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N&SS - Neuro & Stroke > Less Common Neurological Problems > Flashcards

Less Common Neurological Problems Flashcards

1
Q

What is the classic triad of Horner’s syndrome?

A
  • Partial ptosis
  • Miosis
  • Anhidrosis
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2
Q

Which type nerves are affected in Horner’s syndrome?

A

Sympathetic nerves supplying the eye.

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3
Q

Describe the course of the sympathetic fibres of the head and neck that are relevant in Horner’s syndrome.

A
  • Originate in hypothalamus, and descend the cors to C8-T2
  • Synapse onto preganglionic fibres, which leave the cord and ascend the sympathetic chain over the apex of the lung.
  • Synapse to thrid order fibres at C3/4 level/level of carotid artery bifurcation, then travel aling internal carotid, sending branches off to structures in H&N.
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4
Q

Which structures in the H+N have sympathetic innervation?

A

Blood vessels
Sweat glands
Eye (iris dilator)
Occular muscles

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5
Q

Paralysis of which muscle is responsible for the partial ptosis seen in Horner’s syndrome?

A

Superior tarsal muscle

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6
Q

Paralysis of which muscle is responsible for the miosis seen in Horner’s syndrome?

A

Dilator pupillae

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7
Q

What are:

a) anhydrosis
b) miosis
c) partial ptosis?

A

a) decreased sweating
b) constriction of the pupil
c) dropping of the upper eyelid

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8
Q

Other than the classic triad, what symptoms might a pt with Horner’s syndrome present with?

A
  • Facial flushing
  • Orbital pain/headache
  • Neck pain
  • Facial pain

Depends on the cause as to how they present.

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9
Q

How can miosis be detected on examination?

A

Pupil on affected side is more constricted - look at them in a darkened room, then check for pupil response to light source being removed - it will cause less pupil dilation in affected eye.

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10
Q

What sign can indicate anhydrosis on examination?

A

Ipsilateral dry skin on the face - more friction on running fingers over the skin.

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11
Q

According to anatomy, how can we divide the causes of Horner’s syndrome?

A

Into central lesion, preganglionic, and postganglionic nerve lesions.

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12
Q

What are the central causes of Horner’s syndrome?

A
  • CVA
  • Multiple sclerosis
  • Pituitary/basal skull tumours
  • Neck trauma
  • Syringomyelia
  • Spinal cord tumours
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13
Q

What are the preganglionic causes of Horner’s syndrome?

A
  • Apical lung tumours
  • Lymphadenopathy
  • Lower brachial plexus trauma
  • Aortic/subclavian/carotid aneurysms
  • Neck or chest surgery/trauma
  • Neuroblastoma
  • Mandibular dental abscess
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14
Q

What are the postganglionic causes of Horner’s syndrome?

A
  • Cluster headache/migraine
  • Herpes zoster infection
  • Internal carotid dissection
  • Carotid-cavernous fistula
  • Temporal arteritis
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15
Q

What differentials should you have for a presentation of Horner’s syndrome with pain?

A

Arm/shoulder/hand pain -> Pancoast tumour

Face/neck -> carotid dissection

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16
Q

How should Horner’s syndrome be investigated?

A

According to suspected cause:

  • CXR if suspecting apical lung cancer
  • CT/MRI for CVA
  • CT angiography/carotid USS for carotid dissection
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17
Q

Is Horner’s syndrome a symptom, sign, or diagnosis?

A

It is a physical sign

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18
Q

What is a cerebellopontine angle lesion?

A

Something present within the posterior fossa of the brain. Most of them are benign.

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19
Q

What are the 4 most common cerebellopontine angle lesions?

A
  • Vestibular schwannomas (80%)
  • Lipomas
  • Vascular malformations
  • Haemangiomas
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20
Q

What are the common presenting symptoms of cerebellopontine angle lesions?

A
  • Hearing loss (95%)
  • Tinnitus (80%)
  • Vertigo
  • Headache
  • Facial hypesthesia
  • Diplopia

Exact symptoms vary according to size and location of lesion.

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21
Q

What is a vestibular schwannoma also called?

A

Acoustic neuroma

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22
Q

What is an acoustic neuroma?

A

A tumour of the vestibulocochlear nerve arising from the Schwann cells of the nerve sheath.

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23
Q

What are the 2 risk factors for developing an acoustic neuroma?

A
  • Neurofibromatosis

- High-dose ionising radiation

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24
Q

What is the classic presentation of an acoustic neuroma?

A
  • Unilateral hearing loss
  • Vestibular dysfunction
  • Tinnitus
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25
Q

How do symptoms develop/get worse over time with an acoustic neuroma? Why?

A
  • Develop facial pain due to trigeminal nerve involvement
  • Facial weakness (uncommon even with facial nerve compression)
  • Earache
  • Ataxia due to cerebellar compression
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26
Q

What are the differentials for an acoustic neuroma?

A

Other cerebellopontine angle lesions

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27
Q

What Ix should be done for a cerebellopontine angle lesion?

A
  • Audiology to qualify that hearing loss is sensorineural

- MRI/CT depending on the suspected cause

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28
Q

Are most cerebellopontine angle lesions benign or malignant?

A

Benign

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29
Q

Where is the cerebellopontine angle?

A

Within the posterior fossa of the cranium, between the cerebellum and the pons.

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30
Q

Can cerobellopontine lesions be removed surgically?

A

Yes some of them can - it depends where they are and what structures they are involved with. Partial resection can also be an option, especially as a form of debulking.

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31
Q

How can a cerebellopontine lesion be imaged?

A

CT is usually sufficient - may be hypo or hyper dense structures depending on specific diagnosis.

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32
Q

What medical therapy can be done for patients with cerebellopontine angle lesions?

A

Serial imaging for observation
Diuretic therapy can be used if there is a symptomatic arachnoid cyst.
Radiotherapy and surgery can also be considered.

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33
Q

Why imaging modality is the best for diagnosing an acoustic neuroma?

A

MRI

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34
Q

What % of acoustic neuromas do not get bigger over time?

A

Around 75%

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35
Q

What are the 3 treatment options for acoustic neuromas?

A
  1. Observation
  2. Stereotactic radiosurgery
  3. Microsurgery
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36
Q

Who is most appropriate for observation with an acoustic neuroma?

A

Pts with small neuromas and good hearing preservation.

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37
Q

Is microsurgery or stereotactic radiosurgery more commonly done for an acoustic neuroma?

A

Microsurgery

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38
Q

What are the risks of surgery on an acoustic neuroma?

A
  • 1% mortality risk
  • CSF leak
  • Cerebellar injury
  • Stroke
  • Epilepsy
  • Facial paralysis
  • Hearing loss
  • Balance impairment
  • Persistent headache

Sounds like a bundle of laughs!

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39
Q

What is stereotactic radiosurgery?

A

Targets a tumour with single large dose of radiation, which aims to control or slow the growth of the tumour.

40
Q

What is subacute combined degeneration of the spinal cord?

A

Degeneration of posterior and lateral columns of the spinal cord, most commonly due to vitamin B12 deficiency.

41
Q

What causes subacute combined degeneration of the spinal cord?

A

Vit B12 deficiency (most common)
Vit E deficiency
Copper deficiency

42
Q

Which senses are lost in subacute combined degeneration of the spinal cord?

A

Joint position sensation and vibration sense first.

Later on distal parasthesia develops.

43
Q

What signs do pt with subacute combined degeneration of the spinal cord develop?

A

Upper motor neurone signs in the legs

44
Q

How does subacute combined degeneration of the spinal cord present?

A

Weakness of arms, legs, and trunk, and progressively worsening tingling and numbness.

PMHx of pernicious anaemia or alcohol abuse may be present.

45
Q

How can B12 causing subacute combined degeneration of the spinal cord be diagnosed?

A

Serum B12 and FBC showing macrocytic anaemia to confirm B12 deficiency.

46
Q

How can subacute combined degeneration of the spinal cord be managed?

A

If caused by B12 deficiency, replace B12 - the efficacy of this depends on the duration and extent of the neurodegeneration.

47
Q

Where are the cavernous sinuses situated?

A

On the body of the sphenoid bone.

48
Q

Which structures does the cavernous sinus run between?

A

The superior orbital fissure and the petrous temporal bone.

49
Q

What sits medial to the cavernous sinuses?

A

The pituitary fossa and sphenoid sinus

50
Q

What sits lateral to the cavernous sinuses?

A

The temporal lobe of the brain

51
Q

Which cranial nerves pass through the cavernous sinuses?

A

Oculomotor nerve
Trochlear
Ophthalmic
Maxillary

Abducens nerves passes through the sinus, the others sit in the lateral wall.

52
Q

Where do the cranial nerves pass through the cavernous sinus?

A

Lateral wall of each cavernous sinus.

53
Q

What do the cavernous sinuses contain (medial to lateral)?

A

Internal carotid artery (and sympathetic plexus)

Abducens nerve

54
Q

Which veins supply the cavernous sinuses?

A

Ophthalmic vein, superficial cortical veins, and basilar plexus. These then drain into internal jugular vie the superior and inferior petrosal sinuses.

55
Q

What is the classic triad of Wernicke’s encephalopathy?

A

Mental confusion
Ataxia
Ophthalmoplegia

56
Q

What develops if Wernicke’s encephalopathy is indequately treated?

A

Wernicke-Korsakoff syndrome

57
Q

What is Wernicke-Korsakoff syndrome?

A

A specturm of disease resulting from thiamine deficiency, usually related to alcohol abuse.

58
Q

How does chronic alcohol consumption cause a thiamine deficiency?

A
  • Reduced oral intake of dietary thiamine
  • Decreased absorption from GI tract
  • Impaired utilisation of thiamine by cells
59
Q

A patient with a hx of alcohol misuse presents with confusion, weakness, and vomiting. What should come high up on the lost of differentials?

A

Wernicke’s encephalopathy

60
Q

What are the symptoms of Wernicke’s encephalopathy?

A
  • Visual changes (diplopia, movement disorders, ptosis)
  • Loos of muscle co-ordination
  • Memory loss
  • Inability to form new memories
  • Hallucinations
  • N+V
61
Q

What are the signs of Wernicke’s encephalopathy?

A
  • Neurological signs in line with symptoms experienced
  • Abnormal reflexes
  • Hypotension
  • Hypothermia
  • Tachycardia
  • Cachexia
62
Q

What is the diagnostic criteria for Wernicke’s encephalopathy?

A

2 of the following 4 should be present:

  • Dietary deficiency
  • Oculomotor abnormalities
  • Cerebella dysfunction
  • Altered mental state or memory impairment
63
Q

How should suspected Wernicke’s encephalopathy be investiagted?

A

Bloods - FBC looking at MCV, U&Es to exclude electrolyte imbalance, LFTs, glucose, and blood gas. Serum thiamine (B1) and cholesterol should also be performed.

64
Q

How should Wernicke’s encephalopathy be managed?

A
  • MDT approach to include alcohol services where needed.
  • Address issues with alcohol and diet.
  • Oral thiamine and vit B complex long term
  • Lactulose (increases bowel clearance for reduced nitrogen absorption to prevent hyperuricaemia).
65
Q

A patient comes to his GP with recurrent very severe headaches behind one eye, with episodes lasting for half an hour or so. What diagnosis is top of your differential list?

A

Cluster Headaches

66
Q

How long does a period of cluster headaches typically last?

A

Between 2 to 12 weeks

67
Q

Are cluster headaches more common in women or men?

A

Men, by about 4.3 times.

68
Q

What lifestyle factors are associated with a poorer prognosis for cluster headaches?

A

Smoking and alcohol use

69
Q

Can cluster headaches run in a family?

A

Yes, there is a genetic link but no clear inheritence pattern.

70
Q

When is the most common time for a cluster headache to occur?

A

At night a few hours after falling asleep, hence the nickname “alarm clock headache”

71
Q

Describe the onset of a cluster headache.

A

Onset of very severe unilateral headache over about ten minutes without aura, lasting up to about 3 hours.

72
Q

What symptoms are common to get alingside a cluster headache?

A

Autonomic symtpoms on the ipsilateral side i.e. lacrimation, nasal congestion and rhinorrhoea, facial swelling/flushing, partial ptosis, miosis.

73
Q

Does sititng still help a cluster headache?

A

No - pts with cluster headaches are often described as restless.

74
Q

What are some of the common known triggers of cluster headaches?

A
  • Alcohol (during a cluster period)
  • Histamine
  • Nitroglycerine
  • Heat
  • Exercise
  • Solvents
  • Disturbed sleep patterns
75
Q

Do cluster headaches need investiagting?

A

No - the diagnosis can be made clinically as long as there are no red flags

76
Q

What are the red flags that would cause you to investiagte a patient with ?cluster headaches?

A
  • Change in pattern of headaches
  • New headaches over age 50
  • Seizures
  • Concurrent systemic illness
  • Perosnality change
  • Sx of RICP
  • Thunderclap presentation
77
Q

How can cluster headaches be managed?

A

These treatments may not work for all patients:

  • Reassurance, smoking cessation, alcohol avoidance, and sleep hygiene.
  • High flow oxygen and SC sumatriptan for acute attacks.
  • Verapamil for prophylaxis
78
Q

If a pt presents with ?cluster headaches to their GP, what should the GP do?

A

Give lifestyle advice and urgently refer to neurologist.

79
Q

What is the pathophysiology of prion disease?

A

Accumulation of small infectious protein-containing pathogens causing neurodegenertive illnesses

80
Q

What is the most commonly known prion disease?

A

Creutzfeldt-Jakob disease i.e. mad cow diease or bovine spongiform encephalopathy

81
Q

What is important to remember about Creutzfeldt-Jacob disease?

A

It is a notifiable disease - the CDC should be informed if someone is even being investigated for it.

82
Q

How does CJD present?

A

Neurological disturbance alongside rapidly progressive cognitive and functional impairment

83
Q

What neurological disturbances can be seen in CJD?

A 
Myoclonus
Visual disturbance
Cerebellar signs
Pyramidal signs
Extra-pyramidal signs
84
Q

How is CJD investiagted?

A

CSF biochemical markers
EEG has specific waveform in some variants
Brain biopsy is only considered if there is a good chance of another diagnosis

85
Q

How is CJD managed?

A

Supportively

86
Q

What is the name of the peripheral neuropathy that sometimes follows an infection, typically a respiratory or GI infection?

A

Guillain-Barré syndrome

87
Q

What is the pathophysiology of Guillain-Barré syndrome?

A

Peripheral nerve tissue demyelination and axonal degenration caused possibly by antibodies to infectious organisms, causing acute and progressive ascending neuropathy

88
Q

What risk factors are there for developing Guillain-Barré syndrome?

A
  • GI/resp tract infection in preceeding 1-3 weeks.
  • Zika virus
  • Some vaccinations
  • Malignancy
  • Post-partum period
89
Q

Is Guillain-Barré syndrome weakness symmetrical or not?

A

Yes it is symmetrical

90
Q

Where does peripheral weakness usually start in Guillain-Barré syndrome?

A

Lower extremities, then works it’s way up.

91
Q

Where do patients with Guillain-Barré syndrome typically experience pain? What kind?

A

Neuropathic pain usually in legs, but also the back.

92
Q

What pattern of abnormal reflexes is seen with Guillain-Barré syndrome?

A

Hyporeflexia or absent reflexes.

93
Q

Other than weakness, pain, and abnormal reflexes, what symptoms can be caused by Guillain-Barré syndrome?

A

Parasthesiae
Sensory loss

These both start peripherally and work upwards like the weakness.

94
Q

What are the differentials for Guillain-Barré syndrome?

A
  • Stroke
  • Encephalitis
  • Brainstem compression
  • SCC
  • Vasculitis
  • Lead poisoning
  • Porphyria
  • Myasthenia gravis
  • Hypokalaemia
95
Q

How is Guillain-Barré syndrome investigated?

A

Diagnosis usually made on clinical grounds.
U&Es may be derranged due to SIADH
Antibodies to peripheral and central nerves may be seen
Nerve conduction studies abnormal in 85% of cases.

96
Q

How is Guillain-Barré syndrome managed?

A

IV Ig to induce remission
DVT prophylaxis and supportive care
Pain relief
Admission to ITU if ventilation required.

N&SS - Neuro & Stroke (10 decks)

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