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Neurology Flashcards

1
Q

what are the types of stroke?

A

ischemic 85%
haemorragic 15%
transient ischemic attack

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2
Q

what is Transient Ischemic Attack (TIA)?

A
  • “mini-stroke”
  • stroke symptoms but temporary, last minutes to hours
  • importan warning sign to developing future strokes
  • preventative measures need to be established eg antiplatelets/anticoagulants, managing BP etc.
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3
Q

what techinque is used to diagnose/differentiate strokes?

A

MRI/CT

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4
Q

what can cause an ischaemic stroke?

A

Interruption of cerebral blood supply:
Embolism
Thrombosis
Systemic hypoperfusion

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5
Q

what is the Oxford Community Stroke Project (OCSP) Classification (Bamford et al)?

A

classification of stroke
- Anterior Circulation Infarction - Partial (PACI), Total (TACI)
- Posterior Circulation Infarction (POCI)
- Lacunar Infarction (LACI)

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6
Q

what are signs of Anterior Circulation Infarction?

A

(middle/anterior cereberal arteries)
Contralateral weakness
Contralateral sensory loss/sensory inattention
Dysarthria
Dysphasia (receptive, expressive)
Homonymous Hemianopia/visual inattention
Higher cortical dysfunction

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7
Q

what are signs of Posterior Circulation Infarction ?

A
  • cranial nerve damage
  • cerebellar dysfunction
  • Conjugate eye movement disorder (e.g. horizontal gaze palsy)
  • Isolated homonymous hemianopia
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8
Q

what is Lacunar Infarction ?

A
  • Occlusion of deep penetrating arteries
  • affects small volume of subcortical white matter
  • doesn not present with cortical features eg dysphasia, visual field loss
  • pure sensory/motor stroke
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9
Q

what tests investigations are required for stroke?

A
  • CT head
  • bloods - BM, LFTs, CRP
  • BP - if over 180 thrombolysis not given due to bleeding risk
  • Carotid Doppler USS (carotid stenosis)
  • echo/ECG - endocarditis/thrombus
  • NIHSS - severity of stroke
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10
Q

what are modfifiable risk factors for stroke?

A
  • high BP
  • smoking
  • diabetes
  • high cholesterol levels
  • heavy alcohol consumption
  • obesity
  • physical inactivity.
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11
Q

what are non-modifiable risk factors for stroke?

A
  • Age
  • family history
  • race (African Americans)
  • sex (men)
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12
Q

what are symptoms of a stroke?

A
  • numbness/weakness in face, arm, leg, often one-sided
  • Confusion, trouble speaking, or difficulty understanding speech.
  • Trouble seeing in one or both eyes
  • Difficulty walking, dizziness, loss of balance, or lack of coordination.
  • Severe headache
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13
Q

what is Alberta Stroke Program Early CT Score?

A
  • segments brain into parts and score based on areas affected
  • 10 is normal - going down
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14
Q

what is given if ischaemic stroke is suspected?

A

thrombolysis

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15
Q

what is the definition of a stroke?

A
  • rapidly developing clinical signs of focal disturbance of cerebral function
  • lasting more than 24 hours or leading to death
  • no apparent cause other than a vascular origin
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16
Q

what is another treatment for stroke other than medication?

A
  • Mechanical Thrombectomy - catheter that removes blood clot
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17
Q

what is Ischaemic Penumbra?

A
  • reverisble area of damage around the core (irreverable damage)
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18
Q

what is the management of a stroke?

A
  • preventing complication (infection, pressure sores, depression etc.)
  • secondary prevention - lifestyle etc.
  • rehabilitation - physio, occupational therapy, speech/language
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19
Q

what is the ABCD2 score for stroke?

A

Estimates the risk of stroke after a suspected transient ischemic attack (TIA)
A - age over 60
B - over 140/90
C - clinical features - speach/weakness
D - duration ie over 60 mins
D - diabetes

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20
Q

what are Pathological subtypes of ischaemic stroke ?

A
  • Large vessel disease (50%)
  • Small vessel disease (25%)
  • Cardioembolic (20%)
  • Unknown (cryptogenic) (3%)
  • Rare causes (2%) e.g. dissection, CVST, vasculitis
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21
Q

what are secondary preventative measures for stroke?

A
  • antiplatelets - aspirin/clopidogrel
  • anticoagulation
  • hypertension management
  • cholesterol management - statins
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22
Q

what is the surgical management for stroke?

A
  • Carotid endarterectomy (CEA) or carotid artery stenting - for Carotid Stenosis - prevetative
  • Decompressive hemicraniectomy - part of skull removed if stroke is very large/swelling
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23
Q

what are the risks of Posterior circulation infarction?

A
  • hydrocephalus
  • treated with EVD/posterior fossa decompression
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24
Q

how are brain tumours graded?

A
  • WHO classification – histology (cell type), molecular markers and genetic factors (not tumour-node-metastasis)
  • 1 = non-malignant
  • 2 = cytological atypia
  • 3 = anaplasia and mitotic activity
  • 4 = Anaplasia, mitotic activity with microvascular proliferation, and/or necrosis - v aggressive malignant
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25
Q

what are prognostic factors of brain tumours?

A

Histology type
Age *
Size of tumour *
Rate of growth
Location *
Cross midline
Presenting features
Performance status

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26
Q

what are the main types of gliomas?

A
  • Astrocytomas - Glioblastoma (GBM) v aggressive
  • Oligodendrogliomas - more responsive to treatment
  • Ependymomas - easier to surgicallly remove
  • mixed
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27
Q

what are symptoms of brain tumour?

A
  • headache
  • seziures
  • motor loss
  • confusion/weakness/memory loss
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28
Q

what are the presentations of a headache with brain tumours?

A

Woken by headache,
worse in the morning,
worse lying down,
associated with N&V,
exacerbated by coughing, sneezing, drowsiness

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29
Q

what are causes/risk factors of brain tumours?

A

mostly no causes found
risk factors/association
- ionising radiation exposure
- family history
- Immunosuppression (CNS lymphoma)

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30
Q

what is Papilloedema?

A
  • swelling of the optic disc due to elevated intracranial pressure (ICP)
  • seen with brain tumours
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31
Q

what are signs of raised intracranial pressure?

A
  • VIth nerve palsy - hearing loss one sided
  • papilloedema
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32
Q

what are the investigations for brain tumours?

A
  • CT/MRI
  • brain biopsy
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33
Q

what is the treatment of high grade glioma?

A
  • Steroids – reduce oedema
  • surgery - to relieve IC, survival prolongation
  • chemo/radio
    (non curative but prolongs survival)
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34
Q

what is the treatment of low grade glioma?

A

Surgery – early resection (Awake craniotomy)
radio/chemo

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35
Q

what are types of brain tumours?

A
  • gliomas
  • meningomas
  • Schwannomas
  • pituitary tumours
  • Secondary (Metastatic) Brain Tumors
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36
Q

what are the types of traumatic head injury?

A
  • blunt vs penetarting
  • focal vs diffuse
  • primary vs secondary eg due to poor care
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37
Q

what are diffuse axonal injuries?

A
  • white matter lesions on grey/white margins
  • loss of consciousness
  • little haemmorage - better seen on MRI not CT
  • in high impact/shaking incidents
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38
Q

what are tbi contusions?

A
  • brain tissue injured due to brain/skull collision
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39
Q

what are the types of intracranial bleeds?

A
  • extradural (lemon shaped)
  • subdural (banana shaped) - more gradual
  • subarachnoid - from aneurysm/trauma
  • intracerebral/intraventrcular
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40
Q

what is the management of a head injury?

A
  • CT/MRI
  • control seziures if present
  • surgical treatment (rarely)
  • prophylaxis - due to meningitis risk
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41
Q

what is the glasgow coma scale?

A

scale for head injury
- includes assesment of eye, verbal and motor response
- low=more severe, coma likely
- 9-12 moderate

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42
Q

what are potenital complications after TBI?

A
  • endocrinopathy - hormone deficiencies etc.
  • Post-traumatic epilepsy
  • infections
  • gi - peptic ulcers, dysphagia
  • heterotopic ossification
  • congnative changes - memory/personality
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43
Q

what are the typical causes of different bleeds?

A

Extradural Hematoma - arterial bleeding - skull fracture
Subdural Hematoma - vein rupture - rotational injury
Subarachnoid Hemorrhage - rupture of an aneurysm or trauma
Intracerebral Hemorrhage - trauma, hypertension, vascular malformations

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44
Q

what is characteristic of chronic traumatic encephalopathy?

A

p-tau aggregates

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45
Q

what causes parkinsons disease?

A
  • loss of dopamine producing neurones
  • in substantia nigra
  • lewy bodies detected
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46
Q

what are symptoms of parkinsons?

A

- bradykinesia (shuffeling gait, hypomimia)
- resting tremor - asymmetrical
- rigidity
- Postural instability
- sleep disturbances
- Mood/cognitive symptoms

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47
Q

what are types of tremor?

A

rest
action - postrual, kinetic - intention

essential - inherited
dystonic
cerebellar
functional

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48
Q

how is parkinsons diagnosed?

A
  • clinical - classical motor symptoms
  • Datscan
  • tests for infections/electrolystes, thyroid
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49
Q

what is the treatment of parkinsons?

A
  • L-dopa
    taken with carbidopa to reduce metabolism
  • MOA-B inhibitors stop breakdown of dopamine
    (time sensative medication_
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50
Q

what is a complication of stopping parkinsons medication?

A
  • freezing
  • neuroleptic malignant syndrome
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51
Q

what conditions are associated with parkinsons?

A
  • depression/anxiety/psychosis
  • dementia
  • orthostatic hypotension
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52
Q

how are essential tremors treated?

A

primidone
beta-blockers

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53
Q

what are the non-infective causes of meningitis

A
  • neoplastic - cancers
  • drug induced- NSAIDS
  • autoimmune/systemic - SLE
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54
Q

what are symptoms of meningitis?

A
  • fever
  • headache
  • neck stiffness
  • photophobia
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55
Q

what are permenant complications from meningitis?

A
  • skin scars
  • amputation
  • hearing loss
  • seziures
  • Hydrocephalus
  • motor deficit
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56
Q

investigations for meninigitis

A
  • GCS
  • vital signs/glucose levels
  • blood culture
  • lumbar puncture - definitive
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57
Q

treatment of meningitis

A
  • benzylpenicillin
  • supportive treatment - fluids, analgesia
    (notify public health)
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58
Q

what are contraidications of lumbar puncture?

A
  • platelet count less than 20,000 mm3or heparin use within 24hr
  • vertebral trauma
  • infection at LP site
  • raised intracranial pressure
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59
Q

what bacteria cuases meningitis?

A

-ve bacteria
- neisseria meningitidis - young adults
- haemophilis influenza B
- e.coli

+ve bacteria
step.pneumonia
- listeria spp.
- group B step

chronic:
- TB
- syphilis

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60
Q

meningococcal septicaemia symptoms/signs?

A
  • rash: non-blanching, red/brown pin-prick rash then large purple
  • nausea/vomiting
  • hypotension
  • fever
  • septic shock
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61
Q

what are differential diagnosis of meningitis?

A
  • subarachnoid haemorrhage - trauma, thunderclap
  • flu
  • sinusitis
  • malaria
  • brain abscess
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62
Q

what is encephalitis?

A

inflammation of brain

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63
Q

what are the symptoms of encephalitis (different to meningitis)?

A
  • confusion
  • behaviour changes
  • memory loss
  • seziures
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64
Q

types of viruses ect.

what are causes of encephalitis?

A
  • herpes simplex
  • varicella zoster
  • if travelling - ticks, rabies, etc.
  • Enteroviruses
  • measels
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65
Q

what are investigations for encephalitis?

A
  • MRI
  • LP - CSF, viral PCR
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66
Q

what are the main symptoms of huntingtons disease?

A
  • chorea - Uncontrolled movements, poor coordination, speech
  • dementia
  • psychiatric problems - depression/anxiety/OCD
    only start to appear at ages 30-50, then patient starts to deteriorate
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67
Q

what gene is affected in huntingtons disease?

A

HTT

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68
Q

what is the treatment of huntingtons disease?

A
  • Neuroleptics:
    Sulpiride for chorea
    haloparidol for psychosis
  • SSRIs for depression
  • Risperidone for aggression
  • therapy eg speech, physical, occupational
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69
Q

what is Cerebellar ataxia?

A
  • lack of muscle coordination and control
  • originates from the cerebellum
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70
Q

what causes Cerebellar ataxia?

A
  • Genetic disorders: Friedreich’s ataxia, spinocerebellar ataxia
  • damage to cerebellum from stroke, MS, tumors, alcohol, infections
  • inflammation of cerebllum from autoimmune conditions
  • toxins
  • E/B12 deficiency
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71
Q

what is Generalized dystonia?

A
  • movement disorder
  • twisting, muscle contraction, repetitive movement, abnormal posture
  • starts in one limb then effects body
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72
Q

what causes Generalized dystonia?

A
  • genetic: DYT1 dystonia - mutation in TOR1A gene
  • secondary: Wilson’s disease, cerebral palsy, brain injury, medication
73
Q

how is generalised dystonia treated?

A
  • muscle relaxants, anticholinergic drugs
  • Botulinum toxin injections for muscle spams
  • physical/speech therapy
74
Q

what are primary headaches?

A

Migraine, Cluster,
Tension Type - most common

75
Q

what causes secondary headaches?

A

Meningitis, Subarachnoid Haemorrhage, GCA, Idiopathic Intracranial Hypertension
Medication Overuse Headache

76
Q

what features suggest secondary headache?

A
  • sudden thunderclap headache
  • infection - meningitis (neck stiffness, photophobia)
  • Red eye - acute glaucoma
  • Papilloedema
  • seziures
77
Q

what can cause transient loss of consciousness other than epilepsy?

A
  • low bp/heart conditions
  • syncope
78
Q

types of epilepsy

A
  • Genetic generalised epilepsy
  • Unclassifiable epilepsy
  • Structural / metabolic epilepsy
79
Q

what is epilepsy

A
  • Primary disturbance of brain function - excessive hypersynchronous neuronal firing
  • changes of behaviour, sensation and cognition
80
Q

how long do eplieptic seizures commonly last?

A

30 - 120 seconds

81
Q

types of seizures?

A
  • focal
  • generalised
  • eplieptic
  • Convulsive status epilepticus
82
Q

what is Convulsive status epilepticus

A

prolonged convulsive seizure lasting for 5 minutes or longer, or recurrent seizures one after the other without recovery in between

83
Q

what does tonic clonic seizure mean

A

stiffening & jerking

84
Q

what is Functional / dissociative seizure

A
  • caused by mental processes triggered by internal/external stimuli
  • eg from PTSD
85
Q

what presentations are more common in epilepsy rather than syncope

A
  • tongue biting
  • head turning
  • muscle pain
  • loss of conciousness over 5 min
86
Q

symptoms that indicate syncope not epilepsy

A
  • sweating prior
  • prolonged upright position
  • nausea
  • pallor
87
Q

presentations indicating Functional / Dissociative Seizures (FDS) rather than epilepsy

A
  • pre anxiety, crying etc.
  • long duration
  • closed eyes/mouth
  • Surprisingly rapid or slow postictal recovery
  • no cyanosis - blue fingers
88
Q

what are types of epilepsy

A
  • focal (Structural / metabolic) - with/without impairment of consciousness/Secondary generalised seizures
  • Genetic (idiopathic) generalised epilepsy - Absence/Myoclonic/Primary generalised tonic clonic seizures
89
Q

first line treatment of Structural / metabolic (focal) epilepsy

A

Lamotrigine / carbamazepine / levetiracetam

90
Q

neuropathic finding in focal epilepsy

A

Hippocampal sclerosis especially temporal lobe seziures

91
Q

first line treatment of Genetic (idiopathic) generalised epilepsy

A

Lamotrigine / levetiracetam / valproate

92
Q

treatment if drugs not effective for epilepsy

A
  • surgery - Hemispherectomy
  • vagus nerve Electrostimulation - less effective
93
Q

what causes ataxia

A

cerebellar degeneration
purkinje cell loss

94
Q

autosmall recessive ataxia

A

Friedreich’s ataxia

95
Q

autosomal dominant ataxia

A
  • spinocerebellar ataxias
    SCA 6
  • episodic ataxias
    EA 2
96
Q

what drug can cause ataxia

97
Q

immmune mediated ataxia

A
  • paraneoplastic
    cerebellar
    degeneration
  • gluten related
98
Q

degenerative ataxia

A

multi-system atrophy cerebellar variant
(MSA-C)

99
Q

Symptoms of cerebellar dysfunction

A
  • dizzy – unsteady / wobbly / clumsy
  • falls, stumbles
  • difficulty focusing / double vision / ‘oscillopsia’
  • slurred speech
  • problems with swallowing
  • tremor
  • problems with dexterity / fine motor skills
100
Q

clinical signs of ataxia

A
  • nystagmus - uncontrolled eye movement
  • intention tremor
  • heel - shin ataxia
  • gait
  • Dysarthria - speech disorder
101
Q

ataxia investiagtions

A
  • MRI brain
  • blood tests - gluten serology, HLA DQ8, autoimmune screen, CRP etc.
102
Q

cause of motor neurone disease

A

degeneration and loss of upper and lower motor neurons

103
Q

motor neurone disease risk factors

A

age 50-70
male
genetic

104
Q

signs/symptoms of motor neurone disease

A
  • muscle weakness/wasting (LMN)
  • Fasciculations (LMN)
  • spascicity, hyperreflexia (UMN)
  • Dysarthria, dysphagia
  • emotional lability - Inappropriate laughing or crying
  • respiratory failure
105
Q

motor neurone disease investigations

A
  • Electromyography (EMG) and Nerve Conduction Studies (NCS)
  • MRI - rule out lesions
  • blood tests - exlude other
106
Q

motor neurone disease treatment

A
  • Riluzole: An antiglutamatergic drug (glutamate stims neurones)
  • Baclofen or tizanidine for spasticity (GABA (cns inhibitor) agonist)
  • Non-invasive ventilation
  • Multi-disciplinary specialist care
107
Q

cell body location of motor neurones

A

brain/spinal cord

108
Q

main type of motor neurone disease

A
  • ALS (amyotrophic lateral sclerosis)
109
Q

motor neuone disease alternate diagnosis

A
  • FTD
  • Parkinson’s disease
  • Myasthenia gravis
  • Muscular dystrophies
  • Spinomuscular atrophy
  • Polio
110
Q

gene mutations associated with motor neurone disease

A
  • C9orf72
  • SOD1 (Superoxide Dismutase 1)
  • TDP-43
111
Q

what does primary lateral sclerosis effect

A

upper motor neurones

112
Q

what does primary muscular atrophy effect

A

lower motor neurones

113
Q

what does Amyotrophic lateral sclerosis effect

A

upper and lower motor neurones - 90% of MND

114
Q

what are bulbar symptoms of MND

A
  • Dysarthria
  • dysphagia
  • Bulbar pseudobulbar affect - inappropriate emotions
  • facial/tongue weakness
  • jaw jerk reflex test UMN
115
Q

what nucleus are not affected by MND

A

oculomotor
onuf
(MND do not lose continance)

116
Q

histological features of Alzheimer’s dementia

A

amyloid plaques
neurofibrillary tangles

117
Q

types of dementia in order of prevelance

A

Alzheimer’s dementia
Vascular dementia
Lewy body dementia
Frontotemporal dementia (including Pick’s disease)

118
Q

risk factor for vascular dementia

119
Q

Vascular dementia presentation

A

stepwise fashion - stability then decline then stability
- Mood disturbances - depression
- cognative impairment

120
Q

lewy body presentation

A
  • visual hallucinations
  • cognative problems - less memory
  • sleep disorders
  • death within 7 years
121
Q

treatment of alzheimers

A
  • Acetylcholinesterase (AChE) inhibitors
  • Memantine - NMDA antagonist regulates glutamate
  • Cognitive rehabilitation
  • Cognitive stimulation therapy
122
Q

alzheimers disease prevention

A
  • reduce CVD risk - smoking, diet etc.
  • treat depression
  • no loneliness or social isolation
  • staying mentally active
123
Q

what tests assess memory/cognative function in alzheimers

A

Mini-Mental State Examination (MMSE)
Montreal Cognitive Assessment (MoCA)

124
Q

imaging for alzheimers

A
  • Positron Emission Tomography (PET) Scans - show amyloid-beta plaque
  • CT/MRI scan - atrophy, tumours, stroke
125
Q

gene mutations in alzheimers

A

APP, PSEN1, PSEN2

126
Q

CSF analysis in alzheimers

A
  • Total Tau (t-Tau) - elevated = dementia etc.
  • Phosphorylated Tau (p-Tau) - elevated = AD
  • Beta-Amyloid (Aβ) Peptides - low Aβ42
127
Q

what asseses power/strength

A

The Medical Research Council (MRC) Scale of
Muscle Strength
0 - no mevement
5 - (full movement against full resistance)

128
Q

lesions and pulmonary compliactions

A

high thoracic T2-T4 - vital capacity of 30-50%
T11 - strong cough, minimal dysfunction

129
Q

lesions causing neurogenic shock

A

high thoracic
cervical

130
Q

what is spinal shock

A

loss of motor, sensory, autonomic and reflex function at or below the level of injury

131
Q

Brown-Sequard presentations

A
  • UMN signs - lesion side
  • weakness/paralysis, proprioceptive deficits on lesion side
  • loss of pain and temperature sensation on the contralateral side
132
Q

Non Compressive Myelopathy types

A
  • inflammatory: MS, NMO, acute disseminated encephalomyelitis (ADEM)
  • infectious: syphilis, Lyme, HIV, HSV, EBV, enteroviruses
  • infarction: blockage in blood supply or spinal arteriovenous malformations (AVMs)
133
Q

inflammation of spinal cord CSF analysis

A
  • pleocytosis (WBCs)
  • elevated igG
  • gadolinium enhancement (on MRI_
134
Q

Transverse Myelitis signs/symptoms

A
  • numbness, tingling, or pain,weakness - normally bilateral
  • Clearly defined sensory level
  • Bowel and Bladder Dysfunction
  • Autonomic Dysregulation
  • rapid onset
135
Q

causes of Transverse Myelitis

A
  • infections
  • autoimmune eg SLE, MS, NMOS
  • idiopathic
136
Q

Transverse Myelitis on MRI

A
  • Gadolinium Enhancement (more in acute)
  • Hyperintense lesions on T2-weighted images - large area of cords cross-section
  • Spinal Cord Swelling/expanded
  • Longitudinally Extensive - 3 or more vertabrae
  • thoracic spinal cord most common
137
Q

transverse myelitis treatment

A
  • high-dose corticosteroids - Methyl Prednisolone
  • plasma exchagne, IVIg
  • bowel/bladder care
  • rehab
138
Q

Diagnostic Criteria for Neuromyelitis Optica

A
  • Optic neuritis
  • Acute myelitis
  • And at least two of:
    1. Contiguous spinal cord MRI lesion extends over 3 vertebral
    segments.
    2. Brain MRI not multiple
    sclerosis.
    3. AGP4-IgG
139
Q

Conus Medullaris Syndrome (CMS) and Cauda Equina Syndrome (CES) comparison

A
  • impotence = CMS
  • reflexes: CMS dimished at level, brisk below, CES absent
  • symetrical = CMS
  • asymetrical = CES
  • pain: CES - severe radicular pain, CMS - back pain
  • saddle anesthesia - both
140
Q

what is Syringomyelia

A
  • fluid filled cysts - syrinx in spinal cord
  • most commonly due to obstruction of CSF
  • eg Chiari malformation
141
Q

nitrous oxide-induced subacute combined degeneration causes and treatment

A
  • n2o effects b12 metabolism and cuases demyelination
  • Hydroxocobalamin as b12 supplement
  • c3-c5 most commonly affected, axial slices show inverted V
142
Q

what can cuase loss of light touch, vibration and joint position

A

copper/b12 deficiency

143
Q

compensatory mechanism for increased intracranial pressure

A
  • increased CNS drainage via ventricular system
  • increased venous drainage via dural venous sinuses
144
Q

what is Monro-Kellie Doctrine

A

relationship between the contents of the cranium and intracranial pressure.

145
Q

intracranial volume and distribution

A
  • 1700ml total
  • CSF 150ml
  • blood 150ml
  • brain parenchyma 1400ml
146
Q

normal value for intracranial pressure

147
Q

what is herniation due to a tumour

A
  • tumour growing caused raised intracranial pressure
  • parenchyma shift in position and become displaced
  • Uncal herniation - temporal lobe displaced
  • Tonsillar herniation - cereballar tonsils displaced - compression on brainsetm
148
Q

what brain tumours have/not IDH mutation

A

IDH mutation:
- Astrocytoma
- Oligodendroglioma + 1p/19q-codeleted
No IDH mutation:
- Glioblastoma - aggresive, grade 4 gliomas

149
Q

what is dissociation?

A

involutary disruption in the normal integration of identity, sensation, perception, affacts, thoughts, memories, control of body
- feeling of being disconnected from one/world

150
Q

what is mild/common dissociation

A

daydreaming

151
Q

what are the symptom groups of functional neurological disorders

A

sensory
motor
seizures
cognative - memory, concentration, fatigue

152
Q

what is functional neurological disorders likely cause

A

traumatic events
insoluble/intolerable problems
disturbed relationships

153
Q

what is hoovers signs

A

voluntary and automatic movement inconsitency
- seen in functional neurological disorders

154
Q

what are some presenations of functional neurological disorders

A

whack a mole sign - tremor moves when stopped
dystonia
falling towards support
exessive exabaration eg huffing and puffing

155
Q

treatment of functional neurological disorders

A
  • managing physical symptoms eg headaches
  • physio/OT/SALT
  • therapy, CBT
  • hypnosis - some evidence
156
Q

Myasthenia gravis symptoms

A
  • Ptosis: Drooping of one or both eyelids.
  • Diplopia: Double vision
  • facial weakness - difficulty speaking/swallowing etc.
  • generalised weakness - proximal muscles of the limbs
157
Q

most common antibody in MG

A

Acetylcholine Receptor (AChR) Antibodies
- affect nicotinic acetylcholine receptors (AChRs) at the neuromuscular junction of skeletal muscles

158
Q

investigation for MG

A
  • antibody test
  • A CT or MRI of the thymus gland is used to look for a thymoma.
  • Edrophonium Test - improves muscle strength = +ve
159
Q

what tumours is MG associated with?

160
Q

other MG antibodies

A

Muscle-specific kinase (MuSK) antibodies
Low-density lipoprotein receptor-related protein 4 (LRP4) antibodies

161
Q

ways to elicit fatiguability in the muscles

A

Repeated blinking will exacerbate ptosis
Prolonged upward gazing will exacerbate diplopia on further testing
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

162
Q

treatment of MG

A
  • Pyridostigmine - cholinesterase inhibitor - prolongs acetylcholine
  • Immunosuppression (e.g., prednisolone or azathioprine)
  • Thymectomy can improve symptoms, even in patients without a thymoma
  • Rituximab
163
Q

treatment of Myasthenic Crisis

A
  • non-invasive ventilation or mechanical ventilation
  • IV immunoglobulins
  • plasmapheresis
164
Q

Guillain-Barré syndrome trigger

A

infection eg
Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV).

165
Q

Guillain-Barré pathophysiology

A

molecular mimicry
- B cells produce antibodies against pathogen
- also attack myelin sheath or the nerve axon itself

166
Q

Guillain-Barré syndrome symptoms

A
  • Symmetrical ascending weakness
  • Reduced reflexes
  • loss of sensation
  • pain
167
Q

Guillain-Barré syndrome investiagtion

A
  • CSF - raised protein, normal glucose & cell count
  • Nerve conduction studies - reduced signals
168
Q

Guillain-Barré syndrome treatment

A
  • Supportive care
  • VTE prophylaxis (pulmonary embolism is a leading cause of death)
  • IV immunoglobulins (IVIG) first-line
  • Plasmapheresis
169
Q

what is multiple sclerosis

A
  • autoimmune
  • causes demylination
  • affects the central nervous system (the oligodendrocytes)
170
Q

potential causes of MS

A

Multiple genes
Epstein–Barr virus (EBV)
Low vitamin D
Smoking
Obesity

171
Q

optic neuritis in MS

A

Central scotoma (an enlarged central blind spot)
Pain with eye movement
Impaired colour vision
Relative afferent pupillary defect - pupils react differently

172
Q

focal symptoms/signs in MS

A

Incontinence
Horner syndrome - ptosis, anhidrosis and miosis
Facial nerve palsy
Limb paralysis
Trigeminal neuralgia - severe facial pain
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign - electric shock sensation

173
Q

types of symptoms in MS

A
  • optic
  • focal
  • ataxia
174
Q

diagnosis of MS

A
  • MRI scans -typical lesions
  • Lumbar puncture - oligoclonal bands in CSF
175
Q

MS treatment

A
  • steroids in relapse
  • physio/OT
  • treat depression, pain, fatigue etc.
176
Q

causes of compressive myelopathy

A
  • herniated disc
  • spinal stenosis
  • Spondylolisthesis - displacement vertabrae
  • tumours
  • infection - abscesses - potts disease
  • osteoartheritis
177
Q

symptoms of sciatica and spinal nerves

A
  • unilateral pain: worse with movement, burning/jolt
  • Numbness or Tingling in leg/foot
  • weakness (leg)
    (from spinal nerves L4 – S3)
178
Q

sciatica investigation

A

MRI - shows herniations or bulges, stenosis etc.

179
Q

what is Bilateral sciatica a red flag for?

A

cauda equina syndrome

2A (9 decks)

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