Neurology and Geriatrics Flashcards

1
Q

list 3 things that may cause disruption of blood supply

A
  • thrombus formation/embolus
  • AF
  • atherosclerosis
  • shock
  • vasculitits
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2
Q

sudden onset of what symptoms (4) indicate a stroke?

A

asymmetrical

  1. weakness of limbs
  2. facial weakness
  3. dysphasia
  4. visual or sensory loss
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3
Q

4 RF for stroke

A
  • previous stroke TIA
  • CVD - angina/MI/PVD
  • AF
  • carotid artery disease
    -HTN
  • DM
  • smoking
    0 vasculitis
  • combined oral contraceptive pill
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4
Q

scoring tool for stroke in community?

A

FAST

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5
Q

scoring tool for recognition of stroke in emergency room

A

ROSIER (>0 = likely)

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6
Q

immediate imaging and medication for stroke management

A
immediate ct (exclude primary intracerebral haemorrhage) 
aspirin 300mg stat - 2wks
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7
Q

2 main surgical managements for stroke?

A
  • thrombolysis
  • thrombectomy
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8
Q

2 medications given for secondary prevention of stroke

A
  • clopidogrel 75mg 1x day
  • atorvastatin 80mg
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9
Q

classification system for ischaemic stroke?

A

bamford classification

based on presenting s/s

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10
Q

what three signs must all be present to diagnose a total anterior circulation stroke

A
  • unilateral weakness (and or sensory deficit) of face, arms, leg
  • homonymous hemianopia
  • higher cerebral dysfunction (dysphasia )
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11
Q

what are the 5 s/s you may see in posterior circulation syndrome

A

-Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

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12
Q

list the 4 s/s used to diagnose a lacunar stroke

A
  • pure sensory stroke
  • pure motor stroke
  • sensori-motor stroke
  • ataxic hemiparesis
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13
Q

3 investigations for epilepsy

A

EEG, MRI brain, ECG (exclude heart probs)

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14
Q

associated features of tonic-clonic seizures (3)

A
  • tongue biting
  • incontinence
  • groaning
  • irregular breathing
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15
Q

first and second line treatment for tonic-clonic seizures

A
1st = sodium valproate 
2nd = carbamazepine or lamotrigine
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16
Q

in what lobe of the brain do focal seizures start?

A

temporal lobe

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17
Q

what can a focal seizure effect (4)

A

hearing
speech
memory
emotions

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18
Q

1st and 2nd line treatment for focal seizures?

A

1st - carbamazepine or lamotrigine
2nd - sodium valproate or levetiracetam

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19
Q

what type of seizure is typically seen in children?

A

absence seizure

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20
Q

first line absence seizure treatment

A
  • sodium valproate
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21
Q

what type of seizure is also known as a “drop attack”

A

atonic seizure

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22
Q

first line treatment for atonic seizure

A

sodium valproate

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23
Q

1st line treatment for myoclonic seizure

A

sodium valproate

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24
Q

SE of sodium valproate (4)

A
  • teratogenic
  • liver damage and hep
  • hair loss
  • tremor
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25
Q

how does sodium valproate work?

A

increases activivity of gaba which relaxes the brain

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26
Q

why is sodium valproate avoided in women or girls unless no suitable alternative is available?

A

teratogenic

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27
Q

SE of carbamazepine (3)

A

agranulocytosis
aplastic anaemia
induce p450 -> many drug interactions

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28
Q

3 phenytoin SE

A
  • folate and vit d deficiency
  • megoblastic anaemia
  • osteomalacia
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29
Q

what is a myasthenic crisis

A

severe, life threatening complication of myasthenia gravis (acute worsening of symptoms)

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30
Q

usual cause of myasthenic crisis

A

triggered by another illness - respiratory tract infection

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31
Q

what organ failure can occur due to myasthenic crisis

A

respiratory failure as weakness in resp muscles

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32
Q

what management may be needed for a myasthenic crisis

A

bipap or full intubation/ventilation

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33
Q

medical treatment for myasthenic crisis?

A

IV immunoglobulins and plasma exchange

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34
Q

pathophysiology of guillian-barre

A

b cells create antibodies against antigen on pathogen

these antibodies also match proteins on nerve cell
- these may target myelin sheath of motor cell or nerve axon

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35
Q

presentation of gullian-baree syndrome (4)

A
  1. symmetrical ascending weakness
  2. reduced reflexes
  3. peripheral loss of sensation or neuropathic pain
  4. progress to cranial nerves -> facial nerve weakness
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36
Q

how long after infection do guillian-barre symptoms typically occur?

A

within 4 weeks of the preceding infection

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37
Q

what is the criteria used for guillian-barre diagnosis

A

the brighton criteria

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38
Q

what two investigations can be used to support diagnosis of guillian-barre syndrome and what is seen?

A
  1. nerve conduction studies (reduced signal through nerves)
  2. lumbar puncture for CSF (raised protein, normal cell count and glucose)
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39
Q

management options for guillian-barre syndrome (4)

A
  1. IV immunoglobulins
  2. plasma exchange (alternative to iv ig)
  3. supportive care
  4. VTE prophylaxis (PE is leading cause of death)
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40
Q

leading cause of death in guillian-barre syndrome

A

PE

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41
Q

what is the most common type of spinal stenosis

A

lumbar spinal stenosis

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42
Q

what type of spinal stenosis causes narrowing of the nerve root canals?

A

lateral stenosis

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43
Q

list 2 causes of spinal stenosis

A

Congenital spinal stenosis

Degenerative changes, including facet joint changes, disc disease and bone spurs

Herniated discs

Thickening of the ligamenta flava or posterior longitudinal ligament

Spinal fractures

Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)

Tumours

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44
Q

3 s/s of cauda equina syndrome

A
  • saddle anaesthesia
  • sexual dysfunction
  • incontinence of the bladder and bowel
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45
Q

3 typical symptoms of pseudoclaudication

A
  • lower back pain
  • buttock and leg pain
  • leg weakness
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46
Q

define radiculopathy

A

compression of the nerve root as they exit spinal cord/column -> motor/sensory probs

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47
Q

how to spot difference between spinal stenosis and peripheral arterial disease? (2)

A
  • AKBI normal -> think spinal stenosis
  • struggling with back pain -> think spinal stenosis
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48
Q

primary imaging investigation for diagnosing spinal stenosis

A

MRI

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49
Q

management for spinal stenosis

A
  • exercise and weight loss
  • analgesia
  • physio
  • decompression surgery if conservative treatment fails
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50
Q

at what level does the spinal cord terminate?

A

L2/L3

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51
Q

what do the nerves of the cauda equina supply? (3)

A

Sensation to the lower limbs, perineum, bladder and rectum

Motor innervation to the lower limbs and the anal and urethral sphincters

Parasympathetic innervation of the bladder and rectum

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52
Q

3 causes of spinal compression

A
  1. herniated disc (most common)
  2. tumour, metastasis
  3. spondylolisthesis
  4. abscess
  5. trauma
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53
Q

4 red flags for cauda equina syndrome

A
  1. saddle anaesthesia
  2. loss of sensation in bladder/rectum (not knowing when theyre full)
  3. urinary incontinence or retention
  4. faecal incontinence
  5. bilateral sciatica
  6. bilateral or severe motor weakness in legs
  7. reduced anal tone on PR exam
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54
Q

emergency management of cauda equina (3)

A
  • immediate hospital admission
  • emergency MRI
  • neurosurgical input to consider lumbar decompression surgery
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55
Q

key differentiating feature between cauda equina and metastatic spinal cord compression

A

back pain worse on cough or strain in MSSC

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56
Q

what are the three domains on the GCS used to measure a coma?

A
  • eye opening
  • motor respone
  • verbal response
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57
Q

what number on the GCS suggests a coma?

A

coma <8

(usually E2,M4,V2 or less)

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58
Q

what is meant by the term “AVPU”

A

scoring system of a persons consciousness

Alert

responsive to Voice

responsive only to Pain

Unresponsive

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59
Q

4 common causes of coma

A
  • drugs/toxins (opiates, EtOH)
  • anoxia (post arrest)
  • mass lesions (bleeds)
  • head injury
  • infections (bact meningitis)
  • brainstem infarct
  • metabolic
  • SAH
  • seizures
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60
Q

microbiology of neisseria meningitidis

A

gram negative diplococcus

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61
Q

what does a non-blanching rash represent in meningococcal septicaemia?

A

disseminated intravascular coagulopathy (DIC) and sc haemorrhages

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62
Q

most common cause of bacterial meningitis in:

  1. children and adults (2)
  2. neonates (1)
A
  1. neisseria meningitidis (meningococcus)
  2. strep pneumoniae
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63
Q

presentation of meningitis (6)

A
  1. fever
  2. neck stiffness
  3. vomiting
  4. headache
  5. photophobia
  6. altered consciousness and seizures
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64
Q

what should be part of your investigation for meningitis for all children

A

lumbar puncture as can be non-specific signs

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65
Q

what 2 tests can you do for meningeal irritation? define them

A

kernigs test: patient lies on back and flexes one hip and knee 90 degrees -> spinal pain or resistance to movement

Brudzinski’s test: pt lies flat on back as dr lifts head/neck off bed and flex chin 2 chest -? involuntary flexion of hips and knees

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66
Q

usual choice of post mengititis exposure prophylaxis

A

single dose ciprofloxacin within 24hr inital diagnosis

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67
Q

most common cause of viral meningitis (3)

A
  1. herpes simplex virus
  2. enterovirus
  3. varicella zoster virus
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68
Q

what is the standard difference in appearance of CSF for bacterial vs viral meningitis

A

bacterial is cloudy, viral is clear

bacterial (high protein, low glucose, high neutrophils + bacteria)

viral ( high white cell count, negative for bacteria)

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69
Q

3 complications of meningitis

A
  1. hearing loss is a key one
  2. seizures and epilepsy
  3. cognitive impairment and learning disability
  4. memory loss
  5. focal neuro deficit e.g limb weakness or spasticity
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70
Q

3 possible symptoms of a brain abscess

A
  1. headache
  2. lethargy
  3. fever
  4. focal neurological deficit
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71
Q

investigations for diagnosis of brain abscess

A

contrast-enhanced MRI or CT

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72
Q

2 causes of a brain abscess

A
  • cranial infection (osteomyelitis, sinusitis)
  • penetrating head wounds
  • haematogenous spread (bacterial endocarditis)
  • unknown
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73
Q

treatment of brain abscess

A
  1. abx - cefotaxime or ceftriaxone + metronidazole or vancomycin for staph. aureus
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74
Q

a pt presents with an unusual change in personality and behaviour, what type of tumour may be present?

A

frontal lobe tumour

(frontal lobe responsible for personality and higher-level decision making)

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75
Q

what is the key finding on fundoscopy in a pt with raised intracranial pressure which suggests a diagnosis of a brain tumour

A

papilloedema

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76
Q

3 causes of raised intracranial pressure

A
  1. brain tumours
  2. intracranial haemorrhage
  3. idiopathic intracranial hypertension
  4. abscesses or infection
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77
Q

5 headache red flags

A
  1. constant
  2. nocturnal
  3. worse on waking
  4. worse on cough, straining or bending forward
  5. vomiting
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78
Q

define papiloedema

A

swelling of the optic disc due to raised intracranial pressure

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79
Q

2 fundoscopic changes seen with raised intra-cranial pressure

A
  1. blurring of optic disc margin
  2. elevated optic disc
  3. loss of venous pulsation
  4. engorged retinal veins
  5. haemorrhages around optic disc
  6. patons lines
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80
Q

the four common cancers which metastasise to the brain

A
  1. lung
  2. breast
  3. renal cell carcinoma
  4. melanoma
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81
Q

the three types of gliomas

A
  1. astrocytoma (gliobastoma multiform is most common)
  2. oligodendroglioma
  3. ependymoma
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82
Q

optic field defect seen when a pituitary tumour grows large enough

A

bitemporal hemianopia (presses on optic chiasm)

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83
Q

4 hormone deficiences caused by pituitary tumour

A

acromegaly

hyperprolactinaemia

cushings disease

thyrotoxicosis

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84
Q

define an acoustic neruoma

A

tumours of the schwann cells surrounding the auditory nerve that innervates the inner ear

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85
Q

triad of symptoms for acoustic neuroma

A
  1. hearing loss
  2. tinnitus
  3. balance problems
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86
Q

treatment for pit tumours (4)

A
  1. trans-sphenoidal surgery
  2. radiotherapy
  3. bromocriptine (block prolactin secreting tumours)
  4. somatostatin analogues
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87
Q

3 RF for an intracranial bleed

A
  • head injury
  • HTN
  • aneurysm
  • ischaemic stroke -> haemorrhage
  • brain tumour
  • anticoag e.g. warfarin
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88
Q

main presentation of an intracranial bleed

A

sudden onset headache

think also:

Seizures

Weakness

Vomiting

Reduced consciousness

Other sudden onset neurological symptoms

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89
Q

GCS score signalling you may need to secure the airway as theres a riskt they may not maintain on their own

A

= 8

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90
Q

what will be seen on a CT scan of a subdural haemorrhage

A

crescent shape

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91
Q

patients most at risk of subdural haemorrhage?

A

elderly and alcoholics as increased atrophy = more likely to rupture

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92
Q

what fracture can cause an extradural haemorrhage and how do they present on CT?

A

fracture of the temporal bone

CT: bi-convex shape and limited by cranial structures

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93
Q

what type of haemorrhage is seen here

A

intracerebral

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94
Q

what type of haemorrhage is seen below

A

SAH

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95
Q

what is the usual cause of a SAH

A

ruptured cerebral aneurysm

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96
Q

what headache is associated with SAH

what else is associated with SAH

A

thunderclap headache

cocaine and sickle cell anaemia also associated

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97
Q

4 features of a SAH

A
  1. thunderclap headache
  2. neck stiffness
  3. photophobia
  4. vision changes
  5. neuro symptoms e.g. speech changes, weakness, seizures and LOC
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98
Q

3 RF for SAH

A
  1. HTN
  2. smoking
  3. excessive alcohol consumption
  4. cocaine use
  5. family history
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99
Q

first line investigation for SAH

A

CT head

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100
Q

CSF results in a SAH?

A
  • red cell count RAISED
  • xanthochromia (yellow coloured csf caused by bilirubin)
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101
Q

surgical management of a SAH

medication option for SAH

A

surgery - coiling or clipping

meds - nimodipine (CCB prevent vasospasm)

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102
Q

common complication which can result in brain ischaemia following a SAH

A

vasospasm

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103
Q

what cells produce myelin

A

schwann cells in peripheral nervous system

oligodendrocytes in CNS

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104
Q

what part of the nervous system is affected in MS

A

CNS (oligodendrocytes)

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105
Q

3 causes of MS

A
  1. multiple genes
  2. Epstein-barr virus
  3. low vit D
  4. smoking
  5. obestiy
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106
Q

what is the most common presentation of MS

A

optic neuritis

involves demyelination of the optic nerve and loss od vision in one eye

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107
Q

what two key phrases are used to describe a sixth nerve palsy (seen in MS)

A
  • intranuclear opthalmoplegia
  • conjugate lateral gaze disorder
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108
Q

2 focal sensory symptoms seen in MS

A
  1. trigeminal neuralgia
  2. numbness
  3. paraesthesia
    - lhermittes sign
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109
Q

what is Lhermitte’s sign and what condition is it associated with?

A

electric shock down spine into limbs when flexing the neck = disease in cervical spinal cord dorsal column

seen in MS

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110
Q

what is the most common pattern of MS

A

relapsing-remitting

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111
Q

describe secondary progressive MS

A

Secondary progressive MS is where there was relapsing-remitting disease at first, but now there is a progressive worsening of symptoms with incomplete remissions. Symptoms become more and more permanent.

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112
Q

main cause of optic neuritis

A

MS

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113
Q

how long to symptoms have to be progressive to diagnose primary progressive MS

A

1 year

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114
Q

4 key features of optic neuritis

A
  1. central scotoma (enlarged blind spot)
  2. pain on eye movement
  3. impaired colour vision
  4. relative afferent pupillary defect
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115
Q

list 2 causes of optic neuritis aside from MS

A
  • sarcoidosis
  • SLE
  • DM
  • syphilis

_ measles

  • mumps
  • lyme disease
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116
Q

treatment of optic neuritis

A

steroids (recovery 2-6wks)

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117
Q

NICE recommendation for treatment of relapsed MS

A

steroids = Methylprednisolone 500mg oral 5 days,

(1g IV daily 3-5 days if oral treatment failed previous or severe)

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118
Q

what is the most common specific motor neurone disease

A

amyotrophic lateral sclerosis (ALS)

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119
Q

what muscles are affected by progressive bulbar palsy?

A

affects primarily muscles of talking and swallowing

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120
Q

why is family history important when taking a hx for MND

A

5-10% of cases of MND are inherited

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121
Q

where is weakness first noticed in MND

A

upper limbs noted first (progressive weakness affecting limbs, trunk, face, speech)

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122
Q

4 presentation symptoms of MND

A
  1. progressive upper limb weaknes
  2. increased fatigue when exercising
  3. clumsiness
  4. slurred speech (dysarthia)
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123
Q

4 signs of MND

A
  1. muscle wasting
  2. reduced tone
  3. fasciculations (muscle twitch)
  4. reduced reflexes
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124
Q

what are three signs of upper MND

A
  1. increased tone and spasticity
  2. brisk reflexes
  3. upgoing plantar responses
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125
Q

what medication can slow progession of MND and increase survival for few months

A

Riluzole

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126
Q

usual cause of death in pts with MND

A

respiratory failure or pneumonia

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127
Q

what are the five branches of the facial nerve?

A
  1. temporal
  2. zygomatic
  3. buccal
  4. marginal mandibular
  5. cervical
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128
Q

what type of neurone facial nerve palsy should be referred urgently as a stroke risk?

A

upper motor neurone facial nerve palsy

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129
Q

in what type of motor neurone lesion is the forehead spared?

A

UMN lesion = forehead sparing

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130
Q

unilateral motor lesions occur in ____ and ____

bilateral upper motor neurone lesions occur in _____ and ______

A
  1. cerebrovascular accidents (stroke) and tumours
  2. peudobulbar palsies and MND
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131
Q

what type of palsy presents as a unilateral LMN facial nerve palsy?

A

bells palsy

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132
Q

pt presents with bells palsy within 72 hrs of symptom development - what is the treatment as per NICE guidlines

A
  • prednisolone:
  • 50mg 10 days
  • 60mg for 5 days followed by 5 day reducing regime of 10mg a day
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133
Q

what is the concern regarding pain in the eye following a bells palsy

A

exposure keratopathy

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134
Q

what is the cause of Ramsey-hunt syndrome?

A

varicella zoster virus

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135
Q

how does ramsay-hunt syndrome present (2)

A
  • unilateral lower motor neurone facial nerve palsy
  • painful/tender vesicular rash in the ear canal, pinna and around ear on affected side (check tongue and hard palate too)
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136
Q

what treatments are administered within 72hr onset of ramsay-hunt syndrome

A
  • prednisolone
  • acicilovir
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137
Q

list 2 infection causes of LMN facial nerve palsy

A
  • otitis media
  • malignant otitis externa
  • HIV
  • lymes disease
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138
Q

list 2 systemic diseases which may cause LMN facial nerve palsy

A
  • diabetes
  • sarcoidosis
  • leukaemia
  • MS
  • guillain-barre syndrome
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139
Q

list 1 antenatal, perinatal and postnatal cause of cerebral palsy

A

antenatal: maternal inf. trauma in pregnancy
perinatal: birth asphyxia, pre-term birth
postnatal: meningitis, severe neonatal jaundice, head injury

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140
Q

what are the four types of cerebral palsy

A
  1. spastic hypertonia ( from damage of UMN)
  2. dyskinetic (from damage to basal ganglia)
  3. ataxic (damage to cerebellum)
  4. mixed
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141
Q

what is the difference between monoplegia and hemiplegia

A

mono - one limb affected

hemiplegia - one side of body affected

diplegia - four limbs, mainly legs

quadriplegia - four limbs more severe (seizures, speech distrubed, other imapirments)

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142
Q

3 s/s of cerebral palsy

A
  1. failure to meet milestone
  2. increased/decreased tone (general or specific)
  3. hand preference UNDER 18 MONTHS (key sign)
  4. feeding/swallow issues
  5. learning difficulties
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143
Q

what type of gait suggests foot drop or LMN lesion

A

high stepping gate

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144
Q

what gait suggests pelvic muscle weakness due to myopathy

A

waddling gait

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145
Q

what are the findings of a LMN lesion on examination

A
  1. inspection = reduced muscle bulk with fasciculations
  2. tone - hypotonia
  3. power - dramatically reduced
  4. reflex = reduced
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146
Q

reflex findings with an UMN lesion

A

brisk reflexes

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147
Q

2 differentials of UMN lesion

A

brain injury or tumour

148
Q

4 complications and associated conditions with cerebral palsy

A
  1. learning disability
  2. epilepsy
  3. kyphoscoliosis
  4. muscle contractures
  5. hearing/visual impairement
  6. gastro-oesophageal reflux
149
Q

why may baclofen be prescribed in cerebral palsy?

A

muscle relaxant for muscle spasticity and contractures

150
Q

on what chromosome is the neurofibromatosis type 1 gene found

A

chromosome 17

151
Q

what type of protein is neurofibromin

A

tumour suppressor protein

152
Q

name 5 features that indicate a diagnosis of neurofibromatosis (hint: CRABBING)

A

c- cafe-au-lait spots (>6)

r - relative with NF1

A - axillary or inguinal freckles

BB - bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia

i - iris hamartomas (yellow/brown spots on iris)

N - neurofibromas (2+)

g - glioma of optic nerve

153
Q

what imaging techniques are used for neurofibromatosis and what is seen?

A

xray = bone pain and lesion investigation

ct/mri = lesions in brain, spinal cord or elsewhere in body

154
Q

2 complications of neurofibromatosis

A
  1. Renal artery stenosis -> HTN
  2. malignant peripheral nerve sheath tumours
  3. GI stromal tumour
  4. migraines
  5. epilepsy
  6. vision loss (2ndary to optic nerve gliomas)
155
Q

what chromosiome is neurofibromatosis type 2 gene found and what does it code for>

A

found on chromosome 22 and codes for merlin protein (tumour supressor protein in schwann cells)

156
Q

what neuroma is commonly found in neurofibromatosis type 2

A

acoustic neuroma -> hearing loss, tinnitus and balance problems

157
Q

what does a pt presenting with BILATERAL acoustic neuroma certainly indicate?

A

neurofibromatosis type 2

158
Q

what type of bacteria is neisseria meningitidis?

A

gram negative diplococcus (meningococcus)

159
Q

what type of meningitis causes the non-blanching rash and what does it suggest?

A

meningococcal septicaemia causes a non-blanching rash and indicates inf. has -> disseminated intravascular coagulopathy (DIC) and SC haemorrhages

160
Q

what is the most common cause of bacterial meningitis in children and adults? in neonates?

A

children and adults - neisseria meningitidis and strep pneumonia

neonates - group B strep

161
Q

5 symptoms of meningitis

A
  1. fever
  2. neck stiffness
  3. vomiting
  4. headache
  5. photophobia
  6. altered consciousness and seizures
162
Q

what investigation must be utilised in all children <1m with fever, 1-3m with fever and unwell and <1yr with unexplained fever and other serious illness features

A

lumbar puncture

163
Q

what two tests can be performed to look for meningeal irritation

A
  • kernigs sign
  • brudzinski’s sign
164
Q

treatment of children seen in primary care with suspected meningitis AND a non-blanching rash ?

A

urgent stat injection (IM or IV) of benzylpenicillin prior to hospital transfer

165
Q

treatment for meningitis <3m ? >3m?

A

<3m = cefotaxime + amoxicillin

>3m = ceftriaxone

166
Q

what is given as post-exposure prophylaxis for meningococcal infection of close contact

A

single dose ciprofloxacin ideally within 24hr initial diagnosis

167
Q

what are the most common causes of viral meningitis

A
  • herpes simplex virus
  • enterovirus
  • varicella zoster virus
168
Q

what is used to treat suspected of confirmed HSV meningitis

A

aciclovir

169
Q

at what level is a lumbar puncture inserted?

A

L3-L4 intervertebral space

170
Q

difference in CSF appearance between viral and bacterial meningitis

A

bacterial CSF - cloudy

viral CSF - clear

171
Q

4 complications of meningitis

A
  1. memory loss
  2. HEARING LOSS
  3. seizures and epilepsy
  4. cognitive impairment and learning difficulty
  5. focal neuro deficity such as limb weakness or spasticity
172
Q

squint is also known as ….

A

strabismus

173
Q

what is the cause of a concomitant squint

A

difference in control of the extra-ocular muscles

174
Q

define amblyopia

A

affected eye becomes passive and has reduced function compared to other dominant eye

175
Q

name some non-idiopathic causes of squint (3)

A
  1. hydrocephalus
  2. cerebral palsy
  3. space occupying lesions (e.g retinoblastoma)
  4. trauma
176
Q

what 2 tests can be used to examine a squint?

A
  • hirschbergs test
  • cover test
177
Q

what management options may be considered in a squint of a child ?

A

occlusive patch (covers good eye helps weaker eye to develop)

atropine drops - good eye is blurry allows weaker eye to develop

178
Q

define myasthenia gravis

A

autoimmune condition that causes muscle weakness that gets worse with activity sand improves with rest

179
Q

what links the thymus and myasthenia gravis?

A

strong link between thyoma and myasthenia gravis (10-20% will have)

180
Q

what antibodies are produced in pts with myasthenia gravis?

A

85% = acetylcholine receptor antibodies

181
Q

what are the three antibodies with cause myasthenia gravis

A
  1. acetylcholine receptor antibodies
  2. muscle-specific kinase ab (MuSK)
  3. lipoprotein receptor-related protein 4 (LRP4)
182
Q

4 facial symptoms of myasthenia gravis

A
  1. extraocular muscle weakness -> double vision (diplopia)
  2. eyelid weakness -> ptosis
  3. weak facial movement
  4. difficulty swallowing
  5. fatigue in jaw when chew
  6. slurred speech
  7. progressive weakness with competitive movement
183
Q

how is myasthenia gravis diagnosed?

A

testing directly for relevant antibodies

  • 85% ACh-R
  • 10% MuSK
  • <5% LRP4

ct or mri of thymus to look for thyoma

184
Q

if in doubt about diagnosis of myasthenia gravis what test can be done which will show a brief and temporary relief of weakness?

A

edrophonium test (IV dose of edrophonium hydrochloride)

185
Q

what are the treatment options for myasthenia gravis (4)

A
  • reversible acetylcholinesterase inhibitors (pyridostigmine or neostigmine)
  • immosuppression (prednisolone or azathioprine)
  • thymectomy
  • MONOCLONAL ANTIBODIES (rituximab, eculizumab)
186
Q

what is a myasthenic crisis

A

severe complication of myasthenia gravis -> acute worsening of symptoms and often triggered by another illness (resp inf) 0-> resp fail

187
Q

what is the medical treatment of myasthenic crisis

A

immunomodulatory therapies (IV immunoglobulins and plasma exchange)

188
Q

define parkinsons disease

A

progressive reduction of dopammine in the basal ganglia -> disorders of movement

189
Q

what is the triad of parkinsons disease

A
  1. resting tremor
  2. rigidity
  3. bradykinesia
190
Q

4 features of parkinsons disease

A
  1. shuffling gait
  2. unilateral tremor “pill-roll tremor”
  3. cogwheel rigidity
  4. bradykinesia
191
Q

if a tremor presents symmetrical, improving at rest and alcohol what type of tremor is most likely?

A

benign essential tremor

192
Q

what type of tremor is asymmetrical, worse at rest and improves with intentional movement?

A

parkinsons tremor

193
Q

whar types of dysfunction are caused by multiple system atrophy (2)

A
  1. autonomic dysfunction (postural hypotension, constipation, abnormal sweat)
  2. cerebellar dysfunction (causing ataxia)
194
Q

what type of associated symptoms are seen with dementia with lewy bodies (3)

A
  1. visual hallucinations
  2. delusions
  3. disorders of REM sleep
  4. fluctuating consciousness
195
Q

combined medication options for parkinsons

A

co-benyldopa (levodopa and benserazide)

co-careldopa (levodopa and carbidopa)

196
Q

three examples of side effects of dopamine

A
  1. dystonia (excessibe muscle contraction -> abnormal postures)
  2. chorea (involuntary jerking and random)
  3. athetosis (involuntary twisting or writhing)
197
Q

what is the action of COMTi entacapone?

A

taken with levodopa to slow breakdown of levodopa in the brain -> extends effective duration of the levodopa

198
Q

name a notable side effect of prolonged use of dopamine agonists

A

pulmonary fibrosis

199
Q

list 5 differentials of headache

A
  1. tension headache
  2. migraine
  3. cluster headache
  4. raised intracranial pressure
  5. GCA
  6. SAH
  7. meningitis
200
Q

list 4 key red flags to note on a “headache” presentation

A
  1. fever, photophobia or neck stiffness (meningitis or encephalitis)
  2. new neuro symptoms (haemorrhage, malignancy, stroke)
  3. dizziness (stroke)
  4. visual disturbance (temporal arteritis or glaucoma)
  5. sudden onset occipital headache (SAH)
  6. postural, worse on standing, lying, bending over (raised ICP)
201
Q

what important assessment is done for a headache presentation via fundoscopy and why is it done?

A

look for papilloedema - indicates raised ICP -> brain tumour, benign IC HTN, intracrania bleed

202
Q

describe the sensation of a tension headache

A

mild ache around forehead in a band like pattern around the head

203
Q

list 3 causes of a secondary headache

A
  1. underlying medical condition (inf. obstructive sleep apnoea, pre-eclampsia)
  2. alcohol
  3. head injury
  4. carbon monoxide poisoning
204
Q

how may an analgesic headache present?

A

similar non-specific features to a tension headache

205
Q

what is the general cause of a hormonal headache and what treatment may improve them

A

related to low level oestrogen

oral contraceptive pill can improve headaches

206
Q

what condition is caused by degenerative changes in cervical spine and often presents with a headache

A

cervical spondylosis

207
Q

how is the pain of trigeminal neuralgia typically described as

A

electricity-like shooting pain, attacks worsen over time and come on spontaneously, lasting few seconds -> hours

208
Q

first line treatment for trigeminal neuralgia?

A

carbamazepine

(surgery can be used to decompress or damage trigeminal nerve)

209
Q

list the 4 types of migraine

A
  • migraine without aura
  • migraine with aura
  • silent migraine
  • hemiplegic migraine
210
Q

how long will a migraine last?

describe 4 features of a migraine

A

4-72hrs

  • pounding or throbbing
  • unilateral (can be bi)
  • photophobia
  • phonophobia
  • with/without aura
  • nausea and vomiting
211
Q

3 signs of a hemiplegic migraine and what condition do they typically mimic?

A
  1. migraine symptoms
  2. sudden or gradual onset
  3. hemiplegia
  4. ataxia
  5. changes in consciousness
212
Q

list the 5 stages of migraine

A
  1. premonitory or prodromal
  2. aura
  3. headache
  4. resolution stage (headache fades or relieved by vomiting or sleep_
  5. postdromal or recovery phase
213
Q

4 acute management options for migraine

A
  1. paracetamol
  2. triptans (e.g sumitriptan)
  3. NSAIDs (e.g. ibruprofen or naproxen)
  4. anti-emetics
214
Q

3 ways triptans work

A
  1. smooth muscle in arterties -> vasoconstriction
  2. peripheral pain receptors to inhibit activation of pain receptors
  3. reduce neuronal activity in CNS
215
Q

3 medications used in migraine prophylaxis

A
  • propranolol
  • topiramate
  • amitriptyline
216
Q

define the sensation of a cluster headache

A

severe and unbearable unilateral headache, usually around the eye

217
Q

define the typical patient presenting with cluster headache

A

30-50yr old male smoker, attacks triggered by alcohol/strong smells/exercise

218
Q

4 symptoms of cluster headache

A
  1. red, swollen and watering eye
  2. pupil constriction (miosis)
  3. eyelid drooping (ptosis)
  4. nasal discharge
  5. facial sweating
219
Q

what are the two acute managements for a cluster headache

A
  1. triptans (e.g. sumitriptan 6mg SC)
  2. 100% high flow o2 for 15-20 min (can be given at home)
220
Q

3 prophylaxis options for a cluster headache

A
  • verapamil
  • lithium
  • prednisolone (2-3wks to break the cycle during cluster)
221
Q

what is temporal arteritis (GCA) strongly linked with?

A

polymyalgia rheumatica

pts at higher risk are white female >50

222
Q

key complication of GCA

A

vision loss (irreversible) - high dose steroids given as soon as diagnosis is SUSPECTED

223
Q

4 features of GCA

A
  1. severe unilateral headache around forehead/ temple
  2. scalp tenderness (think hair brushing)
  3. jaw claudication
  4. blurred or doublev vision
  5. irreversible painless complete sight loss can occur rapidly
224
Q

a definitive diagnosis of GCA is made via that 3 investigations

A
  1. clinical presentation
  2. raised ESR
  3. temporal artery biopsy findings
225
Q

what are found on the temporal artery biopsy in GCA

A

multinucleated giant cells

226
Q

what anaemia may be seen with GCA and what may be seen on duplex ultrasound

A

FBC = normocytic anaemia

duplex uss = hypoechoic halo sign

227
Q

aside from steroids what 2 other medications may be given in GCA

A
  • aspirin
  • ppi
228
Q

list 2 late complications of GCA

A
  • relapses
  • steroid related SE/comps
  • cerebrovascular accident (stroke)
  • aortitis -> aortic anaeurysm and aortic dissection
229
Q

what type of genetic condition is huntingtons chorea

A

autosomal dominant

230
Q

what gene is mutated in huntingtons and on what chromosome

A

HTT gene on chromosome 4

231
Q

define what is meant by anticipation in the case of huntingtons chorea

A

successive generations have more repeats in gene ->

  • earlier age of onset
  • increased severity of diease
232
Q

what 4 movement disorders may be seen in huntingtons

A
  • chorea (involuntary abnormal movement)
  • eye movement disorders
  • speech difficulty (dysarthia)
  • swallow difficulty (dysphagia)
233
Q

what is the medical treatment for huntingtons

A
  • based on symptomatic relief, no treatment for stopping or slowing progression
234
Q

3 medications which may be given in huntingtons to suppress the disordered movement

A
  • antipsychotics (olanzapine)
  • benzodiazepines (diazepam)
  • dopamine-depleting agents (tetrabenazine)
235
Q

life expectancy for huntingtons and leading cause of death in these pts

A

15-20yrs after onset of symptoms

death often due to respiratory disease (pneumonia)

suicide risk higher

236
Q

where does charcot-marie-tooth disease cause dysfunction?

A

myelin or the axons

237
Q

typical age pts present with charcot-marie-tooth disease symptoms

A

<10yrs, can be delayed to >40yrs

238
Q

3 features to look for in assessing charcot-marie-tooth disease

A
  • high arched foot (pes cavus)
  • distal muscle wasting “inverted champagne bottle legs”
  • weakness in lower legs (loss of ankle dorsiflexion)
  • weakness in hands
  • reduced tendon reflexes
  • reduced muscle tone
  • peripheral sensory loss
239
Q

causes of peripheral neuropathy (hint: ABCDE)

A
  • alcohol
  • B12 deficiency
  • Cancer and CKD
  • Diabetes and Drugs (isonazid, amiodarone, cisplatin)
  • Every vasculitis

TOM TIP: This is a common OSCE scenario. You will have to perform a neurological examination on a patient that has a peripheral neuropathy. Charcot-Marie-Tooth is a relatively common (1 in 2,500 people) condition with good signs that has a high chance of appearing in your exams. Look for the other features, suggest the diagnosis, then run through the ABCDE mnemonic to suggest the possible other causes.

240
Q

the spinal nerves _______ come together to form the sciatic nerve

A

L4-S3

241
Q

what does the sciatic nerve divide in to?

A

tibial nerve and the common peroneal nerve

242
Q

what does the sciatic nerve supply for?

A

sensation to lateral lower leg and foot

motor function to posterior thigh, lower leg and foot

243
Q

3 symptoms of sciatica

A
  • unilateral pain from buttock down back of thigh -> below knee/feet
  • paraesthesia
  • numbness and motor weakness
  • reflexes may be effected
244
Q

3 main causes of sciatica are lumbosacral nerve root compression by? (3)

A
  • herniated disc
  • spondylolisthesis
  • spinal stenosis
245
Q

what type of sciatica is a red flag for cauda equina syndrome

A

bilateral sciatica

246
Q

what 5 main cancers metastasise to the bone

A

PoRTaBLe

prostate

renal

thyroid

breast

lung

247
Q

test to help diagnose sciatice?

A

sciatica stretch test

248
Q

3 types of muscular dystrophy

A
  1. duchennes muscular dystrophy (worth knowing)
  2. beckers muscular dystrophy
  3. myotonic dystrophy
249
Q

what sign is seen in children with proximal muscle weakness (may be seen in muscular dystrophy)

A

Gowers sign

x-linked recessive inheritance

250
Q

what is the cause of duchennes muscular dystrophy

A

defective gene for dystrophin on the x-chromosome

251
Q

where is weakness first noticed in a child with DMD?

A

3-5 yrs old with weakness in muscles around the PELVIS

wheelchair bound by a teen

25-35yrs life expectancy with good management

252
Q

what medication has been shown to slow progression of muscle weakness in DMD?

A

steroids

253
Q

4 typical features of myotonic dystrophy

A
  1. progressive muscle weakness
  2. PROLONGED MUSCLE CONTRACTIONS
  3. cataracts
  4. cardiac arrhythmia

TOM TIP: The key feature of myotonic dystrophy to remember is the prolonged muscle contraction. This may present in exams with a patient that is unable to let go after shaking someones hand, or unable to release their grip on a doorknob after opening a door. When doing an upper limb neurological examination always shake the patients hand and observe for difficulty releasing their grip.

254
Q

what type of muscular dystrophy typically presents with childhood facial weakness -> shoulders and arms (e.g. sleep with eyes slightly open)

A

facioscapulohumeral muscular dystrophy

255
Q

define how oculopharyngeal muscular dystrophy typically presents

A

weakness of the ocular muscles and pharynx

bilateral ptosis, restriced eye movement and swallowing problems

256
Q

what age does limb-girdle muscular dystrophy typically present?

A

teenage years

257
Q

how does emery-dreifuss muscular dystrophy typically present

A

childhood with contractures, commonly elbows and ankles

258
Q

how does blood enter the brain?

A

internal carotid arteries and the vertebral arteries in the neck

259
Q

4 causes of dementia

A
  1. increasing age
  2. alzheimers
  3. vascular dementia
  4. lewy body dementia
  5. frontotemporal dementia
260
Q

common causes of dementia (hint: DEMENTIA)

A

Diabetes

Ethanol

Medication

Environmental (CO poisoning)

Nutritional

Trauma

Infection

Alzheimers

261
Q

5 S/S of dementia

A
  1. memory loss, difficulty retaining new info
  2. language impairement
  3. executive dysfunction (handling complex tasks etc)
  4. visiospatial ability impairment
  5. behavioural disturbance
  6. personality change
262
Q

what is seen on CT for vascular dementia

A

microinfarcts

263
Q

diagnostic tests for dementia (3)

A
  1. mental state examination
  2. montreal cognitive assessment (MoCA)
  3. mini-mental state examination (MMSE)
264
Q

why are acetlycholinesterase inhibitors used in alzheimers

A

increase acetylcholine (brains primary neurotransmitter) levels

265
Q

what medication is given in advanced dementia

A

N-methyl-D-asperate (NMDA) receptor antagonist

266
Q

most common form of dementia?

A

alzheimers

267
Q

how does amyloid precursor protein -> alzheimers disease

A
  • abnormal APP degredation via b-secretase
  • APP cut into insoluble fragments
  • -> beta amyloid plaque
268
Q

3 RF for alzheimers disease

A
  • age>60
  • family history
  • trisomy 21 (downs syndrome)
  • gene mutations affecting APP
  • hx of HTN, dyslipidemia, cerebrovascular disease, altered glucose metabolism, brain trauma
269
Q

how many years after symptom onset is life expectancy for alzheimers

A

5-10yrs

270
Q

diagnostic imaging for alzheimers and results?

A

CT/MRI

  • excludes other dementias
  • brain scans show DIFFFUSE CORTICAL ATROPHY, GYRI NARROWING, SULCI WIDENING, VENTRICLE ENLARGEMENT
271
Q

there is no cure for alzheimers, what medications may be given to pt? (3)

A
  1. acetylcholinesterase inhibitors
  2. vitamin E supplementation may provide benefit
  3. memantine (advanced)
272
Q

cause of lewy body dementia

A

alpha-synuclein protein aggregation in the neurons (particularly cortex, substantia nigra) forming lewy bodies -> apoptosis

273
Q

3 complications of lewy body dementia

A
  1. persistent psychotic symptoms (especially visual hallucinations)
  2. depression
  3. complete debilitation, dependence on others
  4. debilitation -> death, decreased life expectancy
  5. neuroleptic-agent sensitivity (adverse effects, parkinsonism)
274
Q

what type of dementia motor symptoms mimic parkinsons disease

A

lewy-body dementia (resting tremor, stiffness, slow movement, reduced facial expressions)

275
Q

3 medications used to alleviate symptoms of lewy-body dementia

A
  • acetylcholinesterase inhibitors
  • dopamine analogue
  • atypical neuroleptic agents
276
Q

diagnostic imaging for lewy body dementia

A

single-photon emission computerized tomography (SPECT) scanning

277
Q

define frontotemporal dementia

A

heterogenous degenerative frontal/temporal lobe disease

278
Q

what specific protein cellular inclusions are seen in frontotemporal dementia (2)

A
  • TAU proteins (Pick disease)
  • TAR DNA-binding protein 43 (TDP43)
279
Q

diagnostic imaging for frontotemporal dementia?

A

MRI

SPECT/perfusion-MRI/PET

280
Q

how do pick cells in frontotemporal dementia affect the neurons

A

swollen (ballooned) neurons

281
Q

features of pick disease (hint:PICK)

A

Progressive degeneration of neurons

Intracytoplasmic degeneration of neurons

Cortical atrophy

Knife edge gyri

282
Q

what is the second most common dementia in the elderly

A

vascular dementia

283
Q

4 causes of vascular dementia

A
  1. cerebral artery atherosclerosis
  2. carotid artery/heart embolization
  3. chronic HTN
  4. vasculitis
284
Q

3 RF for vascular dementia

A
  1. smoking
  2. HTN
  3. DM
  4. insulin resistance
  5. hyperlipidaemia
285
Q

vaguely define the S/S of vascular dementia

A

progressive, stepwise cognitive function impairment

286
Q

what is seen on MRI/CT in vascular dementia

A

multiple cortical, subcortical infarcts

287
Q

what is the cause of shingles

A

varicella zoster virus

288
Q

when and how does shingles occur

A
  • dominant VSZ reactivates

reactivation in dorsal root -> cranial nerve ganglia -> down axons -> local skin inflammation innervated by ganglion

  • prodromal 2-4 day tingle/localized pain b4 rash onset
289
Q

3 RF for shingles

A
  1. primary varicella infection history
  2. more common in adults >50
  3. immunocomprimised
  4. stress
290
Q

3 complications of shingles

A
  1. ramsay hunt syndrome
  2. postherpetic neuralgia
  3. herpes zoster opthalmicus (sight-threatening)
291
Q

appearance of shingles

A

erythematous, maculopapular lesions evolve into a painful vesicular rash

292
Q

4 medication options for shingles

A
  • oral/IV antiviral therapy
  • analgesia (paracetamol/ibuprofen etc)
  • calamine lotion
  • varicella-zoster immune globulin
293
Q

pathophysiology of normal pressure hydrocephalus

A

CSF accumulation -> progressive lateral ventricle enlargement

294
Q

main RF for normal pressure hydrocephalus

A

prevelance largest among elderly

295
Q

3 main s/s of normal pressure hydrocephalus

A
  • unsteady gait (glue-footed)
  • urinary incontinence
  • cognitive impairment
296
Q

what is seen on CT/MRI in normal pressure hydrocephalus (3)

A
  • ventriculomegaly
  • enlarged sylvian fissure
  • enlarged sulci with no cortical atrophy
297
Q

2 treatment options in normal pressure hydrocephalus

A

surgery in some situations

ventriculoperitoneal shunt (increase ICP relief)

298
Q

cause of wenicke-kosakoff syndrome

A

vitamin B1 or thiamine deficiency

299
Q

name the acute-reversible stage of wenicke-korsakoff syndrome?

A

wernickes encephalopathy -> korsakoff syndrome (chronic, irreversible)

300
Q

where is thiamine stored and absorbed

A

stored in liver

absorbed in duodenum

301
Q

major cause of thiamine deficiency

A

alcohol abuse

302
Q

how does thiamine deficiency affect the cerebellum

A

movement and balance affected

303
Q

2 later findings in thiamine deficiency

A
  • haemorrhage
  • necrosis of mamillary bodies -> affect memory/emotion/behaviour
304
Q

define the triad of wernickes encephalopathy

A
  1. opthalmoplegia (weakness or paralysis of eye muscles)
  2. ataxia or unsteady gait
  3. changes in mental state (confusion, apathy, difficulty concentrating)
305
Q

what is the main impairment caused by korsakoff syndrome

A

mainly targets limbic system = severe memory impairment (anterograde/retrograde amnesia)

confabulation

306
Q

what is the most common cause of encephalitis

A

viral - HSV-1 (herpes simplex virus)

307
Q

one bacterial cause of encephalitis

A
  • listeria monocytogenes
  • mycobacteria
  • spirochetes (syphilis)
308
Q

3 RF for encephalitis

A
  1. immunosuppression
  2. travel to low-income nations
  3. exposure to disease vectors in endemic areas
309
Q

3 complications of encephalitis

A
  1. seizures
  2. SIADH
  3. increased ICP
  4. coma
310
Q

how is meningism seen in encephalitis

A

nuchal rigidity (cant flex neck forward passively due to increased tone/stiffness)

311
Q

what is seen in a brain MRI for viral (HSV) encephalitis

A

increased T2 signal intensity in fronto-temporal region

312
Q

what is seen in the CSF chemistry in viral encephalitis

A

lymphocytosis (>5 WBC/ml) with normal glucose

313
Q

how can a definitive diagnosis be made for viral encephalitis

A

brain biopsy

  • cowdry type A inclusions
  • haemorrhagic necrosis in temporal, orbitofrontal lobes (HSV)
314
Q

what is seen in this CT scan

A

HSV encephalitis

315
Q

what medication is given for HSV encephalitis

A

acylcovir

316
Q

what medication is given for CMV encephalitis

A

ganciclovir/foscarnet

317
Q

medication for bacterial encephalitis

A

targeted abx

318
Q

1 cause of a first order lesion horners syndrome:

1 cause of 2nd order lesion horners syndrome

1 cause of 3rd order lesion horners syndrome

A

1st - arnold-chiari malformation, cerebrovascular insult, basal skull tumor

2nd - trauma, cervical rib, pancoast tumour, neuroblastoma, aortic dissection

3rd - herpes zoster, internal carotid artery dissection, cluster headache

319
Q

triad of horners syndrome

A

ptosis, miosis and anhidrosis

320
Q

2 diagnostic imagings used for horners syndrome investigation

A

x-ray - detect pancoast tumour/shoulder trauma

mri - detects aneurysm/dissection

321
Q

define narcolepsy

A

recurrent sleep phenomena during wakefulness

322
Q

what neuropeptide is narcolepsy associated with and what is the action of this peptide

A

associated with lack of orexin

orexin (A&B): increase state of wakefulness when binding to polysnynaptic neurons

323
Q

cause of narcolepsy

A

damage to orexin-transporting neurons (by autoimmune process/injury)

324
Q

2 RF for narcolepsy

A
  • genetics
  • low levels of histamine
  • infections
  • autoimmune diseases
325
Q

3s/s of narcolepsy

A
  1. daytime sleepiness
  2. cataplexy
  3. hallucinations
  4. sleep paralysis
326
Q

how to diagnose narcolepsy

A

recurrent feeling of sleepiness in daytime >3x week >3m

+ at least 1:

  • cataplexy
  • hypocretin deficiency
  • short rapid eye movements (REM)
327
Q

treatment for narcolepsy (2)

A

SSRI’s

stimulants (modafinil)

328
Q

define cataplexy

A

muscles go weak or limp with no warning - typically experienced during a strong emotion or emotional sensation

329
Q

what is cataplexy often associated with

A

narcolepsy

330
Q

3 symptoms of cataplexy

A

drooping eyelids

jaw dropping

head falling to the side due to neck muscle weakness

whole body falling to the ground

various muscles around your body twitching without an obvious cause

331
Q

define NEAD

A

non-epileptic attack disorder

look like epileptic seizures but not caused by electrical activity in the brain

332
Q

what is the current understanded cause of NEAD (2)

A

brains response to overwhelming stress

traumatic events

333
Q

what cranial nerves are typically affected in bulbar palsy

A

nerves that arise from brainstem

9,10,11,12

334
Q

name two affects of a damaged CN9

A

dysphagia (difficulty swallowing)

reduced gag reflex

335
Q

what type of palsy may you see a nasal speech that lacks in modulation (e.g. controlling or adjusting of one’s speech)

A

bulbar palsy

336
Q

how is pseudobulbar palsy characterised

A

atypical expression of emotion displayed by unusual outbursts of laughing/crying (emotional lability)

337
Q

2 most common causes of bulbar palsy

A

brainstem strokes and tumours

338
Q

briefly define radiculopathy

A

pain/numbness/tingling/weakness in arms or legs caused by compression of a nerve root in the spinal column

339
Q

what is the most common type of lumbar radiculopathy

A

sciatica

340
Q

where is cervical radiculopathy commonly seen

A

c5-c7

341
Q

two forms of cervical radiculopathy

A

disc degeneration and spondylosis

342
Q

define radiculopathy pain

A

sharp and spreads from specific locations to other parts of the body

343
Q

typical treatment for radiculopathy (3)

A
  • nsaids
  • physical therapy
  • surgical procedures to relieve nerve compression if necessary
344
Q

define mononeuropathy

A

damage or dysfunction of a single peripheral nerve that connects the CNS to the body

345
Q

what are the two most common mononeuropathies and briefly define them

A

cubital tunnel syndrome = neuropathy of the ulnar nerve (sensation to 4th/5th finger, part of palm and underside forearm)

carpel tunnel syndrome = neuropathy of median nerve (sensation to 1st/2nd/3rd/4th fingers)

346
Q

3 non-compression related causes of mononeuropathy

A

infection

radiation

cold

347
Q

what is the main cause of a fixed mononeuropathy

A

nerve compression against a hard surface (i.e. tumour/cast/cramped posture for long time)

348
Q

3 RF for entrapment of a nerve in a restricted anatomical structure

A

pregnancy

hypothyroidism

RA

349
Q

define delerium

A

fast decline in attention/consciousness thinking

350
Q

3 categories that are a RF for delirium and 1 example of each

A

disease (dementia, pneumonia, UTI)

post-surgical complication (meds like anticholinergics)or chronic fatigue

increase falls risk (head injuries etc)

351
Q

3 S/S of delirium

A
  • difficulties with attention span, concentration, remaining conscious
  • disorganised and delayed thinking
  • hyperactive symptoms
  • hypoactive symptoms
352
Q

treatment option for severe symptoms of delerium

A

haloperidol/second gen antipsychotics

353
Q

what medication must be avoided in delirium

A

opiates (increased risk delirium)

354
Q

list 3 medication types that can increase the risk of osteoporosis

A
  • long term corticosteroids
  • SSRI’s
  • PPI
  • anti-epileptics
355
Q

why are post-menopausal women at higher risk of osteoporosis than pre-menopausal women?

A

post-menopause have reduced oestrogen

(oestrogen is a protective factor against osteoporosis)

356
Q

assessment tool for identify osteoporisis risk over 10yrs?

A

FRAX tool

357
Q

investigation for bone mineral density

A

DEXA scan

358
Q

what is the bone mineral density result for a patient with a T score of -2

A

osteopenia

T-score of -1 to -2.5 is osteopenia

359
Q

what is the bone mineral density result for a patient with a T score of -2.7

A

osteoporosis

(less than -2.5 is osteoprosis

less than-2.5 + # is severe osteoporosis)

360
Q

supplementation for patients at risk of fragility #

A

vitamin D and calcium

361
Q

first line treatment for osteoporosis

A

bisphosponates

362
Q

3 notible SE of osteoporosis

A
  • reflux and oesophageal erosions
  • atypical #
  • necrosis of the jaw
  • osteonecrosis of external auditory canal
363
Q

3 examples of bisphonates

A
  • alendronate
  • risedronate
  • zolendronic acid
364
Q

what areas of the body are mainly affected by pressure ulcers

A

bony prominences

  • sacrum/heels/hips/elbows
365
Q

3 RF for pressure ulcers

A
  • reduced mobility (e.g. parkinsons, hip #, stroke)
  • reduced perfusion (atherosclerosis, smoking,)
  • factors affecting skin structure (malnutrition, skin moisture)
366
Q

what type of medication has an increase risk of mortality in dementia patients

A

anti-psychotics

367
Q

What type of drug is memantine

A

NMDA agonist