Neurology 3 Flashcards
1
Q
How do you investigate a migraine?
A
Mainly clinical
Exclude differentials - bloods, consider for CT/MRI
2
Q
If you take the OCP and have a migraine with aura, what are you at risk of?
A
Ischaemic stroke
3
Q
What triggers a migraine?
A
CHOCOLATE
CHeese
OCP
Caffeine
AlcohOL
Anxiety/stress
Travel
Exercise
Also too much/little sleep, sensory stimuli, dehydration
4
Q
What are migraines?
A
Recurrent acute attacks of unilateral frontal pulsating headache
5
Q
What worsens migraines?
A
Head movement or physical activity
6
Q
What are migraines associated with?
A
N+V + photo/phonophobia
7
Q
What are the features of migraines?
A
POUND
Pulsating
Onset 4-72hrs
Unilateral
Nausea
Disabling
8
Q
How do migraines start?
A
25% with an aura
9
Q
What is an aura of a migraine like?
A
Usually visual - flashes/lines/zigzags = fortification spectra, scotoma (black hole in visual field)
10
Q
What are the less common features of migraines?
A
Paraesthesia, dysphasia etc
11
Q
What is the acute management of a migraine?
A
Triptans (sumatriptan) + NSAIDs +/- anti-emetic if nauseous
12
Q
What is the non-medicated prophylaxis for migraines?
A
Reduce triggers
Stop OCP
13
Q
What is the 1st line medicated prophylaxis for migraines?
A
Beta blocker (propranolol)
14
Q
What are the other options for medicated prophylaxis of migraines?
A
Anticonvulsant (topiramate), amitriptyline, botulinum toxin type A
15
Q
What is there a risk of when treating a migraine?
A
Medication overuse headache - avoid offering opioids or ergots
16
Q
What is the most common headache?
A
Tension headache
17
Q
What triggers a tension headache?
A
Stress/anxiety, sleep deprivation, eye strain, noise etc.
18
Q
How does a tension headache present?
A
Bilateral tight pressing band-like sensation +/- scalp tenderness
19
Q
How long do tension headaches last?
A
30 mins to 7 days, can be chronic or episodic
20
Q
What are the key differentials of a tension headache from a migraine?
A
Non-pulsatile
Not worsened on head movement/physical activity
No N+V
21
Q
How do you diagnose a tension headache?
A
Clinical diagnosis from history
22
Q
How do you manage a tension headache?
A
Lifestyle advice e.g. regular exercise, avoid triggers
Stress relief
NSAIDs for symptoms
23
Q
How do you reduce the risk of a medication overuse headache?
A
Limit use of analgesia to no more than 6 days/month
Avoid opioids
24
Q
Where is a tension headache felt?
A
25
Where is a migraine felt?
26
What is the most disabling primary headache?
Cluster headache
27
What triggers a cluster headache?
Alcohol
28
How do you diagnose a cluster headache?
Clinical
29
How does a cluster headache present?
Rapid abrupt onset excruciating pain around one eye, temple or forehead - always unilateral, usually affects same side + ipsilateral autonomic features
30
What are the autonomic features of cluster headaches?
Bloodshot eye, miosis, ptosis, lacrimation, rhinorrhea
31
How long do cluster headaches last?
15-60 mins
32
When do cluster headaches occur?
A couple of times a day, usually at the same time - often nocturnal/wakes patient from sleep
Last several weeks, followed by pain-free periods before next cluster
33
What is the acute management of a cluster headache?
100% oxygen for 15 mins via non-rebreathable mask + SC sumatriptan
Analgesics unhelpful
34
How do you prevent a cluster headache?
Verapamil (CCB) = 1st line
Avoid alcohol during
35
How does trigeminal neuralgia present?
Paroxysmal severe sharp stabbing pain
Unilateral in distribution of trigeminal nerve branches - patient's face screws up with pain
36
How long does trigeminal neuralgia last?
seconds - 2 mins
37
What causes trigeminal neuralgia?
Due to compression of trigeminal nerve usually due to loop of vein/artery
Can be secondary e.g. aneurysm, tumour
38
What triggers trigeminal neuralgia?
Cutaneous stimuli e.g. touch, shaving, washing face, eating etc.
39
How do you treat trigeminal neuralgia?
Anticonvulsants - carbamazepine
Analgesics do not work
40
What is giant cell arteritis?
Granulomatous arteritis of large arteries
41
Which artery is commonly affected in giant cell arteritis?
Temporal artery
42
What is the epidemiology of giant cell arteritis?
F\>M
\>50
Caucasian
43
What condition is GCA strongly associated with?
Polymyalgia rheumatica
44
How do you treat GCA?
Corticosteroids - prednisolone immediately
45
What do you prescribe alongside steroids for GCA?
PPI for gastric protection
Bisphosphonates/vitamin D for osteoporosis prophylaxis
46
How do you investigate GCA?
Bloods - ESR/CRP raised
Gold standard - temporal artery biopsy
47
How does GCA present?
Headache
Scalp tenderness - often noticed when brushing hair
Jaw claudication
Malaise
Visual disturbance
48
What is a serious complication that can occur with GCA?
Vision loss - irreversible + painless, monocular
Can happen rapidly + suddenly
49
What visual disturbances can happen with GCA?
Blurred/double vision, diplopia, amaurosis fugax
50
How does the affected vessel in GCA present?
Palpable, tender and non-pulsatile
51
What is Parkinson's disease?
Degenerative movement disorder caused by the loss of dopaminergic neurons in the substantia nigra
52
What are the 2 main pathological hallmarks of Parkinson's disease?
Presence of lewy bodies
Dopaminergic neuron loss
53
How do you investigate parkinson's disease?
Diagnosis is clinical
MRI head/DaTscan may help differentiate
54
How does Parkinson's disease present?
Rigidity (lead-pipe)
Bradykinesia
Resting tremor
55
What is bradykinesia?
Slow to initiate movement (especially repetitive ones), fine movements e.g. micrographia, expressionless face
56
Where is resting tremor in PD patients most obvious?
In hands (pill-rolling tremor), improves on movement
57
Describe the onset of PD.
Asymmetrical, one side is always worse
58
Describe the gait of a PD patient.
Short shuffling gait with stooped posture, narrow base and reduced arm swing
59
What symptoms present first in a PD patient?
Anosmia, depression/dementia, pain, REM sleep disorders, urinary symptoms, constipation
60
How is PD managed?
Co-careldopa (levodopa + carbidopa - decarboxylase inhibitor) - symptom relief, doesn't alter disease progression
MAO-B inhibitors and COMT inhibitors - inhibit dopamine breakdown
61
What are the side effects of co-careldopa?
Causes serious long-term mbility complications - start as late as possible
62
What is the 1st line treatment for PD patients \<60?
Dopamine agonist
63
How does carbidopa work?
Prevents peripheral breakdown of levodopa before it gets to the brain. Allows for lower dose of L-dopa to cause less side effects.
64
What is HD?
Hereditary hyperkinetic neurodegenerative disorder affecting the striatum and other areas
65
What is the inheritance pattern of HD?
Autosomal dominant
66
What causes HD?
CAG repeat in Huntington gene
67
Describe the onset of HD.
100% penetrance
Number of repeats increases as disease passed on so symptoms beccome more severe and appear earlier with each generation (anticipation)
68
How does HD present?
Hyperkinesia - chorea, dystonia, incoordination
Psychiatric issues e.g. psychosis, depression, dementia
Behavioural difficulties, cognitive impairment
69
What is chorea?
Involuntary, irregular, unpredictable jerky muscle movements
70
How is HD treated medically?
No cure, symptom control
Chorea - benzodiazepines
Neuroleptic drugs - haloperidol for psychosis
71
What is MS?
Chronic inflammatory disorder involving a T-cell mediated immune response (autoimmune) causing demyelination in the CNS
72
What is the typical onset of MS?
20-40 yrs
73
What are the different types of MS?
RRMS (80%)
Primary progressive
Secondary progressive
74
Describe the presentation of RRMS.
Partial/complete recovery between attacks, gets worse with each epidsode, attack must last \>48 hours
75
What is primary progressive MS?
Gradually worsens from onset without relapse/remissions
76
What is secondary progressive MS?
Follows on from RRMS, late stage with gradually worsening symptoms and fewer remissions
77
What is clinically isolated syndrome?
First episode of MS, must last \>24 hours, about half progress on to MS
78
What are the visual S+S of MS?
Optic neuritis (often first sign), internuclear ophthalmoplegia, Uhtoff's phenomenon
79
What is Uhtoff's phenomenon?
Worsening of visual symptoms when body temperature is increased e.g. hot bath, fever
80
What are the sensory S+S of MS?
Numbness, tingling, Lhermitte's sign
81
What is Lhermitte's sign?
Electric shock like sensation spreads from neck to limbs on neck flexion
82
What are the motor S+S of MS?
UMN signs - brisk reflexes, hypertonia, spastic weakness
83
What are the cerebellar S+S of MS?
Ataxia, diplopia, nystagmus, intention tremor, vertigo
84
What are the spinal cord S+S of MS?
Urinary incontinence, sexual dysfunction
85
What are the miscellaneous S+S of MS?
Fatigue, intellectual impairment
86
How do you manage an acute relapse of MS?
Methylprednisolone for 5 days (shortens relapse)
87
What is the long term management of MS?
DMARDs e.g. beta interferon, glatiramer acetate, natalizumab
88
What do you treat MS spasticity with?
Baclofen
89
What do you treat MS urinary issues with?
Self-catheterisation, laxatives, anti-cholinergic alpha blockers e.g. doxazosin for urinary incontinence
90
What do you treat MS fatigue with?
Amantidine. physio, exercise
91
What do you treat MS neuropathic pain with?
Gabapentin, amitriptyline
92
What do you treat MS depression with?
SSRI, psychotherapy
93
How do you investigate MS?
McDonald's criteria
MRI - diagnostic \> demyelination
LP - oligoclonal IgG bands \> inflammation
94
What is McDonald's criteria?
Evidence of damage to CNS that is disseminated in time and space
Time - shown by relapses or new lesions on MRI compared to previous one
Space - shown by lesions in different places on MRI or symptoms indicating damage to a new part of CNS
95
What is optic neuritis?
Unilateral eye pain on movement, loss of central vision
96
What is internuclear ophthalmoplegia?
Decreased adduction of IL eye + nystagmus on abduction of CL eye
97
What is MND?
Progressive degeneration of motor neurons in the brain and spinal cord
98
What causes MND?
Unknown, could be familial
99
What is the most common MND?
Amyotrophic lateral sclerosis (ALS)
100
What is ALS?
Asymmetrical patchy distribution of both UMN and LMN features with evidence of spread to other regions
101
What muscles does MND involve?
Weakness and atrophy eventually involves muscles of all 4 extremities, trunk and bulbar muscles
102
How is MND diagnosed?
Diagnosis based on clinical findings - no diagnostic test
Nerve conduction studies + EMG to support diagnosis
MRI/LP/bloods to exclude differentials
103
How is MND managed without medication?
MDT care, feeding and respiratory support when required
104
What is the prognosis of MND?
Involvement of respiratoy muscles associated with poor prognosis - death usually respiratory failure due to bulbar palsy
105
MND significantly overlaps with what condition?
Frontotemporal dementia
106
How do you differentiate MND from MS/polyneuropathies?
No sensory loss or sphincter disturbance in MND
107
How do you differentiate MND from myasthenia gravis?
No effect on eye movement in MND
108
How is electromyography (EMG) used for MND?
Shows denervation of muscles due to degeneration of LMNs
109
What is bulbar palsy?
LMN lesion of CN 9-12 (affects muscles of mouth and throat responsible for speech and swallowing)
110
What is meningitis?
Inflammation of the meninges due to infection
111
Who is meningitis most common in?
Infants then teenagers/young adults
112
What are the common bacteria which cause meningitis?
Neisseria meningitidis (meningicoccus), strep. pneumoniae, haemophilus influenzae type B, listeria monocytogenes
113
What are the common viruses that can cause meningitis?
HSV, enterovirus, varicella zoster, EBV
114
Which meningitis is more serious?
Bacterial
115
How does meningitis present early on?
Fevers, rigors, headache
116
What are the signs of meningism (meningitis)?
Neck stiffness
Photophobia
Non-blanching purpura rash (meningococcal only)
Kernig's sign
117
What are the other signs of meningitis?
Raised ICP - vomiting, altered consciousness, seizures
Risk of septic shock (suggestive of meningococcal septicaemia) - tachycardia, hypotensive, slow cap refill etc.
118
How do you investigate meningitis?
Bloods - blood cultures ASAP (first line)
LP - gold standard. Done ASAP but shouldn't delay treatment
119
When is an LP contradicated?
Raised ICP - may cause coning
120
How does viral meningitis present?
Much more mild than bacterial
121
How is bacterial meningitis treated?
All cases treated as bacterial until proven otherwise
In community - urgent injection of benzylpenicillin + transfer to hospital
Hospital - treat empirically immediately - IV ceftriaxone
Once organism is confirmed, treat according to this
122
What happens after a confirmed case of bacterial meningitis?
Notify public health
Prophylactic antibiotics for close contacts - ciprofloxacin
123
What are the features of CSF in bacterial meningitis?
Cloudy
High protein
Low glucose
High neutrophils
Bacteria
124
What are the features of CSF in viral meningitis?
Clear
Mildly raised or normal protein
Normal glucose
High lymphocytes
Negative for bacteria
125
How is viral meningitis managed?
Often only requires supportive treatment, no specific treatment
Aciclovir for suspected HSV meningitis/concerned about encephalitis
126
What organism is neisseria meningitidis?
Gram -ve diplococci
127
What organism is strep pneumoniae?
Gram +ve diplococci
128
What is Kernig's sign?
Lie patient on back, flex one hip and knee to 90 degrees, slowly straighten knee whilst keeping hip flexed (stretches meninges) \> +ve = spinal pain/resistance to movement
129
What causes meningococcal septicaemia?
Neisseria meningitidis
130
What is meningococcal septicaemia?
Infection is in bloodstream = cause of non-blanching rash (bad news!)
131
What is the prognosis of meningitis?
Treat ASAP, high mortality rate especially in children
132
What are the long term complications of meningitis?
Hearing loss, seizures, learning disabilities/cognitive impairment, focal neuro deficits
133
What is encephalitis?
Inflammation of cerebral cortex due to infection
134
What viruses can cause encephalitis?
HSV, enterovirus, EBV
135
What is the most common cause of encephalitis?
Virus
136
What other organisms can cause encephalitis?
Bacteria e.g. listeria monocytogenes or parasitic/fungal/non-infectious
137
How does encephalitis present?
1st symptoms = fever, flu-like symptoms, headache
Focal neurological deficits
Seizures
Behavioural change, confusion, coma
138
How do you investigate encephalitis?
Bloods and blood cultures
LP - CSF shows lymphocytosis
Viral PCR to identify virus
CT/MRI - asymmetrical but often bilateral inflammation
139
How is encephalitis treated?
Aciclovir if viral cause
140
What causes spinal cord compression?
Central disc protrusion (mostly lumbar) - disc herniation, bulging
Degenerative discs \> osteophyte formation in osteoarthritis/spondylosis
Tumour/haematoma/abscess
Trauma
141
What cancers are most likely to metastasise to the spine?
Breast, prostate, lung
142
How do you treat spinal cord compression?
Surgery ASAP - doesn't improve condition, stops progression e.g. laminectomy, decompression
Pain relief
Treat underlying cause e.g. tumour
143
How do you investigate spinal cord compression?
MRI spine
144
How does spinal cord compression present?
Motor deficit below level of compression
UMN signs e.g. cervical myelopathy \> clumsy hands, difficulty walking
Sensory loss up to level of compression
Aching back pain radiating distally
145
What is the presentation of spinal cord compression dependent on?
Location and injury type
146
How is MND managed with medication?
Antiglutametergic drugs e.g. riluzole
Symptomatic relief
147
Describe the headache of GCA.
New onset severe unilateral headache around temple/forehead
