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MD2 > Neurology and neurosurg > Flashcards

Neurology and neurosurg Flashcards

1
Q

Difference between a stroke and a TIA

A

TIA: episode <24hours without brain damage on imaging or neurological deficits
Stroke: brief episode with brain injury or neurological deficits still existing at 72 hours.

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2
Q

When do you call a code stroke and what does this mean?

A

If <4.5hours from symptom onset -> thrombolysis (if ischaemic)

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3
Q

What does fast stand for?

A

Facial weakness (can they smile? Any mouth or eye droop?)
Arm weakness (can they raise both arms and hold it there)
Speech difficulity
Time to act fast!

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4
Q

What are some DDX that can mimic stroke? (list 5)

A

Seizure
Sepsis
Syncope/pre-syncope
Space occupying lesion (haemmhorage or tumour)
Toxic/metabolic derangement (hypoglycaemia, hyponatraemia)

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5
Q

Initial management (in ED) of stroke

A 
ABCs and vitals
BSL, FBE, UEC
CODE STROKE  -> mobilise stroke team
ECG (AF?)
CT brain 
Medications (aspirin 100mg, ACEi, statin)
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6
Q

What are the 2 main types of stroke and their sub categories?

A
  1. Ischaemic
    - intracerebral
    - subarachnoid
  2. Haemmhoragic
    - Large artery thromboembolism
    - Cardiogenic embolism (AF)
    - Lacunar infarct
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7
Q

Which type of stroke is most lethal?

A

Intracerebral

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8
Q

What is the hallmark of a SA haemmhorage?
What is this due to?

CT findings

A

Thunderclap headache
-ruptured berry

Aneurism (around circle of willis) or AV malformation

CT: Hyperdense blood in fissures, commonly around COW.

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9
Q

What type of stroke is associted w HTN?

A

Deep intracerebral haemmhorage (putamen, thalamus, brainstem, cerebellum)

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10
Q

Should patients be able to recall what they were doing at the moment their stroke SX began, or is this is a sign of a mimic?

A

Yes they should with a stroke.

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11
Q

In stroke MX, what agent do you use for thrombolysis? What is the aim of thrombolysis?

A

Recominant tpa

Aim to salvage the ischaemic penumbra (tissue surrounding the dead core, not yet but will die if left without treatment)

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12
Q

Contraindications for thrombolysis (4)

A

Haemmhorage (stroke or elsewhere)
Recent surgery
Known aneurysm
Stroke mimics (must rule these out first!)

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13
Q

What further investigations would you do if the stroke is ischaemic?

A

ECG +/- echo (AF/clot of cardiac origin?)

Carotid doppler U/S +/- CTA (internal carotid stenosis?)

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14
Q

What medications do you give in ED for stroke?

A

ASPIRIN 100mg
ACE inhibitor
Statin

+/-Warfarin/NOAC if in AF

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15
Q

Primary prevention of stroke (before any stroke has occurred)

A
  1. Reduce stroke risk factors
    -weight loss (diet and exercise)
    -smoking cessation
    Statin (reduce cholesterol)
    Good blood sugar control
    ACE-inhibitior (BP control)
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16
Q

What is the CHADS2 score?

A

Stroke risk for people in AF:

  • Congestive cardiac failure (1 point)
  • HTN (1)
  • Age (>75) (1)
  • Diabetes (1)
  • Prior TIA or stroke (2 points)

□ 0 = very low risk -> antiplatelet
□ 1 = 1 low risk -> anticoag or antiplatelet
□ >2 = mod-high risk -> anticoag

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17
Q

Secondary prevention of stroke (after stroke/TIA)

A
  • Antiplatelet (Aspirin) is FIRST LINE
  • BP lowering (ACEi, thiazide diuretics)
  • Cholesterol: Statins
  • If in AFIB: CHADS2 score to determine antiplatelet and/or anticoagulant
    +/- Carotid revascularisation (endarterectomy and stenting if symptomatic and stenosis >70%)
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18
Q

MX of haemmhoragic stroke

A

Keep BP low (SBP 120-130
Control raised ICP
Admit to neurosurg -> may need craniotomy

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19
Q

What are the different types of brain bleeds?

Which is associated w old age and alcoholism?
Which with trauma?
Which with ruptured berry aneurysm?
Which with HTN?

A

Epidural -> trauma
Subdural -> old age, alcohol, anticoag
Subarachnoid -> ruptured berry aneurysm/AVM
Intracranial -> HTN (aneurysm/AVM to lesser degree)

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20
Q

Characteristic présentation of an epidural haematoma and CT finding

A

Lucid interval before altered conscioussness

Hyperdense lenticular (lemon shaped) mass limited by suture lines

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21
Q

Characteristic présentation of an subdural haematoma and CT finding

A

No lucid period
Altered consciousness
Pupil irregularities
Hemiparesis

Hyperdense concave crescentic (crescent moon shaped) mass
Crosses suture lines

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22
Q

How do intracranial bleeds present?

A

TIA like SX and signs of raised ICP

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23
Q

DDX for headache

A

Tension-type
Migraine
Cluster
Analgesic overuse

Encephalitis/meningitis
SAH
Subdural haemmhorage
Giant cell arteritis
Raised ICP
Glaucoma
Stroke/TIA 
Space occupying lesion - tumour of abscess 
Systemic disorders -thyroid, THN, pheochromocytoma
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24
Q

Clinical presentation of meningitis vs encephalitis

A

Meningitis: severe headache
+/- neck stiffness, photophobia, rash, fever, systemic illness

Encephalitis: confusion, drowsiness, altered LOC, focal neurological signs, seizures, headaches, signs of systemic illness and fever

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25
Q

Causes of meningitis - how do signs and treatment differ?

A

Acute Bacterial
+/- Altered mental state and focal neurological signs
- Strep pneumonia, neisseria meningiditis, listeria, meningococcus (commonly in teens)
- Needs antibiotics

Viral

  • no altered conscious state or focal neurological signs
  • benign except in cases of HSV, VZV
  • Self-limiting within 1-2 weeks
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26
Q

Investigating suspected meningitis

A

Blood tests and blood culture

Empiracle dexamethasone and empiracle antibiotics before CT

CT followed by LP (ensures no increased ICP which is a CI for LP)

** probably can skip CT if they don’t have risk factors for incr ICP and go straight to LP

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27
Q

What is empiracle treatment for bacterial meningitis

A

Ceftriazone (covers S. pneumonia and N. miningiditis)

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28
Q

How does CSF content differ between acute bacterial meningitis and viral meningitis?

Appearance
WCC
Protein
Glucose

A

Bacterial

  • Cloudy
  • > 1000 WBC/microL
  • > 95% PMN
  • Protein >1g/L
  • Glucose decr (used up)

Viral

  • Clear
  • <500 WBC/microL
  • Mostly lymphocytes
  • Protein 0.4-1g/L
  • Glucose normal
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29
Q

Where does HSV encephalitis typically affect?

A

Temporal lobe

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30
Q

Causes of altered mental state + Fever

A 
Encephalitis
Meningitis
Brain abscess
Intracranial tumour or haemmhorage
Seizures
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31
Q

MX of brain abscess

A

Drainage by neurosurgery
Prolonged antibiotics
Anticonvulsants
Follow up CT

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32
Q

Source of bacteria from brain abscess

A

Continuous (sinusitis, dental abscess, mastoiditis etc)
Haematogenous
Direct implantation (post-op, post LP etc)

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33
Q

How can sinusitis lead to headaches and sepsis?

A

Focus of inflammation is in the sphenoid sinus, with para-meningeal involvement, immediately adjacent to CSF space.

Inflammation has incr vascular permeability and polymorphs have leaked across into CSF space. Bacteria may also leak across into CSF and/or blood via this method, causing encephalitis and/or sepsis.

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34
Q

Social implications of eplilepsy

A

Lose license (impacts ability to work, socialise, ADLs etc)

Reduced libido, depression, anxiety

Limited relationships, friendships etc

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35
Q

Simple vs complex partial seizures

A

Partial - limited to one hemisphere or lobe.

Simple: awareness/consciousness not affected (they are awake and alert- often remember)

Complex: consciousness/awareness affected (may not remember

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36
Q

Focal vs generalised seizures (how do they begin, and what is the underlying cause)

A

Focal

  • begins w focal features referral to part of one hemisphere (aura)
  • often w underlying structural disease

General

  • no aura, comes without warning
  • electrical discharge throughout cortex bilaterally, not localising to one hemisphere
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37
Q

What are the subtypes of focal vs general seizures

A

Focal (partial)

  • Simple partial
  • complex partial/dyscognitive
  • secondary generalised

General

  • Generalised tonic clonic
  • myoclonus
  • Absence seizures (spaced out)
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38
Q

How does epilepsy differ from seizure?

A

Seizure: sudden hyper synchronous neural activity

Epilepsy: tendency to stereotypical, repeated spontaneous seizures (2 +)

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39
Q

DDX to first seizure presentation

A

Seizure

Syncope - awaken rapidly, no post-ictal period/confusion

TIA - sudden focal neurological deficit

Psychogenic/psedo seizure

  • consciousness retained
  • long duration of seizure
  • respond to you

-substance use/withdrawal

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40
Q

Triggers of seizures

A

Alcohol
Lack of sleep
Antidepressants and anticonvulsants

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41
Q

MX of seizures

A

Don’t treat the first seizure - await recurrence UNLESS you see and epileptiform EEG or MRI lesion

Treatment:

  • Terminate status epilepticus in ED w benzodiazepine (carbamazepine)
  • Prophylaxis: benzo and phenytoin
  • Surgery in some cases to remove cause (tumour etc)
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42
Q

How do you diagnose epilepsy?

A

Interictal EEG + MRI /CT (anatomical cause)

Ictal EEG not of use because almost almost abnormal in seizure of any type

43
Q

Pathophys of PD and post-mortem findings

A

Degeneration of DA-ergic neurone in substantial nigra -> decr DA in striatum -> lewy bodies present at post-mortem

44
Q

Clinical Ft of PD

A
  1. Resting tremor (pill-rolling tremor occurs between thumb and index finger)
  2. Rigidity (cog-wheel when moved passively)
  3. Bradykinesia, hypokinesia, akinesia.
  4. Postural instability

Weakness is not a feature of PD

\+
Depression
Trouble smelling 
Trouble sleeping
Dementia
45
Q

Different tremor types

A

Resting tremor - worse with rest, better with movement (PD)

Acting/Essential tremor - worse with movement, not present at rest (cerebellar diseases)

46
Q

Treatment of PD

A

Levodopa + Carbidopa

Amantadine (produces endogenous DA production)

Bromocryptine (DA R agonist)

Entecapone (COMT inhibitor, inhibits DA breakdown)

Selegiline (Mao-B inhibitor)

Deep brain stimulation

Anticholinergics treat the tremor

47
Q

Why is L-DOPA given with Carbidopa

A

Carbidopa is a Dopa decarboxylase inhibitor that can’t cross the BBB, so it inhibits conversion of LDOPA to DA in the periphery.

This limits the peripheral side-effects of levodopa conversion to Da or adrenaline (GI upset, arrhythmias)

48
Q

What are things/conditions that cause ‘Parkinsonism’

A

Lewy body dementia, Wilson disease

Haloperidol (blocks DA receptors)
Metaclopromide (Da antagonist treats nausea, vomiting)

49
Q

Pathophysiology of Alzheimers

A

Neurodegeneration in the cortex caused by: plaques and tangles

Outside neuron
- Amyloid precursor protein (APP) helps neuron grow and repair after injury. Gets used, broken down and recycled. Broken down into monomers called beta amyloid which forms clumps -> Beta amyloid plaque -> disrupt signalling
beta amyloid also deposit in walls of vessels in brain -> Amyloid angiopathy -> incr risk of haemmhorage

INSIDE neuron: tangles (tau protein inside neuron forms neurofibrillary tangles)

50
Q

Macro changes to brain in AD

A

Brain atrophies

  • ventricles and sulci widen
  • gyrus narrow
51
Q

Genetic predispositions to AD

A
  1. Apo-E
  2. Presenelin 1 and 2 (PSEN1/2)
  3. Down syndrome (trisomy 21)
52
Q

Symptoms of AD (in order of progression)

A

Short-term memory loss

Loss of some motor skills and language

Long-term memory loss

Disorientation, wandering

Bed ridden

53
Q

Definitive diagnosis of AD

A

Exclude other causes of dementia

Definitive diagnosis is post-mortem biopsy

54
Q

Symptoms following seizure

A

Todd’s paralysis

Post-ictal confusion

55
Q

What is MS?

What is the underlying pathophys?

A

A progressive, demyelinating disease of the CNS causing relapsing and remitting or clinically progressive CNS symptoms.

Discreet plaques of demyelination occur at multiple CNS sites, caused inflammation and/or degeneration

56
Q

Presentation of MS

A

Usually get one of the following that is relapsing and remitting (with full recovery) not assoc w fever or other illness.
-May be stress induced:

  1. Unilateral optic neuritis (pain on eye movement and decr central vision)
  2. transverse myelitis - (Numb/tingling in limbs or Limb weakness)
  3. Brainstem/cerebellar (Diplopia, ataxia, nystagmus, vertigo)

Over time recovery becomes incomplete and disability accumulates.

57
Q

Investigations for MS

A

MRI brain and spine with gadolinium contrast: shows lesions and excludes other causes (T2 -fluid- shows plaques as hyperintense areas)

CSF evaluation - presence of oligoclonal bands

Basic bloods (+TSH, B12) normal

58
Q

Diagnosis of MS

A

Dissemination in space (clinical evidence of 2 or more lesions) and in time (2 or more attacks, > 1 month apart) as based on the revised McDonald criteria

Backed up by MRI findings

59
Q

Management of MS

  • acute
  • chronic (long-term therapy)
A

Treat acute exacerbations
- IV methylprednisilone 3-5 days followed by oral prednisilone

Long-term therapy slows disease progression (but can’t reverse pre-existing plaques)

  • IFNs (SE: Depression)
  • Monoclonal antibodies (Natalizumab and alemtuzumab but SE: JC virus)
  • Azathioprine
  • Non-immunosuppressives
  • Monitor with MRI
  • psychosocial and physio support

+ Treat SX (palliative) + REHAB

60
Q

What functions reside in the anterolateral spinothalamic tract?

A

Pain and temperature laterally

Crude touch anterior

61
Q

What resides in the dorsal root ganglion?

A

Sensory cell bodies

62
Q

What modalities reside in the dorsal column medial lemniscus pathway?

A

Proprioception, light touch and vibration

63
Q

How does diabetes cause nerve palsies?

A

Vasanavorum are affected -> ischaemia of neutrons -> nerve palsy

64
Q

What nerve does carpal tunnel syndrome affect?

A

Median nerve compression

65
Q

Neuromuscular conditions in which you get diplopia and ptosis

A

MG
CNIII palsy
Thyroid eye disease
NOT MND

66
Q

Neuromuscular conditions with proximal weakness

A 
Myopathy (Duchennes muscular dystrophy)
Myasthenia graves (fatiguability)
67
Q

Neuromuscular conditions with distal weakness?

A

Neuropathy

MND

68
Q

Neuromuscular conditions ft. dysphagia and dysarthria?

A

MG

MND

69
Q

Pathophys of MG

A

Post-synaptic anti-AchR Ab inhibit transmission at NMJ

70
Q

What is the presentation of MG?

A 
FATIGUABLE WEAKNESS is main finding.
Prox -> distal
Early involvement of EOM and lid-opening muscles
(Ptosis and diplopia)
Dysarthria

(no change in sensation, reflex, coordination)

71
Q

Investigations for Diagnosis of MG

A

Tensilon Test (Ach-esterase antagonist) GOLD STANDARD

EMG

Bloods: anti-Ach R antibody, MUSK Ab

CT chest (assoc w thymoma)

72
Q

Investigations to diagnose a myopathy

A

Electrophysiology studies (needle EMG)

Serum CK

Genetic tests (myotonic and duchenne’s dystrophy)

Muscle biopsy

73
Q

What will you see on a biopsy of a myopathic muscle

A

Varying muscle fibre size

Increasing fibrosis

74
Q

HX features suggestive of NMD

A

Muscle weakness/wasting
Fasciculation’s
Stiffness
Fatigue

Sensory loss/numbness
Burning/tingling

Clumsiness
Poor balance, falls

Diplopia/blurred vision
Dysphagia
Dyspnoea

75
Q

What causes foot drop

A

Focal single nerve root neuropathy

  • L5 radiculopathy
  • Perineal neuropathy
76
Q

Examples of NMJ disease

A

Pre-synaptic

  • Botulism (degrades the SNARE complex so Ach can’t be released into NMJ)
  • LEMS: Lambert Eaton Myasthenia Syndrome (Ab against pre-synaptic Ca channels)

Post-synaptic

  • MG
  • MuSK Myasthenia
77
Q

What is LEMS associated with 50% of the time?

A

Neoplasm (small cell lung cancer often)

78
Q

Examples of myopathies

A

Duchennes
Beckers
Myotonic dystrophy

79
Q

Investigations of neuromuscular conditions

A

Electrophysiology
Laboratory blood tests
LP
Muscle biopsy/MRI if myopathy suspected

80
Q

What is the main side-effect of Levodopa?

A

Motor fluctuations and dyskinesia develop in 50% of patients after 5-10 years on drug, so start L-DOPA later in disease progress when SX start to seriously interfere w life

  • wearing off earlier
  • on/off syndrome
  • failure to turn ‘on’
  • acute akinesia
81
Q

Potential causes of raised ICP

A

Cerebral oedema (reactive swelling that occurs with trauma, tumour, infarct, haemmhorage, infection)

Overproduction of CSF

Decreased absorption of CSF

82
Q

What type of cerebral oedema and causes responds to steroid therapy?

A

Vasogenic oedema secondary to tumours, trauma.

83
Q

Steps of herniation

A

Steps

  1. Internal herniations first in attempt to compensate
    - Subfalcine
    - Transtentorial (penetration of brain into where cerebellum are meant to be)
  2. Coning -> death because squashes and injures brainstem
    +/- Basilar artery tears and you get haemmhorage within brainstem
84
Q

What is hydrocephalus?

A

Enlarged ventricles

85
Q

2 main types of cerebral oedema

A
  1. Vasogenic (BBB disruption with incr permeability due to tumours, trauma)
    - responds to steroids
  2. Cytotoxic (brain swells due to electrolyte imbalance, often due to infarcts)
    - no response to steroids
86
Q

Cushing’s triad - what does this indicate?

A

Near brain herniation and imminent death

  1. Bradycardia
  2. High SBP (wide Pulse pressure)
  3. Irregular respiration
87
Q

What is Guillan Barre and what is the basic pathophys?

Trigger

A

Acute rapidly evolving polyneuropathy starting distally and ascending proximally.

Autoimmune attack and damage to peripheral nerve myelin, sometimes preceded by viral/bacterial infection.

88
Q

Management of GBS

A

IvIg or plasmapheresis +/- analgesia

89
Q

Presentation of GBS

A

Sensory: distal, symmetric parasthesia and neuropathic pain

Motor: distal weakness, areflexia

Autonomic dysregulation of BP, heart rhythm, bladder

90
Q

MX of myasthenia gravis

A

Steroids or immunosuppressants (azathioprine, cyclophosphamide, mycophenolate)

Thymectomy (85% patients show improvement/remission)

Ach-Esterase inhibitors (SX relief)

Short-term IVIg and plasmapheresis for crises

91
Q

Brain tumours

A

Primary:

  • Most common: Astrocytoma
  • Glioblastoma (high grade astrocytoma)
  • oligodenroglioma
  • schwannoma
  • meningioma
  • pituitary adenoma

Secondary

  • Lung
  • BReast
  • RCC
  • GI
  • Melanoma
92
Q

DDX for ring enhancing lesion on CT with contrast

A

MAGICAL DR

Metastases
Abscess
Glioblastoma 
Infarct
Contusion
AIDS
Lymphoma
Demyelination
Resolving hematoma
93
Q

Treatment for Brain tumours

A

Monitor - serial imaging

Steroids (reduce cytotoxic oedema)
Surgery - decompressive, palliative
Radiotherapy
Chemotherapy

94
Q

Presentation of prolactinoma

A

Young woman
Amenorrhea
Galactorrhea

95
Q

Investigation of galactorrhea

A

Prolactin levels and MRI

BetaHCG, TSH/T4 (r/o pregnancy and hypothyroid)

96
Q

Presentation of pituitary apoplexy

A

Headache (episodic, severe)
Visual Loss
Endocrine Issues (hypotension)

97
Q

Associated SX with migraine

A 
Pulsative, photophobia 
Over 4-72 hours
Unilateral
Nausea and Vomiting
Disabling intensity

aggravated by stress, food, wine, sleep deprivation, hormones, fatigue, exercise

98
Q

Treatment for migraine

  • acute
  • prophylactic
A

Acute: Acetaminophen, ASA
or NSAIDs
+/- antiemetic

Prophylactic: beta blockers or TCAs

99
Q

Treatment for tension type headache

A

Rest and relaxation
NSAIDs
Exercise (prophylactic)

100
Q

Facial nerve palsy symptoms

A

Complete ipsilateral facial weakness:

  • Facial droop
  • Flattened forehead
  • Flattened nasolabial fold
  • Inability to close eyes
101
Q

Supra nuclear facial nerve palsy SX (UMN)

A

forehead sparing with contralateral facial weakness (opposite side)

102
Q

Causes of facial nerve palsy

A

80-90% Bell’s palsy (idiopathic)
but often related to HSV

May also be related to CMV, HZV, EBV, temporal bone fracture, otitis media/mastoiditis

103
Q

Differentials of MS

A 
Neuromyelitis optica
Other systemic autoimmune diseases
Acute disseminated encephalomyelitis
Sarcoidosis
Infections
Tumours
Conversion Disorder
104
Q

Common permanent MS symptoms

A 
Fatigue
Walking problems
Bowel and bladder symptoms
Pain and paraesthesias
Cognitive problems 
Visual disturbances

MD2 (16 decks)

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