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Y4 NSS > Neuro conditions - high yield > Flashcards

Neuro conditions - high yield Flashcards

1
Q

what is motor neurone disease? (MND)

A

cluster of neurodegenerative diseases, which affects lower and upper motor neurones, often as a result of protein misfolding, affecting voluntary movement

*sensory not affected (MS diff) and eyes not affected (MG)

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2
Q

what are the types of MND?

A
  • amyloid lateral sclerosis: most common
  • progressive bulbar palsy
  • progressive muscular atrophy
  • primary lateral sclerosis
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3
Q

what is the classic presentation of MND?

A

> 40 (in UK >60), insidious progressive muscle weakness affecting limbs first, trunk, face and speech, slurred speech, clumsiness

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4
Q

what upper motor neurone signs might you see with MND?

A

spasticity and increased tone
brisk reflexes
upward plantars

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5
Q

what lower motor neurone signs might you see with MND?

A

muscle wasting
fasciculations of tongue, abdomen, back, thigh
reduced tone

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6
Q

what investigations might you carry out for MND?

A

electromyography - fasciculations
nerve conduction studies
genetic testing
MRI - ALS changes
antibodies to rule out MG, Lambert-eaton etc

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7
Q

how is MDN managed?

A

*MDT with neurologist, palliative nurse, hospice, physio, OT, SALT, dietician, social services & GP

  • Riluzole a glutamate release inhibitor, DMARD to improve survival (3m av)
  • botox injections + baclofen for spasticity
  • secretions: positioning, oral care, suctioning, glycopyrronium
  • gastrostomy for dysphagia
  • physio for spasticity
  • augmentative and alternative communication equipment
  • EOL care, ALD
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8
Q

what is Guillain-barre syndrome?

A

acute, immune-mediated demyelinating polyneuropathy typically characterised by progressive, symmetrically ascending neuropathy resulting in weakness and reduced reflexes

*often triggered by an infection (classically Campylobacter jejuni)

*subtypes AIDP, AMAN, AMSAN, MFS

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8
Q

what is the pathophysiology of GBS?
*triggers

A

seen 1-3 weeks after immune system stimulation - URTI or GI infection
*esp campylobacter jejuni, CMV

  • this triggers cause antibodies to attack nerves
  • AIDP affects myelin sheath
  • AMA and AMSAN cause axonal degeneration
  • MFS causes eye sx
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9
Q

how does GBS present?

A

*symmetrical, proximal muscles more affected eg: trunk, resp, cranial nerves
- areflexia or hyporeflexia
- pain common eg: back and limbs
- autonomic dysfunction: sweating, tachy, BP, arrhythmias
- nerve conduction: slow
- is resp involved ITU! FVC!

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10
Q

how is GBS investigated?

A
  • electromyography, nerve conduction studies
  • LP shows high protein, normal WCC
  • FVC for resp inv.
  • antibodies
  • stool cultures
  • throat swab if still sx
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11
Q

how is GBS managed?

A
  • IV immunoglobulins + plasma exchange to remove antibodies
  • ventilation sooner than later
  • DVT prophylaxis
  • analgesia
  • CVS care

*good prognosis, nearly 85% full recovery

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12
Q

what are some complications of GBS?

A
  • autonomic dysfunction - cardiac arrhythmias, postural hypotension, hypertension, urinary retention, ileus
  • respiratory - RF so monitor bedside spirometry, FVC
  • pain
  • DVT, PE
  • SIADH
  • renal failure - secondary to IVIG
  • hypercalcaemia
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13
Q

what is myasthenia gravis?

A

autoimmune disease mediated by antibodies to nicotinic acetylcholine receptors on post-synaptic side of neuromuscular junction

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14
Q

what is the physiological role of Ach in muscle contraction?

A

presynaptic depolarisation through action potential → activated CA2+ channels and causes exocytosis of ACh into synaptic cleft →
ACh binds to receptor → confirmational change and sodium influx and depolarisation →
invades t-tubules and activated calcium channels → mechanical contraction

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15
Q

what is the pathophysiology of MG?

A
  • autoimmune disorder which is due to antibody-mediated blockage of neuromuscular transmission *type 2 hypersensitivity reaction
  • prevents the binding of ACh and depolarisation needed for muscular contraction
  • fatiguability which refers to increasing muscle weakness with repeated use
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16
Q

what other conditions is MG associated with?

A

thyroiditis, graves, RA, SLE, pernicious anaemia

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17
Q

what muscles does MG affect?

A

affects skeletal muscle groups

  • extraocular muscles - commonest
  • bulbar involvement - dysphagia, dysphonia, dysarthria
  • limb weakness - proximal symmetric
  • respiratory muscle involvement
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18
Q

how does MG present?

A

*often noticed with watching TV or reading and eyes getting tired and closing, needing to keep eyebrows raised, driving as well

  • ptosis, diplopia
  • myasthenia snarl, fatiguability
  • bulbar sx
  • breathing difficulties
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19
Q

when might MG symptoms be exacerbated?

A

pregnancy
low potassium
infection
over-tx
changes in climate
emotion
exercise
gentamicin, opiates, tetracycline, quinine, BB

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20
Q

how might you investigate suspected MG?

A
  • antibodies: anti-Ach
  • EMG for repeated nerve stimulation
  • imaging: CT exclude thymoma
  • ice pack test
  • tensilon *rarely used
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21
Q

how is MG managed?

A
  • pyridostigmine!!
  • immunosuppression: prednisolone for relapses
  • thymectomy
  • azathioprine - TPMT before!
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22
Q

what is a myasthenic crisis?

A

life threatening weakness of respiratory muscles during a relapse
- triggers: infection, BB/ abx/ calcium blockers etc, stress, electrolyte abnormalities

  • monitor FVC!!
  • SALT assess
  • differentiate from cholinergic crisis
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23
Q

how would you manage a myasthenic crisis?

A

ventilatory support
plasmapheresis
IVIg
identify triggers for relapse - infection or medications

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24
Q

what is Lambert-eaton myasthenia crisis?

A

paraneoplastic associations with lung cancer or autoimmune

  • antibodies are to voltage-gated calcium channels or pre-synaptic membrane of peripheral nervous system
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25
Q

What is epilepsy?

A

recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as a seizure

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26
Q

What are the elements of a seizure?

A
  • prodrome: which may last hours to days, change in behaviour
    eg: strange feeling in gut, deja vu, strange smells, flashing lights
  • seizure
  • post-ictal: headache, confusion, myalgia, temporary weakness, dysphasia
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27
Q

what could cause epilepsy?

A

idiopathic
structural: cortical scarring, developmental, space-occupying lesion, stroke, hippocampal sclerosis
tubal sclerosis, sarcoidosis etc

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28
Q

what are some issues that come with misdiagnosis of epilepsy?

A
  • employment prospects
  • driving ban
  • stigmatisation
  • side effects of inappropriate medication
  • teratogenicity
  • denial of access to appropriate treatment
  • risk of sudden death if cardiac conditions are missed
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29
Q

what are the sub-types of focal seizures?

A

*one hemisphere, often seen with underlying structural disease
- without impaired consciousness -> no post-ictal
- with impaired consciousness
- evolving to b/L

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30
Q

what are some sub-types of generalised seizures?

A

*originates at same point, rapidly engages b/L hemispheres
- absence seizures
- tonic clonic seizures
- myoclonic seizures
- atonic
- infantile spasms

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31
Q

what are some identifying features of focal seizures originating from temporal lobe?

A
  • automatisms: lip smacking, fiddling, grabbing
  • dysphasia
  • de ja vu
  • emotional disturbance
  • hallucinations like smell, taste or sound
  • delusional behaviour
  • bizarre associations
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32
Q

what are some identifying features of focal seizures originating from fontal lobe?

A
  • motor: posting, peddling legs
  • Jacksonian march
  • motor arrest
  • subtle behavioural disturbances
  • post-ictal Todd’s palsy
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33
Q

what are some identifying features of focal seizures originating from parietal lobe?

A
  • sensory disturbances like tingling, numbness, pain
  • motor sx if pre-central gyrus involved
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34
Q

how is focal seizures managed?

A

1st: or levetiracetam lamotrigine

2nd: carbamazepine

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35
Q

how is generalised seizures managed?

A

1st: sodium valproate, lamotrigine

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36
Q

how is absence seizure managed?

A

sodum valproate or ethuximide

*carbamazepine exacerbates!

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37
Q

how is myoclonic seizures managed?

A

males: sodium valproate
females: levetiracetam

38
Q

how Is tonic/ atonic seizures managed?

A

males: sodium valproate
females: lamotrigine

39
Q

what is Lennox-gastaut?

A
  • severe for of epilepsy
  • causes: tuberculous sclerosis
  • tonic seizures during sleep, drop attacks and atypical absences common
40
Q

how is epilepsy diagnosed?

A

if any of following apply

  • Criteria 1:≥2 unprovoked (or reflex) seizures occurring more than 24 hours apart
  • Criteria 2: 1 unprovoked (or reflex) seizure with a probability of further seizures felt to be at a similar recurrence risk to patients with ≥2 unprovoked seizures over the next 10 years
  • Criteria 3: A diagnosed epilepsy syndrome
41
Q

how is epilepsy investigated?

A
  • ECG
  • bloods - FBC, U&E, LFT, glucose, bone profile
  • toxicology screen
  • other - depending on aetiology, age of presentation
  • EEG
  • MRI or CT
42
Q

What are some side effects to be aware of for anti-epileptics?

A
  1. sodium valproate - teratogenic, drug induced liver injury, pancreatitis, increased suicide risk
  2. carbamazepine - sodium channel antagonist, teratogenic, agranulocytosis, SIADH
  3. lamotrigine - sodium channel antagonist, low but still teratogenic, severe skin reactions
  4. levetiracetam - CNS disturbance, neuropsychiatric disturbance
  5. phenytoin - sodium channel antagonist, teratogenic, arrhythmia, gum hyperplasia, cerebellar atrophy
43
Q

what would you do at epilepsy drug reviews?

A
  • has dose been optimised?
  • reconsider diagnosis - is it epilepsy?
  • is compliance adequate?
  • side effects or no response - change drugs
  • partial response at max tolerable dose - add second drug
    • only known synergistic combination valproate and lamotrigine
44
Q

what advice you give someone with epilepsy?

A
  • driving - you must be seizure free for at least 12 months, before you’re allowed to drive
    • if you have a seizure, stop driving and inform DVLA
  • water safety - swimming with buddy, showers not baths
  • fire safety
  • environment - arrange home accordingly
  • care with heights
  • high risk recreational activities with caution
  • contraception with certain meds
45
Q

what is the most serious complication of epilepsy?

A

Sudden unexplained death in epilepsy is the result of sudden death in a patient with epilepsy with no identifiable cause

It is themost common cause of death in young adults with epilepsy

SUDEP has been linked touncontrolledepilepsyand nocturnal seizures

Seizure control is pivotal to reduce risk.

46
Q

what is the advice regarding driving and epilepsy?

A

first unprovoked/isolated seizure: 6 months off without structural abnormality, If these conditions are not met then this is increased to 12 months

for patients with established epilepsy or those with multiple unprovoked seizures:
may qualify for a driving licence if they have been free from any seizure for 12 months

47
Q

what is Parkinson’s disease?

A

condition where there is a progressive neurodegenerative condition due to destruction of dopaminergic neurones in the basal ganglia, resulting in asymmetrical triad of resting tremor, rigidity and bradykinesia

48
Q

what is the physiology of the basal ganglia?

A

basal ganglia are a series of cell bodies (grey matter) located together within the deep subcortical white matter of the brain

  • responsible for kick-starting and coordinating slow, sustains movements like walking
  • inhibition of muscle tone to suppress useless patterns of movement

*dopamine plays a vital role in the basal ganglia

49
Q

how might Parkinson’s present?

A
  • unilateral resting tremor “pill rolling”
  • “cogwheel” rigidity
  • bradykinesia: movement slower and smaller
    eg -> micrographia, shuffling gait, difficulty initiating movement, mask-like face
  • bowel and bladder sx, autonomic dysfunction, memory problems
50
Q

when might you consider a different diagnosis to PD?

A
  • Early and prominent cognitive dysfunction - Lewy bodies
  • rapid development gait impairment
  • early bulbar dysfunction
  • non-progressive motor symptoms
  • respiratory dysfunction
  • fasciculations
  • no improvement with tx
  • symmetrical, intentional tremor
51
Q

what are some Parkinson’s syndromes and what would make you consider those over PD?

A
  • multi-system atrophy: Very prominent autonomic dysfunction, early postural instability, poor response to levodopa
  • Progressive supranuclear palsy: Early gait instability and falls, vertical gaze palsy, prominent axial rigidity, tremors rare
  • Lewy body: dementia first, visual hallucinations, delusions, fluctuating cognition
  • Corticobasilar Degeneration: May have predominant apraxia, aphasia and ‘alien hand’ syndrome
52
Q

what other things could cause ‘parkinsonism’?

A

drug induced: anti-psychotics, anti-emetics, lithium, methyldopa
*motor symptoms are generally rapid onset and bilateral
rigidity and rest tremor are uncommon

other: post-encephalitis, tumour, vascular causes

53
Q

what are the differences between parkinsons tremor and essential tremor?

A
  • PD asymmetrical and ET symmetrical
  • PD worse at rest and ET improves
  • PD resting tremor and ET intentional tremor
  • PD no change with alcohol and ET improves with alcohol
54
Q

how might you investigate PD?

A

clinical diagnosis

  • CT/ MRI to rule out other causes
  • An absolute failure to respond to 1-1.5g of levodopa daily almost excludes a diagnosis of idiopathic Parkinson’s disease
  • DaTscan: see dopiaminergic transporters by radioactive tagging
  • SPECT: detailed 3D images of brain with radioactive tagging if atypical
55
Q

how is PD managed?

A
  • if QOL affected levodopa with COMT-i, if not levodopa, dopamine agonists like ropinarole and monoamine oxidase inhibitor like selegiline
  • surgical: deep brain stimulation to basal ganglia to reverse akinesia, rigidity, tremor
  • care package if required
  • AD, LPA etc
  • support groups
  • mobility aids etc
  • advice on taking medication and importance to not omit
56
Q

what are some side effects of L-dopa?

A
  • peripheral: postural hypotension, N+V (domperidone can be given)
  • central: confusion, dyskinesia, hallucinations, psychosis, chorea
  • on-off phenomenon

*less effective overtime (4-6y)

57
Q

what drug classes are used to treat PD and why?

A
  • synthetic dopamine
    • decarboxylase inhibitor: to prevent conversion of levodopa to dopamine peripherally
  • COMT inihibitor - inhibit COMT that metabolises levodopa
  • Glutamate antagonist - amantadine to manage dyskinesia with levadopa
  • Dopamine agonists: mimic action of dopamine in basal ganglia
  • Monoamine oxidase-B inhibitor: helping to increase circulating dopamine
  • Antimuscarinics: drug induced
58
Q

what are some complications of PD?

A
  • motor - “on-off” fluctuations, dyskinesia, freezing gait, falls
  • non-motor - aspiration pneumonia, nutritional deficiency, bladder and bowel dysfunction, pressure sores, sleeping disorders, dementia, postural hypotension
  • sudden cessation causing NMS
59
Q

what is neuroleptic malignant syndrome?

A

dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced -> sudden reduction in dopamine

*pyrexia, muscle rigidity, hypertension, tachycardia and tachypnoea, agitated delirium with confusion

*RAISED CK!

60
Q

what is multiple sclerosis?

A

chronic, inflammatory, autoimmune disease of the central nervous system, characterised by the demyelination and axonal loss of neurons

61
Q

how can you classify MS?

A
  • relapsing remitting (which may become secondary): attacks last 1-2m then remission, 85% of cases
  • primary progressive: progressive deterioration from onset
  • secondary progressive: neurological signs and symptoms between relapses
62
Q

what is the pathophysiology of MS?

A

immune reaction leads to damage to oligodendrocytes with subsequent demyelination and formation of MS plaques

*clinical manifestations of MS depend on the location of these plaques

63
Q

how does MS present?

A
  • 70% have lethargy
  • visual: optic neuritis, Uhthoff’s phenomenon
  • sensory: pins/needles, numbness, trigeminal neuralgia, Lhermitte phenomenon
  • cognitive: depression, memory problems
  • cerebellar: ataxia and tremor
  • motor: incontinence, spastic weakness, mostly in legs
64
Q

how is MS diagnosed?

A

The diagnosis of multiple sclerosis is based on at least two of:

  • Clinical history/examination
  • Imaging findings - periventricular white matter lesions seen on MRI

*Oligoclonal bands in the CSF

65
Q

what are some differentials for MS?

A
  • demyelinating: transverse myelitis
  • infections: Lyme disease, tertiary syphilis
  • metabolic: B12, diabetic neuropathy
  • systemic: SLE, sarcoid
  • other: neoplasia, stroke
66
Q

how is MS investigated?

A
  • MRI: high signal T2 lesions, periventricular plaques, Dawson fingers
  • CSF: oligoclonal bands (and not in serum)
  • FBC, CRP, ESR, LFT, U&E, glucose, TFT, B12
  • visual evoked response - electrical activity in occipital response to light
67
Q

how is MS managed? - acute

A
  • Glucocorticoids: 1g of intravenous methylprednisolone every 24 hours for 3 days
  • plasma exchange?
68
Q

how is chronic MS managed?

A
  • MDT - neurologists, specialist nurses, physio, OT
  • DMT: injectable beta-interferon, MAB etc
  • Physiotherapy
  • Baclofen and Botox for spasticity
  • Modafinil and exercise therapy for fatigue
  • Anticholinergics for bladder dysfunction
  • SSRIs for depression
  • Sildenafil for erectile dysfunction
  • soliefenacin for incontinence
  • Clonazepam for tremor
69
Q

what is Bell’s palsy?

A

idiopathic, unilateral lower motor neurone facial palsy

  • most recover within several weeks-12m
70
Q

what is the physiology of the facial nerve?

A

*5 branches - temporal, zygomatic, buccal, marginal mandibular and cervical

  • motor function - facial expression, stapedius, posterior digastric, platysma and stylohoid muscles
  • sensory - taste from anterior 2/3 tongue
  • parasympathetic - submandibular and sublingual salivary, lacrimal gland
71
Q

how do you differentiate bells from a stroke?

A

UMN-> forehead has UMN innervation bilaterally from corticobulbar tracts, forehead spared - can move on affected side

lower motor facial nerve palsy Bothe. innervations to forehead affected, forehead NOT spared

72
Q

how does Bell’s present?

A
  • unilateral facial weakness
  • post-auricular pain
  • difficulty chewing
  • incomplete eye closure
  • drooling
  • tingling
  • hyperacusis - heightened sensitivity to sound
73
Q

what does someone with a Bell’s palsy look like?

A
  • forehead affected
  • drooping of eyelid, exposing the eye
  • loss of nasolabial fold
  • drooping of corner of mouth
  • asymmetrical smile
74
Q

what are some differentials for Bell’s?

A
  • Ramsay hunt with ear rash
  • infection: HIV (b/L), otitis media
  • systemic: DM, MS
  • tumours: acoustic neuroma, parotid tumour, cholesteotoma
  • trauma: surgery, injury, basal skull #
75
Q

what investigations are carried out for bells?

A
  • Full blood count (FBC)
  • Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)
  • Viral serology (e.g. HSV-1, EBV, VZV)
  • Lyme serology (if suggestive symptoms or exposure)
  • Otoscopy to see if any vesicular lesions in external auditory meatus
  • Electromyography (EMG)
  • Imaging studies (e.g., magnetic resonance imaging (MRI) or computed tomography (CT))
76
Q

how is Bell’s managed?

A
  • prednisolone in those 72h from onset
    • 50mg 10 days PO
    • antivirals may be considered
  • eye care: lubricating drops, tape for sleep
  • Pain management with analgesics or anticonvulsants for severe otalgia or neuropathic pain
  • Physical therapy, including facial exercises and massage, to maintain muscle tone and prevent contractures
  • Psychological support and counselling may be beneficial
77
Q

what is an intracranial venous thrombosis?

A

Intracranial venous thrombosis refers to occlusion of venous vessels in the cranial cavity

  • women affected more as pregnancy and the use of the COCP
78
Q

how does a venous thrombosis present?

A

headache (may be sudden onset)
nausea & vomiting
reduced consciousness

79
Q

how would you investigate a venous thrombosis?

A

Non-contrast CT reveals a hyperdensity in the affected sinus

MRI venogram gold standard
*is used to look for a filling defect (‘the empty delta sign’)

80
Q

how s venous thrombosis managed?

A

anticoagulation
typically with low molecular weight heparin acutely
*address risk factors

81
Q

how does sagittal sinus thrombosis present?

A
  • seizures and hemiplegia
  • parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
  • ‘empty delta sign’ seen on venography
82
Q

how does cavernous sinus thrombosis present?

A
  • periorbital erythema and oedema
  • ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
  • trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
  • central retinal vein thrombosis

*causes: local infection (e.g. sinusitis), neoplasia, trauma

83
Q

how might lateral sinus thrombosis present?

A

6th and 7th cranial nerve palsies

84
Q

what causes space occupying lesions?

A
  • Neoplasia, both metastatic (typically from breast, lung, or melanoma primaries) and primary central nervous system (CNS) tumours
    • Primary CNS tumours can be benign, like meningiomas, or malignant, such as glioblastomas
  • Vascular lesions
  • Infective processes - cerebral abscesses and less common diseases such as cysticercosis, amoebiasis, tuberculosis, among others
  • Granulomata e.g. Tuberculosis
85
Q

how might a space occupying lesion present?

A

Headache- waking, lying down, coughing/straining, associated with vomiting

Cranial nerve palsies, notably the abducens nerve

advanced drowsiness, seizures, pupillary abnormalities, and papilloedema may be seen

Cushing’s reflex - raised blood pressure, bradycardia, and abnormal breathing patterns, including Cheyne-Stokes respiration

personality changes

86
Q

how is space occupying lesions investigated?

A
  • CT Head: new seizure
  • MRI with contrast is generally more useful than CT for detecting and characterising lesions
  • CT Chest Abdomen Pelvis to distinguish primary or secondary lesions
  • PET Scans
87
Q

what is the pathophysiology of Wernickes encephalopathy?

A

neurological disorder resulting from thiamine (vitamin B1) deficiency, often caused by conditions such as chronic alcohol abuse, malnutrition and AN, bariatric surgery, or hyperemesis gravidum (Persistent severe vomiting in pregnancy may lead to nutrient deficiencies)

88
Q

what is the triad in Wernicke’s?

A
  • ataxia
  • opthalmoplegia
    • nystagmus - horizontal and vertical
    • conjugate gaze problems
  • confusion
89
Q

what are some differentials for Wernicke’s?

A

meningitis
encephalitis
stroke
Korsakoff’s

90
Q

how is Wernickes investigated?

A

Neurological examination: Assessment of the characteristic triad of symptoms

MRI Head: May show characteristic changes in specific brain regions, such as the mammillary bodies and periaqueductal area

Blood tests: Although not definitive, they can reveal low thiamine levels and other signs of malnutrition or alcohol abuse

91
Q

how is Wernickes managed?

A
  • replacement of thiamine: High-dose intravenous thiamine, commonly given as Pabrinex IV, is the standard treatment
  • be wary of hypoglycaemia - give thiamine before glucose as glucose may precipitate Wernicke’s in susceptible patients
92
Q

what is Korsakoff’s?

A

chronic memory disorder, often occurring as a late complication of untreated Wernicke’s encephalopathy

*It is characterised by profound anterograde amnesia, limited retrograde amnesia, and confabulation

93
Q

how is Korsakoff’s managed?

A

thiamine and adequate hydration, 20% fully recover
- Cognitive rehabilitation
- Careful management of the patient’s environment: To reduce confusion and disorientation
- Treatment of underlying causes, like alcoholism: counselling and support to cease alcohol consumption

Y4 NSS (11 decks)

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