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Neurology > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the diagnostic criteria for medication overuse headache?

A
  1. Headache present for >15 days/month.
  2. Regular use for >3 months of >1 symptomatic treatment drugs.
  3. Headache has developed or markedly worsened during drug use.
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2
Q

What features might be present in the history of a headache that make you suspect meningitis?

A
  1. Pyrexia.
  2. Photophobia.
  3. Neck stiffness.
  4. Non-blanching purpura rash.
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3
Q

What muscle is essential for correcting the extorsion action of lateral rectus when walking downstairs?

A

Super oblique (Cn 4 innervation).

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4
Q

What muscle needs to be working in order to test the action of superior and inferior rectus?

A

Lateral rectus.

To test superior and inferior rectus the patient is asked to abduct their eye 30 degrees first, this requires lateral rectus.

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5
Q

Superior and inferior oblique can never have isolated action. How can they be tested?

A

Position the eye so that superior and inferior recti are giving maximal rotation and look for complete correction.

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6
Q

Give 4 symptoms of rabies.

A
  1. Fever.
  2. Anxiety.
  3. Confusion.
  4. Hydrophobia.
  5. Hyperactivity.
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7
Q

Name the organism responsible for causing tetanus.

A

Clostridium tetani (gram positive anaerobe).

It infects via dirty wounds.

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8
Q

Give 3 symptoms of tetanus.

A
  1. Trismus (lockjaw).
  2. Sustained muscle contraction.
  3. Facial muscle involvement.
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9
Q

Name the organism responsible for causing botulism.

A

Clostridium botulinum.

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10
Q

Give 3 symptoms of botulism.

A
  1. Diplopia (double vision).
  2. Dysphagia.
  3. Peripheral weakness.
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11
Q

If a patient has aphasia what region in the brain has been affected?

A

Broca’s area.

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12
Q

If a patient has receptive dysphasia what region in the brain has been affected?

A

Wernicke’s area.

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13
Q

How does carbamazepine work as an AED?

A

It inhibits pre-synaptic Na+ channels and so prevents axonal firing.

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14
Q

What can be the affect of non missile trauma to the scalp?

A

Contusions and lacerations.

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15
Q

What can be the affect of non missile trauma to the skull?

A

Fracture.

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16
Q

Give 2 risks associated with skull fracture.

A
  1. Haematoma.

2. Infection.

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17
Q

What can be the affect of non missile trauma to the meninges?

A

Haemorrhage and infection (due to skull fracture).

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18
Q

What can be the affect of non missile trauma to the brain?

A

Contusions, lacerations, haemorrhage and infection (due to skull fracture).

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19
Q

Describe the aetiology of diffuse traumatic axonal injury.

A

Acceleration/deceleration -> shearing rotational forces -> axons tear.

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20
Q

Give a sign of diffuse vascular injury due to non missile trauma.

A

Multiple petechial haemorrhages.

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21
Q

What is more severe: diffuse traumatic axonal injury or diffuse vascular injury?

A

Diffuse vascular injury is MUCH more severe. It can result in near immediate death.

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22
Q

Describe the mechanism behind acceleration/deceleration damage.

A

A force to the head can cause differential brain movements -> shearing, traction and compressive stresses -> risk of axon tear and blood vessel damage.

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23
Q

What is contusion?

A

Superficial ‘bruises’ of the brain.

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24
Q

What is laceration?

A

When a contusion is severe enough to tear the pia mater.

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25
Q

What is the cause of chronic traumatic encephalopathy?

A

Often seen following repetitive mild traumatic brain injury.

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26
Q

Give 3 initial symptoms of chronic traumatic encephalopathy.

A
  1. Irritable.
  2. Impulsive.
  3. Aggressive.
  4. Depressed.
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27
Q

Give 3 later symptoms of chronic traumatic encephalopathy.

A
  1. Dementia.
  2. Gait and speech problems.
  3. PD symptoms.
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28
Q

Give 3 signs of chronic traumatic encephalopathy.

A
  1. Atrophy of deep brain structures.
  2. Enlarged ventricles.
  3. Tau deposited in sulci.
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29
Q

You see a patient who you suspect has meningitis. It is noted that they have raised ICP. Would you do a lumbar puncture?

A

NO! You would not do a lumbar puncture in someone with raised ICP due to the risk of coning.

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30
Q

Give 4 signs of raised intra-cranial pressure.

A
  1. Papilloedema.
  2. Focal neurological signs.
  3. Loss of consciousness.
  4. New onset seizures.
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31
Q 
What drug is prescribed in sub-arachnoid haematoma to prevent arterial spasm and subsequent ischaemia? 
What class of drugs does this come from?
A

Nimodipine – CCB.

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32
Q

Give 3 differences in the presentation of a patient with a subdural haemorrhage in comparison to an extradural haemorrhage.

A
  1. Time frame: extra-dural symptoms are more acute.
  2. GCS: sub-dural GCS will fluctuate whereas GCS will drop suddenly in someone with an extra-dural haematoma.
  3. CT: extra-dural haematoma will have a rounder more contained appearance.
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33
Q

What are the 3 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP.
  2. Progressive neurological deficit.
  3. Epilepsy.
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34
Q

Give 3 symptoms of raised ICP.

A
  1. Headache.
  2. Drowsiness.
  3. +/- vomiting.
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35
Q

You ask a patient with a brain tumour about any factors that aggravate their headache. What might they say?

A
  1. Worst first thing in the morning.

2. Worst when coughing, straining or bending forward.

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36
Q

What is the cardinal physical sign of raised ICP?

A

Papilloedema.

Due to obstruction of venous return from the retina.

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37
Q

Where might secondary brain tumours arise from?

A
  1. Lung (NSCC).
  2. Breast.
  3. Malignant melanoma.
  4. Kidney.
  5. Gut.
38
Q

Describe the treatment for secondary brain tumours.

A
  1. Surgery and adjuvant radiotherapy.
  2. Chemotherapy.
  3. Supportive care.
39
Q

From what cell do primary brain tumours originate?

A

Glial cells:

  • Astrocytoma (90%).
  • Oligodendroglioma (<5%).
40
Q

Which primary brain tumour do you associate with genetic defects in chromosomes in 1 and 19?

A

Oligodendroglioma.

41
Q

Give 3 features of oligodendroglioma’s.

A
  1. Genetic defects in chromosomes 1 and 19.
  2. All IDH1 mutation positive.
  3. Chemo sensitive.
  4. 10-15 year survival.
42
Q

Describe the WHO glioma grading.

A
  1. Grade 1: benign paediatric tumour.
  2. Grade 2: pre-malignant tumour.
  3. Grade 3: ‘anaplastic astrocytoma’ - cancer.
  4. Grade 4: glioblastoma multiforme (GBM).
43
Q

Describe the epidemiology of grade 2 gliomas.

A

Disease of young adults.

44
Q

What is often the first symptom that someone with a grade 2 glioma presents with?

A

Seizures.

45
Q

Give 3 causes of grade 2 glioma deterioration.

A
  1. Tumour transformation to a malignant phenotype.
  2. Progressive mass effect due to slow growth.
  3. Progressive neurological deficit from functional brain destruction.
46
Q

Describe the common pathway to GBM.

A

Initial genetic error of glucose glycolysis -> IDH 1 mutation -> excessive build up of 2-hydroxyglutarate -> genetic instability in glial cells triggered.

47
Q

Give 5 good prognostic factors for GBM.

A
  1. <45 y/o.
  2. Aggressive surgical therapy.
  3. Good performance post surgery.
  4. Secondary GBM.
  5. MGMT ‘mutant’ - will respond well to chemo.
48
Q

Give 5 poor prognostic factors for GBM.

A
  1. > 50 y/o.
  2. Poor neurological function after surgery.
  3. Non-radical surgery treatment.
  4. Primary GBM.
  5. MGMT ‘wild type’ - no response to chemo.
49
Q

Describe the treatment for GBM.

A
  1. Resective surgery.
  2. Adjuvant chemotherapy with Temozolomide.
  3. Palliative care.
50
Q

What drug is used as adjuvant chemotherapy for people undergoing GBM resection?

A

Temozolomide.

51
Q

How long do you wait for before doing a lumbar puncture in someone with a suspected SAH?

A

At least 12 hours! You need to wait for the Hb to break down and then CSF will become yellow, this is a sign that there is bleeding in the sub-arachnoid space - xanthochromia.

52
Q

Will GCS drop rapidly or slowly in someone with an extra-dural haematoma?

A

GCS will drop suddenly - there is a rapid deterioration in consciousness with focal neurological signs.

53
Q

A 60-year-old man has just had surgery on his carotids and is complaining of difficulty speaking and swallowing. OE his tongue is deviated to the right. Which nerve has most likely been damaged during the operation?

A

Right hypoglossal.

54
Q

What is the function of the cerebellum?

A

The cerebellum is responsible for precise control, fine adjustment and co-ordination of motor activity based on continual sensory feedback. The cerebellum decides HOW you do something. It computes motor error, adjusts commands and projects this information back to the motor cortex.

55
Q

What are the 3 layers of the cerebellum?

A
  • Molecular layer.
  • Purkinje layer.
  • Granular layer.
56
Q

Give 5 signs of cerebellar dysfunction.

A
  1. Dysdiadochokinesis.
  2. Ataxia.
  3. Nystagmus.
  4. Intention tremor.
  5. Slurred speech.
  6. Hypotonia.
57
Q

How can the severity of ataxia be classified?

A
  • Mild: patient is independent or requires 1 walking aid.
  • Moderate: patient requires 2 walking aids.
  • Severe: patient is wheelchair dependent.

SARA scale can also be used, looks at gait, stance, sitting and speech.

58
Q

What investigations might you do in someone who is presenting with signs of cerebellar dysfunction?

A

MRI - will show cerebellar atrophy and will exclude other causes e.g. CV, tumour, hydrocephalus.

59
Q

Give an example of an AR inherited cerebellar ataxia.

A

Friedreich’s ataxia (FA) - presents early in childhood. Motor and sensory problems. Patients are at increased risk of diabetes/CV problems.

60
Q

Give an example of an AD inherited cerebellar ataxia.

A

Spino-cerebellar ataxia 6 (SCA6) and episodic ataxia (presents with difficulty focusing and migraines).

61
Q

Give 4 causes of acquired cerebellar ataxia.

A
  1. Toxic e.g. alcohol, lithium.
  2. Idiopathic.
  3. Neurodegenerative.
  4. Immune mediated.
62
Q

Give 3 examples of immune mediated cerebellar ataxia.

A
  1. Post-infection cerebellitis.
  2. Gluten ataxia.
  3. Para-neoplastic cerebellar degeneration (secondary from lung or breast, look for a tumour on MRI. Rapid onset).
  4. Primary autoimmune cerebellar ataxia.
63
Q

Briefly describe the physiology of muscle contraction.

A

Ca2+ is released from the sarcoplasmic reticulum -> T-tubules -> binds to troponin C. Troponin C moves tropomyosin to expose myosin binding site. Myosin binds to specific sites on actin (requires ATP) and there is a cross bridge formation and detachment cycle.

64
Q

What is the function of dystrophin?

A

Dystrophin links the ECM to the cytoskeleton of the muscle fibre.

65
Q

What protein is affected to produce the signs and symptoms seen in duchenne muscular dystrophy?

A

Dystrophin.

66
Q

Describe the inheritance pattern of Duchenne muscular dystrophy.

A

X linked recessive. (Xp21).

67
Q

At what age do people present with duchenne muscular dystrophy?

A

<5 y/o. There are delayed milestones and the patient is often in a wheelchair by the time they are 13.

68
Q

What cardiac problems might someone with duchenne muscular dystrophy have?

A
  • Arrhythmias.
  • Conduction block.
  • Cardiomyopathy.
69
Q

What would you see histologically in someone with duchenne muscular dystrophy?

A

Muscle cell nuclei all over the place (not just around the edge of the cell). Muscle cells all different shapes and sizes. Absence of dystrophin.

70
Q

Describe the pathophysiology of duchenne muscular dystrophy.

A

Large deletions, duplications and mutations disrupt the reading frame -> ‘out of frame’ mutations -> dystrophin not produced -> DMD phenotype.

71
Q

What is the treatment for duchenne muscular dystrophy?

A
  • Supportive - physio, OT, home adaptations.
  • Scoliosis corrective surgery.
  • Manage cardiac problems.
  • Steroids.
  • Gene therapy.
72
Q

Describe the inheritance pattern of Becker muscular dystrophy.

A

X linked recessive - milder form of Duchenne.

73
Q

At what age do people present with becker muscular dystrophy?

A

5-15 y/o. Most are still ambulant in their 20’s.

74
Q

What cardiac problems might someone with becker muscular dystrophy have?

A
  • Arrhythmia.

- Cardiomyopathy.

75
Q

Describe the pathophysiology of becker muscular dystrophy.

A

In frame mutations mean dystrophin is still produced but it is defective/shortened.

76
Q

Describe the inheritance pattern of myotonic dystrophy.

A

Autosomal dominant.

77
Q

Describe the pathophysiology of myotonic dystrophy.

A

Tri-nucleotide repeats: CTG expansion in non-coding region of DMPK -> down-steam affects -> mis-splicing of proteins -> Cl channel gene (CLCN1) affected -> myotonia.

Myotonic dystrophy is a SPLICEOPATHY!

78
Q

Give 5 adult onset symptoms of myotonic dystrophy.

A
  1. Myotonia - delayed relaxation after contraction, hard to release grasp after shaking hands.
  2. DISTAL muscle weakness.
  3. Cataracts.
  4. Male hypogonadism.
  5. Frontal baldness.
  6. Diabetes.
  7. Cardiac problems.
79
Q

What is the treatment for myotonic dystrophy?

A
  • Supportive care.
  • Treat cardiac problems.
  • Anti-convulsants for myotonia.
80
Q

What is myotonia?

A

Delayed muscle relaxation after contraction. Characteristic sign - unable to release grasp after shaking hands.

81
Q

What site does brain stimulation affect?

A

The sub-thalamic nucleus.

82
Q

Give 3 signs of normal pressure hydrocephalus.

A
  1. Magnetic gait.
  2. Incontinence.
  3. Dementia.
83
Q

Describe the treatment for essential tremor.

A
  • Beta blockers.

- Primidone.

84
Q

Name a thrombolytic drug that can be used in the treatment of ischaemic stroke.

A

Alteplase.

85
Q

How does alteplase work?

A

It converts plasminogen to plasmin and so promotes the break down of a fibrin clot.

86
Q

What is alteplase used for?

A

Thrombolysis in someone with an ischaemic stroke.

87
Q

When can you do thrombolysis in someone with an ischaemic stroke?

A

Up to 4.5 HOURS post onset of symptoms.

88
Q

Name 3 groups of people who are at increased risk of a sub-dural haematoma.

A
  1. Elderly people.
  2. Alcoholics.
  3. Shaken babies.
89
Q

Why are elderly people and alcoholics at increased risk of a sub-dural haematoma?

A

Both of these groups have cerebral atrophy which leads to an increased tension on cerebral veins.

90
Q

What are the 4 stages of a seizure?

A
  1. Prodromal - often emotional signs.
  2. Aura.
  3. Ictal.
  4. Post-ictal - often drowsy and confused.
91
Q

What is the treatment for raised ICP?

A

Osmotic diuresis with mannitol.

Neurology (20 decks)

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