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6th Yr Neuro MJ > PassMed > Flashcards

PassMed Flashcards

1
Q

IIH RF (5 + list 5 drugs)

A 
Young
Overweight
F
Pregnant
Drugs - COCP, Steroids, Tetracyclines, Vit A, Lithium
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2
Q

IIH Features

A

H, Blurred V, Papilloedema, Enlarged blind spot, 6th nerve palsy

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3
Q

IIH Mx

A

C- Weight loss
M- Diuretics (acetazolamide), Topiramate
S - Repeat LP, ON sheath decompression + fenestration to prevent damage, LP or VP shunt to reduce ICP

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4
Q

GBS define

A

immune mediated demyelination of PNS

  • asc weakness - progressive - symmetrical
  • reflex RED or ABSENT - sensory sx MILD
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5
Q

TIA new definition

A

transient ep of neurological dysftn caused by focal brain, SC, or retinal ischaemia without acute infection
i.e TISSUE - based NOT TIME - based

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6
Q

6 drugs worsening MG

A

6X drugs that may exacerbate myasthenia:

  1. penicillamine
  2. quinidine, procainamide
  3. beta-blockers
  4. lithium
  5. phenytoin
  6. ABx: gentamicin, macrolides, quinolones, tetracyclines
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7
Q

Raised ICP features (5)

A
  1. headache
  2. vomiting
  3. reduced levels of consciousness
  4. papilloedema
  5. Cushing’s triad = WIDE pulse pressure, BRADYCARDIA, irregular breathing, HTN
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8
Q

Raised ICP patho + normal range

A
  • the normal ICP is 7-15 mmHg in adults in the supine position
  • cerebral perfusion pressure (CPP) is the net pressure gradient causing cerebral blood flow to the brain
  • CPP = mean arterial pressure - ICP
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9
Q

Raised ICP Mx

A

-investigate and treat the underlying cause
-HEAD ELEVATION to 30º
-IV MANNITOL may be used as an osmotic diuretic
-controlled HYPERVENTILATION: aim is to reduce pCO2 → VC of the cerebral arteries → reduced ICP
(Caution needed as may reduce blood flow to already ischaemic parts of the brain)
-REMOVAL of CSF, different techniques include:
—drain from intraventricular monitor
—repeated LP (e.g. IIH)
—VP shunt (for hydrocephalus)

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10
Q

MG Mx

A

Management
1-long-acting acetylcholinesterase inhibitors
pyridostigmine is first-line
2-immunosuppression:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
3-thymectomy

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11
Q

Causes of LMN facial palsy

A 
Lower motor neuron:
Bell's palsy
Ramsay-Hunt syndrome (due to reactivation of herpes zoster)
acoustic neuroma
parotid tumours
HIV
multiple sclerosis*
diabetes mellitus
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12
Q

Facial Nerve supplies what

A

Supply - ‘FACE, EAR, TASTE, TEAR’

face: muscles of facial expression
ear: nerve to stapedius
taste: supplies anterior two-thirds of tongue
tear: parasympathetic fibres to lacrimal glands, also salivary glands

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13
Q

Differences between pseudoseizures/psychogenic nonepileptic seizures and true seizures

A 
Factors favouring pseudoseizures:
pelvic thrusting
family member with epilepsy
much more common in F
crying after seizure
don't occur when alone
GRADUAL onset

Factors favouring true epileptic seizures:
SUDDEN onset
tongue biting
raised serum PROLACTION

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14
Q

WE

A

Confusion, ataxia, nystagmus + ophthalmoplegia

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15
Q

Ataxic gait causes

A

Ataxic gaits typically occur following cerebellar injury, the causes of which can be remembered by the mnemonic ‘pastries’

P - Posterior fossa tumour
A - Alcohol
S - Multiple sclerosis
T - Trauma
R - Rare causes
I - Inherited (e.g. Friedreich's ataxia)
E - Epilepsy treatments
S - Stroke
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16
Q

Ataxic gait feat

A

A wide-based gait with loss of heel to toe walking is called an ataxic gait

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17
Q

Temporal lobe seizure features

A

Lip smacking + post-ictal dysphasia are localising features of a temporal lobe seizure

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18
Q

spinal cord compression features

A

most comm from extradural compression from spinal mets

  • feat: 1st = back pain (worse on lying down and coughing)
  • lower limb weakness
  • sensory changes: sensory loss and numbness
  • neurological signs depend on the level of the lesion
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19
Q

how does level of spinal cord compression affect neurological sign presentations

A
  • Lesions above L1 usually result in upper motor neuron signs in the legs and a sensory level
  • Lesions below L1 usually cause lower motor neuron signs in the legs and perianal numbness
  • Tendon reflexes tend to be increased below the level of the lesion and absent at the level of the lesion
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20
Q

bone mets

A

Most common tumour causing bone metastases (in descending order)
prostate
breast
lung

Most common site (in descending order)
spine
pelvis
ribs
skull
long bones
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21
Q

Encephalitis features + immed Mx

A
  • F, H, psychiatric Sx, seiz, vom
  • focal features e.g. aphasia
  • peripheral lesions (e.g. cold sores) have no relation to presence of HSV encephalitis
  • compl by temporal L seizures: motionless staring, confusion and disorientation, altered ability to respond to others) accompanied by an aura (jamais vu - a feeling of unfamiliarity

MX: intravenous aciclovir should be started in all cases of suspected encephalitis

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22
Q

Pituitary apoplexy define + precipitating factors

A

Sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction.

Precipitating factors:

  • HTN
  • pregnancy
  • trauma
  • anticoagulation
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23
Q

Pituitary apoplexy features + Ix

A
  • sudden onset H similar to that seen in SAH
  • vom
  • neck stiffness
  • VF defects: classically bitemporal superior quadrantic defect
  • extraocular nerve palsies
  • feat of pituitary insufficiency
    e. g. hypotension/hyponatraemia secondary to hypoadrenalism

Ix: MRI is dx

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24
Q

Pituitary apoplexy Mx

A

urgent steroid replacement due to loss of ACTH
careful fluid balance
surgery

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25
Q

Restless Legs Syndrome causes + assoc

A 
Causes and associations:
\+FHx in 50% of pts with idiopathic RLS
IDA
uraemia
DM
pregnancy
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26
Q

Restless Legs Syndrome mx

A

Mx:

  • simple measures: walking, stretching, massaging affected limbs
  • treat any iron defic
  • dopamine AGONISTS are first-line treatment (e.g. PRAMIPEXOLE, ROPINIROLE)
  • benzos
  • gabapentin
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27
Q

what scale to measure disability or dependence in ADLs

A

Barthel Index

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28
Q

Wernicke’s vs Brocas

A

Wernicke’s sounds like ‘What?’ as the patient doesn’t understand a command.

Broca sounds like ‘broken’ as the patient’s word-flow is broken.

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29
Q

Thoracic outlet syndrome define

A

-disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet. -TOS can be neurogenic or vascular; the former accounts for 90% of the cases.

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30
Q

NEUROGENIC Thoracic outlet syndrome clinic pres

A

painless muscle wasting of hand muscles, with patients complaining of hand weakness e.g. grasping
sensory symptoms such as numbness and tingling may be present
if autonomic nerves are involved, the patient may experience cold hands, blanching or swelling

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31
Q

VASCULAR Thoracic Outlet Syndrome clin pres

A

subclavian vein compression leads to painful diffuse arm swelling with distended veins
subclavian artery compression leads to painful arm claudication and in severe cases, ulceration and gangrene

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32
Q

Thoracic Outlet Syndrome causes

A

TOS occurs when you get neck trauma to pts with anatomical predispositions eg SOFT TISSUE (70%) eg scalene muscle hypertrophy or OSSEOUS structures (30%) eg cervical rib

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33
Q

CN6 palsy manifesting as diplopia could be the first sign of what?

A

BRAIN METS

  • CN6 (ABDUCENS) is thinnest CN + longest intracranial course
  • v susceptible to compression when SOL develoop
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34
Q

ACUTE mx of stroke

A
  • BL GL, hydration, O2 sats + T should be maint within normal limits
  • BP should not be lowered in the acute phase unless there are compl e.g. Hypertensive encephalopathy*
  • aspirin 300mg orally or rectally should be given asap if a haemorrhagic stroke has been EXCL
  • w/rto AF, anticoagulants should not be started until brain imaging has EXCLUDED HAEMORRHAGE, and usu not until 14 days have passed from the onset of an ischaemic stroke’
  • if the cholesterol is > 3.5 mmol/l pts should be commenced on a STATIN. Many physicians will delay tx until after at least 48 hours due to the risk of HAEMORRHAGIC TRANSFORMATION
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35
Q

autonomic dysreflexia is what

A
  • clinical syndr occurs in pts who have had a SCI at, or ABOVE T6 spinal level.
  • Briefly, afferent signals, most comm triggered by FAECAL IMPACTION or URINARY RETENTION (but many other triggers have been reported) cause a SYMP spinal reflex via thoracolumbar outflow.
  • The usual, centrally mediated, parasymp response however is prevented by the cord lesion.
  • The result is an UNBALANCED physiological response, characterised by extreme HTN, FLUSHING + SWEATING above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme HTN have been reported, e.g. haemorrhagic stroke
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36
Q

Mx of autonomic dysreflexia

A

Mx involves removal/control of the stimulus + tx of any life-threatening HTN +/or BRADY.

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37
Q

Mx of neuropathic pain

A
  • 1st-line tx*: amitriptyline, duloxetine, gabapentin or pregabalin
  • if the 1st-line drug tx does not work try DIFF ONE
  • in contrast to standard analgesics, drugs for neuropathic pain are typically used as monotherapy, i.e. if not working then drugs should be switched, not added
  • tramadol may be used as ‘RESCUE tx’ for exacerbations of neuropathic pain
  • topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
  • pain mx clinics may be useful in pts with resistant problems
38
Q

syringomyelia define

A

collection of CSF (fluid filled cyst) within the SC

39
Q

syringomyelia causes

A
  • Chiara malformation - strong association
  • trauma
  • tumours
  • idiopathic
40
Q

syringomyelia features

A

-a ‘CAPE-LIKE’ (neck, shoulders and arms)
LOSS of SENSATION to PAIN + TEMPERATURE but the preservation of light touch, proprioception and vibration
-classic examples are of patients who accidentally burn their hands without realising
-this is due to the crossing SPINOTHALAMIC TRACTS in the anterior commissure of the spinal cord being the 1st tracts to be affected
-SPASTIC WEAKNESS (predominantly of the lower limbs)
-NEUROPATHIC PAIN
-UPGOING PLANTARS
-autonomic features: HS due to compression of the sympathetic chain, but this is rare
—-bowel and bladder dysfunction
-scoliosis will occur over a matter of years if the syrinx is not treated
NB. associated with Arnold-Chiari malformation

41
Q

stroke thrombolysis for acute ischaemic stroke when to give

A

-Thrombolysis with alteplase should only be given if:
it is administered within 4.5 hours of onset of stroke symptoms (unless as part of a clinical trial)
-haemorrhage has been definitively excluded (i.e. Imaging has been performed)

42
Q

ABSOLUTE CI to thrombolysis

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke or traumatic brain injury in preceding 3 months
  • LP in preceding 7 days
  • GI haemorrhage in preceding 3 weeks
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled hypertension >200/120mmHg
43
Q

RELATIVE CI to thrombolysis

A
  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery / trauma in the preceding 2 weeks
44
Q

Thrombectomy for acute ischaemic stroke must take into account pts overall clinical status HOW

A

NICE recommend that all decisions about thrombectomy take into account a patient’s overall clinical status:
-NICE recommend a pre-stroke functional status of less than 3 on the modified Rankin scale and a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)

45
Q

for PROXIMAL ANTERIOR CIRC strokes on CTA or MRA when to offer thrombectomy

A

ASAP + < 6 hours of SX onset, + IV thrombolysis (if within 4.5 hours)

46
Q

in what cases can you give thrombectomy between 6 and 24h previously (incl wake up strokes)

A

-confirmed occlusion of proximal anterior circulation on CTA or MRA AND if potential to salvage brain tissue as shown by CT perfusion or diffusion weighted mRI showing LIMITED INFARCT CORE VOLUME

47
Q

for wake up strokes what time do you assume stroke occurred

A

time they went to sleep

48
Q

when to CONSIDER thrombectomy together with intravenous thrombolysis (if within 4.5 hours) ASAP for people last known to be well up to 24 hours previously (including wake-up strokes)?

A
  • Ppl who have acute ischaemic stroke and confirmed occlusion of the PROXIMAL POSTERIOR CIRCULATION (that is, basilar or posterior cerebral artery) demonstrated by CTA or MRA AND
  • if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume
49
Q

vestibular schwannoma (acoustic neuroma) features

A

TRIAD

  1. vertigo
  2. hearing loss, tinnitus
  3. absent corneal reflex.

-unilateral SNHL that is progressive - raises suspicion

Features can be predicted by the affected cranial nerves:

  • cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
  • cranial nerve V: absent corneal reflex
  • cranial nerve VII: facial palsy
50
Q

generalised T-C seiz mx

A

sodium valproate
second line: lamotrigine, carbamazepine
F–> 1ST = LAMOTRIGINE

51
Q

ABSENCE seizures mx

A

=SV or ethosuximide

  • SV particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy
  • carbamazepine can WORSEN
52
Q

MYOCLONIC seizures mx

A

-SV
2nd line: clonazepam, lamotrigine
-carbamazepine can WORSEN

53
Q

FOCAL seizures mx

A
  • carbamazepine or lamotrigine

- 2nd line: levetiracetam, oxcarbazepine or sodium valproate

54
Q

VF defects: left homonoymous hemianopia

A

means visual defect to the left, ie lesion of RIGHT optic tract

  • congruous = complete or symmetrical VF loss = lesion of OPTIC RADIATION OR OCCIPITAL CORTEX
  • incongruous = incomplete or asymmetric = OPTIC TRACT lesion
  • macula sparing = lesion of OCCIPITAL CORTEX (glaucoma + retinitis pigmentosa)
55
Q

VF defects - homonoymous QUADRANTANOPIAS

A

PITS
parietal - inferior
temporal - superior

56
Q

MS gold std imaging

A

MRI WITH CONTRAST

-to view plaques showing areas of demyelination

57
Q

brain abscess mx

A

IV 3rd gen cephalosporin + metronidazole

+ Dex for ICP Mx

58
Q

loss of corneal reflex - controlled by what nerve

A

trigeminal - CN V

59
Q

hoovers sign is used for what, and what is it

A

differentiate bet ORGANIC + NON-ORGANIC lower leg weakness

  • based on synergistic contraction
  • if pt was genuinely trying to lift their weak leg then you would feel the NORMAL limb pushing DOWN against your hand = ORGANIC cause of paresis
60
Q

mx of pt on warfarin/DOAC/bleeding disorder presenting with TIA

A

ADMIT imemdiately for imaging to exclude a haemorrhage

61
Q

defective downward gaze + vertical diplopia

A

CN 4 = TROCHLEAR

  • problem with SO
  • cause can be poorly controlled diabetes
62
Q

neuroleptic malignant syndrome tetrad

A

1/hyperthermia
2/muscle rigidity
3/autonomic instability
4/altered mental status

63
Q

defective eye abduction + horizontal diplopia

A

CN 6 = ABDUCENS

64
Q

anterior cerebral artery x1

A

contralateral hemiparesis + sensory loss, lower extremity>upper

65
Q

middle cerebral artery x 3

A
  1. contralateral hemiparesis + sensory loss, upper extremity>lower
  2. contralateral homonoymous hemianopia
  3. aphasia
66
Q

posterior cerebral artery

A
  1. contralateral homonymous hemianopia with macular sparing

2. visual agnosia

67
Q

Weber’s syndrome (branches of posterior cerebral artery that supply the midbrain)

A
  1. Ipsilateral CN III palsy

2. Contralateral weakness of upper and lower extremity

68
Q

Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenburg syndrome)

A
  1. Ipsilateral: facial pain and temperature loss
  2. Contralateral: limb/torso pain and temperature loss
  3. Ataxia, nystagmus
69
Q

Anterior inferior cerebellar artery (lateral pontine syndrome)

A

SX similar to Wallenburg’s

  • BUT
  • ipsilateral: facial paralysis + deafness
70
Q

retinal/opthalmic artery

A

amaurosis fugax

71
Q

basilar artery

A

locked in syndrome

72
Q

Raised ICP Mx

A
  • ix and treat cause
  • HEAD ELEVATION to 30 degrees
  • IV MANNITOL can be used as an osmotic iduretic
  • CONTROLLED HYPERVENTILATION - aim to reduce pCO2– > VC of cerebral arteries –> reduced ICP
  • REMOVAL OF CSF –> drain from IV monitor, repeat LP, VP shunt
73
Q

what is Lhermitte syndrome in MS - L for LIMBS

A

paraesthesia in LIMBS on NECK FLEXION

74
Q

what is Uhthoffs phenomenon in MS - U for EYES

A

worsening of VISION after RISE IN BODY TEMP

75
Q

what can common peroneal nerve lesion cause weakness of

A

Loss of foot dorsiflexion + foot eversion

76
Q

how do chronic SDH look on CT head

A

HYPODENSE (dark)
CRESCENTERIC in shape
NOT restricted by suture lines

77
Q

Oxford stroke classification = Bamford Classification - classifies stroke based on initial Sx - what are the 3 criteria

A
  1. Unilateral hemiparesis +/or hemisensory loss of F, A, Leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction eg dysphasia
78
Q

TOTAL anterior circulation infarcts - 15% strokes

A

involve middle + anterior cerebral arteries

-all 3 of Oxford stroke classification present

79
Q

PARTIAL anterior circulation infarcts (PACI) - 25% strokes

A
  • involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
  • 2 of the above criteria are present
80
Q

LACUNAR infarcts - 25% strokes

A
  • involves perforating arteries around the internal capsule, thalamus and BG
  • presents with 1 of the following:
    1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
    2. pure sensory stroke.
    3. ataxic hemiparesis
81
Q

POSTERIOR circulation infarcts - 25%

A 
-involves vertebrobasilar arteries
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia
82
Q

other recognised stroke patterns - LATERAL MEDULLARY SYNDROME

A

Lateral medullary syndrome (posterior inferior cerebellar artery)
aka Wallenberg’s syndrome
-ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
-contralateral: limb sensory loss

83
Q

other recognised stroke patterns - Weber’s syndrome

A
  • ipsilateral III palsy

- contralateral weakness

84
Q

PHENYTOIN MOA and adverse effects - acute, chronic, idiosyncratic, teratogenic

A

MOA: induces p450
ACUTE: intially - dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures

CHRONIC: common - gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia

IDIOSYNCRATIC:

  • F
  • rashes, including severe reactions such as toxic
  • epidermal necrolysis
  • hepatitis
  • Dupuytren’s contracture*
  • aplastic anaemia
  • drug-induced lupus

TERATOGENIC:
-associated with cleft palate + CHD

85
Q

if pt has aphasia with stroke - most likely site of stroke is where?

A
  • for aphasia to be present it means dominant hemisphere affected–> most commonly LEFT (regardless of handedness)
  • MCA on dominant side–> supplies both Wernicke’s + Broca’s areas of the cortex
  • responsible for understanding + production of speech
86
Q

NPH triad mnemonic

A

WET - urinary incontinence
WACKY - dementia + bradyphrenia (pathological slowing of mental processes)
WOBBLY - gait abnormality (can be like PD)

87
Q

before starting phenytoin what should you ensure is on pt

A

CARDIAC MONITORING

-due to pro-arrythmogenic effects

88
Q

Secondary prevention of stroke

A

1st line = CLOPI - in ischaemic stroke
2nd line = Aspirin + MR dipyridamole if Clop CI or not tolerated - in ischaemic stroke
3rd line = just MR dipyridamole - if aspirin or clop CI or not tolerated

89
Q

what lobes are Wernickes and brocas

A

WC - wernickes responsible for comprehension/understanding - so it is located near the ear in the TEMPORAL LOBE

  • then signal to arcuate fasciculus to Broca’s
  • BP - Brocas resp for production of speech - so it is located near the mouth in the FRONT LOBE
90
Q

in trauma what quick test determines if fluid is CSF

A

checking fro glucose - it is NOT present in MUCUS but is present in CSF
-beta 2 transferrin would be gold standard

6th Yr Neuro MJ (3 decks)

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