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Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the function of the frontal lobe?

A
  • Voluntary movement on contralateral side of body.
  • Dominant hemisphere controls speech (Broca’s area) + writing.
  • Intellectual functioning, thought processes, reasoning + memory.
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2
Q

What is the function of the parietal lobe?

A
  • Receive + interprets sensations including touch, pressure, size + shape.
  • Body-part awareness (proprioception).
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3
Q

What is the function of the temporal lobe?

A
  • Understanding spoken word (Wernicke’s area), sounds, memory + emotion.
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4
Q

What is the function of the occipital lobe?

A
  • Understanding visual images + meaning of written words.
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5
Q

What is the function of the cerebellum?

A
  • Responsible for precise control, fine adjustment + co-ordination of motor activity based on continual sensory feedback.
  • Computes motor error, adjusts commands + projects this information back to motor cortex.
  • Decides HOW you do something.
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6
Q

What is cerebellar dysfunction characterised by?

A

DANISH…

  • Dysdiadochokinesia.
  • Ataxia.
  • Nystagmus.
  • Intention tremor.
  • Slurred speech.
  • Hypotonia.
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7
Q

How is ataxia severity shown? How does cerebellar dysfunction present on MRI brain?

A
  • Mild = independent/1 walking aid, moderate = 2 aids, severe = wheelchair.
  • Cerebellar atrophy (excludes tumour, hydrocephalus).
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8
Q

What part of the brain does the…

i) anterior cerebral artery
ii) middle cerebral artery
iii) posterior cerebral artery

supply?

A

i) Antero-medial aspect.
ii) Lateral portions of cerebrum, basal ganglia.
iii) Occipital lobe, posteromedial parietal lobe.

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9
Q

What is Duchenne muscular dystrophy?

A
  • Dystrophin affected (out-of-frame mutation), scattered cell nuclei, muscle cells all have different morphologies.
  • X-linked recessive.
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10
Q

What is the clinical presentation + treatment for Duchenne muscular dystrophy?

A
  • <5y/o, delayed milestones, wheelchair by teenager, arrhythmias/heart block.
  • Supportive with PT, OT, scoliosis corrective surgery.
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11
Q

What is the corticospinal tract?

A

Descending UMN…

  • Motor.
  • UMN originate in motor cortex.
  • 75% decussate at medulla.
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12
Q

What is the dorsal column medial lemniscus (DCML) tract?

A

Ascending sensory…

  • Proprioception, vibration + 2-point discrimination.
  • Fasciculus cuneatus (lateral, info from upper body to cuneate tubercle).
  • Fasciculus gracilis (medial, info from lower body to gracile tubercle).
  • Decussates at medulla, ascends to thalamus, then cortex.
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13
Q

What is the spinothalamic tract?

A

Ascending sensory tract…

  • Lateral = pain + temperature, medial = crude touch.
  • Enters spinal cord, ascends 1–2 levels + then decussates.
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14
Q

What is Brown-Sequard syndrome?

A
  • Hemi-section of spinal cord.
  • Ipsilateral loss of proprioception, motor + fine touch below lesion (DCML/corticospinal).
  • Contralateral loss of pain, temperature + crude touch a few levels below lesion (spinothalamic).
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15
Q

Describe the process of dopamine production. Where does the substantia nigra project to? What site is affected by brain stimulation?

A
  • Tyrosine > L-dopa > Dopamine.
  • Substantia nigra projects to striatum.
  • Subthalamic nucleus.
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16
Q

What neurotransmitters are excitatory/inhibitory? What site is affected by brain stimulation?

A
  • Glutamate = excitatory.
  • GABA = inhibitory.
  • Dopamine D1 = excitatory.
  • Dopamine D2 = inhibitory.
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17
Q

CEREBROVASCULAR ACCIDENT

What is a CVA?

A
  • A stroke is a rapid onset of neurological deficit which is the result of a vascular lesion + is associated with infarction of central nervous tissue.
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18
Q

CEREBROVASCULAR ACCIDENT

What are the two types of CVA and how do they differ?

A
  • Ischaemic = ischaemia leading to infarction + death of neural tissue leading to loss of functionality.
  • Haemorrhagic = primarily intracerebral haemorrhage, risk factors lead to small vessel damage + aneurysms where a rupture may occur > haemorrhage.
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19
Q

CEREBROVASCULAR ACCIDENT

What is the aetiology of CVA?

A

Cerebral infarction due to embolism/thrombosis (85%)
- Cardiac emboli (AF, endocarditis), atherothromboembolism.
Intracerebral/sub-arachnoid haemorrhage (15%)
- Primary = Hypertensive, lobar haemorrhages due to amyloid depositions.
- Secondary = anticoagulants, tumours (metastases).

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20
Q

CEREBROVASCULAR ACCIDENT

What is Charcot-Bouchard aneurysms?

A
  • Often found in basal ganglia due to chronic HTN.
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21
Q

CEREBROVASCULAR ACCIDENT

What are the risk factors for CVA?

A
  • HTN.
  • DM.
  • Smoking + alcohol.
  • Hyperlipidaemia.
  • Obesity.
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22
Q

CEREBROVASCULAR ACCIDENT

How would an anterior cerebral artery CVA present?

A
  • Lower limb weakness + loss of sensation (contralateral).
  • Gait apraxia (unable to initiate walking).
  • Incontinence.
  • Drowsiness.
  • Decrease in spontaneous speech.
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23
Q

CEREBROVASCULAR ACCIDENT

How would a middle cerebral artery stroke present?

A
  • Upper limb weakness + loss of sensation (contralateral).
  • Hemianopia.
  • Aphasia (inability to understand or produce speech = Broca’s area).
  • Dysphasia (deficiency in speech generation = Wernicke’s area).
  • Facial droop.
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24
Q

CEREBROVASCULAR ACCIDENT

How would a posterior cerebral artery present?

A
  • Visual field defects (contralateral homonymous hemianopia).
  • Cortical blindness.
  • Visual agnosia (Cannot interpret visual information but can see).
  • Prosopagnosia (inability to recognise familiar face).
  • Unilateral headache.
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25
Q

CEREBROVASCULAR ACCIDENT

What are the investigations for CVA?

A
  • Recognise – think F.A.S.T.
  • CT head to identify if haemorrhagic/ischaemic BEFORE treatment.
  • Bloods – FBC for thrombocytopenia + polycythaemia, blood glucose.
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26
Q

CEREBROVASCULAR ACCIDENT

What is the treatment for an ischaemic stroke?

A
  • Thrombolysis with IV alteplase (tissue plasminogen activator) within 4.5 hours.
  • Alteplase converts plasminogen into plasmin + so promotes breakdown of fibrin clot.
  • 300mg aspirin for 2 weeks post-stroke + lifelong clopidogrel.
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27
Q

CEREBROVASCULAR ACCIDENT

What is the treatment for a haemorrhagic stroke?

A
  • Stop anticoagulants, warfarin reversal with beriplex.
  • Control BP with beta-blocker.
  • Surgical = clipping or coiling.
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28
Q

CEREBROVASCULAR ACCIDENT

What risk factor management is there for CVA + post-stroke what professionals work with the patient?

A
  • Anti-hypertensives + statins.
  • PT for physiotherapy
  • OT for home modifications.
  • SALT for swallowing + speech help.
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29
Q

CEREBROVASCULAR ACCIDENT

What are some contraindications to thrombolysis?

A
  • Haemorrhage.
  • Active bleeding.
  • Warfarin/heparin.
  • Aneurysm.
  • Pregnant.
  • HTN.
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30
Q

TIA

What is the pathophysiology of a transient ischaemic attack (TIA)?

A
  • Acute loss of focal neurological deficit with symptoms lasting <24h + with a complete clinical recovery.
  • Symptoms often most severe at start.
  • Caused by inadequate cerebral blood supply > ischaemia + so oxygen deprivation of tissue + transient loss of function with resolution but possible remittance.
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31
Q

TIA

What is the aetiology of TIA?

A
  • Atherothromboembolism from carotid.
  • Cardioembolism – mural thrombus post-MI, AF.
  • Hyperviscosity – polycthaemia, sickle-cell anaemia.
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32
Q

TIA

What are the risk factors for TIA?

A
  • HTN.
  • DM.
  • Smoking + alcohol.
  • Hyperlipidaemia.
  • Obesity.
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33
Q

TIA

What is the clinical presentation of a TIA in the carotid territory?

A
  • Amaurosis fugax (sudden transient loss of vision in one eye).
  • Aphasia.
  • Hemiparesis.
  • Hemisensory loss.
  • Hemianopic visual loss.
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34
Q

TIA

What is the clinical presentation of a TIA in the vertebrobasilar territory?

A
  • Diplopia, vertigo, vomiting.
  • Choking + dysarthria (unclear articulation of speech but understandable).
  • Ataxia (no control of body movement).
  • Hemisensory/hemianopic visual loss.
  • Tetraparesis.
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35
Q

TIA

What are the investigations for TIA?

A
  • Bloods – FBC for polycythaemia, glucose for hypoglycaemia.
  • Carotid doppler ± angiography.
  • CT head.
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36
Q

TIA

What score can be used to assess someone’s 7-day stroke risk post-TIA?

A 
ABCD2...
- Age >60 (1)
- BP >140/90mmHg (1)
- Clinical features (1)
- Duration – ≥60 (2), 10-59 (1)
- Diabetes (1)
Score >6 = specialist immediately, >4 specialist 24h, rest seen within 1w.
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37
Q

TIA

What is the anti-thrombotic treatment given for TIA?

A
  • Aspirin 300mg immediately then 75mg continued long-term.

- Clopidogrel 75mg if intolerant.

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38
Q

TIA

What is the secondary prevention for TIA? What other treatment can be given? Recommendations to patient who drives?

A
  • Control HTN, treatment of statin for patients with high cholesterol.
  • Carotid edarterectomy if ICA stenosis >70%.
  • Do not drive for AT LEAST 1 MONTH following a TIA.
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39
Q

SAH

What is the pathophysiology of a subarachnoid haemorrhage (SAH)?

A
  • Spontaneous rupture causes a rapid release of arterial blood into subarachnoid space causing an increased intracranial pressure + possibly CVA.
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40
Q

SAH

What is the aetiology of SAH?

A

Berry aneurysm rupture (80%)
- Common sites = bifurcations like anterior communicating + anterior cerebral, middle cerebral or posterior communicating + ICA.
Congenital arteriovenous malformations
Other – tumour, vasculitis.

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41
Q

SAH

What are the risk factors of SAH?

A
  • HTN.

- Polycystic kidney disease, coarctation of aorta, Ehler’s Danlos syndrome.

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42
Q

SAH

What are the symptoms of SAH?

A
  • Sudden-onset excruciating headache = thunderclap.
  • Nausea, loss of consciousness, seizures.
  • Preceding ‘sentinel’ headache = small warning leak from offending aneurysm.
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43
Q

SAH

What are the signs of SAH?

A
  • Neck stiffness.
  • Kernig’s (unable to extend patients leg at knee when thigh flexed).
  • Retinal bleeds.
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44
Q

SAH

What are complications of SAH?

A
  • Rebleeding.
  • Cerebral ischaemia due to vasospasm.
  • Hydrocephalus due to blockage of arachnoid granulations.
  • Hyponatraemia.
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45
Q

SAH

What are the investigations for SAH?

A

CT head = gold standard…
- Star-shaped lesion due to blood filling in gyro patterns around brain + ventricles.
Lumbar puncture if CT-ve, wait 12 hours for Hb to break down, 3 samples = no bloody tap..
- Xanthochromic (yellow due to bilirubin) confirms.
CT angiography.

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46
Q

SAH

What is the treatment for SAH?

A
  • Neurosurgery immediately (endovascular coiling vs. surgical clipping).
  • Maintain cerebral perfusion IV fluids but BP <160mmHg.
  • Nimodipine (CCB) to reduce vasospasm.
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47
Q

EXTRA-DURAL HAEMATOMA

What is the pathophysiology of extra-dural haematoma? What is the ventricles mechanism in this?

A
  • Fractured temporal/parietal bone leads to rupture of the middle meningeal artery causing a bleed ABOVE the dura.
  • Ventricles compensate by getting rid of their CSF to prevent rise in intracranial pressure.
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48
Q

EXTRA-DURAL HAEMATOMA

What is the aetiology of extra-dural haematoma?

A
  • Traumatic head injury or skull fracture.
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49
Q

EXTRA-DURAL HAEMATOMA

What is the clinical presentation of extra-dural haematoma?

A
  • Lucid interval pattern where progressive decrease (rapid) in GCS from rising intracranial pressure.
  • Papilloedema (cardinal physical sign due to obstruction of venous return from retina).
  • Increasingly severe headache, vomiting, confusion + seizures.
  • Ipsilateral pupil dilation.
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50
Q

EXTRA-DURAL HAEMATOMA

What are the complications of extra-dural haematoma?

A
  • Brainstem compression causing breathing to become deep + irregular.
  • Death may follow a period of coma due to respiratory arrest.
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51
Q

EXTRA-DURAL HAEMATOMA

What are the investigations for extra-dural haematoma?

A
  • CT head = biconvex/lens-shaped haematoma.
  • Skull X-ray may show fracture lines crossing course of middle meningeal artery.
  • Lumpar puncture C/I.
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52
Q

EXTRA-DURAL HAEMATOMA

What is the treatment for extra-dural haematoma?

A
  • IV mannitol for increased intracranial pressure.

- Surgery for clot removal.

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53
Q

SUBDURAL HAEMATOMA

What is the pathophysiology of subdural haematoma?

A
  • Rupture of a vein running from the hemisphere to the sagittal sinus (bridging veins) that’s beneath the dura.
  • Often latent period after head injury + then clot starts to breakdown + massive increase in oncotic pressure so water is sucked up into haematoma causing symptoms > gradual rise in intracranial pressure.
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54
Q

SUBDURAL HAEMATOMA

What is the aetiology of subdural haematoma? In what group of people are they most common in?

A
  • Almost always head injury (often minor), can occur 9 months post-incident.
  • Patients with small brains, at risk of falls + on anti-coagulation therapy (alcoholics, elderly with dementia).
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55
Q

SUBDURAL HAEMATOMA

What are the symptoms of subdural haematoma?

A
  • Fluctuating level of consciousness (GCS) ± insidious physical/intellectual slowing.
  • Sleepiness.
  • Headache.
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56
Q

SUBDURAL HAEMATOMA

What are the signs of subdural haematoma?

A
  • Increased intracranial pressure (headache, reduced GCS, papilloedema).
  • Localising neurological symptoms (unequal pupils).
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57
Q

SUBDURAL HAEMATOMA

What are the investigations + treatment of subdural haematoma?

A
  • CT head = clot ± mid-line shift, crescent-shaped collection of blood.
  • Surgical remove of clot – 1st line clot evacuation, 2nd line craniotomy, IV mannitol if increased intracranial pressure.
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58
Q

EPILEPSY

What is the pathophysiology of epilepsy?

A
  • Epilepsy is a recurrent tendency to spontaneous, intermittent, abnormal electrical activity in parts of the brain, manifesting as seizures where convulsions are the motor signs of electrical discharges.
  • Innervation of muscle fibres cause physical movements (tonic clonic seizures) + sensory disturbance (partial seizures).
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59
Q

EPILEPSY

What is the aetiology of epilepsy?

A
  • 2/3rd idiopathic.
  • Flashing lights (trigger).
  • CNS infection like meningitis.
  • Trauma.
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60
Q

EPILEPSY

What are the two broad categories of seizures?

A
  • Focal seizures where one hemisphere of the brain is affected.
  • Generalised seizures where the whole brain is affected.
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61
Q

EPILEPSY

What are the different types of focal seizures?

A
  • Simple-partial = with counsciousness.
  • Complex-partial = without consciousness.
  • Secondary generalised seizures.
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62
Q

EPILEPSY

What is the clinical presentation of a temporal lobe seizure?

A
  • Aura.
  • Deja-vu.
  • Auditory hallucinations.
  • Funny smells.
  • Automatisms (chewing, picking at clothes).
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63
Q

EPILEPSY

What is the clinical presentation of a frontal lobe seizure?

A
  • Jacksonian march (starts in small area + spreads to larger).
  • Post-ictal Todd’s palsy (paralysis of limbs involved in seizure for several hours).
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64
Q

EPILEPSY

What is the clinical presentation of a parietal lobe seizure?

A
  • Tingling/numbness.
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65
Q

EPILEPSY

What are the different types of generalised seizures?

A

Absence seizures (petite mals)…
- Brief (≤10s) pauses, presents in childhood.
Tonic-clonic seizures (grand mals)…
- Loss of consciousness, limbs stiffen (tonic) > jerk (clonic).
- Up to 120s, associated with tongue biting + incontinence.
Myoclonic seizures…
- Sudden jerk of a limb/face/trunk, patient may be thrown suddenly to ground.
Atonic (akinetic) seizures…
- Sudden loss of muscle tone causing full but conscious.

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66
Q

EPILEPSY

How can you differentiate between epilepsy + syncope?

A
  • Epilepsy aura, syncope light-headedness, faint.
  • Epilepsy sudden, syncope avoidable with posture change.
  • Epilepsy eyes open, convulsions, syncope eyes closed, falls forwad.
  • Epilepsy recovery is confused + sleepy, syncope is pale, sweaty, cold.
  • Epilepsy involves tongue biting, incontinence, rare in syncope.
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67
Q

EPILEPSY

What is the major complication of epilepsy?

A
  • Status epilepticus > medical emergency with continuous seizures >30m or ≥2 seizures without recovery over similar time period.
  • Risk of death from cardiorespiratory failure – IV lorazepam.
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68
Q

EPILEPSY

What are the investigations for epilepsy?

A
  • Consider electroencephalogram (EEG).
  • CT brain in emergencies.
  • MRI brain.
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69
Q

EPILEPSY

What is the treatment for epilepsy?

A 
Focal seizures...
- 1st line = carbamazepine/lamotrigine.
- 2nd line = sodium valporate.
Generalised...
- 1st line = sodium valporate.
- 2nd line lamotrigine.
Seizure control...
- Diazepam (rectal), IV lorazepam.
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70
Q

PARKINSON’S DISEASE

What is the pathophysiology of Parkinson’s disease?

A
  • There is progressive loss of dopamine secreting cells from the substantia nigra causing an alteration in neural circuits within the basal ganglia which regulates movement.
  • Presence of Lewy bodies.
  • Loss from non-striatal pathways for neuropsychiatric pathology.
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71
Q

PARKINSON’S DISEASE

What is the aetiology of Parkinson’s disease?

A
  • Unknown, genetic link.

- Parkinson’s disease is less prevalent in tobacco smokers than in life long abstainers.

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72
Q

PARKINSON’S DISEASE

What is the clinical presentation of Parkinson’s disease? What are the typical Parkinsonism features?

A
  • Asymmetrical, symptoms on one side always worse.
  • Problems doing up buttons, writing smaller.
    Parkinsonism…
  • Bradykinesia.
  • Rigidity (pain, problems turning in bed).
  • Resting tremor (‘pill-rolling’ of thumbs over fingers).
  • Postural changes (stooped).
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73
Q

PARKINSON’S DISEASE

What are the gait issues in Parkinson’s disease?

A
  • Small steps/shuffling.

- Walking slowly, reduce arm swing (asymmetrical).

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74
Q

PARKINSON’S DISEASE

What are the pre-motor symptoms of Parkinson’s disease?

A
  • Anosmia (loss of sense of smell).
  • Depression.
  • REM sleep behaviour disorder.
  • Autonomic features (urinary urgency, hypotension).
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75
Q

PARKINSON’S DISEASE

What are the investigations for Parkinson’s disease?

A
  • Diagnosis = clinical.

- Idiopathic Parkinson’s disease shows a normal CT/MRI.

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76
Q

PARKINSON’S DISEASE

What is the treatment in Parkinson’s disease to increase the amount of dopamine in CNS?

A
  • Levodopa (dopamine precursor) can cross BBB to be converted to dopamine by dopa-decarboxylase.
  • Combined with peripheral dopa-decarboxylase inhibitor (carbidopa) so it crosses BBB first.
  • Drug = co-careldopa (levodopa + carbidopa).
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77
Q

PARKINSON’S DISEASE

What is the treatment in Parkinson’s disease that mimics the action of dopamine? What is used for tremor management?

A
  • Dopamine receptor antagonists like ropinirole.

- Anticholinergic like amantadine.

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78
Q

PARKINSON’S DISEASE

What is the treatment in Parkinson’s disease that inhibits enzymatic breakdown of dopamine?

A
  • COMT inhibitor (tolcapone).

- MAO inhibitor selegiline.

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79
Q

HEADACHES

What is the pathophysiology of headaches?

A

Primary…
- No underlying cause relevant to headache.
- Migraine, cluster + tension (most common).
Secondary…
- Underlying cause needs identifying.
- Meningitis, SAH, giant cell arteritis, medication overuse.

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80
Q

HEADACHES

What are the red flags of a secondary headache?

A
  • Thunderclap headache.
  • Seizure/altered GCS.
  • Papilloedema.
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81
Q 
HEADACHES
What is the aetiology of...
i) cluster
ii) tension
iii) medication overuse

headaches?

A

i) More common in men + smokers.
ii) Commonest primary headache, precipitated by missed meals, stress, conflict, lack of sleep.
iii) Commonest secondary headache.

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82
Q

HEADACHES

What is the clinical presentation of cluster headache?

A

15m–3h…

  • Rapid onset excruciating pain around one eye, may be watery + bloodshot.
  • Pain is unilateral, often nocturnally.
  • Cranial autonomic features (lacrimation, lid swelling, facial flushing).
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83
Q

HEADACHES

What is the clinical presentation of tension headache?

A

30m–7d…

  • Bilateral.
  • Pressing/tight band-like sensation.
  • Mild-moderate intensity.
  • Non-pulsatile.
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84
Q 
HEADACHES
What are the investigations for...
i) cluster
ii) tension
iii) medication overuse

headaches?

A

i) ≥5 headaches fulfilling clinical presentation.
ii) Clinical diagnosis.
iii) Headache present for >15d/month
- Regular use for >3m of >1 symptomatic treatment drugs.
- Headache developed/markedly worsened during drug use.

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85
Q

HEADACHES

What is the treatment + prevention for cluster headaches?

A
  • Acute attack give 100% oxygen + sumatriptan s/c (serotonin receptor antagonist).
  • Prevention use verapamil (CCB) as first line prophylaxis, avoid alcohol during cluster period.
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86
Q

HEADACHES

What is the treatment for tension headaches?

A
  • Reassurance + lifestyle advice (avoid triggers, exercise).

- Symptomatic treatment for episodes like aspirin, paracetamol.

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87
Q

MIGRAINE

What is the pathophysiology of migraines?

A
  • Changes in brainstem blood flow lead to an unstable trigeminal nerve nucleus + nuclei in basal thalamus.
  • Leads to release of vasoactive neuropeptides CGRP + substance P > neurogenic inflammation > vasodilation + plasma protein extravasation leading to pain propagating all over cerebral cortex.
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88
Q

MIGRAINE

How long does a migraine tend to last? Who is more at risk?

A

4–72h, more common in females.

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89
Q

MIGRAINE

What is the aetiology of migraines?

A

CHOCOLATE…

  • Chocolate.
  • Hangovers.
  • Orgasms.
  • Cheese/caffeine.
  • Oral contraceptives.
  • Lie-ins.
  • Alcohol.
  • Travel.
  • Exercise.
90
Q

MIGRAINE

What are the three types of migraines?

A
  • Episodic migraine without aura (80%).
  • Episodic migraine with aura (20%).
  • Migraine variant.
91
Q

MIGRAINE

What is the clinical presentation of episodic migraine without aura?

A 
≥2 of these...
- Unilateral.
- Pulsatiles.
- Moderate/severe pain.
- Aggravated by physical activity.
≥1 of these...
- Photophobia + phonophobia, 
- Nausea ± vomiting.
92
Q

MIGRAINE

What is the clinical presentation of episodic migraine with aura?

A 
≥2 of these...
- ≥1 aura symptom is unilateral.
- Aura accompanied/followed within 60mins by headache.
≥1 of these...
- Visual disturbances like flashing lights, zig-zag lines.
- Paraesthesia.
- Aphasia.
Motor weakness (hemiplegic migraine).
93
Q

MIGRAINE

What is the clinical presentation of migraine variant?

A
  • Characterised by unilateral motor/sensory symptoms resembling a stroke.
94
Q

MIGRAINE

What is the treatment for migraines?

A 
Avoid triggers.
Prophylaxis...
- Propranolol (1st line).
- Acupuncture (2nd line).
- Amitryptyline (3rd line).
During an attack...
- Oral sumatriptan combined with NSAID/paracetamol.
95
Q

TRIGEMINAL NEURALGIA

What is the pathophysiology of trigeminal neuralgia? Which branch is most affected?

A
  • Compression of the trigeminal nerve resulting in demyelination + excitation of the nerve resulting in erratic pain signalling.
  • Mandibular branch.
96
Q

TRIGEMINAL NEURALGIA

What is the aetiology of trigeminal neuralgia?

A
  • Can be idiopathic or secondary to tumour, MS.

- Triggers = washing affected area, shaving, eating, talking + dental prostheses.

97
Q

TRIGEMINAL NEURALGIA

What is the clinical presentation of trigeminal neuralgia?

A
  • Paroxysms of intense, stabbing pain, lasting seconds in the trigeminal distribution.
  • Unilateral.
  • Knife-like/shooting pain – no neurological deficit.
98
Q

TRIGEMINAL NEURALGIA

What are the investigations + treatment for trigeminal neuralgia?

A
  • MRI head to exclude secondary, clinical diagnosis of ≥3 attacks, pain in ≥1 division + symptoms.
  • Anti-convulsant carbamazepine, if drugs fail microvascular decompression or stereotactic radiation.
99
Q

MULTIPLE SCLEROSIS

What is the pathophysiology of MS?

A
  • Chronic autoimmune inflammatory disorder of CNS due to T-cell mediated immune response.
  • Demyelination heals poorly with thinner, inefficient myelin, eventually causing axonal loss of oligodendrocytes.
100
Q

MULTIPLE SCLEROSIS

Where do you find MS plaques? Are PNS myelinated nerves affected and why?

A

Plaques are perivenular + have predilection for distinct sites…
- Optic nerves.
- Around ventricles.
- Corpus callosum.
- Brainstem + Cerebellar connections.
- Cervical cord.
No as their myelin is Schwann cell based + have different antigens to that of CNS myelin from oligodendrocytes.

101
Q

MULTIPLE SCLEROSIS

What is the epidemiology of MS?

A
  • Presents 20–40y/o.

- Females > males.

102
Q

MULTIPLE SCLEROSIS

What is the aetiology of MS?

A
  • Enviroment (EBV shown to be associated).

- Genetic predisposition.

103
Q

MULTIPLE SCLEROSIS

What are the different types of MS?

A

Relapsing + remitting…
- Periods of remission followed by sudden relapses.
- Patients may accumulate disability over time if they don’t fully recover from relapses.
Secondary progressive MS…
- Follows on from relapsing + remitting consisting of gradually worsening symptoms with fever remissions.
Primary progressive…
- Gradually worsening disability without relapses or remissions.
Progressive relapsing…
- Steady decline since onset with super-imposed attacks

104
Q

MULTIPLE SCLEROSIS

What is the clinical presnetation of MS?

A

DEMYELINATION, usually monosymptomatic…

  • Diplopia.
  • Eye movements painful (optic neuritis).
  • Motor weakness.
  • nYstagmus.
  • Elevated temp worsens (Uhtoff’s phenomenon.
  • Lhermitte’s sign (neck movement = shock).
  • Intention tremor.
  • Neuropathic pain.
  • Ataxia.
  • Talking slurred.
  • Impotence.
  • Overactive bladder.
  • Numbness.
105
Q

MULTIPLE SCLEROSIS

What are the investigations for MS?

A
  • MRI brain + spinal cord to see demyelination plaques.
  • Lumbar puncture with CSF electrophoresis = oligoclonal bands of IgG on electrophoresis.
  • Evoked potentials = delayed visual, brainstem, auditory + somatosensory potentials.
106
Q

MULTIPLE SCLEROSIS

What is the treatment for MS?

A

Lifestyle…
- Regular exercise, smoking cessation, avoid stress, CBT.
Mediciation…
- Relpases = steroids (methylprednisolone).
- Chronic = 1st, beta-interferon, 2nd, natalizumab (monoclonal antibody).

107
Q

MULTIPLE SCLEROSIS

What treatments are used for symptom control in MS?

A
  • Baclofen = spasticity.
  • Gabapentin = neuropathic pain.
  • Beta-blocker = tremor.
108
Q

MOTOR NEURONE DISEASE

What is the pathophysiology of motor neurone disease?

A
  • The relentless destruction/degeneration of motor neurones in…
  • Motor cortex = UMN signs.
  • Anterior horn cells = LMN signs.
  • Cranial nerve nuclei = mixed.
109
Q

MOTOR NEURONE DISEASE

What are the different types of MND?

A 
Amyotrophic lateral sclerosis (ALS)...
- Motor cortex + anterior horn so UMN + LMN.
Primary lateral sclerosis (PLS)...
- Motor cortex
Progressive bulbar palsy (PBP)
- Destruction of CN9–12 + so UMN + LMN of them.
Progressive muscular atrophy (PMA)
- Anterior horn cell lesion so LMN.
110
Q

MOTOR NEURONE DISEASE

What is the clinical presentation of ALS?

A
  • Progressive focal wasting, weakness + fasciculation spreading to other limbs.
  • Cramps.
  • Spasticity + brisk reflexes (Babinski present).
111
Q

MOTOR NEURONE DISEASE

What is the clinical presentation of PLS?

A
  • Slow progressive tetraparesis.

- Pseudobulbar palsy (dysarthria, dysphagia, choking).

112
Q

MOTOR NEURONE DISEASE

What is the clinical presentation of PMA?

A
  • Weakness + fasciculations starting in one limb + progressing to ajacent spinal segments.
113
Q

MOTOR NEURONE DISEASE

What is the clinical presentation of PBP?

A
  • Dysarthria (slurred speech).
  • Dysphagia.
  • Choking.
114
Q

MOTOR NEURONE DISEASE

What are the investigations for motor neurone disease?

A
  • EMG + nerve conductiion studies = muscle denervation.
  • Increased creatinine kinase due to muscle breakdown.
  • LP excludes inflammatory causes.
  • Brain/cord MRI excludes structural causes.
115
Q

MOTOR NEURONE DISEASE

What features of motor neurone disease help distinguish it from MS/myasthenia gravis?

A
  • No sensory loss.
  • No disturbances in eye movements.
  • No sphincter disturbances.
116
Q

MOTOR NEURONE DISEASE

What is the treatment for motor neurone disease?

A
  • Riluzole = Na+ blocker inhibits glutamate release + slows disease progression.
  • Symptomatic > dysphagia = NG/PEG tube, drooling = amitryptyline, pain = analgesics.
117
Q

MENINGITIS

What is the pathophysiology of meningitis? Who must all recorded cases of meningitis be reported to and why?

A
  • Infection of the meninges leads to inflammation of the tissue.
  • Microrganisms can reach the meninges either by direct extension from ears, nasopharynx or via bloodstream spread.
  • Public Health England as it’s a notifiable disease.
118
Q

MENINGITIS

What is the aetiology of bacterial meningitis?

A
  • N. meningitidis, gram-ve diplococci (meningococcal meningitis).
  • S. pneumoniae, gram+ve cocci chain (pneumococcal meningitis, most common).
  • Listeria monocytogenes, gram+ve bacilli.
119
Q

MENINGITIS

What is the aetiology of viral meningitis?

A
  • Enteroviruses (commonest), herpes simplex virus, TB.
120
Q

MENINGITIS

What is the clinical presentation of bacterial meningitis?

A
  • Headache, papilloedema.
  • Fever.
  • Menigism = neck stiffness, photophobia, Kernig’s sign.
  • Non-blanching rash (+ signs of sepsis = meningococcal septicaemia).
121
Q

MENINGITIS

What is the clinical presentation of viral + TB meningitis?

A
  • Blurred vision/headache, often benign + self-limited for about a week.
  • Long history + vague symptoms (headache, vomiting) with meningism later on.
122
Q

MENINGITIS

What are the complications of meningitis infection?

A
  • Cerebral oedema or abscess.

- Later in life = recurring headaches, fatigue.

123
Q

MENINGITIS

What are the investigations for meningitis?

A
  • Blood cultures before LP + Abx.
  • Bloods = FBC, U+E, CRP, glucose.
  • LP (L4/5 level) w/ CSF culture.
  • CT head if other signs like papilloedema.
124
Q

MENINGITIS

In what situations is a lumbar puncture contraindicated in meningitis and why?

A
  • Drowsy/seizures/signs of increased intracranial pressure + meningococcal septicaemia.
  • Coning of cerebellar tonsils.
125
Q 
MENINGITIS
What would the lumbar puncture result look like for...
i) Bacterial.
ii) Viral.
iii) TB.

meningitis?

A

i) Turbid (cloudy), polymorphs, protein +, glucose –
ii) Clear, lymphocytes, protein, normal, glucose normal.
iii) Fibrin web, lymphocytes, protein +, glucose –/normal.

126
Q

MENINGITIS

What is the community treatment for someone suspected of meningitis?

A
  • IM benzylpenicillin.
127
Q

MENINGITIS

What is the immediate hospital treatment for someone with bacterial meningitis?

A
  • IV cefotaxime.

- Add amoxicillin to cover listeria.

128
Q

MENINGITIS

What is the treatment for viral meningitis?

A
  • Supportive therapy + aciclovir for herpetic infection.
129
Q

MENINGITIS

What is the prevention against meningitis?

A
  • Children are vaccinated against meningitis B (8/16w), C (12w+12m) + ACWY (14y).
  • Prophylactic rifampicin give to anyone in droplet range as effective against N. meningitidis.
130
Q

ENCEPHALITIS

What is the pathophysiology of encephalitis?

A

Infection + inflammation of the brain parenchyma (cortex/white matter/brainstem/basal ganglia).

131
Q

ENCEPHALITIS

What is the aetiology of encephalitis?

A

More common in immunocompromised.

  • Mainly viral (Herpes simplex virus 1+2, EBV, HIV).
  • Non viral = any bacterial meningitis, TB, malaria.
132
Q

ENCEPHALITIS

What is the clinical presentation of encephalitis?

A
  • Fever, hedache + altered mental state (personality/behaviour changes).
  • Reduced GCS compared to meningitis.
  • Focal neurological deficit like hemiparesis, dysphasia.
133
Q

ENCEPHALITIS

What are the investigations for encephalitis?

A
  • Viral PCR.
  • Blood cultures.
  • CT head.
  • LP = increased CSF protein + lymphocytes, decreased glucose, send for CSF viral PCR.
134
Q

ENCEPHALITIS

What is the treatment for encephalitis?

A
  • Immediate high dose IV aciclovir.
135
Q

SHINGLES

What is the pathophysiology of shingles?

A
  • Caused by reactivation of varicella zoster virus (chickenpox), usually within dorsal root ganglia where it’s been dormant.
  • When it flares up, virus travels down affected nerve over 3–4 days, causing peri/intraneural inflammation.
136
Q

SHINGLES

What are the risk factors of reactivation in shingles?

A
  • Old age.

- Immunocompromised.

137
Q

SHINGLES

What is the clinical presentation for shingles?

A

Pre-eruptive…
- No skin lesions but burning itch in one dermatome.
Eruptive…
- Erythematous plaques that does not cross dermatomes, pain + paraesthesia.

138
Q

SHINGLES

What are the complications, investigations + treatment for shingles?

A
  • Opthalmic branch of trigeminal nerve damaged it will affect sight.
  • Clinical based on rash within dermatome.
  • Antivirals like aciclovir, analgesia for pain.
139
Q

DEMENTIA

What is the epidemiology of dementia?

A
  • Prevalence rises w/ age.
  • Alzheimer’s disease more common in females.
  • Vascular + mixed more common in males.
140
Q

DEMENTIA

What are the 4 types of dementia?

A
  • Alzheimer’s disease (commonest).
  • Vascular.
  • Lewy-body.
  • Fronto-temporal.
141
Q

DEMENTIA

What is the aetiology of Alzheimer’s disease?

A
  • Accumulation of beta-amyloid peptide resulting in degeneration of cerebral cortex with cortical atrophy, loss of acetylcholine.
  • Temporal lobe affected.
  • 25% develop Parkinsonism.
142
Q 
DEMENTIA
What is the aetiology of...
i) Vascular
ii) Lewy-body
iii) Fronto-temporal

dementia?

A

i) Cumulative effect of many small strokes.
ii) Characterised by Lewy-body deposition, associated with Parkinson’s.
iii) Frontal + temporal lobe atrophy, associated with motor neurone disease.

143
Q

DEMENTIA

What is the clinical presentation of Alzheimer’s disease?

A
  • Insidious onset, short-term memory loss often first cognitive marker.
  • Aphasia, agnosia (can’t interpret sensory information), apraxia (difficult with motor planning).
144
Q

DEMENTIA

What is the clinical presentation of vascular dementia?

A
  • Stepwise deterioration with short periods of stability, sudden onset.
145
Q

DEMENTIA

What is the clinical presentation of Lewy body dementia?

A
  • Fluctuating congitive impairment.
  • Detailed visual hallucinations.
  • Parkinson’s.
146
Q

DEMENTIA

What is the clinical presentation of fronto-temporal dementia?

A
  • Behavioural/personality change.

- Disinhibition.

147
Q

DEMENTIA

How can you differentiate between dementia and delirium?

A
  • Dementia is insidious + progressive, delirium is acute + fluctuating.
  • Dementa lasts months-years, delirium lasts hours-weeks.
  • Dementia has normal consciousness, delirium doens’t.
148
Q

DEMENTIA

What are the investigations for dementia?

A
  • Clinical diagnosis.
  • MMSE <17/30 = serious cognitive impairment.
  • 6CIT = year? month? address? count 20-1? months in reverse? address?
  • Alzheimer’s shows plaques of amyloid + neuronal reduction.
149
Q

DEMENTIA

What is the treatment for dementia?

A
  • Regular exercise, healthy diet, smoking/alcohol cessation.
  • Acetylcholinesterase inhibitor (donepezil).
  • BP control if vascular.
150
Q

DEPRESSION

What are the risk factors for depression?

A
  • Genetic (family history).
  • Death or loss.
  • Conflict/abuse.
  • Medical illness/substance abuse.
  • Life events (positive or negative).
151
Q 
DEPRESSION
What are the...
i) Psychological
ii) Physical
iii) Social

symptoms of depression?

A

i) Continuous low mood/sadness, low self-esteem, feeling suicidal/tearful.
ii) Changes in appetite/weight, constipation, loss of libido.
iii) Not doing well at work, avoiding contact with friends.

152
Q

DEPRESSION

What are the investigations for depression?

A 
PHQ-9, GAD-7 questionnaires.
DSM-IV criteria...
- Symptoms occurring ≥2w.
- Baseline mood change.
- Impaired function social/occupational/educational.
153
Q

DEPRESSION

What are the non-pharmacological treatments for depression?

A
  • CBT (online).
  • Mental health apps.
  • Exercise.
  • Counselling.
154
Q

DEPRESSION

What 2 drug classes are used for depression? Give examples.

A
  • Selective serotonin reuptake inhibitors = citalopram.

- Tricyclic antidepressants = amitriptyline.

155
Q

DEPRESSION

What is the mechanism of citalopram? What are the side effects?

A
  • Preferentially inhibit neuronal reuptake of serotonin (5-HT) from synaptic cleft.
  • GI disturbances, suicidal thoughts increased initially, prolong QT.
156
Q

DEPRESSION

What is the mechanism of amitriptyline? What are the side effects?

A
  • Inhibit neuronal uptake of serotonin + noradrenaline from synaptic cleft + so increase availability for neurotransmission.
  • QT prolongation, sexual dysfunction, sedation.
157
Q

PRIMARY BRAIN TUMOURS

What cell origin are the majority of primary brain tumours? What are benign brain tumours?

A
  • Gliomas (glial cell in origin) like astrocytoma (most common) or oligodendroglioma.
  • Benign tumours = meningiomas + neurofibromas (schwannomas).
158
Q

PRIMARY BRAIN TUMOURS

Describe the aetiology of malignant gliomas.

A
  • Initial genetic error with mutation of IDH-1 resulting in genetic instability + inappropriate mitosis.
    OR
  • No IDH mutation, catastrophic genetic mutation.
159
Q

PRIMARY BRAIN TUMOURS

What is the WHO glioma grading?

A
  • I = benign paediatric tumour (pilocytic astrocytoma).
  • II = premalignant tumour (diffuse astrocytoma).
  • III = anaplastic astrocytoma.
  • IV = glioblastoma multiforme (GBE), all gliomas except grade I eventually lead to this very malignant cancer.
160
Q

PRIMARY BRAIN TUMOURS
What is a medulloblastoma?
What is the advantage of the IDH-1 mutation?

A
  • Cerebellum tumour.

- Good prognostic factor, chemosensitive.

161
Q

PRIMARY BRAIN TUMOURS

What are the three cardinal signs of a primary brain tumour?

A
  • Progressive focal neurological deficit.
  • Raised intracranial pressure.
  • Epilepsy (generalised or partial).
162
Q

PRIMARY BRAIN TUMOURS

Explain the mechanism behind progressive focal neurological deficit.

A
  • Result of mass effect of tumour + surrounding cerebral oedema.
  • Frontal = personality change, hemiparaesis, Broac’s dysphasia.
  • Temporal = dysphasia, amnesia.
  • Parietal = hemisensory lsos, dysphasia.
  • Occipital = contralateral visual defects.
  • Cerebellum = DANISH.
163
Q

PRIMARY BRAIN TUMOURS

Explain the effects of raised intracranial pressure.

A
  • Papilloedema.
  • Headache (worst first thing in morning, coughing + bending forward).
  • Nausea.
164
Q

PRIMARY BRAIN TUMOURS

What are the investigations for primary brain tumours?

A
  • Histological.
  • CT/MRI head.
  • MR angiography.
165
Q

PRIMARY BRAIN TUMOURS

What is the treatment for primary brain tumours?

A
  • Exploration, removal or biopsy.
  • Meningiomas can be removed completely.
  • Radiotherapy (all gliomas) + chemotherapy.
  • Cerebral oedema reduced by corticosteroids.
166
Q

SECONDARY BRAIN TUMOURS

What’s the pathophysiology of brain tumours?

A

Neoplasms which have metastasised to the CNS…

  • Non-small cell carcinoma (most common).
  • Breast.
  • Malignant melanoma.
  • RCC.
  • GI.
167
Q

SECONDARY BRAIN TUMOURS

What’s the clinical presentation of secondary brain tumours?

A
  • Headache (often worse in morning, coughing, bending).
  • Focal neurologcail signs.
  • Ataxia.
  • Fits, nausea, vomiting, papilloedema.
168
Q

SECONDARY BRAIN TUMOURS

What are the investigations + treatment for secondary brain tumours?

A
  • CT/MRI chest, abdomen.
  • Surgery + adjuvant radiotherapy, chemotherapy.
  • Supportive care like dexamethasone to reduce cerebral oedema.
169
Q

GIANT CELL ARTERITIS

What is the pathophysiology of GCA?

A
  • Chronic inflammation of the medium-large arteries, particularly the aorta + its extracranial branches.
170
Q

GIANT CELL ARTERITIS

What is the aetiology of GCA?

A
  • Unknown but associated with polymyalgia rheumatica.
  • Secondary to SLE, RA, HIV.
  • Principally affects >50y/o, incidence increases with age.
171
Q

GIANT CELL ARTERITIS

What is the clinical presentation of GCA?

A
  • Temporal artery + scalp tenderness.
  • Tongue/jaw claudication.
  • Headache.
  • Superficial temporal artery firm + pulseless.
172
Q

GIANT CELL ARTERITIS

What are the complications with GCA?

A
  • Blindness can occur due to inflammation + occlusion of the ciliary and/or central retinal artery = amaurosis fugax.
  • Optic disc pale + swollen.
173
Q

GIANT CELL ARTERITIS

What are the investigations of GCA?

A
  • Bloods, ESR/CRP raised (50/50 = over 50y/o, ESR over 50).

- Temporal artery biopsy = diagnostic.

174
Q

GIANT CELL ARTERITIS

What is the treatment for GCA?

A
  • Prompt corticosteroids + aspirin.
  • PPI to prevent GI toxicity.
  • Osteoporosis prophylaxis important (vitamin D, lifestyle advice).
175
Q

SPINAL CORD COMPRESSION

What is the pathophysiology of spinal cord compression?

A
  • Myelopathy = compression of spinal cord resulting in UMN signs + specific symptoms based on compression.
176
Q

SPINAL CORD COMPRESSION

What is the aetiology of spinal cord compression?

A
  • Osteophytes.
  • Disc prolapse.
  • Tumour.
177
Q

SPINAL CORD COMPRESSION

What is the clinical presentation of spinal cord compression?

A
  • Progressive weakness of legs + UMN signs.

- Sensory loss below level of lesion.

178
Q

SPINAL CORD COMPRESSION

What are the investigations + treatment for spinal cord compression?

A
  • MRI spine instantly.

- Surgical decompression + dexamethasone.

179
Q

CAUDA EQUINA SYNDROME

What is the pathophysiology + aetiology of cauda equina? What is radiculopathy?

A
  • Nerve root compression caudal to termination of spinal cord at L1/2.
  • Herniation of lumbar disc (commonly L4/5, L5/S1), tumour or trauma.
  • Radiculopathy = spinal nerve root disease.
180
Q

CAUDA EQUINA SYNDROME

What is the clinical presentation of cauda equina?

A
  • LMN SIGNS.
  • Bilateral sciatica = sensory loss/pain in back of thigh/leg + lateral aspect of little toe.
  • Bladder/bowel dysfunction.
  • Saddle anaesthesia (bum).
  • Erectile dysfunction.
181
Q

CAUDA EQUINA SYNDROME

What are the investigations + treatment for cauda equina?

A
  • MRI spinal cord to localise lesion.

- Surgery for emergency pressure relief, conservative management.

182
Q

CARPAL TUNNEL SYNDROME

What is the pathophysiology + aetiology of carpal tunnel syndrome?

A
  • Inflammation of carpal tunnel leading to entrapment of median nerve + so pain + loss of sensation.
  • Often idiopathic, associated with hypothyroidism, DM + RA.
183
Q

CARPAL TUNNEL SYNDROME

What is the clinical presentation of carpal tunnel syndrome?

A
  • Aching pain in hand + arm (esp. night).
  • Paraesthesia in thumb, index + middle fingers relieved by dangling hand over edge of bed + shaking (WAKE + SHAKE).
  • ?wasting of thenar eminence.
184
Q

CARPAL TUNNEL SYNDROME

What are the investigations + treatment for carpal tunnel syndrome?

A
  • Neurophysiological exam (nerve conduction studies).
  • Phalen’s test = maximally flex wrist for 1 min, Tinel’s test = tapping on nerve at wrist induces tingling.
  • Splinting, local steroid injection ± decompression surgery.
185
Q 
PERIPHERAL NEUROPATHIES
Define...
i) Mononeuropathy.
ii) Polyneuropathy.
iii) Demyelinating.
iv) Axonal.
A

i) 1 nerve involved.
ii) Multiple/systemic nerves involved, diabetes, MS, GB.
iii) Slow conduction velocities.
iv) Reduced amplitudes of potentials.

186
Q

PERIPHERAL NEUROPATHIES

What is the aetiology of peripheral neuropathies?

A

DAVID…

  • Diabetes.
  • Alcohol.
  • Vitamin deficiency (B12).
  • Infective.
  • Drugs.
187
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a median nerve mononeuropathy.

A
  • Nerve of precision grip (LLOAF) = 2 lumbricals, opponens pollicis, abductor/flexor pollicis brevis.
  • Sensory loss of radial 3.5 fingers + palm.
188
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a ulnar nerve mononeuropathy.

A
  • Elbow trauma.
  • Weakness/wasting of interossei (good luck sign).
  • Medial lumbricals (claw hand).
  • Hypothenar eminence.
189
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a radial nerve mononeuropathy.

A
  • Compression against humerus, nerve opens fist.

- Test for wrist + finger drop.

190
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a brachial plexus mononeuropathy.

A
  • Trauma/radiotherapy/heavy rucksack.

- Pain/paraesthesia + weakness in affected arm.

191
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a phrenic nerve mononeuropathy.

A
  • Cancer/myeloma/thymoma.

- Orthopnoea with raised hemidiaphragm on CXR.

192
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a lateral cutaneous nerve of thigh mononeuropathy.

A
  • Meralgia paraesthetica = Antero-lateral burning thigh pain from entrapment under inguinal ligament.
193
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a scaitic nerve mononeuropathy.

A
  • Pelvic tumour/fracture.

- Sensory loss below knee laterally, foot drop.

194
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a common peroneal nerve mononeuropathy.

A
  • Cross-legged, trauma.

- Foot drop, weak ankle dorsiflexion/eversion, sensory loss over dorsal foot.

195
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a tibial nerve mononeuropathy.

A
  • Inability to tiptoe (plantarflexion), invert foot, flex toes, sensory loss over sole.
196
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of an olfactory nerve mononeuropathy.

A
  • Anosmia (lost sense of smell).
197
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of an optic nerve mononeuropathy.

A
  • L optic nerve lesion = no vision through left eye.
  • Optic chiasma lesion = bitemporal hemianopia.
  • L optic tract lesion = contralateral (right) homonymous hemianopia.
  • L Baum’s (parietal) loop = inferior right homonymous quadrantanopia.
  • L Meyer’s (temporal) loop = superior right homonymous quadrantanopia.
198
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of an oculomotor nerve mononeuropathy.

A
  • Tramps palsy = eye down + out.
  • Ptsosis.
  • Fixed dilated pupil = loss of parasymp outflow.
199
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a facial nerve mononeuropathy.

A
  • Post-viral.
    Bell’s palsy, muscles of facial expression…
  • Diff from stroke as NO forehead sparring.
    Tx = steroids.
200
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a glossopharyngeal/vagus nerve mononeuropathy.

A
  • Swallow, gag, cough issues.

- Uvula deviated AWAY from side of lesion.

201
Q

PERIPHERAL NEUROPATHIES

Explain the pathophysiology of a hypoglassal nerve mononeuropathy.

A
  • Tongue deviates TOWARDS side of lesion.
202
Q

PERIPHERAL NEUROPATHIES

What are the investigations for peripheral neuropathies?

A
  • Clinical examination, nerve conduction studies, MRI.

- Conservative management.

203
Q

MYASTHENIA GRAVIS

What is the pathophysiology of myasthenia gravis?

A
  • Autoimmune disorder against nicotinic acetylcholine receptors (AChR) in the neuromuscular junction where anti-AChR antibodies (IgG) interfere with the neuromuscular junction via depletion of working post-synaptic receptor sites.
  • This leads to fewer action potentials firing + so blocks the excitatory effect of ACh on nicotininc receptors – all or nothing principle.
  • Both T + B cells implicated.
204
Q

MYASTHENIA GRAVIS

What is the aetiology of myasthenia gravis?

A
  • Associated with autoimmune disease, esp. RA + SLE.
  • If <50y/o commoner in females + associated w/ thymic hyperplasia.
  • If >50y/o commoner in males + associated with thymic atrophy/tumour.
205
Q

MYASTHENIA GRAVIS

What muscle groups are affected in order?

A
  • Extra-ocular > bulbar (swallowing, chewing) > face > neck > trunk.
206
Q

MYASTHENIA GRAVIS

What are the symptoms of myasthenia gravis?

A
  • Slowly increasing muscle fatigue + weakness, improves after rest.
  • Weakness exacerbated by pregnancy, infection, emotion + exercise.
207
Q

MYASTHENIA GRAVIS

What are the signs of myasthenia gravis?

A
  • Ptosis, diplopia (extra-ocular).

- Dysphasia, dysarthria (bulbar).

208
Q

MYASTHENIA GRAVIS

What are the investigations for myasthenia gravis?

A

Serum antibodies…
- Increased anti-AChR.
- Muscle-specific tyrosine kinase (MuSK), esp. males.
Electromyogram (EMG) shows decremental muscle response to repetitive nerve stimulation.
Count to 50 – voice fades.
CT chest to exclude thymoma.

209
Q

MYASTHENIA GRAVIS

What is the treatment for myasthenia gravis?

A 
Symptom control...
- Anticholinesterase (pyridostigmine).
Immunosuppression...
- Treat relapses with prednisolone.
Thymectomy.
210
Q

HUNTINGTON’S DISEASE

What is the pathophysiology of HD?

A
  • Presence of mutant Huntingtin protein which causes loss of neurones in the striatum (caudate nucleus + putamen) of basal ganglia causing depletion of GABA (inhibitory neurotransmitter) + acetylcholine.
  • Dopamine is sparred.
211
Q

HUNTINGTON’S DISEASE

What is the impact of GABA depletion?

A
  • Less regulation of dopamine to striatum causing increased movements.
212
Q

HUNTINGTON’S DISEASE

What is the aetiology of HD?

A
  • Autosomal dominant inheritance.
  • CAG repeart in Huntingtin protein gene on chromosome 4.
  • > 35 CAG repeats = HD.
  • Number of repeats = indicative of age of onset.
  • Presents middle age.
213
Q

HUNTINGTON’S DISEASE

What is the clinical presentation of HD?

A 
Early signs...
- Irritability + depression.
- Personality change.
Later...
- Chorea (fidgety).
- Dementia.
- Psychiatric problems
214
Q

HUNTINGTON’S DISEASE

What are the investigations for HD?

A
  • Genetic diagnosis.

- MRI brain shows atrophy of striatum.

215
Q

HUNTINGTON’S DISEASE

What is the treatment for HD?

A
  • Treat chorea w/ benzodiazepines, sodium valporate.
  • Treat depression with SSRI (citalopram).
  • Treat aggressive behaviour with antipsychotics like risperidone.
  • Genetic counselling.
216
Q

GUILLAIN-BARRÉ SYNDROME

What is the pathophysiology of Guillain-Barré syndrome?

A
  • Acute inflammatory demyelinating polyneuropathy, Schwann cells targeted.
  • Demyelination + axonal degeneration due to a trigger causing antibodies to attack nerves.
  • Causes ascending + progressive neuropathy.
217
Q

GUILLAIN-BARRÉ SYNDROME

What is the aetiology of Guillain-Barré syndrome?

A

Often post-infection…

  • Campylobacter jejuni.
  • CMV.
  • EBV.
218
Q

GUILLAIN-BARRÉ SYNDROME

What is the clinical presentation of Guillain-Barré syndrome?

A
  • Progressive symmetrical ascending muscle weakness a few weeks post-infection.
  • Pain.
  • Proximal muscles more affected like trunk, respiratory, cranial nerves.
  • Sweating, tachycardia, BP changes.
219
Q

GUILLAIN-BARRÉ SYNDROME

What are the investigations for Guillain-Barré syndrome?

A
  • Nerve conduction studies (slow).
  • Lumbar puncture (raised protein, WCC normal).
  • Monitor FVC for respiratory involvement.
220
Q

GUILLAIN-BARRÉ SYNDROME

What is the treatment for Guillain-Barré syndrome?

A
  • IV immunoglobulin.

- Ventilation if respiratory muscles involved.

221
Q

ANTI-EPILEPTIC DRUGS

Name 2 anti-epileptic drugs + explain their mechanisms.

A
  • Carbamazepine – inhibits pre-synaptic Na+ channels + so prevents axonal firing.
  • Sodium valporate – teratogenic.
222
Q

ANTI-EPILEPTIC DRUGS

What are the side effects of anti-epileptic drugs?

A
  • Cognitive disturbances (blurred vision, diplopia).
  • Drowsiness.
  • Photosensitivity.

Phase 2a (12 decks)

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