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Phase 2a diseases > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a TIA?

A
  • Transient ischaemic attack.
  • A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia.
  • Symptoms resolve within 24 hours, usually within 1 hour.
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2
Q

What is the clinical presentation of a TIA?

A
  • Sudden onset and brief duration of symptoms.
  • Symptoms will represent a focal neurological deficit.
  • Basically a shorter version of a stroke.
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3
Q

What are the risk factors for a TIA?

A
  • Atrial fibrillation.
  • Mitral valve stenosis.
  • Carotid stenosis.
  • Congestive heart failure.
  • Hypertension.
  • Diabtes mellitus.
  • Smoking.
  • Older age.
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4
Q

What is the pathophysiology of TIA?

A
  • Partial blood flow restriction.
  • Leads to neuronal dysfunction, but delays neuronal death (infarction) as there is still a partial supply of blood.
  • If the partially occluding thrombus is autolysed quickly enough, blood flow is restored and neuronal death will be prevented.
  • Causes reversal of neurological symptoms.
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5
Q

What are the investigations used in a TIA?

A

TIA is a clinical diagnosis primarily.

  • ROSIER (ER assessment)/ FAST (outside of hospital) used to screen/diagnose TIA.
  • Blood glucose levels checked (hypoglycaemia can mimic the symtpoms of a TIA/stroke).
  • Non-contrast CT head not typically used. However, will be used if the patient has a bleeding disorder/ is currently taking anticoagulants (e.g. warfarin) as they are at higher risk of haemorrhage.
  • ABCD2 can be used after a TIA to calculate the risk of stroke in
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6
Q

What is the ABCD2 score?

A

Assesses risk of stroke following a TIA:

A - Age>60? +1
B - BP>140/90? +1
C - Clinical features of TIA.
Speech disturbance without weakness? +1
Unilateral weakness? +2
D - Duration of symptoms.
>10 mins? +1
>60 mins? +2
^2 - History of diabetes? +1

6 or more is high risk.

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7
Q

What treatment can be given for a TIA?

A
  • Give a loading dose of aspirin (an antiplatelet) if TIA suspected.
  • When TIA confirmed, swap aspirin to clopidogrel (P2Y12 inhibitor) and continue clopidogrel as secondary prevention from this point onwards.
  • Start atorvastatin immediately (and continue as secondary prevention).
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8
Q

What is a stroke?

A
  • Rapid onset of either focal or global neurological deficit with no apparent cause other than that of vascular origin.
  • Symptoms last MORE THAN 24 HOURS (unlike a TIA).
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9
Q

What are the two types of stroke?

A
  • Ischaemic (Caused by vascular occlusion/stenosis leading to ischaemia of the brain).
  • Haemorrhagic (vascular rupture causes subarachnoid or intraparenchymal haemorrhage.
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10
Q

What are the risk factors for stroke?

A
  • Old age.
  • FH of stroke.
  • Previous stroke/TIA.
  • Diabetes mellitus.
  • Smoking.
  • High BP.
  • Atrial fibrillation (AF).
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11
Q

What is the general clinical presentation of a stroke?

A
  • Unilateral weakness in face, arm, leg.
  • Unilateral sensory loss.
  • Extremely painful headache.
  • Speech impairments (dysarthria, dysphasia etc.)
  • Loss of coordination/change of gait.
  • Vertigo/loss of balance.
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12
Q

What is the pathophysiology of an ischaemic stroke?

A
  • Stroke is caused by either a permanent or transient occlusion of blood flow due to arterial occlusion or stenosis. There are three main mechanisms for this:
  • Primary vascular pathology (e.g. vasculitis, atherosclerosis).
  • Cardiac pathology (E.g. AF, patent foreamen ovale).
  • Haematological pathology (e.g. sickle cell anaemia, hypercoagulapathies).
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13
Q

What is the pathophysiology of a haemorrhagic stroke?

A
  • Vascular rupture with bleeding into the brain parenchyma, causing primary mechanical brain damage.
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14
Q

What are the two tools used to initially recognise/diagnose stroke in the community and in a hospital?

A
  • FAST (Face, arms, speech test) is used in the community to screen for a potential stroke.
  • ROSIER (Recognition of stroke in emergency room) is used in the ER to quickly diagnose stroke.
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15
Q

What is the initial management of a suspected stroke?

A
  • Admit to specialist acute stroke unit.
  • GCS (Glasgow coma score).
  • Measure blood glucose (to exclude hypoglycaemia, which can mirror the presentation of stroke).
  • Refer for urgent non-contrast CT head scan. This will determine if the stroke is haemorrhagic or ischaemic.
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16
Q

What is the management following confirmation a stroke is ischaemic?

A
  • IF WITHIN 4.5 HOURS OF SYMPTOM ONSET give altepase (a thrombolytic drug).
  • Aspirin ASAP (or clopidogrel if aspirin not tolerated).
  • Thrombectomy if there is potential to save some of the brain tissue.
  • After 48 hours, start high dose atorvastatin.
  • ANTCOAGULANTS (WARFARIN, HEPARIN) ARE NOT INDICATED.
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17
Q

What is the treatment following confirmation a stroke is haemorrhagic?

A
  • Supportive treatment (O2, fluids, BP monitoring, ICP monitoring etc.)
    NOTE: Only give O2 if <94%
  • Urgent reversal of anticoagulants (warfarin is reversed using vit K/prothrombin complex concentrate.
  • Immediate referral to neurosurgery.
  • DO NOT START A STATIN.
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18
Q

What are the key symptoms suggestive of disrupted blood supply in each of the cerebral arteries?

A
  • Anterior cerebral artery (ACA) will generally present with contralateral leg weakness.
  • Medial cerebral artery (MCA) will generally with contralateral face/arm weakness.
  • Posterior cerebral artery (PCA) will generally present with homonymous hemianopia and memory loss (hippocampus supplied by the PCA).
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19
Q

What is a subarachnoid haemorrhage?

How does it present on a CT scan?

A
  • Spontaneous arterial bleeding into the subarachnoid space, between the pia and the arachnoid layers.
  • Presents as a star pattern on a CT scan.
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20
Q

What is a subdural haemorrhage?

How does it present on a CT scan?

A
  • Bleeding occurring between the dura and arachnoid layers.
  • Presents as a crescent on a CT scan.
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21
Q

What is a extradural haemorrhage?

How does it present on a CT scan?

A
  • Bleeding occurring in the potential space between the skull and the dura.
  • Presents as a convex lens (otherwise known as lentiform) shape.
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22
Q

What are the four categories of stroke within the Bamford classification?

A
  • Total anterior circulation stroke (TACS).
  • Partial anterior circulation stroke (PACS).
  • Posterior circulation syndrome (POCS).
  • Lancunar Stroke (LACS
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23
Q

How is the Bamford classification used?

A

Anterior stroke criteria. Total anterior circulation stroke (TACS) needs 3/3, partial anterior circulation stroke (PACS) needs 2/3:

  • Unilateral loss of motor and/or sensory function in face, arm and leg.
  • Homonymous hemianopia.
  • Higher cerebral disfunction (e.g. speech difficulty).

Posterior circulation syndrome criteria. POCS must meet 1 of the following criteria:

  • ISOLATED homonymous hemianopia.
  • Bilateral motor/sensory deficit.
  • Cranial nerve palsy that is contralateral to the motor/sensory deficit.
  • Cerebellar dysfunction (nystagmus, ataxia etc.)
  • Conjugate gaze palsy (Inability to move both eyes in the same direction).

Lancunar stroke criteria. LACS must meet one of the following criteria:

  • Purely motor and/or sensory stroke with NO LOSS OF HIGHER CEREBELLAR FUNCTIONS.
  • Ataxia hemiparesis. (This is ataxia on one side of the body).
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24
Q

What is higher cerebral function?

A

Refers to conscious mental activities. For example:

  • Thinking.
  • Remembering.
  • Reasoning.
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25
Q

Which type of heamorrhage causes thunderclap headache?

A
  • Subarachnoid haemorrhage.
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26
Q

What are the typical causes of each type of haemorrhage?

A

Extradural haemorrhage - Middle meningeal artery rupture due to temporal bone break.

Subdural haemorrhage - Due to bridging vein rupture (e.g. shaken baby, old, alcoholics).

Subarachnoid haemorrhage - Caused by rupture of berry aneurysms.

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27
Q

Which type of haemorrhage is associated with CN III palsy?

A
  • Extradural haemorrhage.
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28
Q

Which type of haemorrhage is associated with Marfan’s syndrome?

Briefly, what is Marfan’s syndrome and how does it relate to brain haemorrhage?

A
  • Subarachnoid haemorrhage.
  • Marfan’s syndrome. An inherited condition that affects the connective tissues of the body. This weakens the blood vessel walls, making them susceptible to aneurysm.
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29
Q

What is a lucid interval and which type of cerebral haemorrhage is it associated with?

A
  • Extradural haemorrhage.
  • Patient initially is knocked unconscious.
  • Then, brain compensates and the patient will appear to briefly recover. This is the “lucid recovery”.
  • Then, as the haemorrhage expands and ICP builds, the patient will again be knocked unconscious.
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30
Q

What is the relationship between brain haemorrhage and haemorrhagic stroke?

A

Haemorrhage CAN cause haemorrhagic stroke, but not all haemorrhages are strokes.

Treatment for a haemorrhage refers to a haemorrhage alone, rather than a haemorrhagic stroke.

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31
Q

What is the management for a subarachnoid haemorrhage (non-stroke)?

A
  • Monitor GCS.
  • ABC
  • Nimodipine (A CCB). Used to reduce risk of late-onset cerebral ischaemia.
  • Reverse anticoagulation/antiplatelets (e.g. warfarin reversal with vit K).
  • Paracetamol for analgesia (AVOID NSAIDS, can affect the clotting cascade).
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32
Q

What is the management of a subdural haemorrhage?

A
  • Continue to assess GCS.
  • ABC.
  • Phenytoin (an anti-convulsant) should be given prophylactically to prevent seizure.
  • Reversal of anticoagulation/antiplatelets (e.g. reverse warfarin with “Prothrombin Complex Concentrate” - this is vit. K).
  • Raise bed to 30 degrees to lower ICP. 2nd line is mannitol.
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33
Q

What is epilepsy?

A
  • Umbrella term for a condition where there is a tendancy to have seixures.
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34
Q

What are the 5 main types of seizures seen in epilepsy and what do they present like?

A

Tonic-clonic - Period of stiffness followed by period of jerking. Most common type of seizure.

Focal - Occurs in the temporal lobe. Affects emotions, memory, speech and hearing (Deja vu, hallucinations, memory flashbacks, strange actions).

Absence - Loses awareness of surrounding and becomes unresponsive for a short period of time. Most common in children and usually resolves as they get older.

Myoclonic - Period of muscles tensing, stiffness.

Atonic - Muscles relax and person goes “floppy”.

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35
Q

What is status elepticus?

Management?

A
  • A seizure that lasts over 5 minutes
    OR
  • More than one seizure in the space of 5 mins, where consciousness is regained briefly between the seizures.
  • THIS IS CONSIDERED A MEDICAL EMERGENCY.

Management:

0-5 mins:

  • ABC (especially high flow oxygen, secure airway).
  • Monitor GCS.
  • Glucose + B1 (thiamine - to prevent Wernicke’s encephalopathy).
  • Manage acidosis.

5-20 mins:

  • Lorazepam (benzodiazepam)
  • Dose of 1st line anticonvulsant (normally sodium valproate - a GABA receptor agonist).
  • Consider CT head if there is focal pathology/patient has no seizure history.

20-40 mins:

  • 2nd line anticonvulsant (usually carbamazepine/lamotrigine - a sodium channel blocker).
  • Notify ICU.
  • Potentially LP if CNS infection suspected.

40 mins+:

  • Transfer to ICU.
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36
Q

What is the treatment for epilepsy?

A

FOR ALL TYPES EXCEPT FOCAL:

  • Sodium valproate is 1st line (GABA receptor agonist).
  • Carbamazepine/lamotrigine is 2nd line (Sodium channel blocker).

FOR FOCAL:

  • Carbamazepine/lamotrigine is 1st line.
  • Sodium valporate is 2nd line.

FOR MID-SEIZURE CONTROL:

  • Lorazepam (1st line) or diazepam (2nd line) (benzodiazepam)
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37
Q

What are some of the most common epileptic triggers?

A

3 most common are:

  • Alcohol.
  • Lack of sleep.
  • Poor adherance to treatment.

Other causes are:

  • Flashing lights
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38
Q

What are the diagnostic tests used for epilepsy?

A
  • EEG (+ video is GS).
  • MRI brain (check for structural abnormality and cancers).
  • ECG (check for cardiac abnormalities, potentially causing syncope).
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39
Q

What are the risk factors for epilepsy?

A
  • Family history.
  • Trauma affecting the brain.
  • Previous CNS infection.
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40
Q

What is Parkinson’s disease?

A

The neurodegenerative loss of dopamine-secreting cells from the substantia nigra.

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41
Q

What is the clinical presentation of Parkinson’s disease?

A
  • Rest tremor
  • Rigidity and bradykinesia, developed over several months
  • Characteristic stoop.
  • Pill rolling tremor

Remember “TRAP”:

  • Tremor
  • Rigidity
  • Akinesia
  • Postural instability (tendency to fall).
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42
Q

What is the pathophysiology of Parkinson’s disease?

A
  • Progressive loss of dopamine secreting cells from the substantia nigra.
  • Leads to alteration in the neural circuits that control movement/coordination.
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43
Q

What is the substantia nigra?

A

A basal ganglia structure, responsible for movement and coordination.

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44
Q

What is the aetiology of Parkinson’s disease?

A
  • Unknown
  • Some genetic link
  • Some environmental link.
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45
Q

What is the epidemiology of Parkinson’s disease?

A
  • Less common in smokers!
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46
Q

What are the diagnostic tests for Parkinson’s disease?

A

1st line:
- Clinical diagnosis, followed by trial of a dopaminergic agent to see if there is an improvement.

2nd line:
- MRI or CT scan to assess any atrophy of the substantia nigra.

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47
Q

What are the treatment options for Parkinson’s disease?

A

1st line:
- carbidopa (decarboxylase inhibitor) AND levidopa (CNS agent) in the same pill. Often called L-DOPA.

2nd line:
- Ropinirole (dopamine agonist).

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48
Q

What is migraine?

A
  • Recurrent headache for 4-72 hours with visual and/or GI disturbance.
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49
Q

What are the 3 main subtypes of migraine and what makes each one different?

A
  • Aura. Unilateral migraine with visual disturbance. Can also make person photosensitive and nauseated.
  • Without aura. Unilateral migraine WITHOUT visual disturbance. Can also make the person photosensitive and nauseated.
  • Variant. Unilateral migraine with various motor and sensory symptoms resembling a stroke.
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50
Q

What is the pathophysiology of migraine?

A
  • Changes in brainstem blood flow, leading to the release of vasoactive neuropeptides (CGRO and substance P).
  • This causes neurogenic inflammation, vasodilation and extravasation, resulting in the pain experienced during a migraine.
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51
Q

What is the aetiology of migraine?

A
  • Genetic and environmental factors.
  • Can be triggered by a variety of things, such as chocolate, cheese and too much/little sleep.
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52
Q

What is the epidemiology of migraine?

A
  • Most common in women.
  • Usually presents before 40.
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53
Q

What are the investigations used to diagnose migraine?

A

1st line:
- Clinical diagnosis

2nd line:
- Neuro imaging. Can be used to rule out potential lesions.

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54
Q

What are the treatment options for migraine?

A
  • Sometimes will pass in sleep.

If moderate:
- Painkillers (Paracetamol/NSAIDs)

If severe:
- Serotonin agonist (such as triptan) will suppress the inflammation causing the migraine.

  • Ensure patient stays hydrated and consider anti-emetics if they are feeling nauseas.
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55
Q

What is multiple sclerosis?

A
  • Autoimmune demyelination of the CNS.
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56
Q

What are the different types of MS and what are their characteristics?

A
  • Benign. Disease relapse/remits but the general trend is neutral (not getting worse over time).
  • Relapsing-remitting. Disease cycles through being better/worse, but the general trend is to get worse over time.
  • Primary progressive. Disease is steadily progressing over time, with no relapse-remitting.
  • Secondary progressive. Initially had relapsing/remitting MS, but it then became progressive.
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57
Q

What is the clinical presentation of MS?

A
  • Typically seen in young adults.
  • Lhermitte’s sign = Tingling down the back into limbs on flexion of the neck.

May present in three ways:

  • Optic. Blurred vision, unilateral eye pain.
  • Brainstem. Diplopia (double vision), vertigo, dysphagia, nystagmus (repetitive, uncontrolled eye movements).
  • Spinal cord. Numbness, pins and needles, potentially spastic paresis.
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58
Q

What is the pathophysiology of MS?

A
  • Inflammation, demyelination and axonal loss of oligodendrocytes.

Occurs in particular sites more commonly:

  • Optic nerve
  • Periventricular white matter
  • Brainstem
  • Cerebellar connections
  • Cervical spinal cord.

PERIPHERAL NERVES NEVER AFFECTED.

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59
Q

What is the aetiology of MS?

A
  • Precise mechanism is unknown.
  • Appears to be as a result of an inflammatory process in the CNS mediated by CD4 T and B cells.
  • Exposure to EBV in early life predisposes MS development.
60
Q

What is the epidemiology of MS?

A
  • More common in women
  • More common in populations further from the equator.
  • More common in the young.
61
Q

What investigations are used to diagnose MS?

A
  • MRI of CNS (brain + spinal cord)
62
Q

What is the treatment for MS?

A

For an acute relapse:
- Methylprednisolone (Short course of steroids).

For relapsing-remitting MS:
- Use immunomodulators: B-interferon or immunosuppressants (e.g. rituximab).

63
Q

What is myasthenia gravis?

A
  • Chronic autoimmune attack against the post-synaptic Ach receptors at the neuromuscular junctions.
  • Causes weakness and rapid fatigue in the skeletal muscles.
64
Q

What is the clinical presentation of myasthenia gravis?

A

Weakness in skeletal muscles. Causes:

  • Ptosis
  • Dysphasia and dysarthria.
  • Weakness/ rapid fatigue in limbs

Symptoms improve after rest.

65
Q

What is the pathophysiology of myasthenia gravis?

A
  • Autoantibody-mediated attack on Ach receptors at the post-synaptic membranes of the NMJs.
  • This causes the blockage/ loss of Ach receptors at the junctions, impairing signal transmission to the skeletal muscles.
66
Q

What is the aetiology of myasthenia gravis?

A

Strong association with thymic hyperplasia:

  • 10% of people with MG have thymic hyperplasia.
  • 50% of people with thymic hyperplasia have MG.
67
Q

What is the epidemiology of myasthenia gravis?

A
  • Women more likely to have myasthenia gravis than men.
68
Q

What are the diagnostic tests for myasthenia gravis?

A

1st line:
- AchR antibody analysis.

If normal, perform MuSK antibody analysis.

69
Q

How is myasthenia gravis treated?

A

1st line:
- Anti-cholinesterase (pyridostigmine).

If severe:
- Immunosuppressant drugs (such as azathioprine).

If there is a myasthenia crisis:

  • Intubation/ventilation
  • Plasma exchange (removes autoantibodies, reducing the autoimmune response).
70
Q

What is myasthenia crisis?

A
  • Worsening of myasthenic weakness, resulting in the need for intubation/ventilation due to respiratory failure.
71
Q

What is MND?

A
  • Motor neurone disease
  • Relentless destruction of motor neurones in brain and spinal cord.
72
Q

What are the 4 types of MND I need to know about?

Which motor neurons does each type affect?

A
  • Amyotrophic lateral sclerosis (Most common). Affects UMN and LMN.
  • Primary lateral sclerosis. Affects UMN only.
  • Progressive muscular atrophy. Affects LMN only
  • Progressive bulbar palsy. Affects UMN and LMN of the lower cranial nerves (CN IX - XII).
73
Q

What is the typical clinical presentation of MND?

A

Varies depending on the type of MND. Generally:

UPPER LIMBS:

  • Reduced dexterity
  • Stiffness
  • Wasting of intrinsic muscles of the hand.

LOWER LIMBS:

  • Tripping
  • Stumbling gait
  • Foot drop

BULBAR:

  • Slurred speech
  • Hoarseness
  • Dysphagia

OVERALL MUSCLE ATROPHY AND SPASTICITY.

74
Q

What is the pathophysiology of MND?

A
  • Destruction of the motor neurones.
  • Leads to LMN and UMN dysfunction (depending on type of MND).
  • Mixed picture of muscular paralysis/atrophy.
75
Q

What us the aetiology of MND?

A

Unknown. Some variants involve genetic mutations.

76
Q

What is the epidemiology of MND?

A
  • Middle age
  • More common in men.
77
Q

What are the investigations used in suspected MND?

A

1st line:
- Clinical (fasciculations are present even in the early stages of MND).

If unsure:
- EMG (electromyography)

78
Q

What treatments are available for MND?

A

1st line:
- Sodium channel blockers (e.g. Riluzole)

If struggling with muscle spasticity:
- Baclofen (a skeletal muscle relaxant).

79
Q

What are the potential complications of MND?

A
  • Most die within 3 years, due to respiratory failure as a result of bulbar palsy and pneumonia.
80
Q

What is meningitis?

A

Infection of the meninges.

81
Q

What are the two different pathogens that can cause meningitis?

A
  • Viruses
  • Bacteria
82
Q

What are the symptoms of meningitis?

A

Bacterial meningitis:

  • Headache
  • Neck stiffness
  • Fever
  • Photophobia
  • Vomiting
  • Kernig’s sign (inability to straighten leg when knee flexed to 90 degrees)
  • Progressive drowsiness
  • Purpuric, non-blanching rash

Viral meningitis:
Same as above, except:
- No rash
- More benign and self-limiting.

83
Q

Is meningitis a notifiable disease?

A

Yes

84
Q

What is the pathophysiology of meningitis?

A
  • Infection of the meninges leads to inflammation of the tissue.
85
Q

What is the aetiology of bacterial meningitis?

A

Infective agents can reach the meninges from:

  • Ears
  • Nasopharynx
  • Cranial injury
  • Bloodstream

The two most common bacterial causes of meningitis in adults are:

  • Neiserria meningitis
  • Streptococcus pneumoniae
86
Q

What is the aetiology of viral meningitis?

A
  • Herpes simplex virus.
  • Enterovirus.
87
Q

What investigations are done to diagnose meningitis?

A
  • Lumbar puncture, and subsequent CSF culture. NOT IF RAISED ICP ON CT.
  • Blood culture and meningococcal and pneumococcal probe PCR.
88
Q

What is the treatment for bacterial meningitis?

A

When suspected:

  • ABC
  • Corticosteroids (dexamethasone)
  • Empirical antibiotics (cefotaxime)

After cultures arrive back, choose more pathogen specific antibiotics.

89
Q

What is the treatment for viral meningitis?

A

When suspected:
- treat with empirical antibiotics until viral cause has been confirmed (cefotaxime).

When confirmed:

  • ABCs
  • Analgesics (Ibuprofen/paracetamol)

If viral meningitis is recurrent:
- Consider specialist referral for antibiotics.

90
Q

What is encephalitis?

A
  • Inflammation of the brain parenchyma (functional tissue).
91
Q

What are the symptoms of encephalitis?

A

Most common:

  • Fever
  • Headache
  • Altered behaviour and altered mental status

Can cause:

  • Hemiparesis
  • Dysphagia
  • Seizure/coma
92
Q

What is the pathophysiology of encephalitis?

A
  • Infection of the brain parenchyma, leading to inflammation.
93
Q

What is the aetiology of encephalitis?

A

Often presumed viral. Common viral causes are:

  • Herpes simplex virus
  • Coxsackie virus
  • ECHO
  • Mumps
94
Q

What investigations are used to diagnose encephalitis?

A

FBC:
- Elevated WCC.

MRI brain (gold standard), but CT if not available: 
- Check for space-occupying regions.

Viral serology:
- LP and CSF analysis

95
Q

What is the treatment for encephalitis?

A
  • ABCs
  • Immediate start on aciclovir as soon as viral encephalitis is suspected. This is because most of the time it is due to HSV, and aciclovir is an antiviral for herpes.
  • Make antiviral therapy more specific when the exact viral cause has been established.
  • If ICP elevated, give steroids and mannitol.
96
Q

What is herpes zoster (Shingles)?

A
  • Reactivation of the varicella zoster virus (chickenpox).
97
Q

What are the symptoms of herpes zoster virus in each of the different phases?

A

Pre-eruptive:

  • No skin lesions yet, but burning and itching in one dermatome.
  • Usually a day or two before eruption.

Eruptive phase:

  • Skin lesions appear (they are infectious until dried).
  • Erythematous swollen plaques.
  • RASH DOES NOT CROSS DERMATOMES.
98
Q

What is the pathophysiology of Herpes Zoster virus (shingles)?

A
  • After infection, the virus lies dormant in the sensory nervous system ganglia.
  • Eventually flares up, virus travels down the affected nerve over 3-4 days, causing perineural and intraneural inflammation.
  • Eventually, the virus reaches the skin, and the typical dermatomal rash will present.
99
Q

What is the aetiology of shingles?

A
  • Varicella-zoster virus reactivation (now called herpes-zoster)
  • Gives rise to chickenpox in childhood, but then if reactivated in adulthood can cause shingles.
100
Q

How is shingles investigated?

A
  • No investigation needed.
  • Diagnosed based on the stereotypical rash, present within one dermatome only.
101
Q

What is the treatment for shingles?

A
  • Famciclovir (antiviral) 1st line.
  • Aciclovir (antiviral) 2nd line.
  • Analgesia as required (NSAID/paracetamol for moderate, oxycodone opiate for severe).
102
Q

What is a primary brain tumour?

A

Tumour in the brain that arose from associated tissue.

103
Q

What is a secondary brain tumour?

A

Tumour in the brain that metastasised from elsewhere.

104
Q

What are the types of primary brain tumour?

A
  • Glioma. Originates from glial cells.
  • Meningioma. Tumour that arrises from the meninges surrounding the CNS (brain + spinal cord).
  • Pituitary adenoma. Benign tumour of the pituitary gland.
105
Q

What are the symptoms of a brain tumour?

A

Progressive focal neurological deficit:

  • Symptoms depend on location.
  • Speed of deterioration is proportional to growth of tumour.

Raised ICP:

  • Headaches (worse on coughing/ leaning forwards).
  • Vomiting.
  • Papilloedema (optic disc swelling).

May develop epilepsy

General cancer symptoms:

  • Weight loss
  • Malaise
  • Anaemia
106
Q

What are false localising signs?

A
  • Signs that occur due to raised ICP or tumour presence that reflect more distant pathology.
  • For example, a tumour of the temporal lobe may cause a CN III palsy.
107
Q

What is the pathophysiology of a tumour?

A
  • Progressive focal neurological deficit is caused directly by the tumour, and will impact the area of the brain the tumour is in.
  • As the tumour grows, ICP increases and the brain will be downwardly displaced.
  • This puts pressure on the brainstem, causing drowsiness. Eventually, it can even cause respiratory depression, coma and death.
  • Tumours can generate pathological electrical signals, causing epilepsy.
108
Q

What is the aetiology of a primary brain tumour?

A
  • Derived either from the skull itself or the adjacent structures.
  • 95% of primary tumours are gliomas or meningiomas.
109
Q

What is the aetiology of a secondary brain tumour?

A

Metastases from: bronchi, breast, kidney, thyroid, stomach and prostate.

110
Q

What are the investigations used when a brain tumour is suspected?

A
  • CT and MRI scan
  • Biopsy (surgery)
111
Q

What are the therapeutic options for a brain tumour?

A
  • Surgery (removal or biopsy)
  • Radiotherapy or chemotherapy.
112
Q

What is giant cell arteritis?

A
  • Granulomatous arteritis.
113
Q

What is the clinical presentation of giant cell arteritis?

A
  • Headache
  • Tender scalp
  • Jaw claudication
  • Superficial temporal artery may be firm, tender and pulseless.
  • Weight loss
  • Malaise
  • Fever
  • Blindness occurs in 25% if left untreated.
114
Q

What is the pathophysiology of giant cell arteritis?

A
  • Chronic inflammation of the medium-large arteries, particularly the aorta and its extra cranial branches.
  • The blindness can occur as a result of ciliary and/or central retinal artery occlusion.
115
Q

What are the investigations used when giant cell arteritis is suspected?

A

Blood tests:

  • Elevated ESR/CRP

If available, conduct rapid-access ultrasonography (gold standard):

  • Non-compressible halo sign indicates giant cell arteritis.
  • Wall thickening, stenosis and/or occlusion also indicate potential giant cell arteritis.
116
Q

What is the treatment for giant cell arteritis?

A
  • Administer high dose prednisolone IMMEDIATELY, even before diagnosis confirmation.
  • Specialist may consider use of methotrexate if the patient is high risk/experiencing a relapse of giant cell arteritis.
117
Q

What areas of the brain do the anterior cerebral, middle cerebral and posterior cerebral artery supply?

A

Anterior cerebral:

  • Medial portions of frontal lobe and superior medial parietal lobe.
  • Occlusion of this artery causes contralateral lower limb weakness.

Middle cerebral:

  • Supplies areas of the frontal, temporal and parietal lobes.
  • Occlusion causes speech impairment, contralateral weakness and hemiparesis of the lower contralateral face (with forehead sparring).

Posterior cerebral:

  • Supplies occipital lobe and the hippocampus.
  • Occlusion causes acute vision loss and memory impairment.
118
Q

What does cerebellar stroke cause?

A
  • Impairs balance and coordination.
119
Q

What does brain stem stroke cause?

A
  • Hemiparesis (inability to move on one side of the body)
  • Can cause quadriplegia (Paralysis from the neck down)
120
Q

What is a cluster headache?

A
  • Attack of severe pain localised to the unilateral orbital, supra-orbital and/or temporal areas.
  • Lasts 15 mins to 3 hours.
  • Occurs between once every 2 days and 8 times a day.
121
Q

What is the clinical presentation of a cluster headache?

A
  • Attacks occur at the same time for a period of weeks (called the cluster period).
  • Most patients are restless or agitated.
  • Can cause ptosis, facial swelling and sweating.
  • Extremely painful headaches.
122
Q

What differentiates a cluster headache from a migraine?

A
  • Migraine patients usually report motion sensitivity so try to remain still.
  • Cluster headache patients are usually restless and agitated during an attack.
123
Q

What is the pathophysiology of cluster headache?

A
  • Hypothalamic activation, along with secondary trigeminal and autonomic activation.
124
Q

What is the aetiology of cluster headache?

A

Cluster period attacks can be induced by:

  • Alcohol
  • Volatile smells
  • Warm temperatures
  • Sleep
125
Q

What are the risk factors associated with cluster headache?

A
  • Family history
  • Male
  • Head trauma
  • Smoking
  • Alcohol
126
Q

How is a cluster headache normally investigated?

A
  • Usually just a clinical diagnosis.
  • MRI may be used to eliminate secondary causes.
127
Q

What is the treatment for cluster headaches?

A

ONGOING MANAGEMENT:

  • CCB (1st line) such as verapamil.
  • Lithium (2nd line).

ACUTE ATTACK MANAGEMENT:

  • Subcutaneous sumatriptan (a triptan) and high flow oxygen.
128
Q

What is a tension headache?

A
  • Tension headache can be either episodic or chronic.
  • Pain is described as a tight band around the head.
  • Pain does not worsen with physical activity.
129
Q

What is the clinical presentation of a tension headache?

A
  • Dull, non-pulsatile, bilateral, constricting pain (not severe).
  • Pain is typically seen in the frontal or occipital areas, but can be anywhere.
130
Q

Why are tension headaches rarely seen in clinic?

A
  • They are usually self-managed, and very rarely disabling.
  • Therefore, patients do no usually seek medical care.
131
Q

What are the common triggers of a tension headache?

A
  • Stress
  • Mental tension
  • Missing meals
  • Fatigue
132
Q

What investigations are typically performed for tension headache?

A

Clinical diagnosis:
- Look for a headache without nausea and vomiting.

133
Q

What is the treatment for a tension headache?

A

Simple analgesics for an acute attack (aspirin/paracetamol/ibuprofen).

For chronic headache (>7 days per month), consider using low dose antidepressants such as amitriptyline (tricyclic antidepressant).

134
Q

What are the symptoms of:

1) A temporal seizure?
2) A frontal lobe seizure?
3) A parietal lobe seizure?
4) A occipital lobe seizure?

A

1) Temporal = Head
- Hallucinations
- Epigastric rising (stomach sensation).
- Emotional
- Automatisms (e.g. lip smacking)
- Deja Vu

2) Frontal lobe = motor
- Head/leg movements
- Posturing
- Post-ictal (period after seizure) weakness

3) Parietal lobe = sensory
- Parasthesia (burning/prickling sensation).

4) Occipital lobe = visual
- Eye floaters
- Flashes

135
Q

What does CN III innervate?

What eye syndrome occurs if there is a lesion in CN III?

A
  • All eye muscles except for lateral rectus (CN XI) and superior oblique (CN IV).
  • Causes “down and out” eye syndrome if lesion.
136
Q

What is CN IV called and what does it innervate?

What does a lesion of CN IV cause?

A
  • Trochlear nerve
  • Innervates Superior oblique muscle.
  • Causes double vision on looking down, and upwards/outwards rotation of the affected eye.
137
Q

What is the name of CN VI and what does it innervate?

What does a lesion of CN VI cause?

A
  • Abducens nerve
  • Innervates lateral rectus muscle.
  • Eye cannot be abducted, leading to it pointing inwards.
138
Q

What is the name of CN V and what does it innervate?

A
  • Trigeminal nerve.

Sensory:
- Face, sinuses and teeth.

Motor:
- Muscles of mastication.

139
Q

What is the name of CN VII and what does it innervate?

A
  • Facial nerve.

Sensory:
- Anterior 2/3 of tongue, and soft (posterior) palette.

Motor:
- Facial muscles (facial expression).

140
Q

What is the name of CN VIII and what does it innervate?

A
  • Vestibulocochlear nerve.

Sensory:

  • Carries information from hearing and equilibrium (balance).
141
Q

What is CN IX called and what does it innervate?

A
  • Glossopharyngeal nerve

Sensory:

  • Posterior 1/3 of tongue. (GAG REFLEX)
  • Pharynx.
  • Epiglottis.

Motor:

  • Stylopharyngeus
  • Pharyngeal constrictors
  • Parotid gland
142
Q

Which is the only cranial nerve to innervate contralateral structures?

A
  • CN IV (Trochlear nerve)
143
Q

What does CN X damage. cause?

A
  • Soft palette droop. (uvula will therefore deviate towards the normal side.
  • Gag reflex loss.
  • Hoarse/nasal voice.
144
Q

What is CN XI and what does it innervate?

A
  • Accessory nerve.

Motor:
- Laryngeal muscles, trapezius (damage makes shrugging shoulders hard).

145
Q

What is CN XII and what does it innervate?

A
  • Hypoglossal nerve

Motor:
- Intrinsic and extrinsic tongue muscles. (damage causes tongue paralysis and eventually atrophy).

Phase 2a diseases (18 decks)

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