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NP- Phase 3a Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

what are some red flags in a headache history?

A
  • new onset headache + history of cancer
  • cluster headache
  • seizures
  • altered conciousness/ memory/ confusion/ coordination
  • papilloedema
  • abnormal neurological examination
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2
Q

features of a migraine

A
  • 4-72 hours
  • must occur at least 5 times for diagnosis
  • painful, unilateral, pulsating, aggravated by routine physical activity
  • associated with nausea, photophobia, phonophobia
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3
Q

features of a tension headache

A
  • 30 mins- 7 days
  • bilateral pressing pain, not aggravated by routine physical activity
  • no nausea/ vomiting
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4
Q

features of a cluster headache

A
  • 15-180 minutes
  • severe unilateral orbital/ supraorbital pain
  • accompanied by ipsilateral cranial autonomic features and a sense of restlessness/ agitation
  • attacks occur in a ‘cluster’ then are separated by a ‘pain free’ period
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5
Q

features of trigeminal neuralgia

A
  • unilateral face pain in the distribution of the trigeminal nerve
  • lasts up to 2 minutes
  • like an electric shock
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6
Q

which headaches are classed as primary headaches?

A

migraine, cluster and tension

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7
Q

how are primary headaches treated?

A 
- lifestyle modification 
pharmacological:
- oral triptans- NSAIDS/ paracetamol 
- anti-emetics
- topiramate/ propanolol 
- botulinum toxin injections
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8
Q

features of idiopathic intercranial hypertension?

A
  • pain is worse on walking, coughing, sneezing and straining
  • nausea and vomiting
  • pappiloedema
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9
Q

how is idiopathic intercranial hypertension treated?

A

acetazolamide
topiramate
diuretics

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10
Q

features of GCA

A 
new onset headache
localised pain 
tenderness 
jaw claudication
visual disturbance
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11
Q

treatment of giant cell arteritis

A

prednisolone

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12
Q

features of medication overuse headache

A
  • headache present over 15 days/ month
  • caused by regular use of drugs (more than 3 months)
  • headaches worse during drug use
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13
Q

clinical features of MS

A
  • more common in females (usual age around 30)
  • monosymptomatic- most commonly optic neuritis
  • symptoms worsen on heat/ exercise
  • relapsing/ remitting- monosymptomatic followed by a period of no symptoms
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14
Q

diagnosis of MS

A
  • clinical
  • lesions disseminated in time and space attributed to no other known cause
  • MRI- identifies plaques
  • CSF- oligoclonal bands of IgG on electrophoresis
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15
Q

treatment of MS

A
  • vitamin D supplements
  • methylprednisolone to treat relapses
  • IFN- 1b and IFN 1a to decrease relapses
  • monoclonal antibodies- alemuzumab/ rituximab
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16
Q

what is myasthenia gravis?

A

autoimmune disease in which antibodies to nicotinic acetylcholine receptors are produced

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17
Q

clinical presentation of myasthenia gravis?

A
  • muscular weakness/ fatigue
  • ‘moves down’ e.g. symptoms begin extra ocularly and progress down the body towards the trunk
  • ptosis, diplopia, myasthenic snarl
  • voice fades on counting to 50
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18
Q

how is myasthenia gravis diagnosed?

A
  • anti-AChR antibodies found in 90%

anti- muscle specific Kinase (MuSK) antibodies

Large thymus/ clusters of immune cells in thymus - Thymomas (tumours)

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19
Q

treatment of myasthenia gravis?

A
  • symptom control- anticholinesterase medication= pyridostigmine
  • treat relapses with prednisolone +azathioprine/ methotrexate
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20
Q

what can exacerbate symptoms in myasthenia gravis?

A
  • pregnancy
  • hypokalaemia
  • infection
  • drugs- tetracycline, quinine, B-blockers
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21
Q

how is MND distinguished from MS and polyneuropathies?

A

affects UMN and LMN, but NO sensory loss or sphincter disturbance

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22
Q

clinical presentation of amyotrophic lateral sclerosis (ALS)

A
  • loss of motor neurons in motor cortex and anterior horn of spinal cord
  • weakness + UMN signs (upgoing plantars etc) +LMN wasting/ fasciculations
  • split hand sign- thumbs side of the hand seems to separate from the rest due to excessive wasting
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23
Q

clinical presentation of progressive bulbar palsy

A
  • cranial nerves IX-XII
  • LMN lesion of the tongue and muscles and talking -results in a flaccid, fasciculating tongue, absent jaw jerk, speech changes- quiet, horse, nasal
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24
Q

clinical presentation of progressive muscular atrophy

A
  • anterior horn cell lesions only
  • LMN only
  • affects distal muscle groups before proximal
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25
Q

clinical presentation of primary lateral sclerosis

A
  • loss of betz cells in motor cortex
  • UMN signs
  • spastic leg weakness and pseudo-bulbar palsy
  • no cognitive decline
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26
Q

How is MND generally diagnosed?

A

clinical findings and EMG/ nerve conduction studies

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27
Q

what is the El Escorial Criteria for the diagnosis of ALS?

A
  • signs of LMN and UMN degeneration
  • progressive spread of signs together with the ABSENCE of:
    • elctrophysiological evidence of other disease processes that may explain the signs
  • neuroimaging evidence of other disease pocess that may explain the observed signs
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28
Q

management of MND

A
  • riluzole- extends life by around 3 month
  • baclofen for spasms
  • PEG tube for feeding if needed
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29
Q

UMN signs

A 
weakness 
brisk reflexes 
hypertoni 
upgoing plantars (positive babinski)
clonus
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30
Q

LMN signs

A 
weakness 
depressed/ absent reflexes 
decreased tone
wasting
fasciculations
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31
Q

what is Guillain-Barre syndrome?

A

acute, inflammatory, demyelinating, ascending polyneuropathy that affects the PNS following an upper respiratory tract infection/ GI infection

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32
Q

what are some common infections that can trigger GBS?

A
  • campylobacter jejuni
  • CMV
  • herpes zoster
  • EBV
  • HIV
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33
Q

clinical features of GBS

A
  • post infection
  • symmetrical, ascending muscle weakness, begninning in the distal limb muscles and progresses proximally
  • loss of reflexes, neuropathic pain and autonomic dysfunction
  • can also affect respiratory muscles
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34
Q

diagnosis of GBS

A
  • nerve conduction studies

- lumbar puncture- CSF- high proteins, normal WCC

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35
Q

how is GBS managed?

A
  • IV immunoglobulin (IVIg) for 5 days

- monitor ventilation

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36
Q

clinical features of Huntingtons

A
  • chorea- jerky, explosive, figidity movements
  • dysarthria, dysphagia, abnormal eye movements
  • dementia
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37
Q

what is the difference between spinal cord and spinal root compression?

A

spinal cord compression- myelopathy with UMN

spinal root compression- radiculopathy with LMN

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38
Q

Clinical features of a subarachnoid haemorrhage

A
  • thunderclap headache/ sudden onset severe headache
  • vomiting
  • collapse
  • seizures
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39
Q

clinical signs of a subarachnoid haemorrhage

A
  • neck stiffness (Kernigs sign)
  • retinal bleeds
  • photophobia
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40
Q

diagnosis of SAH

A

star on CT

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41
Q

management of SAH

A
  • surgery- endovascular coiling
  • maintain cerebral perfusion
  • nimodipine
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42
Q

features of a subdrual haematoma

A
  • fluctuating conciousness
  • bleeding from bridging veins
  • symptoms occur late- a while after the initial injury
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43
Q

features of an extradural haematoma

A
  • traumatic skull fracture

- lucid internal for a few days after injury

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44
Q

what is Lhermitte’s phenomenon?

A

Neck flexion brings on a sudden sensation of an electric shock running down your spine

Sign of MS

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45
Q

What is Uhthoffs phenomenon?

A

Temporary worsening of symptoms caused by an increase in temperature

(e.g. - MS patient in hot bath)

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46
Q

what is clinically located syndrome?

A

First episode of MS characteristics that must last 24 hours.

first attack of demyelination

A diagnosis of MS can be made afterwards if the MRI shows lesions similar to those of MS

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47
Q

what is secondary progressive MS?

A

SPMS follows relapsing remitting. Relapsing remitting will transition into progressive worsening of neurological functioning

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48
Q

what is primary progressive MS?

A

Worsening of neurological functioning from the onset of symptoms, without early relapses or remissions

15% of diagnosis

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49
Q

What is relapsing remitting MS?

A

clearly defined attacks of new or increasing neurologic symptoms.
These attacks – also called relapses or exacerbations – are followed by periods of partial or complete recovery (remissions).

During remissions, there may be no symptoms, and no apparent progression of the disease

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50
Q

describe GCS scoring

A

Eye Opening (E)

4 = spontaneous
3 = to sound
2 = to pressure
1 = none
NT = not testable

Verbal Response (V)

5 = orientated
4 = confused
3 = words, but not coherent
2 = sounds, but no words
1 = none
NT = not testable

Motor Response (M)

6 = obeys command
5 = localizing
4 = normal flexion
3 = abnormal flexion
2 = extension
1 = none
NT = not testable
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51
Q

what condition is due to a CCG repeat?

A

fragile X syndrome

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52
Q

headache red flags

A

1) Sudden onset + severe
2) Age >50
3) Neck pain/stiffness, photophobia
4) Fever
5) Papilloedema
6) New onset neuro deficit
7) Vomiting
8) Dizziness and visual disturbances / atypical aura (over an hour)

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53
Q

what is giant cell arteritis?

A

Granulomatous medium/large vessel vasculitis

large vessel vasculitis of the head, scalp, arms, neck

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54
Q

what is a common association with GCA?

A

Polymyalgia Rheumatica - (neck, shoulders,back,hip)

1) Stiffness
2) Aching
3) Pain

Jaw/ Tongue claudication
Fever
Headache

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55
Q

what anaemia is seen in GCA?

A

normocytic normochromic

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56
Q

what is the difference between a facial palsy caused by an upper or lower motor neurone lesion?

A

Upper motor neurone lesion spares the upper head e.g ‘wrinkle forehead/ raise eyebrows’

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57
Q

what is Bells palsy?

A

Lower motor neurone palsy of the facial nerve (7th)

Causing:

1) Facial droop on one side of the face
2) Cant close one eyelid
3) flat wrinkles on one side of forehead

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58
Q

how is Bells palsy diagnosed?

A

diagnosis of exclusion- rule out other possible causes

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59
Q

management of Bells palsy

A
  • eye drops
  • wear sunglasses
  • corticosteroids- prednisolone
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60
Q

median nerve palsy

A

C6-T1

carpal tunnel syndrome

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61
Q

ulnar nerve palsy

A

C7-T1
claw hand
weakness/ wasting of medial wrist flexors

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62
Q

radial nerve palsy

A

C5-T1

wrist and finger drop

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63
Q

Lat. cutaneous nerve of the thigh palsy

A

L2-L3

meralgia paraesthesia- lateral burning thigh pain

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64
Q

sciatic nerve palsy

A

L4-S3

foot drop

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65
Q

common peroneal nerve palsy

A

L4-S1

foot drop, weak dorsiflexion, sensory loss

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66
Q

tibial nerve palsy

A

L4-S3

failure of plantarflexion (tiptoes)

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67
Q

in which type of myopathy does spontaneous pain at rest occur?

A

inflammatory myopathy

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68
Q

which types of myopathy have a rapid onset?

A

toxic, drug or metabolic myopathies

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69
Q

what myopathy does pain on exercise relate to?

A
  • ischeamia/ metabolic myopathy (McArdle’s disease)
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70
Q

what myopathy does ‘firm; muscles imply?

A

pseudo-hypertrophic muscular dystrophies (Duchenne’s)

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71
Q

how does Duchene’s muscular dystrophy present?

A
  • young (around 4)
  • clumsy walking
  • diffuclty in standing
  • progresses to respiratory failure
  • pseudohypertrophy is also seen- in the calves
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72
Q

what marker is significantly raised in Duchennes?

A

serum creatinine kinase (over 40 times)

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73
Q

what is the inheritance pattern seen in duchenne’s and beckers’ muscular dystrophy?

A

x- linked recessive

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74
Q

how does myotonic dystrophy present?

A
  • 20-40 years old
  • distal weakness (hand/foot drop)
  • weak sternocleidomastoids
  • facial weakness
  • cataracts
  • develop respiratory and cardiac problems
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75
Q

clinical presentation of inflammatory myopathies

A
  • weakness of quadriceps, finger flexors

- poor response to therapy

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76
Q

drug causes of myopathy

A

alcohol, statins, steroids, chloroquine, zidovudine, vincristine, cocaine

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77
Q

clinical features of facioscapulohumeral muscular dystrophy?

A
  • onset 12-14
  • inabiltiy to puff out cheeks
  • cant raise arms over head
  • foot drop
  • scapular winging
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78
Q

what is dermatomyositis?

A

insidious onset of progressive symmetrical proximal muscle weakness plus ‘skin signs’ macular rash, purple eyelids

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79
Q

how are polymyositis and dermatomyositis investigated?

A
  • ALT, AST, LDH, CK all raised
  • muscle biopsy confirms diagnosis
  • MRI shows some muscle oedema
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80
Q

how are polymyositis and dermatomyositis managed?

A

prednisolone

use hydroxychloroquine in dermatomyositis

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81
Q

what is status epilepticus?

A

a seizure lasting more than 30 minutes or repeated seizures without regaining consciousness

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82
Q

how is a diagnosis of status epilepticus confirmed?

A

EEG

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83
Q

how is status epilepticus managed?

A
  • lorazepam
  • buccal midazolam
  • phenytoin infusion
  • dexamethasone
84
Q

what is myasthenic crisis?

A

life-threatening weakness of the respiratory muscles during relapse

85
Q

how is a myasthenic crisis monitored and treated?

A
  • monitor FVC
  • treat with plasmapheresis (removes AChR antibodies from circulation) or give IVIg and identify and treat trigger of relapse (e.g. infection, medication)
86
Q

how is the femoral nerve root tested?

A

L1,L2,L3 - iliopsoas- flex hip against resistance with knee flexed

L2,L3,L4- quadriceps femoris- extend knee against resistance

87
Q

how is the obturator nerve root tested?

A

L2,L3,L4- hip adductors- adduct leg against resistance

88
Q

how is the inferior gluteal nerve tested?

A

L5,S1,S2- gluteus maximus- hip extension (bury heel into bed)

89
Q

how is the superior gluteal nerve tested?

A

L4, L5, S1- gluteus maximum and minimus- abduction and internal hip rotation with leg flexed at hip and knee

90
Q

Where do you test sensation in the following dermatomes on the arm?

C5-T2

A

C5 - Over deltoid

C6 - index finger

C7 - middle finger

C8 - little finger

T1 - inside arm

T2 - apex of axilla

91
Q

Where do you test sensation in the following dermatomes on the leg?

L2-S2

A

L2 - anterior medial thigh

L3 - over knee

L4 - medial tibia

L5 - dorsum of foot running to big toe

S1 - lateral heel

S2 - popliteal fossa

92
Q

Where do you test movement in the following myotomes on the arm?

C5-T1

A

C5 - shoulder abduction

C6 - elbow flexion

C7 - elbow extension

C8 - finger flexion

T1 - finger abduction

93
Q

Where do you test movement in the following myotomes on the leg?

L2-S2

A

L2- Hip flexion

L3- Knee extension

L4- Ankle dorsiflexion

L5- Extension of big toe

S1- Ankle plantar flexion

S2- Knee flexion

94
Q

What muscles does the radial nerve innervate

A

Triceps and finger extensors

95
Q

What muscles do the median nerve innervate?

A

LOAF

Lateral 2 lumbricals

Oppenens brevis

Abductor pollicis brevis

Flexor pollicis brevis

96
Q

What muscles do the ulnar nerve innervate?

A

Intrinsic muscles of the hand, lumbricals, hypothenar and interossei

97
Q

What nerve is responsible for:

Finger flexion?

Finger extension?

Finger abduction?

A

Median

Radial

Ulnar

98
Q

What is the most common winged scapula nerve lesion?

A

Long thoracic nerve (serratus anterior)

99
Q

What nerve is responsible for the following movements?

knee extension

knee flexion

ankle dorsiflexion

Big toe extension

ankle plantar flexion

A

knee extension - femoral L3

knee flexion - sciatic/tibial L5, S1/2

ankle dorsiflexion - peroneal L4

Big toe extension - peroneal L5

ankle plantar flexion - tibial S1

100
Q

Name some foot drop differentials?

A

Muscle: myopathy

Nerve: peroneal nerve, sciatic nerve

Root: L4/5

Anterior horn: MND

Brain: parasaggital mengingioma

101
Q

Which lobe is Brocas area in and what is its function?

A

region in the frontal lobe of the dominant hemisphere, usually the left, of the brain with functions linked to speech production

102
Q

Which lobe is Wernicke’s area in and what is its function?

A

located in the temporal lobe on the left side of the brain and is responsible for the comprehension of speech

103
Q

What are Kernigs and Brudzinkis sign?

A
  • Kernig’s (inability to straighten knee when hip flexed 90 degrees)
  • Brudzinski’s- neck stiffness - flex neck and knee+hip flex too
104
Q

Symptoms of Optic Neuritis?

A

1) Reduced visual acuity over days
2) Pain on moving eye
3) Exacerbated by heat/exercise
4) Afferent pupillary defect
5) Dyschromatopsia (especially red)

105
Q

How does Huntingtons occur?

A

autosomal dominant

1) Chromosome 4 produces Huntingtin protein
2) Mutation to the Huntington gene on chromosome 4 results in CAG nucleotide repeats
3) This leads to an abnormal Huntingtin protein & neurodegenerative disorder

106
Q

What type of hypersensitivity reaction is Myasthenia Gravis and Multiple Sclerosis?

A

MG - type II (antibody mediated - AChR / MuSK)

MS - type IV (cell-mediated- T cell crosses brain barrier, activated by myelin, sends signal to allow more T cells across barrier)

107
Q

what are 3 risk factors of MS?

A

Female
Vit D deficiency
HLA-DR2

108
Q

What is Charcots Neurological Triad?

A

1) Dysarthria (dysfunctional eating, talking, swallowing)
2) intention tremor (muscle weakness, spasms, ataxia, paralysis)
3) Nystagmus (Optic Neuritis, greying of vision, pain, double vision)

Linked to MS

109
Q

What visual defects are caused by:

Temporal lesions?

A

contralateral superior quadranopia

PITS (Parietal-Inferior, Temporal-Superior)

110
Q

What visual defects are caused by:

Parietal lesions?

A

contralateral inferior quadranopia

PITS (Parietal-Inferior, Temporal-Superior)

111
Q

What visual defects are caused by:

Diabetes Insipidus due to craniopharyngioma

A

lower bitemporal hemianopia

112
Q

What visual defects are caused by:

Pituitary macroadenoma

A

Upper bitemporal hemianopia

113
Q

What visual defects are caused by:

Occipital cortex lesion?

A

Macula sparing homonymous hemianopia

114
Q

What visual defects are caused by:

compression of the optic chiasm

A

Bitemporal hemianopia

115
Q

treatment of migraines

A

NSAIDS- ketoprofen, aspirin
- triptans (5HT agonists)- rizatriptan, sumatriptan

1st line- propanolol, amitryptilline, CCB’s
2nd line- valporate, pizotifen, gabapentin

116
Q

treatment of trigeminal neuralgia

A

carbamazepine, lamotrigine, phenytoin

surgery

117
Q

causes of spinal cord compression

A
  • secondary malignancy- breast, lung, prostate, thyroid, kidney
  • infection- epidural abscess
  • cervical disc collapse
  • haematoma
  • intrinsic cord tumour
  • atlanto-axial subluxation
  • myeloma
118
Q

treatment of spinal cord compression

A
  • If malignancy – give dexamethasone IV while waiting for radio/chemotherapy ± decompressive laminectomy
  • Epidural abscess – surgical decompression and abx
119
Q

what is cauda equina and how does it present?

A
  • damage to the spine at or distal to L1
  • presents with leg weakness, back pain, radicular pain down legs, asymmetrical, atorphic, arereflexic paralysis of legs, sensory loss in root distribution, decreased sphincter tone
120
Q

causes of cauda equina syndrome

A
  • trauma
  • congenital lumbar disc disease
  • lumbosacral nerve lesions
  • lumbar disc prolapse
121
Q

examples of primary malignant brain tumours

A
  • glioma
  • embryonal tumours- medulloblastoma
  • lymphoma
122
Q

examples of benign brain tumours

A
  • meningioma

- neurofibroma

123
Q

what cancers metastasise to the brain?

A
  • bronchial
  • breast
  • stomach
  • prostate
  • thyroid
  • kidney
124
Q

what are the clinical features of a brain tumour and what causes these?

A
  • neurological deficit- due to mass effect of tumour and surrounding cerebral oedema
  • raised ICP- results in headache, vomiting and papilloedema
  • epilepsy
125
Q

how can a brain tumour cause respiratory depression?

A

raised ICP- brain is displaced downwards, which puts pressure on the brainstem. This causes drowsiness, resulting in respiratory depression, braycardia and death

126
Q

differential diagnosis for a brain mass

A
  • tumour
  • cerebral abcess
  • tuberculoma
  • subdural haematoma
  • intracranial haematoma
127
Q

what organisms can cause meningitis

A
  • meningococcus or pneumococcus

less common:

  • hemophilus influenzae
  • listeria monocytogenes
  • HSV
  • VZV
128
Q

differential diagnosis for meningitis

A
  • malaria
  • encephalitis
  • septicaemia
  • tetanus
129
Q

what are the clinical features of meningitis (early and later)?

A

early- headache, fever, leg pains, cold peripheries, palor

later:

  • meningism- neck stiffness, photophobia, Kernigs sign
  • decreased GCS, come
  • seizures and focal CNS signs
  • non-blanching petechial rash
  • prolonged CRT
130
Q

Management of meningitis

A
  • early Abx- cefotaxime and ampicillin
  • dexamethasone
  • fluid rescucitation
  • contact tracing prophylaxis- rifampicin ciprofloxacin
131
Q

lumbar puncture- differences in:

  • appearance
  • protein

between bacterial, tuberculous and viral meningitis

A

appearance:

  • bacterial- turbid
  • tuberculous- fibrin web
  • viral- clear

protein (g/L)

  • bacterial- >1.5
  • tuberculous- 1-5
  • viral- <1
132
Q

what is encephalitis?

A

inflammation of the brain parenchyma

133
Q

how does encephalitis present?

A
  • abnormal cerebral function with altered mental status, motor and sensory deficits
  • fever, headache, drowsiness
  • focal neurological signs
  • seizures
134
Q

causes of encephalitis?

A

look for history of recent travel/ animal bite

usually viral:

  • herpes simplex
  • CMV
  • EBV
  • VZV
  • HIV
  • measles

non-viral causes:

  • bacterial meningitis
  • TB
  • malaria
  • listeria
135
Q

investigations in encephalitis

A
  • CT/ MRI
  • viral serology of CSF and blood
  • EEG
136
Q

Tx of encephalitis

A

IV acyclovir

137
Q

what is shingles?

A

re-activation of the herpes zoster virus after a previous primary infection with chickenpox

virus remains dormant in dorsal root ganglia/ cranial nerve ganglia

138
Q

what is the dermatome distribution seen in shingles?

A
  • rash- papules and vesicles
  • pain and tingling
  • lower thoracic dermatomes and opthalmic division of trigeminal nerve
139
Q

treatment of shingles

A

oral acyclovir

140
Q

what is the most common complication in shingles and how is it treated?

A
  • post-herpetic neuralgia (PHN)

- tx- carbamazepine

141
Q

features of an ataxic gait

A
  • wide based
  • falls
  • cannot walk heel to toe
  • worse in dark/ with eyes closed
142
Q

2 main causes of an ataxic gait

A
  • cerebellar dysfunction

- proprioceptive issues

143
Q

what are the cerebellar causes of an ataxic gait?

A
  • MS
  • posterior fossa tumour
  • alcohol
  • phenytoin toxicity

deficit is ipsilateral to cerebellar lesion

144
Q

what are the features of cerebellar syndrome?

A

ataxia plus nystagmus

145
Q

what are the proprioceptive causes of an ataxic gait?

A
  • sensory neuropathies (low B12)

- inner ear problem- affecting the vestibular system

146
Q

what test helps you distinguish between proprioceptive and cerebellar causes of ataxic gait?

A
  • if they can walk normally with their eyes open but not when they close= proprioceptive
  • if the problem is there regardless= cerebellar
147
Q

what are the features and cause of a circumduction (spastic) gait?

A
  • features- stiff gait, circumduction of legs (scuffing of the toes of the shoes)
  • cause- stroke (hemiplegia)
148
Q

what are the features and cause of a shuffling (extra-pyramidal) gait?

A
  • features- flexed posture, shuffling feet, postural instability, difficulty initiating movements
  • causes- Parkinsons disease
149
Q

what is and what are the causes of an antalgic gait?

A
  • limping

- MSK- pain

150
Q

what are the features and causes of a high stepping gait?

A
  • features- trip over often, lift feet high to avoid tripping over
  • cause- common peroneal palsy- foot drop
151
Q

what are the features and causes of trendelenberg gait?

A
  • features- unstable hip, ‘sound side sags’ on tendelenberg test
  • causes- hip dislocation, DDH
152
Q

what are the features and causes of an apraxic gait?

A
  • features- ‘feet glued to floor’, wide based unsteady gait with a tendency to fall
  • causes- normal pressure hydrocephalus, multi-infarct states, Alzheimers
153
Q

How does mononeuritis multiplex present and what are some causes?

A
  • individual nerves picked off randomly – wrist drop, leg numbness, foot drop
  • Subacute presentation – months rather than years
  • Inflammatory/immune mediated

Causes –inflammation of the vasa nervorum can block off the blood supply to the nerve causing sudden deficit

  • Vasculitis (wegner’s, PAN, RA), sarcoidosis
154
Q

causes of a myasthenic crisis

A
  • infection
  • progression of disease
  • under/overdosing medication
155
Q

what is the definition of a coma/ brain death?

A

unarousable unresponsiveness

156
Q

what are lateralising signs in neurology?

A
  • occur from one hemisphere of the brain but not another
157
Q

what causes a fixed dilated pupil?

A
  • 3rd nerve palsy
158
Q

metabolic causes of a coma

A
  • drugs, posioning
  • hypo/hyperglycaemia (HONK, ketoacidosis)
  • hypoxia
  • CO2 narcosis- COPD- if hypoxic drive decreases, CO2 builds up
  • septicaemia
  • hypothermia
  • addisonian crisis
  • encephalopathy
159
Q

neurological causes of coma

A
  • trauma
  • finection- meningitis, encephalitis etc
  • trauma
  • vascular- stroke, haemorrhages etc
  • epilepsy
160
Q

how is the unconscious patient managed?

A

ABC – life support
IV access
Stabilise cervical spine (especially if trauma is likely)
Control any seizures – phenytoin loading etc
Treat potential causes – IV glucose, thiamine, nalaxone if pupils small
Brief collateral history and examination
Vital signs and pupils checked often
Investigations – Bloods, cultures, CXR, CT head
Continually re-assess and plan investigations

161
Q

what is the definition of vertigo?

A

an illusion of movement, often rotary, of the patient of their surroundings

162
Q

causes of vertigo

A
  • motion sickness
  • alcohol
  • benign positional vertigo
  • meniere’s disease
163
Q

how does acute glaucoma present?

A
  • in elderly
  • constant aching pain develops rapidly around 1 eye
  • reduced vision, visual halos, nausea
  • red, congested eye, cloudy cornea, non-responsive dilated pupil, decreased acuity
164
Q

how is acute glaucoma treated

A

IV acetazolamide

165
Q

what are tardive syndromes and what causes them?

A
  • Tardive = delayed onset, occurs due to chronic exposure to dopamine antagonists (antipsychotics, anti-emetics)
  • May be permanent – even once the causative medication has been stopped
  • Tardive dyskinesia – chewing and grimacing movements involving the face, mouth and tongue- common in schizophrenics or have been on long-term typical anti-psychotics
  • Tardive dystonia – twisting/turning of the limbs and back
  • Tardive myoclonic, tourettism and tremor can also occur
166
Q

what is dysphasia?

A

impairment of language

167
Q

what is dysarthria?

A

difficulty with articulation of speech- slurred speech

168
Q

what is dysphonia?

A

difficulty with speech volume due to weakness of respiratory muscles or vocal cords (MG, GBS)

169
Q

what is the difference between bulbar and pseudobulbar palsy?

A

psuedo- UMN
- bulbar- LMN

Pseudobulbar dysarthria – slow, nasal, effortful ‘hot potato’ voice

Bulbar dysarthria – nasal speech due to paralysis of the palate

170
Q

What is dysphagia?

A

difficulty swallowing

171
Q

what is Miller- Fisher syndrome?

A

related variant to GBS that affects the CNS and eye muscles

characterised by opthalmoplegia and ataxia

172
Q

what is hydrocephalus and what are the 3 subtypes?

A
  • Hydrocephalus = abnormal build-up of CSF around the brain

Subtypes:
- Congenital hydrocephalus – born with excess fluid on the brain

  • Acquired – develops at some point after birth due to injury or illness
  • Normal pressure hydrocephalus – uncommon and poorly understood, usually only develops in >60 year olds
173
Q

what causes congenital hydrocephalus?

A
  • spina bifida

- infection during pregnancy (mumps, rubella)

174
Q

what causes acquired hydrocephalus?

A

develops after illness or injury (brain tumour/ head injury)

175
Q

causes of normal pressure hydrocephalus

A
  • develops after head injury/ stroke
176
Q

symptoms of normal pressure hydrocephalus

A
  • abnormal gait
  • urinary incontinence
  • dementia
177
Q

general symptoms of hydrocephalus

A

headache
vomiting
blurred vision
difficulty walking

178
Q

how is hydrocephalus investigated?

A
  • CT and MRI scans used to diagnose congenital and acquired hydrocephalus
  • NPH – diagnostic criteria = walking, mental ability and bladder control (important to diagnose NPF correctly because unlike Alzheimer’s the symptoms can be relieved with treatment)
179
Q

how is hydrocephalus managed?

A
  • Vetriculo-peritoneal shunt – surgically implanted into the brain to drain away excess fluid
  • Endoscopic third ventriculostomy – alternative to shunt surgery – hole made in the floor of the third ventricle to allowed trapped CSF to escape to the surface where it can be re-absorbed
180
Q

what is Gelineau’s syndrome?

A

Narcolepsy

irresistible attacks of innaprorpiate sleep with vivid hypnogognic hallucinations and sleep paralysis

181
Q

treatment of Gelineau’s syndrome

A
  • regular sleeping routine
  • avoid excess caffiene and alcohol
  • pharmacological- methylphenidate/ modafinil
182
Q

what is cataplexy?

A

sudden loss of muscle tone while a person is awake leads to weakness and a loss of voluntary muscle control. It is often triggered by sudden, strong emotions such as laughter, fear, anger, stress, or excitement

183
Q

treatment of cataplexy

A

sodium oxybate

184
Q

inheritance pattern in neurofibromatosis

A

autosomal dominant

185
Q

clinical signs of neurofibromatosis T1

A
  • cafe-au-lait spots- coffee coloured patches seen on skin in 1st year of life
  • freckling
  • dermal neurofibromas
    lisch nodules
    -
186
Q

complications of neurofibromatosis T1

A
  • mild learning disabilitiy
  • nerve root compresssion
  • GI bleeds
  • bone lesions
  • increased risk of epilepsy
187
Q

what is neurofibromatosis?

A

genetic disorder of the nervous system that results in tumours forming on nerves

188
Q

what are T1 and T2 neurofibromatosis also referred to as?

A

T1- recklinghausen disease

T2- bilateral acoustic neurofibromatosis

189
Q

how can T2 neurofibromatosis be differentiated from T1?

A
  • characterised by multiple tumours on the cranial and spinal nerves
  • first symptoms occur in early 20’s- usually hearing loss
190
Q

treatment of neurofibromatosis

A
  • surgery to remove problem tumours
  • chemotherapy
  • physical therapy
191
Q

describe the history, symptoms before, during and after in syncope

A

history- previous faints, poor oral intake, PMH

before- hot, dizzy, visual crowding, visual blurring, ringing in ears, pale

during- LoC, seconds to minutes, occasional jerks, pale, clammy, no tongue biting, no incontinence

after- quick recovery, no confusion

192
Q

describe the history, symptoms before, during and after a seizure

A

History- childhood development, head injury, neurosurgery, stroke, malignancy

before- aura

during- 2-3 mins LoC, convulsions depending on type of seizure, automatisms (lip smacking), eye deviation, tongue biting, urinary incontinence

after- post ictal confusion, disorientated, headache

193
Q

describe the history, symptoms before, during and after in a NEAD

A

history- MUS, history of trauma

before- aura

during- can last a long time, symptoms not localisable, pelvic thrusting, screaming, crying, responsive (sometimes), thrashing around

after- atypically quick, emotionally labile, minimal confusion

194
Q

what is an essential tremor?

A

element of postural tremor which continues through movement (e..g hands shaking when drinking a cup of tea)

does not occur at rest

195
Q

how are essential tremors managed?

A

propanolol/ primidone/ pregabalin/ gabapentin

196
Q

what other conditions can present with Parkinsonism?

A
  • idiopathic parkinsons disease
  • vascular parkinsonism
  • normal pressure hydrocephalus
  • Parkinsons plus (progressive supranuclear palsy, multiple system atrophy)
  • iatrogenic
197
Q

how does Parkinsonism present?

A
  • shuffling gait
  • pill rolling tremor
  • bradycardia
  • cogwheel rigidity
  • micrograhpia
  • cramping
  • non-motor symptoms- mood, sleep etc
198
Q

how is REM sleep behaviour disorder treated?

A

clonazepam/ melatonin

199
Q

what autonomic symptoms are associated with parkinsonism?

A 
orthostatic hypotension
constipation
nausea
vomiting
heat intolerance
urinary frequency
urinary incontinence
nocturia 
sexual dysfunction
200
Q

what presents with worsening symptoms with movement and stress, but symptom relief upon sleep and alcohol consumption?

A

essential tremor

201
Q

what mutations are seen in familial MND?

A

SOD1- association between this and fronto-temporal dementia

C9ORF72

202
Q

mutation seen in Huntingtons disease

A
  • chromosome 4
  • autosomal dominant
  • CAG trinucleotide repeat
203
Q

what is Hoffman’s sign and what is it commonly seen in?

A

flicking of the patient’s middle finger illicts contraction of the thumb (UMN sign), seen in MS

204
Q

other than huntingtons, what else can cause chroea?

A
  • wilsons
  • ataxic telanglectasia
  • SLE
  • rheumatic fever
  • OCP, L-dopa
  • pregnancy
  • thyrotoxicosis
  • polycythaemia rubra vera
  • CO poisoning
  • cerebralvascular disease
205
Q

what medications must be avoided in Parkinsons?

A

anti-physcotic meds (e.g. halopiderol)- anti-dopaminergic

NP- Phase 3a Medicine (22 decks)

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