu Sx (will decrease after first few months)
Mild lymphopenia
Mild-mod rise in liver enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Mechanism Alemtuzumab

A

CD52 monoclonal antibody that targets T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Mechanism Natalizumab

A

acts against VLA-4 receptors that allow immune cells
to cross the BBB and therefore reduces number of immune cells that
can enter the CNS and cause damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Myasthenia Gravis?

A

Autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Patho MS

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is Guillain-Barre Syndrome?

A

Acute, inflamm demyelination polyneuropathy
Affects PNS - Schwann cells
Following URTI or GI tract infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Signs / Symptoms GB syndrome

A

Within 4 weeks of URTI or GI tract infection
Symmetrical, ascending muscle weakness
Proximal muscles more commonly affects - trunk, resp and Cranial nerve esp CN7

REFLEXES LOST (deep tendon refleces)
RESP INVOLVEMENT - affects diaphragm = death!!

Paraesthesia, numbness
Back/limb pain
Cranial nerve involvement - Diplopia, dysarthria
Autonomic fts - Sweating, ↑Pulse, postural hypotension, arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Comp GB syndrome

A

Clots - PE!!
Resp system - if affects diaphragm = death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Causes GB syndrome

A

Triggered by infection! - usually GI tract or Upper resp tract

Campylobacter jejuni MC
Cytomegalovirus
EBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pathophysiology GB

A

MOLECULAR MIMICRY
Infection occurs
∴ immune response
Body produces antibodies against antigens
But these antigens similar to those on Schwann cells
∴ attacks Schwann cell
∴ Demyelination + Acute polyneuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Monitoring GB

A

MONITOR BREATHING BC RESP INVOLVEMENT!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Ix GB syndrome

A

Clinical diagnosis, no GS

Nerve conduction studies
Lumbar puncture (L3/4) to test CSF - ↑protein, normal WCC, normal glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Tx GB

A

IV Ig for 5 days
Plasma exchange - remove Abs
(CI in IgA def patients!! will cause allergic reaction)

Supportive care
VTW prophylaxis (LMWH) e.g. SC enoxaparin and compression stockings - bc clots are common

Spirometry!
If FVC < 0.8, consider intubation and ITU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Prognosis GB

A

80% recover completely - bc myelin sheath recovers
15% lasting weakness
5% die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Quick!
Symmetrical limb weakness, Absent tendon reflexes and ↓ Sensation
What is it?

A

GB syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

In whom does Myasthenia Gravis usually present in?

A

Female < 40
Males > 60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How can you distinguish from Motor Neurone disease and Myasthenia Gravis?

A

MND never affects eye movements!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What type of HS reaction is Myasthenia Gravis?

A

Type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Signs / Symptoms Myasthenia Gravis

A

MUSCLE WEAKNESS
Worse at end of day/with exertion
Better with rest
Starts w/ head and neck! then progresses to lower body

Eye muscle weakness - diplopia
Ptosis
Myasthenic snarl - hard to smile, looks weird
Jaw fatigue
Dysphagia - bulbar weakness
Dysphasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Pathophysiology Myasthenia Gravis

A

Normally, acetylcholine crosses synaptic gap and attaches to receptors

MC!! - Immune system produces Nicotinic Ach-R antibodies, bind to receptors and blocks!
∴ ↓ muscle contraction
As muscles are used, more receptors are blocked!
∴ ↑ ACTIVITY = ↑ WEAKNESS

ALSO : Muscle Specific Kinase (MuSK) and low-density lipoprotein receptor related protein 4 (LRP4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Ix Myasthenia Gravis

A

Serology - Anti-AchR and Anti-MuSK

Tensilon/Edrophonium test!
Administer Edrophonium, POS test = ↑↑muscle power for a few seconds

Also, repeatedly blink causes ptosis
Look up for a while causes diplopia
Repeatedly abduct arm causes unilateral muscle weakness when compare arms
Count to 50 - as higher numbers, voice get less audible

ALSO : FVC! to test resp muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Tx Myasthenia Gravis

A

1st Line = ACh inhibitors!
NEOSTIGMINE, PYRIDOSTIGMINE

2nd Line = Immunosuppression - steroids (prednisolone/azathioprine)

Monoclonal Abs - Rituximab, eculizumab

Thymectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Myasthenia Gravis assoc disease

A

Lambert-Eaton Myasthenic Syndrome!
Paraneoplastic condition, SCLC
Weakness will improve AFTER exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

RF Myasthenia Gravis

Other than F 20-40

A

Thymoma! / Thymic hyperplasia
Autoimmune disease - RA, SLE, pernicious anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Tx Myasthenia Crisis

A

IV Ig
Plasmapheresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Pathophysiology Lambert-Eaton Syndrome

A

Autoantibodies against calcium channels in SCLC cells
Also target calcium channels in presynaptic terminals
∴ ↓ ACh released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Signs / Symptoms Lambert-Eaton Syndrome

A

Same as Myasthenia Gravis
But start w extremities rather than head and neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Ix Lambert-Eaton Syndrome

A

Rule Myasthenia Gravis out !! (aka if ACh-R antibodies = Myasthenia Gravis)

MRI - SCLC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Tx Lambert-Eaton Syndrome

A

Treat any malignancy

ACh inhibitors - pyridostigmine, neostigmine

Amifampridine - improves muscle strength

If v severe - immunosuppression/IV Ig/Plasmapheresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Pathophysiology Parkinson’s disease
SIMPLE

A

Progressive reduction of dopamine in the basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pathophysiology Parkinson’s disease
MORE DETAIL

A

Neurodegen loss of substantia nigra in pars compacta
∴ ↓ Dopamine levels

∴ Thalamus is inhibited
∴ ↓ Movement
∴ Symptoms of Parkinson’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Triad of Parkinson’s

A
  1. Resting tremor
  2. Bradykinesia
  3. Rigidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Parkinson’s : TRAP

A

Tremor - pin-rolling
Rigidity - cogwheel
Akinesia
Postural instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Causes ParkinsonISM

A

Parkinson’s disease
Vascular parkinsonism
Infections - encephalitis, creutxfeldt-Jakob disease
Toxin induced - carbon monoxide, drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Why is Parkinson’s thought to double in the next gen?

A

People are getting older
Population is increasing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Parts of basal ganglia

A

Striatum - putamen and caudate nucleus
Globus pallidus - external and internal
Substantia nigra - produces dopamine
Subthalamic nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Signs / Symptoms Parkinson’s disease

A

TRAP - ASYMM tremor, rigidity, akinesia, postural instability

Small shuffling steps
Reduced arm swing
Difficulty initiating movement - struggle to start walking
Hypomimia - ↓ facial expressions, mask-like face
Depression
Memory problems
Anosmia
Constipation
↑ Urinary freq, NOT incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What should NOT be present at the beginning of Parkinson’s disease?
If these symptoms ARE present, what are you thinking of instead?

A

TIDES
Tremor in action
Incontinence
Dementia
Early falls
Symmetry
–
Normal pressure hydrocephalus
Essential tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Signs / Symptoms Essential tremor

A

Better with alcohol
Action tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Tx Essential tremor

A

Deep brain stimulation
BB
Primidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Tx Normal Pressure hydrocephalus

A

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Ix Parkinson’s disease

A

Usually from history and exams

DaTSCAN
Head CT/MRI

Microscopy - Lewy bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

RF Parkinson’s disease

A

FHx
Male
↑ Age
Smoking seems to be protective!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Parkinsonism Cardinal signs

A

Resting tremor
Bradykinesia
Rigidity
Postural instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Tx Parkinson’s disease

A

LEVODOPA + Carbidopa
Can cross BBB, dopamine can’t
NOT GIVEN INITIALLY bc effect will wear off after a while ∴ saved for when symptoms are rlly bad
Has on/off fluctuations!! - Sx can be well controlled, then suddenly not controlled
–
Dopamine agonists - Bromocriptine, Ropinirole

COMT inhibitors - entacapone, rasagiline
MAO-B inhibitors - selegiline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Why can’t you just give dopamine to treat Parkinson’s disease?

A

silly
you can’t do that bc dopamine can’t cross the BBB
and will cause arrhythmias etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Why MUST you give Carbidopa with Levodopa when treating Parkinson’s disease?

A

Carbidopa ensures Levodopa is not metabolised peripherally, otherwise can cause arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Parkinson Sx THEN dementia = ?

A

Parkinson’s dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Dementia THEN Parkinson’s Sx = ?

A

Lewy Body dementia w Parkinsonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Mechanism of COMT/MAO-B inhibitors

A

Inhibit the inhibition of dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

DDx TIA

A

Obvs stroke
Hypoglycaemia
Migrainous aura
Mass lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Causes Ischaemic Stroke

A

Atherosclerotic rupture
Thrombus, embolus
Shock
Cardiac emboli - AF, MI, IE (blood stasis)
Atherothromboembolism - from carotid artery
Vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

RF Ischaemic stroke

A

Atherosclerosis RF
Ethnicity - black or asian
HTN
Smoking
DM
Age
Alcohol
Past TIA
Heart disease
AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe the ABCD^2 score

A

Age > 60 (1)
BP > 140/90 (1)
Clinical Sx - unilateral weakness (2), slurred speech, no weakness (1)
Duration Sx - 1 hour (2), 1 hour (1)
DMT2 (1)

> 6 REFER TO NEUROLOGY ASAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Describe Glasgow Come Scale

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Signs / Symptoms Ischaemic Stroke
Anterior cerebral artery

A

D CLIT

Drowsiness
Contralateral leg weakness +/- sensory loss (arms probs not affected too but could happen)
Logical thinking and personality affected
Incontinence
Truncal/Gait ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Signs / Symptoms Ischaemic Stroke
Middle cerebral artery

A

MOST COMMON PRESENTATION!!
CASH

Contralateral motor weakness/sensory loss - both arms and legs
Aphasia - Wernicke’s or Broca’s
Smile droop (facial droop)
Hemiplagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Signs / Symptoms Ischaemic Stroke
Posterior cerebral artery - Occipital lobe

A

VIP

Visual agnosia - can’t interpret visual info
Isolated homonymous hemianopia or cortical blindness
Propagnosia - can’t recog faces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Signs / Symptoms Ischaemic Stroke
Posterior circulation - vertebrobasilar artery

A

Balance disorder
Coordination disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

If the posterior circulation (Vertebrobasilar artery) is affected in ischaemic stroke, why is this more concerning?

A

Larger region supplied by this artery
∴ More catastrophic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Signs / Symptoms Lateral Medullary Syndrome

A

Sudden vomiting
Vertigo
Ipsilateral Horner’s syndrome
Facial numbness
Limb ataxia
Dysphagia
Dysarthria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Tx Ischaemic Stroke

A

Urgent NCCT!!!!! EXCLUDE HAEMORRHAGE
Immediate 300mg loading dose Aspirin
Then continue this for 2 weeks

Thrombolysis w IV Alteplase - WITHIN 4.5 HOURS OF SX ONSET !!!!

Lifelong Clopidogrel after 2 weeks of aspirin (75mg)

–
Thrombectomy - within 6 hours of symptom onset!!
Only indicated if severe - large artery has been affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

CI Thrombolysis w IV alteplase

A

History of stroke in DM patients
Severe stroke
Stroke in last 3 months
Active malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

A patient on anticoags has a stroke and presents to the hospital. Thoughts?

A

if Px on anticoags, always suspect to be haemorrhagic stroke until proven otherwise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Causes Haemorrhagic strokes

A

Anything that increases risk of vessel rupture

HTN
2º to ischaemic stroke! - causes stiff, brittle vessels prone to rupture
Head trauma
AV malformations
Vasculitis
Vascular/Brain tumours
Cerebral amyloid angiopathy
Carotid artery dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Presentation of ↑ICP

A

Virtually indistinguishable from Ischaemic infarct
LoC and headache more likely
Papilloedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Extradural haemorrhage
Rupture of?

A

Middle meningeal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Subdural haemorrhage
Rupture of?

A

Bridging cranial veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Subarachnoid haemorrhage
Rupture of?

A

Berry aneurysm in circle of Willis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

go do haemmorhages from table

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Causes Dementia

A

Alzheimer’s - MC!
Vascular
Lewy-Body
Fronto-Temporal (Pick’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

QUICK!
Headache, photophobia and neck stiffness
What is it?

A

MENINGITIS!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What must you make sure you do if a patient has meningitis?

A

Notify Public Health!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

RF Meningitis

A

Elderly or very young children
Immunocompromised
Non-vaccinated
Crowded environments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Meningism Triad

A
  1. Headaches
  2. Photophobia
  3. Neck stiffness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Non-Infective Causes Meningitis

A

Paraneoplastic
Drug S/E
Autoimmune e.g. RA, SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Causes Bacterial Meningitis

A

Neisseria Meningitis
Strep. Pneumoniae
Listeria spp
Group B strep
Haemophilus influenzae B
E. Coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Causes Viral Meningitis

A

Herpes Simplex Virus
Varicella zoster virus
Enterovirus - Coxsackie

106
Q

Causes Meningitis
Chronic presentation

A

Mycobacterium Tuberculosis
Syphilis

107
Q

If Neisseria Meningitidis is found in the bloodstream, what does it indicate?

A

MENINGOCOCCAL SEPTICAEMIA !!

108
Q

How does Meningococcal Septicaemia present?

A

Non-Blanching Purpuric Rash
Disseminated Intravascular clotting - v easy bleeding

109
Q

How does ↑ICP present?

A

Papilloedema
GCS < 12
Focal neuro signs
Continuous or uncontrolled seizures

110
Q

Go through bacterial causes of Meningitis and in what groups you are likely to find them in

A

Neisseria Meningitidis - Kids/Teenagers

Step Pneumoniae - Young children OR adults

Listeria spp - Immunocomp, pregnancy

Group B Strep - neonates
bc colonises maternal vagina

111
Q

Shape and gram stain
Neisseria Meningitidis

A

Gram Neg
Diplococcus

112
Q

Shape and gram stain
Strep Pneumoniae

A

Gram Pos
Diplococcus

113
Q

Shape and gram stain
Group B Strep

A

Gram Pos
Coccus in chains

114
Q

Shape and gram stain
Listeria monocytogenes

A

Gram Pos
Bacillus

115
Q

Signs / Symptoms Meningitis

A

HEADACHE, NECK STIFFNESS, PHOTOPHOBIA
Fever
Kernig’s sign
Brudzinski’s sign

116
Q

If patient presents to GP with Meningism, what should they do immediately?

A

Give IM Benzylpenicillin + admit to hospital!!!

117
Q

Where can Listeria monocytogenes be found?

A

CHEESE
∴ pregnant women advised to try and avoid

118
Q

Describe the steps taken once a patient arrives at hospital with suspected meningitis

A
  1. ABCDE + GCS score
  2. Blood cultures!
  3. Broad spec Abx (don’t wait for results) - IV ceftriaxone or Cefotaxime
    If immunocomp - ADD high dose amoxicillin
    If recent travel - ADD IV Vancomycin
    If pencillin allergy (severe - anaphylaxis) - Give Chloramphenicol
  4. Steroids - IV Dexamethasone (↓Neuro comps)
  5. LUMBAR PUNCTURE!
119
Q

When treating Meningitis with broad spec Abc (aka with cephalosporins), why would you give Chloramphenicol if a patient has a severe penicillin allergy?

A

BC there is a 10% chance that if they react to penicillins, they will react to cephalosporins

120
Q

Why do you give IV Vancomycin if recent travel when treating Meningitis?

A

Bc recent travel increases chance of penicillin resistance

121
Q

CI Lumbar Puncture

A

Abnormal clotting
If on anti-coags
Petechial rash (Indicates meningococcal sepsis - DIC)
Infection at LP site (e.g. shingles)
↑ ICP - bc risk of coning

122
Q

Ix Meningitis

A

LP TABLE !!!!!

123
Q

What should you do after treating a meningitis patient?

A

Inform Public health

And identify close contacts! (Living together esp in first 7 days of infection!)
Give prophylaxis Abx - Ciprofloxacin or Rifampicin if CI !!

124
Q

DDx Meningitis

A

SAH! - thunderclap
Migraine
Flu
Sinusitis - facial pain
Brain abscess
Malaria

125
Q

Big diff between syncope and epilepsy

A

Epilepsy usually has amnesia - forget what happened straight after episode

126
Q

Causes Encephalitis

A

HERPES SIMPLEX (MC by far!!)
Varicella zoster (chicken pox)
Measles, Mumps
Rubella
EBV
HIV
CMV
Coxsackie

ALSO : TB, Malaria, Rabies

Non-Infective : Autoimmune, paraneoplastic

127
Q

Presentation of Encephalitis

A

Hours to Days Preceding : Flu-like illness

THEN, triad of :
1. Altered GCS - confusion, drowsiness, coma
2. Fever
3. Headache

Also : Seizures, Memory loss +/- history of meningism (may have progressed from meningitis)

128
Q

Ix Encephalitis

A

MRI head - shows swelling/inflamm + midline shift (bc ↑ICP)

ECG - periodic sharp and slow waves
Lumbar puncture - done after, ↑lymphocytes
HIV test

129
Q

Tx Encephalitis

A

Mostly supportive

IV Aciclovir - if HSV or VZV
If seizures - carbamazepine

If meningitis sus - IM benzylpenicillin

130
Q

Triggers of a Migraine

A

CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese
Oral contraception
Lie-ins
Alcohol
Tumult - loud noises
Exercise

131
Q

Describe a migraine

A

Unilateral, recurrent throbbing headache +/- aura
Mod - Severe pain

Often w vision changes
Usually bc of specific trigger
MC cause of recurrent headache

132
Q

Describe a typical patient of migraine

A

Women under 40
If over 50, should be sus of underlying cause

133
Q

Describe the difference between 1º and 2ºheadaches

A

1º - syndrome is based on Sx
2º - symptoms bc of underlying cause e.g. SAH

134
Q

Describe the diagnostic criteria for migraines WITHOUT aura

A

A - 5 attacks of

B - 4 - 72 hours

C - 2 of :
Unilateral, pulsing, mod/severe, aggravated by routine physical activity

D - Headache comes w/ N+V OR Photophobia + Phonophobia

135
Q

Describe the diagnostic criteria for migraines WITH aura

A

A - At least 2 attacks fulfilling B + C :

B - At LEAST 1 reversible aura Sx :
Visual - zigzags, spots
Unilateral sensory - tingling, numbness
Speech - aphasia
Motor weakness - hemiplegic migraine (rule out stroke/TIA)

C - AT LEAST 2 of following :
* ≥ 1 aura Sx spread gradually over 5 mins +/- ≥ 2 aura Sx in succession
* Each aura Sx = 5 - 60 mins
* ≥ 1 aura Sx is unilateral
* Aura accompanied/followed within 1hr of headache

136
Q

Ix Migraine

A

Clinical diagnosis
Diagnostic criteria w/ normal neuro exam!

Exclude other causes e.g. SAH

137
Q

If a patient presents with a migraine, what are the indications for a lumbar puncture?

A

Worst headache of life - thunderclap
Rapid onset
Progressive headaches
Unresponsive headaches

138
Q

Tx Migraines

A

Conservative - avoid triggers

ACUTE :
Mild - NSAIDs, paracetamol
Severe - oral triptan e.g. sumatriptan

Avoid opioids if possible! bc risk of dependence and worsens nausea

139
Q

Prophylaxis Migraines

A

1st Line - propanolol or topiramate (anti-convulsant)
2nd Line - acupuncture
3rd Line - Amitriptyline
4th Line - Botulinum toxin Type A

140
Q

What’s the most common headache?

A

Tension headache

141
Q

Trigger Tension headache

A

Stress !!

142
Q

Describe a tension headache

A

Bilateral generalised headache, radiates to neck / trapezius
Like a rubber band / clamp around head

NO motion sickness / N+V / aura

143
Q

Tx Tension headache

A

SImple analgesia - aspirin, paracetamol
Avoid opioids! (dependence!!)

144
Q

Causes Tension Headache

A

MC SCOLD

Missed meals
Conflict

Stress
Clenched jaw
Overexertion
Lack of sleep
Depression

145
Q

Which is the most disabling headache?

A

Cluster

146
Q

Describe a cluster headache

A

Unilateral periorbital pain w/ autonomic features (15 - 160 mins)
Rises in severity
Excruciating pain - hot/boring poker characteristic
Usually in middle of night/morning hours
Rare-ish

147
Q

Describe some autonomic features found in a cluster headache

A

Conjunctival infection + lacrimation (watery bloodshot eyes)
Ptosis
Miosis (dilated unilateral pupil)
Rhinorrhoea

148
Q

Ix Cluster headaches

A

At least 5 similar attacks confirms diagnosis

149
Q

Tx Cluster headaches

A

Acute :
SC sumatriptan
IM Zolmitriptan
100% O2 therapy! (unless COPD)

150
Q

Prophylaxis Cluster headaches

A

Verapamil
Lithium
Corticosteroids

151
Q

Describe Trigeminal Neuralgia

A

Chronic, debilitating condition
Causes intense and extreme episodes of pain
Almost always unilateral

152
Q

Age of Trigeminal Neuralgia normally

A

50 - 60 years

153
Q

RF Trigeminal Neuralgia

A

MS!!!!!!!!!
↑ Age
Female

154
Q

Triggers Trigeminal Neuralgia

A

Eating
Shaving
Talking
Brushing teeth

155
Q

Presentation Trigeminal Neuralgia

A

Electric shock pain (seconds-mins)

156
Q

Diagnostic criteria Trigeminal Neuralgia

A

At least 3 attacks

157
Q

Tx Trigeminal Neuralgia

A

Carbamazepine
Surgery if nothing else works

158
Q

Name types of Generalised seizures

A

Tonic-Clonic
Myoclonic
Absence
Tonic
Atonic

159
Q

Define Epilepsy

A

Recurrent tendency to have spontaneous, intermittent, abnormal electrical activity that manifests as seizures
**AT LEAST 2 SEIZURES TO BE EPILEPTIC **

160
Q

Define an Epileptic Seizure

A

Spontaneous, intermittent, uncontrolled electrical brain activity

161
Q

What is Ictus?

A

The epilepsy attack

162
Q

What is Prodrome?

A

Non-specific symptoms that precede an epileptic attack

163
Q

What is Aura?

A

Sensory disturbances that precede an epileptic attack, usually by minutes
More specific than Prodrome

164
Q

What age group is Epilepsy common?

A

Can happen at age
Highest < 20 and > 60

165
Q

RF Epilepsy

A

FHx
Premature birth
Developmental abnormalities
Trauma
Drugs e.g. cocaine
Space occupying lesion - tumour, infection, haematoma
Alzheimer’s /Dementia

166
Q

Types of Epileptic Seizures
Briefly describe

A
  1. Primary Generalised
    Originates in midbrain/brainstem
    Electrical discharge in both hemispheres
    Assoc w/ LOC
  2. Partial/Focal - MC
    Electrical discharge restricted to one hemisphere
    May develop into generalised (2º)
167
Q

Types of Partial/Focal Seizures

A

Partial WITHOUT impairment of conciousness e.g. déjà vu, Jacksonian seizures

Partial WITH impairment of consciousness e.g. psychomotor seizures

168
Q

Describe how a Tonic-Clonic seizure presents

A

Often no aura
Tonic : stiffening of the limbs, tongue biting, incontinence, no breathing (10-60s)

Clonic : Convulsions, limb jerking, eye rolling, uncoordinated breathing (secs-mins)

169
Q

Potential physical injuries of a Tonic-Clonic seizure

A

Common!
Drowsy
Confusion
Headache

170
Q

Describe the presentation of Absence seizures

A

Childhood
Conscious but unresponsive
Can occur many times a day
Usually very short, normal function resolves quickly

171
Q

Describe a Myoclonic seizure

A

Sudden isolated jerk of limb, face or trunk
May fall suddenly to the ground

172
Q

Describe a Tonic seizure

A

Sudden increased tone, RIGID
No jerking!

173
Q

Describe an Atonic seizure

A

Sudden loss of muscle tone + movement
RESULTS IN A FALL

174
Q

Describe a Simple Partial/Focal seizure

A

No LOC or loss of memory
Isolated limb jerking
Head turning! (away from side of seizure)
Isolated paraesthesia
TODD’s PARALYSIS - temporary paralysis/weakness

175
Q

Describe a Complex Partial/Focal seizure

A

Usually from temporal lobe
Can affect awareness +/- memory - before, during or after!
Visual/auditory halluciations
LIP SMACKING
Automatism
Post-ictal confusion/drowsiness

Sx depend on lobe involved!

176
Q

Describe a 2º Generalised seixure

A

Partial seizure that spread to lower brain area
∴ Initial a generalised seizure
usually tonic-clonic

177
Q

What is Status Epilepticus?

A

Seizure lasting longer than 5 minutes or more than 1 within 5 minutes without returning to normal consciousness in between

178
Q

Types of Status Epilepticus
Brief description

A

Convulsive :
Jerking, grunting, drooling, nystagmus

Non-Convulsive :
NO jerking, confusion, unable to speak, behavioural changes

179
Q

Tx Status Epilepticus

A

IV benzodiazepine - Lorazepam, diazepam

Rectal benzodiazepine - Buccal midazolam

Phenobarbital - 2nd Line
Phenytoin - 3rd Line

180
Q

Comp of Phenobarbital

A

Can cause circulatory depression

181
Q

Comp of Phenytoin

A

Can cause severe cardiac arrythmia

182
Q

Ix Epilepsy

A

Clinical diagnosis - AT LEAST 2 or more unprovoked seizures > 24 hours apart !!

EEG - Not diagnostic
Can support diagnosis but might show false negatives

MRI/CT - can show focal lesions to identify cause

Bloods - FBC, U&E, LFTs, BM
(to look for potential cause)

183
Q

Tx Generalised Tonic-Clonic

A

Sodium Valproate

UNLESS female of childbearing age - Lamotrogine

184
Q

Tx Tonic

A

Sodium Valproate

UNLESS female of childbearing age - Lamotrogine

185
Q

Tx Atonic

A

Sodium Valproate

UNLESS female of childbearing age - Lamotrogine

186
Q

Tx Myoclonic

A

Sodium Valproate

UNLESS female of childbearing age - Levetiracetam or Topiramate

187
Q

Tx Absence

A
  1. Ethosuximide
  2. Sodium Valproate

UNLESS female of childbearing age - Ethosuximide

188
Q

Tx Partial/Focal Seizures

A

Lamotrigine or Carbamazepine

189
Q

Types of Motor Neuron Disease
Brief description of area affected

A

1. Amyotrophic Lateral Sclerosis (ALS)
Loss of MN in motor cortex + ant. horn
UMN + LMN SIGNS

2. Progressive Bulbar Palsy
Affects brainstem motor nuclei, CN nerves 9-12 !! UMN + LMN

3. Progressive Muscular Atrophy
LMN only!
Distal muscles before proximal

4. Primary Lateral Sclerosis
UMN signs only!

190
Q

Types of MND and how they present ish

A

1. ALS
Progressive focal wasting, weakness and fasciculations spreading to other limbs!
Cramps
Spasticity
Brisk reflexes

2. Progressive Bulbar Palsy
CN 9-12 affected ∴ PALSY of the tongue, chewing/swallowing and facial muscles

3. Progressive Muscular Atrophy
Weakness + Fasciulations starts in one limb, progresses to adjacent spinal segments
Distal before proximal!!
LMN only!

4. Primary Lateral Sclerosis
Slow progressive tetraparesis and pseudobulbar palsy
UMN only!

191
Q

UMN lesion signs

A

↑Muscle tone = spasticity
Hyperreflexia (overrative/overresponsive reflexes)
NO Fasciculations!
++POS BABINSKI SIGN - Extensor plantar response
Pyramidal/Pronator drift
CORTICAL SENSORY LOSS
Maybe emotional lability

Upper limb extensor weaker than flexor!
Lower limb flexors weaker than extensor!
Fine movements impaired

192
Q

LMN lesion signs

A

Everything goes DOWN

↓Muscle tone (Hypotonia) - Flaccid (can be normal)
HYPOreflexia (reduction or absence of reflex)
FASCICULATIONS !
Muscle wasting! Can be Bulbar (speech/swallowing muscles), Upper limb (hand), Lower limb

RESPIRATORY! - weakness of breathing muscles, most patients will die bc of this
Diaphragm higher up!!

193
Q

What is a Positive Babinski sign?

A

When you stroke sole of foot, normally big toe will go down
If positive = will go up = UMN lesion

194
Q

Describe Pyramidal/Pronator drift

A

Hold arms out w palms up, eyes closed
Arm will “drift” away (or turn so palm down? idk need to check this)

195
Q

What can lower limb wasting look like?
Esp with LMN lesions

A

Wasting of tibialis anterior muscle = BILATERAL FOOT DROP
& Prominent tibial bones

196
Q

DDx MND

A

Cervical spine lesion - can present with UMN + LMN in arms and legs

Idiopathic multifocal motor neuropathy - weakness in hands and profuse fasciculations

197
Q

Ix MND

A

MRI of brain/spine
Nerve conduction studies
Electromyography - can confirm LMN

198
Q

By itself, are fasciculations enough to diagnose LMN lesions?

A

NO
NEED WEAKNESS TOO!!!!!

199
Q

Median age on onset MND?

A

60 years

200
Q

Prognosis MND

A

Usually fatal within 2-4 years

201
Q

RF MND

A

Usually sporadic, no known RF
MIGHT be linked to a mutation in SOD-1 (scavenging enzyme superoxide)

202
Q

Diagnostic tips for differentating DDx and MND!

A
  1. No sensory loss = RULE OUT MS or MYELOPATHY
  2. No disturbances in eye movements = RULE OUT MYASTHENIA GRAVIA OR MS
  3. No sphincter disturbances = RULE OUT MS
203
Q

Tx MND

A

NO CURE!

Oral Riluzole
Palliative :(

204
Q

Symptom Tx for MND

A

NG/PEG tube - Dysphagia
Oral amitriptyline - Drooling (bulbar palsy)
Baclofen - spasticity
Analgesic ladder - Joint pain

205
Q

MOA Riluzole

A

Na+ channel blocker
Inhibits Glutamate release

206
Q

Big difference in Bell’s Palsy vs Stroke

A

Bell’s = Lesion in CN 7
NOT FOREHEAD SPARING - forehead and lip droop

Stroke = Central lesion
FOREHEAD SPARING - ONLY lip droop

207
Q

Causes Peripheral Neuropathy

A

ABCDE

Alcohol
B12 deficiency
Cancer and CKD
DM and Drugs - isoniazid, amiodarone, cisplatin
Every vasculitis

208
Q

Signs / Symptoms Peripheral Neuropathy

A

2 Patterns - Axonal Loss and Demyelination

  1. Axonal loss
    Sensory changes - symmetrical numbness, burning or pins and needles
    THEN progresses to motor symptoms
  2. Demyelination
    Motor changes - Weakness
    THEN progresses to motor symptoms

–
Slow healing
Sensitivity to touch
Persistent injury
Lack of sensation
Burning pain
Ulcers

209
Q

Ix Peripheral Neuropathy

A

Nerve conduction studies
Rule out DDx

210
Q

CN 1
What is it?
How does CN1 Palsy present?

A

Olfactory
Anosmia - Can’t smell

211
Q

CN 2
What is it?
How does CN2 Palsy present?

A

Optic
Visual defect - depends on location of lesion!
LEARN

212
Q

CN 3
What is it?
How does CN3 Palsy present?

A

Occulomotor
Ptosis - drooping eyelid
Fixed dilated pupil
Eye down and out

213
Q

What might cause a CN3 palsy?

A

↑ICP
DM
HTN
Giant cell arteritis

214
Q

CN 4
What is it?
How does CN4 Palsy present?

A

Trochlea
Diplopia when looking down (e.g. walking downstairs)

215
Q

CN 5
What is it?
How does CN5 Palsy present?

A

Trigeminal
Jaw deviates to side of lesion
Loss of corneal relex

216
Q

CN 7
What is it?
How does CN7 Palsy present?

A

Facial
Facial droop and weakness (BELL’S)
Dribbling at side of mouth

217
Q

CN 8
What is it?
How does CN8 Palsy present?

A

Vestibulocochlear
Hearing impairment, Vertigo, Lack of balance

218
Q

Causes of CN8 Palsy?

A

Local tumours - if tumour in internal acoustic meatus, will press on CN7+8
Skull fracture - CN8 close to bone
Ear infections

219
Q

CN 9 + 10
What is it?
How does CN 9 + 10 Palsy present?

A

Glossopharyngeal + Vagus
Gag reflex issues
Dysphagia - Uvula deviates AWAY from side of lesion
Vocal issues

220
Q

Which might cause a CN 9 +/- 10 lesion?

A

Jugular foramen lesion

221
Q

CN 11
What is it?
How does CN11 Palsy present?

A

Accessory
Sternocleidomastoid and Trapezius palsy
Can’t shrug shoulders or shake head

222
Q

CN 12
What is it?
How does CN12 Palsy present?

A

Hypoglossal
Tongue deviates towards side of lesion

223
Q

Types of Dementia

A

Alzheimer’s - MC !! (50%)
Vascular
Lewy-Body
Fronto-Temporal

Can be mixed - more than one cause

224
Q

Epilepsy
What must we do once a patient has been diagnosed?

A

Must inform DVLA!!!
Can’t drive until seizure free for one year!!

225
Q

What’s another name for Fronto-Temporal Dementia?

A

Pick’s

226
Q

RF Alzheimer’s

A

↑ Age - usually develops after 60
FHx
Mutations in amyloid precursor protein
Apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian
Down’s

227
Q

Pathophysiology Alzheimer’s

A

Beta amyloid plaques and neurofibrillary tangles accumulate causing neuronal death
Also, loss of ACh

228
Q

Signs / Symptoms Alzheimer’s

A

4 A’s

Amnesia - recent mems lost first
Aphasia - speech muddled/disjointed
Agnosia - recog problems
Apraxia - can’t carry out fine/skilled tasks despite normal motor function
–
gradual onset!

229
Q

Ix Alzheimer’s

A

MRI !!
Degen of cerebral cortex w/ Cortical atrophy

230
Q

Tx Alzheimer’s

A

Acetylcholine inhibitor e.g. Donepezil, Rivastigmine
Memantine
Social support

231
Q

Onset of Alzheimer’s

A

Gradual

232
Q

What is Fronto-Temporal Dementia?

A

Atrophy to frontal and temporal lobes!

233
Q

Presentation Fronto-Temporal Dementia

A

Onset BEFORE 65
Memory + Visuospatial skills are preserved
Personality changes and social conduct problems !!

234
Q

Onset of Fronto-Temporal Dementia

A

Insidious onset
Rapid progress

235
Q

Tx Fronto-Temporal Dementia

A

Supportive

236
Q

What is Vascular dementia?

A

Brain damage from a cerebroVASCULAR disease

237
Q

RF Vascular Dementia

A

Hx of Stroke/TIA
HTN
DM
Smoking
Obesity
Coronary hear disease
FHx of Stroke

238
Q

Signs / Symptoms Vascular Dementia

A

STEPWISE DETERIORATION OF COGNITION - w short periods of stability
Attention deficits
Loss of exec function (kinda like organising, scheduling, memory - stuff for work)

239
Q

Ix Vascular Dementia

A

MRI - infarcts

240
Q

Tx Vascular Dementia

A

↓ RF

241
Q

Pathophysiology Lewy-Body Dementia

A

ALPHA-SYNUCLEIN AGGREGATES
form Lewy body deposits within neurons

Found in substantia nigra and cortex!!

242
Q

Signs / Symptoms Lewy-Body Dementia

A

After onset of dementia, PARKINSONISM follows ! :(

Cog fluctuations
Visuospatial abilities impaired
REM sleep affected
Visual hallucinations
↑↑Exec dysfunction!

243
Q

Ix Lewy-Body Dementia

A

Usually clinical diagnosis

244
Q

Onset of Vascular Dementia

A

Abrupt OR Gradual

245
Q

Onset of Lewy-Body Dementia

A

Insiduous

246
Q

Tx Lewy-Body Dementia

A

Acetylcholinesterase inhibitors - rivastigmine, donepexil

Memantine

247
Q

Typical age of onset Lewy-Body Dementia

A

50+

248
Q

Vascular Dementia typical age of onset

A

65+

249
Q

What is Huntingtons Disease?

A

Autosomal dominant neurodegen movement disorder
FULL PENETRANCE - all gene carriers WILL get the disease

250
Q

Pathophysiology Huntington’s

A

↑ CAG repeats !
< 28 = normal
28 - 35 - high risk
> 36 = DIAGNOSTIC !
–
CAG repeats form faulty protein
This protein builds up in striatum
∴ cell death + loss of cholinergic + GABA-nergic neurons
∴ ↓ACH and ↓ GABA synthesis in striatum

↓ GABA = less regulation of dopamine
∴ XS dopamine
∴ chorea

251
Q

What is Chorea?

A

Continuous flow of involuntary, jerky, semi-purposeful movements
Cease during sleep

252
Q

Huntingtons - If early onset i.e. from childhood, how many CAG repeats would we expect to see?

A

60+

253
Q

Define Anticipation in terms of Huntington’s

A

More repeats each generation

254
Q

If ONE parent has Huntington’s, what’s the chance of the child getting it?

A

50%
ONLY IF THEY HAVE THE GENE THEY WILL GET IT

255
Q

Presentation Huntington’s

A

1st Phase
Depression
Incoordination
Personality change

2nd Phase
Chorea
Abnormal eye movement
Loss of coord
Dysarthria
Dementia
Depression
Rigidity

256
Q

Ix Huntington’s

A

PCR testing - shows CAG repeats

MRI/CT - shows atrophy of striatum (caudate and putamen)

257
Q

Tx Huntington’s

A

No cure.

Symptoms management =
FOR CHOREA - Antipsychotics e.g. Risperidone or Tetrabenazine

FOR DEPRESSION - SSRI e.g. Sertraline

FOR AGGRESSIVE BEHAVIOUR - Antipsychotics e.g. Risperidone

258
Q

Most common death of Huntington’s :(

A

Suicide :((( rlly rlly sad :(
Aspiration pneumonia also common cause

259
Q

MOA Risperidone

A

Dopamine receptor antagonists

260
Q

MOA Tetrabenazine

A

Depletes dopamine

261
Q
A

Phase 2 Quick (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions