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Phase 3a Jemima > Neurology > Flashcards

Neurology Flashcards

1
Q

what is a acoustic neuroma

A

it is a rare tumour of the vestibulocochlear nerve

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2
Q

what cells does an acoustic neuroma arise from

A

schwann cells of the nerve sheath

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3
Q

are acoustic neuromas benign/malignant

A

they are benign and slow growing
however they can occur at the cerebellopontine angle which can compress local structures and lead to life threatening conditions

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4
Q

are acoustic neuromas unilateral or bilateral

A

they are usually unilateral
if bilateral think of neurofibromatosis type 2

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5
Q

what are the clinical features of an acoustic neuroma

A

hearing loss - unilateral
unilateral tinnitus
vestibular disturbance - dizziness or imbalance
sensation of fullness in the ear
can also be associated with facial nerve palsy (forehead NOT spared)
Can headaches nausea and vomiting due to increased intercranial pressure

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6
Q

what are risk factors of developing an acoustic neuroma

A

high dose ionising radiation to the head and neck
neurofibromatosis type 2

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7
Q

what would be differential diagnosis be for acoustic neuroma

A

meningioma
ectodermal inclusion tumours
neuromas originating from other cranial nerves
extension of nearby lesions

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8
Q

what investigations should be done with suspected acoustic neuroma

A

MRI head
pure tone audiometry - sensorineural pattern of hearing loss

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9
Q

what is the management of acoustic neuroma

A

active observation
microsurgery
radiosurgery

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10
Q

what does the management of an acoustic neuroma depend on

A

size of tumour
patient factors - age and future quality of life
involvement of local structures

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11
Q

what microsurgery options are there for acoustic neuromas

A

retrosigmoid, translabyrinthine and middle fossa approach to the tumour
- which one is chosen will depend on location and size of tumour

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12
Q

what is conservative treatment for acoustic neuromas and when is it done

A

active surveillance with annual neuroimaging - MRI
this is done in patients with small tumours with no impairment or in elderly patients with multiple medical co morbidities

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13
Q

what are the risks of microsurgery for acoustic neuroma

A

cerebrospinal fluid leak
cerebellar injury
meningitis
hearing loss and/or facial paralysis
death

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14
Q

what is stereotactic radiosurgery for acoustic neuroma

A

it is used for tumours <3cm and it involves high energy gamma rays to deliver a singe dose of radiation to the tumour (gamma knife)

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15
Q

what are the risks associated with stereotactic radiosurgery for acoustic neuroma

A

radiation necrosis to the brain
malignant change of the neuroma to glioblastoma

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16
Q

what are complications of acoustic neuroma

A

hearing loss
facial paralysis
hydrocephalus
compression of the cerebellar peduncles, cerebellum, brainstem and cranial nerves IX-XI

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17
Q

what is anterior cord syndrome

A

it is incomplete spinal cord injury

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18
Q

how does anterior cord syndrome present

A

with impairments in the pain and temperature sensations while vibration and proprioceptive sensations are preserved
motor deficits are seen both at and below the level of injury

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19
Q

what causes anterior cord syndrome

A

ischaemia within the anterior spinal artery

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20
Q

what does the anterior spinal artery supply

A

the bilateral anterior and lateral horns of the spinal cord
the spinothalamic tracts
the corticospinal tracts

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21
Q

what are causes of anterior cord syndrome

A

iatrogenic - cross clamping of the aorta during aneurysm repair
direct injury - crash, burst, knife
indirect injury - occlusion or hypoperfusion due to severe hypotension, atherothrombotic disease or vasculitis

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22
Q

what is the mechanism of a bust injury (anterior cord syndrome)

A

forces coming from above or below the vertebral body
nucleus pulposus of the intervertebral disc is forced into the vertebral body
causes it to shatter and cause spinal cord injury

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23
Q

what are the two phases of mechanical trauma to the spinal cord in anterior cord syndrome

A

the initial direct trauma results in acute compression and disruption of vasculature
second phase there is inflammation, oedema, haemorrhage, demyelination changes in the neurones
a later stage consists of scar formation, wallerian degeneration and development of cysts

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24
Q

how does anterior cord syndrome present

A

varying degrees of muscle weakness and sensory loss
- pain sensation is decreased or absent
- proprioception is maintained
- loss of motor power usually mimics same pattern of pain loss
chance of autonomic dysreflexia, movement and sexual impairments, neuropathic pain, bladder and bowel dysfunction

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25
Q

what motor effects will there be in anterior cord syndrome

A

below the level of spinal injury there will be bilateral motor dysfunction
- flaccidity with absent reflexes which may return with increased tone or spasticity

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26
Q

what sensory effects will there be in anterior cord syndrome

A

alterations in pain and temperature sensation present two to three dermatomal segments below the level of the injury

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27
Q

how is anterior cord syndrome diagnosed

A

detailed history and exam
MRI - pencil like hyper intensities
axial MRI will show owls eye
lumbar puncture
echo
bloods and U+E

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28
Q

how is anterior cord syndrome managed

A

mainly supportive
need to address the limitations in mobility and activities of daily living

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29
Q

whats the non surgical management of anterior cord syndrome

A

management of anticoagulation
antiplatelet and thromboprophylaxis
fever and glycemic control
blood pressure support
rehabilitation focused on improving independence and quality of life

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30
Q

where does the facial nerve leave the brainstem

A

at the cerebellopontine angle, passes through the temporal bone and the parotid gland

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31
Q

what are the five branches of the facial nerve

A

temporal
zygomatic
buccal
marginal mandibular
cervical

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32
Q

what is the motor function of the facial nerve

A

facial expression
stapedius in the inner ear
posterior digastric, stylohyoid and platysma muscles

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33
Q

what is the sensory function of the facial nerve

A

taste from the anterior 2/3 of the tongue

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34
Q

what is the parasympathetic function of the facial nerve

A

submandibular and sublingual salivary glands
lacrimal gland

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35
Q

is the forehead spared in a lower motor neurone lesion

A

NO !!!!!!!!!!!!!!!!!!!!!!!!!

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36
Q

what is bells palsy

A

it is a unilateral lower motor neurone facial nerve palsy

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37
Q

what is the cause of bells palsy

A

it is idiopathic - no apparent cause

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38
Q

how long is the recovery of bells palsy

A

most patients fully recover over several weeks but recovery may take up to 12 months
- 1/3 are left with some residual weakness

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39
Q

what is the treatment for bells palsy

A

if the patient presents within 72 hours of symptom development then prednisolone for
- 50mg for 10 days
- 60 mg for 5 days followed by a 5 day reducing regime dropping the dose by 10mg each day
patients also require lubricating eye drops

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40
Q

what is Ramsay-hunt syndrome

A

it is caused by VZV and causes a unilateral lower motor neurone facial nerve palsy

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41
Q

what are symptoms of ramsay hunt syndrome

A

painful and tender vesicular rash in the ear canal, pinna and round the ear. this rash can extend to the anterior two thirds of the tongue and hard palate
have facial drop like in bells palsy

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42
Q

what is the treatment of |Ramsay hunt syndrome

A

aciclovir
prednisolone
lubricating eye drops

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43
Q

what are other infectious causes of lower motor neurone facial nerve palsy

A

otitis media
otitis externa
HIV
lyme disease

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44
Q

what are systemic causes of lower motor neurone facial nerve palsy

A

diabetes
sarcoidosis
leukemia
multiple sclerosis
guillian barre

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45
Q

what tumours can cause lower motor neurone facial nerve palsy

A

acoustic neuroma
parotid tumour
cholesteatoma

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46
Q

what trauma can cause lower motor neurone facial nerve palsy

A

direct nerve trauma
surgery
base of skull fractures

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47
Q

what is a brain abscess

A

it is a pus filled swelling in the brain

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48
Q

what are causes of a brain abscess

A

direct extension of cranial infections - osteomyelitis, mastoiditis, sinusitis
penetrating head wounds
hematogenous spread
unknown cause

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49
Q

what bacteria commonly cause brain abscess

A

staphylococci - due to trauma, surgery or endocarditis
enterobacteriaceae - chronic ear infections
fungi (aspergillus) and protozoa (toxoplasma gondii) in HIV infected patients

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50
Q

what are symptoms of a brain abscess

A

headache
nausea
vomiting
lethargy
seizures
personality changes
papilloedema
focal neurological deficits
fever
chills
leukocystosis

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51
Q

how do you diagnose a brain abscess

A

Contrast enhanced MRI
if unavailable then contrast enhanced CT
CT guided aspiration and culture

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52
Q

what will a brain abscess look like on MRI

A

oedematous mass with ring enhancement - can look similar to tumour or infarction

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53
Q

how is a brain abscess treated

A

antibiotics - initially cefotaxime or ceftriaxone plus metronidazole/vancomycin
CT guided aspiration/surgical drainage
corticosteroids
anti seizure medication

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54
Q

how long should antibiotics be given for with a brain abscess

A

4-8 weeks
cefotaxime 2g IV every 4 hours
ceftriaxone 2g IV every 12 hours

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55
Q

what are the clinical features of a brain tumour

A

signs relating to raised intercranial pressure are common
- headache: worse on waking, lying down, bending forward or coughing
- nausea and vomiting
- papilloedema
- coma

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56
Q

what is a meningioma

A

it is a slow growing tumour that forms from the arachnoid cell cap found on the meninges

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57
Q

what are the clinical features of a meningioma

A

they are usually benign and surgically viable

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58
Q

when are meningiomas most common

A

peak incidence occurs at 45 yrs
2;1 female ratio

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59
Q

how might someone with a meningioma present

A

may be asymptomatic
headache
seizure
spastic weakness or numbness in both leg
gait abnormalities
visual loss

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60
Q

what investigations are done for a meningioma

A

MRI with gadolinium contrast (+/- CT)
angiography

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61
Q

how is meningioma managed

A

usually conservative unless symptoms develop
surgical excision
radiotherapy

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62
Q

what is a pituitary adenoma

A

it is a cancer that occurs in the pituitary gland
they can be functional and secrete hormones

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63
Q

what are the clinical presentations of pituitary adenomas

A
  • cushingoid symptoms
  • acromegaly
  • diabetes insipidus
  • hyperpituitarism
  • amenorheoa/galactorrhoea/impotence
  • bitemporal hemianopia
  • hydrocephalus
  • diplopia
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64
Q

what investigations are done for suspected pituitary adenoma

A

endocrine lab tests
MRI with contrast (+/- CT)

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65
Q

how is a pituitary adenoma managed

A

dopamine agonists to treat prolactinomas
surgery
radiation therapy

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66
Q

what are complications of pituitary adenoma

A

pituitary apoplexy - when haemorrhage causes a rapid increase in the size of the lesion and surrounding vasogenic oedema
due to this is causes tissue necrosis with sudden onset visual loss, headache and hydrocephalus

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67
Q

what is a craniopharyngioma

A

it arises in the pituitary stalk and can affect the hypothalamus and the pituitary

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68
Q

what is a craniopharyngioma derived from

A

residual cells of Rathkes pouch

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69
Q

what is the age of onset of craniopharyngiomas

A

bimodal age of onset 5-14 and 50-70

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70
Q

what are the symptoms of craniopharyngiomas

A

growth failure in children
diabetes insipidus
sexual dysfunction in adults
hydrocephalus
bitemporal hemianopia
pituitary insufficiency
headache

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71
Q

what investigations are done for craniopharyngiomas

A

MRI with contrast (+/- CT)
endocrine lab investigations

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72
Q

what is the management for craniopharyngiomas

A

surgical removal
radiotherapy

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73
Q

what is primary CNS lymphoma

A

it is usually a large B cell lymphoma

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74
Q

what are the clinical features of primary CNS lymphoma

A

seizures
headache
altered mental status
systemic symptoms: fever, night sweats, unintentional weight loss
diplopia
vertigo
dysphagia

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75
Q

what investigations are done for primary CNS lymphoma

A

MRI +/- CT
HIV testing
lumbar puncture - may show increased WCC
EBV virus PCR

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76
Q

what is the management of primary CNS lymphoma

A

chemotherapy - methotrexate (+ cytarabine)
radiation therapy
steroids - dexamethasone
surgery

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77
Q

what is a medulloblastoma

A

it is thought to arise from cerebellar stem cells and tend to seed within CSF pathways giving rise to a high metastatic propensity

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78
Q

what population is medulloblastoma most common in

A

children

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79
Q

what are the clinical features of medulloblastoma

A

hydrocephalus: worsening headache and decreased consciousness
cerebellar signs - incoordination and gait abnormalities
mass effect symptoms - speech and vision issues, unilateral weakness, headache, drowsiness, nausea and vomiting
extraocular muscle palsies

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80
Q

what investigations are done for medulloblastoma

A

lumbar puncture
MRI +/- CT

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81
Q

what is the management for medulloblastoma

A

surgical removal of the tumour
radiotherapy
chemotherapy

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82
Q

what is a glioma

A

it is an umbrella term for a variety of tumour subtypes consisting of malignant tumours of the glial tissue of the nervous system

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83
Q

what are different types of gliomas

A

astrocytoma’s
glioblastoma multiforme
pilocytic astrocytoma
ependymomas
oligodendrogliomas

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84
Q

what is the mean age of onset for gliomas

A

about 55

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85
Q

how to gliomas metastisise

A

all gliomas metasisise via the CSF

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86
Q

what are the clinical features of gliomas

A

headache
vomiting
seizures
focal neurological deficit including vision loss
cranial nerve dysfunction

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87
Q

what investigations are done for suspected glioma

A

MRI with contrast

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88
Q

what is the management for gliomas

A

surgery - complete excision often challenging. Carmustine implants can be added which can help reduce rate of tumour spread
Radiotherapy
Chemotherapy - temozolomide

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89
Q

what is the prognosis for gliomas

A

overall poor prognosis as they are rarely curable

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90
Q

what are causes of increased intercranial pressure

A

brain tumours
intercranial haemorrhage
idiopathic intercranial hypertension
abscess of infection

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91
Q

what are symptoms of raised intercranial pressure

A

constant headache which is nocturnal, worse on waking, worse on coughing, straining or bending forward
vomiting
papilloedema on fundoscopy
altered mental status
visual field defects
seizures
unilateral ptosis
third and sixth nerve palsies

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92
Q

what is papilloedema

A

it is swelling of the optic disc secondary to raised intercranial pressure

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93
Q

how is papilloedema seen on fundoscopy

A

blurring of the optic disc margin
elevated optic disc
loss of venous pulsation
engorged retinal veins
haemorrhages around the optic disc
patons lines - creases or folds in the retina around the optic disc

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94
Q

what are the three main types of glioma

A

astrocytoma - most common and aggressive
oligodendroglioma
ependymoma

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95
Q

what cancers most often spread to the brain

A

lung
breast
renal cell carcinoma
melanoma

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96
Q

what is bulbar palsy

A

it is a lower motor neurone impairment in nerves 9, 10, 11 and 12

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97
Q

what are symptoms of bulbar palsy

A

depends on nerve damaged
- swallowing difficulties
- reduced gag reflex
- difficulty chewing
- nasal regurgitation
- slurred speech
- difficult in handling secretions
- aspiration of secretions
- altered vocal ability
- difficulty articulating words
- nasal speech that lacks in modulation
- difficulty with consonants
- wasting tongue
- drooling
- weakness of jaw and facial muscles
- absent or abnormal jaw reflex

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98
Q

what are the two types of bulbar palsy

A

progressive and non progressive
- progressive is more common

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99
Q

what is pseudobulbar palsy

A

it is a result of damage to the upper motor neurons

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100
Q

what is the difference between bulbar palsy and pseudobulbar palsy

A

in pseudobulbar palsy the patient often has atypical expression of emotion displaying unusual outbursts of laughing or crying

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101
Q

what are causes of bulbar palsy

A

brainstem strokes
tumours
degenerative diseases - ALS
autoimmune diseases - guillian barre
genetic diseases - kennedy disease, brown-vialetto-van laere syndrome, fazio-londe syndrome

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102
Q

what is Kennedy disease

A

it is a lower motor neurone disease that can affect transmission signals between the brain and spinal cord
- x linked

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103
Q

how do you diagnose bulbar palsy

A

history and exam
CSF analysis
MRI of brain

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104
Q

how is bulbar palsy treated

A

currently no known treatments
supportive management - feeding tube, speech and language therapy, medications to prevent drooling
condition specific treatment

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105
Q

is bulbar palsy fatal

A

it can be in progressive cases - can occur 1-3 years from the start of the disorder and normally attributed to aspiration pneumonia

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106
Q

what are the three parts of the cerebellum

A

Archicerebellum/vestibulocerebellum
midline vermis
lateral hemispheres

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107
Q

what is the role of the archicerebellum

A

maintains equilibrium and coordinated eye, head and neck movements

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108
Q

what is the role of the midline vermis (cerebellum)

A

coordinates trunk and leg movements

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109
Q

what is the role of the lateral hemispheres (cerebellum)

A

control quick and finely coordinated limb movements predominantly the arms and legs

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110
Q

what is the most common cause of cerebellar disorders

A

alcoholic cerebellar degeneration

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111
Q

what are causes of cerebellar disorders

A

alcoholic cerebellar degeneration
congenital malformations
hereditary ataxias
acquired ataxias - MS, stroke, traumatic brain injury, toxin exposure, celiac disease, hypothyroidism
paraneoplastic syndrome

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112
Q

what toxins can cause cerebellar dysfunction

A

carbon monoxide
heavy metals
lithium
phenytoin
solvents

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113
Q

what are symptoms of cerebellar degeneration

A

balance problems
decreased muscle tone
eye problems - double vision and nystagmus
poor muscle coordination in arms and legs
problems with motor skills such as holding your head up
slow and slurred speech

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114
Q

how id cerebellar degeneration diagnosed

A

MRI or CT
CSF analysis
bloods - immune issues

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115
Q

how is cerebellar degeneration managed

A

treatment of possible cause
usually supportive
Riluzole 50mg every 12 hours for short term ataxia treatment
chemo if paraneoplastic syndrome
alcohol abstinence
physical, occupational or speech therapy

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116
Q

what is cerebral palsy

A

it is a non progressive permanent neurological condition commonly affecting normal movement and posture

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117
Q

what causes cerebral palsy

A

it is caused by damage to the developing brain which can occur while the baby is in utero, during birth or in the neonatal period
- hypoxia, haemorrhage, infection

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118
Q

what are the antenatal risk factors of cerebral palsy

A

multiple gestation
chorioamnionitis
maternal infections - toxoplasmosis, rubella, CMV and herpes simplex

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119
Q

what are the perinatal risk factors for cerebral palsy

A

prematurity
low birth weight
birth asphyxia
neonatal sepsis

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120
Q

what are the clinical features of cerebral palsy

A

delayed motor milestones
- not siting by 8 months
- not walking by 18 months
- hand preference before 12 months
tone abnormalities
abnormal movements
feeding issues such as choking/dysphagia
persistent toe walking

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121
Q

what are postnatal risk factors for cerebral palsy

A

meningitis
severe hyperbilirubinaemia

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122
Q

what are the different types of cerebral palsy

A

spastic cerebral palsy
dyskinetic cerebral palsy
ataxic cerebral palsy

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123
Q

what is spastic cerebral palsy

A

it is charactised by velocity dependent hypertonia and hyperreflexia
it is the most common type
when a limb is moved quickly the muscle can suddenly increase in tone and stop further movement

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124
Q

what is dyskinetic cerebral palsy

A

it is charactised by involuntary, uncontrolled, recurring movements, fluctuating muscle tone and persistent primitive reflexes

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125
Q

what are the two subtypes of dyskinetic cerebral palsy

A

dystonic - abnormal posturing and hypertonia
choreoathetotic - chorea and athetosis

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126
Q

what is ataxic cerebral palsy

A

it is characterised by a loss of muscle coordination resulting in ataxia and tremor

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127
Q

what are the classifications of cerebral palsy depending on limbs affected

A

monoplegic
hemiplegic
dipelgic
quadraplegic

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128
Q

what is hypertonia

A

it is a general term for increased resistance to movement

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129
Q

what is spasticity

A

velocity dependent
the faster you move a limb the higher the tone you will feel

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130
Q

what is dystonia

A

it is abnormal postures which are worse on intention

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131
Q

what investigations are done for cerebral palsy

A

it is a clinical diagnosis
MRI brain - may show damage

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132
Q

what is conservative management for cerebral palsy

A

physiotherapy - improve function
occupational therapy
speech and language therapy
dietician input

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133
Q

what is the medical management for cerebral palsy

A

hyoscine hydrobromide - excess drooling
diazepam - pain
baclofen: hypertonia
botulinum toxin type A injections for spasticity

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134
Q

what surgical management is done for cerebral palsy

A

hip displacement is very common and surgical intervention may be required

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135
Q

what are complications of cerebral palsy

A

problems with eating or drinking
drooling
constipation
virtual and hearing issues
epilepsy
learning disability
speech difficulty
osteopenia and osteoporosis
sleep disturbance

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136
Q

what is hypoxic ischaemic encephalopathy

A

it is brain injury that occurs when the brain doesnt get enough oxygen/blood and permanently affect brain unction

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137
Q

what are causes of hypoxic ischaemic encephalopathy

A

traumatic birth
neonatal encephalopathy
perinatal hypoxia

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138
Q

what are signs/symptoms of hypoxic ischaemic encephalopathy

A

a floppy, weak muscle tone or tense muscles
difficulty feeding
fatigue
irritability
a weak cry
a pale blue or gray tone to the skin, fingers and lips
little to no response to sound
poor reflexes
irregular or slow HR
abnormal breathing
seizures
LOC

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139
Q

what are causes of hypoxic ischaemic encephalopathy during foetal development

A

abnormal development or function of fetus heart or lung
an infection - toxoplasmosis or CMV
blood pressure thats too high or too low
low oxygen levels in pregnant parent

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140
Q

what acre causes of hypoxic ischaemic encephalopathy during birth

A

umbilical cord prolapse
umbilical cord compression
placental abruption
uterine rupture
placenta praevia

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141
Q

what are causes of hypoxic iscaemic encephalopathy in older children and adults

A

arrhythmia
asphyxiation
overdose
poisoning
shock

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142
Q

what are risks of hypoxic ischaemic encephalopathy

A

low birth weight
amniotic fluid contamination
delayed fetal development
preeclampsia
gestational diabetes
prolonged labour
substance use disorder

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143
Q

what are complications of hypoxic ischaemic encephalopathy

A

developmental delays
problems with growth
hearing or vision loss
issues with cognitive function
difficulty paying attention
epilepsy
cerebral palsy
infections

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144
Q

how is hypoxic ischaemic encephalopathy diagnosed

A

medical emergency
physical exam
fetal heart monitoring
placenta bloods
newborn wellness assessment
cord blood and gasses
MRI
EEG

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145
Q

how is hypoxic ischaemic encephalopathy treated

A

cooling babies body followed by rewarming body to protect brain from further injury
EEG monitoring and antiseizure medication
supportive treatment - oxygen
physical and occupational therapy
speech therapy
early intervention educational programs

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146
Q

what is chronic fatigue syndrome

A

it is extreme fatigue that lasts for at least six months
symptoms worsen with physical or mental activity but dont fully improve with rest

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147
Q

what are the symptoms of chronic fatigue syndrome

A

extreme exhaustion after physical or mental exercise
problems with memory or thinking
dizziness that worsens with moving from lying down or sitting to standing
muscle or joint pain
unrefreshing sleep
headaches
sore throats
tender lymph nodes

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148
Q

what are causes of chronic fatigue syndrome

A

genetics
infections
physical or emotional trauma
problems with energy storage

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149
Q

what are risk factors of chronic fatigue syndrome

A

age - young to middle aged adults
sex- women more common
other medical conditions - fibromyalgia or PoTS

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150
Q

what is the diagnostic criteria for chronic fatigue syndrome

A
  • so severe that it interferes with the ability to engage in pre illness activities
  • new or definite onset
  • not substantially alleviated by rest
  • worsened by physical, mental or emotional exertions
  • difficulties with memory, focus and concentration
  • dizziness that worsens with moving from lying down o from sitting to standing
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151
Q

how long do symptoms need to be present for before a diagnosis of chronic fatigue syndrome is made

A

at least six months and occur at least half the time at moderate, substantial or severe intensity

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152
Q

what is the treatment for chronic fatigue syndrome

A

there is no cure treatment focuses on symptom relief
- pain: ibuprofen, naproxen, pregabalin, gabapentin
- orthostatic intolerance: bp regulation
- depression: antidepressants

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153
Q

what is diabetic neuropathy

A

it is a type of nerve damage that can occur with diabetes

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154
Q

what are the four main types of diabetic neuropathy

A

peripheral neuropathy
autonomic neuropathy
proximal neuropathy
mononeuropathy/ focal neuropathy

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155
Q

what is peripheral neuropathy

A

it is the most common type of diabetic neuropathy and it affects the feet and the legs first

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156
Q

what are symptoms of peripheral neuropathy

A

numbness or reduced ability to feel pain or temperature changes
tingling or burning feeling
sharp pains or cramps
muscle weakness
extreme sensitivity to touch
serious foot problems

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157
Q

what are symptoms of autonomic neuropathy

A

a lack of awareness that blood sugar is low
drops in blood pressure when rising from sitting or lying down that may cause dizziness
bladder or bowel issues
slow stomach emptying causing N+V
difficulty swallowing
changes in the way the eyes adjust to light/dark/things far away
increased or decreased sweating
problems with sexual response, vaginal dryness in women and erectile dysfunction in men

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158
Q

what is proximal neuropathy

A

it is a type of neuropathy that affects the nerves in the thighs, hips, buttocks or legs
symptoms are normally on one side of the body

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159
Q

what are symptoms of proximal neuropathy

A

severe pain in the buttock, hip or thigh
weak and shrinking thigh muscles
difficulty rising from a sitting position
chest or abdominal wall pain

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160
Q

what is mononeuropathy

A

it is damage to a single specific nerve

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161
Q

what are signs of mononeuropathy

A

difficulty focusing or double vision
paralysis on one side of the face
numbness or tingling in hands or fee
weakness in the hand
pain in the shin or foot
foot drop
pain in the front of the thigh

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162
Q

what are risk factors or developing diabetic neuropathy

A

poor blood sugar control
diabetes history
kidney disease
being overweight
smoking

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163
Q

what are complications of diabetic neuropathy

A

hypoglycaemic unawareness
loss of toe, foot or leg
urinary tract infections and urinary incontinence
sharp drops in blood pressure
digestive issues
sexual dysfunction
increased/decreased sweating

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164
Q

how can you prevent diabetic neuropathy

A

blood sugar control
foot care

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165
Q

how is diabetic neuropathy diagnosed

A

filament testing
sensory testing
nerve conduction testing
electromyography
autonomic testing

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166
Q

how is diabetic neuropathy treated

A

slow progression of disease - maintaining blood sugars, maintaining healthy weight, regular physical activity
relieving pain - gabapentin, pregabalin, amitriptyline, SNRIs
managing complications and restoring function

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167
Q

what is encephalitis

A

it is inflammation of the brain

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168
Q

what are symptoms of infective encephalitis

A

headache
fever
chills
aches in muscles
fatigue or weakness
stiff neck
confusion, agitation, hallucinations
seizures
irregular movements
loss of consciousness

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169
Q

how might infective encephalitis preset in an infant

A

bulging of the fontanelle
nausea and vomiting
stiffness affecting the whole body
poor feeding or not waking for feeding
irritability

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170
Q

what are symptoms of autoimmune encephalitis

A

changes in personality
memory loss
psychosis
hallucinations
seizures
changes in vision
sleep issues
muscle weakness
trouble waking
irregular movements
bladder and bowel dysfunction

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171
Q

what are causes of encephalitis

A

infections - viruses mc
autoimmune - can be triggered by tumours, infection or idiopathic

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172
Q

what are viruses that can cause encephalitis

A

HSV 1 and 2
EBV
VZV
enteroviruses
mosquito borne viruses - west nile
tick borne viruses
rabies virus

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173
Q

what are risk factors for developing encephalitis

A

age - extremes of age
weakened immune system - HIV/AIDS
geographical regions - mosquito/tic causes
autoimmune disease
smoking

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174
Q

what are complications of encephalitis

A

chronic disease
weakness or lack of muscle coordination
personality change
memory issues
hearing or vision changes
trouble with speech

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175
Q

how is encephalitis diagnosed

A

MIR/CT
CSF analysis
bloods, U+E, sputum sample
EEG
brain biopsy (rare)
body imaging

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176
Q

how is encephalitis managed

A

bed rest
fluids
antivirals- acyclovir, ganciclovir
steroids and IV Ig

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177
Q

what follow up therapy may be done for those with encephalitis

A

brain rehabilitation
physical therapy
occupational therapy
speech therapy
psychotherapy

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178
Q

what is the pathophysiology of seizures

A

imbalance between excitatory (glutamatergic) and inhibitory (GABAergic) neuronal signaling at the synaptic level resulting in a reduced threshold for neurotransmission

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179
Q

what are structural abnormalities which can increase risk of seizures

A

head injury
stroke
space occupying lesion - tumours
neurodegenerative disease
genetic syndromes - tuberous sclerosis or neurofibromatosis

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180
Q

what genetic disorders can affect neurological conduction and cause epilepsy

A

Dravet syndrome - mutation affecting sodium voltage gated channels
tuberous sclerosis
neurofibromatosis

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181
Q

what can change seizure threshold in patients with epilepsy/all patients

A

metabolic or electrolyte abnormalities - hyponatraemia, hypoglycaemia
central nervous system infection - encephalitis, meningitis
alcohol withdrawal

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182
Q

what does the international league against epilepsy classify seizures as

A

according to onset
- focal
- generalised
- unknown

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183
Q

what is a focal seizure

A

it is a seizure that begins from a specific focus

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184
Q

what are features of a focal seizure

A

the patient remains conscious during
awareness may be impaired
may have motor or non motor onset
may spread to a generalised seizure

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185
Q

what is a general seizure

A

it affects both hemispheres
often motor and have characteristic abnormal movements

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186
Q

what are types of generalised seizures

A

tonic clonic
myoclonic
atonic
absence

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187
Q

what may be seen in a motor onset focal seizure

A

automatisms - repeated stereotypes movements
atonic movement
clonic movement
epileptic spasms
hyperkinetic
myoclonic
tonic

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188
Q

what what might be seen in a non motor onset focal seizure

A

autonomic behaviours
behaviour arrest
cognitive change
emotional change
sensory issues

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189
Q

what are key questions to ask in a seizure history

A

prodrome - any sensory aura pre fit
seizure itself - what happened
post ictal period - confusion/disorientation. how long for

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190
Q

what is Todds paralysis

A

post ictal limb weakness

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191
Q

what are dissociative seizures

A

type of functional neurological disorder which have distinctive features and lack abnormal electrical activity in the brain

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192
Q

what are features of functional seizures

A

long duration of seizure
quick recovery
retained awareness with bilateral arm movement
back arching
eye opening during events
dissociation
often very emotional after the event as well

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193
Q

what investigations should be done post epileptic fit

A

basic obs
capillary blood glucose
FBC, U+E, Bone profile, venous blood gas
CT/MRI head
EEG
video telemetry
patient videos

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194
Q

what are the criteria that needs to be met for someone to be diagnosed with epilepsy

A

two or more unprovoked seizures more than 24 hours apart

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195
Q

what does anti seizure medication primarily target

A

sodium channels or modulate GABAergic neurotransmission

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196
Q

what are complications of epilepsy

A

accidental self injury
status epilepticus
sudden death in epilepsy

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197
Q

whats something you always need to check with someone who has had a seizure

A

DRIVING
will have license removed until they are one year seizure free

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198
Q

what is the general treatment for tonic clonic seizures

A

Sodium valproate
in women - lamotrigine or levetiracetam

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199
Q

what is the general treatment for partial seizures

A

lamotrigine or levetiracetam

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200
Q

what is the treatment for myoclonic seizures

A

sodium valproate
in women levetiracetam

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201
Q

what is the treatment for tonic and atonic seizures

A

sodium valproate
in women lamotrigine

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202
Q

what is the treatment for absence seizures

A

ethosuximide

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203
Q

what is carbamazepine used for

A

epilepsy - partial seizures with complex symptoms, general tonic clonic and mixed patterns
trigeminal neuralgia
acute manic and mixed bipolar disorder

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204
Q

what are the different antiseizure medications

A

sodium valproate
lamotrigine
levetiracetam
ethosuximide
carbamazepine
phenytoin
topiramate

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205
Q

how does sodium valproate work

A

it increases activity of GAMA which reduces activity in the brain

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206
Q

what are the side effects of sodium valproate

A

teratogenic
liver damage and hepatitis
hair loss
tremor
reduced fertility - not given to under 55 anymore

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207
Q

how is sodium valproate teratogenic

A

it causes neural tube defects and developmental delay

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208
Q

what is status epilepticus

A

it is a seizure lasting more than 5 minutes or multiple seizures without regaining consciousness in the interim

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209
Q

how do you treat status epilepticus

A

ABCDE approach
IV benzodiazepine repeat after 5-10 mins
IV phenytoin, levetiracetam or sodium valproate
general anaesthesia

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210
Q

what are the different benzodiazepine options in status epilepticus

A

IV lorazepam
rectal diazepam
buccal midazolam

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211
Q

what is essential tremor

A

it is a fine tremor that affects all voluntary muscles
- common in elderly

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212
Q

what are the features of essential tremor

A

fine tremor - 6-12 Hz
symmetrical
more prominent with voluntary movement
worse when tired, stressed or after caffeine
improved by alcohol
absent during sleep

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213
Q

what are differential diagnosis for essential tremor

A

parkinsons
multiple sclerosis
huntingtons
hyperthyroidism
fever
dopamine antagonists - antipsychotics

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214
Q

what is the treatment for benign essential tremor

A

no definitive treatment - not harmful so doesnt require treatment unless its causing functional or psychological issues
- propranolol
- primidone

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215
Q

what is an extradural haemotoma

A

it is an acute haemorrhage between the dura and the inner surface of the skull

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216
Q

what is an extradural haemotoma commonly caused by

A

skull trauma in the temporal region - fall, assault, sporting injury

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217
Q

what is the most common artery to rupture in extradural haemotomas

A

middle meningeal artery

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218
Q

what does an extradural haemotoma look like on CT

A

lemon shaped haemotoma
- bi-convex
- can get midline shift and brainstem herniation

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219
Q

what is the pathophysiology of an extradural haemotoma

A

as blood leaks into extradural space it begins to strip the dura mater away from the skull
as this grows it increases the intercranial pressure
this can cause midline shift and tentoria herniation
this can eventually lead to brainstem death

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220
Q

what is the typical history of someone with extradural haemotoma

A

headache
nausea and vomiting
confusion
loss of consciousness followed by a period of lucidity
progressive decreasing level of consciousness

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221
Q

what are the typical clinical findings in extradural haematoma

A

tenderness of the skull
confusion
reduced GCS
cranial nerve deficits
motor or sensory deficits of the upper and/or lower limbs
hyperreflexia and spasticity
upgoing planter reflex
cushings triad

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222
Q

what is cushings triad

A

it is a physiological response to raised intercranial pressure
bradycardia
hypertension
irregular breathing pattern

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223
Q

what investigations would be done on someone with suspected extradural haemorrhage

A

capillary blood glucose
ECG
FBC, U+E, CRP, coagulation, group and save
CT head

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224
Q

what is the initial management for an extradural haemorrhage

A

ABCDE
patients on anticoagulation will require reversal
prophylactic antibiotics
temporary anticonvulsant medication
IV MANNITOL to reduce intercranial pressure

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225
Q

what is the definitive management for extradural haematoma

A

conservative - small bleeds with minimal mass effects
burr hole craniotomy
trauma craniotomy
will need close observation during post operative period

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226
Q

what are complications of an extradural haematoma

A

infection
cerebral infarct
seizures
cognitive impairment
hemiparesis
hydrocephalus
brainstem injury

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227
Q

what clinical features in extradural haemorrhage are associated with poorer prognosis

A

low GCS at presentation
no history of lucid interval
pupil abnormalities
decerebrate rigidity
pre-existing brain injury

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228
Q

what is a febrile seizure

A

it is a convulsion that occurs in a febrile child (between 6 months and 5 years) and is not caused by a CNS infection

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229
Q

what are most febrile seizures caused by

A

viral infections
- human herpes virus 6 and influenza mc

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230
Q

what are risk factors for febrile seizures

A

family history of febrile seizures
high fever
viral infection
recent immunisation (rare)

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231
Q

what are the clinical features of febrile seizures

A

most occur within 24 hours of the child developing a fever
depends on whether it is a simple or complex febrile seizure

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232
Q

what is a simple febrile seizure

A

most common (80-85%)
the duration is less than 15 minutes
generalised seizure - normally tonic-clonic
occurs only once in 24 hours

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233
Q

what is a complex febrile seizure

A

15-20%
duration longer than 15 minutes
focal seizure
prolonged post ictal state
more than one seizure in 24 hours

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234
Q

what is febrile status epilepticus

A

a seizure lasting over 30 minutes or multiple seizures without recovery

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235
Q

what is the immediate management of a febrile seizure

A

most will have resolved by the time of presentation
same management of normal seizure in practice - ABCDE

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236
Q

what is the management of febrile seizure after the seizure has occurred

A

need to find the source of the fever !
parental education - explain the benign nature
give info on managing seizures and basic first aid
can give rescue medication - rescue midazolam

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237
Q

what are complications of febrile seizures

A

injury while seizing
aspiration while seizing
small increased risk of epilepsy compared to the general population (2% risk)
risk of recurrence

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238
Q

what is giant cell arteritis

A

it is a systemic vasculitis that can affect large and medium sized vessels
it commonly affects the extracranial branches of the carotid artery

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239
Q

what other condition in giant cell arteritis associated with

A

polymyalgia rheumatica

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240
Q

what are risk factors of giant cell arteritis

A

age: mostly round 50 years old
female sex
polymyalgia rheumatica

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241
Q

what are typical symptoms of giant cell arteritis

A

subacute onset unilateral headache typically affecting temporal region
tongue and jaw claudication
scalp tenderness
painless complete or partial vision loss in one/both eyes
diplopia
systemic symptoms - malaise, weight loss, fatigue, anorexia, depression

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242
Q

what are symptoms of polymyalgia rheumatica

A

bilateral shoulder stiffness
pelvic girdle pain
worse in morning

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243
Q

what are clinical findings seen in giant cell arteritis

A

scalp/temporal artery tenderness
reduced or absent temporal artery pulse
fundoscopy: oedema and pallor of the optic disc
auscultation: axillary, brachial and carotid bruits may be heard
asymmetrical blood pressure

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244
Q

what investigations are done for suspected giant cell arteritis

A

full blood count
CRP - typically increased
ESR - over 50mm/hour seen as significant
LFTs - alkaline phosphatase and transaminases may be slightly increased
temporal artery ultrasound - thickening of wall (halo sign)
temporal artery biopsy - multinucleated giant cells

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245
Q

what is the initial management of giant cell arteritis

A

Medical emergency !
urgent referral to rheumatologist
oral prednisolone - visual symptoms
IV methylprednisolone - vision loss

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246
Q

if someone has vision symptoms in GCA what is given to them

A

same day 60-100mg one off dose of prednisolone

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247
Q

what is given to someone with GCA that presents with vision loss

A

500mg IV methylprednisolone OD for 3 days
follow with prednisolone regime

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248
Q

what is given to someone who presents with GCA but doesnt have visual symptoms

A

a dose 40-60mg prednisolone per day

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249
Q

what is the on going management for GCA

A

gradually taper prednisolone down to 0 over a period of 12-18 months
patient has regular monitoring every 2-8 weeks after diagnosis
side effects of prednisolone are monitored

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250
Q

what are complications of temporal arteritis

A

irreversible vision loss
aortic dissections, aortic aneurysms, large artery stenosis
cardiovascular events - stroke/MI
complications from steroid treatment - bruising, diabetes, hypertension, osteoporosis

251
Q

what is Guillian barre syndrome

A

it is an acute inflammatory neuropathy which primarily affects the peripheral nervous system

252
Q

what is the cause of GBS

A

about 66% o cases involve previous history of either upper respiratory tract infection or gastrointestinal infection
- CMV, EBV, mycoplasma, campylobacter jejuni

253
Q

what is the pathophysiology of GBS

A

it is considered an autoimmune condition
immune system activation against pathogens where molecular mimicry occurs and immune system attacks components of the peripheral nerves
this results in demyelination of motor and sensory peripheral nerves

254
Q

what are the 4 subtypes of GBS

A
  1. acute inflammatory demyelinating polyneuropathy - MC
  2. acute motor axonal neuropathy - motor presentation
  3. Acute motor sensory axonal neuropathy
  4. Miller fisher syndrome - antibodies to GQIb ganglioside
255
Q

what is the triad which is typically associated with Miller-Fisher GBS syndrome

A

ophthalmoplegia
ataxia
areflexia

256
Q

what are the typical symptoms of GBS

A

rapidly progressive symmetrical weakness typically in an ascending pattern
paraesthesia in lower limbs and hands (tingling)
issues with balance or coordination
back pain or limb pain which can be worse at night
difficulties with vision
difficulties with speech, swallowing or chewing
autonomic dysfunction - palpitations, heart failure, bowel and bladder dysfunction

257
Q

what typical examination findings are found in those with GBS

A
  • symmetrical bilateral weakness ascending from the lower limbs first up to arms, trunk, bulbar and ocular muscles
  • reduced sensation over area of weakness
  • areflexia: absent/reduced reflexes
  • autonomic dysfunction
258
Q

what are differential diagnosis to think of or GBS

A

stroke
encephalitis
myasthenia gravis
polymyositis
myelopathy
botulism

259
Q

what investigations should be done on someone with suspected GBS

A

clinical diagnosis
serial lung function tests - regular FVC
electrocardiogram
continuous BP monitoring
FBC, U+E, LFT, glucose, creatinine kinase
MRI spine to rule out myelopathy
nerve conduction studies
lumbar puncture - increased protein and normal cell count

260
Q

what is the general management of GBS

A

serial lung function tests
supportive treatment - IV fluids
VTE prophylaxis
eye care
pressure sore screening and relief
physiotherapy
swallow assessment
plasma exchange
IV IG

261
Q

when should someone with GBS be admitted to intensive care

A

requirement of significant respiratory support
rapidly progressing muscle weakness
rapidly fluctuating blood pressure/arrhythmias
swallow dysfunction

262
Q

what are complications of GBS

A

respiratory compromise
VTE
infection
aspiration pneumonia
cardiac arrhythmias
ileus
long term disability
persistent neuropathic pain or fatigue
psychological trauma

263
Q

what is looked at in the motor section of the GCS

A

5 - obeys commands
4 - localises to pain
3 - flexes to pain
2 - extends away from pain
1 - none

264
Q

what is looked at in the verbal portion of the GCS

A

5 - orientated to time place and person
4 - confused
3 - inappropriate words
2 - incomprehensible sounds
1 - none

265
Q

what is looked at in the eye response portion of the GCS

A

4 - eyes open spontaneously
3 - eyes open to speech
2 - eyes open to pain
1 - none

266
Q

what causes shingles

A

re activation of herpes zoster virus

267
Q

who is more at risk of shingles

A

those with a weakened immune system
those over 50
other illness
trauma
those under stress

268
Q

what are the symptoms of shingles

A

fever
chills
headache
fatigue
sensitivity to light
stomach upset
itching, tingling or burning in area of skin
redness on affected skin area
raised rash
fluid filled blisters
mild to severe pain

269
Q

what is the shingles disease course

A
  1. few days before rash there may be pain on the skin which is itching, burning, stabbing or shooting
  2. raised rash occurs on one side of body only on one dermatome
  3. within 3-4 days the rash develops into red, fluid filled painful open blisters
  4. these blisters begin to dry out/scab over within about 10 days
  5. scabs clear up about 2-3 weeks later
270
Q

what is the most common long term complication of shingles

A

long term nerve pain - postherpetic neuralgia

271
Q

how is shingles diagnosed

A

history and exam - clinical diagnosis
can scape/swab blisters and do lab tests

272
Q

how is shingles treated

A

no cure
can use acyclovir, famciclovir or valacyclovir within 72 hours of first signs of shingles
ibuprofen can help with pain
prednisolone can be used if shingles affect eyes or other parts of the face

273
Q

how many people who get shingles develop postherpetic neuralgia

A

over 10% of people

274
Q

other than postherpetic neuralgia what other complications can occur because of shingles

A

numbness or itching
bacterial infection of the shingles rash
eye/ear inflammation

275
Q

how is postherpetic neuralgia treated

A

lidocaine or capsaicin cream
antidepressants - amitriptyline
antiepileptics
nerve blocks
steroid injections

276
Q

what is Horners syndrome

A

it is a characteristic triad of ptosis, anhidrosis and miosis caused by a lesions in the sympathetic chain supplying the eye

277
Q

what three structures does the sympathetic nervous system innervate in the eye

A
  1. dilator pupillae: involved in mydriasis or dilation of the pupil
  2. superior tarsal muscle: aids in elevating the upper eyelid with the levator palpebrae superioris
  3. sweat glands
278
Q

how can you tell if Horners syndrome is caused by first, second or third order neurone lesions

A

by the sites affected by anhidrosis
Central/first order = anhidrosis of the face, arm and trunk
Anhidrosis of face = second order
No anhidrosis = third order

279
Q

what causes central horners

A

a lesion in the first order neurone which spans from the hypothalamus to the T1 segment of the spinal cord

280
Q

what can cause central horners

A

multiple sclerosis
brain tumours - Wallenbers syndrome

281
Q

what causes second order horners

A

a lesion in the second order neurone which leaves the spinal cord and travels towards head via the cervical sympathetic chain, terminating at the superior central ganglion

282
Q

what can cause second order horners syndrome

A

pancoast tumours - apical lung cancer
thyroid malignancies
iatrogenic
trauma causes

283
Q

what causes third order horners syndrome (postganglionic)

A

lesion in the postganglionic neurone which arises from the superior cervical ganglion and travels along the internal carotid artery to the cavernous sinus where it joins the ophthalmic nerve V1

284
Q

what are causes of postganglionic horners syndrome

A

carotid artery dissection
cavernous sinus thrombosis
cluster headaches - rare

285
Q

what is congenital horners

A

this is very rare, when horners is present at birth
it can be due to birth trauma or due to an unknown cause
classic finding is iris heterochromia

286
Q

what investigations are done for horners syndrome

A

clinical diagnosis + presence of anhidrosis
if unclear can be diagnosed using eye drops
- Apraclonidine given which reverses the pupillary constriction in horners as its an aloha 2 receptor agonist
- hydroxyamphetamine drops can be used to identify the location of the lesion as it will dilate a constricted horners pupil if there is an underlying preganglionic lesion

287
Q

what is the management of horners

A

management depends on underlying cause
accurate and timely investigation aids in reducing morbidity and mortality

288
Q

what is the genetic inheritance pattern of huntingtons

A

autosomal dominant

289
Q

what is the genetic abnormality in huntingtons

A

a trinucleotide repeat disorder
genetic mutation in the HTT gene on chromosome 4

290
Q

when do symptoms typically begin in huntingtons

A

30-50

291
Q

what are other examples of trinucleotide repeat disorders

A

fragile X syndrome
spinocerebellar ataxia
myotonic dystrophy
friedrich ataxia

292
Q

what is anticipation

A

it is when successive generations have
- earlier age of onset
- increased severity of disease
due to more repeats

293
Q

how does huntingtons present

A

cognitive, psychiatric or mood problems
chorea - involuntary, random, abnormal
dystonia - abnormal muscle tone
rigidity
eye movement disorders
dysarthria - speech issues
dysphagia - swallowing issues

294
Q

how is huntingtons diagnosed

A

genetic testing
- involves pre and post test counselling

295
Q

how is huntingtons managed

A

there is currently no treatment options for slowing or stopping the progression of the disease
- counselling
- physiotherapy
- speech and language therapy
- tetrabenazine : helps chorea
- antidepressants
- advanced directives
- end of life care

296
Q

what is the prognosis of huntingtons

A

life expectancy is about 10-20 years after the onset of symptoms

297
Q

what is malaria caused by

A

plasmodium family of protozoan parasites

298
Q

how is malaria spread

A

through bites from the female anopheles mosquitos

299
Q

what are the types of malaria

A

plasmodium falciparum - most common and severe
plasmodium vivax
plasmodium ovale
plasmodium malariae
plasmodium knowlesi

300
Q

what is the malaria life cycle

A
  1. sporozoites from the mosquitos gut are injected into someone as they are bitten
  2. they travel to the liver of the infected person
  3. here they mature into merozoites which enter the blood and infect red blood cells
  4. in the RBC the merozoites reproduce, and the RBC ruptures releasing them
  5. this causes haemolytic anaemia
301
Q

what malaria types can lie dormant in someones liver

A

P. vivax and P. ovale

302
Q

what are symptoms of malaria

A

fever - up to 41oC with sweats and rigors
fatigue
myalgia
headache
nausea and vomiting

303
Q

what signs on examination would you see in someone with malaria

A

pallor due to anaemia
hepatosplenomegaly
jaundice

304
Q

how is malaria diagnosed

A

malaria blood film - in EDTA bottle
- three negative samples over three consecutive days is requires to exclude malaria

305
Q

how is uncomplicated malaria managed

A

inform infectious diseases
- artemether with lumefantrine
- quinine plus doxycycline
- quinine plus clindamycin
- chloroquine (increasing resistance)

306
Q

what is the management of severe or complicated sepsis

A

admission to HDU or ICU
IV artesunate
IV quinine dihydrochloride

307
Q

what are the complications of malaria (p.falciparum)

A

cerebral malaria
seizures
reduced consciousness
AKI
pulmonary oedema
disseminated intravascular coagulopathy
severe haemolytic anaemia
multi organ failure and death

308
Q

what prophylaxis is given to those travelling to areas where malaria is present

A
  • mosquito spray
  • mosquito nets and barriers when sleeping
  • seek medical advice
  • take antimalarials: proguanil with atovaquone, doxycycline, mefloquine, chloroquine with proguanil
309
Q

what is the treatment course of proguanil/atovaquone

A

taken two days before until 7 days after travel to an endemic area

310
Q

what are the side effects of doxycycline

A

skin sensitivity to sun
diarrhoea
thrush

311
Q

what is the treatment course of doxycycline

A

two days before until four weeks after travel to an endemic area

312
Q

what are the side effects of mefloquine

A

psychiatric side effects - anxiety, depression, abnormal dreams

313
Q

what is the treatment course of mefloquine

A

two weeks before until four weeks after travel to an endemic area

314
Q

what is Merieres disease

A

it is a common cause of peripheral vertigo

315
Q

what is the treat that Menieres presents with

A

vertigo
tinnitus
hearing loss

316
Q

what is the cause of Menieres disease

A

not fully known
significant number of patients have endolymph build up in the membranous labyrinth

317
Q

what are the typical symptoms of menieres disease

A

recurrent spontaneous vertigo lasting between 20 minutes to several hours
progressive or fluctuating hearing loss
tinnitus
aural fullness

318
Q

what are risk factors of Menieres disease

A

family history of the disease

319
Q

what are differential diagnosis for menieres disease

A

vestibular migraine
labyrinthitis
benign paroxysmal positional vertigo
stroke
vestibular schwannoma

320
Q

what investigations are done to diagnose menieres disease

A

no specific investigations are required to diagnose the disease
- most patients receive formal audiology assessment
- MRI imaging to exclude abnormalities

321
Q

what hearing loss is common in menieres

A

in early disease either low frequency sensorineural hearing loss or combined low and high frequency sensorineural hearing loss
later disease the hearing loss is at all frequencies

322
Q

how is menieres disease diagnosed

A
  • two or more spontaneous episodes of vertigo, with each episode lasting between 20 minutes to 12 hours
  • audiological assessment demonstrating low to moderate sensorineural hearing loss on affected side
  • aural fullness
323
Q

what is the medical management of menieres disease

A

lifestyle and dietary changes - minimise salt and caffeine intake
betahistine can be used
vestibular sedatives (prochlorperazine) can be used in acute episodes of vertigo
vestibular rehabilitation

324
Q

what is the surgical management of Menieres disease

A

involves the injection of medication intratympanically - either dexamethasone or methylprednisolone or gentamicin
intratympanic steroids
labyrinthectomy
vestibular neurotomy

325
Q

what are complications of Menieres disease

A

intermittent flares
long term intermittent tinnitus
long term hearing loss

326
Q

what is meningitis

A

it is inflammation o the meninges- the outer membranes that cover the brain and spinal cord

327
Q

what can meningitis be caused by

A

bacteria
viruses
fungo
leukaemia and lymphoma
autoimmune disease
drugs

328
Q

what is the common causes of bacterial meningitis

A

in neonates - Group B streptococcus, E.coli, Strep.pneumoniae, listeria monocytogenes
in children and adults - Neisseria meningitidis, strep. pneumoniae and haem. influenzae B

329
Q

what is aseptic meningitis

A

this is when the CSF has white cells on microscopy but the gram stain is negative
- viral
- fungal

330
Q

what are the common causes of viral meningitis

A

enteroviruses - echovirus, coxackievirus
mumps
HSV
herpes zoster
HIV
measles
influenza

331
Q

what are causes of fungal meningitis

A

cryptococcus

332
Q

what are clinical features of meningitis

A

neck stiffness
non blanching rash in meningococcal disease
photophobia
leg pain
altered mental state
ever
seizures
general flu like illness
bulging fontanelle in infants
Kernig and Brudzinski sign

333
Q

what is Kernigs sign

A

pain and resistance on passive knee extension with hips fully flexed

334
Q

what is brudzinskis sign

A

knees and hips flex on bending the head forward

335
Q

what investigations should be done for suspected meningitis

A

vital signs
blood sugar
FBC, U+E, CRP, blood culture
CT
lumbar puncture

336
Q

what are contraindications to performing a lumbar puncture in meningitis

A

raised intercranial pressure - reduced or fluctuating consciousness, bradycardia and hypertension, focal neurological signs, abnormal posturing, abnormal pupil reflexes, papilloedema, bulging fontanelle
convulsions
coagulation abnormalities
shock
extensive purpura

337
Q

how do you treat bacterial meningitis in hospital

A

children three months and older - IV ceftriaxone
children under 3 months - IV ceftriaxone + amoxicillin/ampicillin (covers listeria)

338
Q

how do you treat bacterial meningitis in primary care

A

urgent transfer to hospital
IM/IV benzylpenicillin if meningococcal sepsis is suspected

339
Q

how do you treat contacts of someone with bacterial meningitis

A

ciprofloxacin/rifampicin within 24 hours

340
Q

what is the treatment of viral meningitis

A

supportive therapy
if concerns of encephalitis then IV aciclovir

341
Q

what are the acute complications of meningitis

A

sepsis
septic shock
disseminated intravascular coagulation
coma
cerebral oedema
raised ICP
subdural effusions
SIADH
seizures
peripheral gangrene
death

342
Q

what are complications of bacterial meningitis

A

30-50% survivors have permanent neurological sequelae
- hearing loss
- seizures
- motor deficit
- cognitive impairment
- hydrocephalus
- visual disturbance

343
Q

what are complications of viral meningitis

A

usually complete resolution within 10 days but you can get
- headaches
- cognitive and psychological issues

344
Q

what are the four main types of migraine

A

migraine with aura
migraine without aura
silent migraine
hemiplegic migraine

345
Q

what are the five stages of a migraine

A

premonitory or prodromal stage
aura
headache
resolution
postdromal or recovery stage

346
Q

what are the typical symptoms of a migraine

A

unilateral
- moderate to severe in intensity
- pounding or throbbing
- photophobia
- phonophobia
- osmophobia - discomfort of strong smells
- aura
- nausea and vomiting

347
Q

what is an aura

A

it is a sensation change that occurs pre migraine
it can affect vision, sensation and language

348
Q

what are examples of aura in migraine

A

sparks in the vision
blurred vision
lines across the vision
loss of visual fields
dysphagia
tingling or numbness

349
Q

what is a hemiplegic migraine

A

where you get unilateral limb weakness (can also include ataxia and LOC) associated with the migraine

350
Q

what is familial hemiplegic migraine

A

it is an autosomal dominant genetic condition characterised by hemiplegic migraines which run in families

351
Q

what are migraine triggers

A

stress
bright lights
strong smells
certain foods - chocolate, cheese, caffeine
dehydration
menstruation
disrupted sleep
trauma

352
Q

what is the acute management of a migraine

A

dark, quiet room, sleeping
NSAIDS
paracetamol
triptans
antiemetics - metoclopramide or prochlorperazine

353
Q

what are triptans used for in migraines

A

they are used to abort migraines when they start to develop (5HT receptor agonists)
- taken as soon as the headache starts

354
Q

what are the main contraindications o triptan use

A

relate to risks associated with vasoconstriction
- hypertension
- CAD
- previous stroke or TIA
- MI

355
Q

what prophylaxis can be used for migraines

A

propranolol - not in asthmatics
amitriptyline
topiramate - teratogenic and very effective contraception is needed

356
Q

what specialist medications can be used in migraine prophylaxis if regular prophylaxis doesnt work

A

pizotifen
candesartan
sodium valproate
monoclonal antibodies - erenumab

357
Q

when might prophylactic triptans be used in migraine

A

for menstrual migraines
- taken two days before until three days after the start of menstruation

358
Q

what is mononeuropathy

A

it is damage to a single nerve, which results in the loss of movement, sensation or other function of that nerve
- damage that occurs outside the brain and spinal cord

359
Q

what can cause mononeuropathy

A

most common cause is injury/trauma
systemic disease can damage isolated nerves

360
Q

what are common forms of mononeuropathy

A

axillary nerve dysfunction
common peroneal nerve dysfunction
carpal tunnel syndrome
cranial mononeuropathy III,IV
cranial mononeuropathy VI
cranial mononeuropathy VII
femoral nerve dysfunction
radial nerve dysfunction
sciatic nerve dysfunction
ulnar nerve dysfunction

361
Q

what does axillary nerve dysfunction cause

A

loss of movement or sensation in the shoulder

362
Q

what does common peroneal nerve dysfunction cause

A

loss of movement or sensation in the foot and leg

363
Q

what causes carpal tunnel syndrome

A

median nerve dysfunction
- numbness, tingling, weakness in hand and fingers

364
Q

what does cranial mononeuropathy VI cause

A

double vision

365
Q

what does cranial mononeuropathy VII cause

A

facial paralysis

366
Q

what does femoral nerve dysfunction cause

A

loss of movement or sensation in part of the leg

367
Q

what does radial nerve dysfunction cause

A

problems with movement in the arm and wrist and with sensation in the back of the arm or hand

368
Q

what does sciatic nerve dysfunction cause

A

problems with the muscles of the back of the knee and the lower leg, and sensation to the back of the thigh, part of the lower leg and the sole of the foot

369
Q

what does ulnar nerve dysfunction cause

A

cubital tunnel syndrome
- numbness, tingling, weakness of outer and underside of the arm, palm, ring and little fingers

370
Q

what are symptoms of mononeuropathies

A

loss of sensation
paralysis
tingling, burning, pain, abnormal sensations
weakness

371
Q

what investigations can be done for a mononeuropathy

A

electromyograms
nerve conduction studies
nerve ultrasound
X-ray, MRI, CT
bloods - glucose
nerve biopsy
CSF examination
skin biopsy

372
Q

what are treatment options of mononeuropathy

A

painkillers
antidepressants - amitriptyline
steroid injections
surgery to relieve the pressure on the nerve
physical therapy to maintain muscle strength
braces, splints
TENS to improve nerve pain

373
Q

what are possible complications of mononeuropathy

A

deformity - loss of tissue mass
medicine side effects
repeated or unnoticed injury to the affected area due to lack of sensation

374
Q

what is motor neurone disease

A

it is a term that encompasses a variety of specific diseases affecting the motor nerves
it is progressive and eventually fatal condition where motor neurones stop functioning

375
Q

what are the different types of motor neurone disease

A

amyotrophic lateral sclerosis (ALS)
progressive bulbar palsy
progressive muscular atrophy
primary lateral sclerosis

376
Q

how does ALS present

A

begins with muscle twitching and weakness in an arm or leg, trouble swallowing and slurred speech
- tripping and falling
- weakness in legs, feet or ankles
- hand weakness or clumsiness
- slurred speech or trouble swallowing
- muscle cramps and twitching
- thinking or behavioural change

377
Q

what are risk factors for developing ALS

A

genetics - 10%
age
sex - men>women
smoking
environmental toxin exposure - lead

378
Q

what are the symptoms of progressive bulbar palsy

A

wasting of tongue
weakness/stiffness of tongue
difficulty speaking
difficulty swallowing
problems with the thickness/amount of saliva

379
Q

how does motor neurone disease often present

A

late middle aged man
insidious progressive weakness or the muscles though out the body affecting the limbs, trunk, face and speech
weakness often first noticed in the upper limbs
increased fatigue when exercising
clumsiness
dropping things or tripping over
dysarthria

380
Q

what are signs of motor neurone disease

A

have both upper and lower signs
lower - muscle wasting, reduced tone, fasciculations, reduced reflexes
upper - increased tone or spasticity, brink reflexes, upgoing plantar reflex

381
Q

how is motor neurone disease managed

A

no effective treatment in halting/reversing the disease
- Riluzole can help slow progression and extend survival by several months in ALS
- non invasive ventilation
- symptom control: baclofen for muscle spasticity and antimuscarinics for saliva
- benzodiazepines
- advanced directives
- end of life care

382
Q

what is multiple sclerosis

A

autoimmune inflammatory disease of the CNS which is characterised by demylination

383
Q

what is the pathophysiology of MS

A

thought to be mediated by T cell activation although underlying cause is unclear
- attacks central nervous system causing demyelination and eventually cell death

384
Q

what are the four main groups of MS

A

relapsing remitting
secondary progressive
primary progressive
clinically isolated syndrome

385
Q

what is clinically isolated syndrome in MS

A

this is the first episode of demyelination and neurological signs that cant be explained by something else
patients with this may never go on to having MS but they are more likely to than the general population

386
Q

what is relapsing remitting MS

A

this is when there are unpredictable attacks of neurological dysfunction lasting over 24 hours followed by relief of symptoms
- patients may not fully return to previous baseline

387
Q

what is secondary progressive MS

A

this is when MS initially presents as relapsing remitting and then later steadily declines and progressively without remission in between attacks

388
Q

what is primary progressive MS

A

this is when there is a steady, progressive worsening of disease severity from the onset without remission

389
Q

what are risk factors for developing MS

A

family history
sex F>M
age - between 25-35
other co existing auto immune disease
smoking
previous EBV infection
latitude of habitat
vitamin D deficiency

390
Q

what are common symptoms of MS

A

limb weakness
limb tingling/numbness
cerebellar symptoms
fatigue
nystagmus
optic neuritis
diplopia
dysphagia
slurring/stuttering speech
spasm
urinary incontinence
retention
constipation/diarrhoea

391
Q

what two phenomina are characteristic to MS

A

Uhthoffs phenomenon
Lhermittes phenomenon

392
Q

what is Uhthoffs phenomenon

A

this is when there is worsening of symptoms on exercise/in warm environments such as the bath

393
Q

what is Lhermittes phenomenon

A

this is a lightning shock sensation down the spine on flexion of the neck secondary to cervical cord plaque formation

394
Q

what is often the first sign of MS

A

optic neuritis

395
Q

what is optic neuritis

A

it is demyelination of the optic nerve and presents with unilateral reduced vision developing over hours

396
Q

what are key features of optic neuritis

A

central scotoma - enlarged central blind spot
pain with eye movement
impaired colour vision
relative afferent pupillary defect -

397
Q

what is a relative afferent pupillary defect

A

this is when the pupil of the affected eye constricts more when shining light in the contralateral eye then when shining it in the affected eye

398
Q

what other eye movement abnormalities can you get with MS

A
  • lesions affecting CN III, IV, VI can cause double vision and nystagmus
  • internuclear ophthalmoplegia caused by a lesion in the medial longitudinal fasciculus causing impaired adduction on the ipsilateral eye and nystagmus in the contralateral eye
  • CN VI lesion causes conjugate lateral gaze disorder
399
Q

what focal weaknesses may present in MS

A

incontinence
horners syndrome
facial nerve palsy
limb paralysis

400
Q

what focal sensory symptoms may be present in multiple sclerosis

A

trigeminal neuralgia
numbness
paraesthesia (pins and needles)
Lhermittes sign

401
Q

what cerebellar signs may be present in MS

A

nystagmus
intention tremor
scanning dysarthria

402
Q

what investigations are done to diagnose MS

A

FBC, CRP, U+E, LFT, calcium, TFT, vit B12, HIV
MRI of the brain and spinal cord
lumbar puncture with CSF analysis

403
Q

what is the typical CSF finding in someone with MS

A

high protein content
oligoclonal bands of immunoglobulin

404
Q

what is the McDonald criteria for MS

A

for a diagnoses the symptoms need to be disseminated in both time and space

405
Q

what is the management of an acute MS attack

A

if symptoms are severe - high dose steroid therapy with methylprednisolone (500mg oral 5 days)
plasmapheresis
look to see if there is an underlying cause i.e infection

406
Q

what is the long term management of MS

A

Beta interferon and glatiramer acetate - DMARDS which reduce relapses in RRMS
other DMARDS - dimethyl fumarate, cladribine
moAbs - alemtuzumab, natalizumab
exercise
physiotherapy
neuropathic pain - amitriptyline or gabapentin
spasticity - gabapentin
urge incontinence - antimuscarinics: solifenacin

407
Q

what are complications of MS

A

majority of those diagnosed with MS become unemployed within 15 years
depression (50%)
cognitive deficits
reduced life expectancy

408
Q

what is muscular dystrophy

A

it is a group of genetic diseases associated with progressive weakness and loss of muscle mass
- occurs with mutations in genes responsible for the production of proteins key to healthy muscle development

409
Q

what are the types of muscular dystrophy

A

duchenne muscular dystrophy
becker muscular dystrophy
emery dreifuss muscular dystrophy
limb girdle muscular dystrophy
facioscapulohumeral muscular dystrophy

410
Q

what are the two most common types of muscular dystrophy

A

Duchennes muscular dystrophy
Beckers muscular dystrophy

411
Q

what is the genetic inheritance of duchennes muscular dystrophy and becker muscular dystrophy

A

x linked recessive conditions

412
Q

what are typical presenting features of muscular dystrophy

A

progressive weakness - starting proximally and moving distally with the lower limbs being affected before upper limbs
delayed motor milestones
waddling gait
faltering growth
fatigue
intellectual impairment
behavioural issues
leg pain

413
Q

what is important to check in children who cannot walk by 18 months of age

A

their creatinine kinase levels

414
Q

at what age to people with duchennes muscular dystrophy become wheelchair users

A

typically about 12 years of age

415
Q

what are clinical findings in patients with muscular dystrophy

A

weakness - typically the proximal and distal leg muscles
calf pseudohypertrophy - accumulation of connective tissue and fat replacing muscle
waddling gait
tip toe walking
hyporeflexia or areflexia
loss of arches of the feet
difficulty of inability to squat

416
Q

what are clinical findings associated with facioscapulohumeral MD

A

winging of the scapula
upper extremity weakness
facial weakness

417
Q

what are clinical findings associated with oculopharyngeal MD

A

dysarthria
dysphagia

418
Q

what are clinical findings associated with emery-dreifuss MD

A

contractures affecting the ankles, elbows and neck extension
increased tone in the lumbar and paravertebral muscles
cardiac abnormalities

419
Q

what investigations are done in suspected muscular dystrophy

A

serum creatinine kinase - increases with more muscle damage
genetic analysis
muscle biopsy
clinical exam
electromyography
ECG and echo
lung function testing

420
Q

what is the early management of muscular dystrophy - when the child is still walking

A

corticosteroids - prolong walking by 6-24 months
vitamin D and calcium supplements
physiotherapy
orthoses - stabilise the knee, ankle and foot
serial casting of the ankles - prevent shortening of the achilles tendon

421
Q

what is the later stage management of muscular dystrophy

A

wheelchair aid
counselling
orthopaedic input - orthotics and surgery
cardiac and respiratory surveillance
advanced planning and palliative care

422
Q

what is Gowers sign

A

this is a technique children with proximal muscle weakness use to stand up
- get onto their hands and knees
- then push their hips up and back
- they shift their weight back and put their hands onto their knees
- whilst keeping their legs straight they then walk their hands up their legs to stand up

423
Q

what is the genetic abnormality that causes duchennes muscular dystrophy

A

defective dystrophin gene which normally holds muscle together at a cellular level

424
Q

what is beckers muscular dystrophy

A

it is similar to duchennes however the dystrophin gene is less severely affected and maintains some function
- clinical course is less predictable and symptoms only appear between 8-12

425
Q

what are contractures (seen in emery-dreifuss MD)

A

they are the shortening of muscles and tendons that restrict the range of movement in limbs
- patients suffer with progressive weakness and washing of muscles

426
Q

what is myasthenia gravis

A

it is an autoimmune condition affecting the neuromuscular junction
causes muscle weakness and progressively worsens with activity and improves with rest

427
Q

what other condition does myasthenia gravis have a strong link with

A

thymomas - thymus gland tumours

428
Q

what is the pathophysiology of myasthenia gravis

A

In the NMJ acetylcholine is released and binds to acetylcholine receptors on the post synaptic membrane stimulating muscle contraction
in MG there are acetylcholine receptor antibodies which bind to the post synaptic receptors, blocking them and preventing stimulation, and muscle contraction

429
Q

what is the link between exercise and myasthenia gravis

A

the more activity the more acetylcholine receptors are used, and therefore the more they become blocked
- MG worsens with exercise

430
Q

other than blocking postsynaptic preceptors what else do the autoantibodies do in MG

A

they activate the compliment system within the NMJ leading to cell damage at the postsynaptic membrane and further worsening symptoms

431
Q

what two other antibodies can cause myasthenia gravis other than acetylcholine receptor antibodies

A

muscle specific kinase antibodies
low density lipoprotein receptor related protein 4 (LRP4)

432
Q

how does myasthenia gravis present

A

difficulty climbing the stairs, standing from a seat or raising their hands above their head
extraocular muscle weakness causing dipolpia
eyelid weakness causing ptosis
weakness in facial movements
difficulty with swallowing
fatigue in the jaw when chewing
slurred speech

433
Q

what muscles are most affected in myasthenia gravis

A

proximal muscles of the limbs and small muscles of the head and neck

434
Q

how do you elicit muscle weakness in people with myasthenia gravis

A

repeated blinking
prolonged upward gazing
repeated abduction of one arm 20 times will result in unilateral weakness

435
Q

what investigations are done in someone with suspected myasthenia gravis

A

AchR antibodies
MuSK antibodies
LRP4 antibodies
CT/MRI of the thymus to look for thymoma
edrophonium test

436
Q

what is the edrophonium test

A

patient is given IV edrophonium chloride (neostigmine) which blocks cholinesterase enzymes and reduces acetylcholine breakdown. As a result there is temporary relied of weakness

437
Q

How do you treat myasthenia gravis

A

pyridostigmine - cholinesterase inhibitor
immunosuppression - prednisolone
thymectomy - even without thymoma
rituximab - monoclonal antibody against B cells

438
Q

what is a myasthenic crisis

A

it is a potentially life threatening complication of myasthenia gravis
it is an acute worsening to symptoms often triggered by another illness
respiratory muscle weakness can lead to respiratory failure

439
Q

what is the treatment for a myasthenic crisis

A

non invasive ventilation or mechanical ventilation
IV immunoglobulins
plasmapheresis

440
Q

what is narcolepsy

A

it is a sleep disorder that makes people very drowsy during the day - suddenly fall asleep or loss of muscle tone (cataplexy)

441
Q

what are the two types of narcolepsy

A

type 1 - with cataplexy
type 2 - without cataplexy

442
Q

what are symptoms of narcolepsy

A

excessive daytime sleepiness - can fall asleep without warning
sudden loss of muscle tone - can cause slurred speech or complete weakness of most muscles
triggered by intense emotions
sleep paralysis
hallucinations
changes in REM sleep

443
Q

what is the cause of narcolepsy

A

not fully known
people with type 1 narcolepsy have low levels of hypocretin (orexin) which is a chemical in the brain that helps control being awake and when you enter REM sleep

444
Q

what is the link between narcolepsy an REM sleep

A

in narcolepsy you may suddenly enter REM sleep without going through non REM sleep

445
Q

what are risk factors for narcolepsy

A

age - between 10-30
family history - 20-40 times higher if a close family has it

446
Q

how is narcolepsy diagnosed

A

clinical history - sleep history (epworth sleepiness scale)
looking at sleep records
a sleep study - polysomnography
multiple sleep latency test
genetic tests and lumbar puncture

447
Q

what is the treatment for narcolepsy

A

there is no cure - medication and lifestyle changes
- stimulants: modafinil or armodafinil/ solriamfetol (new)
- SNRI/SSRI
- tricyclic antidepressants
sodium oxybate and oxybate salts: relieve cataplexy

448
Q

what is neurofibromatosis

A

it is a genetic condition that causes nerve tumours to develop throughout the nervous system
- benign but can cause neurological and structural issues

449
Q

what are the two types of Neurofibromatosis

A

type 1 - chromosome 17, Auto dominant
type 2 - chromosome 22, Auto dominant

450
Q

what does the neurofibromatosis type 1 gene code for

A

a protein called neurofibromin which is a tumour suppressor protein

451
Q

what are the features of neurofibromatosis type 1

A

CRABBING
Cafe au lait spots (>15mm diameter in adults)
Relative with NF1
Axillary or inguinal freckling
Bony dysplasia such as Bowing of long bone/sphenoid wing dysplasia
Iris hamartomas - yellow/brown spots on iris
Neurofibromas
Glioma of the optic pathway

452
Q

where can neurofibromas be seen

A

they can be seen on the skin - skin coloured, raised nodules or papules with a smooth regular surface
- two or more are significant
- one plexiform neurofibroma is significant (larger, irregular, complex)

453
Q

what is the management of neurofibromatosis

A

no treatment
- managing symptoms, monitoring and treating complications

454
Q

what are complications of neurofibromatosis

A

migraines
epilepsy
renal artery stenosis - hypertension
learning disability
behavioural issues
vision less - secondary to optic nerve gliomas
malignant peripheral nerve sheath tumours
gastrointestinal stromal tumours
brain tumours
spinal cord tumours
increased risk of cancer

455
Q

what does neurofibromatosis type 2 gene code for

A

merlin which is a tumour suppressor protein which is important in schwann cells
- mutations lead to schwannomas

456
Q

how does a temporal lobe seizure present

A

flushing sweating, pallor, butterflies in stomach
hallucinations
feeling intense emotions
stereotypic behaviours - chewing, lip smacking, swallowing, scratching, fumbling

457
Q

how does a frontal lobe seizure present

A

motor symptoms
- arm/hand stiffness or rigidity and abnormal posturing
- abnormal movements of the arm
- head turning or abnormal posturing

458
Q

how does a parietal lobe seizure present

A

sensory symptoms - warmth, paraesthesia, pain up one side of the body

459
Q

how does an occipital lobe seizure present

A

visual disturbance - lashes, floaters, vision loss, change in colour vision

460
Q

what does primary lateral sclerosis present as

A

movements becoming slow
pseudobulbar effect
- affects the upper motor neurones of the arms, face and legs

461
Q

how does progressive muscular atrophy present

A

muscle wasting, clumsy hand movements, fasciculations, muscle cramps
- progressive degeneration of only the lower motor neurones

462
Q

who are at the highest risk of carpal tunnel syndrome

A

females between the age of 40-60

463
Q

what are risk factors for carpal tunnel

A

smoking
over 30 years old
high BMI
smoking
acromegaly
hypothyroidism
rheumatoid arthritis
diabetes
pregnancy
occupation

464
Q

what is normal pressure hydrocephalus

A

this is when CSF slowly builds up within your skull putting pressure on the brain
there is a slow build up meaning while pressure increases it remains within normal range

464
Q

what are symptoms of normal pressure hydrocephalus

A

symptoms start gradually and develop over about 6 months
Triad:
Gait issues, Urinary incontinence, Cognitive issues

465
Q

what gait issues are present in normal pressure hydrocephalus

A

trouble lifting the feet
steps are shorter and unsteady
freeze/walk uncertainty
rotate toes out as they walk

466
Q

what cognitive difficulties may be present in normal pressure hydrocephalus

A

mental or physical slowness
memory issues
executive dysfunction
emotional change

467
Q

what are causes of primary normal pressure hydrocephalus

A

idiopathic - think its to do with age
may have a connection to lewy body dementia or Alzheimer’s

468
Q

what are causes of secondary normal pressure hydrocephalus

A

brain aneurysm
intercranial haemorrhage
brain tumours
encephalitis or meningitis
stroke
traumatic brain injury

469
Q

how do you diagnose normal pressure hydrocephalus

A

history and exam
MRI and lumbar puncture

470
Q

how do you treat normal pressure hydrocephalus

A

primary - use a shunt. They drill a hole in the skull and the shunt runs down under the skin and drains into the abdomen or the chest
secondary - need to treat underlying cause

471
Q

what are side effects of a shunt to treat normal pressure hydrocephalus

A

infection
shunt malfunction or failure
position shit of the valve/catheters
too much CSF draining out the shunt

472
Q

is normal pressure hydrocephalus reversible

A

if it is caught and treated early then it is reversible however delay can lead to more permanent brain damage due to prolonged pressure and compression of the brain

473
Q

what are causes of headache

A

tension headache
migraines
cluster headaches
secondary headaches - drug induced
sinusitis
GCA
glaucoma
intercranial haemorrhage
subarachnoid haemorrhage
venous sinus thrombosis
hormonal headache
cervical spondylitis
trigeminal neuralgia
raised ICP
tumour
meningitis
encephalitis
abscess
pre eclampsia

474
Q

what are red flags in a headache

A

fever, photophobia or neck stiffness
new neurological symptoms
visual disturbance
sudden onset occipital headache
postural, worse on standing, lying or bending over
vomiting
history of trauma
history of cancer
pregnancy

475
Q

what is a tension headache

A

it is common type of headache that typically causes a mild ache or pressure in a band like pattern around the head
- develop and resolve gradually and dont produce visual change

476
Q

what may tension headaches be associated with

A

stress
depression
alcohol
skipping meals
dehydration

477
Q

what are symptoms of tension headache

A

Dull, aching head pain.
Feeling of tightness or pressure across the forehead or on the sides and back of the head.
Tenderness in the scalp, neck and shoulder muscles.

478
Q

what is the management for tension headache

A

simple analgesia - ibuprofen or paracetamol
amitriptyline is offered first line in chronic or frequent headaches

479
Q

what are causes of secondary headache

A

infections
obstructive sleep apnoea
pre elampsia
head injury
carbon monoxide poisoning

480
Q

what is sinusitis

A

it is inflammation in the paranasal sinuses which typically causes pain and pressure following a viral upper resp. tract infection

481
Q

what is hormonal headache

A

it is a headache related to low oestrogen
- similar features to migraine
- occur two days before and the first three days of the menstrual period, in the perimenopausal period and in early pregnancy

482
Q

what is the treatment for hormonal headaches

A

triptans and NSAIDS (mefenamic acid)

483
Q

what is cervical spondylosis

A

it is a common condition caused by degenerative changes in the cervical spine. It usually causes neck pain made worse by movement and headaches

484
Q

what are cluster headaches

A

severe unilateral headaches centered around the eye which come on in clusters of attacks

485
Q

how long does a cluster headache last for

A

between 15 minutes and 3 hours

486
Q

what are symptoms of cluster headaches

A

severe pain - suicide headaches
read swollen and watering eye
pupil constriction (miosis)
eyelid drooping (ptosis)
nasal discharge
facial sweating

487
Q

what is the treatment for an acute cluster headache attack

A

Triptans - subcut or intranasal sumatriptan
high flow 100% oxygen - reservoir mask

488
Q

what is used for cluster headache prophylaxis

A

verapamil (calcium channel blocker)
occipital nerve block
prednisolone
lithium

489
Q

what is parkinson’s disease

A

it is a neurodegenerative disorder occurring due to the loss of dopaminergic cells from the substantia nigra

490
Q

what is the aetiology of parkinsons

A

typically presents in those above 55 years old
higher prevalence in men

491
Q

what is the pathophysiology of parkinsons disease

A
  • in parkinsons there is a progressive loss of dopaminergic neurones
  • the motor signs of parkinsons occur due to the loss of dopaminergic neurons in the nigrostriatal pathway
  • physiologically dopamine acts to upregulate the thalamus and the motor cortex via the direct pathway which results in increased movement
  • loss of neurones results in a reduction in the action of the direct pathway and increase in the antagonistic indirect pathway which restricts movement
492
Q

what are the symptoms of parkingsons

A

motor symptoms: bradykinesia, stiffness, resting tremor, instability, falls
constipation
lightheadedness
excess salivation or sweating
urinary and sexual dysfunction
mood symptoms: low mood, anxiety, sleepiness
sleep disturbance
anosmia or reduced sense of smell
micrographia

493
Q

what are the typical clinical findings in someone with parkinsons

A

bradykinesia
tremor: pill rolling
rigidity (cog wheel)
abnormal gait: shuffling
postural instability
hypomimia - decreased facial activity
confusion
reduced dexterity

494
Q

what are differential diagnosis for parkinsonism

A

lewy body dementia
multiple system atrophy
progressive supranuclear palsy
vascular parkinsonism
drug induced parkinsonism

495
Q

what drugs can cause drug induced parkinsonism

A

antipsychotics
anti emetics - prochlorperazine or metoclopramide

496
Q

what investigations do you do in someone with suspected parkinsons disease

A

bedside investigations and cognitive assessment
FBC, U+E, LFT, CRP, Glucose, TFT, calcium, B12
Dopamine active transporter scans

497
Q

what medical management can be used for parkinsons

A

Levodopa
Monoamine oxidase B inhibitors
dopamine agonists
catechol-o-methyl transferase inhibitors - always taken with levodopa

498
Q

what is often used with levodopa to extend its life

A

it is often used with carbidopa which is a dopamine decarboxylase inhibitor to reduce metabolism of levodopa

499
Q

what else can be done for parkinsons other than medication

A

physiotherapy
speech and language therapy
deep brain stimulation

500
Q

what are complications of parkinsons

A

increased fall risk
increased risk of dementia with lewy bodies
hallucinations
aspiration pneumonia

501
Q

what type of tremor is present in parkinsons

A

pill rolling, worse on one side, 4-6 hz

502
Q

what is the main side effect of levodopa

A

dyskinesia
- dystonia
- chorea
- athetosis

503
Q

what can be used to manage the dyskinesia associated with levodopa

A

amantadine - glutamate antagonist

504
Q

what is the main side effect of dopamine agonists

A

pulmonary fibrosis with prolonged use

505
Q

what are examples of dopamine agonists

A

bromocriptine
pergolide
cabergoline

506
Q

what are examples of monoamine oxidase B inhibitors

A

selegiline
rasagiline

507
Q

what are symptoms of a motor nerve peripheral neuropathy

A

muscle weakness
cramps
muscle twitching

508
Q

what are symptoms of a sensory nerve peripheral neuropathy

A

numbness or tingling
trouble walking or keeping your balance
issues fastening buttons
issues with sensing pain or changes in temperature
injury of sensory nerves may cause pain

509
Q

what can autonomic nerve peripheral neuropathy cause

A

excessive sweating
changes in blood pressure
inability to tolerate heat
GI symptoms

510
Q

what are causes of peripheral neuropathy

A

injury - compress, crush or cut nerves
medical conditions - diabetes, guillian barrre, carpal tunnel
autoimmune disease - lupus, RA, sjogren syndrome

511
Q

how are peripheral neuropathies diagnosed

A

history and exam
electromyography
nerve conduction studies
MRI
US
glucose monitoring

512
Q

what treatment may be required for a peripheral neuropathy

A

medication - aspirin, ibuprofen, amitriptyline
physical therapy
surgery - nerve repair or graft
braces or splints
electrical stimulators
exercise

513
Q

what is radiculopathy

A

it describes a range of symptoms which is produced by the pinching of a nerve root in the spinal column

514
Q

what is a lumbar radiculopathy

A

it is sciatica

515
Q

what are different types of radiculopathy

A

cervical - affects arms and hands most commonly
thoracic - pain and numbness that wraps round to the front of your body
lumbar - sciatica

516
Q

what are symptoms of radiculopathy

A

sharp pain in the back, arms, legs or shoulders that worsen with certain activities
weakness or loss of reflexes in the arms or legs
numbness of the skin, pins and needles or other abnormal sensations

517
Q

what are causes of radiculopathies

A

herniated disc
bone spurs - extra bone growth
ossification of spinal ligaments
spinal infection
cancer/non cancer growths

518
Q

how is radiculopathy diagnosed

A

physical exam and history
imaging - X-ray, CT, MRI
nerve conduction studies

519
Q

how is radiculopathy treated

A

NSAIDs, opioids, muscle relaxants
weight loss
physical therapy
steroid injections
surgery - releases the pressure on the nerve root by widening the foramina it exits out of

520
Q

what is the difference between a radiculopathy and myelopathy

A

radiculopathy is a temporary issue caused by a pinched nerve root near your spine
myelopathy is compression of your spinal cord caused by trauma, tumour, generation or infection

521
Q

what is the acute treatment for a seizure

A

insert nasogastric tube into the nose
provide supplemental oxygen
ensure IV access
attach O2 sats and watch for hypoxia

522
Q

whats the best benzodiazepine to use in status epilepticus

A

IV midazolam as its short acting
- test dose of 1ml

523
Q

what is mannitol

A

an osmotic diuretic and is used short term to treat rising ICP

524
Q

what is given before an operation for patients undergoing surgery for intercranial tumours

A

dexamethasone
- 4mg QDS or 8mg BD

525
Q

what can be used in cranial diabetes insipidus to help prevent sx

A

desmopressin

526
Q

what is often used to treat radicular pain

A

gabapentin and pregabelin

527
Q

what is first line treatment for trigeminal neuralgia

A

carbamazepine
can also be used in combination with amitriptyline

528
Q

when might intubation/ventilation be required in neurosurgery

A
  1. agitated and CNS imaging required
  2. in circumstances of acute neurologic deterioration
  3. persisting poor level of consciousness
  4. where the patient is at risk or has resp. failure
  5. status epilepticus
  6. significant intra-operative brain swelling
529
Q

where is the pain/numbness felt in a patient with carpal tunnel syndrome

A

thumb, index and middle finger and the palm

530
Q

what will a patient with vertebral pain syndrome complain of

A

localising aching pain with limited radiation
stiffness
restriction of movement
worse with activity
abscence of associated neurological sx

531
Q

what are causes of vertebral pain syndrome

A

most commonly just due to wear and tear/degenerative changes
TB
bacterial discitis
osteomyelitis
osteoporotic fractures
metastatic disease

532
Q

what two nerve roots are commonly affected in cervical radiculopathy

A

C6 and 7

533
Q

what to nerve roots are commonly affected in lumbar radiculopathy

A

L5 and S1

534
Q

how will patients with spinal claudication present

A

bilateral radiating leg pain or paraesthesia that comes on with walking
symptoms often relieved by sitting forward

535
Q

what are red flag symptoms of spinal claudication

A

constant bilateral leg pain
perineal numbness
foot weakness
urinary incontinence

536
Q

what is the c6 myotome, dermatome and reflex

A

myotome - thumb
dermatome - biceps
reflex - biceps jerk

537
Q

what is the c7 myotome, dermatome and reflex

A

myotome - middle finger
dermatome - triceps
reflex - triceps reflex

538
Q

what is the L5 myotome, dermatome and reflex

A

myotome - dorsum of the foot/big toe
dermatome - dorsiflexion (stand on heels)
reflex

539
Q

what is the S1 myotome, dermatome and reflex

A

myotome - ankle, lateral aspect of foot/sole of foot/ little toe
dermatome - plantar flexion (stand on toes)
reflex - ankle jerk

540
Q

what will be found on examination if someone has raised ICP

A

drowsiness
papilloedema
paralytic squint
fixed dilated pupil
reduced levels of consciousness

541
Q

what area of the brain is broccas area in

A

frontal

542
Q

how do you calculate the cerebral perfusion pressure

A

the mean arterial pressure - intercranial pressure

543
Q

what are predisposing factors for chronic subdural haemotoma

A

aspirin
anticoagulation

544
Q

what can cause late secondary brain injury

A

brain swelling
delayed hydrocephalus
CNS infection
post operative haemotoma
systemic infection - pneumonia

545
Q

what is the most common brain tumour type

A

gliomas

546
Q

what is the most common form of glioma

A

glioblastoma multiform - high grade/grade 4

547
Q

what are the major categories of extra-axial/extrinsic tumours

A

meningiomas
pituitary adenomas
nerve sheath tumours - schwannomas

548
Q

what causes spinal degenerative disease

A
  1. hard disc osteophyte formation - osteoarthritis or wear and tear
  2. soft disc prolapse
    both of which result in canal stenosis, lateral recess stenosis or foraminal stenosis
549
Q

what are causes of spinal cord compression

A

osteoarthritis - wear and tear
abnormal spine alignment - scoliosis
injury to the spine
spinal tumour
bone diseases
rheumatoid arthritis
infection

550
Q

what are symptoms of spinal cord compression

A

pain and stiffness in the back, neck or lower back
burning pain that spreads to the arms, legs, buttocks
numbness, cramping or weakness
loss of sensation in the feet
trouble with hand or leg coordination
foot drop
loss of sexual ability

551
Q

how is spinal cord compression diagnosed

A

X ray of the spine
CT/MRI
bone scan, myelogram, electromyography

552
Q

how is spinal cord compression treated

A

NSAIDs
high dose steroids
radiation used to shrink tumours
physical therapy
surgery - removal or bone spurs

553
Q

what is cauda equina syndrome

A

it is compression of the nerve roots in the cauda equina
- surgical emergency

554
Q

what are causes of cauda equina syndrome

A

lumbar disc herniation - L4/5 L5/S1
spinal vertebral fractures of subluxation
malignancy
spinal infection: abscess, meningitis, tuberculosis
iatrogenic: anaesthesia, post operation

555
Q

what cancers most commonly metastasise to the spine

A

breast, prostate, lung

556
Q

what are the typical features of cauda equina

A

severe back pain
bilateral sciatica
perineal (saddle) anaesthesia
bowel and bladder dysfunction
sexual dysfunction

557
Q

what is the difference between incomplete and complete cauda equina syndrome

A

incomplete - urinary difficulties, altered urinary sensation, loss of desire to void, hesitancy, urgency
complete - definitive urinary retention with associated overflow incontinence

558
Q

what is the management of cauda equina syndrome

A

ABCDE
analgesia
catheter insertion
surgery = surgical decompression (laminectomy - removal of vertebral lamina, or discectomy - removal of intervertebral disc, or both)

559
Q

what are complications of cauda equina syndrome

A

paraplegia
lower limb numbness
chronic urinary retention or incontinence
chronic sexual dysfunction

560
Q

what are the ascending tracts of the spine

A

dorsal columns - fine touch, vibration sense and proprioception
spinothalamic tracts - pain and temperature

561
Q

what are the descending tracts

A

corticospinal tract - motor information
corticobulbar
rubrospinal
tectospinal
reticulospinal
vestibulospinal

562
Q

what is brown sequard syndrome

A

it is damage to one lateral half of the spinal cord - mostly occurs in cervical region

563
Q

what is the classical clinical presentation of brown-sequard syndrome

A

ipsilateral spastic paralysis below level of lesion
ipsilateral loss of fine touch, proprioception and vibration
contralateral loss of pain and temperature sensation

564
Q

what deficiency is posterior cord syndrome seen in

A

B12 deficiency - due to subacute combined degeneration of the spinal cord

565
Q

What is a TIA

A

it is a sudden onset focal neurological deficit of vascular origin that lasts less than 24 hours

566
Q

what are the most important causes of TIA to identify

A

atrial fibrillation
carotid stenosis

567
Q

what are risk factors for developing a TIA

A

age
sex: M>F
smoking
hypertension
atrial fibrillation
diabetes
family history of TIA
previous TIA
vasculitis

568
Q

what are the clinical features of a TIA

A

sudden onset and short duration
weakness
numbness or tingling
speech issues
vision changes
dizziness or loss of balance
headache

569
Q

what investigations need to be done in someone with suspected TIA

A

12 lead EGC
FBC, blood glucose, lipid profile, coagulation screen
CT brain, MRI brain, carotid US and echo

570
Q

what is the management of a TIA

A

300mg aspirin immediately
referral for assessment within 24 hours
screen for AF and carotid stenosis
if TIA confirmed and not at high risk of haemorrhage then duel antiplatelet for 21 days - aspirin and clopidogrel 75mg daily
secondary prevention: lifestyle advice, statins, smoking cessation, htn and diabetes management

571
Q

what is carotid endarterectomy and when is it performed

A

it is a surgical procedure that removes atherosclerotic plaque from the carotid artery
recommended if:
70-99% internal carotid artery stenosis
50-69% stenosis recommended but only at centres with perioperative complication rate of <6%

572
Q

what is trigeminal neuralgia

A

it is a form of neuropathic pain that is characterised by sharp, shooting sensation affecting the face
the pain is very intense

573
Q

what are the three branches of the trigeminal nerve

A

ophthalmic branch - cornea, scalp and forehead
maxillary branch - cheek, upper jaw, upper lip, teeth, gums, lateral aspect of nose
mandibular branch - lower jaw, teeth, gums and lower lip

574
Q

what are three types of trigeminal neuralgia

A

classic trigeminal neuralgia - vascular compression by artery/vein
secondary trigeminal neuralgia - tumour
idiopathic trigeminal neuralgia

575
Q

what artery/vein most commonly causes classic trigeminal neuralgia

A

superior cerebellar artery

576
Q

what are risk factors for trigeminal neuralgia

A

female
age (>50)
multiple sclerosis

577
Q

what are symptoms of trigeminal neuralgia

A

unilateral, sharp facial pain

578
Q

what are common triggers of trigeminal neuralgia

A

talking
washing the face
shaving
brushing teeth
exposure to cold air

579
Q

how is trigeminal neuralgia managed

A

1st line - carbamazepine
other treatments: oxcarbazepine, lamotrigine, gabapentin, pregabalin
surgery - decompression, gamma ray knife

580
Q

what is idiopathic intracranial hypertension

A

it is a raised intracranial pressure in the absence of intracranial mass or hydrocephalus

581
Q

what is idiopathic intracranial hypertension associated with

A

female sex
obesity

582
Q

what is the pathophysiology of idiopathic intracranial hypertension

A

several mechanisms proposed to explain it:
- overproduction of CSF
- obstruction of outflow of CSF
- raised pressure in the venous sinuses
- dysfunction in the glymphatic pathway
- hormonal alteration

583
Q

what is the normal mechanism of CSF production and distribution

A

CSF is secreted by the choroid plexus in the lateral, third and fourth ventricles
this then moves into the subarachnoid space and acts as a cushion
CSF absorption mainly occurs via the arachnoid granulations when pressure exceeds the venous sinus pressure

584
Q

what are risk factors for idiopathic intracranial hypertension

A

obesity
female sex
medications - COCP, tetracyclines, vitamin A, retinoids, lithium, thyroxine, nitrofurantoin

585
Q

what are symptoms of idiopathic intracranial hypertension

A

headache - most common (non specific, diffuse)
nausea and vomiting
retrobulbar pain
pressure like sensation behind the eyes, worse on bending forward
transient visual loss/burring of vision
pulsatile tinnitus
visual disturbance
ocular motility disturbance - horizontal diplopia

586
Q

what clinical findings might you see in idiopathic intracranial hypertension

A

papilloedema - bilateral and symmetrical
enlargement of the blind spot
peripheral visual field defects
horizontal diplopia

587
Q

what are differential diagnosis for IIH

A

intracranial mass lesions
increased CFS production
reduced CSF absorption
obstruction of venous outflow
malignant hypertension
obstructive sleep apnoea

588
Q

what investigations should be done for IIH

A

MRI/CT
lumbar puncture
blood pressure
magnetic resonance venogram of the head
perimetry
ocular coherent tomography

589
Q

how is IIH diagnosed

A

signs and symptoms of raised intracranial pressure
absence of localising findings on neurological examination
normal CSF composition
absence of deformity, displacement or obstruction of ventricular system
normal neuroimaging
no other cause of increased ICP

590
Q

how is IIH managed

A

conservative - weight loss
medical - Acetazolamide (first line), topiramate, furosemide, serial lumbar punctures
surgical - given to those with rapidly declining function: CSF diversion procedures, optic nerve sheath fenestration

591
Q

what are complications of IIH

A

permanent visual loss

592
Q

what is the most of action of acetazolamide

A

it is a carbonic anhydrase inhibitor and is believed to reduce the rate of CSF production

593
Q

what is a stroke

A

it is an acute neurological deficit attributed to an acute focal injury of the brain, spinal cord or retina by either a vascular occlusion or haemorrhage

594
Q

what are causes of ischaemic stroke

A

large vessel atherosclerosis
small vessel occlusion
cardioembolic ischaemic stroke
arterial dissection
non atherosclerotic arterial wall disease
non inflammatory vasculopathy
haematological disorders
cryptogenic

595
Q

in western population where is the most common site of atherosclerosis with stroke

A

the internal carotid artery, however the circle of willis, vertebral arteries and the aortic arch may also be sources

596
Q

what are risk factors for stroke

A

high BMI
high fasting plasma glucose
high systolic blood pressure
high LDL
kidney dysfunction
tabacco smoking
low physical activity
diet high in sodium and red meat, low in fruit and veggies
alcohol consumption
air pollution, lead exposure

597
Q

what initial investigations should be done for someone presenting with a stroke

A

blood sugar - check for hypoglycaemia
CT head !!
CT angiogram and perfusion
chest X ray
ECH - AF
bloods - U+E, LFT, pregnancy

598
Q

how is stroke diagnosed

A

history of symptom onset - acute deficit in keeping with a vascular event
radiological data to back it up

599
Q

what is the management for ischaemic stroke

A

ABCDE !!!
- thrombolysis with administration of a tissue plasminogen activator such as alteplase. This is given within 4.5 hours or may be given up to 9 hours after stroke
- thrombectomy can be performed up to 24 hours after the stroke
- aspirin - 300mg immediately or after 24 hours if thrombolysis has been given
- decompressive hemicraniectomy

600
Q

what is the initial ward care for patients coming in with stroke

A

should be admitted to acute or hyperacute stroke unit
need to manage aspiration risk, blood sugar control and VTE risk
blood pressure control in intercranial haemorrhage
cardiac rhythm monitoring

601
Q

when is endarterectomy used in ischaemic stroke

A

if the carotid vessel is occluded by over 50% on the side where a stroke has happened

602
Q

what is the long term medical care for ischaemic stroke

A

modifying risk factors
blood pressure - want systolic <130mmHg
lipids - 80mg atorvastatin
antiplatelets - 75mg clopidogrel OD long term
anticoagulation - DOAC

603
Q

what is a total anterior circulation stroke

A

large cortical stroke affecting areas of the brain supplied by both the middle and anterior cerebral arteries

604
Q

what are the criteria for something to be diagnosed as a total anterior stroke

A
  1. unilateral weakness (and/or sensory deficit) of the face, arm and leg
  2. Homonymous hemianopia
  3. higher cerebral dysfunction (dysphagia, visuospatial disorder)
605
Q

what is a partial anterior circulation stroke

A

it is a less severe form of TACS in which only part of the anterior circulation has been compromised

606
Q

what is the criteria needed for a partial anterior circulation stroke to be diagnosed

A

two of the following need to be present:
1. unilateral weakness (and/or sensory deficit) of the face, arm and leg
2. Homonymous hemianopia
3. higher cerebral dysfunction (dysphagia, visuospatial disorder)

607
Q

what is posterior circulation syndrome

A

it involves damage to the area of the brain supplied by the posterior circulation (e.g cerebellum and the brainstem)

608
Q

what needs to be present for a diagnosis of posterior circulation syndrome

A

one of the following need to be present:
1. cranial nerve palsy and contralateral motor/sensory deficit
2. bilateral motor/sensory deficit
3. conjugate eye movement disorder
4. cerebellar dysfunction
4. isolated homonymous hemianopia

609
Q

what is a lacunar stroke

A

this is a subcortical stroke that occurs secondary to small vessel disease. there is no loss of higher cerebral functions

610
Q

what needs to be present for a diagnosis of lacunar stroke

A

one of the following needs to be present:
1. pure sensory deficit
2. pure motor deficit
3. sensori-motor stroke
4. ataxic hemiparesis

611
Q

what is lateral medullary syndrome

A

clinical syndrome caused by acute ischaemia or infarction of the lateral medulla oblongata due to occlusion of the intracranial portion of the vertebral artery, posterior inferior cerebellar artery or its branches
- also known as wallenberg syndrome

612
Q

what are risk factors of lateral medullary syndrome

A

hypertension is the commonest risk factor
smoking
diabetes

613
Q

what is the clinical presentation

A
  1. vestibulocerebellar symptoms: ipsilateral hemiataxia, vertigo, falling towards the side of the lesion, multidirectional nystagmus
  2. autonomic dysfunction: ipsilateral horner syndrome, hiccups
  3. sensory symptoms: loss of pain and temperature over the ipsilateral face and contralateral side of the body
  4. ipsilateral bulbar muscle weakness: hoarseness, dysphonia, dysphagia and dysarthria, reduced gag reflex
614
Q

what structures can be affected in lateral medullary syndrome

A

inferior cerebellar peduncle
dorsolateral medulla
descending spinal tract
nucleus of the trigeminal nerve
vagus nucleus and nerve
glossopharyngeal nucleus and nerve
descending sympathetic tract fibres

615
Q

what causes lateral medullar syndrome

A

vertebral artery disease - atherosclerosis, cerebral embolism, dissection, hypoplastic vertebral artery

616
Q

how is lateral medullary syndrome diagnosed

A

clinical history and examination
MRI evaluation including diffusion weighted imaging (will look bright)

617
Q

how is lateral medullary syndrome treated

A

similar management to any acute stroke
- rapid evaluation and treatment

618
Q

what are the two pared arteries which are responsible for the blood supply to the brain

A

the vertebral arteries and the internal carotid arteries

619
Q

where do the internal carotid arteries originate

A

at the bifurcation of the left and the right common carotid arteries at the level of C4

620
Q

what arteries does the internal carotid artery give rise to

A

ophthalmic artery - structures in the orbit
posterior communicating artery - connecting vessel in circle of willis
anterior choroidal artery - brain important for motor and vision
anterior cerebral artery - cerebrum (parts)
the internal carotids then continue as the middle cerebral artery and supplies the lateral portions of the cerebrum

621
Q

what are the branches of the vertebral arteries

A

meningeal branch - supplies falx cerebelli
anterior and posterior spinal arteries
posterior inferior cerebellar artery - supplies the cerebellum
the two vertebral arteries converge to form the basilar artery which supplies the pons and cerebellum

622
Q
A

Phase 3a Jemima (16 decks)

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