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Y4 Neuro and Special Senses > Neurology 1 > Flashcards

Neurology 1 Flashcards

1
Q

How do migraines typically present?

A

Recurrent, severe headache which is usually unilateral and throbbing in nature
May be be associated with aura, nausea and photosensitivity
Aggravated by, or causes avoidance of, routine activities of daily living. Patients often describe ‘going to bed’.
In women may be associated with menstruation

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2
Q

How do tension headaches typically present?

A

Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living

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3
Q

How do cluster headaches typically present?

A

Pain occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
More common in men and smokers

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4
Q

How does temporal arteritis typically present?

A

Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
Tender, palpable temporal artery
Raised ESR

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5
Q

How does a medication overuse headache typically present?

A

Present for 15 days or more per month
Developed or worsened whilst taking regular symptomatic medication
Patients using opioids and triptans are at most risk
May be psychiatric co-morbidity

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6
Q

Give some causes of an acute onset single episode of headache

A

meningitis / encephalitis
subarachnoid haemorrhage
head injury
sinusitis
glaucoma (acute closed-angle)

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7
Q

Give some causes of chronic headache

A

chronically raised ICP
Paget’s disease
psychological causes

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8
Q

Give some red flags for a headache

A

Fever, photophobia or neck stiffness (meningitis)
History of head trauma (haemorrhage)
History of cancer (brain mets)
Postural , triggered by coughing / straining (raised ICP)
Visual disturbance (GCA, glaucoma, tumours)
New-onset neurological deficit
Change in personality
Impaired level of consciousness

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9
Q

What may tension headache be associated with?

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

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10
Q

How can tension headaches be managed?

A

Reassurance
Simple analgesia (e.g., ibuprofen or paracetamol)
Low dose amitriptyline is generally first-line for chronic or frequent tension headaches

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11
Q

What is a common trigger for cluster headaches?

A

drinking alcohol

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12
Q

How should cluster headaches be investigated?

A

most patients will have neuroimaging - underlying brain lesions are sometimes found even if the clinical symptoms are typical for cluster headache

MRI with gadolinium contrast is the investigation of choice

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13
Q

How should cluster headaches be managed?

A

NICE recommend seeking specialist advice from a neurologist

acute:
100% oxygen (80% response rate within 15 minutes)
subcutaneous triptan (75% response rate within 15 minutes)

prophylaxis: verapamil

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14
Q

Which patients are most at risk of developing medication overuse headaches?

A

patients using opioids and triptans are at most risk

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15
Q

How should medication overuse headaches be managed? What is the risk with this?

A

simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)

opioid analgesics should be gradually withdrawn

Withdrawal symptoms such as vomiting, hypotension, tachycardia, restlessness, sleep disturbances and anxiety may occur

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16
Q

Headache following lumbar puncture (LP) occurs in approximately one-third of patients.

What features does it present with?

A

usually develops within 24-48 hours following LP but may occur up to one week later
may last several days
worsens with upright position
improves with recumbent position

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17
Q

How can headache following LP be managed?

A

supportive initially (analgesia, rest)

if pain continues for more than 72 hours then specific treatment is indicated, to prevent subdural haematoma

treatment options include: blood patch, epidural saline and IV caffeine

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18
Q

Migraine is a complex neurological condition causing episodes of headache and associated symptoms. It tends to affect women more than men and is most common in young adults.

What are the 4 main types?

A

Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine

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19
Q

What are the 5 stages of migraine?

A

Premonitory or prodromal stage (can begin several days before the headache)
Aura (lasting up to 60 minutes)
Headache stage (lasts 4 to 72 hours)
Resolution stage (the headache may fade away or be relieved abruptly by vomiting or sleeping)
Postdromal or recovery phase

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20
Q

Give some typical features of migraine

A

Usually unilateral but can be bilateral
Pounding or throbbing in nature
Photophobia (discomfort with lights)
Phonophobia (discomfort with loud noises)
Osmophobia (discomfort with strong smells)
Aura (visual changes)
Nausea and vomiting

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21
Q

What is aura?

A

sensory disturbance commonly associated with migraines

Visual symptoms are the most common.
These may be:
Sparks in the vision
Blurred vision
Lines across the vision
Loss of visual fields (e.g., scotoma)

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22
Q

What are hemiplegic migraines?

A

migraines associated with hemiplegia (unilateral limb weakness). Other symptoms may include ataxia and impaired consciousness

may be familial

can mimic a stroke or TIA so should be investigated urgently

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23
Q

Give some common migraine triggers

A

Stress
Bright lights
Strong smells
Certain foods (e.g., chocolate, cheese and caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma

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24
Q

What are the medical options for managing an acute migraine attack?

A

NSAIDs (e.g., ibuprofen or naproxen)
Paracetamol
Triptans (e.g., sumatriptan)
Antiemetics if vomiting occurs (e.g., metoclopramide or prochlorperazine)

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25
Q

What are triptans?
How do they work to treat migraines?

A

5-HT receptor agonists (they bind to and stimulate serotonin receptors)

They have various mechanisms of action:
Cranial vasoconstriction
Inhibiting the transmission of pain signals
Inhibiting the release of inflammatory neuropeptides

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26
Q

When can you NOT use triptans in migraine mx?

A

Triptans are taken as soon as a migraine starts and should halt the attack. If the attack resolves and then reoccurs, another dose can be taken. If it does not work the first time, another second dose should NOT be taken for the same attack.

Risks associated with vasoconstriction:
hypertension, coronary artery disease or previous stroke, TIA or MI

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27
Q

What can be used in migraine prophylaxis?

A

headache diary to identify and avoid triggers

Propranolol (a non-selective BB)
Amitriptyline (TCA)
Topiramate (teratogenic!!!)

CBT, mindfullness and acupuncture may also be used

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28
Q

What is Parkinson’s disease?

A

a chronic, progressive, degenerative neurological condition leading to disorders of movement

due to reduction in dopamine in the basal ganglia

symptoms are characteristically asymmetrical, with one side of the body affected more

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29
Q

What is the Parkinson’s disease (PD) triad?

A

Resting tremor
Rigidity (resisting passive movement)
Bradykinesia (slowness of movement)

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30
Q

What factors are thought to be protective against developing PD?

A

smoking
caffeine
aerobic exercise

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31
Q

What factors are thought to increase risk of developing PD?

A

Family history
- particularly evident if onset of disease is in people less than 50-years-old

Previous head injury

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32
Q

Outline the pathophsyiology of PD

A

selective loss of dopaminergic neurons in the substantia nigra = in a reduction in dopaminergic output

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33
Q

What features may PD present with?

A

Pill-rolling tremor

Cogwheel rigidity

Bradykinesia: movements getting slower and smaller
Shuffling gait , difficulty in initiating movement
Mask-like facies (hypomimia)
Dysarthria and dysphagia
Micrographia

Postural Instability : increased risk of falls!

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34
Q

Describe the tremor seen in PD

A

‘Pill-rolling’ resting tremor, 4-6 hertz frequency

Usually unilateral or worse on one side than another

Exacerbated by rest, and improves when a person engages in purposeful actions

Exaggerated when the other hand is being used to do something else (can ask someone to mime painting a fence)

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35
Q

How does muscle rigidity in PD manifest for the patient?

A

muscular stiffness, stooped posture, and reduced arm swing when walking

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36
Q

What may a patient who is experiencing bradykinesia due to PD describe in the history?

A

reduction in manual dexterity of finger movements (e.g. fastening buttons, picking up small items), difficulty standing from a seated position, and troubles when walking (e.g. dragging feet)

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37
Q

What non-motor sxs may a patient with PD experience?

A

Depression
Sleep disturbance and insomnia
Loss of the sense of smell (anosmia)
Cognitive impairment and memory problems

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38
Q

How can you differentiate between a Parkinson’s tremor and a Benign Essential tremor?

A
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39
Q

How may Parkinson’s Disease be investigated and diagnosed?

A

Usually a clinical diagnosis: UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria

Investigations to differentiate from other disorders:

Single photon emission computed tomography (SPECT) to distinguish Parkinson’s disease from an essential tremor and Parkinsonism

Structural MRI to exclude structural abnormalities as the cause of the symptoms

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40
Q

What is the diagnostic criteria for PD?

A

Presence of bradykinesia plus at least one of the following:
* Muscular rigidity
* Resting tremor (4-6 Hz frequency)
* Postural instability (not caused by a visual, vestibular, cerebellar or proprioceptive dysfunction)

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41
Q

Give some ddx for PD

A

Essential tremor
Multiple system atrophy
Lewy-body dementia
Secondary Parkinsonism

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42
Q

What are the similarities and differences between Multiple System Atrophy and PD?

A

Similarities:
Both may initially present with Parkinsonian features
Both may respond to levodopa therapy
Both have an element of autonomic dysfunction (although more pronounced in MSA)

Differences:
In MSA, there is usually cerebellar involvement, which is part of the exclusion criteria for Parkinson’s disease
Cognition is well preserved in MSA

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43
Q

What are the differences between Lewy-Body dementia and PD?

A

In Lewy-body dementia, the dementia usually occurs alongside, or prior to, the development of parkinsonism (and must occur no later than a year after onset of motor symptoms)

In PD, motor symptoms appear before cognitive decline

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44
Q

What may cause secondary Parkinsonism?

A

Drug induced: Anti-psychotics and anti-emetic drugs which act via dopaminergic antagonism

Vascular: due to multiple infarcts affecting the basal ganglia

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45
Q

How can drug-induced Parkinsonism be differentiated from PD?

A

Can be distinguished via a thorough medication history

Other movement disorders also caused by these drugs can help differentiate, such as akathisia, tardive dyskinesia and acute dystonia

Usually causes symmetrical symptoms (PD is asymmetrical)

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46
Q

How can vascular Parkinsonism be differentiated from PD?

A

Usually can be identified via a thorough history and radiological findings
Probably step-wise progression rather than continuous

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47
Q

What are the treatment options for PD?

A

Levodopa (combined with peripheral decarboxylase inhibitors)
COMT inhibitors
Dopamine agonists
Monoamine oxidase-B inhibitors

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48
Q

What is Levodopa?

A

precursor to dopamine which is converted both in the CNS and periphery

can be taken orally

patients may build a tolerance so not usually given first line

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49
Q

What are the main side effects of Levodopa?

A

Dyskinesia:
Dystonia (where excessive muscle contraction leads to abnormal postures or exaggerated movements)
Chorea (abnormal involuntary movements that can be jerking and random)
Athetosis (involuntary twisting or writhing movements, usually in the fingers, hands or feet)

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50
Q

What can be used to manage dyskinesia associated with levodopa?

A

Amantadine - a glutamate antagonist

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51
Q

Give some examples of Monoamine oxidase B (MAO-B) inhibitors. How do they work?

A

rasagiline and selegiline

inhibitors of MAO-B which degrades dopamine, therefore increasing the amount of circulating dopamine available

used to delay the use of levodopa, then in combination with levodopa to reduce the “end of dose” worsening of symptoms

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52
Q

Dopamine agonists mimic the action of dopamine in the basal ganglia, stimulating the dopamine receptors.

Give some examples

A

Bromocriptine
Pergolide
Cabergoline

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53
Q

What is the main side effect of prolonged use of dopamine agonists?

A

Pulmonary fibrosis

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54
Q

What are COMT Inhibitors (e.g. entacapone)? How do they work?

A

inhibitors of catechol-o-methyltransferase (COMT) enzyme which metabolises levodopa in both the body and brain

Entacapone is taken with levodopa (and a decarboxylase inhibitor) to slow the breakdown of the levodopa in the brain

Extends the effective duration of the levodopa

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55
Q

The first-line treatment for early stage Parkinson’s disease depends on what?

A

depends on the impact of the motor symptoms on the patient’s quality of life

If motor symptoms impact on quality of life - levodopa
If motor symptoms do not impact on quality of life - dopamine agonist, levodopa or MAO-B inhibitors

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56
Q

What can you use to help guide which medications to use to manage someone’s PD?

A

The patient’s current symptom profile
Patient age (UptoDate indicate that for patients over 65-years-old, levodopa is better tolerated than dopamine agonists)
Current co-morbidities and existing medications (need to consider the risk of polypharmacy and medication interactions)
Possible risks and side effects of each medication

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57
Q

What can be used as an adjuvant to medical therapy for PD?

A

Deep brain stimulation- if sxs not controlled by medication

Physio
Speech therapy
Occupational therapy

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58
Q

What complications may be experienced by patients with PD?

A

Autonomic dysfunction
Recurrent falls
Cognitive impairment

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59
Q

Autonomic dysfunction occurs when the autonomic nervous system fails to work appropriately, and may be seen in patients with progressive PD.

How may this manifest?

A

Postural hypotension with no compensatory tachycardia
- dizziness, light-headedness and subsequent falls

Constipation
-due to dysregulated colonic smooth muscle activity

Urinary dysfunction
- increased urinary frequency and urgency

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60
Q

Why are patients with PD at 2 fold greater risk of falls than their peers?

A

postural instability and impaired corrective reflexes
orthostatic hypotension

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61
Q

What does onset of dementia symptoms at different stages of someone’s PD experience suggest?

A

If dementia develops >1 year after Parkinson’s disease diagnosis, it is considered to be Parkinson’s disease dementia

However, if dementia begins prior or alongside the Parkinson’s disease diagnosis (<1 year), Lewy-body dementia is more likely

62
Q

Motor neuron disease is a neurological condition which can present with both upper and lower motor neuron signs, usually in patients > 40 years old.

What features does it present with?

A

mixture of LMN and UMN signs
asymmetric limb weakness is the most common presentation
wasting of the small hand muscles/tibialis anterior
fasciculations
no sensory signs/symptoms

63
Q

What motor functions are spared in motor neurone disease?

A

doesn’t affect external ocular muscles
no cerebellar signs
abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature

64
Q

Give some signs of lower motor neurone disease

A

Muscle wasting
Reduced tone
Reduced reflexes
Fasciculations (twitches in the muscles)

65
Q

Give some signs of upper motor neurone disease

A

Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex

66
Q

What are the different types of MND?

A

Amyotrophic lateral sclerosis (50% of patients)
Progressive bulbar palsy (second most common)
Primary lateral sclerosis
Progressive muscular atrophy

67
Q

How does ALS present?

A

typically LMN signs in arms and UMN signs in legs
in familial cases the gene responsible lies on chromosome 21

68
Q

How does progressive bulbar palsy present?

A

palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei

carries worst prognosis

69
Q

How can MND be diagnosed?

A

Clinical diagnosis

Nerve conduction studies will show normal motor conduction and can exclude a neuropathy

MRI is usually performed to exclude cervical cord compression and myelopathy

70
Q

How can MND be managed?

A

Riluzole: used mainly in amyotrophic lateral sclerosis

Respiratory care: non-invasive ventilation (usually BIPAP) is used at night

Nutrition: Percutaneous gastrostomy tube (PEG) is the preferred way to support nutrition in patents with MND

71
Q

What is the prognosis like for MND ?

A

Prognosis generally poor: 50% of patients die within 3 years

Riluzole prolongs life by about 3 months

72
Q

What is myasthenia gravis?

A

an autoimmune condition affecting the neuromuscular junction. It causes muscle weakness that progressively worsens with activity and improves with rest.

typically affects women under 40 and men over 60

73
Q

What antibodies are usually found in patients with myasthenia?

A

Acetylcholine receptor (AChR) antibodies

74
Q

What other conditions is myasthenia gravis associated with?

A

thymomas in 15%

thymic hyperplasia in 50-70%

autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE

75
Q

What features does myasthenia present with?

A

proximal muscle weakness that exhibits fatiguability

Difficulty climbing stairs, standing from a seat or raising their hands above their head
Extraocular muscle weakness, causing diplopia
Eyelid weakness causing ptosis
Weakness in facial movements
Difficulty with swallowing
Fatigue in the jaw when chewing
Slurred speech

76
Q

How can you elicit fatiguability in the muscles when examining for myasthenia gravis?

A

Repeated blinking will exacerbate ptosis
Prolonged upward gazing will exacerbate diplopia on further testing
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

77
Q

What should you look for on examination of Myasthenia gravis?

A

Check for a thymectomy scar
Test the forced vital capacity (FVC)

78
Q

How can Myasthenia gravis be investigated?

A

Antibody testing:
AChR antibodies (around 85%)
MuSK antibodies (less than 10%)
LRP4 antibodies (less than 5%)

A CT or MRI of the thymus gland is used to look for a thymoma.

The edrophonium test can be helpful where there is doubt about the diagnosis

79
Q

How can Myasthenia Gravis be managed?

A

Long acting acetylcholinesterase inhibitor (Pyridostigime) that prolongs the action of ACh and improves symptoms

Immunosuppression (e.g., prednisolone or azathioprine) suppresses the production of antibodies

Thymectomy can improve symptoms, even in patients without a thymoma

Rituximab (a monoclonal antibody against B cells) is considered where other treatments fail

80
Q

What is Myasthenic crisis? How can it be managed?

A

a potentially life-threatening complication of myasthenia gravis where there is an acute worsening of symptoms, often triggered by a viral illness

Respiratory muscle weakness can lead to respiratory failure and patients may require NIV or mechanical ventilation.

Treatment is with IV immunoglobulins and plasmapheresis

81
Q

What is Guillain-Barré syndrome?

A

an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)

82
Q

What is the pathophysiology of Guillain-Barré syndrome?

A

molecular mimicry

B cells create antibodies against the antigens on the triggering pathogen. These antibodies also match proteins on the peripheral neurones. They may target proteins on the myelin sheath or the nerve axon itself.

83
Q

What is the timeline of Guillain-Barré syndrome?

A
84
Q

What symptoms does Guillain-Barré syndrome present with?

A

around 65% of patients experience back/leg pain in the initial stages of the illness

progressive, symmetrical weakness of all the limbs

the weakness is classically ascending i.e. the legs are affected first
reflexes are reduced or absent
sensory symptoms tend to be mild (e.g. distal paraesthesia)

85
Q

What less common symptoms may GBS present with?

A

respiratory muscle weakness

cranial nerve involvement:
* diplopia
* bilateral facial nerve palsy
* oropharyngeal weakness

autonomic involvement
urinary retention / diarrhoea

86
Q

How can GBS be investigated?

A

nerve conduction studies:
* decreased motor nerve conduction velocity (due to demyelination)
* prolonged distal motor latency
* increased F wave latency

lumbar puncture (diagnostic)
rise in protein with a normal white blood cell count

87
Q

How can GBS be managed?

A

Supportive care:
VTE prophylaxis (pulmonary embolism is a leading cause of death)
IV immunoglobulins (IVIG) first-line
Plasmapheresis is an alternative to IVIG

Severe cases with respiratory failure may require intubation, ventilation and admission to the intensive care unit

88
Q

What is Duchenne Muscular Dystrophy?

A

an X-linked recessive inherited disorder in the dystrophin genes required for normal muscular function

89
Q

How does Duchenne Muscular Dystrophy present?

A

progressive proximal muscle weakness from 5 years
calf pseudohypertrophy
Gower’s sign: child uses arms to stand up from a squatted position
30% of patients have intellectual impairment

90
Q

How may Duchenne Muscular Dystrophy be investigated and managed?

A

Investigation
raised creatinine kinase
genetic testing to obtain a definitive diagnosis

Management
is largely supportive as unfortunately there is currently no effective treatment

91
Q

What is the prognosis for Duchenne Muscular Dystrophy?

A

most children cannot walk by the age of 12 years
patients typically survive to around the age of 25-30 years
associated with dilated cardiomyopathy

92
Q

What is Becker muscular dystrophy?

A

x-linked recessive dystrophinopathy, often thought of as a ‘less severe’ version of Duchenne muscular dystrophy

develops after the age of 10 years

intellectual impairment much less common than in Duchenne

93
Q

What is Multiple Sclerosis?

A

a chronic cell-mediated autoimmune disorder characterised by demyelination in the central nervous system (immune system attacks myelin sheath)

In early disease, re-myelination can occur, and the symptoms can resolve. In the later stages of the disease, re-myelination is incomplete, and the symptoms gradually become more permanent

MS lesions are described as ‘disseminated in space and time’ - they pop up and affect different sites causing different symptoms

94
Q

What is the epidemiology of MS?

A

3 times more common in women
most commonly diagnosed in people aged 20-40 years
much more common at higher latitudes

95
Q

What are the subtypes of MS?

A

Relapsing-remitting disease (MOST COMMON: 85%)

Secondary progressive disease

Primary progressive disease

96
Q

How does relapsing-remitting MS present?

A

most common form, accounts for around 85% of patients
acute attacks (e.g. last 1-2 months) followed by periods of remission

97
Q

How does secondary progressive MS present?

A

relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses

around 65% of patients with relapsing-remitting disease go on to develop secondary progressive disease within 15 years

gait and bladder disorders are generally seen

98
Q

How does primary progressive MS present?

A

accounts for 10% of patients
progressive deterioration from onset
more common in older people

99
Q

What non-specific feature do patients with MS often experience?

A

75% of patients have significant lethargy

100
Q

What are the visual manifestations of MS?

A

optic neuritis: common presenting feature
optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia

101
Q

Optic neuritis is the most common presentation of MS due to demyelination of the optic nerve.

How does it present?

A

unilateral reduced vision, developing over hours to days

Central scotoma (an enlarged central blind spot)
Pain with eye movement
Impaired colour vision
Relative afferent pupillary defect

102
Q

What sensory symptoms may be caused by MS?

A

pins/needles
numbness
trigeminal neuralgia
Lhermitte’s syndrome: paraesthesiae in limbs on neck flexion

103
Q

What is the most common motor manifestation of MS?

A

spastic weakness: most commonly seen in the legs

104
Q

How may cerebellar MS manifest itself?

A

ataxia: more often seen during an acute relapse than as a presenting symptom
tremor

105
Q

What is Uhthoff’s phenomenon?

A

where neurological symptoms are exacerbated by increases in body temperature

typically associated with multiple sclerosis

106
Q

What is Lhermitte’s syndrome?

A

paraesthesiae in limbs on neck flexion

also known as ‘Barber Chair phenomenon’

may be seen in MS

107
Q

How can MS be investigated?

A

MRI
high signal T2 lesions
periventricular plaques
Dawson fingers: hyperintense lesions perpendicular to the corpus callosum

CSF
oligoclonal bands (and not in serum)

108
Q

What is seen on this MRI?

A

multiple white matter plaques perpendicular to the corpus callosum - Dawson’s fingers

characteristic of MS

109
Q

What is seen on this MRI?

A

multiple high signal T2 lesions

young patient with MS

110
Q

How can acute relapses in MS be managed?

A

High-dose steroids (methylprednisolone 500 mg orally or 1g IV ) may be given for 5 days to shorten the length of an acute relapse

N.B. shortens the duration but does not alter the degree of recovery (i.e. whether a patient returns to baseline function)

111
Q

What are the indications for disease modifying drugs in MS?

A

relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided

secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

112
Q

Give an example of a disease modifying drug that can be used to reduce risk of relapse in MS

A

natalizumab (monoclonal antibody)

113
Q

How can fatigue in MS be managed?

A

exclude other issues e.g. anaemia, thyroid or depression
trial of amantadine
other options include mindfulness training and CBT

114
Q

How can spasticity in MS be managed?

A

baclofen and gabapentin are first-line
physiotherapy is important

115
Q

How can bladder dysfunction in MS be managed?

A

USS first to assess bladder emptying - anticholinergics may worsen symptoms in some patients

if significant residual volume → intermittent self-catheterisation

if no significant residual volume → anticholinergics may improve urinary frequency

116
Q

What is oscillopsia?
How may it be managed?

A

visual fields appear to oscillate - may be seen in MS
gabapentin is first-line

117
Q

Describe diabetic neuropathy

A

sensory loss in a ‘glove and stocking’ distribution

118
Q

How can diabetic neuropathy be managed?

A

first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin

tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain

pain management clinics may be useful in patients with resistant problems

119
Q

As well as the classic peripheral neuropathy, diabetes can cause gastrointestinal autonomic neuropathy.

How may this present?

A

Gastroparesis:
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide and domperidone (prokinetic agents)

Chronic diarrhoea: often occurs at night

GORD: caused by decreased lower oesophageal sphincter pressure

120
Q

Give some causes of peripheral neuropathy

A

A – Alcohol
B – B12 deficiency
C – Cancer (e.g., myeloma) and Chronic kidney disease
D – Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
E – Every vasculitis

121
Q

Give some causes of peripheral neuropathy with predominately motor loss

A

Guillain-Barre syndrome
Charcot-Marie-Tooth
diphtheria
porphyria
lead poisoning
chronic inflammatory demyelinating polyneuropathy (CIDP)

122
Q

Give some causes of peripheral neuropathy with predominately sensory loss

A

diabetes
alcoholism
vitamin B12 deficiency
amyloidosis
uraemia
leprosy

123
Q

How does alcoholism cause peripheral neuropathy?

A

secondary to both direct toxic effects and reduced absorption of B vitamins
sensory symptoms typically present prior to motor symptoms

124
Q

How does B12 deficiency cause peripheral neuropathy?

A

subacute combined degeneration of spinal cord
dorsal column usually affected first (joint position, vibration) prior to distal paraesthesia

125
Q

Give some examples of medications which may cause peripheral neuropathy

A

amiodarone
isoniazid
vincristine
nitrofurantoin
metronidazole

A I’s Very Nearly Mastered

126
Q

What is Charcot-Marie Tooth Disease?

A

the most common hereditary peripheral neuropathy

usually autosomal dominant, results in predominantly motor loss

sxs usually start to appear before the age of 10 but can be delayed until 40 or later

127
Q

What features does Charcot-Marie Tooth present with?

A

Distal muscle weakness and atrophy
There may be a history of frequently sprained ankles
Foot drop (due to weakness of ankle dorsiflexion)
High-arched feet (pes cavus)
Hammer toes
Hyporeflexia
Stork leg deformity

128
Q

How can Charcot-Marie Tooth disease be managed?

A

there is no cure

Analgesia for neuropathic pain (e.g., amitriptyline)
Physiotherapy to maintain muscle strength and joint range of motion
Occupational therapy
Podiatry input for insoles and orthoses to improve symptoms
Orthopaedic surgery for severe joint deformities

129
Q

Cervical spondylosis (degeneration of the cervical vertebrae) is an extremely common condition that results from osteoarthritis.

How does it present?

A

most commonly presents as neck pain although referred pain may mimic headaches

complications include radiculopathy and myelopathy

130
Q

Degenerative disc disease (or spondylosis) refers to the natural deterioration of the intervertebral disc structure over time.

What factors may influence this?

A

Ageing

Environmental factors:
Sedentary lifestyle, occupation, smoking
Increased body weight (especially in lumbar spine)

131
Q

Outline the cascade of changes seen in degenerative disc disease

A

Dysfunction - outer annular tears and cartilage destruction

Instability – disc resorption and loss of disc space height

Restabilisation – osteophyte formation and canal stenosis

132
Q

How may degenerative disc disease (spondylosis) present?

A

localised back pain
radicular pain or paraesthesia

On examination:
local spinal tenderness or contracted paraspinal muscles, hypomobility, or painful extension of the back or neck

133
Q

Lumbar spondylosis may cause a positive Lasegue sign on examination- what is this?

A

When back pain is reproduced by passively raising the extended leg

134
Q

Give some ddx for degenerative disc disease (spondylosis)

A

cauda equina syndrome, infection (such as discitis), or malignancy (including metastatic disease)

135
Q

Give some red flags for back pain

A
136
Q

How may suspected degenerative disc disease (spondylosis) be investigated?

A

Imaging should be warranted in cases of suspected degenerative disc disease if:
Red flags present
Radiculopathy with pain for more than 6 weeks
Evidence of a spinal cord compression
Imaging would significantly alter management

An MRI spine is the gold standard investigation

137
Q

What may be seen on MRI for degenerative disc disease (spondylosis)?

A

signs of degeneration, reduction of disc height, the presence of annular tears, and endplate changes

138
Q

Bell’s palsy may be defined as an acute, unilateral, idiopathic, facial nerve paralysis.

Who does it most commonly present in?

A

peak incidence is 20-40 years and the condition is more common in pregnant women

139
Q

What features does Bell’s palsy present with?

A

lower motor neuron facial nerve palsy → forehead affected (in contrast, an upper motor neuron lesion ‘spares’ the upper face)

patients may also notice:
post-auricular pain (may precede paralysis)
altered taste
dry eyes
hyperacusis

140
Q

How can Bell’s palsy be managed?

A

commence on a course of prednisolone (if present within 72 hours of onset) and give eye care advice

Eye care is important in Bell’s palsy - drops, lubricants and night time taping should be considered to prevent exposure keratopathy

141
Q

How should Bell’s palsy be followed up?

A

if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT

most people with Bell’s palsy make a full recovery within 3-4 months

if untreated around 15% of patients have permanent moderate to severe weakness

142
Q

What does the facial nerve and its branches supply?

A

‘face, ear, taste, tear’
face: muscles of facial expression
ear: nerve to stapedius
taste: supplies anterior two-thirds of tongue
tear: parasympathetic fibres to lacrimal glands, also salivary glands

143
Q

What can cause bilateral facial nerve palsy?

A

sarcoidosis
Guillain-Barre syndrome
Bell’s palsy
Lyme disease
bilateral acoustic neuromas (as in neurofibromatosis type 2)

144
Q

How can you differentiate between upper and lower motor neurone lesions on the facial nerve?

A

upper motor neuron lesion ‘spares’ upper face i.e. forehead
lower motor neuron lesion affects all facial muscles

145
Q

Give some lower motor neurone causes of facial nerve palsy

A

Bell’s palsy
Ramsay-Hunt syndrome (due to herpes zoster)
acoustic neuroma
parotid tumours
HIV
diabetes mellitus

146
Q

What is the main cause of unilateral upper motor neurone facial nerve palsy?

A

Stroke
can also be caused by tumours

147
Q

Carpal tunnel syndrome is caused by compression of median nerve in the carpal tunnel.

What symptoms does it present with?

A

pain/pins and needles in thumb, index, middle finger
unusually the symptoms may ‘ascend’ proximally
patient shakes his hand to obtain relief, classically at night

148
Q

How does carpal tunnel syndrome present on examination?

A

weakness of thumb abduction (abductor pollicis brevis)
wasting of thenar eminence (NOT hypothenar)
Tinel’s sign: tapping causes paraesthesia
Phalen’s sign: flexion of wrist causes symptoms

149
Q

What can cause carpal tunnel syndrome?

A

idiopathic
pregnancy
oedema e.g. heart failure
lunate fracture
rheumatoid arthritis

150
Q

How may carpal tunnel syndrome be investigated and managed?

A

Ix with electrophysiology:
motor + sensory: prolongation of the action potential

Treatment:

6-week trial of conservative treatments if the sxs are mild:
corticosteroid injection
wrist splints at night

Severe/ persistent sxs:
surgical decompression (flexor retinaculum division)

Y4 Neuro and Special Senses (21 decks)

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