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Phase 2a > NEURO > Flashcards

NEURO Flashcards

1
Q

what is a dermatome

A

area of skin supplied by single spinal nerve

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2
Q

what is a myotome

A

volume of muscle supplied by single spinal nerve

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3
Q

what is a somite

A

brick like block on embryo
each form single spinal nerve which gives skin and muscle of each segment individual supply = forms dermatomes and myotomes

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4
Q

what is anencephaly

A

failure of fusion of neural tube at cranial end

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5
Q

what is spina bifida

A

failure of fusion of neural tube at caudal end

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6
Q

at what level is a lumbar puncture performed

A

L3-L4 / L4-L5
performed further down from conus medullaris/corda equina as less likely to cause spinal damage

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7
Q

what are the 3 layers of the meninges

A

dura = firmly adhered to the skull
arachnoid = adhered to the brain
pia = attached to brain cannot be separated

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8
Q

what is horner’s syndrome

A

lesion of sympathetic supply
typically causes small pupils, ptosis, anhidrosis

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9
Q

how does a lesion of cerebral hemispheres typically present

A

unilateral affects the contralateral side

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10
Q

how does a lesion of the internal capsule typically present

A

complete contralateral hemiparesis

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11
Q

how does a lesion of the spinal cord typically present

A

bilateral
typically affects legs
often bladder involvement

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12
Q

how does a lesion of the cerebellum typically present

A

ataxia
loss of coordination

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13
Q

how does a lesion of the brain stem typically present

A

bilateral weakness
bulbar involvement
cranial nerve nuclei commonly affected

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14
Q

how does a lesion of the peripheral nerves typically present

A

gloves and stocking appearance

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15
Q

what are the 3 branches of the aortic arch

A

right brachiocephalic trunk
left common carotid
left subclavian

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16
Q

at what level does the common carotid artery bifurcate

A

C3/4

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17
Q

what are the 4 parts of the internal carotid artery

A

cervical
petrous
cavernous
supraclinoid

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18
Q

what do the extracranial vertabral arteries supply

A

neck muscles
cervical spine meninges
cervical spinal cord

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19
Q

what are the branches of the intercranial vertebral arteries

A

posterior inferior cerebellar artery
anterior spinal artery
small medullary perforators

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20
Q

what are the branches of the basilar artery

A

posterior cerebral arteries
superior cerebellar arteries
anterior inferior cerebellar arteries
pontine perforators

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21
Q

where does the posterior inferior cerebellar artery arise from

A

terminal bifurcation of the basilar artery

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22
Q

what does OTOMCAT stand for

A

in carotid sinus:
occulomotor nerve
trochlear nerve
opthalmic division of trigeminal
maxillary division of trigeminal

cavernous segment of internal carotid
abducens nerve
trochlear nerve

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23
Q

which nerves run through the carotid sinus

A

occulomotor 3
trochlear 4
opthalmic V1
maxillary V2
abducens 6

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24
Q

what are the main types of primary headache

A

cluster
tension
migraine
trigeminal neuralgia

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25
Q

what are the main types of secondary headache

A

subarachnoid haemorrhage
menignitis
encephalitis
idiopathic intercranial hypertension
giant cell arteritis
drug overdose

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26
Q

what signs/symptoms suggest a possible secondary headache

A

Hx of HIV/cancer
vomiting without cause
changing personality/cognitive dysfunction
jaw claudication
severe eye pain

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27
Q

what symptoms of headache are considered to be red flags

A

new headache with history of cancer
thunderclap headache = SAH assume
seizure
significantly altered consciousness, memory, confusion, coordination
papilloedema
abnormal neuro exam or symptom

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28
Q

what are red flags during a clinical headache examination

A

fever
altered conciousness
neck stiffness/kernigs sign
focal neurological signs
ALWAYS CHECK BP

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29
Q

how does idiopathic intercranial hypertension present

A

pain is worse on waking, coughing, sneezing, straining, lying down
presents with nausea/vomiting
papilloedema may present

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30
Q

name 5 bacterial causes of menigitis

A

neisseria meningitidis
strep. pneumoniae
listeria monocytogenes
E.coli
group B strep
(strep agalactiae = neonates)

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31
Q

name 4 viral causes of meningitis

A

enterovirus
mumps
herpes simplex
varicella zoster

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32
Q

when should a lumbar puncture NOT be performed in suspected meningitis

A

if intracranial pressure is raised
if petechial rash is present
if patient has abnormal clotting

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33
Q

what is the prophylaxis for meningitis

A

ciprofloxacin (close contacts)
rifampicin

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34
Q

what is the first line treatment for any suspected meningitis

A

IV Benzylpenicillin

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35
Q

what is the treatment for bacterial meningitis

A

cefotaxime OR ceftriaxone AND dexamethasone
possible add:
chloramphenical (peni allergy)
amoxicillin (immunocomp)
vancomycin (recent travel)

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36
Q

what is the treatment for encephalitis

A

acyclovir in case its herpes simplex virus

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37
Q

what is the most common cause of encephalitis

A

herpes simplex virus

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38
Q

what spores cause tetanus

A

clostridium tetani

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39
Q

what toxins do clostridium tetani spores produced

A

tetanolysin and tetanospasmin = cause tissue lysis and spasms

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40
Q

what drug is used to treat tetanus

A

metranidazole

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41
Q

describe the furious stage of rabies

A

agitated
hydrophobia
aerophobia
hyperactivity

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42
Q

describe the paralytic phase of rabies

A

flaccid
weakness
not really there

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43
Q

how is rabies managed

A

high does sedatives = end of life care
vaccination for pre-exposure prophylaxis
Ig for post exposure prophylaxis

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44
Q

what is herpes zoster

A

viral disease characterised by painful skin rashes with blisters in localised areas

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45
Q

describe the pathophysiology of herpes zoster

A

caused by reactivation of varicella zoster virus which may remain inactive within nerve cells
when reactivate = travel down nerve cells and effects dermatome its present in

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46
Q

how does herpes zoster present

A

headache
pyrexia
malaise
burning pain
itching
hyperesthesia (extra sensitive)
parasthesia

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47
Q

how is herpes zoster treated

A

analgesia = paracetamol, ibuprofen, opiates, topical capsaicin, topical lidocaine, gabapentin
antivirals = acyclovir

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48
Q

what mediates the demyelination in MS

A

macrophages

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49
Q

what are the 3 types of MS

A

relapse remitting MS
primary progressive MS
secondary progressive MS

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50
Q

what is the Lhermitte’s sign

A

electric shock sensation down spinal cord on movement of head
SEEN IN MS

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51
Q

what would be seen on an MS MRI

A

plaques of focal demyelination

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52
Q

what is an epileptic seizure

A

paroxymal event in which excessive hypersynchronous neuronal discharges in brain cause change in behaviour sensation or cognitive processes

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53
Q

what are the differentials for an epileptic seizure

A

syncope
non-epileptic seizure
migraine
hyperventilation
TIA

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54
Q

what is syncope

A

insufficient blood/oxygen to brain
caused by sitting or standing
rarely from sleep
5-30s duration
rapid post ical recovery

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55
Q

what is a non epileptic seizure

A

caused by psychosocial stress
1-20 min duration
closed eyes/mouth or crying/speaking

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56
Q

what would suggest epilepsy over syncope

A

tongue biting
head turning
muscle pain
loss of consciousness more than 5 mins
cyanosis

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57
Q

what would suggest syncope over epilepsy

A

prolonged upright position
sweating prior
nausea
presyncopal symptoms
pallor

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58
Q

how do you differentiate between NES and epileptic seizures

A

CANT use history
video of seizures needed

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59
Q

what is obstructive/non communicating hydrocephalus

A

blockage of ventricles = CSF buildup due to lack of drainage

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60
Q

what can cause obstructive hydrocephalus

A

foreign material in CSF
tumours compressing outflow tract
posterior fossa pathology

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61
Q

how does obstructive hydrocephalus present

A

headaches
seizures
vomiting
downward eyes
loss of coordination
incontinence

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62
Q

what is normal pressure hydrocephalus

A

intermittent increasing of ICP

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63
Q

how does normal pressure hydrocephalus present

A

incontinence
dementia
falls
wide gait
magnetic gait = stuck to floor

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64
Q

how is normal pressure hydrocephalus treated

A

shunt placement = drains extra fluid from ventricles to peritoneum

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65
Q

what is cerebellar syndrome

A

ataxia and nystagmus due to cerebellar injury
appear/feel drunk
deficit is IPSILateral
caused by stroke/tumours/haemorrhage

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66
Q

what is jugular foramen syndrome

A

glossopharyngeal, vagus, accessory palsies present
reticular activation system maybe also affected

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67
Q

what is the reticular activation system

A

involved in:
alertness
sleeping
waking
respiration
cardiovascular drive

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68
Q

what is the difference between focal and generalised seizures

A

focal = occur in one part of brain
generalised = affect whole brain

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69
Q

what are the 2 different types of focal seizures

A

without impaired consc = no post-ictal sympt
with impaired consc = most commonly temporal lobe

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70
Q

what is an obvious feature of 3rd nerve palsy

A

down and out pupil

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71
Q

what would 3rd nerve palsy with pupil dilation suggest

A

space occupying lesion compressing nerve

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72
Q

what is the effect of brown-sequard syndrome

A

lesion in spinal cord causes hemisection of spinal cord:
SPINOTHALAMIC = contralateral loss of pain, temp, crude touch, pressure 2 levels below lesion
DCML = ipsilateral loss of fine touch, proprioception, vibration (decussation in medulla)
DESCENDING TRACTS = ipsilateral hemiparesis/spastic paralysis below lesion
LMN = ipsilateral loss of sensation and flaccid paralysis at level of lesion

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73
Q

what neurological conditions are vaccine preventable

A

polio
tetanus
TB
H.influenzae
measles
meningococcus

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74
Q

what is clinical epidemiology

A

uses information about distribution and determinants in a clinical setting, especially in diagnosis

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75
Q

what is incidence

A

how many cases each year

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76
Q

what is the prevalence

A

proportion of population affected

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77
Q

what is the burden of disease

A

time lost off work

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78
Q

describe the use of epidemiology in neural disease

A
  1. case ascertainment
  2. incidence/prevalence/trends
  3. risk factors
  4. scope for earlier diagnosis and prevention
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79
Q

what are the public health risk factors for migraine

A

age, sex, FHx = female more common
education/income
oral contraceptives

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80
Q

what are the public health risk factors of stroke

A

age, sex = male more common
hypertension
cardiac disease, DM
smoking/alcohol

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81
Q

describe the rehabilitation following a stroke

A

84% return home but not necessarily back to work

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82
Q

what public health interventions are there for dementia

A

opportunistic screening for memory loss in NHS health checks
dementia controversial

83
Q

what are the risk factors for cerebral palsy

A

anoxia
low birth weight

84
Q

which neurological conditions are of public health importance

A

migraine
stroke
dementia
epilepsy
parkinsons
MS
cerebral palsy

85
Q

describe the prevalence of MS

A

directly proportional to distance from equator
uncommon in fishing communities
positive association with some HLA antigens

86
Q

what is Creutz-Jakob disease (CJD)

A

rapidly progressive dementia = very rare
14% associated with gene mutation

87
Q

how is head injury classified

A

type = penetrative/blunt
lesion distribution = focal or diffuse
time course = primary (immediate), secondary (effect after injury

88
Q

what is a contusion injury

A

due to blow of force
essentially brain ‘bruises’
occur at site of injury = coup
occur away from site of injury = contrecoup

89
Q

what is a laceration

A

blow to head lead to tear in tissues (pia mater)

90
Q

what is a diffuse traumatic axonal injury

A

injury to axons due to trauma that occurs throughout the brain
pattern of tears
usually involves acceleration and deceleration of head

91
Q

describe the recovery of mild traumatic axonal injury

A

recovery of consciousness
may be longterm
variable severity deficit

92
Q

describe the recovery of severe traumatic axonal injury

A

unconscious from impact and remain so/severe disability

93
Q

what is the prognosis for diffuse vascular injury

A

usually result in near immediate death
multiple petechial haemorrhages throughout brain

94
Q

what can cause brain swelling

A

congestive brain swelling
vasogenic oedema = fluid leaves damaged blood vessels
cytotoxic oedema = increase water in neurons/glia

95
Q

what is hypoxia-ischaemia

A

lack of oxygen and blood to brain
can be diffuse or focal
results in increased intercranial pressure

96
Q

what is chronic traumatic encephalopathy

A

repetitive low-level blows to the head with or without loss of consciousness which cause neurological deficit later in life

97
Q

how does chronic traumatic encephalopathy present

A

after injury =
personality change
epilepsy
memory issues
later life = parkinsonism

98
Q

what is weakness/paresis

A

impaired ability to move body part in response to will

99
Q

what is paralysis

A

no ability to move body part in response to will

100
Q

what is ataxia

A

willed movements = clumsy and uncontrolled

101
Q

what is apraxia

A

disorder of consciously organised patterns of movement or impaired ability to recall acquired motor skills

102
Q

where are lower motor neurones found

A

cranial nerve nuclei in the brainstem
anterior horn on spinal cord

103
Q

describe the final common pathway

A

LMN then along axon then to neuromuscular junction then to muscle fibres

104
Q

what is a motor unit

A

basic functional unit of muscle activity
includes LMN, axon and several supplied muscle fibres

105
Q

what controls muscle tone

A

stretch receptors detect stretch (afferent nerves)
gamma motor neurons innervate stretch receptors to allow for contraction

106
Q

what is muscle tone

A

resistance of muscles to stretch

107
Q

what are the clinical features of LOWER MN disease

A

= everything goes DOWN
muscle tone reduce
muscle wasting
fasciculation = twitching
reflexes depressed or absent
focal weakness
absent bobinski sign

108
Q

name 5 causes of lower MN lesions

A

polio
guillain-barre syndrome
ALS (motor neurone disease)
myasthenia gravis
vascular disease

109
Q

how are lower motor neurone disease investigated

A

neurophysiology nerve conduction sites
brain and spinal MRI
lumbar puncture
bloods = muscle enzymes, auto-antibodies, peripheral neuropathy screen

110
Q

what are the clinical features of UPPER MN leasions

A

= everything up
muscle tone increased
tendon reflexes/jaw jerk
positive bobinski sign
characteristic pattern of muscle weakness (pyramidal)
emotional liability

111
Q

describe the pyramidal characteristic pattern of weakness seen in UMN lesions

A

legs = weaker flexors than extensors
arms = weaker extensors than flexors

112
Q

name 7 causes of UPPER MN lesions

A

stroke
brain injury
spinal cord injury

cerebral palsy
MS
MND/ALS
CNS tumour

113
Q

how are upper MN lesions investigated

A

LP
Bloods for metabolic disorders
MRI brain/spine

114
Q

what increases chance of brain tunours

A

ionising radiation
family Hx (for gliomas)
immunosuppression
history of cancer

115
Q

where do primary brain tumours arise from (5)

A
  1. germ cell line = craniopharyngioma or medulloblastoma = in children (WHO grade 4)
  2. meninges = meningioma, usually benign (WHO grade 1)
  3. sella region = pituitary adenoma
  4. glial cells = glioma usually astrocytoma/oligodendroglioma (WHO grade 2)
  5. cranial nerves = schwannomas
116
Q

which primary tumours commonly metastasise to the CNS

A

BLT CRM
breast
lung
testicular
colorectal
renal
malignant melanoma

117
Q

how are brain tumours classified

A

WHO classification based on histology
I = most benign
4= most malignant

118
Q

how do low grade gliomas present (I-II)

A

slow growing
allo pathways to move so less deficit
commonly present with seizures

119
Q

how do high grade gliomas present (III-IV)

A

rapidly progress so = neurological deficit
symptoms of raised ICP and focal/non focal neurology

120
Q

what type of brain tumour presents more commonly with seizures

A

low grade tumours

121
Q

what are functional symptoms

A

disorder of function and not structure
structure is normal

122
Q

what are organic symptoms

A

some kind of structural issue with the body
can be detected by physical exam or test

123
Q

what is somatisation

A

converting emotions into physical signs

124
Q

what is dissociation

A

dissociating immediate reality into alternate reality

125
Q

how does cerebellar disease present

A

ataxia
nystagmus
dysarthria (slurred/slow speech)
dysdiadochokinesia
intention tremor

126
Q

what is dysdiadochokinesia

A

inability to perform rapid repetitive tasks

127
Q

what cells are lost in ataxia of the cerebellum

A

purkinje cells

128
Q

what is nystagmus

A

rapid uncontrolled movement of eyes in one direction
most noticeable looking TOWARDS the lesion

129
Q

describe the classification for the severity of ataxia

A

mild = mobilise independently or with 1 walking aid
moderate = mobilise with 2 walking aids or frame
severe = mostly wheelchair bound

130
Q

what is the name of ataxia classification

A

scale for assessment and rating of ataxia (SARA)

131
Q

how is ataxia investigated

A

head MRI = first choice
FBC, U+E, vitamin B12
genetic testing

132
Q

what does a hot cross bun sign on the pons on brain MRI indicate

A

multisystem atrophy cerebellar type MSA-C

133
Q

what causes cerebellar disease

A
  1. tumours
    posterior circulation stroke
    haemorrhage
    head trauma
  2. VZV
  3. alcoholism
    heavy metal poisoning
  4. Friedrich ataxia (autosomal recessive)
    Wilsons disease (excess copper)
134
Q

what causes ataxia (6)

A
  1. cerebrovascular damage = post. circulation stroke
  2. primary/secondary tumours
  3. hydrocephalus
  4. MS
  5. familial ataxia
  6. idiopathic ataxia
135
Q

what is kernigs sign and in what condition would you expect to see it

A

cannot straighten leg past 130 degrees (hip is flexed at 90 degrees but leg cannot extend further without pain)
subarachnoid haemorrhage or meningitis

136
Q

which is the dominant brain hemisphere for language and speech

A

left hemisphere

137
Q

what is the ABCD2 score used for

A

assess risk of further stroke following a TIA
high risk = 4 points or more

138
Q

describe the ABCD score

A

age = 60+
BP = 140/90 +
clinical features = unilateral weakness/speech problems
durations = 60 mins +
diabetes

139
Q

what makes a TIA high risk

A

ABCD 4 points or more
atrial fibrillation
more than 1 TIA in 1 week
TIA whilst on anticoagulant

140
Q

name 8 causes of raised intercranial pressure

A
  1. tumours
  2. head injury
  3. haemorrhage
  4. meningitis
  5. encephalitis
  6. brain abcess
  7. hydrocephalus
  8. cerebral oedema
141
Q

describe the pathophysiology of raised ICP in 6 steps

A
  1. brain compensates = less CSF/more drainage
  2. compensation exhausted = ICP starts to increase
  3. displacement/distortion of brain structures including midline shift
  4. pressure on occulomotor = down+out+dilated pupil
  5. ICP continues to increase = cerebellar tonsils herniate through foramen magnum + midline bleeding of brainstem
  6. DEATH
142
Q

how does raised ICP present

A

headache = worse on coughing/leaning forward
vomiting/nausea
altered GCS
decrease HR, increased BP
pupillary changes
papilloedema
Cheyne-stokes respiration

143
Q

what is cheyne-stokes respiration

A

periods of apnoea followed by increased breath then decreasing breaths

144
Q

how is ICP investigated

A

head CT
blood pressure
lumbar puncture EXCEPT in suspected mass lesions as this can cause brain herniation and DEATH

145
Q

how is raised ICP treated

A

hyperventilation = decrease pCO2 = cause cerebral vasoconstriction
craniotomy/burr holes (definitive treatment)
treat cause

146
Q

what is an essential tremor

A

gradual onset and worsening of intention tremor

147
Q

how is essential tremor different from intention tremor

A

essential at rest
essential are present without associated symptoms
essential effects hands, head/voice, paarkinsons = whole body
intention = present when moving arm e.g. anxiety

148
Q

how are essential tremors treated

A

beta blockers (not in asthma)
primidone = antiepileptic
gabapentin = antiepileptic
deep brain stimulation

149
Q

what is huntingtons disease

A

autosomal dominant neurodegenerative disorder caused by lack of neurotransmitter GABA
decreased GABA and ACh
increased dopamine

150
Q

what causes huntingtons disease

A

repeated CAG sequence
over generations repeat increases = called anticipation = earlier age of onset withe more CAG sequences
caused by HTT gene

151
Q

how does huntingtons present

A

psychiatric = irritability, depression, anxiety
chorea = jerky, dance-like rigid movements, stop in sleep
dementia
dysarthria = unclear speech
dysphagia

incoordination
seizures
abnornmal eye movement

152
Q

how is huntingtons diagnosed

A

mainly clinical with FHx

head CT/MRI shows caudate nucleus atrophy and increase size of ventricles

genetic testing shows CAG sequence repetition or presence of HTT gene

153
Q

what parts of the brain reduce in size in huntingtons

A

caudate nucleus and putamen

154
Q

how is huntingtons managed

A

no cure, just prevent progression
reduce chorea
= RISPERIDONE dopamine receptor agonist)
= benzodiazepines
= dopamine depletion (tetrabenazine)
antidepressants = SSRIs
antipsychotics = neuroleptics (haloperidol)
genetic counselling

155
Q

what signal do A alpha fibers send

A

= large myelinated fibres
proprioception

156
Q

whats signal do A beta fibres send

A

= large myelinated fibres
light touch
pressure
vibration

157
Q

what signal do A gamma fibres send

A

= thin myelinated
pain and cold sensation

158
Q

what signals do C fibres send

A

= thin, unmyelinated
pain and warm sensation (this is why burning sensation is painful)

159
Q

when is ataxia caused by a sensory neuropathy

A

when ataxia gets worse when eyes closed or dark

160
Q

what is guillain barre syndrome

A

rapid onset muscle weakness caused by autoimmune damage to peripheral NS schwann cells

161
Q

what causes guillain barre

A

3-6months after infection
campylobacter jejuni or cytomegalovirus most common

162
Q

how does guillain barre present?

A

intially = numbness/tingling/pain
then = rapid bilateral muscle paralysis
cranial nerve involvement (facial) = weak face, dysphasia/dysarthria, weak eye muscles
back pain
muscle pain
absent reflexes

163
Q

in severe cases of guillain-barre what can muscle weakness lead to

A

respiratory failure

164
Q

how is guillain barre diagnosed

A
  1. clinical
  2. lumbar puncture = elevated protein, low/normal WBC
  3. nerve conduction studies = most useful
  4. spinal MRI to exclude lesions
165
Q

how is guillain barre treated (6)

A
  1. IV immunoglobulins = neutralise harmful antibodies
  2. plasmapharesis = filters out antigens from blood
  3. intubation for resp failure
  4. analgesia
  5. occupational therapy/social work/physical therapy/psychologists
    (6. possible DVT prophylaxis due to immobility)
166
Q

what are the 2 areas a stroke can affect

A

anterior circulation = circle of willis and branches
posterior circulation = basilar artery and branches

167
Q

what is thrombolysis

A

given intravenously to break up clot
give up to 4.5 hours post onset of symptoms

168
Q

what are the contraindications for thrombolysis (8)

A
  1. recent surgery
  2. recent arterial puncture
  3. active malignancy
  4. evidence of brain aneurysm
  5. anticoagulants
  6. severe liver disease
  7. acute pancreatitis
  8. clotting disorder
169
Q

what are 2 key findings that suggest a subarachnoid haemorrhage

A

thunderclap headache = sudden onset
star shape on CT

170
Q

what lobe of the brain is more likely to be the cause of focal epilepsy

A

temporal

171
Q

what is radiculopathy

A

pain in distribution of spinal nerve usually due to compression
most commonly in cervical spine
e.g. sciatica
e.g. spinal stenosis

172
Q

what causes radiculopathy (9)

A

degenerative disk disease
osteoarthritis
face joint degeneration

ligament hypertrophy
disk prolapse
spondylolisthesis

radiation
diabetes mellitus
neoplastic disease

173
Q

how does radiculopathy present and how would you investigate

A

clinical signs of pain, numbness, weakness
reduced reflexes

spinal MRI of suspected area
nerve conduction studies
BOWSTRING TEST

174
Q

how is radiculopathy treated

A

treat underlying cause

175
Q

what is neurofibromatosis

A

genetic disorder causes tumours to form on nerve tissue = on brain, spinal cord, nerves

176
Q

describe type 1 neurofibromatosis

A

= recklinghausens disease
nerve tissue grows neurofibromas which may be benign
cause damage by compressing nerves and other tissue

177
Q

describe type 2 neurofibromatosis

A

bilateral acoustic neuromas develop = hearing loss

178
Q

how does type 1 neurofibromatosis present (8)

A
  1. cafe au lait spots
  2. freckling = axilla, groin, neck base, sub-mammary
  3. dermal fibromas = brown nodules on skin, may itch
  4. nodular neurofibromas = firm clear brown skin growths on trunk may cause parasthesia
  5. lisch nodules = brown translucent mounds on iris
  6. short stature
  7. microcephaly
  8. nerve root compression
179
Q

how does type 2 neurofibromatosis present

A

cafe au lait spots
deafness
vertigo
tinnitus
signs of raising ICP

180
Q

what are cafe au lait spots

A

flat light brown patches of skin seen in first year of life
size increase with age

181
Q

what causes brown-sequard syndorme

A

intervertebral disc prolapse = most common
MS
tumour
trauma
TB

182
Q

what is cervical spondylosis

A

degeneration of annulus fibrosis and osteophyte formation on adjacent vertabra = narrowing of spinal canal and intervetebral foramina
spinal cord dragged over bony spurs and indented when neck flexes and extends = painful

183
Q

what is carpal tunnel syndrome

A

inflammation in carpal tunnel = median nerve trapped
most common entrapmetn neuropathy
more women:men
associated with hypothyroidism, DM, pregnancy, RA, acromegaly and obesity

184
Q

how does carpal tunnel present

A

pain/parastesia of hand and arm
worse at night, relieved by shaking = SHAKE AND WAKE
loss of sensation in median supplied territories

185
Q

what investigations are done for carpal tunnel syndrome

A

phalens test = 1 min maximal wrist flection causes symptoms
tinels test = tapping over nerve at risk = tingling

186
Q

how is carpal tunnel treated

A

splinting
steroid injections
decompression surgery

187
Q

what questionnaires are used in the diagnosis of depression

A

PHQ-9
GAD-7

188
Q

what is the sudden loss of vision (like a curtain descending) called?

A

amaurosis fugax

189
Q

what is giant cell arteritis and how is it treated

A

granulomatous arteritis of large vessels
Female, White, over 50, Temporal artery
throbbing headache, tender scalp, jaw claudication
biopsy needed
Tx = prednisolone

190
Q

what is cushings triad

A

physiological response to critically high ICP
- hypertension
- bradycardia
- deep/irregular breathing

191
Q

parkinsons aetiology

A

lack of dopaminergic neurones in the substantia nigra
associated with lewy bodies

192
Q

what is significant in prescribing sodium valproate

A

must NOT be given to female of childbearing age

193
Q

what is narcolepsy and what is the aetiology

A

excessive sleepiness due to normal sleep pattern disruption
peptide hypocretin (orexin)
familial link
head trauma/infection/change in sleep habits trigger
= sleep paralysis occurs in 1/3rd

194
Q

what is cataplexy

A

sudden loss of voluntary muscle tone triggered by emotion
consciousness is maintained
can ONLY occur with narcolepsy (70% of narcolepsy cases)
slurring speech/double vision/blurred vision can be present
frequency of attacks vary

195
Q

what investigations are used in narcolepsy/cataplexy

A

epworth sleepiness scale
sleep studies
EEG
brain MRI to exclude other causes

196
Q

what is the diagnostic criteria for narcolepsy with cataplexy and without

A

excessive daytime sleepy >3months
cataplexy symptoms
hypersomnia not better explained by another condition
WITHOUT CATAPLEXY
not present/uncertain episodes

197
Q

what is the management for narcolepsy

A

EDS
good sleep hygeine
strategic naps
education and exercise
DRUG
1. modafinil 200mg/day not in pregnancy
2. methylphenidate
3. modafinil + sodium oxybate
others:
SSRI
solriamfetol if modafinil CI
stimulants (amfetamines) but SE

198
Q

what is the drug treatment for cataplexy

A

sodium oxybate (GHB)
antidepressents particularly Tricyclic

199
Q

what is a squint and what are the 2 types

A

= misalignment of the visual axes
concomitant = common = imbalance in extraocular muscles
paralytic = rare = paralysis of extraocular muscles

200
Q

how is a squint diagnosed and managed

A

corneal light reflection test = light 30cm from childs face to see if light refelcts symmetrically
cover test
= refer to secondary care
= eye patches

201
Q

what is anterior cord syndrome and which tracts are damaged

A

incomplete spinal cord injury results in infarction of anterior 2/3rds of cord
bilateral spinothalamic and spinocerebellar damage (ascending) = sensory deficits
bilateral corticospinal (descending) = motor deficits

202
Q

what are the effects of anterior cord syndrome/injury

A

MOTOR
= sudden onset with PAIN
= motor deficits below level of injury - varies from paraplegia to quadriplegia
SENSORY
= temperature and pain sensation altered 2-3 dermatomes below level of injury
vibration/fine touch/proprioception maintained as tracts are in posterior

203
Q

what investigation for anterior cord synrome

A

MRI
= thin pencil-like hyperintensities on sagittal T2
= two bright dots either side of anteiror horn on axial T2

Phase 2a (15 decks)

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