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Finals > Neurology > Flashcards

Neurology Flashcards

1
Q

Guillain Barre syndrome presents how long after an URTI or gastroenteritis

A

1-4 weeks

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2
Q

Pathogens associated with Guillain Barre syndrome

A

Viral - CMV, EBV, HIV, influenza, HSV, cytomegalovirus
Bacteria - campylobacter, mycoplasma pneumoniae, E.coli
Parasites - toxoplasmosis

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3
Q

Non-infectious triggers for Guillain Barre syndrome

A

Systemic illness - Hodgkins lymphoma, CLL, hyperthyroidism, sarcoid, renal disease
Pregnancy
Surgery
Immunisation

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4
Q

Pathogenesis of Guillain Barre syndrome

A

Post-infectious autoimmune reaction that generates cross-reactive antibodies (molecular mimicry)

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5
Q

Clinical features of Guillain Barre syndrome

A

Symmetrical/bilateral ascending flaccid paralysis, stocking glove distribution from lower limbs to upper limbs
Back and limb pain
Neuropathic pain
Peripheral symmetrical paraesthesia hands/feet
Reduced/absent reflexes
Cranial nerve involvement - bilateral facial nerve paralysis/facial diplegia, ophthalmoplegia - Miller Fisher syndrome
Involvement of respiratory muscles
Voiding dysfunction
Intestinal dysfunction
Arrhythmia

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6
Q

CSF findings in Guillain Barre syndrome

A

Cytoalbuminologic dissociation - normal cell count but raised protein level
Cell counts <50

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7
Q

Antibodies associated with Guillain Barre syndrome

A

Anti-GM1 antibodies (antibodies directed against gangliosides)

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8
Q

What happens to nerves in Guillain Barre syndrome

A

Demyelination

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9
Q

Differential diagnosis for Guillain Barre syndrome

A

Acute myelopathies (would have sensory levels and bowel/bladder involvement)
Botulism (would be descending)
Diphtheria
Lyme disease
Porphyria (would have abdo pain and prominent ANS fluctuation)

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10
Q

Management of Guillain Barre syndrome

A 
Monitor cardiac and respiratory function
Consider ICU/HDU care
VTE prophylaxis
High dose IV immunoglobulins
Plasmapheresis
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11
Q

Prognosis of Guillain Barre syndrome

A

Progression peaks around 2-4 weeks after symptom onset
Symptoms recede in reverse order of their development
80% recover by 6 months
3-5% mortality
15% get severe disability

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12
Q

At how many weeks does disability peak in a) acute b) subacute c) chronic Guillain Barre syndrome

A

a) 4 weeks
b) 4-8 weeks
c) >8 weeks

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13
Q

Features that suggest an UMN lesion

A 
Increased tone (spasticity)
Weakness (variable)
Brisk reflexes
Sustained clonus
Babinski reflex
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14
Q

Features that suggest a LMN lesion

A 
Decreased/normal tone
Weakness
Reduced/absent reflexes 
Muscle wasting 
Fasciculations
No pathological reflexes
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15
Q

GBS mimics

A

Poliomyelitis: prodromal flu symptoms, rapid deterioration, proximal > distal asymmetrical paralysis, no sensory deficit, recent travel
Enterovirus 71: prodromal illness, acute flaccid paraparesis, outbreaks in Australia and Cambodia
Rabies: acute flaccid paraparesis 1-2 months after exposure
C
Acute transverse myelitis
Anterior spinal artery occlusion

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16
Q

What blood tests would you order if a patient presents with limb weakness

A 
FBC
U+E
LFTs
CRP/ESR
K
Ca
PO4
Mg
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17
Q

Inheritence pattern of Charcot-Marie-Tooth

A

Autosomal dominant

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18
Q

What is the most common inherited peripheral neuropathy

A

Charcot-Marie-Tooth

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19
Q

Features of Charcot-Marie-Tooth

A 
Predominantly distal weakness 
Distal muscle wasting
Sensory loss
Proximally progresses 
Foot deformities - pes cavus, high arch, hammer toes, pes plantus
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20
Q

Causes of a predominant sensory loss with a glove and stocking distribution

A

Diabetes
Alcohol
B12 deficiency

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21
Q

Features of carpal tunnel

A

Pain and paraesthesia in the distribution of the medial nerve
Tinnels test positive
Phalens test positive

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22
Q

Where do you insert the needle for lumbar puncture

A

Above or below L4

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23
Q

Risks of lumbar puncture

A 
Post lumbar puncture headache
Infection
Bleed
Neuropathy
Brain herniation
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24
Q

Description of CSF in MS

A

Clear
Normal pressure, lactate, glucose
Normal/slightly raised protein
WBCs raised <50

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25
Q

Description of CSF in GBS

A

Clear
Normal pressure, lactate, glucose
Really high protein
WBC raised <10

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26
Q

Description of CSF in SAH/stroke

A 
Bloody/pink/yellow (xanthochromia)
Pressure normal/slightly increased
Normal lactate and glucose
Raised gamma globulin protein
Raised RBCs and WBCs
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27
Q

Lumbar puncture is most sensitive for SAH if performed how long after symptom onset?

A

12 hours

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28
Q

Description of CSF in bacterial meningitis

A 
WBCs really raised >100-5000
Neutrophil predominant
Raised protein
Very low glucose
Very low CSF:plasma glucose ratio
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29
Q

Description of CSF in viral meningitis

A 
WBCs raised 5-1000
Lymphocyte predominant
Mildly raised protein
Normal/low glucose
Normal/low CSF:plasma glucose ratio
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30
Q

What is Bells Palsy

A

An acute facial nerve palsy
Cause unknown but thought to be viral
Diagnosis of exclusion

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31
Q

Prognosis of Bells Palsy

A

70% completely recover (without treatment). 13% minor permanent, 16% major permanent

32
Q

Onset of Bells Palsy

A

Evolved within 72hours

Symptoms may worsen in the first few days

33
Q

When does recovery tend to start after Bells Palsy

A

4-6 months after symptom onset

34
Q

What features would make Bells Palsy less likely to be the diagnosis of facial droop

A

Forehead sparing
Waxing and waning
Facial zones unevenly affected

35
Q

Differential diagnosis for Bells Palsy

A

Stroke
Ramsay Hunt Syndrome
Lyme disease
Facial nerve schwannoma (benign facial tumour)

36
Q

Management of Bells Palsy

A

Steroids early on
Consider Acyclovir
Tape eye shut at night
Artificial tears

37
Q

What is Ramsay Hunt syndrome

A

Herpez zoster (shingles) affecting the geniculate ganglion of the facial nerve

38
Q

What can trigger reactivation of shingles

A

Immunosuppression

Stress

39
Q

Clinical features of Ramsay Hunt syndrome

A

Rash/blisters in or around ear, scalp, hair line, inside mouth
Painful
Generalised burning sensation in the area
Unilateral facial weakness, drooping, difficulty closing eye/blinking, altered taste, difficulty eating/drinking/speaking
Hearing loss, dizziness, vertigo, tinnitus

40
Q

Management of Ramsay Hunt syndrome

A 
Acyclovir ASAP (ideally within 3 days of symptom onset)
Short course of high dose steroids
Analgesia - consider neuropathic agents
41
Q

Prognosis of Ramsay Hunt syndrome

A

If treated within 3 days 70% fully recover
If treatment delayed >3 days then 50% fully recover
Recovery pattern similar to Bells Palsy

42
Q

You would refer someone with Ramsay Hunt to a specialist if there is no improvement in facial nerve palsy after how long?

A

1 month

43
Q

You would refer someone with Ramsay Hunt to an ophthalmologist if they still can’t close their eye after how long?

A

2-3 weeks

44
Q

Differentials for loss of consciousness

A 
Vasovagal syncope
Cardiogenic syncope 
Unprovoked seizure/epilepsy
Provoked seizure - substance abuse or withdrawal
Non-epileptic attack disorder
Migraine events
Vestibular disorders
TIA
45
Q

Difference between a simple and complex partial seizure

A

Simple - fully aware throughout

Complex - consciousness/awareness impaired during the event

46
Q

Features of temporal lobe seizures

A

Memory disturbance such as déjà vu
Olfactory and auditory hallucinations
A feeling of a rising epigastric sensation/fear
Bizarre psychic phenomena such as derealisation and depersonalisation and even attacks of elation.
Automatisms: absent-mindedly plucking at clothes, lip-smacking, repetitive mumbling or repetition of a stereotypical phrase. More complex automatisms can occur (for example getting undressed), with no or only partial awareness/recollection subsequently

47
Q

What is mesial temporal sclerosis

A

Atrophy and scarring in the temporal lobe, typically hippocampus
Is a cause and effect of temporal lobe seizures/epilepsy
Gliosis (structural lesion) can be seen on MRI

48
Q

Risk factors for patients with epilepsy having a seizure

A

Intercurrent illness (chest infection, UTI – check temp + inflammatory markers)
Missing medication (common cause of breakthrough seizure)
New meds that interact with anticonvulsants or lower seizure threshold (tramadol and amitriptyline lower seizure threshold)
Alcohol excess acute binge/chronic heavy drinking (withdrawal seizures)
Use of recreational drugs
Hyponatraemia
Hypoglycaemia
Broken sleep/fatigue/jetlag
GI disturbance that alters absorption
NB: photosensitive epilepsy syndromes are small minority

49
Q

Sodium Valproate can have serious interactions with which other anticonvulsant?

A

Lamotrigine

50
Q

How do you change a patients anticonvulsants

A

Gradually reduce the dose of one whilst simultaneously gradually increasing the dose of the new one

51
Q

DVLA advice regarding changing anticonvulsants

A

If have breakthrough seizure have to stop driving and inform DVLA + licence withheld for 6 months. The DVLA recommend, (but do not legally enforce) that when a patient is changing epilepsy drugs that they stop driving during the changeover period and for six months thereafter: this is because of the recognised risk of breakthrough seizures

52
Q

If a patient is changing epilepsy meds, what sort of activities do they need to be careful of due to the risk of breakthrough seizures

A

Working at height, cycling in traffic, working with dangerous machinery, or being alone beside deep water, less obvious things like taking a bath (shower with door open or someone nearby), parents with young children may have to consider activities such as help supervising the child’s bath-time

53
Q

Definition of epilepsy

A

Two or more unprovoked seizures separated by more than 24 hours, One unprovoked seizure with an underlying predisposition to seizures (recurrence risk over the next 10 years that is similar to the recurrence risk after two unprovoked seizures), Diagnosis of an epilepsy syndrome

54
Q

Causes of provoked seizures

A

Metabolic and electrolyte disturbances: hypoglycemia and hyperglycemia, hyponatremia and hypernatremia, hypocalcemia, uremia, thyroid storm, hyperthermia, water intoxication
Mass: brain tumors and metastases, hippocampal sclerosis
Withdrawal: Alcohol withdrawal (most common trigger in adults), noncompliance with anticonvulsant treatment, medication withdrawal
Intoxication: cocaine, ecstasy, carbon monoxide poisoning, metal poisoning
Meds: amitriptyline, penicillin, maprotiline, lithium, lidocaine, antipsychotics, theophylline
Infections: encephalitis, brain abscess, meningitis, septic shock
Ischemia: stroke, perinatal injuries
Trauma: traumatic brain injury
Increased ICP and cerebral edema: eclampsia, hypertensive encephalopathy, cerebrovascular malformation
Fever in infants and children (see febrile seizures)

55
Q

What is Todds paralysis

A

Post-ictal weakness or paralysis of the affected limb or facial muscles. Lasts for minutes up to hours

56
Q

When do tonic seizures often occur

A

When the person is drowsy/asleep/waking up

57
Q

What is a relative afferent pupillary defect and how do you detect it

A

Its a sign of optic (CNII) neuropathy
Detected with swinging light test - in normal circumstances the pupil remains constricted because of equal direct (light shone into that eye) or indirect (light shone into the other eye) stimulation. In an eye affected by optic neuropathy the pupil paradoxically dilates when light is shone into that eye as the direct stimulus (light via ipsilateral damaged optic nerve) is weaker than the indirect stimulus (light via intact contralateral optic nerve).

58
Q

Differentials for optic neuritis

A

MS
B12 deficieny
Systemic inflammatory diseases
Infection (rare)

59
Q

MRI findings of MS

A

High signal lesions in the periventricular white matter - represent demyelination
Lesions perpendicular with long axis of lateral ventricles

60
Q

How can cerebellar lesions affect speech

A

Can cause staccato speech

61
Q

What is L’Hermitte’s phenomenon

A

A sudden electric shock like sensation radiating down and up the spine, provoked by flexion and extension of the neck
It is a characteristic symptom of a patch of inflammation in the cervical spinal cord

62
Q

Which medication can be used to ease spasticity

A

Baclofen

Dantrolene

63
Q

Which medication can be used for neurogenic bladder (common in MS)

A

Oxybutinin (anticholinergic)

64
Q

What is MS

A

A chronic degenerative CNS disease

Auto-immune inflammatory demyelination of white matter in brain and spinal cord

65
Q

Mean age onset of MS

A

20-40

66
Q

Clinical features of multiple sclerosis

A

Optic neuritis - impaired vision, colour blindness
Internuclear ophthalmoplegia (INO) - affected eye has impaired adduction and when they try the other eye gets nystagmus
Lhermitte’s sign
Absent abdominal reflex
Pyramidal tract lesion - UMN signs
Dorsal column lesion - loss of vibration and fine touch, numbness, paraesthesia, sensory ataxia
Cerebellar - staccato speech, nystagmus, intention tremors
Cranial nerve palsies
Autonomic dysfunction
Cognitive changes
Uhthoff’s phenomenon

67
Q

What is Uhthoff’s phenomenon

A

A feature of MS (but can also be triggered by a viral infection)
A reversible exacerbation of neurological symptoms following physical exertion, a warm bath, or fever

68
Q

What contrast can be used with MRI to differentiate old Vs new MS lesions

A

Gadolinium contrast

69
Q

Electrophoresis of CSF in MS shows what

A

Oligoclonal bands

70
Q

What are the 3 main types of MS

A

Relapsing remitting
Secondary progressive
Primary progressive

71
Q

Definition of an MS relapse/exacerbation

A

New symptoms or significant worsening of existing symptoms, both of which last at least 24 hours and are preceded by at least 30 days of relative clinical stability

72
Q

Escalation Vs induction therapy for MS

A

Escalation - you start with disease modifying drugs first then use stronger meds if not controlled
Induction - if severe at presentation, use strong meds/immunosuppressants at first then long term maintenance with disease modifying drugs

73
Q

What meds can be used for painful paraesthesias in MS

A

Carbamazepine

Amitriptylline

74
Q

How does pregnancy affect MS

A

Decreased rate of relapses during pregnancy but higher rate in the postpartum period
Long-term clinical course doesn’t change

75
Q

Treatment for an acute exacerbation of MS

A

High dose glucocorticoids (methylprednisolone)

Second line: plasmapheresis

76
Q

Main drug used as a disease-modifying-drug for MS

A

Interferon beta

Finals (32 decks)

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