Neurology/Neurosurgery Flashcards

1
Q

what are the features of wernicke’s encephalopathy?

A
  • opthalmoplegia
  • reduced GCS/confusion
  • nystagmus
  • ataxia
  • peripheral sensory neuropathy
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2
Q

how would you manage Charcot-Marie-Tooth disease?

A

there is no treatment to cure or slow the disease

management is for symptomatic relief, and should be coordinated by a specialist neurologist involving the MDT of orthopaedic surgeons, and PT/OT

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3
Q

what is the role of steroids in managing guillian-barre syndrome?

A

should not use steroids

only treatment is IVIG or plasma exchange

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4
Q

what does coning mean?

A

coning = herniation of the cerebellar tonsils through the foramen magnum

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5
Q

what is usually the first feature of parkinsons?

unilateral or bilateral?

A

unilateral pill-rolling tremor (60%)

asymmetrical signs support parkinson’s rather than parkinsonism

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6
Q

what sort of medication leads to acute dystonia?

what is the neural mechanism?

what is the management?

A

anti-dopaminergics (typical antipsychoitcs and metaclopramide)

blockade of negrostriatal D2 leads to compensatory excess production of basal ganglia catecholamines, resulting in prolonged, forceful contractions of the muscles around the face, head, neck and arms

treatment is with anticholinergic - procyclidine

written paper 2014

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7
Q

does pain behind the ear increase or decrease the likelihood of a diagnosis of bell’s palsy?

A

pain behind the ear is consistent with Bell’s palsy

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8
Q

what are the features of vestibular schwannoma (acoustic neuroma)?

A
  • cranial nerve VIII: hearing loss, vertigo, tinnitus
  • cranial nerve V: absent corneal reflex
  • cranial nerve VII: facial palsy
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9
Q

what are the causes of parkinsonism?

A
  • idiopathic
  • lewy body dementia
  • drugs/toxins
    • MPTP
    • typical > atypical antipsychotics
    • chlorpromazine, prochlorperazine
    • metaclopramide
  • basal ganglia tumour
  • wilson’s disease
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10
Q

name two Parkinson’s Plus syndromes

A
  • progressive supranuclear palsy
  • multisystem atrophy
  • corticobasal degeneration
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11
Q

other than better soft tissue resolution, what is the benefit of MR imaging over CT in the brain?

A

MR has better sensitivity for posterior fossa masses/bleeds

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12
Q

what two conditions increase the rate of Bell’s palsy?

A

pregnancy and diabetes

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13
Q

what are the causes of bilateral facial nerve palsy?

what are the causes of unilateral facial nerve palsy?

A

lyme disease, giullian-barre syndrome, sarcoidosis or trauma

bell’s, ramsey-hunt, parotid surgery/tumour, diabetes, stroke, middle ear (otitis media or cholesteatoma)

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14
Q

typical side effects of lamotrigine

A
  • skin: maculopapular rash / SJS / TEN
  • head: diplopia, blurred vision, photosensitivity
  • tremor
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15
Q

side effects of valproate

A

pregnancy: teratogenic

GI: liver failure, pancreatitis

skin: hair loss, regrows curly
nerves: tremor, ataxia, encephalopathy
haem: thrombocytopenia

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16
Q

what is the definition of ‘parkinsonism’

A

movement disorder characterised by bradykinesia and at least one of tremor, rigidity, postural instability

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17
Q

describe what you see (3)

A
  • wasting of the distal leg muscles, specifically the anterolateral compartment with relative sparing of the quadraceps, giving an ‘inverted champagne bottle’ appearance
  • bilateral pes cavus
  • clawing of the toes

the diagnosis is Charcot-Marie-Tooth disease

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18
Q

cerebellar lesions - hyper or hypotonia?

A

hypotonia

loss of supplimental cerebellar bacgkround reinforcing signals leaves motor cortex to send tonic signals out unaided, resulting in temporary hypotonia in the early/medium term. eventually the motor cortex adjusts and the hypotonia becomes less marked

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19
Q

what physcial sign helps identify the location of the lesion in Horner’s syndrome?

A

anhidrosis

  • central lesion - anhidrosis of arm, trunk and face
  • pre-ganglionic lesion - anhidrosis of the face
  • post-ganglionic lesion - no anhidrosis
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20
Q

what are the investigations for guillian-barre syndrome?

A

FVC every 4 hours

LP demonstrates elevated protein (>5.5 g/L), normal WCC

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21
Q

if the diagnosis is parkinson’s, what other tests would you like to complete the examination? (4)

A
  • assess handwriting - micrographia
  • lying and sitting blood pressure - autonomic dysfunction
  • seborrhoeic dermatitis - autonomic dysfunction
  • mini-mental test score - cognition/dementia with Lewy bodies
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22
Q

what is dysmetria?

A

incorrect velocity and amplitude of planned movements

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23
Q

what is the eye sign in parkinson’s disease?

A

blepharoclonus

tremor of the eyelid when the eyes are gently closed

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24
Q

what are the driving rules for epilepsy?

what is other general safety advice for a newly diagnosed epileptic?

A

must contact the DVLA and stop driving until they are seizure free for >1 year

avoid swimming, becoming pregnant, driving (esp HGVs), extreme sport, occupational hazards (pylon engineers, window cleaners etc)

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25
Q

how can you demonstrate bradykinesia in parkinsonism?

A

patient to open and close hands repeatedly. movements become slower and smaller in amplitude

patient to tap foot on the floor repeatedly. movements become slower and smaller in amplitude

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26
Q

what is Todd’s palsy?

A

temporary weakness following a focal seizure in the primary motor cortex

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27
Q

what nerve roots are affected in Erb’s palsy?

what are the classic findings on inspection of the upper limb?

A

C5-6

upper limb held in pronation and medial rotation

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28
Q

what are the types of seizures?

A
  • focal - start in a specific part of the brain and remain on one side
    • focal aware, focal impaired awareness , focal awareness unknown
    • focal motor (Jacksonian march), focal non-motor (deja-vu, jamais-vu)
    • aura - implies the seizure starts in the temporal lobe
    • focal to bilateral
  • generalised - involves both hemispheres of the brain, consciousness is lost immediately
    • motor or absence
    • motor subtypes: tonic-clonic, tonic, clonic, atonic, myoclonic
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29
Q

what is the gold standard diagnostic test for degenerative cervical myelopathy?

A

MRI cervical spine

disc degeneration, ligament hypertrophy, cord signal change

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30
Q

side effects of levetiracetam/keppra

A
  • psych: depression and agitation (common)
  • GI: dyspepsia, D&V
  • head: diplopia, drowsiness
  • haem: blood dyscrasia
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31
Q

what are the complications of ventriculoperitoneal shunt placement?

A

failure/malfunction requiring revision

shunt infection with staph epidermidis

other: over/under drainage, subdural haematoma, seizures

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32
Q

what does an aura preceeding a seizure tell you about the neuropathology?

A

often, but not always, indicates focal seizure starting in the temporal lobe

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33
Q

what is the principle of investigating epilepsy?

A

trying to identify a provoking factor - unprovoked is basically diagnosing epilepsy and that needs prophylactic medication and a driving ban

bedside - emergency EEG to include non-convulsive status epilepticus

bloods: U&E, glucose, anti-epileptic drug level
urine: dip, MC&S and 5-panel drug screen
images: MRI brain for ?SOL

special tests: LP and blood cultures if infection is suspected

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34
Q

what tests should be done for facial nerve palsy/Bell’s ?

A

rule out more sinister causes

look in the ear for vesicular rash on/aorund tympanic membrane (site of viral replication is the geniculate nucleus)

ESR and glucose.

varicella and boriella antibodies

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35
Q

what is classically found in Weber’s syndrome (stroke)?

A
  • ipsilateral: CN III palsy
  • contralateral: limb weakness
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36
Q

what is the summary of clinical findings that strongly suggests a diagnosis of motor neuron disease?

what are some types of motor neuron disease?

A

this patient has a combination of upper and lower motor neuron signs in the face, arms and legs with no sensory involvement. the diagnosis is motor neuron disease.

  • amyotrophic lateral sclerosis (UMN and LMN)
  • primary lateral sclerosis (mostly UMN)
  • progressive muscular atrophy (mostly LMN)
  • progressive bulbar palsy (mostly bulbar/pseudobulbar)
37
Q

what sort of drugs are used to treat movement disorders (e.g. huntington’s)?

A

dopamine antagonists

unlicenced use of antipsychotics that have an anti-DA mechanism of action can also help control movement disorders
(e.g. haloperidol, olanzapine, risperidone)

note on Huntington’s - no treatment can slow the progression of disease

(e.g. tetrabenazine)

38
Q

where is the tumour?

  • grasp reflex
  • dysphasia, perseveration
  • decreased verbal fluency

…what is the grasp reflex?

A

frontal lobe

dysphasia - expressive dysphasia (Broca’s), receptive/fluent (Wernicke’s)

grasp reflex - running fingers across palm triggers the hand to grasp the examiner’s fingers

39
Q

typical side effects of carbemazepine

A
  • haem: leucopenia
  • head: diplopia & blurred vision, balance, drowsiness
  • skin: generalised erythematous rash
40
Q

what is the treatment for Bell’s palsy?

A

conservative

  • education - 95% make a full recovery but can take up to 6 months in some cases
  • protect the eye - taping shut at night, sunglasses, arteficial tears

medical

  • prednisolone given within 72 hours of onset of symptoms
    • 60 mg OD PO for 5 days, then taper down by 10 mg/day
  • if ramsey-hunt, give aciclovir
41
Q

what is the consideration in migraine management for a woman of childbaring age?

A

for prophylaxis - propranolol is preferred to topiramate

usually topiramate is first class though

42
Q

where is the tumour?

  • hemisensory loss, decreased two-point descrimination
  • sensory inattention
  • astereognosis
  • dysphasia

…what is astereognosis?

A

parietal lobe

astereogonosis - inability to descriminate objects based on touch alone

43
Q

what are the causes of cerebellar syndrome?

A

ADULT

  • posterior circulation CVA
  • demyelination (MS)
  • alcoholic cerebellar degeneration

PAEDS

  • hereditary
    • fredrich ataxia
    • ataxia telengiectasia
  • developmental malformations
    • arnold-chiari
    • dandy-walker
  • posterior fossa tumour
    • medulloblastoma
    • astrocytoma
      *
44
Q

what are some complications of epilepsy?

A

sudden unexpected death in epilepsy (SUDEP) - apnoea or asystole during nocturnal seizure

5% risk of foetal abnormalities in women suffering from epilepsy during pregnancy

45
Q

what are the eye signs of cerebellar disease?

how would you elicit these clinically?

A

nystagmus, fast beat toward the side of the lesion
test as usual

loss of smooth persuit: hyper/hypometric saccades
ask patient to alternate gaze between two fingers held up shoulder width apart

46
Q

where is the tumour?

  • dysphasia
  • homonomous hemianopia
  • amnesia
A

temporal lobe

47
Q

what medication is used for acute termination of migraine?

what medication is used first line for prophylaxis?

A

termination - triptans + NSAID or triptan + paracetamol

prophylaxis: topiramate or propranolol

48
Q

what are the localising signs of cerebellar disease?

A
  • vermis - truncal ataxia
    • test with propulsion and retropulsion when standing
  • neocortex - ipsilateral limb ataxia
49
Q

what is the gait in cerebellar disease?

A

broad-based, ataxic, ‘drunken’ gait

tendency to fall toward the side of the lesion

50
Q

what is the management plan for a CNS tumour?

A

conservative

  • ?palliation maybe the best option

medical

  • prevent seizures - anti-epileptics
  • treat headaches
    • opiates appropriate (codeine 60 mg prn max QDS)
  • cerebral oedema?
    • chronic = dexamethasone
    • acute = mannitol

surgical

  • resection if possible
  • debulking and carmustine wafer insertion (deilvery of local chemotherapy)
  • biopsy for tissue diagnosis and genotyping to optimise medical treatment
  • ventriculo-peritoneal shunt placement for hydrocephalus
  • neoadjuvant chemo/radiotherapy, or curative/palliative when tumour is inaccessable surgically
51
Q

what is the prognosis of a CNS tumour?

A

poor: <50% survival at 5 years

…getting better

52
Q

what is the result of Romberg’s test in cerebellar disease?

mechanism?

A

Romberg negative

Romberg is a test of proprioception: closing the patient’s eyes removes the second of three position senses, so with only the vestibular system functioning they will lose balance quickly

cerebellar lesions do not affect proprioception.

N.B. alcoholic cerebellar degeneration with co-morbid vit B12 deficiency and subacute combined degeneration of the spinal cord

53
Q

what is the prognosis of guillian-barre syndrome?

A

10% die

85% make a complete/near-complete recovery

10% are unable to walk alone at 1 year

54
Q

what are the risk factors for degenerative cervical myelopathy?

A

smoking, genetics and occupation that exposes patients to high axial weight loads

55
Q

what is classically found in lateral medullary syndrome? (stroke)

A
  • ipsilateral: ataxia, dysphagia, facial numbness, cranial nerve palsy (horner’s)
  • contalateral: loss of limb pain and temperature sensation

structures affected - nucleus ambiguous (CN IX and X), cerebellar peduncle, spinothalamic tract, CN VIII nucleus

56
Q

what is the pathology of normal pressure hydrocephalus?

what is the definitive treatment?

A

decreased absorbtion of CSF by the arachnoid villi

ventriculo-peritoneal shunting

57
Q

what are the drug treatments for parkinson’s?

A
  • dopaminergic drugs
    • Levodopa
    • dopamine agonists (bromocriptine, pramipexole)
    • MAO-B inhibitors (rasagline)
  • anticholinergics (procyclidine)
  • COMT inhibitors (entacapone, tolcapone)
    • decrease the peripheral degradation of levodopa, increasing the on:off ratio
58
Q

what are the complications of myotonic dystophy?

A
  • cardiac
    • conduction (arrythmia, heart block)
    • valves (mitral valve prolapse)
    • cardiomyopathy (LVH and myocardial myotonia)
  • endocrine
    • diabetes mellitus
    • hypogonadism
  • gastrointestinal
    • dysphagia and reflux
    • hypomotility/delayed gastric emptying
  • respiratory
    • respiratory failure following anaesthesia
    • hypoventilation (weakness)
59
Q

personal or family history of respiratory complications following anaesthesia should make you suspect…

A

myotonic dystrophy

60
Q

define epilepsy

A

neurological condition characterised by recurrent episodes of abnormal, uncontrolled, intermittent electrical activity in the brain leading to multiple seizures.

convulsions are the motor sign of electrical discharges in the brain

61
Q

what are the archetypal features of myotonic dystrophy

A
  • myotonic facies
    • wasting of small facial muscles, temporalis, masseter and SCMs
  • frontotemporal balding
  • cateracts
  • delayed hand grip release
  • delayed eye opening followng forceful closure
  • distal muscle wasting, foot drop & high steppage gait
62
Q

side effects of phenytoin

A

psych: decreased intellect, depression
skin: acne, gum hyperplasia, coarse facial features
haem: blood dyscrasia
nerves: polyneuropathy

63
Q

what are the aetiologies of a space occupying lesion in the brain?

A
  • tumour
    • primary
    • metastasis
  • vascular
    • aneurysm
    • chronic subdural haematoma
  • infection
    • abscess
    • granuloma
    • cyst (cysticersosis)
64
Q

what are some disease that present with diffuse LMN signs ONLY?

A
  • multifocal motor neuropathy
  • chronic inflammatory demyelinating polyneuropathy
  • old poliomyelitis
  • syphilis
  • spinal muscular atrophy
65
Q

what are the principles of managing restless leg syndrome?

A
  • stretch and massage the legs
  • treat any iron deficiency
  • dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
  • benzodiazepines
  • gabapentin
66
Q

what are the investigations of Wernicke’s encephalopathy?

A
  • decreased RBC transketolase (rarely done)
  • MRI brain (periaqueductal punctate haemorrhage)
67
Q

how do you describe the arms in parkinson’s?

how do you describe the gait in parkinson’s?

A

asymmetrical pill rolling temor, lead pipe rigidity at the elbow, cogwheel rigidity in the wrist, bradykinesia accentuated by voluntary movement of the opposite arm

unsteady, shuffling, narrow-based, stooped posture, accentuation of the pill-rolling tremor

68
Q

what’s the diagnosis?

  • pain
  • opthalmoplegia
  • horner’s syndrome
  • trigeminal nerve (V1) palsy
  • proptosis
A

cavernous sinus syndrome

69
Q

what are the diagnostic findings that would support MS?

A

MRI - hyperintensities in the periventricular white matter

CSF - oligoclonal IgG bands that are not present in the serum, suggest CNS inflammation

70
Q

what is the medical management of MS?

A

DMARDs

  • if mild… dimethyl fumarate
  • alemtuzumab (anti-T cell)
  • natalizumab (anti-leukocyte migration)

acute

  • pulse methylprednisolone

symptom control

  • tremor - botox A
  • spasticity - baclofen/gabpentin
  • urinary retention, PVRV >100 mL = self-catheterisation
  • urinary retention, PVRV <100 mL = tolterodine
  • fatigue = amantadine, CBT, exercise
71
Q

what are Lhermitte’s sign and Uhthoff phenomenon?

A

both seen in MS

Lhermitte’s sign = flexion of the neck causes electric shock like feeling down the trunk and limbs

Uhthoff phenomenon = worsening of sypmtoms with heat

72
Q

what are the layers of the scalp?

A

use SCALP

Pericranium

  • Skin
  • Connective tissue (dense)
  • Aponeurotic layer (galea)
  • Loose connective tissue
73
Q

what is the origin of the middle meningeal artery?

A

external carotid

maxillary artery

middle meningeal

74
Q

which branches of the trigeminal nerve are commonly affected in trigeminal neuralgia?

A

V2 and V3

opthalmic division is rarely affected.
pain felt in the upper nose, eyelid, forehead and scalp are unusual.

75
Q

what is the normal CSF opening pressure?

A

8-14 mmHg

76
Q

what are the layers through which the needle will pass for a lumber puncture?

A

skin

subcut fat

supraspinous ligament and intraspinous ligament

ligamentum flavum

extradural space

dura mater

arachnoid mater

subarachnoid space (with CSF)

77
Q

compression of which nerve root affects knee jerk reflex?

compression of which nerve root affects ankle jerk reflex?

A

L4

S1

78
Q

what are the causes of peripheral neuropathy?

A

metabolic

  • diabetes
  • vitamin B12 deficiency

drugs/toxins

  • isoniazid
  • phenytoin
  • nitrofurantoin
  • metronidazole
  • alcohol
  • heavy metals: lead/mercury

inflammatory

  • chronic inflammatory demyelinating neuropathy

infectious

  • guillian-barre syndrome
  • neurosyphilis
  • leprosy

hereditary

  • charcot-marie-tooth disease
79
Q

patient has UMN and LMN signs.

what 3 things should you look for/ask the examiner to confirm the diagnosis of MND?

A

never invovlement of the bladder

never involvement of the extra-ocular muscles

never any sensory signs

80
Q

what are the causes of a ptosis?

A

unilateral

  • CN III
  • horner’s
  • multiple sclerosis

(distiguishing question: is the pupil large, small or normal?)

bilateral

  • dystrophia myotonica
  • myaesthenia gravis, lambert eaton myaesthenic syndrome
  • bialteral horner’s syndrome
81
Q

what are the causes of a CN III palsy?

A

medical (eye movements first)

  • diabetes
  • hypertension
  • microembolism from carotid arteries

surgical (mydriasis first)

  • painful = aneurysm (posterior communicating artery)
  • trauma
  • bleed
82
Q

what are the causes of a CN VI palsy?

A

medical

  • diabetes
  • hypertension
  • multiple sclerosis
  • intracranial hypertension
    • has longest intracranial course. pressure will compress the nerve against the petrous part of the temporal bone -> palsy
83
Q

what are the physical signs associated with intracranial hypertension?

A
  1. loss of retinal vein pulsation on fundoscopy
  2. reduced GCS
  3. CN VI palsy
  4. CN III palsy
  5. papilloedema (late)
  6. cushing’s triad
    • hypertension
    • bradycardia
    • Cheyne-Stokes respiration)
84
Q

what is the differential diagnosis for spastic paraparesis?

A

brain

  • stroke
  • multiple sclerosis

cord

  • cervical spondylosis
  • cerebral palsy
  • motor neuron disease
  • syringomyelia

emergency

  • cord compression
85
Q

what are the questions you have to ask to rule out a sinister cause of spinal back pain?

A
  • erectile dysfunction (nocturnal erections)
  • urinary retention
  • faecal incontinence
  • change in the sensation as you pass urine?
  • perianal sensation
86
Q

genetics of neurofibromatosis

A

type 1 - autosomal dominant, micodeletion syndrome of a gene on chromosome 17

type 2 - autosomal dominant, mincrodeletion syndrome of a gene on chromosome 22

both can arise de novo in a significant proportion of patients

87
Q

what are the rules for the cafe-au-lait spots in NF?

A

must have more than 5

must be >15 mm diameter

88
Q

what are the medical complications of type 1 NF?

A
  • hypertension (phaeochromocytoma)
  • SpLD
  • malignant transformation in 10% of cases
  • thoracic kyposis, T2RF
89
Q

which is the muscle in the inner ear affected by CN VII lesions that leads to hyperacusis?

A

stapedius