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3A > Neuro > Flashcards

Neuro Flashcards

1
Q

What structure is damaged in Bell’s palsy?

A

Cranial nerve 7 (facial)

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2
Q

What is the presentation of Bell’s palsy?

A

Weakness of the facial muscles responsible for expression

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3
Q

LMN presentation vs UMN presentation

bells palsy vs stroke

A

LMN - no forehead sparing

UMN - forehead sparing ie can wrinkle forehead

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4
Q

What is the management for Bell’s palsy?

A

Steroids

Surgery if there is residual symptoms 6-9 months after initial symptoms

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5
Q

Bulbar palsy vs Peudobulbar palsy

A

Bulbar palsy - lower motor neurone dysarthria (difficult/unclear articulation of speech) and dysphagia (difficulties swallowing)
Pseudobulbar palsy - upper motor neurone dysarthria and dysphagia

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6
Q

What is the aetiology of Bulbar palsy?

A 
Diphtheria
Poliomyelitis
Motor neurone disease
Cerebrovascular event
Brainstem tumours
Gullain-Barre syndrome
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7
Q

Aetiology of Pseudobulbar palsy?

A 
Cerebrovascular event
demyelinating disorders
motor neurone disease
head injuries
neurosyphillis
high brainstem tumours
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8
Q

What are the investigations for bulbar/pseudobulbar palsy?

A

CT/MRI
electropalatography
electromagnetic articulography

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9
Q

What is the management for bulbar/pseudobulbar palsy?

A

Treat directing cause
SALT
Baclofen for spasticity, anticholinergics for drooling
Dietician

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10
Q

What is cerebral palsy?

A

A brain disease causing paralysis

Lesion in an immature brain any time up to the postnatal period

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11
Q

What causes cerebral palsy?

A 
Vascular
hypoxic-ischaemic
teratogenic
exposure to radiation
infection ie meningitis
toxins
metabollic problems
trauma ie head injury
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12
Q

What are the different characteristics of cerebral palsy?

A
  • Spastic (70% of types): scissor gait
  • Dyskinetic: hyperkinesia - dystonia and chorea
  • Ataxic: without order/control
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13
Q

Epidemiology of cerebral palsy?

A

More likely in new borns <2500g

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14
Q

What are the risk factors for cerebral palsy?

A
  • antenatal: preterm birth, intrauterine infections, multiple births
  • perinatal: low birth weight, neonatal sepsis, chorioamnionitis
  • postnatal: meningitis, intracranial haemorrhage, seizures
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15
Q

Presentation of cerebral palsy?

A
  • associated with low Apgar score
  • delay in reaching developmental milestones
  • abnormal tone
  • excessively fidgety
  • feeding difficulties
  • emotional and behavioural difficulties in later childhood
  • epilepsy
  • sleep disturbance
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16
Q

Investigations for cerebral palsy?

A

Neuroimaging: USS, CT, MRI, PET

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17
Q

Managment for cerebral palsy?

A

Treat/support symptoms: wheelchairs, splints, physio
medical treatment: diazepam/baclofen for spastic pain
Surgical treatment

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18
Q

What is churg-strauss/Eosinophilic Granulomatosis with Polyangiitis ?

A

diffuse vasculitic disease affecting coronary, pulmonary, cerebral, abdominal and visceral circulations

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19
Q

what’s the aetiology of churg-strauss?

A

unknown - thought to be autoimmune and have a genetic factor

drugs known to cause churg-strauss: mesalazine, leukotriene receptor antagonists

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20
Q

What are the 3 features that characterise churg strauss?

A

eosinophillia
asthma
peripheral neuropathy
*can also have paranasal sinusitis

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21
Q

Presentation of churg strauss..

A

depends on the system affected
peripheral neuropathy presents as mononeuritis multiplex,
pulmonary system presents as asthma,
cardiac: heart failure, myocarditis, mi.
renal: glomerulonephritis
general symptoms include: fatigue, malaise, weight loss, fever

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22
Q

Investigations of churg strauss

A

antineutrophil cypoplasmic antibodies

bloods: eosinophillia, raised inflammatory markers

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23
Q

Management of churg strauss?

A

high dose steroids
cyclophosphamide for severe/life threatening disease
IVIg, interferon-alpha, plasma exchange
rituximab

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24
Q

What is Horner’s syndrome?

A

Lesion which affects the sympathetic nervous supply to the eye.
TRIAD: partial ptosis, miosis and hemifacial anhidrosis

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25
Q

What are some of the causes of Horner’s syndrome

A 
Anything that can cause a lesion to the sympathetic nervous system
Apical lung tumours
cerebrovascular accidents
cluster headaches/migraines
internal carotid artery dissection
\+ many more
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26
Q

What is the presentation of Horner’s syndrome?

A

TRIAD: miosis, partial ptosis, hemifacial anhidrosis

pain

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27
Q

What are the investigations for Horner’s syndrome?

A

guided by suspected underlying aetiology
CXR for suspected lung tumour
CT/MRI for suspected cerebrovascular event
Ct angiography for suspected carotid artery dissection

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28
Q

Management for Horner’s syndrome?

A

treat underlying cause

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29
Q

What is hydrocelphalus?

A

an increase in CSF in the cerebral ventricles.
due to impaired absorption or increased secretion.
obstructive vs communicating

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30
Q

Epidemiology of hydrocephalus?

A

occurs in neonates

-absence of neonatal care, maternal hypertension during pregnancy, alcohol use during pregnancy

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31
Q

Presentation of hydrocephalus

A

Acute onset: headache and vomiting, papilloedema
gradual onset: unsteady gait, large head
cognitive deterioration, neck pain, blurred/double vision, incontinence

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32
Q

investigations for hydrocephalus?

A

HEAD CT

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33
Q

Management for hydrocephalus?

A

lumbar puncture (once ct is done and if hydrocephalus is communicating)
furesomide - inhibits further csf secretion
surgery - shunt and venrticular drain

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34
Q

What is a mononeuropathy?

A

a local lesion that causes focal involvement of a nerve

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35
Q

What is the aetiology of mononeuropathies?

A 
mechanical ie compression, constriction, trauma
entrapment
diabetes mellitus
hypothyroidism
rheumatoid arthritis
vasculitis
pregnancy
sarcoidosis
amyloidosis
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36
Q

How does carpal tunnel present?

A
  • lesion of the median nerve
  • caused by excessive use of the wrist, obesity, tenosynovitis
  • presents with NOCTURNAL PARASTHESIA affecting the thumb, index and middle fingers
  • in severe cases: wasting of abductor pollicis brevis
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37
Q

How does ulnar nerve palsy present?

A
  • lesion of the ulnar nerve
  • also known as claw hand
  • causes complete paralysis and sensory loss in 4th/5th fingers, wasting and weakness of the small muscles of the hands
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38
Q

How does radial nerve palsy present?

A
  • saturday night palsy (occurs after a night out if slept on a chair and compressed raidal nerve against the humerus)
  • wrist and finger drop
  • variable parasthesia
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39
Q

How does common peroneal nerve present?

A
  • foot drop
  • commonly caused by surgery or trauma
  • weakness on the everting foot
  • inability to extend the toes
  • parastheisa over the dorsum of the foot
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40
Q

What are the investigations for a mononeuropathy?

A
  • nerve conduction studies
  • electromyography
  • ultrasounds
  • MRI
  • nerve biopsy
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41
Q

What is the conservative management for a mononeuropathy?

A

NSAIDS
Splints
local steroid injections
(done if there is no history of trauma, if the onset is sudden, if there are no or few sensory findings and no motor deficit)

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42
Q

What is the surgical management for a mononeuropathy?

A

decompression

-done in carpal tunnel if conservative management is ineffective

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43
Q

What is narcolepsy?

A

chronic neurological condition producing abnormal disruption in normal sleep patterns

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44
Q

What is cataplexy?

A

sudden loss of muscle tone and power in response to strong emotion
-always occurs alongside narcolepsy

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45
Q

What is the epidemiology of narcolepsy?

A

onset is usually in adulthood
usually affects males
genetic component

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46
Q

What is the pathology behind narcolepsy?

A
  • patients enter REM sleep a lot faster than usual

- REM sleep intrudes into wakefulness

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47
Q

What’s the presentation of narcolepsy?

A
  • excessive daytime sleepiness (napping during daytime activities ie eating and talking)
  • cataplexy (attacks can be triggered by emotion and last from seconds to minutes)
  • hypnagogic hallucinations (at onset of sleep)
  • sleep paralysis
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48
Q

Investigations for narcolepsy?

A

CLINICAL DIAGNOSIS: >3 months excessive daytime sleepiness, cataplexy, hypersomnia not attributive to another condition, biomarkers present in tests
Epsworth sleepiness scale
Sleep studies
Brain MRI

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49
Q

Management of narcolepsy?

A

inform the DVLA
referral to sleep services
good sleep hygeine, regular exercise, strategic day time naps
drug treatment: modafinil, antidepressants, benzodiazapines (at night)

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50
Q

What is neurofibromatosis?

A

lesions on the skin, nervous system and skeleton

  • genetic disorder (autosomal dominant)
  • NF1 - most common causing skin lesions
  • NF2 - CNS tumours
  • schwannomatosis - benign nerve sheath tumour
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51
Q

what is the epidemiology of neurofibromatosis?

A

NF1>NF2
white caucasion
autosomal dominantly inherited
(50% of new cases do not have a family history)

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52
Q

presentation of NF1?

A

at least 2/7 of the following:

  • > 6 cafe-au-lait spots or hyperpigmented macules
  • Axillary or inguinal freckles
  • > 2 typical neurofibromas or one plexiform neurofibroma (from nervous tissue)
  • Optic nerve glioma
  • > 2 iris hamartomas - Lisch nodules
  • Sphenoid dysplasia
  • First degree relative with NF1
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53
Q

presentation of NF2

A

at least 1/3 of the following:

  • Bilateral 8th nerve masses on MRI scan
  • 1st degree relative with NF2 for a unilateral 8th nerve mass
  • 1st degree relative with NF2 with at least 2 of the following: Meningioma, Glioma, Schwannoma, Juvenile cataracts
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54
Q

What are the investigations for neurofibromatosis?

A

plain x ray
ct/mri head
genetic testing
histology

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55
Q

Management for neurofibramotosis?

A

monitor for malignant change
monitor multisystem involvement
surgical management for compression of tumours on other structures
pain management

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56
Q

What is non-epileptic attack disorder?

A

Attacks that have no epileptical activity in the brain

are usually pscyhologically related - known as dissociative seizures

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57
Q

How do non-epileptic attacks present?

A
  • often longer than 2 minutes
  • flapping movements (like a fish out of water)
  • eyes closed
  • have limited information about the event
  • gradual onset
  • if collapse (dramatic fall, won’t hurt themselves, legs collapse)
  • fluctuating course
  • pelvic thrusting
  • asynchronous movements (no symmetry involved)
  • can identify a trigger in some cases ie emotions
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58
Q

Investigations for non-epileptic attack?

A
  • exclude epilepsy (eeg studies)
  • mri
  • investigate other physiological causes of attacks ie syncope
  • psychiatric assessment
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59
Q

management for non-epileptic attack disorder?

A
  • education
  • anti-anxiety and antidepressant medications
  • psychological therapies ie cbt
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60
Q

What is normal pressure hydrocephalus?

A

-ventricular dilatation in the absence of increased csf pressure

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61
Q

What is the aetiology of normal pressure hydrocephalus?

A
  • idiopathic
  • SAH
  • meningitis
  • head injury
  • CNS tumour
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62
Q

How does normal pressure hydrocephalus present?

A

TRIAD:
gait disturbance - dilated ventricles cause distrubance to corona radiata
sphincter disturbance - urinary incontinence > bowel incontinence
dementia - memory loss, inattention, slow progression

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63
Q

investigations for normal pressure hydrocephalus?

A

CT/MRI - dilated ventricles
lumbar puncture - csf pressure should be normal
intraventricular pressure monitoring

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64
Q

management of normal pressure hydrocephalus

A

short term management: carbonic anhydrase inhibitors, repeated lumbar puncture
surgical management: CSF shunt

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65
Q

What is a polyneuropathy?

A

a general degeneration of peripheral nerves that spreads towards the centre of the body.
chronic and generally slow progression

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66
Q

what are the common causes of peripheral neuropathy?

A

diabetes
alcohol
leprosy (worldwide)

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67
Q

presentation of diabetic neuropathy?

A

parasthesiae, numbness, burning pain

may not have symptoms and signs picked up on check up - loss of sensation

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68
Q

What are examples of motor polyneuropathies?

A

guillain-barre syndrome
charcot-marie-tooth syndrome
-lead poisoning
-diphtheria

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69
Q

What are examples of painful peripheral neuropathies?

A
  • alcoholic neuropathy
  • diabetic myotrophy
  • vitamin b1 and b12 deficiency
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70
Q

examples of causes of peripheral neuropathies?

A
  • diabetic neuropathy

- nutritional deficiencies ie alcohol, vit b1/b12 deficiency,

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71
Q

What are some other causes of polyneuropathies?

A
  • heavy metal poisoning
  • infection
  • chronic vascular disease
  • iatrogenic
  • idiopathic
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72
Q

investigations for polyneuropathy?

A

-distal and proximal nerve stimulation tests
-immunology
-nerve biopsy
VASCULITIS SCREEN:
-glucose
-rheumatoid factors, anca
-inflammatory markers
-fbc (anaemia)
-b12
-U&Es, LFTs
-paraneoplastic antibodies and PET scan

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73
Q

management of polyneuropathies?

A
  • treat underlying cause
  • foot care, weight reduction, sensible footwear and foot orthoses
  • OT/PT
  • chronic inflammatory demyelinating polyneuropathy: steroids, IVIg, plasma exchange
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74
Q

What is a common cause of mononeuritis multiplex?

A

VASCULITIS

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75
Q

What are radiculopathies?

A
  • nerve root compression

- C6/C7 and L5/S1 are usually affected

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76
Q

What cause radiculopathies?

A
  • degenerative disc disease = disc prolapse
  • osteoarthritis
  • facet joint degeneration
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77
Q

How do patients describe a radiculopathic pain?

A

SHARP AND SHOOTING, radiating down a limb commonly in the pattern of a dermatome

78
Q

Presentation of C6/C7 radiculopathy?

A

affects the thumb and middle finger

79
Q

presentation of L5/S1 radiculopathy?

A

dorsum of foot/big toe and the ankle, lateral aspect of the foot and the sole

80
Q

What are the investigations for radiculopathy?

A

MRI

nerve conduction studies

81
Q

management for radiculopathy?

A

physio

surgery for herniated discs if appropriate

82
Q

What is shingles?

A

a rash that occurs in a dermatomal pattern following immunosuppression allowing the dormant herpes virus to flare up

83
Q

what are the risk factors for shingles?

A
  • increasing age

- immunocomprimisation

84
Q

How does shingles present?

A
  1. Pre-eruptive phase: no skin lesion, parastheisa in a dermatome, generally unwell, malaise, tender dermatome
  2. eruptive phase: skin lesions with acute neuritic pain, crust formation and drying around 7-10 days
  3. chronic phase: persistent and recurring pain lasting for 30 days
85
Q

Investigations of shingles

A

clinical diagnosis

if presentation is atypical ie extending beyond one dermatome- investigate for immunodeficiency

86
Q

management of shingles?

A

general: keep area clean and dry, when the rash isn’t covered, weeping - stay at home
Oral anti-viral therapy: aciclovir (shortens symptom duration and severity)
analgesia and fluids

87
Q

What is a stroke?

A

a clinical syndrome caused by a disruption of blood supply to the brain causing focal and/or global disturbance or cerebral function
-lasts for more than 24 hours and can be fatal

88
Q

What are the different types of stroke?

A

ischaemic (75%) and haemorrhagic (25%)

89
Q

What causes ischaemic infarctions?

A

-thromboembolisms and atheromas

can rarely be caused by trauma, infection or malignancy

90
Q

What are haemorrhagic stroke features?

A

meningism
severe headache
coma within hours

91
Q

what signs indicate ischaemic stroke?

A

carotid bruits
af
past tia

92
Q

What are the risk factors for stroke?

A
  • hypertension
  • smoking
  • diabetes mellitus
  • heart disease - valvular, ischaemic and AF
  • peripheral artery disease
  • post tia
  • carotid artery occlusion
  • combined oral contraceptive pill
  • hyperlipidaemia
  • excess alcohol
  • family history
  • age
  • gender: female
93
Q

Presentation of cerebral hemisphere infarcts:

A
  • ~2/3 of strokes occur from the middle cerebral artery
  • contralateral hemiplegia
  • facial weakness
  • contralateral sensory loss
  • homonymous hemianopia
  • dysphasia, dysphagia
94
Q

Presentation of posterior circulation infarct?

A 
motor deficit: ipsilateral weakness, lack of coordination
ipsilateral cranial nerve dysfunction
sensory deficit contralaterally
ataxia
vertigo +nausea/vomiting
diplopia
dysphagia
95
Q

investigations for stroke?

A
  • glucose
  • ECG
  • head ct
  • carotid duplex ultrasound
  • echo
  • bloods
96
Q

management of stroke

A

General: blood pressure and blood sugar managment
Ischaemic: aspiring or thrombolysis (once haemorrhage has been excluded), thrombectomy (to push clot out), long term antiplatelet therapy
haemorrhagic: clot evacuation, burr hole

REHABILLITATION with PT/OT

97
Q

indications for thrombolysis:

A
  • within 4.5 hours of initial onset of symptoms

- haemorrhagic stroke has been excluded

98
Q

What is a subarachnoid haemorrhage?

A

spontaneous arterial bleeding into the subarachnoid space usually caused by a rupture of berry aneurysms

99
Q

what are the clinical features of a SAH?

A

-thunder clap headache
nausea and vomiting
sometimes there can be a loss of consciousness
o/e focal neurological signs, papilloedema, meningeal irritation

100
Q

investigations for SAH?

A 
CT scan
lumbar puncture (12 hours after onset of symptoms if ct is clear) - XANTHOCHROMIA
101
Q

management of SAH?

A 
Bed rest
supportive measures ie control hypertension
NIMODIPINE - control artery spasms
IV Saline if hyponatraemic
neurosurgery referral?
102
Q

What is a subdural haematoma?

A

a bleed into the subdural space caused by a rupture of bridging veins
usually caused by a head injury a few weeks previously
elderly and alcoholics are most at risk

103
Q

clinical symptoms of subdural haematoma?

A

headaches
drowsiness
fluctuating confusion

104
Q

how is subdural bleeds diagnosed?

A

CT head - long crescent shaped white bleed

105
Q

treatment of subdural

A

surgery if chronic.

106
Q

what is an extradural haematoma?

A

a bleed in the extradural space - usually caused by trauma causing the underlying middle meningeal artery

107
Q

what is the history of an extradural haematoma?

A

-head injury with brief loss of consciousness, lucid interval recovery and then rapid deterioration focal neurological signs

108
Q

what does an extraduarl haematoma look like on CT?

A

lens shaped

109
Q

how is an extradural haematoma treated?

A

surgical drainage

110
Q

What is temporal arteritis?

A

systemic immune-mediated vasculitis usually affecting the carotid artery and it’s extracranial branches

111
Q

Epidemiology of temporal arteritis?

A

women are commonly affected

112
Q

risk factors for temporal arteritis?

A

european
peak incidence 60-80
genetic factors

113
Q

Presentation of temporal arteritis?

A
  • temporal headache with scalp tenderness - usually noticed when combing hair
  • transient visual symptoms
  • jaw/tongue claudication
  • systeic features: fatigue, malaise, anorexia, fever
114
Q

Investigations for temporal arteritis?

A

ESR - elevated
temporal artery biopsy
colour duplex ultrasonography

115
Q

Management for temporal arteritis

A
  • steroids

- low dose aspirin

116
Q

What are myopathies? What is a common type of muscular dystrophy?

A

a disease of the muscle

Duchenne’s muscular dystrophy

117
Q

Aetiology of myopathies?

A

inherited: Duchenne’s
Acquired: immmunologically mediated ie RA, SLE
non-inflammatory mediated: hyper/hypothyroidism, Cushings
toxic: drugs - steroids, statins
infection: hiv, influenza, LYME DISEASE

118
Q

Clinical features of myopathies?

A

Weakness: usually proximally
variation of strength with exercise
difficulties rising from a chair, climbing stairs, combing hair

119
Q

investigations for myopathy

A 
blood and urine tests: creatinine kinase, renal function, 
ecg
muscle biopsy
electromyopgraphy
mri
genetic testing
120
Q

management of myopathies?

A

treat underlying cause ie treat infection, stop/change drugs
physiotherapy
physical aids
dietary advice

121
Q

what is wernicke korsakoff’s syndrome?

A

a sprectrum of disease resulting from thiamine deficiency

triad: mental confusion, ataxia, ophthalmoplegia

122
Q

epidemiology of wernicke korsakoff’s syndrome?

A

alcoholics

higher prevalence in lower socioeconomic groups

123
Q

pathogenesis wernicke korsakoffs?

A

chronic alcohol misuse = inadequate thiamine intake, decreased absorption, impaired thiamine usage in cells

124
Q

presentation of wernicke korsakoffs?

A
  • confusion,
  • nausea and vomiting
  • weakness and loss of muscle coordination
  • eye problems: diplopia, nystagmus, eye movement abnormalities
125
Q

investigations for wernicke korsakoffs??

A

clinical diagnosis - treat is suspicions are high
bloods - fbc, u&es, lfts, glucose, serum thiamine levels
ct scan
abg

126
Q

management of wernicke korsakoffs?

A

management of alcohol
oral thiamine replacement
dietician input

127
Q

What are the acute causes of headaches?

A
  • infection: meningitis/encephalitis
  • haemorrhage: SAH, extradural
  • venous sinus thrombosis
  • sinusitis
  • low pressure headache: csf leak
  • acute glaucoma
128
Q

what are the causes of chronic headache?

A
  • tension headaches
  • migraine
  • cluster headaches
  • trigeminal neuralgia
  • raised icp
  • medication overuse headache
  • giant cell arteritis
129
Q

what are the triggers for a migraine?

A
  • Chocolate
  • Hangovers
  • Orgasms
  • Cheese
  • Oral contraceptives
  • Lie ins
  • Alcohol
  • Tumult (loud noises)
  • Exercise
130
Q

Treatment for acute migraine?

A

NSAIDs, triptans

131
Q

Prevention for migraine?

A

beta blockers
amitriptyline
topiramate

132
Q

presentation of a cluster headache?

A

unilateral pain around the eye, watery/bloodshot eye, clusters of headaches - followed by pain free periods for months

133
Q

management of a cluster headache?

A

oxygen, sumatriptan

134
Q

what’s the management for trigeminal neuralgia

A

MRI
carbamazepine
microvascular decompression

135
Q

what’s the definition of a TIA?

A

stroke symptoms lasting less than 24 hours

136
Q

TIA management?

A 
reduce blood pressure
reduce cholesterol
control diabetes
control other lifestyle factors
DVLA - can't drive for 1 month
CLOPIDOGREL
carotid endarectomy
137
Q

What are the causes of seizures?

A
  • epilepsy
  • febrile convulsions
  • alcohol withdrawal seizures
  • psychogenic non epileptic seizures
  • brain injury
  • infection
  • trauma
  • metabolic disturbance
138
Q

What are the different partial types of seizures?

A

Focal/partial: seizure activity is limited to one part of a hemisphere
Complex/partial: disturbance of consciousness or awareness
eg. frontal lobe seizure: usually occur from waking, 4-shape, drawing an arrow. very fast recovery

139
Q

what are the different generalised types of seizures?

A

Absence: brief episode where patient appears blank/staring
Tonic-clonic: muscle rigidity followed by repeated contraction and relaxation
Myoclonic: brief, rapid muscle jerks
Atonic: ‘drop attacks’, lose muscle tone and drop to ground

140
Q

Treatment for generalised seizures?

A
  • Sodium valproate

- lamotrigine, carbamazepine

141
Q

Treatment for partial/focal seizures?

A
  • Carbamazepine

- leveritacetam (keppra)

142
Q

treatment for absence seizures?

A
  • sodium valproate

- ethosuximide

143
Q

what is multiple sclerosis?

A

cell mediated demyelination in the cns

144
Q

how does ms present?

A
  • Visual: optic neuritis, optic atrophy, uhtoff’s phenomenon
  • sensory: numbness, tingling, trigeminal neuralgia
  • motor: spastic weakenss
  • cerebellar: ataxia, diplopia, intention tremor
  • urinary incontinence
  • sexual dysfunction
  • intellectual deterioration
145
Q

epidemiology of ms?

A
  • 20-40 year old females

- temperate climate with low vit d levels

146
Q

how is ms investigated?

A

MRI - demyelinated plaques

147
Q

types of ms progression?

A

Relapsing-remitting
Primary progressive
Secondary progressive

148
Q

MS management?

A

Steroids for acute relapses
Disease modifying drugs: beta-interferon, alemtuzimab
Treat symptoms

149
Q

parkinsons pathophysiology?

A

degeneration of dopaminergic neurones in the substantia nigra

150
Q

parkinsons presentation?

A

TRIAD: bradykinesia, cogwheel ridigity, resting tremor

  • postural instability
  • asymmetrical pattern
  • shuffling gait with reduced arm swing
  • difficulty initiating movement
151
Q

What are the histiological findings in parkinsons?

A

lewy bodies

152
Q

management of parkinsons?

A
  • dopamine receptor agonists (bromocriptine, ropinirole)
  • levodopa and dopa-decarboxylase inhibitor (carbadopa)
  • MAO-B inhibitors: selegilline
  • anticholinergics: orphenadrine
  • COMT inhibitors: entacapone
153
Q

what is huntington’s disease?

A

-inherited (autosomal dominant) - defect in huntingtin gene, repeated CAG neurodegenerative, progressive
movement disorder
-loss of GABA mediated inhibition

154
Q

prodrome features of huntingtons?

A
  • personality changes
  • lack of coordination
  • chorea
  • dystonia/hypotonia
  • intention/tremor
  • fits
  • intellectual impairment
  • progressive dementia
155
Q

investigations fo huntingtons disease

A

genetic testing

156
Q

management of huntingtons?

A

MDT approach: genetic counselling, salt, dieticians, physio, ot, psychologists
symptom control: dopamine antagonists

157
Q

what is motor neurone disease?

A

a degenerative condition that affects motor neurones

  • no sensory involvement or cerebellar signs
  • no effect on eye movements
158
Q

what are the different types of motor neurone disease?

A
  • ALS: amyotrophic lateral sclerosis (most common type - both)
  • progressive bulbar palsy (Both)
  • progressive muscular atrophy (LMN)
  • primary lateral sclerosis (UMN)
159
Q

presentation of MND:

A

LMN signs: progressive limb weakness, wasting of thenar/tibialis anterior, fasciculations
UMN signs: hypertonia, brisk reflexes, upgoing plantars, spasticity
CLASSICALLY: stumbling spastic gait, foot drop, proximal myopathy, weak grip, associate with frontotemporal dementia

160
Q

investigations for mnd:

A

nerve conduction studies

mri (exclude cervical cord compression, ms, myelopathy

161
Q

management of mnd:

A 
feeding and respiratory support
mdt approach
RILUZOLE
BACLOFEN
ANTIDEPRESSANTS
162
Q

What is gullain-barre syndrome?

A

acute inflammatory demyelinating polyenuropathy

163
Q

how does guillaine-barre syndrome present?

A 
post-infection: campylobacter 
symmetrical ascending weakness
no or little sensory signs
areflexia
cranial nerve dysfunction ie diplopia
autonomic dysfunction: sweating, tachycardia, arrhythmias, urinary retention
164
Q

investigations for guillain barre?

A

nerve conduction studies: slow
csf: raised protein, normal wcc
anti-gm1 antibodies

165
Q

management for guillain barre?

A

IVIg

Plasma exchange

166
Q

What is myasthenia Gravis?

A

autoimmune neuromuscular disease causing weakness of the muscles

167
Q

pathology of myasthenia gravis?

A

antibodies to post-synaptic nicotinic ACh receptors which interferes with muscular transmission causing fatiguability. This is because of the fewer receptors at the NMJ.

168
Q

what antibodies would be present in myasthenia gravis?

A

ACh-R

MuSK - Muscle-specific receptor tyrosine kinase

169
Q

epidemiology of myasthenia gravis?

A

females
30-50 year old
other autoimmune conditions
associated with a thymic tumour

170
Q

presentation of myasthenia gravis?

A
  • increasing muscular fatigue (especially at the end of the day)
  • in order: extra-ocular (ptosis, diplopia), bulbar (swallowing, chewing, dysphonia) face, neck, limbs (proximal), girdle, trunk
  • normal tendon reflexes
171
Q

What are 2 classic myasthenic signs?

A
  • Peek sign: After 30 seconds of sustained forced eyelid closure, he is unable to keep the lids fully closed.
  • Myasthenic snarl: may occur when patients try to smile. The snarl follows contraction of the middle portion of the upper lip while the upper mouth corners fail to contract.
172
Q

investigations for myasthenia gravis?

A

antibodies: anti-AChR, MuSK
CT Thorax: thymus
Ice test
Tensilon test (short acting antiacetylcholinesterase which improves muscle strength after administration)

173
Q

treatment for myasthenia gravis?

A
  • acetylcholineesterase inhibitors: PYRISTIGMINE
  • immunosuppressants for relapses: prednisolone
  • Thymectomy
174
Q

what is myasthenic crisis?

A
  • weakness of the respiratory muscles
  • may need intubation and ventilation
  • treated with plasmapharesis/IVIg
  • treat trigger ie infection, medications, post-op
175
Q

What are some examples of types of dementia?

A
  • alzheimers
  • vascular
  • lewybody
  • frontotemporal
  • huntingtons, CJD
176
Q

What are some treatable types of dementia?

A
  • Hypothyroid
  • Addisons
  • B12/Folate deficiency
  • Low thiamine
  • Syphillis
  • Brain tumour
  • Normal pressure hydrocephalus
  • Subdural haematoma
  • Depression
  • Drugs
177
Q

Assessment tools for dementia?

A 
Adenbrookes cognitive examination - less than 84 indicates dementia. poor memory and fluency inidicates alzheimers
Abbreviated mental test score (AMTS)
6CIT - 6 item cognitive impairment test
GPCOG- GP assessment of cognition
MMSE - (less than 24/30)
178
Q

What is alzheimer’s disease?

A

progressive global cognitive impairment

179
Q

what is the pathology of alzheimer’s?

A

beta-amyloid plaques
cerebral atrophy in the cortex and hippocampus
defecit in acetylcholine

180
Q

what are the features of alzheimers?

A 
memory loss
decrease in visuospatial skills
verbal abilities decline
reduction in executive function
lack of insight
181
Q

management of alzheimers?

A
  • specialist memory service

- acetylcholineesterase inhibitors: rivistigmine, donepezil, galantamine, memantine (late stages)

182
Q

describe vascular dementia, its associations and management

A
  • cumulative effect of many small strokes, stepwise progression
  • associated with: past history of stroke, hypertension, AF, diabetes, smoking, coronary heart disease, obesity
  • management: modify risk factors, treat symptoms
183
Q

describe lewybody dementia, its features and management

A
  • lewybody: alpha-synuclein cytoplasmic inclusions in brainstem and neocortex
  • features: progressive cognitive impairment, parkinsonism, visual hallucinations
  • management: avoidance of neuroleptics, AChesterase inhibitors,
184
Q

What is dysarthria?

A

difficult or unclear articulation of speech that is otherwise linguistically normal

185
Q

what is dysphonia

A
  • difficulty in speaking due to a physical disorder of the mouth, tongue, throat or vocal cords
  • sounds like donald duck
186
Q

what is dysphagia?

A

difficulties swalloing

187
Q

what is dysphasia?

what are the different types of dysphasia?

A
  • difficulty communicating
  • expressive dysphasia: difficulties with speech - broken sentences that is comprehensible once they’ve said what they want (BROCAS)
  • receptive dyspahsia: difficulties with comprehension. what they say won’t make sense (WERNICKES)
  • NOTE: aphasia and dysphasia are used interchangably
188
Q

what is akinesia?

A

loss or impairment of the power of voluntary movement

189
Q

what is ataxia?

A
  • lack of voluntary coordination of muscle movements

- includes: gait abnormality, speech changes, eye movement abnoralities

190
Q

what is apraxia?

A

difficulty with the motor planning to perform tasks or movements when asked (provided that the request or command is understood and he/she is willing to perform the task.)

191
Q

what is agnoisa?

A

inability to interpret sensations and therefore recognise things ie not recognising people

3A (6 decks)

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