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Y4 Neuro and Special Senses > Neurology 2 > Flashcards

Neurology 2 Flashcards

1
Q

What is essential tremor?
What makes it worse? What makes it better?

A

an autosomal dominant condition which usually affects both upper limbs

Symmetrical fine tremor (6-12 Hz)

postural: worse if arms outstretched
worse with tiredness, caffeine and stress

improved by alcohol and rest, completely absent during sleep

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2
Q

Other than the hands, where may be affceted by essential tremor?

A

head tremor, jaw tremor and vocal tremor

most common cause of titubation (head tremor)

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3
Q

How can essential tremor be managed?

A

propranolol is first-line

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4
Q

Give some ddx for a patient with tremor?

A

Essential tremor
Parkinson’s disease
Dopamine antagonists (e.g. antipsychotics)
Multiple sclerosis
Huntington’s chorea
Hyperthyroidism
Fever
Anxiety

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5
Q

What is Horner’s syndrome?

A

Triad of:
miosis (small pupil)
ptosis
anhidrosis (loss of sweating one side)

May include enophthalmos (sunken eye)

Caused by damage to the sympathetic nervous system supplying the face

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6
Q

How can you distinguish between causes of Horner’s syndrome based on clinical signs alone?

A

heterochromia (difference in iris colour) is seen in congenital Horner’s

Anhidrosis of the face, arm and trunk = central lesion

Anhidrosis of the face = pre-ganglionic lesion

No anhidrosis = post ganglionic lesion

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7
Q

How can you test for Horner’s syndrome pharmacologically?

A

apraclonidine drops (an alpha-adrenergic agonist) can be used: causes pupillary dilation in Horner’s syndrome but produces mild pupillary constriction in the normal pupil

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8
Q

What is the classical history of an acoustic neuroma?

A

a combination of vertigo, hearing loss, tinnitus and an absent corneal reflex

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9
Q

What may cause bilateral acoustic neuromas?

A

neurofibromatosis type 2

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10
Q

How should patients with a suspected acoustic neuroma be investigated and managed?

A

referred urgently to ENT

MRI of the cerebellopontine angle
Audiometry: only 5% of patients will have a normal audiogram.

Mx = surgery, radiotherapy or observation

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11
Q

What can be seen on this MRI?

A

vestibular schwannoma (acoustic neuroma) of the right cerebellopontine angle

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12
Q

What is Subacute combined degeneration of the spinal cord?

A

impairment of the lateral corticospinal tracts, dorsal columns and spinocerebellar tracts due to vitamin B12 deficiency

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13
Q

What sxs may dorsal column involvement in subacute combined degeneration of the cord present with?

A

distal tingling/burning/sensory loss is symmetrical and tends to affect the legs more than the arms
impaired proprioception and vibration sense

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14
Q

What sxs may lateral corticospinal tract involvement in subacute combined degeneration of the cord present with?

A

muscle weakness, hyperreflexia, and spasticity
upper motor neuron signs typically develop in the legs first
brisk knee reflexes
absent ankle jerks
extensor plantars

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15
Q

What sxs may spinocerebellar tract involvement in subacute combined degeneration of the cord present with?

A

sensory ataxia → gait abnormalities
positive Romberg’s sign

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16
Q

How can subacute combined degeneration of the spinal cord be managed?

A

high-dose vitamin B12 supplementation

can help to reverse the neurological symptoms and prevent further damage

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17
Q

Cavernous sinus thrombosis (CST) refers to the formation of a clot within the cavernous sinus.

What causes this?

A

most common cause of CST is infection

typically spreads from an extracranial location such as the orbit, paranasal sinuses, or the ‘danger zone’ of the face

Infection is able to spread due to the anastomosis between the facial vein and superior ophthalmic veins

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18
Q

How may cavernous sinus thrombosis present?

A

headache, unilateral periorbital oedema, proptosis (eye bulging), photophobia and cranial nerve palsies

the abducens nerve (CN VI) is most commonly affected

If it is due to infection, it can rapidly progress to meningitis, so requires prompt tx with abx

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19
Q

A pituitary adenoma is a benign tumour of the pituitary gland. They account for around 10% of adult brain tumours.

How may they be classified?

A

Pituitary adenomas can be classified according to:
size (a microadenoma is <1cm and a macroadenoma is ≥1cm)

hormonal status (a secretory/functioning adenoma produces an excess of a particular hormone and a non-secretory/functioning adenoma does not)

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20
Q

What is the most common type of pituitary tumour?

A

Prolactinomas are the most common type

After prolactinomas, non-secreting adenomas are the next most common, then GH-secreting and then ACTH-secreting adenomas.

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21
Q

How may pituitary tumours present?

A

excess of a hormone (e.g. Cushing’s disease due to excess ACTH, acromegaly due to excess GH or amenorrhea and galactorrhea due to excess prolactin)

depletion of a hormon / generalised hypopituiatrism (due to compression of the normal functioning pituitary gland)

stretching of the dura around the pituitary fossa (causing headaches)

compression of the optic chiasm (causing a bitemporal hemianopia due to crossing nasal fibers)

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22
Q

How may pituitary adenomas be investigated?

A

a pituitary blood profile (including GH, prolactin, ACTH, FSH, LSH and TFTs)
formal visual field testing
MRI brain with contrast

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23
Q

Give some ddx for a pituitary adenoma

A

pituitary hyperplasia
craniopharyngioma
meningioma
brain metastases
lymphoma
hypophysitis
vascular malformation (e.g. aneurysm)

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24
Q

How may pituitary adenomas be managed?

A

medical therapy:
prolactinomas = dopamine agonists (cabergoline or bromocriptine)
GH-secreting adenomas= somatostatin analogues (e.g. octreotide)

transsphenoidal surgery:
non-functioning adenomas are generally diagnosed due to their compressive symptoms - surgery is therefore the first-line treatment

radiotherapy: for residual or recurrent tumours post-surgery

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25
Q

What is Wernicke’s encephalopathy?

A

a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics

classic triad of ophthalmoplegia/nystagmus, ataxia and encephalopathy may occur

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26
Q

What features may Wernicke’s encephalopathy present with?

A

oculomotor dysfunction:
nystagmus (the most common ocular sign)
ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy

gait ataxia

encephalopathy: confusion, disorientation, indifference, and inattentiveness

peripheral sensory neuropathy

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27
Q

How may Wernicke’s encephalopathy be investigated and managed?

A

Investigations:
bloods: decreased red cell transketolase
MRI

Treatment is with urgent replacement of thiamine

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28
Q

What is Korsakoff’s syndrome?

A

Wernicke’s encephalopathy with the addition of antero- and retrograde amnesia and confabulation

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29
Q

What is Argyll Robertson pupil?

A

Classic pupillary syndrome

Small, irregular pupils
Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

Causes: diabetes mellitus, syphilis

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30
Q

What is Creutzfeldt-Jakob disease (CJD)?

A

rapidly progressive neurological condition caused by prion proteins

Sporadic CJD accounts for 85% of cases

presents with dementia (rapid onset) and myoclonus

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31
Q

How can CJD be investigated?

A

CSF is usually normal
EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
MRI: hyperintense signals in the basal ganglia and thalamus

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32
Q

What is Syringomyelia?

What can cause it?

A

Syringomyelia (‘syrinx’ for short) is a collection of CSF within the spinal cord.

Causes include:
a Chiari malformation: strong association
trauma
tumours
idiopathic

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33
Q

How does Syringomyelia present?

A

‘cape-like’ (neck, shoulders and arms) loss of sensation to temperature

spastic weakness (predominantly of the lower limbs)

neuropathic pain

autonomic features:
Horner’s syndrome
bowel and bladder dysfunction

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34
Q

What causes the cape like loss of sensation in Syringomyelia?

A

loss of sensation to temperature but the preservation of light touch, proprioception and vibration

this is due to the crossing spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected

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35
Q

How can Syringomyelia be investigated and managed?

A

Investigations:
full spine MRI with contrast to exclude a tumour or tethered cord
a brain MRI is also needed to exclude a Chiari malformation

Tx: shunt into the Syringomyelia

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36
Q

What is Hypoxic ischaemic encephalopathy (HIE)?

A

prolonged or severe hypoxia leading to ischaemic brain damage in neonates

should be suspected when there are events that could lead to hypoxia during birth, acidosis (pH < 7) on the umbilical artery blood gas, poor Apgar scores, or evidence of multi organ failure

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37
Q

What are the potential complications of HIE?

A

cerebral palsy and death

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38
Q

What may cause HIE?

A

Maternal shock
Intrapartum haemorrhage
Prolapsed cord, causing compression of the cord during birth
Nuchal cord, where the cord is wrapped around the neck of the baby

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39
Q

How can HIE be managed?

A

supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures

therapeutic hypothermia

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40
Q

How does a third nerve (oculomotor) palsy present?

A

eye is deviated ‘down and out’
ptosis
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)

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41
Q

What may cause a third nerve palsy?

A

diabetes mellitus

vasculitis e.g. temporal arteritis, SLE

posterior communicating artery aneurysm (pupil dilated, often associated pain)

cavernous sinus thrombosis

Weber’s syndrome: ipsilateral third nerve palsy with contralateral hemiplegia - caused by midbrain strokes

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42
Q

What is the main function of the 4th cranial nerve (trochlear) ?

A

supplies superior oblique (depresses eye, moves inward)

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43
Q

What are the features of a 4th nerve (trochlear) palsy?

A

when looking straight ahead, the affected eye appears to deviate upwards and is rotated outwards

vertical diplopia
classically noticed when reading a book or going downstairs

subjective tilting of objects (torsional diplopia)

the patient may develop a head tilt

44
Q

What is Progressive supranuclear palsy? (aka Steele-Richardson-Olszewski syndrome)

A

a ‘Parkinson Plus’ syndrome

Parkinsonism: bradykinesia is prominent

postural instability and falls = stiff, broad-based gait

impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)

cognitive impairment: primarily frontal lobe dysfunction

45
Q

What can cause ulnar nerve damage at the elbow?

A

Trauma at the level of the medial epicondyle (e.g. isolated medial epicondyle fracture, supracondylar fracture). It can also be compressed in the cubital tunnel.

46
Q

What can cause ulnar nerve damage at the wrist?

A

Lacerations to the anterior wrist.

47
Q

How does ulnar nerve palsy caused by damage at the wrist present?

A

‘claw hand’ - hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits

wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)

wasting and paralysis of hypothenar muscles

sensory loss to the medial 1 1/2 fingers (palmar and dorsal aspects)

48
Q

How does ulnar nerve palsy present caused by damage at the elbow?

A

less severe claw hand deformity even though the lesion is more proximal (ulnar paradox)

radial deviation of the wrist

49
Q

What is Froment’s Sign?

A

Patient holds a piece of paper between their thumb and index finger which is then pulled away

Tests fo adductor pollicis muscle function

A positive Froment’s sign = the patient is unable to hold the paper and will flex the flexor pollicis longus to compensate (flexion of thumb at interphalangeal joint)

Suggests ulnar nerve palsy

50
Q

What is radiculopathy?

A

a conduction block in the axons of a spinal nerve or its roots, with impact on motor axons causing weakness and on sensory axons causing paraesthesia

51
Q

What red flags should you screen for in patients with radiculopathy?

A

Faecal incontinence
Urinary retention (painless, with secondary overflow incontinence)
Saddle anaesthesia

52
Q

Radiculopathy is most commonly a result of nerve compression, which can be caused by a wide range of pathology.

How can it be managed?

A

Treat underlying cause of the compression

Analgesia for associated radicular pain - Amitriptyline is usually first line, or pregabalin and gabapentin as alternatives

Physiotherapy

53
Q

Foot drop is a result of weakness of the foot dorsiflexors. What can cause this?

A

common peroneal nerve lesion - the most common cause
L5 radiculopathy
sciatic nerve lesion
superficial or deep peroneal nerve lesion
central nerve lesions (e.g. stroke)

54
Q

What can cause common peroneal nerve lesions?

A

secondary to compression at the neck of the fibula

Precipitants:
certain positions such as leg crossing, squatting or kneeling
prolonged confinement
recent weight loss
Baker’s cysts
plaster casts to the lower leg

55
Q

How may foot drop present on examination?

A

isolated peroneal neuropathy = weakness of foot dorsiflexion and eversion, normal reflexes

L5 radiculopathy= weakness of hip abduction

56
Q

How should foot drop be managed?

A

Bilateral symptoms, fasiculations or other abnormal neurological findings (e.g. hyperreflexia) are indications for specialist referral

If the examination suggests a peroneal neuropathy then conservative management
Leg crossing, squatting and kneeling should be avoided Symptoms typically improve over 2-3 months

57
Q

What is thoracic outlet syndrome (TOS)?

A

a disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet

TOS can be neurogenic (90%) or vascular

58
Q

What causes TOS to occur?

A

when neck trauma occurs to individuals with anatomical predispositions

a well-known associated osseous anomaly is the presence of cervical rib

59
Q

How does neurogenic TOS present?

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

60
Q

How can vascular TOS present?

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

61
Q

How should thoracic outlet syndrome patients be examined?

A

neurological examination and musculoskeletal examination are necessary

stress manoeuvres such as Adson’s manoeuvres may be attempted

careful examinations to rule out other pathologies of the cervical spine, the shoulder or peripheral nerves incl. cervical radiculopathy, shoulder injuries and carpal tunnel syndrome

62
Q

How should thoracic outlet syndrome be investigated?

A

chest and cervical spine X rays to check for any obvious osseous abnormalities e.g. cervical ribs, exclude malignant tumours or cervical spine degenerative changes

CT or MRI to rule out cervical root lesions

venography or angiography may be helpful in vascular TOS

an anterior scalene block may be used to confirm neurogenic TOS and check the likelihood of successful surgical treatment

63
Q

How should thoracic outlet syndrome be managed?

A

Neurogenic TOS:
1st line: conservative management with education, rehabilitation, physiotherapy, or taping

surgical decompression where conservative management has failed especially if there is a physical anomaly. Early intervention may prevent brachial plexus degeneration

Vascular TOS:
surgical treatment may be preferred

64
Q

What is the most common cause of brain tumours?

A

metastatic brain cancer

65
Q

Which cancers most commonly metastasise to the brain?

A

lung (most common)
breast
bowel
skin (namely melanoma)

66
Q

Glioblastoma multiforme is the most common primary brain tumour in adults and is associated with a poor prognosis (< 1 yr).

Describe its key features. How can it be managed?

A

Key features:
Imaging: solid tumours with central necrosis and a rim that enhances with contrast
Histology: Pleomorphic tumour cells border necrotic areas

Mx:
surgical with postoperative chemotherapy / radiotherapy
Dexamethasone is used to treat the oedema

67
Q

Meningiomas are the second most common primary brain tumour in adults.

What are their key features?
How can they be investigated and managed?

A

benign CNS tumours
typically located next to the dura and cause symptoms by compression

IX: CT (will show contrast enhancement) and MRI
Mx: observation, radiotherapy or surgical resection

68
Q

What is the most common primary brain tumour in children?

A

Pilocytic astrocytoma

69
Q

What may cause a brain abscess?

A

extension of sepsis from middle ear or sinuses
trauma or surgery to the scalp
penetrating head injuries
embolic events from endocarditis

70
Q

What sxs and signs may suggest the presence of a brain abscess?

A

headache: dull, persistent
fever
focal neurology e.g. oculomotor nerve palsy or abducens nerve palsy secondary to raised ICP

71
Q

How can brain abscesses be investigated and managed?

A

Ix: CT brain

Mx:
craniotomy is performed and the abscess cavity debrided
IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
ICP management: e.g. dexamethasone

72
Q

Brown Sequard syndrome is caused by lateral hemisection of the spinal cord.

What features does it present with?

A

ipsilateral weakness below lesion (loss of corticospinal tracts)
ipsilateral loss of proprioception and vibration sensation (loss of dorsal columns)
contralateral loss of pain and temperature sensation (loss of spinothalamic tracts which decussate)

73
Q

What are the components of the CSF?

A

Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3

74
Q

What are the 4 main types of aphasia?

A
75
Q

What is Wernicke’s aphasia?

A

Also known as receptive aphasia
Occurs due to a lesion of the superior temporal gyrus

The superior temporal gyrus (Wernicke’s area) is where comprehension of speech happens and speech is ‘formed’ before being sent to Broca’s area which is involved in the motor control of speech.

Comprehension is impaired but motor control is intact - speech is fluent but does not make sense (e.g. word salad)

76
Q

What is Broca’s aphasia?

A

Also known as expressive aphasia

Due to a lesion of the inferior frontal gyrus (Broca’s area)

Comprehension is intake, but speech is non-fluent and halting.

77
Q

What is a conduction aphasia?

A

Classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area

Comprehension is normal and speech is fluent but repetition is poor due to delay in the connection between the comprehension and the motor areas.

78
Q

What is global aphasia?

A

Expressive and receptive aphasia

Due to large lesion affected Wernicke’s area, Broca’s area, and the connecting tissue.

79
Q

What is Arnold-Chiari malformation?

A

herniation of the cerebellar tonsils through the foramen magnum - may be congenital or traumatic

Features
non-communicating hydrocephalus may develop as a result of obstruction of CSF outflow
headache
syringomyelia

80
Q

What is autonomic dysreflexia?

A

clinical syndrome that occurs in patients who have had a spinal cord injury at, or above T6 spinal level

Afferent signals, most commonly triggered by faecal impaction or urinary retention cause a sympathetic spinal reflex. The balancing parasympathetic response is blocked by the cord lesion.

81
Q

How does autonomic dysreflexia present? How may it be managed?

A

extreme hypertension (may lead to stroke)
flushing and sweating above the level of the cord lesion
agitation

Mx: removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.

82
Q

Do unilateral cerebellar lesions cause contralateral or ipsilateral signs?

A

Ipsilateral

83
Q

What are the sxs of cerebellar disease?

A

DANISH

D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’
A - Ataxia (limb, truncal)
N - Nystamus (horizontal = ipsilateral hemisphere)
I - Intention tremour
S - Slurred staccato speech, Scanning dysarthria
H - Hypotonia

84
Q

Give some causes of cerebellar syndrome?

A

MD FANS

MS
Drugs

Friedrich’s Ataxia
Alcohol
Neoplasm/paraneoplasms
Stroke

85
Q

What is the DVLA guidance for a first unprovoked seizure in suspected epilepsy?

A

6 months off driving if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG

If these conditions are not met then this is increased to 12 months

86
Q

What is the DVLA guidance for patients with established epilepsy?

A

may qualify for a driving licence if they have been free from any seizure for 12 months

if there have been no seizures for 5 years (with medication if necessary) a ‘til 70 licence is usually restored

87
Q

What is the DVLA guidance for people with epilepsy who are withdrawing from medication ?

A

should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose

88
Q

What is the DVLA guidance post syncope?

A

simple faint: no restriction
single episode, explained and treated: 4 weeks off
single episode, unexplained: 6 months off
two or more episodes: 12 months off

89
Q

What is the DVLA guidance post stroke/TIA?

A

1 month off driving, may not need to inform DVLA if no residual neurological deficit

90
Q

What is the DVLA guidance for patients who have had multiple strokes in a short space of time?

A

3 months off driving and inform DVLA

91
Q

What is the DVLA guidance for patients with chronic neurological disorders e.g. multiple sclerosis, motor neuron disease?

A

DVLA should be informed, complete PK1 form (application for driving licence holders state of health)

92
Q

What is the DVLA guidance post craniotomy?

A

1 year off driving

93
Q

Neurofibromatosis Type 1 is an autosomal dominant genetic condition. How does it present?

A

Cafe-au-lait spots, axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas in > 90%
Scoliosis
Pheochromocytomas

94
Q

Neurofibromatosis Type 2 is also an autosomal genetic condition. How does it present?

A

Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas

95
Q

Pituitary apoplexy is sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction.

What may precipitate this?

A

hypertension
pregnancy
trauma
anticoagulation

96
Q

How does pituitary apoplexy present?

A

sudden onset headache
vomiting
neck stiffness
visual field defects
extraocular nerve palsies
features of pituitary insufficiency
e.g. hypotension secondary to hypoadrenalism

97
Q

How can pituitary apoplexy be investigated and managed?

A

Investigation: MRI is diagnostic

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

98
Q

Outline the spinal tracts affected in Brown Sequard syndrome and the resultant sxs

A
  1. Lateral corticospinal tract - Ipsilateral spastic paresis below lesion
  2. Dorsal columns - Ipsilateral loss of proprioception and vibration sensation
  3. Lateral spinothalamic tract- Contralateral loss of pain and temperature sensation
99
Q

Outline the spinal tracts affected in Subacute Combined Degeneration of the Cord and the resultant sxs

A
  1. Lateral corticospinal tracts - Bilateral spastic paresis
  2. Dorsal columns - Bilateral loss of proprioception and vibration sensation
  3. Spinocerebellar tracts - Bilateral limb ataxia
100
Q

Outline the spinal tracts affected in Anterior Spinal Artery Occlusion and the resultant sxs

A
  1. Lateral corticospinal tracts - Bilateral spastic paresis
  2. Lateral spinothalamic tracts - Bilateral loss of pain and temperature sensation
101
Q

Outline the spinal tracts affected in Syringiomyelia and the resultant sxs

A
  1. Ventral horns - Flacid paresis (typically affecting the intrinsic hand muscles)
  2. Lateral spinothalamic tract - Loss of pain and temperature sensation
102
Q

What part of the spinal cord is affected by Neurosyphilis (tabes dorsalis)? What are the resultant sxs?

A

Dorsal columns - Loss of proprioception and vibration sensation

103
Q

What is Tuberous sclerosis (TS) ?

A

a genetic condition of autosomal dominant inheritance

Cutaneous features:
depigmented ‘ash-leaf’ spots
roughened patches of skin over lumbar spine (Shagreen patches)
adenoma sebaceum (angiofibromas): butterfly distribution over nose
cafe-au-lait spots

Neurological features:
developmental delay, intellectual impairment
epilepsy (infantile spasms or partial)

104
Q

What is Huntington’s disease?

A

an autosomal dominant neurodegenerative condition

trinucleotide repeat disorder: repeat expansion of CAG

typically results in death 20 years after appearance of sxs

105
Q

What features may Huntington’s disease present with?

A

Features typical develop after 35 years of age:
chorea
personality changes (e.g. irritability, apathy, depression) and intellectual impairment
dystonia
saccadic eye movements

106
Q

As Huntington’s disease is a trinucleotide repeat disorder, the phenomenon of anticipation may be seen.

What does this mean?

A

the disease is presents at an earlier age in successive generations

Y4 Neuro and Special Senses (21 decks)

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