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Phase 3a topics > general neuro > Flashcards

general neuro Flashcards

1
Q

what lobe?
seizure

Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing/plucking), Deja vu/Dysphasia post-ictal)

A

Temporal lobe (HEAD)

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2
Q

What lobe seizure?

Head/leg movements, posturing, post-ictal weakness, Jacksonian march

A

Frontal lobe (motor)

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3
Q

what lobe seizure?

paraesthesia

A

Parietal lobe (sensory)

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4
Q

what lobe seizure?

floaters/flashes

A

Occipital lobe (visual)

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5
Q

Brain scan where does encephalitis classically affect

A

temporal lobe

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6
Q

Hypsarrhythmia on EEG

A

Infantile spasms (west’s syndrome)

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7
Q

What birth defects are sodium valproate associated with

A

neural tube defects

hypospadias most common

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8
Q

epilepsy management pregnancy

A

aim for mono therapy

lamotrigine is often best choice

5mg folic acid prior to getting pregnant if possible

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9
Q

Normal lumbar puncture result

A

clear appearance

glucose 70% of plasma

protein 0.3 g/l

WCC 2 per mm^3 (neuts)

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10
Q

Bacterial meningitis LP result

A

Cloudy

Glucose low (< 1/2 plasma) bacteria using up the glucose

Protein high (> 1 g/l) bacteria releasing proteins

WCC 10 - 5,000 polymorphs/mm³ the immune system releases neutrophils in response to bacteria

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11
Q

Viral meningitis LP result

A

Clear/cloudy

Glucose 60-80% of plasma glucose* viruses don’t really use glucose

Protein normal/raised viruses may release a small amount of protein

WCC 15 - 1,000 lymphocytes/mm³ the immune system releases lymphocytes in response to viruses

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12
Q

Tuberculous LP result

A

Slight cloudy, fibrin web

glucose Low (< 1/2 plasma)

Protein high >1g/l

WCC 30-300 lymphocytes/mm3

The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)

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13
Q

Management of brain abscess?

A

surgery - craniotomy

IV antibiotics: IV 3rd-generation cephalosporin + metronidazole

intracranial pressure management: e.g. dexamethasone

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14
Q

EEG : 3Hz generalized, symmetrical

A

absence seizures

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15
Q

EEG centro-temporal spikes

A

Benign rolandic epilepsy

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16
Q

Contraindications to lumbar puncture

A

focal neurological signs
papilloedema
significant bulging of the fontanelle
disseminated intravascular coagulation
signs of cerebral herniation

For patients with meningococcal septicaemia a lumbar puncture is contraindicated - blood cultures and PCR for meningococcus should be obtained.

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17
Q

Degenerative cervical myelopathy

A

Presentation: myelopathy: pain (affecting the neck, upper or lower limbs) loss of fine motor function (dexterity, clumsy) loss of sensory function causing numbness, loss of autonomic function, hoffmans

Causes: Cervical spondylosis (osteophyte), disc herniation

Investigation: MRI

Management: decompressive surgery

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18
Q

Neoplastic spinal cord compression

A

Presentation: cancer patient, back pain, bilateral weakness, UMN signs. First symptom: back pain

Investigation: MRI of whole spine

Management: high dose dexamethasone and oncology assessment

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19
Q

Brown-sequard syndrome

A
  • ipsilateral dorsal column signs
  • ipsilateral corticospinal tract signs
  • contralateral spinothalamic tract signs
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20
Q

Subacute combined degeneration of spinal cord

A

Presentation: bilateral dorsal column signs, may have bilateral corticospinal tract signs (affects posterior cord)

Cause: B12 deficiency

Prevention: Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord

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21
Q

Friedrich’s ataxia

A

Presentation: teenage corticospinal, spinocerebellar, dorsal column and peripheral nerves

Information: autosomal recessive trinucleotide repeat disorder resulting in reduced level or function of the frataxin protein.

Investigation: genetic analysis

Management: supportive

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22
Q

Syringomyelia

A

Pathophysiology: development of a fluid-filled cyst (a syrinx) around the spinal canal.

Causes: Chiari malformation, tumour, trauma

Presentation: ‘central cord syndrome’ bilateral spinothalamic and/or bilateral corticospinal tract symptoms. The upper limbs are affected first whilst the lower limbs are spared until much later. As the fibres of the spinothalamic tract enter the spinal cord and immediately decussate, they pass close to the spinal canal, meaning they are often the first of these white matter fibres to be compressed and damaged. As the cervical cord is the most likely location of the lesion, there is classically said to be a “cape-like” loss of pain and temperature sensation.

Investigation: full spine MRI with contrast and brain MRI

Management: treat cause. If persistent : shunt

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23
Q

Lumbar spinal stenosis

A

Presentation: back pain, bilateral leg weakness or unilateral, positional element: better on walking up hill and sitting forward. Ddx claudication

Investigation: MRI

Management: Laminectomy

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24
Q

Ankylosing spondylitis

A

Presentation: young man, lower back pain and stiffness, worse in morning
Investigation: plain x ray of sacroiliac joints
Management: encourage regular exercise such as swimming, NSAIDs are the first-line treatment, physiotherapy

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25
Q

Myelopathy vs radiculopathy

A

Myelopathy: bilateral as spinal cord and bladder/bowel, not always painful “clumsiness” “loss of manual dexterity”

Radiculopathy: radiating limb pain, often in the pattern of the dermatome, sharp/shooting in character, with only a small proportion (about 5%) having associated neurologic symptoms such as dermatomal sensory loss, and even less commonly myotomal muscle weakness.

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26
Q

Myotomes upper limb

A

C5 – Elbow flexion (and shoulder abduction)
C6 – Wrist extension (and shoulder adduction) (and elbow flexion)
C7 – Elbow extension (and wrist flexion)
C8 – Finger flexion and thumb extension
T1 – Finger abduction

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27
Q

Myotomes lower limb

A

L2 – Hip flexion
L3 – Knee extension
L4 – Ankle dorsiflexion
L5 – Great toe extension
S1 – Ankle plantarflexion

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28
Q

Dermatome Thumb + index finger

A

C6

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29
Q

Dermatome middle finger + palm of hand

A

C7

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30
Q

Dermatome ring + little finger

A

C8

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31
Q

Dermatome nipples

A

T4

T4 at the Teat Pore

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32
Q

Dermatome xyphoid process

A

T6

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33
Q

Dermatome umbillicus

A

T10

BellybuT-TEN

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34
Q

Dermatome inguinal ligament

A

L1

L for ligament, 1 for 1nguinal

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35
Q

Dermatome knee caps

A

L4

Down on aLL fours - L4

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36
Q

Dermatome big toe, dorsum of foot (except lateral aspect)

A

L5

Largest of the 5 toes

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37
Q

Dermatome Lateral foot, small toe

A

S1

the smallest 1

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38
Q

Dermatome genetalia

A

S2, S3

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39
Q

Cauda equina most common cause

A

central disc prolapse at L4/5 or L5/S1

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40
Q

Parkinsons disease tremor

A

Unilateral resting tremor (improves with voluntary movement)

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41
Q

Causes of drug-induced parkinsonism

A

Antipsychotics or antiemetic metoclopramide can cause EPSE.

In patients with parksinons, prescribe antiemetic domperidone as it doesn’t cross BBB therefore doesn’t cause EPSE

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42
Q

Invetsigation lewy-body

A

SPECT/DaTSCAN

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43
Q

Glasgow coma scale components and scoring

A

Glasgow coma scale (GCS) out of 15

Motor response
6. Obeys commands
5. Localises to pain
4. Withdraws from pain
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None

Verbal response
5. Orientated
4. Confused
3. Words
2. Sounds
1. None

Eye opening
4. Spontaneous
3. To speech
2. To pain
1. None

If pt awake:
Hello mr/mrs x, my name is Ailsa I’m…
do you know where you are at the moment?
what year is it?
where do you live?
can you squeeze my finger?

If pt eyes closed:
Hello mr/mrs x, my name is Ailsa I’m…
can you open your eyes for me?
can you squeeze my fingers for me?
do you know where you are at the moment?
test pain repsonse

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44
Q

MRC power grades

A

Grade 0
No muscle movement

Grade 1
Trace of contraction

Grade 2
Movement at the joint with gravity eliminated

Grade 3
Movement against gravity, but not against added resistance

Grade 4
Movement against an external resistance with reduced strength

Grade 5
Normal strength

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45
Q

Reflex nerve roots

A

Ankle = S1
Miss out 2
Knee = L3,4
Brachioradialis = C5,6
Biceps = C5,6
Triceps = C7

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46
Q

Causes and ddx features cranial third nerve palsy

A

Surgical third nerve palsy : painful, dilated pupil
- posterior communicating artery aneurysm

Diabetes : not painful, reactive pupil

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47
Q

Bell’s palsy

presentation and management

A

lower motor neuron facial nerve palsy - forehead affected

oral prednisolone within 72 hours

if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT

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48
Q

When should IV thrombolysis with mechanical thrombectomy be offered for ischaemic stroke?

A

Thrombectomy within 6 hours of onset
Thrombolysis within 4.5 hours onset

Both if occlusion if proximal anterior circulation on CTA or MRA

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49
Q

Wernikes aphasia

Presentation
Location

A

Receptive aphasia

Fluent speech, doesn’t make any sense, comprehension impaired

Lesion in superior temporal gurus

Supplied by inferior division of left MCA

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50
Q

Brocas aphasia

Presentation
Location
Blood supply

A

Non-fluent laboured and halting speech. Repetition impaired (expressive)

Inferior frontal gyrus
Superior division of left MCA

Spoken word is heard at the ear. This passes to Wernicke’s area in the temporal lobe (near the ear) to comprehend what was said. Once understood, the signal passes along the arcuate fasciculus, before reaching Broca’s area. The Broca’s area in the frontal lobe (near the mouth) then generates a signal to coordinate the mouth to speak what is thought (fluent speech).

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51
Q

Conduction aphasia

Presentation
Location

A

Speech fluent but repetition is poor
Aware of errors

Arcuate fasiculus (connection between brocas and wernikes)

Spoken word is heard at the ear. This passes to Wernicke’s area in the temporal lobe (near the ear) to comprehend what was said. Once understood, the signal passes along the arcuate fasciculus, before reaching Broca’s area. The Broca’s area in the frontal lobe (near the mouth) then generates a signal to coordinate the mouth to speak what is thought (fluent speech).

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52
Q

UMN signs

A

Minimal muscle atrophy

Weakness ‘Pyramidal’ pattern i.e. weakness of upper limb extensors, lower limb flexors So upper limb is flexed and lower limb extended (think hemiplegic gait)

Slightly reduced power

Hyperreflexia of deep tendon reflexes- as no UMN regulating that reflex

Absent superficial reflex - babinski positive

Hypertonia + or - clonus (Spasticity occurs in pyramidal tract lesions) such as clonus and clasp-knife rigidity

Pronator drift

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53
Q

management of extradural hematoma

A

stabilising the patient followed by surgical intervention with a burr hole or craniotomy to evacuate the haematoma.

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54
Q

blood vessel implicated by extradural hematoma

A

middle meningeal artery

eminem getting hit by a lemon

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55
Q

ct scan subdural hematoma

A

concave crescent-shaped

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56
Q

blood vessel implicated in subdural hematoma

A

bridging veins

old man drinking alcohol in a cave with a bridge outside and a crescent moon in the sky

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57
Q

management subdural hematoma

A

Small or incidental acute subdurals can be observed conservatively.

If big or signs then surgical options include monitoring of intracranial pressure and decompressive craniectomy.

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58
Q

Causes SAH

A

Ruptured cerebral aneurysm or trauma

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59
Q

conditions associated with berry aneurysms

A

adult polycystic kidney disease

Ehlers-Danlos syndrome

Coarctation of the aorta

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60
Q

ct scan for SAH

A

Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

may be normal - do LP

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61
Q

lumbar puncture for SAH

A

LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).

Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).

As well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure

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62
Q

invetsigation after spontaneous SAH confirmed?

A

CT intracranial angiogram

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63
Q

Management SAH

A
  1. referral to neurosurgery after confirmation
  2. coil by interventional radiologists
  3. or craniotomy
  4. 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature)
  5. Hydrocephalus is temporarily treated with an external ventricular drain
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64
Q

treatment of radiculopathy

A

Similar to that of other musculoskeletal lower back pain: analgesia, physiotherapy, exercises

If symptoms persist after 4-6 weeks then referral for consideration of MRI is appropriate

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65
Q

narcolepsy associations

A

associated with HLA-DR2

it is associated with low levels of orexin (hypocretin), a protein which is responsible for controlling appetite and sleep patterns

early onset of REM sleep

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66
Q

features narcolepsy

A

typical onset in teenage years
hypersomnolence
cataplexy (sudden loss of muscle tone often triggered by emotion)
sleep paralysis
vivid hallucinations on going to sleep or waking up

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67
Q

investiagtions narcolepsy

A

multiple sleep latency EEG

polysomnography

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68
Q

management narcolepsy

A

daytime stimulants (e.g. modafinil) and nighttime sodium oxybate

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69
Q

what CN palsy may be present in IIH

A

6th

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70
Q

Contralateral hemiparesis and sensory loss, lower extremity > upper

A

Anterior cerebral artery

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71
Q

Contralateral hemiparesis and sensory loss, upper extremity > lower, Contralateral homonymous hemianopia, Aphasia

A

Middle cerebral artery

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72
Q

Contralateral homonymous hemianopia with macular sparing, Visual agnosia

A

Posterior cerebral artery

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73
Q

Ipsilateral CN III palsy, Contralateral weakness of upper and lower extremity

A

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

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74
Q

Ipsilateral: facial pain and temperature loss, Contralateral: limb/torso pain and temperature loss, Ataxia, nystagmus

A

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

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75
Q

Ipsilateral: facial paralysis and deafness

vertigo and vomiting

A

Anterior inferior cerebellar artery (lateral pontine syndrome)

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76
Q

a curtain coming down over their vision and episodes often recur.

A

Retinal/ophthalmic artery- Amaurosis fugax is a term used to describe transient monocular visual loss due to atherosclerosis of the ipsilateral internal carotid artery which causes lack of blood flow to central retinal artery

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77
Q

complete paralysis of voluntary muscles, very low GCS

A

Basilar artery- locked in syndrome

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78
Q

contralteral symptoms: either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia

A

“Lacunar strokes - common sites include the basal ganglia, thalamus and internal capsule
“

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79
Q

contralateral hemiparesis/hemisensory loss of face arma dn leg, higher cog dysfunction such as aphasia, homonymous hemianopia

A

total anteroir ciruclation infact, if only 2 = partial

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80
Q

Bitemporal hemianopia

A

Midline lesion at chiasm

upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

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81
Q

Right nasal hemianopia

A

Lesion involving right perichaismal area

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82
Q

Left homonymous hemianopia

A

Lesion or pressure on right optic tract (posterior to chiasm, before optic radiations)

Lesion or pressure across all right optic radiations

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83
Q

Left homonymous hemianopia with macular sparing

A

Lesion in right occipital lobe (both banks of calcarine fissure) posterior cerebral artery

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84
Q

Left superior homonymous quadrantanopia

A

PITS = parietal inferior, temporal superior therefore;
Temporal as superior

Right sided tract

Lesion to the right inferior optic radiations in the temporal lobe (meyer’s loop)

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85
Q

Right inferior homonymous quadrantanopia

A

PITS = parietal inferior, temporal superior therefore;
Parietal as inferior

Right visual field so left optic tract

Lesion to the left superior optic radiations in the parietal lobe

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86
Q

“A 23-year-old man was driving a car at high speed whilst intoxicated, he was wearing a seat belt. The car collides with a brick wall at around 140km/h. When he arrives in the emergency department he is comatose. His CT scan appears to be normal. He remains in a persistent vegetative state.”

A

diffuse axonal injury

if they also have a bleed it will be subdural

About 90% of survivors with severe diffuse axonal injury remain unconscious. The 10% that regain consciousness are often severely impaired.

Management
Preventing secondary brain injury eg swelling etc.

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87
Q

“A 25-year-old male is brought to the emergency department after being struck on the side of the head with a bottle in a nightclub. According to one of his accompanying friends, he was knocked unconscious initially but then regained consciousness. An ambulance was called after the patient lost consciousness again. The admission CT head scan shows an intracranial haemorrhage.”

A

extradural hematoma

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88
Q

hypersensitive in bi-convex/lentiform brain ct

A

extradural hematoma

lemon shape (lemon thrown at head)

bi-convex - if youre vexxed you puff out in anger

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89
Q

“A 59-year-old man attends his GP with increasing mild confusion. This came on 2 weeks ago and has been getting progressively worse, both in his and his husband’s opinion. His past medical history is significant for being in a road traffic collision 6 weeks prior. At the time, he was discharged from the emergency department with no injuries but did suffer a head injury. Since then, he reports no headache, nausea or changes in vision.”

A

subdural hematoma

slow onset, fluctuating conscioussness/confusion

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90
Q

Sudden onset occipital headache (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’
Nausea and vomiting
Meningism (photophobia, neck stiffness)

A

subarachnoid haemorrhage

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91
Q

A 54-year-old man attends the GP complaining of double vision. He says it is worse when he walks down the stairs.

On inspection, he is sitting with his head tilted towards the right. The left eye deviates supero-laterally.

A

left trochlear never palsy

head tilt away from lesion.

Palsy results in defective downward gaze → vertical diplopia.

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92
Q

Palsy results in defective abduction → horizontal diplopia

A

abducens (6th) nerve palsy

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93
Q

uvula deviation and loss of gag reflex

A

vagus nerve

uvula deviates away from lesion

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94
Q

tounge deviation

A

cranial nerve 12

tounge deviates towards lesion

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95
Q

isolated foot drop and may have sensory loss on dorusm of foot

A

common peroneal nerve palsy

conservative management is appropriate. Leg crossing, squatting and kneeling should be avoided. Symptoms typically improve over 2-3 months.*

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96
Q

Sensory loss dorsum of foot
Weakness in foot and big toe dorsiflexion (foot drop)
Reflexes intact
Positive sciatic nerve stretch test

Hip abductors are also likely to be weak (superior gluteal nerve).

A

L5 radiculopathy

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97
Q

Sensory loss over anterior thigh
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test

A

L3 radiculopathy

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98
Q

Sensory loss anterior aspect of knee
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test

A

L4 radiculopathy

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99
Q

Sensory loss posterolateral aspect of leg and lateral aspect of foot
Weakness in plantar flexion of foot
Reduced ankle reflex
Positive sciatic nerve stretch test

A

S1 radiculopathy

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100
Q

Management of generalised tonic-clonic seizures?

A

males: sodium valproate

females: lamotrigine or levetiracetam

girls aged under 10 years and who are unlikely to need treatment when they are old enough to have children or women who are unable to have children may be offered sodium valproate first-line

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101
Q

Management focal seizures?

A

first line: lamotrigine or levetiracetam

second line: carbamazepine, oxcarbazepine or zonisamide

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102
Q

Management of absence seizures?

A

first line: ethosuximide

second line:
male: sodium valproate
female: lamotrigine or levetiracetam

carbamazepine may exacerbate absence seizures

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103
Q

Management atonic seizures?

A

males: sodium valproate
females: lamotrigine

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104
Q

What epilepsy syndrome benefits from ketogenic diet?

A

Lennox-Gastaut syndrome

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105
Q

Management juvenile myoclonic epilepsy/myoclonic

A

males: sodium valproate
females: levetiracetam

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106
Q

Management infantile spasms (west syndrome)

A
  1. Prednisolone or Vigabatrin
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107
Q

Star sign

A

SAH

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108
Q

Sciatic vs femoral tests?

A

The femoral nerve is for the front of the leg, while the sciatic nerve serves the back of the leg.

therefore femoral stretch test stretches the front of the leg (patient prone, knee at 90 degrees, lift up)

sciatica test (straight leg raise) stretches the back of the leg (patient supine, lift leg to elicit pain)

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109
Q

Bacterial meningitis 0-3 months

A

BELS

  1. Group B Streptococcus (most common cause in neonates)
  2. E. coli
  3. Listeria monocytogenes
  4. Strep pneumoniae
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110
Q

Bacterial meningitis 3 months-6 years

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
  3. Haemophilus influenzae
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111
Q

Bacterial meningitis 6-60 years

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
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112
Q

Bacterial meningitis >60 years

A
  1. Streptococcus pneumoniae
  2. Neisseria meningitidis
  3. Listeria monocytogenes
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113
Q

Meningitis in immunocompromised

A

listeria monocytogenes

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114
Q

Children in community meningitis initial management

A

Benzylpenicillin IM or IV

< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg

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115
Q

Meningitis initial empirical therapy < 3 months

A

IV cefotaxime + amoxicillin (or ampicillin)

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116
Q

Meningitis initial empirical therapy 3 months-50 years

A

IV cefotaxime

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117
Q

Meningitis initial empirical therapy > 50 years

A

IV cefotaxime + amoxicillin (or ampicillin)

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118
Q

Meningitis management - listeria

A

IV amoxicillin (or ampicillin)
+ gentamicin

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119
Q

When should dexamethasone be given for meningitis

A

Give if lumbar puncture reveals:
- frankly purulent CSF
-CSF white blood cell count greater than 1000/microlitre
- raised CSF white blood cell count with protein concentration greater than 1 g/litre
- bacteria on Gram stain

Withhold if:
- septic shock
- meningococcal
- septicaemia
immunocompromised

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120
Q

Management meningococcal meningitis

A

IV benzylpenicillin or cefotaxime

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121
Q

Post exposure prophylaxis bacterial meningitis

A

Ciprofloxacin single dose

This risk is highest for people that have had close prolonged contact within the 7 days prior to the onset of the illness

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122
Q

Most common pathogen encephalitis in children and adults

A

herpes simplex HSV-1 from cold sores

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123
Q

Most common pathogen encephalitis in neonates

A

herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth.

think “been passed on 2”

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124
Q

Management ?encephalitis

A

aciclovir (covers HSV and varicella zoster)

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125
Q

Management CMV encephalitis

A

Ganciclovir

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126
Q

Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living

A

tension headache

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127
Q

Recurrent, severe headache which is unilateral and throbbing in nature. Associated with nausea and photosensitivity. Last 4-72 hours
Behaviour: withdrawal, not moving, dark room, no noise

A

migraine

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128
Q

Migraine triggers

A

Chocolate
Hangovers
Orgasms
Cheese
Caffeine
The oral contraceptive pill
Lie-ins
Alcohol
Travel
Exercise

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129
Q

migraine diagnostic criteria

A

At least 5 attacks

Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)

Headache has at least two of the following characteristics:
1. unilateral location*
2. pulsating quality (i.e., varying with the heartbeat)
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)

During headache at least one of the following:
1. nausea and/or vomiting*
2. photophobia and phonophobia

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130
Q

acute management migraine

A
  1. Oral triptan + NSAID/paracetamol
  2. metoclopramide or prochlorperazine and non-oral NSAID or triptan
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131
Q

mechanism triptan

A

5-HT agonist

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132
Q

who should get prophylaxis for migraines

A

> 2 attacks per month

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133
Q

Migraine prophylaxis

A
  1. Topiramate or propranolol (propranolol for women of CBA as topiramate can be teratogenic and can reduce effectiveness of hormonal contraception)
  2. Acupuncture
  • Riboflavin (vit B2) 400 mg may be effective at reducing migraine frequency and intensity for some people
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134
Q

Management of pre-menstrual migraines

A

Frovatriptan (2.5mg twice a day) or zolmitriptan (2.5mg twice or three times a day) as mini-prophylaxis

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135
Q

What type of side effects can occur in children and young adults taking antiemetic metoclopramide?

A

EPSE

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136
Q

Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling

A

cluster headache

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137
Q

triggers for cluster headaches

A

alcohol

nocturnal sleep schedule

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138
Q

Acute management cluster headache

A
  • 100% high flow oxygen (80% response within 15 mins)
  • subcutaneous triptan (75% response within 15 mins)
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139
Q

When are triptans contraindicated

A

triptans are contraindicated in CAD as it may cause vasospasm

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140
Q

Prophylaxis cluster headaches

A

Verapamil
prednisolone

141
Q

Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
(worse when talking for a while, worse when chewing, worse when moving jaw, tender to touch, scalp tenderness, worse when brushing hair, shaving etc)
Tender, palpable temporal artery
Visual disturbance

A

temporal arteritis

142
Q

association temporal arteritis

A

50% have features of PMR : aching, morning stiffness in proximal limb muscles

143
Q

Investigations temporal arteritis

A

Tender palpable temporal artery
Raised ESR >50 (10% of pts don’t have)
CRP may be elevated
Vision testing
Temporal artery biopsy : skip lesions (Histology shows changes that characteristically ‘skips’ certain sections of the affected artery whilst damaging others.) may also be normal

144
Q

Management temporal arteritis

A

Urgent, no vision loss:
High dose oral glucocorticoids eg oral methylprednisolone

Urgent, vision loss:
IV methylprednisolone

145
Q

What do you need to test in temporal arteritis? what may you find?

A

VISION

Amaurosis fugax
Blurring
Double vision

146
Q

Severe unilateral pain, often triggered by touching the skin, brief electric shock like pains, abrupt in onset and termination

A

trigeminal neuralgia

147
Q

Management trigeminal neuralgia

A

Carbamazepine

148
Q

management Herpes zoster ophthalmicus (HZO)

A

oral antiviral treatment for 7-10 days
ideally started within 72 hours

topical corticosteroids may be used to treat any secondary inflammation of the eye

149
Q

Facial ‘fullness’ and tenderness
Nasal discharge, pyrexia or post-nasal drip leading to cough

A

sinusitis

150
Q

Management sinusitis

A

analgesia
if > 10 days - intranasal corticosteroids

severe : abx

151
Q

Management medication overuse headache

A

simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)

opioid analgesics should be gradually withdrawn

152
Q

Management post lumbar puncture headache

A

Caffeine and fluids

if > 72 hours - may develop subdural haematoma - treat

153
Q

Normal ICP

A

7-15 mmHg in adults in the supine position

154
Q

A young, overweight woman is admitted to the medical assessment unit with headaches. Her CT head scan is normal, her lumbar puncture has an opening pressure of 30 cmH2O (reference range 5-25 cmH2O) and papilloedema is found on fundoscopy

A

IIH

155
Q

Management IIH

A
  1. Weight loss
  2. acetazolamide (decreases fluid production)
  3. Topiramate
  4. Repeated lumbar puncture
  5. Surgery : optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.
  6. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
156
Q

Causes of obstructive hydrocephalus

A

tumours

acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage)

developmental abnormalities (e.g. aqueduct stenosis

157
Q

Investigations for raised ICP

A

CT head is used as a first line imaging investigation since it is fast and shows adequate resolution of the brain and ventricles

MRI may be used to investigate hydrocephalus in more detail, particularly if there is a suspected underlying lesion

Lumbar puncture for non-obstructive hydrocephalus is both diagnostic and therapeutic since it allows you to sample CSF, measure the opening pressure, but also to drain CSF to reduce the pressure

158
Q

selegiline, rasagiline

A

MAO-B

parkinsons management

159
Q

Parkinsonism

Autonomic disturbance : erectile dysfunction often early feature, postural hypotension, atonic bladder

Cerebellar signs eg ataxia

A

multi-system atrophy

MSA-P - Predominant Parkinsonian features
MSA-C - Predominant Cerebellar features

160
Q

Parkinsonism: bradykinesia prominent

Postural instability and falls

Stiff, broad-based gait

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

Cognitive impairment, primarily frontal lobe dysfunction

A

Supranucelar palsy / steele-richardson-olszewski syndrome

poor response to l-dopa

161
Q

Urinary incontinence
Gait abnormality (shuffling and freezing)
Dementia and bradyphrenia (slowness of thought)

A

Normal pressure hydrocephalus

ventriculoperitoneal shunting (VP shunt)

162
Q

progressive cognitive impairment (early impairments in attention and executive function rather than just memory loss)

cognition may be fluctuating, in contrast to other forms of dementia

visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

later develops parkinsonism

A

Lewy body dementia

SPECT/DaTSCAN

Both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s

Neuroleptics are contraindicated

May use levodopa for parkinsonism

163
Q

A 19-year-old man is referred to the general medical clinic. For the past six months his family have noted increasing behavioural and speech problems. He himself has noticed that he is more clumsy than normal and reports excessive salivation. His older brother died of liver disease.

disease
inheritance
investigations
management

A

Wilsons disease

autosomal recessive
Defect in ATP7B gene located on chromosome 13

Excessive copper deposition in the tissues (increased copper absorption from SI and decreased hepatic copper excretion

Investigations:
- Slit lamp examination for Kayser-Fleischer rings
- Increased 24hr urinary copper excretion
- Reduced serum ceruloplasmin
- Reduced total serum copper
- Free serum copper is increased

Diagnostic : genetic analysis of ATP7B gene

Penicillamine (chelates copper)

164
Q

Management parkinsons

A

Motor symptoms affecting quality of life:
1. levodopa

Motor symptoms not affecting quality of life:
1. dopamine agonists, levodopa or monoamine oxidase B (MAO‑B) inhibitors

Do not offer ergot-derived dopamine agonists as first-line treatment for Parkinson’s disease

165
Q

Name non-ergot dopamine agnoists

A

pramipexole, ropinirole, rotigotine and apomorphine

166
Q

Name ergot dopamina agonists

what are ergot side effects

A

bromocriptine, pergolide, cabergoline

require monitoring due to fibrosis SE

167
Q

adverse effects dopamine agonists

A

more adverse events eg Impulse control disorders

Excessive sleepiness and sudden onset of sleep

Psychotic symptoms

168
Q

When to consider ergot-derived dopamine agnoists

A

in people who have developed dyskinesia or motor fluctuations despite optimal levodopa therapy and

in people whose symptoms are not adequately controlled with a non-ergot-derived dopamine agonist. [2017]

169
Q

Management dyskinesia parkinsons

A
  1. modify meds
  2. amantadine
170
Q

Management of generalised tonic-clonic seizures?

A

males: sodium valproate

females: lamotrigine or levetiracetam

girls aged under 10 years and who are unlikely to need treatment when they are old enough to have children or women who are unable to have children may be offered sodium valproate first-line

171
Q

Management focal seizures?

A

first line: lamotrigine or levetiracetam

second line: carbamazepine, oxcarbazepine or zonisamide

172
Q

Management of absence seizures?

A

first line: ethosuximide

second line:
male: sodium valproate
female: lamotrigine or levetiracetam

carbamazepine may exacerbate absence seizures

173
Q

Management atonic/tonic seizures?

A

males: sodium valproate
females: lamotrigine

174
Q

What epilepsy syndrome benefits from ketogenic diet?

A

Lennox-Gastaut syndrome

175
Q

Management juvenile myoclonic epilepsy/ myoclonic epilepsy

A

males: sodium valproate
females: levetiracetam

176
Q

Management infantile spasms (west syndrome)

A
  1. Prednisolone or Vigabatrin

vigabatrin - inhibiting the GABA-degrading enzyme, GABA transaminase, resulting in a widespread increase in GABA concentrations in the brain.

177
Q

brachial plexus nerve roots

A

3 musketeers = musculocutaneous nerve C5, C6, C7

2 were assassinated = axillary nerve C5, C6 (gun sign with thumb and finger)

4 men (4 fingers) = median nerve C6, C7, C8, T1

5 rats = radial nerve C5, C6, C7, C8, T1

2 unicorns = ulnar nerve C8, T1

178
Q

low back pain
bilateral sciatica
present in around 50% of cases
reduced sensation/pins-and-needles in the perianal area
decreased anal tone
it is good practice to check anal tone in patients with new-onset back pain
however, studies show this has poor sensitivity and specificity for CES
urinary dysfunction
e.g. incontinence, reduced awareness of bladder filling, loss of urge to void
incontinence is a late sign that may indicate irreversible damage

A

cauda equine

179
Q

Investigation and management cuada equina

A

urgent MRI

surgical decompression

180
Q

MRI finding normal pressure hydrocephalus

A

Ventriculomegaly without sulcal enlargement

181
Q

What factors favour a true epileptic seizure over a psuedoseizure

A

tongue biting
raised serum prolactin

182
Q

Investigations guilian barre

A

lumbar puncture
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
nerve conduction studies may be performed
decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency

183
Q

wasting in his calf muscles and high arches in his feet

A

charcot-marie tooth

184
Q

Management guilian barre

A

IV immunoglobulins or plasma exchange
VTE prophylaxis (pulmonary embolism is a leading cause of death)

185
Q

Symptoms of motor loss polyneuropathy

A

Ascending weakness
“Tripping over feet”
Foot drop
Hyporeflexia

186
Q

Causes of motor loss polyneuropathy

A

Guillain-Barre syndrome
porphyria
lead poisoning
hereditary sensorimotor neuropathies (HSMN) - Charcot-Marie-Tooth
chronic inflammatory demyelinating polyneuropathy (CIDP)
Diphtheria

187
Q

Pathophysiology charcot-marie tooth

A

CMT is caused by mutations in genes that support or produce proteins involved in the structure and function of either the peripheral nerve axon or the myelin sheath.
Because longer nerves are affected first, symptoms usually begin in the feet and lower legs and then can affect the fingers, hands, and arms.
The majority of mutations are inherited in an autosomal dominant pattern.

188
Q

Investigations charcot-marie tooth

A

Diagnosis is made with a combination of nerve conduction studies and genetic testing. Patients with type 1 have reduced conduction velocity, whereas this is normal in type 2.

189
Q

Abdominal pain, peripheral neuropathy motor, blue lines on gum margin

A

lead posioning

190
Q

Causes of sensory polyneuropathy

A

A – Alcohol
B – B12 deficiency
C – Cancer and Chronic Kidney Disease
D – Diabetes and Drugs (e.g. amiodarone, metronidazole, cisplatin, phenytoin, isoniazid, nitrofurantoin, vincrystine)
E – Every vasculitis

191
Q

Management of neuropathic pain

A
  1. amitriptyline, duloxetine, gabapentin or pregabalin
  2. if the first-line drug treatment does not work try one of the other 3 drugs

tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain

topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)

pain management clinics may be useful in patients with resistant problems

192
Q

Presentation of diabetic polyneuropathy

A

Distal Symmetrical Sensory Neuropathy
Most common
Caused by loss of large sensory fibres.
Sensory loss in a glove and stocking distribution.
Often affecting touch, vibration and proprioception.

Small-fibre Predominant Neuropathy
Caused by loss of small sensory fibres.
Presents with deficits in pain and temperature sensation in a glove and stocking distribution along with episodes of burning pain.

193
Q

Autonomic neuropathy in diabetes

A

Presents with postural hypotension, gastroparesis, constipation, urinary retention, arrhythmias and erectile dysfunction.

Gastroparesis:
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)

194
Q

Presentation sensory polyneuropathy

A

Sensory symptoms:
Large fibre (dorsal column): touch, vibration, joint position (proprioceptive ataxia), painless paraesthesia

Small fibre (spinothalamic) : pain, temperature, burning, allodynia, hyperalgesia

Sensory ataxia affects patients with significant proprioceptive loss. Characteristically, the patient looks down and walks as if throwing his feet, which tend to slap on the ground. Smooth, familiar routes cause less trouble than uneven, rough ones.

195
Q

allodynia and hyperalgesia definitons?

A

allodynia: pain due to a stimulus that does not normally provoke pain

hyperalgesia: increased sensitivity to pain

196
Q

Diagnosing MS

A

two or more episodes disseminated in time and place (mcdonald criteria)

MRI with contrast

197
Q

Categories of symptoms MS

A

Visual
Sensory
Motor
Cerebellar
Other

198
Q

Visual symptoms MS

A

optic neuritis: common presenting feature (inflammation of the optic nerve causing sudden vision loss, colour blindness especially of the colour red and retrobulbar pain)

optic atrophy

Uhthoff’s phenomenon: worsening of vision following rise in body temperature

internuclear ophthalmoplegia (impaired lateral gaze due to damage to the medial longitudinal fasciitis) (nystagmus)

199
Q

Sensory symptoms MS

A

pins/needles
numbness
trigeminal neuralgia
Lhermitte’s syndrome: paresthesia in limbs on neck flexion

200
Q

Motor symptoms MS

A

spastic weakness: most commonly seen in the legs

201
Q

Cerebellar symptoms MS

A

ataxia: more often seen during an acute relapse than as a presenting symptom
Tremor
Coordination of movement “off balance” “feels like world it moving”

202
Q

Types of MS

A

Relapsing-remitting: relapse then complete resolution
Secondary progressive: relapses and remission but with ongoing deficit
Primary progressive: progressive, no remission from onset

203
Q

Invetsigations MS

A

MRI (with contrast) periventricualar white plaques
Lesions disseminated in space and time
Oligoclonal bands in CSF

204
Q

Management acute relapse of MS

A

High dose steroids (eg oral or IV methylprednisolone) for 5 days

Steroids shorten the duration of a relapse but don’t alter the degree of recovery

205
Q

Disease modifying drugs MS

A

Natalizumab (a recombinant monoclonal antibody)
Fingolimod

beta interferon
glatiramer

206
Q

Treatment of spasticity MS

A

Baclofen and gabapentin

207
Q

Sudden vision loss, colour blindness especially of the colour red and retrobulbar pain

A

optic neuritis

208
Q

What is internuclear opthalmaplegia

A

Internuclear ophthalmoplegia or ophthalmoparesis (INO) is an ocular movement disorder that presents as an inability to perform conjugate lateral gaze and ophthalmoplegia due to damage to the interneuron (medial longitudinal fasciculus) between two nuclei of cranial nerves (CN) VI and CN III (internuclear)

209
Q

inhertiance charcot-marie tooth

A

autosomal dominant

210
Q

what drugs increase risk of iih

A

combined oral contraceptive pill
steroids
tetracyclines
vitamin A
lithium

211
Q

How does motor neurone disease present?

A

fasciculations
the absence of sensory signs/symptoms*
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
Other features
doesn’t affect external ocular muscles
no cerebellar signs

weakness, changes to reflexess and tone, fasiculations, in the absence of pain…

212
Q

lower motor neurone signs

A

Muscle atrophy
Flaccid paralysis
No plantar response
Absent tendon reflexes
Fasciculations (single muscle fibres of uninjured LMN stimulated)

213
Q

Investiagtions motor neurone disease

A

The diagnosis of motor neuron disease is clinical, but nerve conduction studies will show normal motor conduction and can help exclude neuropathy. Electromyography shows a reduced number of action potentials with increased amplitude. MRI is usually performed to exclude the differential diagnosis of cervical cord compression and myelopathy

214
Q

Amyotrophic lateral sclerosis presentation

A

typically LMN signs in arms and UMN signs in legs

215
Q

Primary lateral sclerosis presentation

A

UMN signs only

216
Q

Progressive muscular atrophy presentation

A

LMN signs only
affects distal muscles before proximal
carries best prognosis

217
Q

Progressive bulbar palsy presentation

A

palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei

carries worst prognosis

218
Q

management motor neurone disease

A

Riluzole
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months

Respiratory care
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months

219
Q

When do you initiate anticoagulation for someone with a stroke and newly diagnosed AF

A

Anticoagulation should be commenced 14 days after an ischaemic stroke. Earlier anticoagulation may exacerbate any secondary haemorrhage.

treat with aspirin as normal

220
Q

management status epilepticus

A

1 Buccal midazolam or PR dizepam (pre-hospital)/ IV lorazepam (hospital)
2 IV lorazepam
3 IV phenytoin (phenobarbital if already on regular phenytoin)
4 Rapid sequence induction of anaesthesia using thiopental sodium

221
Q

cerebellar signs

A

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

222
Q

cranial nerves implicated in acoustic neuroma

A

Cranial nerve V (trigeminal) - V1 (opthalmic) afferent (corneal) - main one for corneal
Cranial nerve VII (facial) efferent (corneal) and facial palsy
Cranial nerve VIII (vestibulocochlear) vertigo, unilateral sensorineural hearing loss, unilateral tinnitus

223
Q

Presentation acoustic neuroma

A

Vertigo, hearing loss, tinnitus and an absent corneal reflex

224
Q

Bilateral vestibular schwannomas

A

neurofibromatosis type 2

225
Q

Investigation and management ?acoustic neuroma

A
  1. urgent referral to ENT
  2. MRI of the cerebellopontine angle - gadalidium enhanced scan
  3. audiogram
  4. surgery, radiotherapy or observation
226
Q

features of tuberus scleorsis

A

Cutaneous features
depigmented ‘ash-leaf’ spots which fluoresce under UV light
roughened patches of skin over lumbar spine (Shagreen patches)
adenoma sebaceum (angiofibromas): butterfly distribution over nose
fibromata beneath nails (subungual fibromata)
café-au-lait spots* may be seen

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

retinal hamartomas: dense white areas on retina (phakomata)
rhabdomyomas of the heart
gliomatous changes can occur in the brain lesions
polycystic kidneys, renal angiomyolipomata
lymphangioleiomyomatosis: multiple lung cysts

227
Q

features of neurofibromatosis T1

A

Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules) in > 90%
Scoliosis
Pheochromocytomas

There must be at least 2 of the 7 features to indicate a diagnosis. You can remember this with the mnemonic CRABBING.
C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults
R – Relative with NF1
A – Axillary or inguinal freckles
BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris
N – Neurofibromas (2 or more) or 1 plexiform neurofibroma
G – Glioma of the optic nerve

228
Q

features of neurofibromatosis T2

A

Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas

229
Q

antiemetic for someone with parkinsons

A

Domperidone

230
Q

what is cushings reflex

A

Bradycardia and hypertension with a wide pulse pressure is the correct answer.

Cushing’s triad, compromised of widening pulse pressure, bradycardia and irregular breathing, is a late sign indicating impending brain herniation.

Systolic hypertension occurs as a reflex to maintain cerebral perfusion pressure in the presence of raised intracranial pressure.

231
Q

what is a pontine haemorrhage

A

Pontine haemorrhage is a life-threatening condition. It often occurs as a complication secondary to chronic hypertension. Patients often present with reduces Glasgow coma score, quadriplegia, miosis, and absent horizontal eye movements.

232
Q

essential tremor presentation

A

bilateral fine intention tremor

233
Q

Pharmacological treatments essential tremor

A

Propranolol (a non-selective beta blocker)
Primidone (a barbiturate anti-epileptic medication)

234
Q

DVLA first unprovoked/isolated seizure

A

6 months off 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

235
Q

DVLA patients with established epilepsy or those with multiple unprovoked seizures

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

236
Q

DVLA withdrawal of epilepsy medication

A

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

237
Q

DVLA 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

238
Q

DVLA stroke/TIA

A

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

239
Q

DVLA multiple TIAs over short period of time

A

3 months off driving and inform DVLA

240
Q

DVLA after craniotomy

A

craniotomy e.g. For meningioma: 1 year off driving
pituitary tumour: craniotomy: 6 months; trans-sphenoidal surgery ‘can drive when there is no debarring residual impairment likely to affect safe driving’

241
Q

DVLA narcolepsy/cataplexy

A

cease driving on diagnosis, can restart once ‘satisfactory control of symptoms’

242
Q

DVLA chronic neuro conditions eg MS, MND

A

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

243
Q

axillary nerve mononeuropathy

A

Normal function:Shoulder abduction (deltoid muscle), sensory to inferior region of the deltoid muscle

Damage: Humerus surgical neck fracture: usually by direct blow or falling on an outstretched hand

Result: flattened deltoid, loss of sensation over deltoid

244
Q

Radial nerve mononeuropathy

A

Normal function: Extension (forearm, wrist, fingers, thumb), (back off sign) sensory to small area between the dorsal aspect of the 1st and 2nd metacarpals

Damage: Humeral midshaft fracture

Result: Extensors become paralysed → unopposed flexion of the wrist ‘wrist drop’

245
Q

Median nerve mononeuropathy

A

Normal function: LOAF* muscles. Wrist flexion, finger flexion, thumb opposition, pronation. (power to the people and okay sign, whip watch me okay) Sensory to Palmar aspect of lateral 3½ fingers

Damage: carpal tunnel syndrome, thenar wasting

246
Q

Ulnar nerve mononeuropathy

A

Normal function: finger abduction and adduction. (peace sign) Sensory to Medial 1½ fingers
Damage: cubital tunnel syndrome/Supracondylar fracture/tardy ulnar palsy

247
Q

how does hyperventilation to reduce icp work?

A

Hyperventilation -> reduce CO2 -> vasoconstriction of the cerebral arteries -> reduced ICP

248
Q

Types of cerebral palsy

A

spastic (70%)
subtypes include hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons

dyskinetic
caused by damage to the basal ganglia and the substantia nigra
athetoid movements and oro-motor problems and dystonia

ataxic
caused by damage to the cerebellum with typical cerebellar signs

mixed

249
Q

Myasthenia gravis associations

A

thymomas 15%

autoimmune conditions

250
Q

Diagnostic investigation myasthenia gravis

A

Specific antibodies against the acetylcholine receptors AChR antibodies

If negative test anti-muscle-specific tyrosine kinase antibodies
single fibre electromyography: high sensitivity (92-100%)
CT thorax to exclude thymoma
CK normal

251
Q

Mnagement myasthenia gravis

A

long-acting acetylcholinesterase inhibitors:
pyridostigmine is first-line

immunosuppression is usually not started at diagnosis, but the majority of patients eventually require it:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
thymectomy

252
Q

Management of a myasthenic crisis

A

plasmapheresis
intravenous immunoglobulins

​​Plasmapheresis removes circulating antibodies, including the autoimmune antibodies responsible for the disease. Immunotherapy with intravenous gammaglobulin appears to diminish the activity of the disease.

253
Q

MG implications for anaesthesia?

A

Suxamethonium is a depolarising NMBD - it acts by binding to and activating the receptor, at first causing muscle contraction, then paralysis. Due to a decreased number of available receptors, MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses.

254
Q

What drugs should be avoided in MG?

A

beta blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

255
Q

What is Lambert-Eaton ?

A

Progressive muscle weakness with increased use due to damage off NMJ. Asosociated with small cell lung cancer. Antibody against cancer attacks NMJ

256
Q

Presentation lambert eaton

A

Insidious onset
proximal muscle weakness
Ptosis
Swallowing difficulties
Autonomic disturbance

257
Q

Management lambert eaton

A

Amifampridine

258
Q

Examination carpal tunnel syndrome

A

weakness of thumb abduction (abductor pollicis brevis)
wasting of thenar eminence (NOT hypothenar)
Tinel’s sign: tapping causes paraesthesia
Phalen’s sign: flexion of wrist causes symptoms

259
Q

Management carpal tunnel syndrome

A

6-week cons if the symptoms are mild-moderate:
1. corticosteroid injection
2. wrist splints at night

Severe symptoms/persistent:
- surgical decompression (flexor retinaculum division)

260
Q

what is frommets sign

A

Assess for ulnar nerve palsy

Adductor pollicis muscle function tested

Hold a piece of paper between their thumb and index finger. The object is then pulled away. If ulnar nerve palsy, unable to hold the paper and will flex the flexor pollicis longus to compensate (flexion of thumb at interphalangeal joint).

261
Q

Management cubital tunnel syndrome

A

Avoid aggravating activity
Physiotherapy
Steroid injections
Surgery in resistant cases

262
Q

Symptoms brain abscess

A

Headache
Fever
focal neurology

263
Q

At what level does spinal lesion cause autonomic disturbance

A

at or above T6

UMN lesion

faecal impactation – urine retention – facial flushed etc

hypotension and tachycardia

264
Q

what is hoovers sign

A

Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.

265
Q

Presentation cavernous sinus/venous sinus thrombosis

A

Headache – classically acute onset, often unilateral, with photophobia

Ophthalmoplegia and/or diplopia
Due to lesions on nerves of eye movements (CN 3, CN 4, CN 6)
Usually unilaterally, later progressing to both eyes

266
Q

Causes cavernous sinus/venous sinus trombosis

A

local infection (e.g. sinusitis), neoplasia, trauma, prothrombotic states

267
Q

What runs within cavernous sinus

A

Internal carotid arteries
Nerves –
CN 3 (oculomotor nerve)
CN 4 (trochlear nerve)
CN 5a & 5b (ophthalmic and maxillary branches of trigeminal nerves)
CN 6 (abducens nerve)
Post-ganglionic sympathetic nerve fibres

268
Q

Investigations venous thromboses

A

MRI venography is the gold standard
CT venography is an alternative
non-contrast CT head is normal in around 70% of patients
D-dimer levels may be elevated

269
Q

Presentation saggital sinus thrombosis

A

Seizures and hemiplegia
parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
‘empty delta sign’ seen on venography

270
Q

Most common cancer to metastise to brain

A

Lung (most common)
Breast
Renal cell carcinoma
Melanoma
Bowel
Kidney

271
Q

What are glial cells

A

provide support and nutrients for neurones

272
Q

what are gliomas

A

tumours of glial cells

273
Q

Most common priamary brain tumour in adults

A

glioblastoma multiforme / grade IV astrocytoma

274
Q

Most malignant glioma

A

glioblastoma multiforme / grade IV astrocytoma

275
Q

glioblastomaon imaging and histology

A

solid tumours with central necrosis and a rim that enhances with contrast

Pleomorphic tumour cells border necrotic areas

276
Q

Management of glioblastoma

A

Treatment is surgical with postoperative chemotherapy and/or radiotherapy. Dexamethasone is used to treat oedema.

277
Q

imaging and histology meningioma

A

CT
* Histology: Spindle cells in concentric whorls and calcified psammoma bodies
* Investigation is with CT (will show contrast enhancement) and MRI

278
Q

location meningiomas

A

falx cerebri, superior sagittal sinus, convexity or skull base

279
Q

Cause of huntingtons

A

more than 38 repeats of the CAG trinucleotide

280
Q

Prevalence huntingtons

A

between 1 in 10,000 and 1 in 20,000.

281
Q

Scan huntingtons

A

MRI and CT scans in moderate to severe disease can show loss of striatal volume and increased size of the frontal horns of the lateral ventricles. (MRI shows atrophy of the caudate nucleus and putamen)

282
Q

Diagnosis huntingtons

A

genetic testing

283
Q

Management chorea

A

tetrabenazine

284
Q

What level controls diaphragm

A

C4 level,

285
Q

Where do meningiomas arise from?

A

arachnoid cap cells of the meninges and are typically located next to the dura

286
Q

Symptoms meningiomas

A

Cause symptoms by compression rather than invasion

Changes in vision, such as seeing double or blurriness.
Headaches, especially those that are worse in the morning.
Hearing loss or ringing in the ears.
Memory loss.
Loss of smell.
Seizures.
Weakness in your arms or legs.

287
Q

Histology acoustic neuroma

A

Antoni A or B patterns are seen. Verocay bodies (acellular areas surrounded by nuclear palisades)

288
Q

Most common primary brain tumour in children?

Histology?

A

Pilocytic astrocytoma

Rosenthal fibres (corkscrew eosinophilic bundle)

289
Q

How do patients with pituitary adenoma present?

A

Patients will present with the consequences of hormone excess (e.g. Cushing’s due to ACTH, or acromegaly due to GH) or depletion. Compression of the optic chiasm will cause a bitemporal hemianopia due to the crossing nasal fibers.

290
Q

What is cushings syndrome

A

excess ACTH –> excess cortisol

291
Q

Most common paediatric supratentorial tumour? how does it present?

A

Craniopharyngioma

hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.

292
Q

Where does craniopharyngioma originate from?

A

Derived from remnants of Rathke pouch

293
Q

Investigations and treatment craniopharyngioma

A

Investigation requires pituitary blood profile and MRI. Treatment is typically surgical with or without postoperative radiotherapy.

294
Q

What are the features of Creutzfeldt-Jakob disease

A

dementia (rapid onset)
myoclonus

295
Q

MRI creutzfeldt-Jakob disease

A

hyperintense signals in the basal ganglia and thalamus.

296
Q

EEG creutzfeldt-Jakob disease

A

biphasic, high amplitude sharp waves

297
Q

CSF creutzfeldt-JAkob disease

A

normal

298
Q

What protein is responsible for creutzfeldt jakob disease

A

prion proteins

299
Q

Define dystonia

A

prolonged, often painful, muscle contraction

300
Q

PResentation Polymyositis/dermatomyositis

A

proximal muscle weakness +/- tenderness
Raynaud’s
respiratory muscle weakness
interstitial lung disease: e.g. fibrosing alveolitis or organising pneumonia
dysphagia, dysphonia

dermatomyositis is a variant of the disease with skin manifestations eg a purple (heliotrope) rash on the cheeks and eyelids

301
Q

First line invetsigation polymyositis/dermatomyositis

A

elevated creatine kinase

302
Q

Definitive diagnosis polymositis/dermatomyositis

A

msucle biopsy

303
Q

Pathophysiology polymyositis/dermatomyositis

A

thought to be a T-cell mediated cytotoxic process directed against muscle fibres

may be idiopathic or associated with connective tissue disorders

associated with malignancy

304
Q

Management polymyositis/dermatomyositis

A
  1. corticosteroids
  2. additional immunosuppressant such as methotrexate or azathioprine as a steroid-sparing agent.
  3. hydroxycloriquine for dermatomyositis
305
Q

What drugs can cause myopathy

A

chronic corticosteroids (CK normal)
acute corticosteroids (CK raised)
statins (CK raised)

306
Q

triad rhabdomyolysis

A

dark urine, generalised weakness and myalgia

307
Q

dianostic rhabdomyolysis

A

CK > 5x normal. this can then cause aki

308
Q

MAnagement rhabdomyolysis

A

IV fluids to maintain good urine output

urinary alkalinization (eg sodium bicarbonate) is sometimes used

management of electrolyte imbalance such as potassium

309
Q

Electrolyte changes rhabdomyolysis

A

Raised LDH (suggestive of muscle damage)
Hyperkalaemia (liberated from the damaged muscle) (aki)
Hyperphosphatemia (liberated from the damaged muscle)
Hyperuricaemia (liberated from damaged muscle)
Hypocalcaemia (calcium is taken into the damaged muscle by several mechanisms)

310
Q

What drug is co-prescribed with levodopa to prevent side effects

A

Dopa decarboxylase inhibitor (e.g. carbidopa or benserazide)

311
Q

side effects levodopa

A
  • hallucinations
  • dyskinesia
  • postural hypotension on starting
  • on/off effect
  • dry mouth
  • palpitations
312
Q

Where is the damage in dyskinetic cerebral palsy

A

results from damage to the basal ganglia and the substantia nigra

313
Q

Klumpke’s paralysis

A

damage to T1

314
Q

Spasticity vs rigidity

A

Spasticity occurs in pyramidal tract lesions and is due to 1. Increased activity of alpha motor neurons and it is velocity dependent
eg. clasp knife and ankle clonus

Rigidity occurs in extrapyramidal lesions and is due to increased activity of gamma neurons 2. Not velocity dependent. eg cogwheel and lead pipe

315
Q

flow of cerebrospinal fluid

A
  1. Lateral ventricles (via foramen of Munro)
  2. 3rd ventricle
  3. Cerebral aqueduct (aqueduct of Sylvius)
  4. 4th ventricle (via foramina of Magendie and Luschka)
  5. Subarachnoid space
  6. Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus
316
Q

BAmford classification total anterior circualtion stroke

A

All three of the following need to be present for a diagnosis of a TACS:

Unilateral weakness (and/or sensory deficit) of the face, arm and leg (at least 2/3)
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)

317
Q

Bamford classification partial anterior cirucaltion stroke

A

Two of the following need to be present for a diagnosis of a PACS:

Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)*
*Higher cerebral dysfunction alone is also classified as PACS.

318
Q

Bamford classification posterior ciruclation stroke

A

One of the following need to be present for a diagnosis of a POCS:

Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

319
Q

Bamford classification lacunar stroke

A

One of the following needs to be present for a diagnosis of a LACS:

Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis

320
Q

cause of anterior cord syndrome

A

ischemia within the anterior spinal artery (ASA)

321
Q

Adverse effects sodium valproate

A

-alopecia
-hepatitis
-pancreatitis
-thrombocytopenia
-teratogenic

-Increased appetite and weight gain
-P450 enzyme inhibitor
-ataxia
-tremor

322
Q

Adverse effects carbmazepine

A

-leucopenia and agranulocytosis

P450 enzyme inducer
-dizziness and ataxia
-drowsiness
-inappropriate ADH secretion
-visual disturbances (diplopia)

323
Q

Adverse effects lamorigine

A

-stevens-johnson syndrome

324
Q

Adverse effcects phenyoin

A

-megaloblastic anaemia

-p450 enzyme inducer
-dizziness and ataxia
-drowsiness
Gingival hyperplasia, hirsutism, coarsening of facial features
-peripheral neuropathy
-enhanced vitamin D metabolism causing osetomalacia
-lymphadenopathy

325
Q

Process of invetsgigating SAH

A
  1. CT head non-contrast (may show star sign)
  2. Lumbar puncture (xnathachromia)
  3. CT angiography (gold standard - shows where lesion is)
326
Q

Adverse effects ethosuximide

A

night terrors

327
Q

In a SAH, what artery would be implicated if they had a occulomotor nerve palsy

A

posterior cmmunicating artery

328
Q

Dysphasia vs dysarthria

A

dysphasia - language problem eg brocas

dysarthria - muscle impairment meaning can’t create sound properly

329
Q

what is tardy ulnar palsy

A

damage to ulnar nerve at the wrist –> unopposed action of upper undamaged ulnar –> flexion of 4th and 5th digits (claw hand)

330
Q

cuases of common peroneal nerve palsy

A

posturing eg crossing legs

fracture of neck of fibula

331
Q

what is tarsal tunnel syndrome

A

damage to tibial nerve - pain numbness and tingling in feet

medial malleous

332
Q

How to ddx peroneal nerve palsy from L5 radiculopathy

A

L5 radiculopathy also has issues with hip abduction and foot inverson

333
Q

whcih radiculopathies are femoral stretch test positive

A

L3 and L4

334
Q

what is ROSIER

A

ROSIER is a clinical scoring tool based on clinical features and duration. Stroke is likely if the patient scores anything above 0.

335
Q

Secondary prevention stroke

A

Anti-platelet:
1. clopidogrel 75 mg daily.
2. Aspirin 75 mg daily with modified-release dipyridamole 200 mg twice daily
3. Modified-release dipyridamole 200 mg twice daily

Statin 80mg

Antihypertensive if required

Anticoagulation after 14 days if indicated eg AF

336
Q

what is keppra

A

brand name for levetiracetam

337
Q

examples of decarboxylase inhibitors

A

Cobeneledopa = levodopa + benserazide

Cocareldopa = levodopa + carbidopa

338
Q

MRI exam buzzword: hot cross bun sign

A

multiple systems atrphy

339
Q

MRI exam buzzword: hummingbird sign

A

progressive supranucelar palsy

340
Q

do CN lesions cause contralateral or ipisilateral symptoms?

A

all ipsilateral apart from trochlear (4th)

341
Q

Which CN at midbrain?

A

3 and 4

342
Q

Which CN at pons

A

5, 6, 7, 8

343
Q

Which CN at medulla

A

9,10, 11, 12

344
Q

BP contraindication for thrombolysis

A

180/110mmHg is a contraindication for thrombolysis.

345
Q

Arnold-Chiari malformation

A

Arnold-Chiari malformation describes the downward displacement, or herniation, of the cerebellar tonsils through the foramen magnum. Malformations may be congenital or acquired through trauma.

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

346
Q

triad parkinsons

A

tremor, rigidity, and bradykinesia

347
Q

what is a colles fracture? what erve can be damaged?

A

Colles’ fracture – The most common type of radial fracture. A fall onto an outstretched hand causing a fracture of the distal radius. The structures distal to the fracture (wrist and hand) are displaced posteriorly. It produces what is known as the ‘dinner fork deformity’.

median eg can’t abduct thumb

348
Q

when is carotid endarterectomy indicated?

A

Carotid endarterectomy is considered in a patient who has had a TIA with carotid artery stenosis exceeding 70%

349
Q

neuro incontinence vs retention?

A

UMN - urinary retention as hypertonic sphincters

LMN - urinary incontinence as hypotonic sphincters

Phase 3a topics (39 decks)

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