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Clinical Years / Progress Test > Neuro > Flashcards

Neuro Flashcards

1
Q

what is status epilepticus?
management?

A

a single seizure lasting >5 minutes, or >= 2 seizures within a 5-minute period
use IV benzodiazepines such as diazepam or lorazepam - can repeat dose after 10-20 mins
if not responding 2nd line = phenytoin
if still not after 45 mins then general anaesthesia

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2
Q

how is a SAH diagnosed?

A

CT head
but need to LP if negative - not all show on CT

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3
Q

What are the general causes of loss of consciousness

A

Cardiovascular including Vasovagal syncope (most common)
Neurological
Psychogenic

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4
Q

First line medication for seizures

A

Lamotrigine 25mg increased by 25mg every two weeks up to 75 mg

Note most common side effect is a hypersensitivity rash

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5
Q

What features indicate syncope?

A

Positional
Provoking factors; dehydration, emotion, heat
Prodrome; dizziness and sweating

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6
Q

Types of seizures

A

Generalised tonic clinic
Myoclonic jerks
Partial seizures
Absent seizures
Focal seizures

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7
Q

Signs of raised ICP

A

Papilloedema
Peripheral field loss and blond spots
6th nerve palsy (other reasons too)
Hypertension
Vomiting
Headache

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8
Q

Investigating headaches

A

CT
MRI
LP - measures CSF pressure

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9
Q

Acute migraine treatment

A

NSAIDs
Antiemetics
Triptans

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10
Q

Migraine secondary prevention

A

Beta blocker or amitriptyline
if unsuccessful can try antiepileptics or antihypertensives

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11
Q

Investigations in meningitis

A

CSF sample via lumbar puncture
Blood cultures
Viral serology
Throat swab
MRI brain if encephalitis likely

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12
Q

Meningitis treatment

A

3rd generation cephalosporin: cefotaxime or ceftriaxone
And dexamethasone

If over 60 add amoxicillin

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13
Q

Treatment for temporal arteritis

A

Immediate oral prednisolone

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14
Q

signs/symptoms of Wernicke’s encephalopathy

A

Confusion
Ataxia
Nystagmus
Ophthalmoplegia
PEripheral
Neuropathy

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15
Q

TIA presents to GP within 7 days?

A

300mg aspirin and refer for specialist review

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16
Q

focal seizures based on where they occur

A

temporal lobe - hallucinations, epigastric/emotional, automatisms, deja vu/dysphasia
frontal lobe - head/leg movements, jacksonian march
parietal lobe - parasthesia/sensory abnormalities
occipital - visual floaters and flashes

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17
Q

cluster headache acute and prophylactic management

A

acute - 100% oxygen and subcut sumatriptan
prophylaxis - verapamil and steroids

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18
Q

trigeminal neuralgia
symptoms + treatment

A

severe, unilateral electric shock pain in face/head precipitated by light touch
treat with carbemazapine

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19
Q

what symptoms are common in syncope

A

presyncopal symtpoms
motor symptoms; twitching/jerking of limbs, tongue biting and incontinence can occur

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20
Q

typical non-epileptic attack disorder history

A
  • prolonged episodes
  • conscious even with profound movements
  • collateral history
  • normal EEG/MRI etc
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21
Q

typical cardiogenic syncope history

A
  • sudden onset
  • no warning
  • short duraiton
  • usualy middle aged or older
  • CV history
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22
Q

Broca’s aphasia

A

expressive aphasia where the patient’s speech is non-fluent and halting, repetition is impaired.

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23
Q

Wernicke’s aphasia

A

fluent speech, impaired comprehension, and impaired ability to repeat back phrases.

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24
Q

prophylaxis for contacts in meningitis

A

rifampicin
note meningitis is a notifiable disease

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25
Q

intracranial space occupying lesions

A

tumours
vascular - haemorrhages
infective
hydrocephalus

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26
Q

brain tumour presentation

A

raised ICP
neurological deficits
cortical/meningeal irritation
hormonal effects

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27
Q

causes of raised ICP

A

increased brain mass/volume

increase in CSF

increase in blood

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28
Q

what is cerebral perfusion pressure

A

CPP = ABP - ICP

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29
Q

management of acute ICP rise

A

ensure all routine measures; position, temperature, BP etc under control
- heavy sedation +/-paralysis
- CSF drainage
- osmotic therapy with mannitol
- hyperventilation
- barbiturate therapy
- decompressive craniotomy

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30
Q

how do extra dural bleeds usually present

A

usually following trauma resulting in an arterial bleed - commonly to side of head and involving middle meningeal artery
lucid interval may be present betwen trauma and patient deteriorating

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31
Q

how does a subdural bleed usually occur

A

venous injruy - may not be very traumatic
often in elderly, alcoholics, etc
haematoma usually develops very slowly

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32
Q

what are the NICE headache red flags

A

-Sudden onset high severity headache
-Headache with fever
-New onset neurological deficit
-New onset cognitive dysfunction
-Change in personality
-Impaired level of consciousness
-Recent head trauma (within past three months)
-Headache triggered by cough, sneeze, exercise, or changes in posture.
-Headache associated with halos around lights or headaches that get worse in the dark.
-Headache associated with jaw claudication and scalp tenderness.

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33
Q

what does increased tone indicate

what is the difference between rigidity and spasticity

A

increased tone indicates as UMN lesion

rigidity; increased tone that is not velocity dependent - indicates an extrapyramidal lesion such as in Parkinson’s disease

spasticity;velocity dependent increase of tone which indicates a pyramidal lesion

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34
Q

what is the nerve root of each movement in the neurological examination

A

Shoulder abduction C5
Elbow flexion C5/C6
Elbow extension Radial nerve C7
Wrist extension Radial nerve C6
Finger extension Posterior interosseous nerve C7
Finger flexion C8
Finger abduction Ulnar nerve T1
Thumb abduction Median nerve T1
Hip flexion L1/L2
Hip extension L5/S1
Knee flexion Sciatic nerve S1
Knee extension Femoral nerve L3/L4
Foot dorsiflexion Deep peroneal nerve L4
Toe dorsiflexion L5
Foot plantarflexion S1

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35
Q

how do reflexes change in pathology

A

Reflexes are decreased or absent in LMN pathology, and exaggerated in UMN pathology.

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36
Q

what are the nerve roots of the reflexes tested

A

Biceps reflex C5-C6
Triceps reflex C7-C8
Supinator reflex C6-C7
Knee reflex L3-L4
Ankle reflex S1

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37
Q

what tracts are impaired in loss of
- vibration sensation
- pinprick sensation

A

vibration - dorsal columns

pinprick - spinothalamic tracts

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38
Q

what is the MRC grading scale for muscle strength

A

0) No power
1) Twitching but no movement
2) Movement, but cannot overcome gravity
3) Can overcome gravity
4) Movement against gravity and resistance
5) Normal muscle strength

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39
Q

what is brown-sequard syndrome

A

a hemisection of the spinal cord

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40
Q

what are the main investigations used in neurology

A

CT
MRI
LP
EEG
EMG

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41
Q

When is global areflexia seen

A

Sensory (+/- motor) poly neuropathy

If length dependent the lower limbs are lost before the upper limbs

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42
Q

What does asymmetric loss of reflexes indicate

A

Mononeuropathy, mononeuropathy multiplex or radiculopathy

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43
Q

What happens to reflexes in
- acute spinal cord lesions “spinal shock”
- Lambert Eaton Myasthenic Syndrome

A
  • loss of reflexes
  • lost but can return after voluntary sustained contraction of the responsible muscle
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44
Q

What is Pes Cavus

A

A sign of chronic neurological disease most commonly seen in Charcot Marie tooth disease. Can also be seen in cerebral palsy, nerve rauma and spinal cord tethering

Foot deformity of an elevated arch, forefoot drop and toe clawing, muscle actions

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45
Q

What is pseudoathetosis

A

Loss of sense of joint position causing slow involuntary movements usually of the arms

Caused by sensory ataxia

Can be seen in ataxic neuropathy, myelopathy, thalami and parietal lesions - ie anywhere along the sensory pathway

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46
Q

What is high stepping gait a sign of

A

peripheral sensory neuropathy

can be motor

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47
Q

What is myotonia? When is it seen

A

Prolonged muscle contraction once activated due to abnormal activity of the muscle fibre membrane

Seen mainly in myotonic dystrophy types 1 & 2

Can be elicited voluntarily (make fist) or by percussion of thenar eminence

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48
Q

What needs to be asked in a neurological systems review

A

Headaches
Fits faints funny turns
Memory
Vision
Hearing
Speech
Numbness, tingling
Weakness
Sensation
Incontinence or erectile dysfunction
Balance and coordination

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49
Q

Where do motor pathways decussate

What will lesions therefore show

A

Medulla

Proximal to medulla = contralateral
Medulla = ipsilateral CN signs and contralateral limb signs
After medulla = ipsilateral signs

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50
Q

Where do the
- dorsal columns
- spinothalamic tracts
decussate

A

Dorsal columns = medulla
Spinothalamic tracts = dorsal root ganglion

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51
Q

What are the main differentials for weakness in all four limbs

A

Acute peripheral neuropathy such as Guillan Barre syndrome
Acute myelopathy (acute spinal cord syndrome) eg transverse myelitis
(Both present with weakness and altered sensation
Reflexes most helpful to distinguish)
Myasthenia Gravis
Acute myosotis

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52
Q

What is the main treatment for guillian barre syndrome

A

Intravenous immunoglobulins

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53
Q

What information does a lumbar puncture give you and normal ranges

A

Opening pressure - <20cm
Blood glucose
WBC - <5 WBCs w/ no neutrophils
RBC - none but occasional blood contamination
Protein - <0.45g/dL
CSF glucose - approx 2/3 of plasma glucose
Appearance - clear

can also do gram stain, cytology, cultures, viral/bacterial PCR, oligoclonal bands which indicates IgG synthesis in the CNS, tests for xanthochromia

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54
Q

How can GBS affect
- CSF / LP results
- breathing

A

LP - increased protein due to albuminocytological dissociation in the CSF. Normal cell count, normal cells and all else

Breathing can be affected by lying flat as neuromuscular ventilatory failure occurs due to a weak diaphragm - shown by increased neck weakened, reduced chest expansion, CO2 retention
FVC can become markedly reduced - consider ICU

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55
Q

acute cervical cord syndrome

A

Mixture of 4 limb motor and sensory signs
May have pain
Many have sphincter symptoms e..g bladder urgency and frequency

Examination expected to show increased tone and brisk reflexes in all four limbs but often can have flaccid tone and absent reflexes - spinal shock

If only posterior cord may have no sensory symptoms - otherwise can find a sensory level with pinprick

Sensory ataxia often present - unsteady gait

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56
Q

Cauda equina syndrome

A

Lower limb lower motor neurone symptoms and signs
Normal upper limbs
Combination of motor and sensory problems, bladder disturbance, saddle anaesthesia
Pain may be present if due to compressive pathology

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57
Q

Myasthenia gravis symptoms

A

Muscle weakness is cardinal symptom
No sensory symptoms
Can affect any muscle but typically eyes, mouth and proximal limbs
Respiratory muscles can be involved especially when lying down due to weak diaphragm
Weakness is fatigable - worse the more the muscle is used ie end of the day

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58
Q

Acute myositis

A

Rare condition with weakness predominantly of the proximal limb
Myalgia may be present
Reflexes and sensation normal

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59
Q

Characterising features of:
1. Migraine
2. Cluster headache
3. Tension headache
4. Temporal arteritis

A
  1. Unilateral, pounding, headache with multiple triggers. Lasts for hours. Aversion to lights, noises and can be preceded by aura
  2. Occur frequently for a couple of weeks. 20 minutes of unilateral, debilitating pain with retro orbital pain, red eye and eye watering
  3. Tight band like sensation triggered by stress
  4. Scalp tenderness, unilateral, jaw Claudication
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60
Q

Characterising features of
1 trigeminal neuralgia
2 acute glaucoma
3 sinusitis

A

1 brief stabbing pain when brushing teeth or chewing
2 pain around eye, blurred vision with halos around lights
3 facial, tenderness and rhinorrhea

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61
Q

Characterising features of
1 meningitis
2 SAH
3 raised ICP

A

1 photophobia, neck stiffness, fever
2 sudden onset excruciating headache
3 headache triggered by positional change or exertion and changes in vision

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62
Q

Characterising features of collapse caused by
1. Hypertrophic cardiomyopathy/ cardiogenic syncope
2. Arrhythmia/ cardiogenic syncope
3. Aortic stenosis
4. Carotid sinus hypersensitivity

A
  1. Triggered by vigorous exercise in a young person
  2. Palpitations or chest pain beforehand - FHx of sudden unexplained death
  3. Older person, chest pain, breahtlessness and collapse of exertion
  4. Collapse on shaving or turning head
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63
Q

what are the defined illnesses within Guillan-Barre syndrome

A

Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) - most common

Acute Motor Axonal Neuropathy (AMAN)

Acute Motor and Sensory Axonal Neuropathy (AMSAN) - severe

Miller-Fisher Syndrome - ophthalmoplegia, arreflexia and ataxia

Pure Sensory Neuropathy

Acute Pandysautomia

all are acute or subacute monophasic illnesses - progress for up to 4 weeks acute or up to 8 weeks subacute

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64
Q

what is AIDP

A

Acute Inflammatory Demyelinating Polyradiculoneuropathy

begins with parasthesia and pains followed by muscle weakness usually beginning with the legs
can start in arms or face rarely

sometimes causes ophthalmaplegia

has autonomic features; labile BP, arrhythmia, constipation, abdominal distention

2/3 have an identifiable trigger

can’t progress for longer than 4 weeks by definition

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65
Q

differential diagnoses of Guillan Barre

A

when examining ensure signs fit with LMN disease otherwise not GB!

differentials;
acute myelopathies
botulism
diphtheria
Lyme disease
Porphyria
vasculitis neuropathy

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66
Q

suspected GBS but…

significant protein elevation in CSF; >5g/dL

significant cell numbers in CSF

A

think impairment of CSF flow - spinal block e.g. epidural infection, disc disease or tumours

some cells normal (10-20) but if >50 think HIV seroconversion which can present similarly or alternative diagnosis

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67
Q

what is the pathophysiology of GBS?

A

Peripheral neuropathy

Demyelinating form; immune attack; macrophage mediated demyelinating disease of the peripheral nerves

Axonal disease particularly at the nodes of Ranvier by plasmalemma

both thought to be caused by a combination of macrophage activity via T cell pathway and of antibody mediated attack via plasma B cells

note in AMSAN there is severe Wallerian degeneration which impairs full recovery

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68
Q

how does GBS generally present?

A

LMN signs
- Arreflexia
- Reduced tone
- reduced power if motor involvement
- reduced sensation if sensory involvement

usually ascending
progresses over days -weeks

80% make a full recovery but long process with physio, OT and neurorehab

69
Q

management for GBS

A
  • prophylaxis for DVT/PE; LMWH
  • monitor respiratory function using FVC; if declining pt may be peri-arrest; ventilate if severely reducing
  • IV immunoglobulins
  • plasma exchange (equivalent outcomes for IVIG)
  • oral steroids not effective
70
Q

what can trigger GBS?

A

Viral infections; EBV, CMV, HIV, influenza
Bacterial infections; campylobacter (stands out as a trigger), mycoplasma pneumonia, E coli
Systemic illnesses; Hodgkins lymphoma, CLL, hyperthyroidism
Others; pregnancy, surgery, bone marrow transplant

71
Q

why is campylobacter infection a particular trigger for GBS?

A

shared epitopes on the bacteria lipo-oligosaccharides with the human gangliosides (abundant cells in neuronal membrane) - target for antigenic attack as body tries to fight infection

some genetic variability in susceptibility

72
Q

what are nerve conduction studies used for

A

highly sensitive in detecting peripheral nervous system disease, allow the precise anatomical localisation of the lesion, and characterise the pathology

sensory and motor studies measuring conduction speed and amplitude,

73
Q

what presentations are LP useful in

A
  • headache particularly measuring pressure
  • neurological infection e..g meningitis
  • inflammatory NS conditions e.g. transverse myelitis
  • GBS
  • Cancer of the CNS
74
Q

CSF analysis results in
- bacterial infection e.g. meningitis
- viral infection
- TB
- fungal infection

A

bacterial - high opening pressure, high protein >1, v high cell count with neutrophils, low glucose

viral - normal opening pressure, slightly raised protein(0.5-1), raised cell count (lymph), normal glucose

TB - v high opening pressure, slightly raised cell count (lymph), high protein 1-5g/dL, low glucose <1/3

fungal - v high opening pressure, raised cell count (lymph), raised protein (0.5-2), slightly low glucose

75
Q

CSF in
-MS
-cancer
-SAH

A

MS; usually normal except in extremely active disease can have 10-20 white cells
oligoclonal bands present

cancer; high WBC and protein, low glucose, abnormal cytology

SAH; RBCs (less sensitive) and xanthochromia; starts after a few hours

76
Q

what are CMAPs and SNAPs in nerve conduction studies

A

CMAP compound muscle action potential
SNAP sensory nerve action potential

77
Q

chronic inflammatory demyelinating polyneuropathy

A

considered the chronic version of GBS
progressive weakness and impaired sensory function in the legs and arms

treated with IV IG

78
Q

how does a Bells palsy present?
cause?
treatment?
prognosis?

A

one sided facial weakness of whole side of face ie. no forehead sparing
sensation in tact
may have hyperacusis, taste change, dry eyes (functions of CNVII)

cause unknown; potentially viral

-if treated early steroids are effective; 1 week of prednisolone 60mg o.d
-advise patient to tape eye closed to avoid corneal damage

facial weakness can worsen over the first few days. The majority recover completely: most cases recover within 4-6 months. The time taken to recover relates to the severity of the initial weakness. Recurrence is uncommon

79
Q

what is Ramsay Hunt syndrome

A

Herpes zoster (“shingles”) of the geniculate ganglion of the facial nerve

typically associated with painful vesicles affecting the external ear and occasionally on the palate

80
Q

common peroneal nerve palsy

background function of the CPN

A

foot drop with weakness
typically painless, the ankle reflex is preserved & often occurs after a period of unaccustomed activity involving prolonged kneeling

The CPN winds round the fibular head and is susceptible to compression at this site. The CPN innervates tibialis anterior, responsible for ankle dorsiflexion, and the peroneal muscles which evert the foot, but not tibialis posterior (tibial nerve), responsible for inversion. It does not subserve the ankle reflex, and hence this is spared.

81
Q

what is the commonest cause of a root lesion (radiculopathy) leading to foot drop

A

vertebral disc prolapse leading to compression of the L5 nerve root
The L5 root contributes a significant number of fibres to tibialis anterior, peroneal muscles and tibialis posterior and hence there is weakness of both inversion and eversion of the foot.
usually also involves S1 to some extent so ankle reflex

82
Q

causes of a foot drop

A

lumbar nerve root lesion
common perineal nerve palsy

83
Q

what will nerve conduction studies show in CPN palsy

A

severe compression can be associated with axonal loss which will show denervation changes on EMG
most are demyelinating and may show slower conduction but usually fully recover

84
Q

presentation of a radial nerve palsy

A

compression of the radial nerve against the mid-shaft of the humerus
causes wrist drop
neurophysiology can be helpful, to confirm the diagnosis and add prognostic information, and a wrist drop splint can greatly improve hand function pending recovery.

85
Q

degenerative cervical myelopathy (DCM)
what is it
symptoms
diagnosis
treatment

A

most common form of spinal cord dysfunction in adults
age-related osteoarthritic changes cause narrowing of the cervical spinal canal, leading to chronic spinal cord compression and neurologic disability.

symptoms
pain
loss of motor function - especially dextrous function
loss of sensory function
loss of autonomic function

MRI gold standard for diagnosis

decompressive surgery

86
Q

what drugs can exacerbate myasthenia gravis

A

lots of different drugs - be careful prescribing

don’t need to learn but examples:
penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

87
Q

what cranial nerves are affected by a vestibular schwannomas
what are the classical symptoms

A

CNs V, VII and VIII

vertigo, sensorineural hearing loss and tinnitus
typically arises from cells of the VIII nerve at the cerebellopontine junction and later involves CNV (absent corneal reflex) and CNVII (facial palsy)

requires urgent ENT referral

88
Q

in what patient group should triptans be avoided as treatment for cluster headaches

A

people with a history of coronary artery disease

89
Q

idiopathic intracranial hypertension
- presentation
- management

A

young, overweight females at risk
presents with headache, blurred vision, papiloedema, possible 6th nerve palsy

management:
advise weight loss
diuretics e..g acetazolamide
repeated LP to reduce pressure

90
Q

What do you need to know from a patient after a loss of consciousness collapse

A

Are they well? Illness can precipitate a seizure
What was she doing at the time? Thinking vasovagal
Any warning or aura
First memory on recovery - after syncope memory is usually retained
Pain, injuries, incontinance, tongue biting - more towards epileptic
Previous attacks?
Other neurological symptoms now or ever

91
Q

What do you need to know from a witness after a LoC collapse

A

Any warning? Pale sweaty nauseous points to syncope. Twitching, blankness, eye movement points to seizure
Fall stiffly or floppily? Stiff more likely seizure. Floppy more likely faint
Shaking? Brief myoclonus jerks syncope. Rhythmic clinic jerks seizure
Cyanosis? More in seizures
Duration? In syncope usually less than a minute seizure linger
Duration of shaking? Prolonged could be NEAD
Condition on recovery

92
Q

Immediate assessments and investigations after a suspected seizure

A

Vital signs, oxygenation and BM
ECG - cardiac rhythm disturbance?
Neurological examination
Bloods for acute metabolic disturbances e.g. hyponatraemia, hypocalcaemia
CT head usually done

93
Q

What is a complex partial seizure / focal impaired awareness seizure

A

Seizure activity confined to one area of the brain
Awareness is impaired without total LoC and may have partial recollection of events
Often staring blankly

94
Q

What is a focal aware seizure

A

Confined to one area of the brain e.g. twitching of the face and arm but the patient is fully aware
Much less common than focal impaired awareness

95
Q

What can focal seizures progress to

A

Can spread to whole brain and develop into a generalised tonic clinic seizure
Patient will then totally lose consciousness and begin to display features of a GTCS

96
Q

What symptoms are typical of a partial seizure of the temporal lobes

A

Auditory symptoms - includes primary auditory cortex
Deja vu - temporal lobe important in memory
Bizarre psychic phenomena e.g. derealisaiton and depersonalisation
Automatism e.g. picking, lip smacking, repetitive mumbling

97
Q

What factors can be important to ask about to identify underlying causes for epilepsy

A

Birth history - ask about prematurity, delivery
Childhood milestones or developmental delay
Seizures in childhood or infancy
Significant head injury
History of CNS infection
FHx of epilepsy
Medications
Recreational drugs and alcohol

98
Q

What are febrile convulsions?

A

Common in early childhood - seizure activity that occurs associated with a high fever
Normally brief convulsions however some can be prolonged activity
Typically occur around 18 months

99
Q

How do febrile convulsions relate to later developing epilepsy

A

Most children with a single and uncomplicated convulsion do not go on to have epilepsy

Some do lead to epilepsy later in life usually with seizures originating in the temporal lobes and associated with scarring in this area - Mesial Temporal Sclerosis
Risk factors for going on to have epilepsy include prolonged and several febrile convulsions, additional features such as transient hemiparesis, FHx epilepsy, convulsions occurring at an atypical age or with only a mild pyrexia

100
Q

When do serum anticonvulsant levels need to be measured

A

Phenytoin is the only one that needs monitoring with close correlation between serum level and efficacy
Others only need measuring if concern about toxicity or overdose, concordance, absorption and a drug interaction causing a drop in levels

101
Q

What group should sodium valproate be completely avoided in and why

A

Any women of childbearing agents
Major congenital defects - especially neural tube defects; spina bifida and anencephaly
Syndrome of dysmorphia, developmental delay and cognitive impairment;t known as foetal valproate syndrome

102
Q

Can people with epilepsy ever be medication free?

A

Some patients who have been seizure free for several years especially those who had childhood epilepsy may be considered to withdraw from anticonvulsants

103
Q

What are the issues with switching anticonvulsant medications

A

Avoiding breakthrough seizures - gradually reduce one whilst gradually increasing the other I.e. taking two drugs for several weeks at adjusting doses

Tolerability of new drug

Potential interactions between the two during changeover period or interaction with any other drugs taken particularly OCP

implications for driving - breakthrough seizure means stopping driving for at least six months and informing DVLA. Either way DVLA recommends stopping driving for six months whist changeover occurs

104
Q

What are the common side effects of lamotrigine and the serious side effects

A

Common dose related: sedation, dizziness, nausea, insomnia
Rarer and serious: allergic skin rash, multisystem hyeprsensitivity reaction. Rapid medical attention and discontinuation needed

105
Q

Risk of lamotrigine in pregnancy

A

No AED can be said to be completely safe in pregnancy

Lamotrigine at 200mg or less a day is said to be minimal risk and out balances risk of seizures to mother and foetus
Take folic acid 5mg daily as soon as contraception stopped and continue throughout first trimester

106
Q

What factors can reduce seizure threshold

A

Current illness eg chest infection or UTI causing pyrexia and raised inflammatory markers

Missing medication

New medication that reacts with AEDs to lower seizure threshold eg tramadol, amitriptylline

Alcohol excess

Recreational drugs

Metabolic disturbance inc hypoglycaemia and hyponatraemia

Broken sleep, fatigue and jet lag

GI disturbances which may impair absorption

107
Q

Driving implications after a breakthrough seizure

A

Tell DVLA
License removed
Need to be seizure free for a year for return of license

108
Q

Doctors duty if patient does not want to inform DVLA

A

Make all efforts to persuade pt to inform DVLA about event seizure - personal, family and public safety
Explain to pt that they will have to break confidentiality and inform the DVLA if not
Record all encounters in medical records
Discuss with medical defence organisation before informing DVLA

109
Q

What is medically refractory epilepsy
How can it be managed

A

Seizures failed to come under control with at least two different anticonvulsant drugs at adequate tried doses

Each new drug less likely to be successful but some respond with 2 or more AEDs

This disorder increases risk if status epilepticus and of sudden unexplained death in epilepsy

110
Q

Hen is epilepsy surgery considered

A

Where a well defined structural cause for seizures is apparent
In a part of the brain that resection may be possible

Further investigation required to assess possible benefit from surgery, without undue risk of damage and input of MDT

111
Q

Treatment pathway for status eplipeticus

A

Benzodiazepine first line (repeated)
IV antipileltic second line eg IV phenytoin or sodium valproate
General anaesthesia third line

112
Q

What is the DVLA advice after a first seizure

A

Inform DVLA and be seizure free for 6 months before driving

113
Q

Where is a lesion that causes a relative afferent pupillary defect
How is it detected

A

Optic neuropathy - damage to CN II
Detected by a swinging light test - when moving light quickly between eyes pupil should remain constricted due to direct and consensual response
In a RAPD the dir3ft response is impaired so the pupil dilates when light shone into that eye

114
Q

What is optic neuritis

A

An area of inflammation that damages the optic nerve

115
Q

What blood tests should be done in optic nerve pathology

A

Serum B12 - optic neuropathy can mimic optic neuritis

Non specific inflammatory markers - CRP, ESR

Specific tests for autoimmune conditions - ANA, ANCA, dsDNA, ENA, anti cardio lipid antibodies, serum ACE levels - optic neuritis could be the first presentation of a multi system autoimmune disease such as SLE, granulomatosis with polyangitis, sarcoidosis

Serology for possible infective triggers - HIV, syphilis, hep B and C

Rare; aquaporin 4 antibodies which can result in an attack in specific parts of the CNS including optic nerves

116
Q

What is the diagnosis of a single demyelinating episode before it can be MS
How can diagnosis of MS be made

A

Clinically isolated syndrome of CNS demyelination (shown on MRI)
Has to happen twice to be MS

If LP is done after first episode and shows oligoclonal bands then a diagnosis of MS could be made immediately
Can also consider scheduled MRI to look for demyelination lesions over time

Clinical attacks of inflammation within the CNS at different times and in different places

117
Q

Where can ataxia arise from?

A

Cerebellar ataxia - cerebellum and it’s connections in the brain
Sensory ataxia - dorsal columns OR peripheral nerves / nerve roots
Vestibular ataxia - vestibular apparatus and its connections

118
Q

How can types of ataxia be distinguished from each other

A

Vertigo and nausea - main presenting symptom in vestibular and made worse with head movements. Often associated with hearing loss and/or tinnitus. V & N can also be present in cerebellar ataxia so ask about coordination in arms and if one side worse .e.g in cerebellar stroke

Sensory disturbance or loss - numbness, pins and needles in limbs or trunk. May be aware balance worse in the dark or closing eyes in shower (Romberg). May additionally have Lhermittes sign(pain on neck flexion) or tight sensation around trunk

Bladder disturbance - sensory ataxia due to a SC lesion in often associated with bladder urgency and frequency. Rarely present due to sensory ataxia from the peripheral nerves so think dorsal columns/SC lesion if bladder disturbance

119
Q

What are the potential risks of high dose steroids

A

GI irritation - give PPI cover
Agitation, restlessness and insomnia

Rarely a steroid psychosis can occur

Hyperglycaemia usually with chronic steroid use but can rarely happen acutely

Very rarely avascular necrosis of the hip can occur with short term high dose steroid use

120
Q

How are high dose steroids given for MS relapse

A

1g methylprednisolone IV in the morning for 3 days in an inpatient setting

As an outpatient can give methylprednisolone 500mg daily for 5 days

121
Q

What tests are needed before giving high dose steroids

A

Ensure no signs of systemic infection before giving steroids which are immunosuppressant - WCC, CRP
FBC, renal function and random glucose along with dipstick for UTI

122
Q

What is secondary progressive MS?
How is treatment approached?

A

Begins relapsing remitting but then transforms to progressive disease - atonal degeneration and loss of nerve cells with minimal inflammation

Once progressive then disease modifying drugs no longer use of and treatment switches to symptomatic relief including for spasticity e.g. baclofen, neuropathic pain e.g. gabapentin, depression e..g sertraline, urinary symptoms e.g oxybutynin

123
Q

What are the range of treatments used for neuropathic pain

A

Anticonvulsants are often used
Pregabalin or gabapentin are effective
Tricyclics antidepressants but note anticholinergic side effects
Trigeminal neuralgia can be managed with carbamazepine or oxcarbazepine
SNRI duloxetine can be helpful
Sometimes nerve blocks, epidurals and surgical options considered

124
Q

Types of MS

A

Relapsing remitting - most common. Acute attacks followed by remission
Secondary progressive - relapsing remitting deteriorating to have signs and symptoms between relapses. 65% of RR patients go on to SP within 15 years
Primary progressive - progressive from onset without remission. More common in older people

125
Q

when do NICE guideline recommend starting anti-epileptics

A

normally after a second seizure but some circumstances after a first seizure…
- pt has remaining neurological deficit
- brain imaging shows a structural abnormality
- EEG shows unequivocal epileptic activity
- patient or their family or carers consider the risk of having a further seizure unacceptable

126
Q

What are the common presenting symptoms of MS

A

Optic neuritis - blurred vision, pain on movement, colour desaturation

Cerebral - fatigue, weakness, sensory disturbance

Brain stem symptoms - vertigo, slurred speech, ataxia, in coordination, double vision

Spinal cord symptoms - weakness, sensory disturbance, autonomic dysfunction

127
Q

How can grey matter involvement happen in MS
what is its significance

A

Neuronal loss and axonal transection can occur - grey matter

Irreversible - may be the primary driver of disability in MS
relevant to cognitive impairment and seizures

128
Q

What are the chronic plaques in MS compared to acute plaques

A

Chronic plaque are an expanding area of microglial cells around an inactive centre- cause of axonal damage

Acute plaques are macrophage mediated inflammation via antigens crossing the blood brain barrier and initiating an autoimmune response

129
Q

What are evoked potentials tests

A

Can be visual or somatosensory
Assess speed of transmission in optic nerve or in posterior columns of the spinal cord, the brain stem and the cerebral cortex

130
Q

What effects do disease modifying agents have in MS

A

Reduce MRI lesion activity
Reduce progressive brain atrophy
Reduce rates of elapses
Reduce sustained disability progression
May increase product of nerve growth factor

131
Q

What are the injectable disease modifying therapies for MS

A

Beta- interferons
- more frequent doses (IM weekly or SC multiple times a week)

Glatiramer acetate (copaxone)
- subcutaneous daily

These first 2 are considered first line therapies. Side effects few and include skin reactions, flu like symptoms and occasionally an acute reaction
Then…

Alemtuzumab (lemtrada)
- IV two courses

Natalizumab (tysabri)
- IV monthly

These two are considered higher efficacy

132
Q

What are the oral disease modifying therapies in MS

A

Dimethyl fumerate (tecfidera)

Teriflunomide (aubagio)

Fingolimod (gilenya)

133
Q

What is the link between alemtuzumab and other diseases

A

Other autoimmune diseases are increased by use of alemtuzumab including thyroid disease, immune thrombocytopenia and goodpasture syndrome which need treating

134
Q

What is the link between natazlizumab (tysabri) and the JC virus

A

JC virus is endemic in the population
But interaction of antibodies from previous infection with natalizumab can cause progressive multifocal leukoencephalopathy which has a 25% mortality rate
Link betwEen duration of treatment and risk

Need to test for antibodies of the JC virus in patients receiving treatment to assess risk and decide whether to change treatments/use a different option

135
Q

Where does the spinal cord terminate

A

L1

136
Q

What conditions can mimic MS

A

Anticardiolipin antibody system

Devics syndrome - neuromyelitis optica

Neurosarcoidosis

Sjögren’s syndrome

For the last two important to ask about systemic symptoms to distinguish from MS e.g rashes, fever, athropathy, weight loss or respiratory difficulties

137
Q

how does juvenile myoclonic epilepsy tend to present

A

unprovoked episodes of myoclonus (jerking) bilaterally in the upper and lower limbs which occur more often early in the morning or near bedtime (i.e. nearing sleep deprivation)

138
Q

Management of myasthenia Gravis

A

First line pyridostigmine - long acting acteylcholinesterase inhibitor

When not controlled start immunosuppressive - prednisolone

Thymectomy if associated thymoma

139
Q

Management of myasthenic crisis

A

Plasmapheresis
IV immunoglobulins

140
Q

Cerebellar symptoms

A

Dysdiodochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

141
Q

where is the lesion in internuclear ophthalmoplegia
what condition is it most common in

A

in the medial longitudinal fasiculus; the communication between the CNIII and CNVI when looking left or right so causes nystagmus of one eye i.e. if L eye nystagmus when looking to left then INO on R side of MLF

most common in MS where a demyleinating lesion occurs here

142
Q

what are the causes of cervical cord syndromes

A

inflammatory
- MS, post infective, neuromyelitis optics
- connective tissue diseases

compressive
- discs
- tumours

infective

metabolic
- B12 or copper deficiencies

143
Q

what are the vascular causes of a sudden onset hemiparesis

A

ischameic stroke
primary intracerebral haemorrhage
extra-cerebral haemorrhage (sub-arachnoid, sub dural, extra dural)
venous sinus thrombosis

143
Q

what are the vascular causes of a sudden onset hemiparesis

A

ischameic stroke
primary intracerebral haemorrhage
extra-cerebral haemorrhage (sub-arachnoid, sub dural, extra dural)
venous sinus thrombosis

143
Q

what are the vascular causes of a sudden onset hemiparesis

A

ischameic stroke
primary intracerebral haemorrhage
extra-cerebral haemorrhage (sub-arachnoid, sub dural, extra dural)
venous sinus thrombosis

144
Q

what are the symptoms of a third nerve palsy

A

dilated pupil (mydriasis)
ptosis
abdcuted eye

145
Q

what is the treatment for a focal seizure

A

lamotrigine or levetiracetam

146
Q

what is Charcot Marie tooth disease

A

an inherited peripheral neuropathy affecting sensory and motor nerves

usually inherited in an autosomal dominant pattern

presents with LMN signs typically in first 2 decades of life

147
Q

A-E causes of peripheral neuropathy

A

Alcohol
B12 deficiency
Cancer and CKD
Diabetes and Drugs
Every Vasculitis

148
Q

What is Lambert Eaton Myasthenic Syndrome

A

typically occurs in patients with small-cell lung cancer
similar presentation to myasthenia gravis but symptoms temporarily improve initially with exercise

149
Q

what is neurofibromatosis

A

inherited condition that causes neuromas to develop throughout the nervous system
type 1 more common than type 2
many neurological symptoms and associations

cafe-au-lait spots on the skin
bony dysplasia
yellow brown sots on the iris
axillary freckling

note type 2 is most associated with acoustic neuromas especially bilateral

150
Q

what is tuberous sclerosis

A

generic condition that causes harmatomas (benign growths) in multiple systems affecting the skin, brain, lungs, heart, kidneys and eyes

associated with epilepsy and developmental delay

151
Q

what group of patients with TIA should be admitted immediately for assessment

A

on warfarin/a DOAC/ or has a bleeding disorder and they are suspected of having a TIA, they should be admitted immediately for imaging to exclude a haemorrhage

152
Q

what are the first line treatments for neuropathic pain

A

amitriptyline, duloxetine, gabapentin, pregabalin

153
Q

what is first line for trigeminal neuralgia

A

carbamazepine

154
Q

trochlear nerve palsy

A

Defective downward gaze and vertical diplopia
patient tilts their head to the opposite side
eye deviates supero-laterally

155
Q

what is syringomyelia

A

a collection of cerebrospinal fluid within the spinal cord

presents with loss of sensation to temperature but the preservation of light touch, proprioception and vibration - classically “cape” like distribution
UMN signs

diagnose with MRI
treat by treating cause e.g. tumour, trauma, or by draining with a shunt if persistent

156
Q

carpal tunnel syndrome

A

compression of the median nerve in the carpal tunnel

  • parasthesia in thumb, index and middle finger
  • pt shakes hand for relief esp at night
  • wasting of thenar evidence
  • weak thumb abduction
  • tapping causes parasthesia (Tinel’s sign)
  • wrist flexion causes symptoma (Phalen’s sign)

treat with corticosteroid injections and last resort surgical decompression

157
Q

What is cataplexy

Strongly associated condition

A

sudden and transient loss of muscular tone caused by strong emotion (e.g. laughter, being frightened)

Around two-thirds of patients with narcolepsy have cataplexy

158
Q

Link between lambert Eaton syndrome and exercise

A

Muscle weakness improves with exercise

159
Q

which anti epileptics affect the p450 system

A

carbamazepine - inducer

phenytoin - inducer

sodium valproate - inhibitor

160
Q

causes of bilateral facial nerve palsy

A

Sarcoidosis
Guillian-Barre
Lyme disease
Bilateral acoustic neuromes - NF type 2

161
Q

subacute combined degeneration of the spinal cord

A
  • due to B12 deficiency
  • dorsal columns and lateral corticospinal tracts affected
  • proprioception and vibration lost first then parasthesia
  • UMN signs develop
162
Q

motor neurone disease presentation

A

can present with both upper and lower motor neurone signs
rarely presents before aged 40

163
Q

drug used in MND

A

riluzole

used mainly in ALS - prolongs life by about 3 months

164
Q

respiratory care and nutrition in MND

A

BIPAP at night

PEG feeding

165
Q

what is spinal stenosis
symptoms/signs

A

pressure on spine from mass, trauma or spondylolisthesis

altered sensation below affected level

LMN signs at affected level
UMN signs below affected level

166
Q

cervical spondylosis signs

A

altered sensation below affected levele
LMN signs in the upper limbs
UMN signs in the lower limbs

Clinical Years / Progress Test (24 decks)

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