Brainscape's Knowledge GenomeTM

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


See full index

Year 6 > Neuro > Flashcards

Neuro Flashcards

1
Q

imaging used in strokes

A

non contrast CT, carotid dopplers

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

scoring systems used in stroke

A

NIHSS

ROSIER - both used acutely to assess severity and guide tx

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

On non contrast CT, difference in appearance of ischaemic vs haemorrhage

A

ischaemia - patch of darker grey

haemorrhage - bright white

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

Mx haemorrhagic stroke (SAH)

A

nimodipine - 60mg every 4h for 21d
1st - coiling
2nd - surgical clipping - need craniotomy

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

Mx ischaemic stroke

A

CT- exclude haemorrhage

Aspirin 300mg OD/PR 2 weeks.
No AF - clopidogrel 75mg OD life + statin
AF - apixaban + statin

<4.5h - thrombolysis (alteplase)
<4.5h and occluded proximal anterior circulation - thrombolysis and thrombectomy
<6h - thrombectomy

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

Parkinsons core symptoms

A

Bradykinesia
Hypertonia
Tremor

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

(Parkinson plus syndromes)

Multiple Systems Atrophy (MSA) / Shy-Drager Syndrome

S+S

A

Autonomic dysfunction (postural hypotension, bladder dysfunction)

Cerebellar ataxia

Rigidity > tremor

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

(Parkinson plus syndromes)

Progressive Supranuclear Palsy (PSP)

S+S

A

Vertical gaze palsy

Postural instability – falls

Speech disturbance, dementia

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

(Parkinson plus syndromes)

Corticobasilar Degeneration (CBD)

S+S

A

Unilateral parkinsonism

Aphasia

Astereognosis (cortical sensory loss) – alien limb phenomenon

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

(Parkinson plus syndromes)

Dementia with Lewy Bodies (DLB)

S+S

A

Visual hallucinations

Fluctuating cognition

Dementia – parkinsonism

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

Difference between Parkinsonism and Parkinson’s disease

DPR - distribution, progression, response

A

Parkinsonism is a general term that refers to
a group of neuro disorders that cause movement problems similar Parkinson’s disease e.g. tremors, slow movement and stiffness

Distribution - symmetrical
Progression - rapid
Response - poor response to levodopa

Parkinson’s disease is a neurodegenerative brain disorder that progresses slowly
Distribution - asymmetrical
Progression - slower
Response - good response to levodopa

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

PD Mx

A

MDT, physio, depression screen

1st

  • levodopa
  • SINEMET/ co-careldopa = Levodopa + Carbidopa . (Combined with dopa decarboxylase inhibiters)
  • MADOPAR = levodopa + benserazide
  • MAO-B inhibitors (i.e. selegiline)
  • DA agonists (i.e. pramipexole, ropinirole)

2nd adjuncts

  • COMT inhibitors e.g. entacapone (peripheral) tolcapone (central and peripheral)
  • give with Levodopa to improve compliance but may increase SE
  • Amantadine (PO; nicotinic antagonist, DA agonist, non-competitive NMDA antagonist)
  • Apomorphine (SC; DA agonist)
  • Deep brain stimulation (of subthalamic nucleus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PD ix

A

CT MRI - rule out vascular

DaTScan = Dopamine Transporter scan - Can exclude other causes of tremor

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

Causes of Parkinsonism

A

drug induced
e.g. antipsychotics, some CCB, cocaine, amphetamines

Other neurodegenerative disorders e.g.multiple system atrophy, Lewy body dementia and progressive supranuclear palsy

Vascular Parkinsonism

Depression - Severe psychomotor retardation can give a parkinsonian appearance, with slow movements and loss of facial expression.

Tumour

Repeated head trauma

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

What medications to avoid in PD

A

metoclopramide, haloperidol

dopamine antagonists

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

Side effects of levodopa

A

DOPAMINE

Dyskinesia
On/off phenomena
Psychosis
Arterial BP down
Mouth dryness
Insomnia 
N&V
Excessive daytime sleepiness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does the Dopa decarboxylase inhibitor help do with levodopa?

Indications?

A

Prevents levodopa being broken down peripherally, but doesn’t cross the BBB allowing levodopa to be broken down releasing dopamine in the brain.

Predominant motor symptoms, less side effects

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

Criteria for epilepsy

A

2 or more epileptic seizures or

1 seizure with epileptogenic markers (EEG or brain malformation)

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

you do not treat the first episode of seizure unless

A

abnormal brain architecture (i.e. MRI) or EEG findings

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

S+S/ stages of tonic clonic seizure

A

1st - behavioural arrest (i.e. stop writing, stop talking)

2nd - head and eyes turn to one side (it looks painful) – the side they turn is the opposite side to the lesion

3rd - Stiffening

4th - Shaking

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

What increases chances of seizure

A

[STRESS]

– ETOH, insomnia,
medications, recreational drugs, trauma, infection, etc.

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

Epilepsy Ix

A

A-E - including glucose, consider pabrinex

  • ECG - cardiac causes
  • MRI - structural causes
  • prolactin - distinguishes dissociative seizure from true CNS seizure (raised in central seizures)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Epilepsy Mx

Tonic clonic (during seizure)

A

Tonic-clonic seizure:

  • 1 = Buccal midazolam, PR diazepam / IV lorazepam if IV access
  • 2 = IV lorazepam
  • 3 = IV phenytoin (phenobarbital if already on regular phenytoin)
  • Rapid sequence induction of anaesthesia using thiopental sodium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When to admit a patient with a seizure

A
  • Poor initial response
  • First seizure
  • Status epilepticus
  • high risk of recurrence (hx of recurrent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Epilepsy Mx

Focal seizure (during seizure)

A

Focal seizure:
• Conservative measures
• Admission if first seizure or lasts longer than 5 minutes

• Review patients once a year

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

Definition of status epilepticus

A

STATUS EPILEPTICUS

- ≥5 minutes OR >3 seizures in an hour (no recovery in between)

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

LT Mx of tonic clonic seizure

A

1st line = valproate

2nd = lamotrigine

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

LT Mx of absence seizure

A

1st line = valproate, ethosuximide

2nd = lamotrigine

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

LT Mx of tonic, atonic or myoclonic seizure

A

1st line = valproate

2nd = levetiracetam

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

LT Mx of focal seizure

A

1st line = lamotrigine

2nd = CBZ

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

SE carbamazepine

A

Hyponatraemia

Rash

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

SE Valproate

A

VALPROATE

V = Vomiting, nausea 
A = Anorexia 
L = Liver toxicity 
P = Pancreatitis 
R = Retain weight 
O = Oedema
A = Alopecia 
T = Teratogen, tremors
E = Enzyme inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

SE levetiracetam

A

mood changes

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

SE Lamotrigine

A

SJS

Dizzy

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

SE phenytoin

A

Enzyme inducer

gum hypertrophy

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

Which part of brain is affected first in Alzheimers

A

hippocampus

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

3 theories for AD

A

Amyloid - beta amyloid protein forms toxic aggregates

Tau - tau tangles cause damage to neurones

Inflammation - microbial cells increased phagocytosis and decrease levels of neuroprotective proteins

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

RF for AD

A

Biological:

  • Age
  • Genetics (92% sporadic though) - Presenilin 1 and 2, Downs, APEN, APP, ApoE
  • Head injury
  • Vascular RF e.g. HTN

Psychosocial

  • Low IQ
  • Poor educational level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

S+S are due to which 4 elements of pathophysiology

A
  • Atrophy (neurone loss)
  • Plaque formation
  • Neurofibrillaty tangle formation
  • Cholinergic loss§
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

S+S presentation of AD

A

4As

Amnesia
- recent memories first, disorientation

Aphasia
- difficulty finding correct words, speech muddled

Agnosia
- visual e.g prosopagnosia

Apraxia
- dressing, skilled tasks

BPSD = mood change, abnormal behaviour, hallucination/ delusion

Psychiatric presentations - delusions, depression, GAD

Behavioural disturbances - aggression, wandering, sexual disinhibition, explosive temper

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

Dementia Ix

A
  • GPCOG
  • AMTS (<8/10)
  • MMSE (20-24 = mild dementia, 13-20 = moderate dementia, and <12 = severe dementia.

Bloods
- LFT, TFT, U+E, HbA1c, B12 and folate

MRI CT

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

Prognostic factors in AD

A

Good - female

Bad - male, depression, behavioural problems, severe focal cognitive defect

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

AD Mx

A

Biological - start low, go slow

1st = anticholinesterases (mild-moderate)

  • Donepezil (reversible)
  • Galantamine (reversible)
  • Rivastigmine (pseudo-reversible)

2nd = NMDA glutamate partial receptor agonist (moderate, 1st line in severe)
- Memantine

Psych
1st = structural group cognitive stimulation sessions (mild-mod)

  • exclude GAD/ depression
  • multisensory therapy
  • group reminiscence therapy
  • validation therapy

Social

  • explain diagnosis
  • optimising health e.g. hearing, vision
  • identify future wishes e.g. AD, LPA
  • carers
  • social support
  • FU every 6m with yourself and a dingle care managed
  • DVLA, insurers

General

  • wear ID
  • dossed boxes
  • change gas to electricity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Anticholinesterases - must check

A

ECG

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

Anticholinesterases SE

A

GI - NV, diarrhoea, anorexia

fatigue, dizziness, headache

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

Anticholinesterases absolute CI

A

anticholinergics (block ACh from binding)

BB

NSAIDs

muscle relaxants

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

Migraine S+S, Mx

A

unilateral, throbbing, severe, 4-72h

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

Migraine Mx

acute, prophylaxis

A

Acute
- oral triptan + NSAID/ paracetamol

Prophylaxis
- topiramate/ propanolol (only if >2 attacks a month)

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

Cluster headache S+S,

A

Intense pain around eye, watering; last 15m-2hrs

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

Cluster headache Mx

acute, prophylaxis

A

Acute: 100% O2, SC triptan
Prophylaxis: verapamil

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

Temporal arteritis S+S

A

Headache, jaw claudication, tender scalp

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

Temporal arteritis Mx

A

Oral prednisolone

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

Medication-overuse headache S+S and Mx

A

≥15 days / month, worsened with medication

stop meds

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

Define MS

A

an autoimmune demyelinating disorder of the CNS characterised by multiple plaques of separate in time and space

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

Classification of MS

A

Relapsing remitting
Primary progressive
Secondary progressive
Progressive relapsing

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

S+S of MS

A

TEAM

Tingling
Eye / optic neuritis
Ataxia (and other cerebellar signs DANISH)
Motor (spastic paraparesis)

INO

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

What is Lhermitte’s sign

A

Neck flexion –> electric shocks in trunk or limb

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

What is Uhthoff’s sign

A

temporary worsening of MS symptoms with increased temperature – i.e. a hot bath, exercise

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

What is INO

A

lesion in the medial longitudinal fasciculus (MLF) connecting CN6 to CN3 (and CN 4) which has S/S of weak adduction of ipsilateral eye and nystagmus of the contralateral eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Criteria for MS

A

McDonald criteria - demonstrating lestions disseminated in time and space

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

MS Ix

A

o Contrast MRI (gadolinium-enhanced, T2-weighted)

o LP (IgG oligoclonal bands)

o Blood antibodies:

  • Anti-MBP (myelin basic protein)
  • NMO-IgG (neuromyelitis optica)  Devic’s syndrome (S/S: MS + transverse myelitis + optic atrophy)

o Evoked potentials

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

MS differentials

A 
stroke
tumour 
CNS sarcoidosis 
SLE
Devic's syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

MS Management

ACute
chronic
Sx Mx

A

Acute
- methyprednisolone 1g IV/PO OD for 3d

Chronic

  • DMARDs - IFN beta
  • Biologics - natalizumab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

MS symptom management

Drug for
Fatigue

A

modafinil

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

MS symptom management

Drug for
Depression

A

SSRI

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

MS symptom management

Drug for pain

A

amitryptiline, gabapentin

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

MS symptom management

Drug for spasticity

A

baclofen + gabapentin

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

MS symptom management

Drug for urgency/ frequency

A

oxybutynin, tolterodine

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

MS symptom management

Drug for
tremor

A

clonazepam

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

MS good and bad prognostic factors

A

Good

  • female
  • <25yo
  • sensory signs at onset
  • long interval in relapses
  • few MRI lesions

Bad

  • male
  • older
  • motor signs at onset
  • short interval in relapses
  • many MRI lesions
  • axonal loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Myasthenia gravis definition

A

Autoimmue disorder characterised by insufficient functioning NACh receptors

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

Myasthenia gravis antibody

A

Anti-ACh-R in 85-90% cases

Anti muscle specific receptor TK AB 40%

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

Myasthenia gravis associations

A

15% thymoma
50-70% thyme hyperplasia
AI disease e.g. RA, SLE, AI thyroid

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

MG S+S

A

Muscle fatiguability
Extraocular (diplopia, ptosis), bulbar, face and neck muscles affected

Proximal myopathy - face neck, limb girdle

Dysphagia

Reflexes normal

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

MG Exacerbating drugs

A 
Penicillamine
BB
Quinidine, procainamide
Lithium 
Phenytoin
Abx - gentamicin, macrolides, quinolones, tetracyclines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Causes of myasthenia crisis

A

emotion, exercise, hypokalaemia, drugs e.g. opiates, BB, abx

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

What happens in myasthenia crisis

S+S

A

RESP FAILURE
risk of sudden apnoea: FVC ≤1L, negative inspiratory force ≤20cmH2O, need ventilation

S+S
- decreased RR
- accessory muscle use
weak cough

78
Q

myasthenia crisis Ix

A

ABG (hypercapnia before hypoxia)

FVC

79
Q

myasthenia crisis Mx

A

Plasmapheresis
IVIG
intubation

80
Q

MG Ix

A
  • single fibre EMG >92% sensitivity
  • Repetitive nerve stimulation (test fatiguability)
  • Serial pulmonary function testing (test fatiguability)
  • Ice pack test - ice pack on affected eyelid - temporary resolution = positive (80% positive rate)

TFTs

81
Q

MG Mx

A

Crisis - IVIG and plasmapheresis

1st line symptomatic - long acting AChE inhibitor
- pyridostigmine, neostigmine

1st line LT control -
- prednisolone
2nd - azathioprine, cyclosporine, mycophenolate mofetil

surgery
- thymectomy

82
Q

Lambert eaton myasthenic syndrome seen in associated with

A

SCLC and breast and ovarian cancer

83
Q

Lambert eaton myasthenic syndrome S+S

A
  • repeated muscle contractions lead to increased muscle strength (in 50% pt)
  • limb girdle weakness (lower limbs first)
  • hyporeflexia
  • ANS symptoms (dry mouth, impotence, difficulty micturating)
  • eye signs rare
84
Q

Lambert eaton myasthenic syndrome Ix

A

EMG

Incremetnal response to repetitive electrical stimulation

85
Q

Lambert eaton myasthenic syndrome Mx

A

Treat cancer

immunosuppression (pred ± azathioprine)

86
Q

MND definition

A

motor neurone loss from cortex, brainstem, spinal cord and ant. horn cells of spinal cord

87
Q

MND classification

A

50% amyotrophic lateral sclerosis

30% primary lateral sclerosis

10% progressive muscular atrophy

10% progressive bulbar palsy

88
Q

MND amyotrophic lateral sclerosis

where is affected?
S+S UMN or LMN?

A

Corticospinal tracts

Mixed UMN LMN

89
Q

MND primary lateral sclerosis

where is affected?
S+S UMN or LMN?

A

Loss of Betz cells in the motor cortex

UMN mainly – spastic leg weakness and pseudo bulbar palsy (CN5, 7, 9-12), no cognitive decline

90
Q

MND Progressive Muscular Atrophy

where is affected?
S+S UMN or LMN?

A

Anterior horn cell lesions

LMN mainly - distal to proximal signs

91
Q

MND progressive bulbar palsy

where is affected?
S+S UMN or LMN?

A

Cranial nerves 9-12

Bulbar palsy

92
Q

MND type with best prognosis

A

Progressive muscular atrophy

93
Q

MND type with worst prognosis

A

Progressive bulbar palsy

94
Q

Difference between bulbar and pseudo bulbar palsy

A

Bulbar = LMN signs
CN 9-12

Pseudobulbar = UMN signs
CN 5, 7
CN 9-12

95
Q

MND S+S

A

S+S
Mixed UMN and LMN

Neuro exam 
	Inspection (wasting & fasciculations – esp. tongue)
	Tone (spastic)
	Power (weak)
	Reflexes (absent, extensor plantars) 
	Sensation (NORMAL)

Cranial nerves:
 Speech (bulbar = nasal; pseudobulbar = hot potato)
 Jaw-jerk (bulbar = absent; pseudobulbar = brisk)
 Eye movements (NORMAL; preserved until very late)

96
Q

Differentials for mixed UMN LMN signs

A

MAST

  • MND
  • Ataxia (Friedrich’s)
  • SCDC (subacute degeneration of the spinal cord)
  • Taboparesis
97
Q

MND Ix/ criteria

A

Diagnostic criteria = revised el Escorial criteria

  • MRI brain/ spinal cord - exclude structural causes
  • EMG (fasciculations)
  • LP - exclude inflammatory conditions
98
Q

MND Mx

A

MDT - neurologist, physio, OT, dietician, GP, specialist nurse

  • Riluzole - extends life by ~3 months
  • Supportive

Drooling - amitriptyline

Resp failure - NIV

Dysphagia - NG/PEG

Spasticity - Baclofen, botulinum

Pain - analgesic ladder

99
Q

Guillan Barre S defintion

A

immune-mediated demyelination of the peripheral nervous system often triggered by an infection (often C. jejuni

100
Q

GBS Initial Sx

Characteristic features

A

65% initially get back/leg pain

o Progressive symmetrical weakness of all limbs
o Ascending weakness (legs affected first)
o Reflexes reduced or absent
o Sensory sx mild e.g. digital paraesthesia with very few sensory signs

• Other features – Hx gastroenteritis, resp muscle weakness, CN involvement diplopia, bilateral facial nerve palsy, oropharyngeal weakness, autonomic involvement e.g. urinary retention and diarrhoea

101
Q

GBS Ix

A

LP = 66% have rise in protein, normal WCC

o Nerve conduction studies – decreased motor nerve conduction velocity (demyelination

102
Q

GBS Mx

A

IVIG

Plasmapheresis

103
Q

Causes of UMN lesion in cortex

A 
functinal
abscess
CVA
tumour 
demyelination
104
Q

Causes of UMN lesion in spine

A 
MS
compression
trauma 
MND (some LMN)
Syringomelia (some LMN)
105
Q

Causes of UMN lesion - anterior horn cell disease

A

spinal muscular atrophy
polio
MND (ALS)

106
Q

UMN bilateral (spastic paresis) causes

A

MS
cord compression
cord trauma
cerebral palsy

107
Q

UMN unilateral hemicord causes

A

MS

cord compression

108
Q

UMN unilateral hemisphere causes

A

MS
stroke
SOL
cerebral palsy

109
Q

Mixed UMN LMN cause

A 
MAST
MND
Ataxia (Friedrich's)
Subacute demyelination of the spinal cord (low b12)
Taboparesis
110
Q

LMN peripheral neuropathy
Predominantly motor

causes

A

Infection e.g. GBS, Polio

Metabolic e.g. porphyria, lead poisoning

congenital (Charcot marie tooth)

Autoimmune./ infection = hepatitis, SLE

111
Q

LMN peripheral neuropathy
Predominantly sensory

causes

A

Infection - leprosy

Metabolic - DM, ETOH, amyloid, uraemia

congenital - Charcot marie tooth

Autoimmune/ metabolic / iatrogenic - vitamin B12 deficiency. isoniazid

112
Q

LMN peripheral neuropathy sensory and motor

causes

A

Alcoholic neuropathy - toxic effects and reduced B vitamin absorption
Sensory –> motor

V B12 deficiency - SCDC - dorsal columns affected first – decreased joint position, vibration sense – later get distal paraesthesia

113
Q

LMN

Proximal myopathy causes

A

Autoimmune - MS, polymyositis

Iatrogenic/ drugs - ETOH, statins, steroids

Neoplastic - paraneoplasm (detmaomyositis, LEMS)

congenital - muscular dystrophy

Endo - cushings, hyperthyroid, acromegaly, osteomalacia, diabetic amyotrophy

114
Q

LMN

Hand wasting causes

A

Anterior horn cell - syringomyelia, MND, polio

Roots (C8, T1) - spondylosis

Brachial plexus - compression by cervical rib, avulsion e.g. Klumpke’s palsy

Neuropathy - hereditary sensory motor neuropathy, mononeuritis multiplex, DM

Muscle - disuse RA, myopathy - myotonic dystrophy

115
Q

Charcot marie tooth types

A

hereditary sensory motor neuropathy 1 and 2

116
Q

Charcot marie tooth types S+S

A

inspection

  • pes cavus
  • distal muscle wasting
  • thickened nerves esp common perineal
  • BL symmetrical distal LMN features – foot drop, high stepping gait, absent ankle jerks
  • stocking distribution loss of sensation
117
Q

Charcot marie tooth Ix

A

nerve conduction studies

  • HSMN1 = demyelination– ↓ conduction velocity
  • HSMN2 = axonal degeneration – ↓ conduction amplitude

Genetic testing (HSMN1 PMP22 gene)

118
Q

Cerebellar syndrome S+S

DANISH

A

Dysdiadochokiensia, dysmetria, dysarthria

Ataxia

Nystagmus

Intention tremor

Speech - scanning, staccato

Hypotonia

119
Q

Cerebellar syndrome

causes

VITAMIN CD

A

Vascular = (vertebrobasilar) stroke

Infection = encephalitis, abscess

Trauma —- raised ICP

Autoimmune - MS, paraneoplasic cerebellar degeneration

Metabolic - ethanol, poisons e.g. phenytoin

Neoplastic - posterior fossa tumour

Degeneration - spinocerebellar ataxia

120
Q

Nystagmus

cerebellar cause/ vestibular cause

  • Fast phase to or away from lesion?
  • Maximal looking toward or away from lesion?
A

Cerebellar = Close

fast phase towards lesion
maximal looking towards lesion

Vestibular = V far

fast phase away from lesion
maximal looking away from lesion

121
Q

Cerebellar syndrome Ix

A

o Bloods

  • ETOH
  • FBC, UE, LFT
  • clotting (thrombophilia)
  • Wilsons (low ceruloplasmin)

o ECG (arrhythmia)

o CSF (oligoclonal bands)

o MRI (posterior cranial fossa)

o Pure tone audiometry (CPA lesion)

122
Q

Spinocerebellum

where are the lesions

A

midline cerebellar lesions

123
Q

Neocerebellum

where are the lesions

A

Lateral cerebellar lesions

124
Q

Spinocerebellum

controls
S+S

A

movement sand posture

truncal ataxia

125
Q

Neocerebellum

controls
S+S

A

motor planning

limb coordination

dysmetria, intention tremor, dysdiadochokiensia

126
Q

Vestibulocerebellum

controls
S+S

A

balance and vision

diplopia, nystagmus, vertigo

127
Q

Lateral medullary syndrome occurs after

A

occlusion of the posterior inferior cerebellar artery

128
Q

Lateral medullary syndrome S+S

A

o Cerebellar:

  • Ataxia
  • Nystagmus

o Brainstem:

  • Ipsilateral: dysphagia, facial numbness, cranial nerve palsy (HORNERS – miosis, anhidrosis, ptosis)
  • Contralateral: limb sensory loss
129
Q

Marcus-Gunn (RAPD)

what is it
causes

A

The afferent pathway of the eye is disrupted which leads to a non-responsive direct stimulation and a responsive indirect stimulation (light in opposite eye)

MS, glaucoma, retinal disease

130
Q

Argyll Robertson pupil

what is it
causes

A

Small, irregular pupils

ARP – Accommodation Reflex Present

PRA– Pupillary Reflex Absent

Diabetes, neurosyphilis

131
Q

Holmes-Adie Pupil

Adie Tonic Pupil

A
  • Dilated pupil (Holmes has a dilated ego)
  • Poorly reactive (accommodation and light)

Idiopathic

132
Q

3rd nerve palsy S+S

A

o ‘Down and out’
o Ptosis
o Dilated pupil (aka: surgical 3rd nerve palsy – due to compression on peripheral PNS fibres)

133
Q

3rd nerve palsy causes

A

DM

Vasculitis (GCA, SLE)

Uncal herniation through tentorium (raised ICP)

Posterior communicating artery aneurysm

Cavernous sinus thrombosis

Amyloid, MS

Weber’s syndrome:

134
Q

What is weber’s syndrome

A

ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain strokes

135
Q

Clostridium botulinum infection

RF
S+S
Mx

A

o RF: IVDU
o S/S: descending paralysis, diplopia, bulbar palsy
o Mx: botox antitoxin

136
Q

Normal pressure hydrocephalus

Onset
S+S

A

quick

“wet, wobbly, wacky” (incontinent, falls, dementia

137
Q

Syringomyelia

causes

A

chiari malformation, trauma, tumours, idiopathic

138
Q

Syringomyelia

S+S

A
  • ‘cape-like’ (neck and arms) loss of sensation to pain & temperature

(preserved light touch, proprioception, vibration)

139
Q

Paroxysmal hemicrania

S+S

A

Cluster headache presentation

140
Q

Paroxysmal hemicrania

Mx

A

Indomethacin (completely resolves)

141
Q

Horner’s syndrome S+S

A

Ptosis, mitosis, anhidrosis, enopthalmos

142
Q

Horner’s syndrome Ix

A

differentiating causes

  • heterochromia (congential horners)
  • anhidrosis presence
143
Q

Degenerative cervical myelopathy aetiology

A

cervical spondylosis

144
Q

Degenerative cervical myelopathy S+S

A
  • Pain neck and limbs
  • Loss of ANS function (incontinence, impotence)
  • Loss of motor function (loss of digital dexterity)
  • Loss of sensory function (numbness)
  • Hoffmans +ve (flick nail of middle finger and there’s flexion of index/ thumb)
145
Q

what is cervical spondylosis

A

age related wear and tear to spinal discs in neck - discs shrink, OA Sx

146
Q

Degenerative cervical myelopathy Ix

A

cervical spine MRI - disc degeneration and ligament hypertrophy, with accompanying cord signal change

147
Q

Degenerative cervical myelopathy Mx

A

Urgent referral (neurosurgery or orthopaedic spinal surgery)

– early <6m decompression surgery

148
Q

Acute meningitis S+S

A

fever
neck pain
confusion

149
Q

Acute meningitis causes

Neonates
Children
Adults

A

Bacterial is most common

Neonates

  • GBS
  • Listeria
  • E coli

Children

  • H influenzae
  • S pneumoniae
  • N meningitidis

Adults

  • S pneumonia
  • N meningitides

Older - Listeria monocytogenes

150
Q

Acute meningitis Mx

A
  • S pneumoniae, N meningitidis –> IV ceftriazone + IM benzylpenicillin (in community)

Elderly (listeria)
- IV amoxicillin/ ampicililn

Neonate (listeria, E coli)
- IV cefotaxime + IV amoxicillin

151
Q

Chronic meningitis causes

A

TB, syphillis, cryptococcus (immunosuppressed)

152
Q

Chronic meningitis Mx

A

Tx cryptococcus neoformans with Ambisome ± flucytosine

153
Q

Viral meningitis causes

A

Enterovirus (Coxsackie A and B, echovirus)

154
Q

Viral meningitis Mx

A

children - self limiting 1-2 weeks

155
Q

Encephalitis S+S

A

Meningitis Sx: Meningism - headache stiff neck, photophobia
Confusion
Fever

+

Focal neuro deficit
Altered mental state

156
Q

Encephalitis causes

UK

Worldwide

A

UK - HSV2

Worldwide - arboviruses, West Nile virus

157
Q

Encephalitis Tx

A

often treat as ‘meningoencephalitis’ as you cannot differentiate them

o IV aciclovir (10mg/kg, TDS) + IV ceftriaxone (2g, BD) ± IV amoxicillin (immunocompromised or >50yo)

158
Q

Cerebral abscess S+S

A
  • fever

- raised ICP (seizures, papilloedema, localising signs)

159
Q

Where are bacterial abscesses

A

peripheral

160
Q

where are Toxoplasma abscesses

A

deeper; basal ganglia

161
Q

Cerebral abscess Ix

A

ESR
WCC
CT MRI- ring enhancing lesion

162
Q

Cerebral abscess mx

A

urent neurosurgical referral

163
Q

Status epilepticus definiton

A

= a seizure that lasts for ≥30 minutes (or multiple seizures in <30 minutes)

164
Q

Status epilepticus

Early status
Established status
Refractory status timeframe and drugs

A

o Early status = 5-30 minutes

–> lorazepam, usual AED medication

o Established status = 30-60 minutes

–>phenytoin

o Refractory status = ≥60 minutes

–>anaesthesia

165
Q

Status epilepticus IX

A

o Initial: CBG, pulse oximetry, cardiac monitor

o Once treatment started: lab glucose, ABG, U&Es, Ca2+, FBC, ECG

o Consider: anticonvulsant levels, toxicology, LP, CT/MRI, urine/blood culture, EEG, CO levels

166
Q

Status epilepticus Mx

A

0 minutes

  • buccal midazolam OR
  • PR diazepam OR
  • IV lorazepam (0.1mg/kg; preferable if IV access)

10-20 minutes

  • IV lorazepam (0.1mg/kg; bolus)
  • anaesthetic help if ≥20 minutes

30 minutes

  • IV phenytoin (15-18mg/kg at 50mg/minute)
  • OR IV phenobarbitone

60 minutes
- Rapid induction anaesthesia (i.e. propofol + ventilation)

167
Q

Head injury + pupils unequal … what do you do

A

diagnose high ICP (i.e. extradural haemorrhage)

neurosurgical emergency

168
Q

Head injury Ix / Mx

A

o ABCDE (if GCS ≤8, intubate)

o Assess events (retrograde + anterograde amnesia)

o Examine CNS

o Early involvement of anaesthetics and ITU

169
Q

Head injury

- when to do CT Head immediately

A
  • GCS (<13 on initial assessment; <15 at 2 hours post-injury)
  • Fracture (suspected open or depressed skull fracture or basal skull fracture)
  • Hemotympanum, ‘panda’ eyes, CSF leakage from ear/nose, Battle sign
  • Seizure (post-traumatic)
  • Focal neurological deficit
  • Vomit >1
170
Q

Head injury

- when to do CT Head soon <8h (if some LOC or amnesia since injury) AND ….

A

ABCD

  • Age ≥65
  • Bleeding or clotting disorders (incl. current anticoagulation medication)
  • (Re-)Collection of events before (>30 minutes’ retrograde amnesia of events before the head injury)
  • Dangerous mechanism of injury:
    • Pedestrian or cyclist struck by a motor vehicle
    • An occupant ejected from a motor vehicle
    • Fall from a height >1m or 5 stairs
    o CT spine immediately (<1 hour):
171
Q

Head injury

- when to do CT Spine immediately <1h

A
  • GCS <13 on initial assessment
  • Patient intubated
  • Ruling out needed (i.e. for surgery)
  • Clinical suspicion and…
    • Age ≥65yo • High-impact injury
    • Focal neurological deficit • Paraesthesia in limbs
172
Q

Head injury Cx

A

Early:

  • Extradural / Subdural haemorrhages
  • Seizures

Late:

  • Subdural haemorrhage
  • Seizures
  • Diabetes insipidus
  • Parkinsonism
  • Dementia
173
Q

Normal ICP

A

<15mmHg

174
Q

Raised ICP causes

A

o Tumours (primary, metastatic)
o Head injury
o Haemorrhage (subdural, extradural, subarachnoid, intracerebral, intraventricular)
o Infection (meningitis, encephalitis, brain abscess)
o Hydrocephalus
o Cerebral oedema
o Status epilepticus

175
Q

Raised ICP S+S

A

o Headache (worst on leaning forward) / vomiting

o Altered GCS, focal neurological deficit

o Trauma history

o Cushing’s response (high BP, low HR), Cheyne-Stokes respiration (period of gradual hyperpnoea then gradual hypopnea then period of apnoea)

o Eye changes:

  • Pupil constriction early –> dilation late
  • Reduced visual acuity, peripheral field loss
  • Papilloedema ± visible venous pulsation LOSS (absent in 50% normally, but LOSS is a useful sign)
176
Q

Raised ICP Ix

A

o U&E, FBC, LFT, glucose, serum osmolality, clotting, BC

o Toxicology screen

o Consider… CXR, CT head –> LP

177
Q

Raised ICP Mx

A

o Urgent neurosurgery referral

o Holding measures:
-Sit up 40 degrees

  • If intubated –> hyperventilate them (reduce PaCO2 –> cerebral vasoconstriction –> reduce ICP)
  • Osmotic agents (mannitol) – n.b. can lead to rebound raised ICP with prolonged use (12-24hrs)
  • Steroids (only useful for oedema surrounding tumours)

o Fluid restriction

178
Q

Cauda Equina Syndrome definiton

A

= a constellation of symptoms due to compression of the Cauda Equina

179
Q

where is then cauda equina

A

L2 and below and film terminale form it

180
Q

Cauda Equina responsible for….

A
  • Lower limb sensation/power

- S2-4 (bladder control, EAS, external genitalia, perianal sensation)

181
Q

Cauda Equina causes

A 
V	
I	abscess 
T	trauma, haematoma 
A
M
I	iatrogenic spinal surgery
N	tumour
C	congenital spinal abnormalities
D	spinal cord disc prolapse (L4/5, L5/S1)
182
Q

Cauda Equina S+S

A
  • Back pain, unilateral/bilateral sciatica (50%)
  • Saddle anaesthesia
  • Urinary retention, urinary/faecal incontinence
  • —- Urinary retention (bladder distension as sensation of fullness lost)
  • —– Urinary incontinence (by loss of sensation when passing urine)
  • —- Faecal incontinence (due to loss of sensation of rectal fullness)
  • Reduced sexual function, lower limb weakness
183
Q

Red flags for Cauda Equina

A

Bilateral sciatica

Saddle anaesthesia

Lower limb weakness

184
Q

White flag for Cauda Equina (too late)

A

Urinary retention or incontinence

185
Q

Cauda Equina Ix

A

Exam

  • lower limb near exam
  • saddle anaesthesia
  • DRE (anal tone, sensation)

Bladder scan (urinary retention)

MRI

186
Q

Cauda Equina Mx

A

PO dexamethasone (if metastatic whilst waiting MRI results)

Decompressive laminectomy (<48h from bladder dysfunction)

187
Q

Spinal cord compression - definition

A

oncological emergency - extradural compression from vertebral body mets - lung, breast and prostate cancer

188
Q

Spinal cord compression S+S

A

o Back pain (earliest, most common, worse on lying down and coughing)

o Above L1 –> UMN signs + sensory level

o Below L1 (as spinal cord ends around L1/2) –> LMN signs + peripheral numbness

o Tendon reflexes = increased below the level of the lesion and absent at the level of the lesion

189
Q

Spinal cord compression Ix

A

Urgent <24h whole spine MRI

190
Q

Spinal cord compression Mx

A

High dose PO/IV dexamethasone ± radiotherapy (frail, multiple lesions) or surgery (non-frail, single/few lesions)

Year 6 (8 decks)

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