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Neurology Flashcards

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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
Description of CSF in GBS
Clear Normal pressure, lactate, glucose Really high protein WBC raised <10
26
Description of CSF in SAH/stroke
``` Bloody/pink/yellow (xanthochromia) Pressure normal/slightly increased Normal lactate and glucose Raised gamma globulin protein Raised RBCs and WBCs ```
27
Lumbar puncture is most sensitive for SAH if performed how long after symptom onset?
12 hours
28
Description of CSF in bacterial meningitis
``` WBCs really raised >100-5000 Neutrophil predominant Raised protein Very low glucose Very low CSF:plasma glucose ratio ```
29
Description of CSF in viral meningitis
``` WBCs raised 5-1000 Lymphocyte predominant Mildly raised protein Normal/low glucose Normal/low CSF:plasma glucose ratio ```
30
What is Bells Palsy
An acute facial nerve palsy Cause unknown but thought to be viral Diagnosis of exclusion
31
Prognosis of Bells Palsy
70% completely recover (without treatment). 13% minor permanent, 16% major permanent
32
Onset of Bells Palsy
Evolved within 72hours | Symptoms may worsen in the first few days
33
When does recovery tend to start after Bells Palsy
4-6 months after symptom onset
34
What features would make Bells Palsy less likely to be the diagnosis of facial droop
Forehead sparing Waxing and waning Facial zones unevenly affected
35
Differential diagnosis for Bells Palsy
Stroke Ramsay Hunt Syndrome Lyme disease Facial nerve schwannoma (benign facial tumour)
36
Management of Bells Palsy
Steroids early on Consider Acyclovir Tape eye shut at night Artificial tears
37
What is Ramsay Hunt syndrome
Herpez zoster (shingles) affecting the geniculate ganglion of the facial nerve
38
What can trigger reactivation of shingles
Immunosuppression | Stress
39
Clinical features of Ramsay Hunt syndrome
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
Management of Ramsay Hunt syndrome
``` Acyclovir ASAP (ideally within 3 days of symptom onset) Short course of high dose steroids Analgesia - consider neuropathic agents ```
41
Prognosis of Ramsay Hunt syndrome
If treated within 3 days 70% fully recover If treatment delayed >3 days then 50% fully recover Recovery pattern similar to Bells Palsy
42
You would refer someone with Ramsay Hunt to a specialist if there is no improvement in facial nerve palsy after how long?
1 month
43
You would refer someone with Ramsay Hunt to an ophthalmologist if they still can't close their eye after how long?
2-3 weeks
44
Differentials for loss of consciousness
``` Vasovagal syncope Cardiogenic syncope Unprovoked seizure/epilepsy Provoked seizure - substance abuse or withdrawal Non-epileptic attack disorder Migraine events Vestibular disorders TIA ```
45
Difference between a simple and complex partial seizure
Simple - fully aware throughout | Complex - consciousness/awareness impaired during the event
46
Features of temporal lobe seizures
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
What is mesial temporal sclerosis
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
Risk factors for patients with epilepsy having a seizure
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
Sodium Valproate can have serious interactions with which other anticonvulsant?
Lamotrigine
50
How do you change a patients anticonvulsants
Gradually reduce the dose of one whilst simultaneously gradually increasing the dose of the new one
51
DVLA advice regarding changing anticonvulsants
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
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
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
Definition of epilepsy
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
Causes of provoked seizures
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
What is Todds paralysis
Post-ictal weakness or paralysis of the affected limb or facial muscles. Lasts for minutes up to hours
56
When do tonic seizures often occur
When the person is drowsy/asleep/waking up
57
What is a relative afferent pupillary defect and how do you detect it
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
Differentials for optic neuritis
MS B12 deficieny Systemic inflammatory diseases Infection (rare)
59
MRI findings of MS
High signal lesions in the periventricular white matter - represent demyelination Lesions perpendicular with long axis of lateral ventricles
60
How can cerebellar lesions affect speech
Can cause staccato speech
61
What is L'Hermitte's phenomenon
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
Which medication can be used to ease spasticity
Baclofen | Dantrolene
63
Which medication can be used for neurogenic bladder (common in MS)
Oxybutinin (anticholinergic)
64
What is MS
A chronic degenerative CNS disease | Auto-immune inflammatory demyelination of white matter in brain and spinal cord
65
Mean age onset of MS
20-40
66
Clinical features of multiple sclerosis
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
What is Uhthoff's phenomenon
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
What contrast can be used with MRI to differentiate old Vs new MS lesions
Gadolinium contrast
69
Electrophoresis of CSF in MS shows what
Oligoclonal bands
70
What are the 3 main types of MS
Relapsing remitting Secondary progressive Primary progressive
71
Definition of an MS relapse/exacerbation
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
Escalation Vs induction therapy for MS
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
What meds can be used for painful paraesthesias in MS
Carbamazepine | Amitriptylline
74
How does pregnancy affect MS
Decreased rate of relapses during pregnancy but higher rate in the postpartum period Long-term clinical course doesn't change
75
Treatment for an acute exacerbation of MS
High dose glucocorticoids (methylprednisolone) | Second line: plasmapheresis
76
Main drug used as a disease-modifying-drug for MS
Interferon beta

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