Common Neurological Conditions Flashcards
Done: To Do: Epilepsy MS Parkinson's Disease Migraine and Headaches Venous Sinus Thrombosis Temporal Arteritis
1
Q
Define epilepsy.
A
2 or more unprovoked seizures occuring more than 24 hours apart.
2
Q
What are the 2 main types of seizure?
A
Focal and generalised
3
Q
How can focal seizures be classified?
A
Simple partial or Complex partial, or secondary generalised seizures.
Further classified by the area of the brain they affect.
4
Q
Which are the 2 main areas in the brain that patients most commonly get focal seizures in?
A
Temporal and frontal
5
Q
How common is epilepsy?
A
0.5% prevalence - it is very common!
6
Q
What are the main types of generalised epilepsy?
A
Absence Myoclonic Atonic Tonic Tonic-Clonic
7
Q
A patient has a seizure. This is the first one they have ever had, and investigation shows no identifiable cause, and no ongoing risk.
How long will the DVLA ask them not to drive for?
A
They must go 6 months without a seizure before they can drive again.
Depending on circumstances, this may be extended to 12 months.
8
Q
A patient who drives HGVs for a living has a seizure. This is the first one they have ever had, and investigation shows no identifiable cause, and no ongoing risk.
How long will the DVLA ask them not to drive for?
A
They cannot drive an HGV/Class II vehicle until they have been seizure-free for 5 years.
If they take medication for the seizures, they must have gone 5 years seizure free without medication.
9
Q
A patient has epilepsy that has been well controlled on medication. Their last seizure was 6 months ago.
How long will the DVLA ask them not to drive for?
A
A further 6 months at least, so be seizure free for 12 months total at least.
10
Q
A patient with epilepsy has some of their medications changed.
The want to know about driving. What can you tell them?
A
They must wait at least 6 months after medication is changed.
Depending on how many seizures they have had, they may need to wait a further 6-12 months after that.
11
Q
A patient has well controlled epilepsy, and has been on the same medications for years. They continue to get seizures at night time however.
How long will the DVLA ask them not to drive for?
A
They need to have gone 3 years seizure free in the DAY TIME/WHILE AWAKE before they can drive again.
12
Q
What are the risk factors for epilepsy?
A
Family Hx Developmental abnormalities Trauma/surgery/hypoxic brain injury Space occupying lesion in skull Drugs CNS infection Metabolic disturbance Vascular abnormalities
13
Q
What factors can lower the seizure threshold in some individuals?
A
- Sleep deprivation
- Alcohol
- Drugs
- Physical/mental exhaustion
- Particular times in menstrual cycle
- Flickering lights
- Infection/metabolic disturbance
14
Q
A patient presents with recurrent episodes of “funny turns”.
They describe them as starting with their head turning to one side, then one limb jerking on the other side of the body. They remain conscious through these episodes.
What seizure type does this sound like?
A
Simple partial seizure
15
Q
A patient with simple partial seizures also finds that after each episode, one side of their face “stops working” for an hour.
They are worried about a stroke. What phenomenon is this more likely to be?
A
Todd’s paralysis - weakness of the limbs/face following a simple partial seizure.
16
Q
A patient with recurrent seizures describes:
- LoC or unaware of surroundings but may appear conscious still
- Vertigo
- Lip smacking
- Tachycardia
What seizure type does this describe, and what other features might they have?
A
Complex partial seizure.
Deja vu Jamais vu Visual or auditory hallucinations Emotional disturbance Automatism (impaired consciousness but motor function not impaired so they wander off)
17
Q
How do secondary generalised seizures occur?
A
Start as a partial seizure then electrical activity spreads to the lower brain areas.
Secondary generalised seizures are usually tonic-clonic.
18
Q
Describe the pattern of activity of a generalised seizure.
A
Start in the midbrain or brainstem, then spread simultaneously to both cortices.
19
Q
Which age and demographic groups is epilepsy more common in?
A
- Onset as children or people over 60.
- People with a learning disability
20
Q
Describe a typical absence seizure.
A
Pt unresponsive to stimuli but no LoC.
Stares, may go pale.
Fairly quick recovery.
May have some muscle jerking during the episode.
21
Q
Describe the EEG pattern of an absence seizure.
A
3Hz spike and wave pattern
22
Q
Describe a typical myoclonic seizure.
A
- Convulsions/limb jerking
- Eye rolling
- Tachycardia
- Breathing is erratic/depressed
23
Q
Describe a typical atonic seizure.
A
May appear to be a faint.
Limb tone suddenly absent, pt drops to the floor.
Often present with nasty facial/head injuries
24
Q
Describe a typical tonic seizure.
A
Rigidity of muscles, may bite tongue
Incontinence occurs
Epileptic cry
Hypoxia/cyanosis
25
Describe a typical tonic-clonic seizure.
Aura before attack.
Tonic phase first (10s-1 minute) (rigidity, tongue biting, incontinence)
Clonic phase second (seconds-minutes) (limb jerking, eye rolling)
26
What are the classic post-ictal symptoms?
Confusion
Drowsiness
Headaches
May be agitated/aggressive
27
How is epilepsy diagnosed?
Clinically i.e. through history
28
What tests would we do to rule out organic pathology causing seizures?
```
ECG
Calcium
Urine dip for diabetes
CT/MRI brain
Bloods - sugar, U&E, LFTs, CK, prolactin
```
29
Name a bunch of AEDs.
```
Levetiracetam
Lamotrigine
Sodium valproate
Carbamazepine
Phenytoin
Pregabalin
Ethosuximide
Phenobarbital
```
30
Which AED is used for absence seizures only?
Ethosuximide
31
When is phenobarbital used? Why?
Rarely - it causes sedation and tolerance over time.
32
Which 3 AEDs ork well for most types of epilepsy?
Levetiracetam
Lamotrigine
Sodium Valproate
33
Which drug is generally first line for generalised epilepsy?
Sodium valproate
34
What is the issue with sodium valproate?
It is much more teratogenic than other AEDs - 10% of children whos mothers use SV during pregnancy have a defect at birth of some description.
35
Which drug is first line for focal seizures?
Carbamazepine
36
A patient presents from GP with suspected epilepsy, but from the history you aren't convinced.
What other causes might there be for these apparent seizures?
```
Syncope
Arrhythmias
TIA
Migraine
Paroxysmal vertigo
Metabolic disorder
Encephalopathy
Panic attacks
Non-epileptic seizures
```
37
When might surger be considered in a pt with epilepsy?
If there is a mass lesion in the brain, or epilepsy is uncontrolled with medications.
38
How common are migraines?
They affect 15% of the population.
M:F 1:2
39
What symptoms are typically associated with migraines?
Nausea
| Photophobia
40
How can a migraine and TIA be distinguished from each other?
TIA's are more sudden in onset, and rare to have headache also.
Migraine usually comes on slowly/deficit occurs gradually.
41
What are some common triggers/risk factors for migraines?
- Times of relaxation
- Foods - chocolate, cheese, alcohol, caffeine.
- Travel
- Exercise
- Noise/lights
- Pregnancy, puberty, menstruation/menopause
- Obesity
42
A patient presents with awful headaches accompanied by bright lights in her vision, and zig-zag lines. What is this likely to be?
Migraine with visual aura
43
Why do visual aura occur?
Reduced blood flow to occipital cortex before an attack
44
Other than visual, what auras are possible with migraines?
Sensory (pins and needles)
| Speech (temporary dysarthria)
45
Do pts with migraines have clinical signs on examination?
No
46
Do pts with migraines always get an aura?
No - they can have a migraine without an aura.
47
What is the management of an acute migraine?
Simple analgesia (paracetamol/aspirin/NSAIDs)
Antiemetics
Triptans may be useful for some patients
48
What can we use for migraine prophylaxis?
Propanol
| Amytriptiline
49
When is migraine prophylaxis suggested?
If the pt experiences more than 2 episodes of migraine per month.
50
What can make migraines worse once treatment has been started?
Overuse of analgesics
51
Describe a cluster headache.
Severe short-lived headache, usually unilateral around one eye.
Often associated with nasal congestion.
52
How can we manage cluster headaches?
```
High dose O2
Triptans
Analgesics
Steroids
Lithium/Verapamil
```
53
How do tension headahces typically present?
With a band-like headache, no aura
54
What is the most common cause of Parkinsonism?
Idiopathic Parkinson's disease
55
What is the classic triad/tetrad of symptoms associated with Parkinson's disease?
Bradykinesia
Rigidity
Tremor
Postural instability
56
Describe the tremor that Parkinson's patients tend to have.
Pill-rolling, resting tremor.
Frequency 5-7 Hz.
57
When is the mean age of onset for IPD?
45-60 years
58
Define IPD.
Progressive neurodegenerative disease caused by loss of dopaminergic neurones in the substantia nigra.
59
Is IPD typically symmetrical?
Nope, usually asymmetrical.
60
How can bradykinesia manifest clinically?
Short, shuffling steps.
Reduced arm swing.
Difficulty initiating movements.
61
Decsribe the rigidity that classically accompanies IPD.
Lead pipe rigidity (i.e. bending arm is like bending a lead pipe, smooth consistent rigidity)
Cogwheel rigidity in wrists when slowly moved.
62
What are some other features of IPD, other than the classic triad?
- Mask-like face
- Flexed posture
- Micrographia
- Drooling
- Psychiatric symptoms
- Impaired smell
- Sleep disturbance
- Postural hypotension
63
How does drug induced parkinsonism differ in presentation to IPD?
Rigidity and rest tremor are uncommon in drug induced parkinsonism.
Drug induced has rapid onset, and bilateral motor symptom onset.
64
What kind of dementia is associated with IPD?
Lewy body dementia
65
What is parkinsonism?
Syndrome clinically similar to IPD, but which have additional features and a known aetiology
66
What are the causes of parkinsonism?
- Drug induced
- Progressive supranucelar palsy
- Multiple systems atrophy
- Wilson's disease
- Toxins
- Post-encephalitis
67
Which drugs are associated with parkinsonism?
- Chlorpromazine
- Prochlorperazine
- Haloperidol
- Droperidol
- Metoclopramide
68
What toxins can cause parkinsonism?
Carbon monoxide
| MPTP
69
What are the steps to managing IPD?
- Exercise and physiotherapy
- Medications
- Symptom control
- Surgery sometimes
70
Which drug tends to be first line in the management of IPD?
Levodopa
71
What is the problem with levodopa?
It requires some functioning neurones to convert it to dopamine, so only works in early stage disease, and may only work for 3-5 years.
72
Which IPD drug shows the most improvement in movement/motor symptoms?
Levodopa
73
Other than levodopa, what drugs can we use in IPD?
MAOIs
Dopamine agonists
COMT inhibitors
Amantadine
74
What can we give with levodopa? Why do we do this?
A decarboxylase inhibitor e.g. carbidopa to prevent peripheral metabolism of levodopa to dopamine.
This maximises the amount of dopamine that reaches the CNS.
75
What can we do to help motor symptoms associated with drug-induced parkinsonism?
Stop the offending drug.
Can also give antimuscarinics (block cholinergic receptors)
76
What imaging can we do to diagnose IPD?
We can't!
MRI will be normal.
PET scans are only for fancy research purposes at the moment.
77
Thinking about the non-motor symptoms of IPD, what can we do to help patients with IPD?
- Physiotherapy
- Pain relief (neuropathic pain)
- Laxatives
- Social support & OT
- SALT assessment
- Psychological support (counselling, antidepressants)
- Manage acute conditions e.g. UTI promptly
78
Define motor neurone disease.
A common condition caused by degeneration of motor neurones in the motor cortex and spinal cord.
79
Does motor neurone disease affect UMNs or LMNs?
Both!
80
What is never caused by motor neurone disease?
Sensory problems
81
What are the different types of motor neurone disease?
- Amyotrophic lateral sclerosis
- Progressive bulbar palsy
- Progressive muscular atrophy
- Spinal muscular atrophy
82
What are the most convincing cause of MND?
Genetic predisposition
83
When MND is inherited, what inheritance pattern does it follow?
Autosommal dominant
84
With what symptoms do 70% of MND patients present?
- Muscle weakness and wasting, usually at extremities
- Cramps
There is not usually any pain
85
O/E of a patient with distal muscle weakness and wasting, what signs might indicate MND?
UMN and LMN signs:
Brisk reflexes
Fasciculations
No sensory loss or sphincter problems.
86
Who does MND tend to affect?
Slightly more males, usually middle aged onset.
87
A 55 year old man presents to you with dysphagia and dysarthria, as well as muscle wasting in his distal legs, and hands.
What does the dysphagia suggest? What pattern of dysphagia would support this?
Bulbar or pseudobulbar MND.
Progressive pattern would support this.
88
How can we distinguish MND from myasthenia gravis?
MND never affects eye movements
89
When are spastic paraparesis and loss of muscle tone seen together?
In motor neurone disease!
Upper limbs tend to be weak in extension, lower in flexion.
90
How is MND diagnosed?
Clinically, sometimes supported by investigations
91
Which investigations can be used to support a diagnosis of MND?
EMG
| Nerve conduction studies
92
What investigations should be done with suspected MND to rule out other differentials?
MRI (foramen magnum/SC compression)
TFTs (hyperthyroid)
Ca (calcium/parathyroid issues)
Bloods for CK for muscle breakdown
93
Why do thyroid and parathyroid issues need to be ruled out when suspecting MND?
Hyperthyroidism and hyperparathyroidism can both cause muscle wasting and hyperreflexia.
94
Other than MND, what conditions exhibit both upper and lower MN signs?
Cervical spondylitis
| Spinal tumours
95
What is the prognosis for MND?
Poor - survival is usually less than 3 years.
96
Which teams should be involved in the care of a pt with MND?
- Specialist nurse
- Physio
- OT
- Orthotics
- SALT
- Dietician
- Respiratory and Gastro teams
Palliative care later on
97
How can we manage MND pharmacologically?
With:
- Riluzole (Na channel blocker)
- Baclofen
- Amitriptyline/propantheline
98
What does riluzole do in the management of MND?
Increase survival by 3-5 months
Delays need for supportive intervention e.g. gastrostomy, ventilatory support
Prolongs muscle strength
99
What does baclofen do in the management of MND?
Help reduce spasticity as a GABA agonist
100
What symptom can amitriptyline/propantheline help with in MND?
Drooling
101
What is multiple sclerosis?
A chronic autoimmune disorder characterised by CNS demyelination.
102
Tell me about the epidemiology of MS.
M:F 1:3
Most commonly presents between ages 20-40
More common at higher latitudes
103
What is the pathophysiology underlying MS?
Autoimmune destruction of oligodendrocites -> axonal loss mediated by antibodies to myelin. Macrophages express a different protein that allows them to cross the BBB.
Active sites of inflammation (plaques) can form anywhere in the CNS.
104
Where do plaques most commonly form in MS?
At the:
- optic nerves
- perventricular lesion
- brainstem
- cerebellar connections
105
How do most cases of multiple sclerosis progress?
In a relapsing-remitting fashion
106
A 30 year old man presents with blurred vision, muscle weakness, and fatigue. He also experiences parasthesia in his left arm.
What would you expect to see on fundoscopy of this patient?
Optic disc swelling
107
What cerebellar sign is commonly exhibited in MS?
Ataxia
108
How long do acute attacks of MS typically last?
1-2 months
109
What are the common features of multiple sclerosis?
```
Optic neuropathy
Optic disc swelling
Worse on hot day/after exercise
UMN signs
Relative afferent pupillary defect
Lethargy
Gait disturbance
Sensory symptoms
Muscle weakness
Ataxia
Tremor
Urinary incontinence
Sexual dysfunction
```
110
A 35 year old woman presents to neurology with gait disturbance, pins and needles down her right leg, and visual disturbance.
What investigations do we need to do, considering the top differential?
MS:
MRI (85% have plaques)
VEP (visual evoked potentials, for optic nerve lesion)
Oligoclonal bands in CSF (LP)
111
How is MS diagnosed?
1. At least one attack + multiple plaques on MRI
Or
2. Single attack/progressive MS + multiple plaques on MRI + additional evidence
112
How do we treat MS?
We can't cure it, but we can induce remssion in acute relapses, prevent relapses, and manage symptoms.
Nothing really alters long term outcomes.
113
What can we do for an acute relapse of MS?
Give a short course of high dose steroids (5 days)
114
What is the problem with using steroids for acute relapses of MS?
They should not be used more than twice a year.
They also don't alter long term outcomes.
115
What drug can we use to reduce the symptoms of MS, and how does it work?
Baclofen - GABA receptor antagonist
116
Other than baclofen, what can we give for MS relapse prevention?
B-interferon
Glatiramer acetate
Natalizumab
Mitoxantrone (experimental)
117
What holistic elements of care do MS patients need?
- Practical changes to living conditions
- Counselling
- Mx of infections esp. UTIs
- OT/PT
- Prevent pressure sores
- Sativea (cannabis extract for symptom relief)
118
How should fatigue be managed in MS patients?
Exclude all other causes e.g. anaemia, thyroid dysfunction, depression.
Mindfullness, CBT
Maximise management of MS.
Ensure good enough support networks.
119
Define dementia.
A syndrome characterised by chronic progressive cognitive impairment, significant enough to impact on a pts ADLs, existing for at least 6 months. No altered level of consciousness.
120
What is the most common cause of dementia?
Alzheimer's disease
121
Other than alzheimer's, what are the other causes of dementia?
Vascular dementia/multi-infarct
Lewy body dementia
Frontal lobe dementia
122
In terms of memory impairment, what kind of memory is most affected in dementia?
Generally short term memory is impaired, but long term memory is preserved.
123
An older gentleman comes to you with low mood, memory loss, and problems with speech that have been progressing.
Other than dementia, what is an important differential here?
Depression - can manifest in similar ways to dementia, or may co-exist.
124
What are some of the cognitive functions impaired in dementia?
```
Memory
Attention
Concentration
Language processing
Speech
Thinking
Judgement
```
125
What % of people over 85 are affected by dementia?
25%
| 20% at 80, 15% at 75, 10% at 70, 5% at 65
126
What is the average time from diagnosis of dementia to death?
10 years
127
Which medical conditions are associated with dementia?
Huntington’s
MS
HIV
Down's syndrome
128
Define Alzheimer’s disease
A form of dementia characterised by insidious onset of symptoms, associated with the formation of amyloid plaques, neurofibrillary tangles, and brain atrophy.
129
What are some of the features of late stage dementia?
- Severe and pervasive memory features/cognitive symptoms
- Marked behavioural changes, both positive and negative
- Severe disability - assistance required almost constantly
- No insight
130
Define frontotemporal dementia
Chronic progressive neurodegenerative syndrome characterised by change in personality and social conduct, with usually preserved memory and visuospatial skills. Due to frontotemporal lobe degeneration.
131
Define vascular dementia
Syndrome of cognitive decline caused by multiple acute ischaemic events that progresses in a step-wise manner.
132
Define Lewy body dementia
Syndrome of cognitive decline characterised by the presence of Lewy bodies in the brainstem and neocortical areas.
133
What is considered when distinguishing between types of dementia?
```
Course
Onset
Initial symptoms
Mood and behavioural changes
Other symptoms
Neurological features
Structural brain imaging
```
134
Can pts get mixed type of dementia? Eg?
Yes
Eg Alzheimer’s with vascular dementia
135
What is an important part of the history to get in a pt with suspected dementia?
Collateral Hx (alongside pts own account)
136
What is the aim of treatment for dementia?
Reduce rate of disease progression and prevent/manage complications/comorbidities in a timely manner.
137
What are the elements of care for dementia patients?
- Reduce disease progression
- Manage risk factors
- Social support
- Promote independance
138
How can we reduce disease progression for a patient with Alzheimer's disease?
Use of anticholinesterase drugs - delay cognitive decline by ~3-6 months in about 40% of patients.
139
Name some anticholinesterase drugs.
Donepezil
Galantamine
Rivastigmine
140
What are the side effects of anticholinesterase drugs?
```
Anorexia
Nausea
Vomiting
Diarrhoea
Abdo pain
Insomnia
Confusion
Agitation
Headache
```
141
Other than anticholinesterase drugs, what can we use pharmacologically for Alzheimer's?
NMDA receptor antagonists e.g. memantine
Antipsychotics for anxiety and sleep disorders
142
How can we prevent vascular dementia?
Reduce vascular risk factors - aspirin/warfarin therapy, control BP, and control cholesterol.
143
What is essential in primary care in a suspected dementia case?
Bloods and full screening for a reversible cause e.g. hypothyroid, metabolic distrubance, infection, depression.
144
What is essential in secondary care in a suspected dementia case?
Structural imaging to rule out reversible conditions, and to guide prognosis and Mx based on aetiology
145
What is a polyneuropathy?
Damage or disease affecting peripheral nerves in roughly the same areas on both sides of the body.
146
How are polyneuropathies classified?
According to which part of the nerve cell is affected; distal axonopathy, myelinopathy, and neuronopathy.
147
Give some examples of distal axonopathies/causes.
```
Diabetic neuropathy
Kidney failure
Connective tissue disease
Deficiency (malnutrition, alcohol)
Chemical (toxins/drugs e.g. chemotherapy)
```
148
Why are the feet often the first affected part of the body with polyneuropathies?
They are the most distal, and therefore have the longest axons, so blood supply is more likel to be compromised.
149
What is the acronym we can use to remember causes of peripheral neuropathies? What does it stand for?
```
DAVID:
Diabetes
Alcoholism
Vitamin B12 deficiency
Infective or Inherited
Drugs
```
150
Give some examples of myelinopathies.
Guillain-Barré syndrome (acute or chronic inflammatory demyelinating polyneuropathy)
151
Give some examples of neuronopathies/causes.
MND
Sensory neuropathies
Toxins/chemotherapy
Autonomic dysfunction
152
Can regeneration occur in peripheral neuropathies?
It can, but it is limited.
Can be via remyelination, or rarely axonal regrowth
153
Which drugs can cause peripheral neuropathy?
Antimicrobials - Isoniazid, ethambutol, nitrofurantoin, metronidazole.
Chemotherapy esp. vinca alkaloids/cisplatin.
Amiodarone
154
Tell me about Guillian-Barré syndrome.
Acute inflammatory demyelinating polyneuropathy, occuring typically several weeks after a viral infection.
155
How can Guillian-Barré syndrome be differentiated from other peripheral neuropathies?
Proximal muscles are more affected in GBS.
Trunk, respiratory, and cranial nerves can also be affected.
156
How is Guillian-Barré syndrome investigated, and what do the results show?
LP -> increased protein in CSF with normal WCC.
Nerve condction studies -> nerve conduction slow.
157
What is the pathophysiology of Guillian-Barré syndrome?
Viral infection -> autoimmune antibodies against peripheral nerves -> myelin damage -> reduced or blocked transmission.
158
How do we manage GBS?
ABCDE -> intubation if respiratory muscles involved.
DON'T GIVE STEROIDS.
IV Ig may help.
Usually recover without specific treatment.
159
What is cervical spondylosis?
Non-specific degenerative process causing stenosis of the spinal canal and/or nerve roots in the cervical spine.
160
Where is cervical spondylosis most common?
C5/C6 or C6/C7
161
How does cervical spondylosis present?
Very common - often presents as neck pain
162
What are the pathological features behind cervical spondylosis?
- Degenerate disc
- Osteophytes
- Hypertrophy of ligaments
- Congenitally narrow canal
163
What are the 2 main causes of pain in cervical spondylosis?
Mechanical/MSK neck pain
| Radiculopathy
164
What are the clinical features of cervical sponylosis -> radiculopathy?
Referred pain in the arm due to nerve root irritation
Sensory symptoms first -> myotomal radicular pain
Weakness and abnormal reflexes
165
What are the red flags we should be aware of with cervical sponylosis?
What might they be signs of?
```
Fever/chills
Weight loss
Relentless nocturnal pain
History of cancer
Immunosuppression
```
Infection or a tumour
166
What investigation is good for suspected cervical spondylosis?
MRI :D
167
How should cervical spondylosis be managed?
Conservative - Hard or soft collar.
Medical - NSAIDs, epidural injections of steroids.
Surgical - decompression
168
When is surgery indicated in cervical spondylosis?
With uncontrollable pain, severe weakness, or failure of other measures after 12 weeks
169
A 30yo man presents to his GP with a sudden onset facial drooping and weakness of his facial muscles on the right hand side. The forehead is also affected.
What do you suspect?
Bell's palsy (idiopathic facial nerve paralysis)
170
What does forehead sparing/affected tell us abiut facial nerve palsy?
If the forehead is affected, it is a LMN facial nerve palsy.
171
Aside from facial muscle weakness/paralysis, what symptoms do pts with Bell's palsy experience?
Post-auricular pain
Altered taste
Dry eyes
Hyperacusis
172
A 30yo man presents to his GP with a sudden onset facial drooping and weakness of his facial muscles on the right hand side. The forehead is also affected.
What is this, and how should it be managed?
Bell's palsy
Prednisolone for 10 days if started within 72 hours of onset of symptoms
Eye care
173
What eye care can we do for pts with Bell's palsy?
Artificial tears and eye lubricants
174
When should a pt with Bell's palsy be referred for specialist assessment?
Refer to ophthalmology if the pt can't close their eye fully.
175
Why is the forehead spared with an UMN lesion in facial nerve palsy?
Due to bilateral innervation of the forehead
176
Which comorbidities confer worse prognosis for a pt with Bell's palsy?
Age over 60
Pregnancy
Diabetes
Hypertension
177
What is the biggest differential to rule out with possible Bell's palsy?
Stroke! Especially in older patients.
178
How can we remember the causes of carpal tunnel syndrome?
MEDIAN TRAP
```
Myoxoedema
Edema
Diabetes
Idiopathic
Acromegaly
Neoplasm
Trauma
Rheumatoid arthritis
Amyloidosis
Pregnancy
```
179
What is the pathophysiology of carpal tunnel syndrome?
Compression of the median nerve as it passes through the carpal tunnel under the flexor retinaculum
180
What are the symptoms of carpal tunnel syndrome?
Pain and parasthesia in lateral 3 fingers
| Parasthesia extends to lateral half of 4th finger also
181
When are carpal tunnel syndrome symptoms typically worse?
At night or when holding objects like a telephone, newspaper, or steering wheel
182
A 30 year old pregnant woman presents with pain in both her hands.
She reports parasethesia in the lateral aspect of her hand on palmar surface, and discomfort extending up the arm into her shoulder.
Considering the likely diagnosis, what might we see on examination?
Sensory impairment in first 3 fingertips
Wasting of the thenar eminences
Weak thumb abduction
Tinel's and
182
A 30 year old pregnant woman presents with pain in both her hands.
She reports parasethesia in the lateral aspect of her hand on palmar surface, and discomfort extending up the arm into her shoulder.
Considering the likely diagnosis, what might we see on examination?
Sensory impairment in first 3 fingertips
Wasting of the thenar eminences
Weak thumb abduction
Tinel's and Phalen's sign positive
Flick sign will very often be positive
183
What is Tinel's sign, and how is it elicited?
Tapping the distal wrist causes parasthesia in the median nerve distribution.
184
What is Phalen's sign, and how is it elicited?
Ask pt to flex the wrist to 90 degrees and hold it there for 60 seconds -> parasthesia.
Fairly specific test for carpal tunnel syndrome.
185
What is the flick sign associated with carpal tunnel syndrome and what does it tell us?
The patient makes a flicking movement with their wrist to alleviate symptoms.it is both very specific and sensitive for carpal tunnel syndrome.
186
A patient presents with parasthesia in the median nerve distribution, which is worse at night. He has no neck or arm pain.
Considering the diagnosis, what investigations would it be sensible to do, and why?
T4 for hypothyroidism
Glucose/HbA1c for diabetes
FBC and CRP forinflammatory or invective causes.
188
A patient presents with parasthesia and pain in the distribution of the median nerve. You suspect carpal tunnel.
What differentials might you want to rule out, and how would you do that?
C6 or C7 radiculopathy - usually bilateral, with neck pain, and symptoms on dorsal aspect of the hand. Not worse at night.
Thoracic outlet syndrome - have concurrent C8 and T1 dermatome sensory disturbance.
Thalamic infarcts - symptoms are constant, associated with perioral parasthesia.
189
What measures can we use to treat carpal tunnel syndrome?
Splinting the wrist for short term symptoms relief.
Intracarpal corticosteroid injection.
Oral prednisolone may have short term benefit.
Surgical release of carpal tunnel.
190
Which management option for carpal tunnel syndrome has the best efficacy?
Surgery - 80-90% of patients improve.
191
Tell me about the ulnar nerve.
Arises from C8 T1 nerve roots.
Passes through lower trunk, and medial cord of brachial plexus.
Runs behind the medial epicondyle of distal humerus.
Most common site of injury is at the elbow.
192
Where does the ulnar nerve supply?
Motor - intrinsic muscles of hand, flexor carpi ulnaris, and medial half of flexor digitorum profundus.
Sensory - medial one and a half fingers and palmar area, on anterior and posterior surfaces.
193
What is ulnar nerve palsy also known as?
Cubital tunnel syndrome
194
What are the clinical features of ulnar neuropathy?
Parasthesia and/or numbness in the medial 1.5 fingers.
Initially intermittent, later constant.
May have pain around the elbow.
195
Which muscles waste in ulnar neuropathy?
First dorsal interosseus
Hypothenar eminence
Forearm muscles
196
O/E of a pt with ulnar neuropathy, what motor abnormality will be seen?
Ulnar claw - on extension of the fingers of the hand, the 4th and 5th fingers remain flexed due to denervation of the lumbricals.
