Week 14 - Neurological Disease Flashcards
(154 cards)
1
Q
What is the difference between primary and secondary headache?
A
Primary = tension-type, migraine, trigeminal autonomic cephalagias (cluster headaches) - a headache that is not caused by a different pathology
Secondary - headache caused by an alternative pathology
2
Q
What are the red flags for headache?
A
3
Q
What tests can you order for headaches?
A
Depends on the possible diagnosis - if just tension or migraine and you’re sure, no need to further test.
If worried about underlying pathology…
4
Q
What are the SNNOOP10 criteria for red flags for headache?
A
5
Q
How do we manage primary headaches?
A
Classify what type
Determine frequency
If frequent - consider Rx - acute / abortive / preventative
6
Q
What are the three types of primary headache?
A
Tension-type
Migraine
Cluster
7
Q
How can you differentiate between different types of headaches?
A
8
Q
What is another name for trigeminal autonomic cephalgia? What are the Sx?
A
Cluster headache - trigeminal autonomic cephalalgia - excruciating stabbing pain - these Ps cant lie still, agitated, cant get comfortable as the pain so severe (unlike other headaches where the P wants to lie still). Is not related to having headaches in clusters.
9
Q
How can you calculate whether a tension headache is frequent, infrequent or chronic?
A
Freq = >10 days / month
Infreq = < 10 days / month
Chronic = >15 days / month for at least 3 months
10
Q
How can you calculate whether migraines are episodic or chronic?
A
15 days
<15 days / per month = episodic
> 15 days / month for at least 3 months
11
Q
What is it called when a migraine lasts for longer than 72 hours?
A
Status migrainosus
12
Q
What structure in the neck is thought to be involved with causing headaches?
A
Trigeminocervical complex
13
Q
Which abortive therapies can be given for tension headaches?
A
Paracetamol
Aspirin
14
Q
Which abortive therapies can be given for migraine?
A
Paracetamol
Aspirin
NSAIDs
Prochlorperazine (Dopa agonist)
Metoclopramide (Dopa agonist)
Triptains
Monoclonal ABs
Nerve block injection
15
Q
What abortive therapies can be given for cluster headaches?
A
High flow O2 therapy
Triptans
NeurostimulationWhat
16
Q
What lifestyle modification can be prescribed for all 3 types of primary headache?
A
Adequate sleep
Hydration
Exercise
Cognitive behavioural therapy
17
Q
Should you give opioids for headache?
A
No
18
Q
What is the maximum that analgesics should be used in a month to prevent overuse headaches?
A
<15 days
19
Q
What preventative medications can be given for tension headaches?
A
Amitryptyline
Acupuncture
20
Q
What preventative medications can be given for migraine?
A
Propanolol
Amitryptyline
Topiramate
Triptans
CGRP mABs
Botulinum toxins
Nerve block injections
Acupuncture
Neurostimulation
21
Q
What preventative medications can be given for cluster headaches?
A
Verapamil
Topiramate
22
Q
What is it called when you get electrical shock-like or stabling pain for anywhere between a few seconds to 2 minutes in the mouth, cheek or gums of the face?
A
Trigeminal neuralgia
23
Q
What are most cases of trigeminal neuralgia attributed to?
A
Idiopathic cause
24
Q
What is the first line treatment for trigeminal neuralgia?
A
Carbamazepine
25
What is second line treatment for trigeminal neuralgia?
Gabapentin
Pregabalin
Lamotrigine
26
What is a seizure?
Abnormal firing of the brain
27
What is the difference between focal and generalised seizures?
Focal = positive motor and visual features
Can be aware or have impaired awareness
Generalised = loss of awareness, synchronous movements, eyes are open
28
Which part of the brain is the most common cause of focal seizures?
Temporal lobe (60%)
Then frontal
Rare - parietal or occipital lobes
29
What is it called when a seizure lasts for longer than 5 minutes?
Status epilepticus
30
In a generalised seizure - which part of the brain is effected?
Both hemispheres are affected.
31
How do seizure symptoms vary by lobe?
32
How is epilepsy defined?
2 or more unprovoked seizures separated by 24 hours
or - 1 unprovoked seizure with a high risk of further seizures (>60%) in the next 10 years
33
How is resolved epilepsy defined?
Seizure free for 10 years inc 5 years post medication free
34
How can you differentiate between non-seizures?
35
What is the commonest cause of seizures occurring in previously well controlled epilepsy?
Inconsistency in taking medication
Also - lifestyle changes, new medications which interact with the antiseizure meds, infection, pregnancy
36
Why does pregnancy affect seizure medication levels?
Pregnancy - inc in circulating volume, dilutes amount of protein and renal clearance - can clear medication quicker and can affect protein binding drugs. During pregnancy P needs to be monitored and dose adjusted to prevent seizures in pregnancy
37
What is SUDEP?
Sudden unexplained death of epilepsy
Responsible for 2-18% of deaths of all Ps with epilepsy - 10x inc risk with those who have generalised tonic-clonic seizures.
38
When is epilepsy deemed to be drug resistant?
When two appropriate anti-seizure meds have failed to stop the seizures.
39
What is an internal sensation of restlessness called?
Akathisia
40
What is asterixis?
Negative myoclonus - associated with sudden drop in tone due to metabolic disturbances - hepatic encephalopathy or renal dysfunction.
Myoclonus is a sudden, brief, involuntary muscle jerk. It is caused by abrupt muscle contraction, in the case of positive myoclonus, or by sudden cessation of ongoing muscular activity, in the case of negative myoclonus (NM).
Clonus = hyperreflexia
41
What are sudden, brief-repetitive, non-rhythmic movements called?
Tic
42
What is involuntary, irregular, non-rhythmic, unpredictable movement flowing between muscles called? Can appear as if Ps are dancing.
Chorea
43
What is the definition of a tremor?
Involuntary rhythmic oscillation of one or more body parts
44
What is myoclonus?
Brief, involuntary, regular twitches
45
What does abrupt or rapid progression of a tremor suggest?
A secondary cause - e.g. drug toxicity
46
What is the difference between pyramidal and extrapyramidal tracts?
Pyramidal = voluntary motor control & fine motor control
Extrapyramidal = Modulate motor functions, especially involuntary movement, posture and tone
47
What are the two main pyramidal tracts?
Corticospinal Tract: Controls voluntary movements of the body.
Corticobulbar Tract: Controls voluntary movements of the face, head, and neck.
48
Which investigations can you do for tremor?
49
Which drugs can commonly cause tremor?
Sodium valpoate
Phenytoin
50
How can you differentiate between an essential tremor and a Parkinsonian tremor?
Essential tremor - happens with movement rather than at rest. Also improves with alcohol and worsened by caffeine.
Parkinsons - happens at rest
51
What is essential tremor plus?
Essential tremor with additional signs such as dystonia, ataxia and Parkinsonism.
52
What scan is 100% specific in determining whether a P has Parkinsons or Essential Tremor?
DaTscan
53
What medications can be given for essential tremor?
Propanolol
Also - primidone, topiramate, botulinum
54
What type of facial paralysis do you get with the following diseases?
- Guillain-Barre
- Lyme
- HIV
- Sarcoid
- MG
All cause bilateral LMN facial nerve palsy
55
How can you determine whether a facial lesion affects an UMN or a LMN?
In upper motor neuron - only the lower half of the face is affected
In a LMN - the entire half of the face is affected
56
What type of lesions (UMN or LMN) are caused by the following?
- stroke
- MS
- Tumour
- Bell's palsy
Stroke, MS & Tumour = UMN
Bell's palsy = LMN
57
Which virus is most commonly associated with Bell's palsy?
Herpes simplex virus
58
What medication can be given in Bell's palsy?
If presenting within 72 hours of first onset - can prescribe prednisolone.
May also prescribe antivirals but seek advice.
59
What complications can occur during recovery of Bell's palsy?
When the nerve recovers - can be some growth or plasticity of the nerve - may no longer innervate the correct part of the face
Can cause synkinesis (involuntary contraction) or Bogorad syndrome (cry when you eat).
60
What causes Wernicke's encephalopathy?
Thiamine deficiency
61
What is the triad of Wernicke's
Mental status changes
Ocular dysfunction
Gait apraxia
62
What are possible differentials for Wernicke's?
63
What is the biochemical implication of giving glucose to patients who are deficient in thiamine?
Thiamine (and magnesium) are needed for co-factors in the breakdown of glucose. Without these - end up down the pyruvate -> lactate pathway = increase of lactate in these patients!
Need to therefore give thiamine before giving glucose in nutritionally deficient patients
64
What would symmetric lesions around the 3rd and 4th ventricles and aqueduct, also affecting mamillary bodies suggest?
Wernicke's encephalopathy
65
What vitamin is thiamine?
B1
66
What complications can arise from thiamine deficiency?
Wernicke encephalopathy
Korsakoff syndrome
Dry & wet beri beri
GI beri beri
Machiafava Bignami disease - ass with Italian Chianti wine abuse
67
How does Korsakoff's present?
Amnestic disorder - confabulation, personality changes and memory loss
68
What is the management for acute alcohol withdrawal?
Correct any metabolic derangements
CXR or CT if concern for head injury
Chlordiazepoxide
Do CIWA
Give IM / IV Pabrinex
69
What factors inc risk of another seizure after a single unprovoked seizure?
If it
- occurred in sleep
- if there are MRI brain abnormalities
- If there is concerning EEG
- If there is an underlying genetic disorder
70
Why do focal seizures occur?
There is a surrounding loss of inhibition - e.g. decrease in GABA transmission - means that transmission is no longer dampened -> abnormal firing
71
What is the difference between a tonic and clonic phase of seizure?
Tonic = stiff phase - due to prolonged depolarisation due to loss of GABA inhibition
Clonic = jerk phase - due to some neuronal repolarisation
72
What is MS?
Inflammatory and progressive demyelinating condition - get episodes of inflammation -> demyelination of nerves.
Occurs in CNS.
Causes focal symptoms +/- neurological disability
73
Do we know what causes MS?
Not entirely - thought to be a combo of genetic, environmental and other issues. No single gene identified.
Poss link to Vit D deficiency
Inc risk poss with EBV
Smoking inc riskh
74
What questions do we need to ask when taking a seizure Hx?
75
What things can present in the post-ictal period?
Drowsiness
Confusion
Psychotic
Bitten tongue
Lost continence
76
Does epilepsy occur in provoked seizures?
No = epilepsy only occurs in unprovoked seizures
77
What is the term of coordinated involuntary motor activity (almost always accompanied by impaired awareness and amnesia)
Automatisms
(e.g. chewing or lip smacking)
78
Are EEGs definitive in diagnosing epilepsy?
They can be supportive but are not definitive - can have normal EEGs in frontal lobe seizures
79
Does a normal EEG exclude epilepsy?
No! Routine EEG can remain negative in 10% of Ps with epilepsy
80
What things can look like a seizure?
81
What is the main treatment for non-epileptic attacks?
Psychotherapy
82
How can you differentiate between non-epileptic attack and seizure on exam?
Non-epileptic attacks - wax and wane lasting over 2 mins
Have motionless unresponsiveness for over 5 mins
Do not respond to drugs!
If true seizure - on exam - eyes should remain deviated to the ground on turning (check with mirror for visual fixation).
If generalised tonic-clonic seizure, should have positive Babinski and absence of corneal reflexes
83
What is convulsive syncope?
Not a seizure or epilepsy
Is cerebral hypoxia that results in myoclonic jerks (usually less than 20)
Usually - there is a lack of BF to brain = cerebral hypoxia = myoclonic jerks.
May see slowing EEG but not epileptiform discharges
84
What percentage of Ps with herpes simplex encephalitis will present with seizures?
Up to 50%
85
What is the first imaging done for Ps presenting to A&E with seizures?
CT
86
What bleed has a biconvex appearance on CT?
Extradural
87
How can you differentiate a subarachnoid bleed from other bleeds on CT?
In subarachnoid the blood can leak into the sulci of the brain
88
If the presentation is not acute, which is the best mode of imaging the brain in seizures?
MRI
89
Which part of the brain is the most common cause for epilepsy?
Temporal lobe
90
What is the most likely cause of mesial temporal sclerosis?
Childhood febrile seizures
91
What is limbic encephalitis?
AI condition that attacks the limbic system (hippocampus, cingulate gyrus, hypothalamus, frontotemporal lobe and insula)
92
Which nuclear medicine scans can be done for seizure and syncope?
FDG PET
SPECT
93
When taking a neurological history - what is the most important thing to ascertain that can help you decipher what is going on?
Speed of presentation
Can use it to differentiate between acute and less acute etc.
94
95
What does a hyperacute presentation suggest in neurology? (Seconds -> minutes)
Vascular pathology
96
What does an acute presentation suggest in neurology? (Hours)
Vascular or inflammatory pathology
97
What does a subacute presentation suggest in neurology? (Days-weeks)
Inflammatory or metabolic pathology
98
What does an acute on chronic presentation suggest in neurology?
Worsening of something preexisting - e.g. metabolic cause
99
What does a chronic presentation suggest in neurology?
Neoplastic or degenerative cause
100
Where do UMN and LMN in the motor pathway synapse? (Where the CNS and PNS meet)
The anterior horn
101
Which is the descending motor tract?
Corticospinal tract
Aka Pyramidal tract
102
What is the path of UMNs in the motor tract?
Fibres come from primary motor cortex and amalgamate into the corticospinal tract - through internal capsule and cerebral peduncles, midbrain, through medulla where they decussate to the contralateral side - synapsing in the anterior horn cell.
103
How does UMN damage present in terms of flexors and extensors in the pyramidal pathway?
Arm - flexors are stronger
Leg - extensors are stronger
Is increased spasticity (velocity dependent)
Brisk reflexes
Get positive Babinksi (extension of the big toe)
Coordination is not impaired
Sensation - will normally have a hemisensory problem as well
104
What is the difference between spasticity and rigidity?
Spasticity = velocity dependant increase in tone. Sign of pyramidal pathology
Rigidity = increased tone that is maintained throughout the movement. Sign of extrapyramidal pathology
105
How do spinal cord lesions present?
Depending on the size of the lesion - may get bilateral or unilateral signs.
Can get sensory level involvement
Bowel and bladder involvement is common.
Arms + legs will only be involved if damage is to the cervical spine. If below this impairment will be to legs only.
106
What is the pathway of the LMN?
Leaves anterior horn as a ventral root -they then join together to form a plexus - brachial plexus or lumbosacral plexus
Nerves then untangle into individual peripheral nerves. These get to NMJ and communicate with muscles.
107
If damage occurs at the point of the anterior horn - what Sx do you get?
Mixed UMN and LMN symptoms
108
What are the signs of LMN pathology?
Muscle wasting or fasciculations
Tone is normal or reduced
Reflexes are normal, reduced or absent
109
110
Which disease is an example of anterior horn pathology?
Motor Neurone Disease
111
How does nerve root pathology present?
With myotome and dermatome loss
Also lose the reflex that those roots innervate
112
What things can cause nerve root pathology?
Compression of the root (e.g. herniated intervertebral disc)
Inflammation
Infiltrative cause (neoplastic)
113
Is plexus pathology common?
No
Consider if there are multiple peripheral nerves involved in a limb.
114
How does peripheral nerve pathology present?
With weakness and sensory Sx in the distribution of the single nerve
115
Which nerve is involved?
116
Which nerve is involved?
117
Which nerve is involved?
118
What is the sensory innervation?
119
What is generalised polyneuropathy?
Weakness that starts distally, moves proximally in a glove and stocking pattern. Sensory and reflexes are also affected.
120
What can cause generalised polyneuropathy?
A - Alcohol
B - B12
C - Connective tissue, Cancer
D - Diabetes
E - Everything else (inc Guillain Barre)
121
Name a pathology of the NMJ
Myaesthenia Gravis
122
What are the Sx of myaesthenia graves?
Fatiguable weakness is the hallmark
Can affect eyes, face, speech, limbs, and SOB.
Is NO SENSORY INVOLVEMENT
123
What is the difference between myopathy and myositis?
Myopathy = non-inflammatory process affecting the muscles
Myositis = inflammation of the muscles
124
What is inflammation of the spinal cord called?
Myelitis
125
Is there a test for MS?
Is no single test - have to come to a clinical diagnosis
126
How can MS affect Ps?
Can affect them in different ways depending on which part of the nervous system is affected.
Has a relapsing / remitting presentation
Exam points towards UMN pattern
127
What is the most common cause of cauda equina syndrome?
Disc herniation
128
How can cauda equina present?
Saddle anaesthesia
Urinary retention
Weakness of ankle dorsiflexion
Absent ankle reflexes
129
Which diagnostic criteria are used for radiological imaging of MS?
McDonald Diagnostic Criteria
130
Which MRI sequence was designed for MS?
MRI FLAIR
131
How does optic neuritis present?
Pain on eye movement
Visual loss
132
If MS attacks the spine - which part is normally affected?
The cervical cord
133
How does cerebral small vessel disease present on MRI?
Patchy white matter changes - bright on T2 and FLAIR
134
Which MRI finding is common with MS?
Dawson fingers
135
What is MS?
Inflammatory and progressive demyelinating condition of CNS.
Occurs in attacks or relapses - where areas of demyelination occur - causes focal symptoms +/- neurological disability
136
How does MS differ from other neurological conditions?
Their lesions are disseminated in both time and space - no other disease does this.
137
What causes MS?
Thought to be a combination of genetic vulnerability + environmental and other insults that lead to the disease forming.
Thought there may be a possible link to Vit D deficiency as the further from the equator you are, the higher the incidence of MS.
Also thought that maybe there is a link between EBV and MS.
138
What are the traditional phenotypes of MS?
Relapsing remitting
Secondary progressive
Primary progressive
139
What are the three goals of Rx for Ps?
Disease modifying - reduce progression
Symptomatic - reduce symptoms
Acute relapse - manage acute Sx
140
Why do we give amytriptyline in MS?
Reduces pain and sensation
141
What is a psuedorelapse / pseudo exacerbation in terms of MS?
A pseudoexacerbation is a temporary worsening of symptoms without actual myelin inflammation or damage, brought on by other influences. These can include other illnesses or infection, exercise, a warm environment, depression, exhaustion, and stress.
We're suspecting that there hasn't been a new area of inflammation but we're suspecting that that old area has just made the patient a little bit more vulnerable to re-experiencing those same symptoms when something else happens.
142
What Rx is given for an MS relapse?
Methylprednisolone
143
What is myasthenia gravis?
144
What is Lambert-Eaton syndrome?
ABs against the voltage gated Ca channels in the pres-synaptic membrane.
Similar to MG but MG causes fatigue over time whereas LE may improve with exercise
145
Where can weakness present in MG?
Ocular
Bulbar / Facial
Diaphragm
Limbs
Generalised
146
What daily Rx is given for MG?
Pyridostigmine (Acetylcholinestease inhibitor)
147
What Rx is given for acute relapse in MG?
Prednisolone
148
What do you need to monitor with predinisolone (or any steroids?)
If P has diabetes - monitor sugars as can inc risk of hyperglycaemia
149
MG is one of the few situations where long term steroids may be used. Which is most commonly used?
Azathioprine
150
How does Azathioprine work?
Inhibits purine synthesis
151
What are the potential SE of Azathioprine?
Bone marrow suppression
Hepatotoxicity
152
How does Mycophenolate work?
What are its SEs?
T & B cell inhibition.
GI side effects are common. Monitor for skin cancer.
153
How does methotrexate work?
What are its SEs?
Inhibits DNA synthesis & T cell mediated inflammation
Can cause interstitial lung disease, bone marrow suppression and hepatotoxicity (but quickest to work)
154
What drugs should be avoided in MG?
Anything that causes neuromuscular blockade
- Cardiac drugs
- Abx
- APs
- β blockers
- Aminoglycosides
