Neurology Flashcards

1
Q

Functions of frontal lobe

A
  1. Motor cortex for contralateral side= precentral gyrus
  2. Broca’s area, speech output inferior frontal gyrus
  3. Emotions
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2
Q

Function of parietal lobe

A
  1. Sensory cortex for contralateral side = postcentral gyrus
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3
Q

Functions of temporal lobe

A
  1. Memory

2. Wernicke’s area, comprehension of speech = superior temporal gyrus

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4
Q

Function of occipital lobe

A
  1. Vision
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5
Q

UMN signs (CNS)

A
  • inc tone (spasticity)
  • weakness, no wasting
  • brisk reflexes + clonus
  • upgoing plantars
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6
Q

LMN signs (PNS)

A
  • Reduced tone
  • weakness, wasting, fasciculation
  • reduced or absent reflexes
  • normal plantar
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7
Q

Name and describe the motor tract

A

Corticospinal
UMN in motor cortex (precentral gyrus) -> medulla where it crosses to contralteral side -> spinal level of action -> ventral root (LMN) -> muscle

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8
Q

Name the 2 sensory pathways and what they transmit

A
  1. Spinothalamic- pain and temp (coarse)

2. Dorsal/posterior column- position and vibration (fine)

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9
Q

Describe the spinothalamic pathway

A

Nociceptors or thermoreceptors detect impulse -> dorsal root -> dorsal horn and crosses to contralateral side AT SAME SPINAL LEVEL -> post central gyrus sensory cortex

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10
Q

Describe the posterior/dorsal column pathway

A

proprioceptors or mechanoreceptors detect stimuli -> afferent to dorsal root ganglion/horn -> up to medulla and CROSSES TO CONTRALATERAL SIDE AT MEDULLA-> thalamus-> sensory cortex

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11
Q

Biceps reflex at level

A

C5

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12
Q

Supinator reflex at level

A

C6

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13
Q

Triceps reflex at level

A

C7

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14
Q

Knee Jerk at level

A

L4

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15
Q

Ankle reflex at level

A

S1

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16
Q

What is a negative symptom

A

Partial or complete failure of impulse conduction leading to loss/reduction of function

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17
Q

What are positive symptoms

A

Exaggeration of a physiological phenomenon eg seizure, tremor, trigeminal neuralgia

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18
Q

Hemiplegia

A

severe/complete loss of strength on one side of body

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19
Q

Hemiparesis

A

slight weakness on one side of body

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20
Q

Paraparesis

A

bilateral leg weakness

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21
Q

Spondylosis

A

AGE RELATED degeneration of intervertebral discs

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22
Q

Define MND

A

Progressive DEGENERATION of ANTERIOR horn cells- where UMN from motor cortex synapse and LMN begin -> muscle.

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23
Q

MND presentation

A
U+LMN signs
Widespread fasciculations
NO sensory signs
Men > women
Chronic and BILATERAL symptoms can include speech
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24
Q

DD for MND

A

Cervical myelopathy (spinal cord compression)

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25
Q

Spinal Shock

A

You get ACUTELY UNEXPECTED SIGNS before correct signs develop. IE flaccid paralysis with loss of sensation and then gradually -> spasticity and reflexes ie LMN -> UMN

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26
Q

Guillan-Barre Syndrome Definiton

A

Acute DEMYELINATION of PERIPHERAL nerve roots and nerves typically post viral infection.

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27
Q

GBS typical presentation

A

LMN signs ONLY
sensory deficit
ascending weakness
generalised, bilateral signs

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28
Q

Causes of peripheral neuropathy (7 categories)

A
  1. congenital
  2. metabolic (b12 deficiency)
  3. Toxic (alcohol, drugs)
  4. Endocrine (DM, thyroid)
  5. Inflammatory (GBS)
  6. Neoplastic
  7. Infective (HIV, Lyme)
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29
Q

Define Myasthenia Gravis

A

Autoimmune condition attacking components of NMJ-> weakness and fatigue of skeletal muscle

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30
Q

Typical presentation of Myasthenia

A

Variable incorrect eye movements
Fatiguability
Difficulty swallowing
ADD PIC

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31
Q

Define functional disorders

A

Symptoms appear not to be caused by PHYSICAL disease, no VISIBLE pathology.
Thought to be a disturbance of FUNCTION

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32
Q

Define Epilepsy

A

A CHRONIC disorder characterised by RECURRENT SEIZURES (2 or more without clear symptomatic provocation eg alcohol withdrawal)

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33
Q

DD of a blackout/sudden collapse

A
  1. Faint = vasovagal syncope
  2. Seizure
  3. Cardiac syncope
    other: cataplexy (temp paralysis, no LOC) and hypoglycaemic attacks
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34
Q

Define vasovagal syncope

A

Sudden and temporary IMPAIRMENT of CONSCIOUSNESS with LOSS of TONE caused by reduction of blood/oxygen to brain.

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35
Q

Define seizure

A

Clinical phenomenon due to abnormal synchronous cortical discharges

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36
Q

Useful features to differentiate between faint and seizure(4)

A
  • POST event CONFUSION >2min
  • Deeply bitten lateral TONGUE
  • LONG T+C phases >1min
  • deep CYANOSOS
    NB NOT:
    twitching/jerking, incontinence, pallor, bitten tongue tip, fatigue
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37
Q

Causes of epilepsy in adults

A
  1. unknown
  2. anything effecting cortical brain eg:
    - stroke
    - trauma
    - tumour
    - infection
    - degenerative
    - congential/genetic
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38
Q

Classification of seizures

A
Focal or Generalised
Generalised: 
- Absence
- Tonic
- Tonic-Clonic
Atonic, myoclonic
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39
Q

Define status epilepticus (acute seizures) and their treatment.

A

seizures 5min+ OR
2+ discrete seizure with incomplete recovery of consciousness between them.
BENZODIAZIPINES ( lorazepam) and PHENYTOIN (block Na channel) nb phenytoin is teratogenic

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40
Q

Mood stabilising drugs in epilepsy

A

CarbaMezepine (block Na channel) and laMotrigine = safe (LLT for epilepsy)

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41
Q

Sodium valproate uses and se

A

pro - best overall drug for epilepsy but teratogenic! neurodevelopment delay

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42
Q

Newer anti-epileptics, safer profile LLT

A

Lamotrigine, Levetiracetam, Topiramate

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43
Q

3 types of pain

A
  1. Nociceptive- caused by stimulation of primary afferent nerves responding to nocious stimuli
  2. Neuropathic- ECTOPIC pain signal generation, often in the ABSENCE of ongoing noxious events,due to PATHOLOGY in the P/CNS
  3. Psychogenic- no apparent organic basis
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44
Q

WHO pain ladder 3 steps

A

1- non opiod eg paracetamol
2. weak opiod + non opiod eg codein + paracetamol
3. Strong opiod + non opiod
adjuvant analgesia eg anticonvulsant/depressant

45
Q

Paracetamol benefits and dosage

A

Analgesic, antipyretic, NO anti inflam

uk tablets are 500mg. LESS for frail, underweight and taking other paracetamol products

46
Q

NSAIDS mechanism of action eg ibruprofen or diclofenac, nb aspirin is antiplatelet nsaid

A

Inhibit prostaglandin synthesis via COX1 (GI lining) and COX2 (controls inflamm response)
-> anti inflamm but GI SE

47
Q

NSAIDs max dose

A

2.4g
tablet is usually 400mg
take after food

48
Q

NSAID SE

A

GI- gastritis, bleeding
CV. may give lansoprazole 15mg once a day (PPI)
Renal (COX2)
Hypersensitivity reactions like rashes, angioedema, bronchospam (ASTHMA contraindication if NSAID use causes attack)

49
Q

Weak opiod examples, mechanism of action + SE

A

Codeine phosphate, dihydrocodeine.
alter perception of pain, no anti infalmm.
SE- nausea, constipation, adr long term

50
Q

Codeine contraindications

A

children, adolescents, breast feeding women because toxic metabolites

51
Q

Tramadol mechanism, Indications and SE

A

STRONG OPIOD (better than codeine, not as good as morphine)
Enhances serotonin and adrenergic pathways.
SE- N+V, drowsiness, resp despression,(SO) hypotension,(SO) abuse with SSRI

52
Q

Strong opiod examples and mechanism of action

A

Morphine, fentanyl, oxycodone, pethidine

Act on Mu and kappa receptors in CNS

53
Q

Tricyclic Antidepressants as adjuvant agents. Example, SE

A

Amitriptyline, nortriptyline, dosulepin

SE- sedation, antimuscarinic (dry mouth, urinary retention)

54
Q

Antiepileptics as adjuvant agents for neuropathic pain. Examples

A

Gabapentin (not acc used in anti-epilepsy)

Carbamazepine- mood stabiliser in epilepsy

55
Q

Anxiolytics - pain disorders and muscle spasm

A

Benzodiazepines eg diazepam

56
Q

Define Multiple Sclerosis

A

Chronic AUTOIMMUNE condition of CNS leading to INFLAMMATION (RR), DEMYELINATION and NEURODEGENERATION (long).
Leads to functional disability that either worsens or has periods of R/R

57
Q

Symptoms of MS

A

Sensory disturbance-numb, tingling (otoff and lhermitte)
Visual - especially 1 eye
Motor- UMN signs and walking difficult (slap)
Bladder and bowel problems
fatigue
pain

58
Q

Epidemiology of MS

A

20-40year olds. Women >men. Further from equator

59
Q

Lhermittes symptom MS

A

neck flexion- electric feeling down spine

60
Q

Uhtoffs phenomenon MS

A

Transient functional disturbance when it’s hot/post excercise

61
Q

Aetiology of MS

A

theory - T cell infiltration of CNS in RR stage then resident cns cells contribute to inflammation long term
Both genetic and env triggers likely (incidence > further from equator)

62
Q

Primary Headache Syndromes- 3 types

A
  1. Tension headaches
  2. Migraine
  3. Trigeminal autonomic cephalagies ( pain on one side of the head in the trigeminal nerve area and symptoms in autonomic systems on the same side, such as eye watering and redness or drooping eyelids.Inc Cluster headache.)
63
Q

Tension Headache

presentation

A
Site - bilateral
O- episodic
C- tight band
R
A
T- chronic
E- stress, caffeine, lack of sleep, dehydration, eyesight etc
S- not debilitating/affecting AODL
64
Q

Causes of tension headache

A

thought to be VASC IRR referred to muscles
May be:
- ANELGESIC OVERUSE but withdrawal can -> rebound headache
- need glasses/ other TRIGGERS
- ongoing migraine
- neck stiffness irritating occipital

65
Q

Treating TTH (3)

A
  1. lifestyle factors
    + paracetamol, NSAID
    2.analgesia withdrawal
  2. neck physio if relevant
66
Q

Migraine cause and presentation

A
cause - vasospasm
S- unilateral
O- Episodic, 
C- disabling
R
A- predrome, aura, nausea, inc sensitivity 
T- hours- days
E- better when lie down, dark
S- bad
67
Q

Assd migraine features

A
- prodrome eg yawn, toilet, irritable
aura- flashing lights
- postdrome - feel shit days
-Nausea
photophobia
phonophobia
osmophobia
= sensitivity!
68
Q

Treating migraine- current (3)

A
  1. lifestyle changes
2. prophylaxis - 
beta blocker(propanolol)
anticonvulsant/antiepileptic topiramate (teratogenic), 
antidepressant amitryptiline
candesartan?
  1. RESCUE treatment=
    IV antiemetic eg metaclopramide + NSAID+ TRIPTAN

NSAID for mild symptoms (aspirin, ibruprofen, naproxen)
Triptan for severe symptoms (sumatriptan)

69
Q

CN1

A

Olfactory- smell

Px - change in smell

70
Q

CN2

A

Optic
AFRO for examination
ADD pictures of visual fields

71
Q

Absent direct and consensual light reflex =

A

optic nerve lesion (CN2)

72
Q

Absent direct light reflex, consensual is present =

A

ipsilateral occulomotor nerve lesion (CN3)

73
Q

CN3,4,6

A

Occulomotor, Trochlear, Abducens
All eye movement except superior oblique (down and out CN4) and lateral rectus (side CN6, squint)
So4Lr6

74
Q

CN5

A

Trigeminal (V1 = Opthalmic, V2 = Maxillary, V3 = Mandibular)
sensation, corneal reflex, muscles of mastication
jaw swings to side of lesion

75
Q

CN7

A

Facial
movement and taste ant 2/3 tongue
NB forehead is spared in UMN lesions like strokes because it receives motor innervation from both hemispheres

76
Q

CN8

A

Vestibulocochlear

perform Webers and Rinnes test

77
Q

Weber’s test (1st)

A

Hit tuning fork, place on forehead.
If heard louder on one side there is either :
a) conductive hearing loss (outer/middle) = on the side louder
or
b) sensorineural (inner ear deficit)= on the quieter side

78
Q

Rinne’s test (2nd)

A

Hit tuning fork, place on mastoid of 1 ear.
should hear ringing.
place it outside the ear and should still hear ringing = +, normal
place it outside ear and no hearing = - Rinne, conductive hearing loss on that side.

79
Q

CN9, 10

A

Glossopharyngeal, Vagus (sensory and motor func mix)
inspect for palate symmetry, cough, speech, swallow
taste post 1/3 = cn9
uvula deviation = away from side of lesion CN10
gag reflex

80
Q

CN11

A

Spinal
SCM and trapezius
get patient to turn head and shrug shoulders against force and look for wasting

81
Q

CN12

A

Hypoglossal
tongue movement
deviates to side of lesion

82
Q

Causes that can affect any CN -> deficit (6)

A

DM, MS, tumour, vasculitis, infection, syphyilis

83
Q

Define Trigeminal Neuralgia and 3 drugs used to treat

A

stabbing pain in one division of trigeminal nerve, without any known pathology.
Often treated with carbamezipine, gabapentin or phenytoin (anti-seizure meds)

84
Q

Define TIA

A

SUDDEN onset of FOCAL NEUROLOGICAL DEFICIT
(usually dysphasia and hemiparesis)
caused by ischaemia.
the deficits are temporary and maximal at onset.
Lasts 5-15 mins.
traditionally <24 hours to define.

85
Q

Risk factors for ischaemic stroke (9)

A

AF, CA stenosis,hypercholestrolemia,obesity, DM, hypertension, age, smoking, FH

all cv risk factors

86
Q

Bamford/Oxford Classification of stroke (4)

NB most of the time these are ischaemic.

A
  1. TACS
  2. PACS
  3. LACS- lacunar
  4. POCs
87
Q

Causes of ischaemic stroke

A
  1. Thrombotic occlusion due to large vessel disease - atherosclerosis
  2. Cardioembolism
  3. Dissection (CA -> intramural haematoma)
88
Q

What is TACs criteria

A
  1. Higher function loss - speech, apraxia,neglect
  2. Homonomyous Hemianopia
  3. Hemi-losses sensory/motor, unilateral
    3/3 = TACs
    2/3 = PACs OR just number 1
89
Q

What is Lacunar Syndrome

A
  1. Hemiplegia
    2.Hemisensory loss
  2. Upgoing plantar
    NB - NO HIGHER FUNCTION LOSS OR HEMIANOPIA
90
Q

SIgns of POC syndrome

A

Brainstem signs: CN involvement ipsilateral eg dizzy, vertigo, dysphagia, ataxia
Cerebellar signs: ipsilateral DANISH
Occipital signs: homonymous hemianopia (isolated), diplopia
CROSS HALLMARK:
contralateral motor weakness and upgoing plantar

91
Q

Forms of POCS

A
  1. PCA stroke
  2. Basilar artery thrombosis
  3. Cerebellar stroke
  4. Brainstem stroke
92
Q

PCA stroke MOA and typical symptom

A

PCA infarct or occipital haemorrhage

-> controlateral homonymous hemianopia

93
Q

Cerebellar stroke- DANISH

A
Dysdiadochokinesia
Ataxia 
Nystagmus
INTENTION TREMOR
Scanning dysarthria
Heel Shin test incoordination
94
Q

Basilar artery thrombosis symptoms

A
Bilateral/uni CN palsy
severe quadriplegia
bilateral upgoing plantar
coma, resp arrest
locked in syndrome
95
Q

Brainstem stroke syndromes

A
  1. Lateral medullary/wallenburg
96
Q

8 causes of hemorrhagic stroke

A
  1. Trauma
  2. Hypertension
  3. Vascular abnormalities
  4. Vasculitis
  5. Impaired coagulation
  6. Amyloid angiopathy
  7. Tumour
  8. Drug induced
97
Q

Types of brain hemorrhage

A
  1. Intracerebral
  2. Subarachnoid
  3. Subdural
  4. Extradural
    add pics
98
Q

Differentials of acute secondary headaches

A
  1. SAH (sudden onset severe headache)
  2. Meningitis (rash, fever, neck stiff)
  3. Encephalitis (fever, fits, strange behaviour, reduced consciousness)
99
Q

Headache warning signs

A
  1. Papilloedema
  2. Seizures, focal neurological signs, cancer, immunosuppression (HIV)
  3. Visual disturbance
  4. Postural change
  5. Pregnancy
  6. N+V
  7. Vasculitis history, DM
  8. Getting worse
  9. morning headache or wakes from sleep
100
Q

CA Dissection signs 5

A
  1. recent trauma
  2. neck stiffness
  3. Horners
  4. TIA symptoms
  5. Thunderclap headache
101
Q

VA Dissection signs

A
  1. recent trauma
  2. neck stiffness
  3. sudden onset vertigo or ataxia
  4. risk of POCS
102
Q

Giant Cell Arteritis/ Temporal arteritis definition and presentation

A

Vasculitis (inflammation in lining of) temporal artery.
THINK in 50+
Generalised aches and pains and unilateral throbbing
May have palpable artery, scalp tenderness and jaw claudication.
if suspected, immediately START STEROIDS to avoid vision loss.

103
Q

Differentials of subacute secondary headaches

A
  1. CVST
  2. GCA
  3. Tumour
  4. Intracanial hypertension (benign or malignant)
  5. Sinusitis
  6. Glaucoma
104
Q

Expressive dysphasia

A

They don’t make sense when you ask them to name 3 objects.

- issue is with Broca’s area frontal lobe

105
Q

Receptive dysphasia

A

can speak normally but cannot understand what you want them to do

  • won’t perform a 3 stage command
  • issue is with comprehension in Wernickes area in temporal lobe
106
Q

Dysarthria

A

Slurred speech

  • cannot articulate well when asked to say a tongue twister
  • issue with muscles
107
Q

Aphasia

A

cannot speak

108
Q

Ischaemic stroke management

A
  1. Thrombolysis /Clot busting within 4.5 hrs = Alteplase
  2. Antiplatelet = Aspirin short term, clopidogrel
  3. Anticoagulants = Short term heparin, warfarin , long term apixaban etc
  4. BP control, cholestrol control if necessary
  5. Thrombectomy if anterior circulation stroke and feasible