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3a > Neurology > Flashcards

Neurology Flashcards

1
Q

Give 3 primary headaches

A

-Migraine
-Cluster
-TensionF

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2
Q

Give 8 typical features of a migraine

A

-Last 4 to 72 hours
-Unilateral
-Pounding/throbbing in nature
-Moderate to severe intensity
-Photophobia
-Phonophobia
-With or without aura
-N&V

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3
Q

Give the 5 stages of a typical migraine

A

-Prodromal stage -> up to 3 days before headache
-Aura -> up to 60mins
-Headache
-Resolution
-Postdromal/recovery phase

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4
Q

Give 8 possible triggers for a migraine

A

-Stress
-Bright lights
-Strong smells
-Certain foods (chocolate, cheese, caffeine)
-Dehydration
-Menstruation
-Abnormal sleep patterns
-Trauma

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5
Q

What is aura ?

A

-Visual changes associated with a migraine
-Can be : sparks in vision, blurring vision, lines across visions and loss of different visual fields

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6
Q

How is a migraine acutely managed ?

A

-Paracetamol, NSAIDs
-Triptans (e.g sumatriptan, 50mg as the migraine starts)
-Antiemetic

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7
Q

What kind of medication is a triptan ?

A

-5HT receptor agonists (serotonin receptor agonists)

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8
Q

What do triptans act on?

A

-Smoot muscle in arteries causing vasoconstriction
-Peripheral pain receptors to inhibit their activation
-Reduce neuronal activity in the CNS

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9
Q

What can be used for migraine prophylaxis ?

A

1st : Propranolol and Topiramate -> teratogenic.
-Amitriptyline
-Acupuncture

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10
Q

What can be used to reduce the frequency and severity of migraines?

A

-Vitamin B2 (Riboflavin)

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11
Q

What can be used for prophylaxis with migraines associated with menstruation ?

A

-NSAIDs (e.g. mefanamic acid)
-Triptans (frovatriptan, zolmitriptan)

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12
Q

What is a cluster headache ?

A

-Severe and unbearable unilateral headache, typically around the eye.
-Lasts 15 mins to 2 hrs

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13
Q

Explain the pattern of occurrence of cluster headaches

A

-Clusters of attacks before disappearing for a while
-E.g 3-4 attacks a day for a week/mnth followed by a pain-free period lasting 1-2 years

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14
Q

What can trigger cluster headaches?

A

-Alcohol
-Strong smells
-Exercise

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15
Q

Give 5 symptoms of a cluster headache

A

-Red, swollen and watering eye
-Pupil constriction (miosis)
-Eyelid dropping (ptosis)
-Nasal discharge
-Facial sweating

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16
Q

How is a cluster headache managed acutely ?

A

-Triptan (e.g. sumatriptan 6mg injected subcut)
-High flow 100% oxygen for 15-20 mins

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17
Q

Give 3 prophylactic options for a cluster headache

A

-Verapamil (CCB)
-Lithium
-Prednisolone (short course for 2-3 wks to break the cycle during clusters)

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18
Q

What is a tension headache ?

A

-Mild headache across the forehead in a band-like pattern around the head
- Lasts mins - days

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19
Q

Give 5 associations of a tension headache

A

-Stress
-Depression
-Alcohol
-Skipping meals
-Dehydration

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20
Q

Give 2 treatment options for a tension headache

A

-Reassurance
-Basic analgesia

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21
Q

Explain sinusitis

A

-Inflammation in the ethmoidal, maxillary, frontal or sphenoidal sinuses can cause a headache
-Usually produces facial pain behind the nose, forehead and eyes (worse on bending forward)
-Often tenderness over affected sinus
- Nasal discharge
- Nasal onstruction

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22
Q

What is an analgesic headache

A

-Headache caused by long term analgesia
-Presents similar to a tension headache

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23
Q

What is cervical spondylosis ?

A

-Common condition caused by degenerative changes in the cervical spine (OA)
-Causes neck pain worse on movement but can also present with a headache

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24
Q

How does trigeminal neuarlgia present ?

A

-Intense facial pain
-Described as electricity-like shooting pain
-90% unilateral

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25
Q

What can trigger trigeminal neuralgia and what is a common association

A

-Triggers : cold weather, spicy food, caffeine and citrus fruit
-5 to 10% of ppl with MS have trigeminal neuralgia

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26
Q

how is trigeminal neuralgia treated ?

A

-1st line -> carbamazapine
-Surgery to decompress or intentionally damage the nerve

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27
Q

Give the 3 branches of the trigeminal nerve

A

-Opthalmic (V1)
-Maxillary (V2)
-Mandibular (V3)

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28
Q

Give 4 causes of an ischaemic stroke

A

-Embolism : embolus from somewhere else in the body
-Thrombosis : blood clot forming locally with in the vessel
-Systemic hypoperfusion (e.g. cardiac arrest)
-Cerebral venous sinus thrombosis : blood clot in veins that drain the brian

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29
Q

Explain the blood supply to the cerebrum

A

-Anteromedial cerebrum : anterior cerebral artery
-Lateral cerebrum : middle cerebral artery
-Posterior cerebrum : posterior cerebral arteries

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30
Q

what classifies as a partial anterior circulation stroke (PACS)?

A

-TWO of the following :

-Unilateral weakness or sensory disturbance
-Homonymous hemianopia
-Higher cerebal dysfunction (dysphagia, visuospatial disorder)

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31
Q

What classifies as a total anterior circulation stroke (TACS)

A

-BOTH the middle and anterior cerebral arteries affected.
-THREE of the following :

-Unilateral weakness or sensory disturbance
-Homonymous hemianopia
-High cerebral dysfunction

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32
Q

Posterior cerebral artery stroke

A
  • Contralateral homonymous hemianopia with macular sparing
  • Visual agnosis
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33
Q

What has to be present for a diagnosis of a lacunar stroke?

A

ONE of the following needs to be present :

  • Pure one-sided sensory loss
  • Unilateral motor disturbance
  • Ataxic hemiparesis
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34
Q

What is the immediate management of an ischaemic stroke ?

A

-Thrombolysis with alteplase if within 4.5 hrs
-300mg of aspirin and continue for 2 wks
-Thrombectomy if thrombolysis is CI

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35
Q

What is the longterm management for an ishcaemic stroke ?

A

-75mg of clopidogrel daily (+PPI)
-80mg atorvostatin but not immediately
-If pt has carotid stenosis -> consider carotid endarterectomy

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36
Q

What are the RF for a stroke (8)

A

-CVD
-Previous stroke or TIA
-AF
-Hypertension
-DM
-Smoking
-Vasculitis
-Combined contraceptive pill

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37
Q

Define MS

A
  • Autoimmune demyelination of the CNS
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38
Q

What cells produce myelin in the CNS and in the PNS ?

A

-CNS : oligodendrocytes
-PNS : schwann

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39
Q

How do the episodes of demyelination present in MS?

A

-Episodes disseminated in time and space

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40
Q

What is optic neuritis ?

A

-Unilateral painful reduced vision developing over hrs to days.

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41
Q

Give 4 key features of optic neuritis

A

-Central scotoma (blind spot)
-Pain on eye movement
-Impaired colour vision
-Relative afferent pupillary defect

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42
Q

Give 7 other causes of optic neuritis other than MS

A

-Sarcoidosis
-SLE
-DM
-Syphilis
-Measles
-Mumps
-Lyme disease

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43
Q

What investigations can support a diagnosis of MS

A
  • MRI -> lesions
  • LP -> oligoclonal bans in CSF
  • McDonald criteria for diagnosing
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44
Q

Give the 4 disease patterns of MS

A

-Clinically isolated syndrome
-Relapsing-Remitting
-Secondary progressive
-Primary progressive

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45
Q

Explain the relapsing-remitting pattern of MS

A

-Episodes of disease followed by recovery. Classified on whether active and/or worsening

-Active : new symptoms developing
-Not active : no new symptoms developing
-Worsening : overall worsening of disability over time
-Not worsening : no worsening of disability over time

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46
Q

Explain secondary progressive pattern of MS

A

-Was relapsing/remitting but now a progressive worsening of symptoms
-Can also be classified as active and/or worsening

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47
Q

Explain primary progressive pattern of MS

A

-Worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions

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48
Q

Give two common characteristics of MS

A

-Lhermitte’s sign : tingling electric shock shooting up the spine when flexing the neck
-Uhthoff’s phenomenon : symptoms are worse when hpt (e.g. in bath, hot weather, exercise).

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49
Q

What can be used to treat relapses in MS?

A

-Methylprednisolone
-500mg orally for 5 days or 1g IV for 3-5 days if treatment fails

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50
Q

What is the pathophysiology behind MND?

A

-Progressive degeneration of both upper and lower motor neurones
-Sensory neurones are spared

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51
Q

What can increase the risk of MND?

A

-Smoking
-Exposure to heavy metals
-Certain persticides

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52
Q

What is a typical presentation of MND

A
  • Late middle aged man
  • Insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech
  • Weakness often first noticed in upper limbs
  • Fatigue when exercising
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53
Q

Give 4 signs of lower MND

A

-Muscle wasting
-Reduced tone
-Fasciculations
-Reduced reflexes

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54
Q

GIve 3 signs of upper MND

A

-Increased tone or spasticity
-Brisk reflexes
-Upgoing plantar responses

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55
Q

What is the most common presentation of MND ?

A

-Amyotrophic lateral sclerosis (ALS)
- Typically LMN signs in the arms and UMN signs in the legs

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56
Q

What can be used to slow the progression of MND ?

A

-Riluzole

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57
Q

What is myasthenia Gravis ?

A

-Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest
- Affects the NMJ

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58
Q

What is strongly associated with myasthenia Gravis?

A

-Thyoma : tumour of the thymus gland

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59
Q

Explain the pathophysiology behind myasthenia gravis

A

-In most cases, acetylcholine receptor antibodies are produced
-These bind to the postsynaptic receptors
-This prevents the stimulation of the receptor and so prevents muscle contraction
-The antibodies also activate the complement system, leading to damage to the cells of the postsynaptic membrane further worsening the symptoms

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60
Q

Why do the symptoms of myasthenia gravis get worse with exercise ?

A

-The receptors are used more during muscle activity and so more of them become blocked up.
-This leads to less effective stimulation of the muscle with increased activity
-There is more muscle weakness the more the muscles are used
-This improves with rest as more receptors are freed up again for use

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61
Q

What are 2 other antibodies involved in myasthenia gravis?

A

-Muscle-specific kinase (MuSK)
-Low density lipoprotein receptor-related protein (LRP4)
-These proteins are imprtant for the creation of acetylcholine receptor
-Destruction of these by the antibodies leads to inadequate acetylcholine receptors

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62
Q

What is a characteristic feature of myasthenia gravis

A

-Weakness that gets worse with muscle use and improves with rest

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63
Q

What muscles are most affected in myasthenia gravis ?

A

-Proximal muscles and small muscles of the head and neck

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64
Q

Give 8 common symptoms of myasthenia gravis

A
  • Diplopia : extraocular muscle weakness
  • Ptosis
  • Weak upwards gaze
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
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65
Q

Give 3 things to assess of examination for myasthenia gravis

A

-Thymectomy scar
-FVC
-Elicit fatiguability of muscles : repeated blinking will exacerbate ptosis ; prolonged upward gaze with exacerbate diplopia ; repeated abduction of one arm 20 times with result in unilateral weaknes when comparing both sides

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66
Q

Give 3 investigations for diagnosing myasthenia gravis

A
  • Test for antibodies
  • CT/MRI of the thymus to check for thymoma
  • Edrophonium test if in doubt (tensilon)
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67
Q

What is the edrophonium test

A

-Used to aid diagnosis of myasthenia gravis

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68
Q

What is the edrophonium test

A

-Used to aid diagnosis of myasthenia gravis
-IV edrophonium chloride is given which will prevent the breakdown of acetylcholine
-Acetycholine levels will rise giving temporary relief from the weakness

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69
Q

Give 3 treatment options for myasthenia gravis

A

-Pyridostigmine -> reversible acetylcholinesterase inhibitors -> increase the amount of acetylcholine at the junction (or rivastigmine)
-Immunosuppression with prednislone or azathioprine : suppress antibody production
-Thymectomy

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70
Q

What 2 monoclonal antibodies can be used in myasthenia gravis ?

A

-Rituximab -> targets b cells reducing antibody production
-Eculizumab -> targets complement protein C5.

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71
Q

What is a myasthenic crisis?

A

-Acute worsening of symptoms often triggered by a viral infection
-Can lead to resp failure due to weakness in the muscle of respiration
- FVC needs monitoring

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72
Q

What is used in the management of a myasthenic crisis?

A
  • IV immunoglobulins
  • Plasmapheresis

If needed :
- BiPAP
- Intubation and ventilation

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73
Q

What is Lambert-Eaton myasthenic syndrome ?

A

autoimmune condition affecting the neuromuscular junction

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74
Q

Who is usually affected by Lambert-Eaton myasthenic syndrome ?

A

-Patients with small cell lung cancer

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75
Q

Explain the pathophysiology behind Lambert-Eaton myasthenic syndrome

A
  • Antibodies against voltage-gated calcium channels in the SCLC are produced.
  • These target and damage the same channels in the presynaptic terminals of the neuromuscular junction
  • This results in less acetylcholine being released into the synapse
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76
Q

How does lambert-eaton syndrome present ?

A

-Proximal muscles most affected -> leg muscle weakness (difficulty climbing stairs)
- Reduced or absent tendon reflexes
-Autonomic dysfunction : dry mouth, blurred vision, impotence and dizziness

-Double vision
-Ptosis
-Dysphagia

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77
Q

What is post-tetanic potentiation ?

A

-In lambert-eaton syndrome, tendon reflexes are normally reduced
-They can become temporarily normal for a short period following a period of strong muscle contraction

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78
Q

How is lambert-eaton syndrome managed?

A

-Treat underlying malignancy if present
-Amifampridine
-Immunosuppressants
-IV immunoglobulins
-Plasmaphersis

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79
Q

How does amifampridine work in the treatment of Lambert-Eaton?

A

-It blocks voltage-gated potassium channels in the presynaptic cells
-This prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action

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80
Q

Define Gullian-Barre syndrome (GBS)

A

-Acute paralytic polyneuropathy affecting the peripheral nervous system

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81
Q

What usually triggers GBS ?

A

-Infection
-Campylobacter jejuni (food poisoning), cytomegalovirus, EBV

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82
Q

How does GBS present ?

A
  • Back/leg pain in initial stages
  • Symmetrical ascending weakness
  • Reduced reflexes
    -+/- peripheral loss of sensation or neuropathic pain
  • May progress to cranial nerves and cause diplopia, bilateral facial nerve palsy and oropharyngeal weakness
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83
Q

What is the clinical course of GBS?

A

-Preceding infection
-Symptoms begin 4 wks later
-Symptoms peak after 2-4 wks
-Recovery period lasting mnths to years

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84
Q

What investigations support the diagnosis of GBS?

A

-Once clinically diagnosed using Brighton criteria :

-Nerve conduction studies showing reduced signal through the nerves
-LP : raised protein with normal cell count and glucose

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85
Q

How is GBS managed ?

A
  • IV immunoglobulins
  • Plasmapheresis can be an alternative to IVIG
  • VTE prophylaxis with LMWH
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86
Q

What are the features of a benign essential tremor ? (6)

A

-Fine tremor
-Symmetrical
- 6-12 Hz
-MORE prominent on VOLUNTARY movement
-Worse when tired, stressed or after caffeine
-Improved by alcohol
-Absent during sleep

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87
Q

Give 6 differentials of a tremor

A

-Parkinson’s
-MS
-Huntington’s chorea
-Hyperthyroidism
-Fever
-Medications (e.g. antipsychotics)

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88
Q

What 2 medications can improve the symptoms of a benign essential tremor ?

A

-Propranolol
-Primidone

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89
Q

What is the cause of parkinson’s ?

A
  • Progressive reduction of dopamine in the basal ganglia
  • Leads to disorders of movement
  • Symptoms are ASYMMETRICAL
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90
Q

What is the classic triad of parkinson’s

A
  • Cogwheel rigidity
  • Pill-rolling resting tremor (4-6Hz)
  • Bradykinesia : smaller handwriting, shuffling gate, difficulty initiating movements, reduced facial expressions (hypomimia)

postural instability is an extra

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91
Q

Where is dopamine produced ?

A

-Substantia nigra of the basal ganglia

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92
Q

Give 5 other features of parkinson’s

A

-Depression
-Sleep disturbance and insomnia
-Anosmia
-Postural instability
-Cognitive impairment and memory problems

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93
Q

Describe a parkinson’s tremor

A

-Asymmetrical
-WORSE at REST
-IMPROVES with INTENTIONAL movement
-No change with alcohol

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94
Q

Give 4 treatment options for parkinson’s

A
  • Co-benyldopa or co-careldopa
  • COMT inhibitors
  • Dopamine agonists
  • Monoamine Oxidase-B Inhibitors
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95
Q

Explain how levodopa works

A

-Synthetic dopamine
-Most effective but becomes less effective over time

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96
Q

What is usually given with levodopa and why?

A

-Peripheral decarboxylase inhibitor
-Stops is being broken down before it reaches the brain
-Examples : carbidopa, benserazide

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97
Q

What is the main side effect of levodopa?

A
  • Too high dopamine = dyskinesias = abnormal movements associated with excessive motor activity.
  • E.g. dystonia, chorea, athetosis
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98
Q

How do COMT inhibitors work?

A

-Example : entacapone
-Inhibits catechol-o-methyltransferase which is responsible for metabolising levodopa
-Extends to duration of levodopa

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99
Q

How do dopamine agonists work ?

A
  • Mimic dopamine in the basal ganglia and stimulate dopamine receptors
  • Less effective than levodopa
  • Examples : bromocryptine, pergolide, cabergoline
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100
Q

What is the most notable side effect of dopamine agonists with prolonged use ?

A
  • Pulmonary fibrosis
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101
Q

How do monoamine Oxidase-B Inhibitors work?

A

-They block Monoamine Oxidase-B enzyme which is responsible for breaking down dopamine
-Examples are selegiline and rasagiline

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102
Q

Name 4 parkinson plug syndromes

A
  • multiple system atrophy
  • Dementia with lewy bodies
  • progressive supranuclear palsy
  • corticobasal degeneration
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103
Q

What is multiple system atrophy

A
  • Neurones of multiple systems in the brain degenerate
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104
Q

What is dementia with lewy bodies

A
  • Dementia w/ features of Parkinsonism
  • Causes progressive cognitive decline
  • Associated symptoms : visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness
  • Anti-parkinson meds may worsen psychosis
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105
Q

Give 6 risk factors for an intracranial bleed

A

-Head injury
-HTN
-Aneurysm
-Brain tumour
-Anticoagulants
-Ishcaemic stroke progressing to haemorrhagic

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106
Q

How does an intracranial bleed present ?

A

-Sudden onset headache
-Seizures
-Weakness
-Vomiting
-Reduced consciousness
-Other sudden onset neurological symptoms

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107
Q

Explain a subdural haemorrhage

A
  • RF : elderly, alcholics, anticoag, recent trauma
  • Rupture of bridging veins between the dura and arachnoid
  • Px : fluctuating conspicuousness, headache, drowsy, can be present for wks
  • Ix : Crescent shaped on CT and do not cross suture lines. Chronic = dark/hypodense. Acute = bright/hyperdense
  • Tx : burr hole craniotomy, stop anticoag and drainage, supportive mannitol
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108
Q

Explain an extradural haemorrhage

A
  • Usual Rupture of middle meningeal artery in the temporal region
  • Px : Traumatic head injury, LOC, lucid period, rapid decline in GCS, headache, N&V
  • Ix : lentiform heterogenous hyper-dense extra-axial collection adjacent to temporal bone (lemon)
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109
Q

Explain an intracerebral haemorrhage

A

-Bleeding into the brain tissue
-Presents similar to an ischaemic stroke

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110
Q

Expain a subarachnoid haemorrhage

A
  • Bleeding into the subarachnoid space between the pia and the arachnoid membrane
  • Usually a result of berry aneurysm (also trauma and atrioventricular malformation)
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111
Q

How does a subarachnoid haemorrhage present ?

A
  • Sudden onset occiptal headache : ‘thunderclap headache’
  • Neck stuffness
  • Photophobia
  • Vision changes
  • Neurological symptoms : speech changes, weakness, seizures and loss of consciousness
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112
Q

What are subarachnoid haemorrhages associated with (5)

A

-Cocaine use
-Sickle cell anaemia
-Connective tissue disorders
-Neurofibromatosis
-Autosomal dominant PKD

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113
Q

What is seen on a CT in a subarachnoid haemorrhage

A

-Hyperattenuation in the subarachnoid space (star shape)

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114
Q

What is seen on an LP in a subarachnoid haemorrhage

A

-Raised red cell count
-Xanthochromia (yellow colour of CSF caused by bilirubin after 12 hrs)

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115
Q

How can a subarchnoid haemorrhage be managed ?

A

-Coiling or clipping of the aneurysm
- Nimodipine (CCB) to prevent vasospasm
- LP or shunt insertion if hydropcephalus occurs
- Antiepileptics for seizures

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116
Q

Give 3 complications of a subarachnoid haemorrhage

A

-Vasospasm
-Hydrocephalus
-Seizures

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117
Q

What is Charcot-Marie-Tooth disease and what is the usual inheritance pattern?

A
  • Hereditary motor and sensory neuropathy
  • Autosomal dominant
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118
Q

Give 7 features of Charcot-Marie-Tooth ?

A

-High foot arches (pes cavus)
-Distal muscle wasting causing ‘inverted champagne bottle legs’
-Weakness in lower legs, particularly loss of ankle dorsifelxion (with high stepping gait due to foot drop)
-Weakness in the hands
-Reduced muscle tone
-Reduced tendon reflexes
-Peripheral sensory loss

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119
Q

Give 5 causes of peripheral neuropathy

A

-A : alcohol
-B : B12 deficiency
-C : cancer and chronic kidney disease
-D : diabetes and drugs (e.g isoniazid, amiodarone & cisplatin)
-E : every vasculitis

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120
Q

What is tuberous sclerosis ?

A
  • Autosomal dominant condition affecting multiple systems, resulting in the development of hamartomas
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121
Q

What are hamartomas and where do they usually occur in tuberous sclerosis

A

-Benign neoplastic growths of the tissue
-Skin, brain, lungs, heart, kidneys and eyes

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122
Q

What causes tuberous sclerosis ?

A

-> Mutations in one of two genes
-> TSC1 on chromosome 9 -> hamartin
-> TSC2 on chromosome 16 -> tuberin
-> Hamartin and tuberin interact with each other to control the size and growth of the cells
-Abnormalities in these lead to abnormal cell size and growth

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123
Q

Give 2 neurological features of tuberous sclerosis

A

-Epilepsy
-Learning disability and developmental delay

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124
Q

Give 3 skin signs of tuberous sclerosis

A

-Ash leaf spots : depigemented areas of skin shaped like ash leaf
-Angiofibromas : papules on nose and cheeks
-Poliosis : white patch of hair on head, eyebrows, eyelashes or beard

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125
Q

What is the preffered way to support nutrition in patients with MND?

A

-Percutaneous gastrostomy tube

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126
Q

What is a pontine haemorrhage ?

A

-Life threatening condition occurring secondary to chronic hypertension
-Patients present with reduced GCS, quadriplegia, miosis and absent horizontal eye movements

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127
Q

What classes as a lacunar infarct?

A

-ONE of the following :

-Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three
-Pure sensory stroke
-Ataxic hemiparesis : weakness and impaired co-ordination on one side

-Involves perforating arteries around the internal capsule, thalamus and basal ganglia

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128
Q

What is Bell’s palsy ?

A
  • Acute, unilateral, idiopathic, lower motor neuron facial nerve palsy -> FOREHEAD AFFECTED
  • Lower motor neuron facial nerve palsy affecting the forehead
  • Possible pain, altered taste, dry eyes and hyperacusis (everyday sounds seem much louder)
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129
Q

How is Bell’s palsy managed ?

A
  • Oral prenisolone within 72 hrs of onset (50mg for 10 days, 60mg for 5 days, followed by 5-day reducing regime of 10mg)
  • Eye care -> eye lubricants, tape closed at night with microporous tape
  • Return to ENT if no improvement within 3 weeks
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130
Q

What is a complication of Bell’s palsy ?

A

-Exposure keratopathy : dry and damaged eye

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131
Q

What is neurofibromatosis ?

A

-Genetic condition causing nerve tumours (neuromas)
-Neurofibromatosis type 1 is more common than type 2
-Usually autosomal dominant inheritance

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132
Q

What is the the role of the neurofibromatosis type 1 gene ?

A

-Codes for neurofibromin -> a tumour suppressor protein
-Found on chromosome 17

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133
Q

What are the diagnostic features for neurofibromatosis type 1 ?

A

-2 of the following :
-CRABBING

-C : Cafe-au-lait spots (>6)
-R : Relative with NF1
-A : Axillary or inguinal freckles
-BB : Bony displasia such as Bowing of a long bone or sphenoid wing displasia
-Iris hamartomas (Lisch nodules)
-Neurofibromas (>2) or 1 plexiform neurofibroma
-G : Glioma of the optic nerve

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134
Q

What is the role of the neurofibromatosis type 2 gene ?

A

-Codes for merlin -> a tumour suppressor gene important in Schwann cells
-Chromosome 22
-Mutations lead to schwannomas

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135
Q

What is a generalised tonic-clonic seizure?

A
  • Loss of consciousness with muscle tensing
  • Followed by clonic phase of muscle jerking
  • Associated tongue biting, incontinence, groaning and irregular breathing
  • Post-ictal period : confusion, drowsy, irritable and depressed
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136
Q

How are tonic-clonic seizures managed ?

A
  • 1st line : sodium valporate
  • 1st line in females = levetiracetam
137
Q

What are focal seizures

A
  • Begin in a certain part of the brain (e.g. temporal lobes)
    -If in temporal lobe can affect hearing, speech, memories and emotions
  • May present with hallucinations, memory flashbacks, deja vu
  • 1st line : carbamazapine or lamotrigine
  • 2nd line : sodium valporate
138
Q

What are absence seizures

A
  • Usually occurs in children (3-10, F>M)
  • Pt becomes blank and stares into space before abruptly returning to normal
  • Unaware of surroundings and won’t respond
  • Can be provoked by hyperventulation or stress
  • 1st line = sodium valporate or ethosuximide
139
Q

What are atonic seizures?

A
  • ‘Drop attacks’ : brief lapses in muscle tone
  • 1st : sodium valporate
  • 2nd : lamotrigine
140
Q

What are myoclonic seizures?

A
  • Sudden brief muscle contractions usually when tired
  • 1st : sodium valporate or in females = levetiracetam
141
Q

What are infantile spasms ?

A

-Known as ‘west syndrome’
-Starts around 6mnths of age
-Characterised by clusters of full body spasms
-Tx : prednislone, vigabatrin

142
Q

What is status epilepticus

A

-Seizure lasting >5 mins or >3 seizures in an hour

143
Q

How is status epilepticus treated in hospital ?

A

-Secure airway
-High-conc oxygen
-Assess cardiac and resp function
-Check glucose levels
-Insert cannula
-IV lorazepam 4mg, repeat after 10 mins if seizures continues
-If seizure persists : IV phenobarbital or phenytoin

144
Q

Give two medical options in community for status epilepticus

A

-Buccal midazolam
-Rectal diazepam

145
Q

What parkinson medication is associated with pulmonary fibrosis ?

A

-Cabergoline

146
Q

What is used in the management of drug-induced parkinsonism

A

-Procyclidine

147
Q

What artery is affected in amaurosis fugax?

A

-Central retinal/opthalmic artery
-Will be caused by atherosclerosis of the internal carotid on the SAME side as the amourosis

148
Q

What antiparkinsonian medications are associated with disinhibition disorders ?

A

-Dopamine receptor agonists (e.g. bromocriptine/rotigotine/cabergoline))

149
Q

What is Bell’s palsy

A

-Unilateral lower motor neurone facial nerve palsy
-Nerve is affected on the same side as the symptoms (e.g. dropping smile to the left, cannot close left eye or wrinke left side of forehead) = left cranial nerve VII LMN lesion

150
Q

How is Bell’s palsy managed ?

A

-If pt presents within 72 hrs of sx onset = prednislone
-50mg for 10 days, then 60mg for 5 days, followed by reducing regime of 10mg a day
-Eye treatment : lubricating eye drops to prevent exposure keratopathy

151
Q

You are examining a patient who complains of double vision. Whilst looking forward the patient’s left eye turns towards the nose. On looking to the patient’s right there is no obvious squint. However, on looking to the left the patient is unable to abduct the left eye and double vision worsens. What is the most likely underlying problem?

A

Left 6th nerve palsy

152
Q

Define wernicke’s dysphasia

A

-Speech fluent, comprehension abnormal, repetition impaired
-It is from damage to the wenicke’s area in the temporal lobe

153
Q

What tumours most commonly spread to the brain (5)

A

-Lung (most common)
-Breast
-Kidney
-Melanoma
-Colorectal cancer

154
Q

What are the RF for idiopathic intracranial hypertension ?

A

-Obesity
-Female sex
-Pregnancy
-Drugs : COCP, steroids, tetracyclines, lithium, vit A
-Exam : young, overweight female

155
Q

How does idiopathic intracranial hypertension present ? (5)

A

-Headache
-Blurred vision (reduced visual acuity)
-Papilloedema
-Enlarged blind spot
-VI nerve palsy may be present - LR6 - unable to abduct eye

156
Q

How is idiopathic intracranial hypertension managed ?

A

-Weight loss
-Diuretics (e.g. acetazolamide)

157
Q

What is the classic history in an acoustic neuroma (vestibular schwannoma)

A

-Vertigo, hearing loss, tinnitus and absent corneal reflex
-Corneal reflex : involuntary blinking caused by stimulation of cornea
-Account for 90% of cerebellopontine angle tumours (MRI is Ix of choice)

158
Q

What is the most likely visual impairment seen in a pt with acromegaly ?

A

-Bi temporal hemianopia
-Pituitary lesion is often the cause = compression of optic chiasm

159
Q

What questionnaire is used to diagnose neuropathic pain ?

A

-DN4
>4 = neuropathic pain

160
Q

What 4 medications are used 1st line in neuropathic pain

A

-Amitriptyline
-Duloxetine
-Gabapentin
-Pregbalin

161
Q

Give 7 features of complex regional pain syndrome

A

Neuropathic pain
Skin flushing
Swelling
Abnormal hair growth
Colour change
Temp change

162
Q

Explain the pathway of the facial nerve

A

-Brainstem -> cerebellopontine angle - temporal bone and parotid gland

163
Q

What are the 5 branches of the facial nerve

A

-Temporal
-Zygomatic
-Buccal
-Marginal mandibular
-Cervical

164
Q

What is the motor function of the facial nerve

A

-Muscle of facial expression, the strapedius, posterior digastric, styohyoid and platysma muscle

165
Q

What is the sensory function of the facial nerve

A

taste from anterior 2/3 of the tongue

166
Q

What is the parasympathetic function of the facial nerve

A

-Supply to submandibular and sublingual salivary glands
-Lacrimal gland

167
Q

What causes a unilateral upper motor facial nerve lesion

A

-STROKE
-tumour

168
Q

How would an upper motor neurone facial lesion present and why

A

-Forehead sparing -> each side of the forehead receives upper motor innervation from both sides of the brain

169
Q

What can cause lower motor neuron facial lesions

A

-Bell’s palsy
-Ramsay-hunt syndrome

170
Q

What causes Ramsay-Hunt syndrome

A

Varicella Zoster Virus - causes inflammation and irritation of facial nerve

171
Q

How does Ramsay-Hunt present

A

-unilateral lower motor neuron facial nerve palsy
-Painful, tender vesicular rash in the ear canal, pinna and around ear on affected side
-Rash to anterior 3/3rd of tongue and hard palate
- sensorineural deafness
- vertigo

172
Q

How is ramsay-hunt treated

A

-Prednisolone
-Aciclovir
-Within 72 hrs

173
Q

What is the inheritance pattern of Huntington’s

A

-Autosomal dominant

174
Q

What causes Huntington’s

A

-Trinucleotide repeat disorder -> genetic mutation in the HTT gene on chromosome 4 (CAG)

175
Q

what is anticipation

A

Successive generations have more repeats in the gene resulting in earlier age of onset and increased severity of disease

176
Q
  • Cognitive, psychotic or mood problems
  • Chorea
  • Eye movement disorders
  • Speech difficulties (dysarthria)
  • Swallowing difficulties (dysphagia)
A

=Huntington’s

177
Q

EEG in absence seizures
Treatment

A

-> Bilateral, symetrical 3Hz spike and wave pattern
-> Sodium valporate and ethosuximide

178
Q

What kind of aphasia is wernicke’s aphasia

A

receptive

179
Q

Sentences that make no sense, word substitutions and neologisms but speech is fluent
Comprehension is impaired

A

Wernicke’s aphasia

180
Q

What causes wernicke’s aphasia

A

-Lesion of superior temporal gyrus
-Supplied by inferior division of left MCA

181
Q

What kind of aphasia is broca’s aphasia

A

Expressive

182
Q

speech is non fluent, laboured and halting
Repetition is impaired
Comprehension is normal

A

Broca’s aphasia

183
Q

What causes broca’s aphasia

A

-Lesion in inferior frontal gyrus
-Supplied by superior division of MCA

184
Q

Conduction aphasia

A

-> Speech is fluent but repetition is poor. Comprehension is normal
-> Cause by stroke affecting arcuate fasiculus

185
Q

What is global aphasia

A

-Large lesion affecting broca’s, wernicke’s and arcuate fasiculus

186
Q

-> Faecal impaction, bladder distention leading to extreme HTN, flushing, sweating, agitation.

A

-Autonomic dysregulation due to spinal cord lesion at, or above T6.
- It is an uninhibited sympathetic nervous system response to a variety of noxious stimuli

187
Q

What are the nerve roots of the brachial plexus and what are it’s sections

A

-C5 to T1
-Roots, trunks, divisions, cords, branches

REAL TEENAGERS DRINKS COLD BEERS

188
Q

Damage to C5,6 roots
Winged scapula
Breech presentation possible cause

A

Erb-Duchenne paralysis

189
Q

Damage to T1
Loss of intrinsic hand muscles
Due to traction

A

Klumpke’s paralysis

190
Q

Sensory inattention
Apraxias
Astereognosis : inability to recgonise objects by touch
Inferior homonymous quadrantanopia

A

Parietal lobe lesion

191
Q

Homonymous hemianopia (with macula sparing)
Cortical blindness
Visual agnosia

A

Occipital lobe lesions

192
Q

Wernicke’s aphasia
Superior homonymous quadrantopia
Auditory agnosia
Prosopagnosia

A

Temporal lobe lesion

193
Q

Broca’s aphasia
Disinhibition
Perseveration
Anosmia
Inability to generate list

A

Frontal lobe lesion

194
Q

What tumour is associated with neurofibromatosis type 2

A

Bilateral vestibular schwannomas

195
Q

What is the most common primary brain tumour

A

Glioblastoma
Solid tumours with central necrosis

196
Q

What kind of brain tumour will cause symptoms of compresion rather than invasion

A

-Meningioma

197
Q

What does brown-sequard syndrome cause

A

-Ipsilateral UMN weakness below lesion (corticospinal)
-Ipsilateral loss of proprioception and vibration sensation (dorsal)
-Contralateral loss of pain and temp sensation (spinothalamic)

=Lateral hemisection of the spinal cord

198
Q

Define cataplexy

A

Sudden and transient loss of muscular tone caused by strong emotion
Ranges from buckling knees to collapse

199
Q

What 3 things travel through the cavernous sinus

A

-Abducens nerve
-carotid plexus
-Internal carotid artery

200
Q

What 3 things travel through the lateral wall of the cavernous sinus

A

Oculomotor nerve
Trochlear nerve
Opthalmic and maxillary branch of trigeminal nerve

201
Q

do cerebellar lesions cause ipsilateral or contralateral signs

A

Ipsilateral

202
Q

Give 6 signs of cerebella syndrome

A

D : dysdiadochokinesia
A : ataxia
N : nystagmus
I : intention tremor
S : slurred speech, scanning dysarthria
H : hypotonia

203
Q

Where is CSF produced

A

Ependymal cells in choroid plexus

204
Q

explain the circulation of the CSF

A
  1. Lateral ventricles (via foramen of munro)
  2. 3rd ventricle
  3. Cerebral aqueduct
  4. 4th ventricle (via foramina of magendie and luschka)
  5. Subarachnoid space
  6. Reabsorbed into venous system via arachnoid granulations into superior sagittal sinus
205
Q

What nerve causes foot drop

A

-> Common peroneal nerve lesion (branch of sciatic nerve)
-> Injury often occurs at neck of fibula
-> Inability to dorsifelx foot
-> Sensory loss over the dorsum of the foot

206
Q

Rapid onset dementia
Myoclonus - quick, involuntary muscle jerks
65yrs old

A
  • Creutzfeldt-Jakob disease
  • Caused by prion proteins that induce formation of amyloid folds resulting in tightly packed beta-pleated sheets
207
Q

pain in the neck, upper or lower limbs
Loss of digital dexterity
Numbness
Urinary or faecal incontinence

A

Degenerative cervical myelopathy -> osteoarthritic changes causing narrowing of the cervical spine = compression

208
Q

What is a test for degenerative cervical myelopathy and what is the gold standard investigation

A

-Hoffman’s sign : flicking one finger results in reflex twitching of other fingers on same hand
-Cervical spine MRI : disc degeneration and ligament hypertrophy

209
Q

How is degenerative cervical myelopathy treated

A

Decompressive surgery

210
Q

What is the nerve roots of the nipple? (dermatome)

A

T4 at the Teat Pore

211
Q

What is the nerve root of the umbilicus

A

T10
BellybuT-TEN

212
Q

What is the nerve root of the knee caps

A

L4
Down on aLL fours

213
Q

What is the nerve root of the big toe and dorsum of foot

A

L5
Largest of the 5 toes

214
Q

What is the nerve root of the little toe and lateal foot

A

S1
Smallest toe

215
Q

Nerve root of thumb and index ringer

A

C6
Make a 6 with left hand by touching thumb to index finger

216
Q

Nerve root of middle finger and palm

A

C7

217
Q

Nerve root of ring and little finger

A

C8

218
Q

Nerve root of inguinal ligament

A

L1
L for Ligament
1 for 1nguinal

219
Q

Name 5 drugs that cause peripheral neuropathy

A

AMY : amiodarone
MET : metronidazole
NATHAN : nitrofurantoin
VIA : Vincristine
INSTAGRAM : Isonizid

220
Q

Epilepsy and DVLA

A
  • Inform DVLA
  • First seizure : 6 mnths off
  • Established epilepsy : apply for licence if 12 mnth seizure free
221
Q

Stroke and DVLA

A

-1 mnth off driving
-No need to inform DVLA

222
Q

Progressive muscular weakness from 5 yrs
Calf pseudohypertrophy
Gower’s sign : child uses arms to stand from squatted position
Intellecutal impairment
X linked recessive

A

Duchenne msucular dystrophy

223
Q

-Fever, headache, psychiatric symptoms, iritability
-seizures, vomiting
Focal features (e.g. aphasia)

A

Encephalitis - if EBV : aciclovir

224
Q

words enter in your ear and goes to wernickes in the temporal lobe to comprehend what was said, before travelling to broca’s area in the frontal lobe to generate speech

A

good way to remember

225
Q

Most common cause of encephalitis in adults

A

-HSV-1 : typically affects temporal lobes

226
Q

What is seen on CSF in encephalitis

A

Lymphocytosis
Elevated protein

227
Q

How is encephalitis treated

A

IV aciclovir

228
Q

Affected eye deviates up and out
Vertical diplopia (reading a book/going upstairs)
Head tilt

A

Fourth nerve palsy
SO4 -> superior oblique (superior oblique usually depresses eye and moves in)

229
Q

10-15 yrs old
Gait ataxia
Kyphoscoliosis

A

Friedreich’s ataxia

230
Q

What are the 3 modalities of the GCS

A

Motor response
Verbal response
Eye opening

231
Q

Explain the possible motor response for the GCS

A
  1. Obeys commands
  2. Localises to pain
  3. Withdraws from pain
  4. Abnormal flexion to pain
  5. Extending to pain
  6. None
232
Q

Explain the verbal response in the GCS

A
  1. Orientated
  2. Confused
  3. Words
  4. Sounds
  5. None
233
Q

Explain the eye opening options in the GCS

A
  1. Spontaneous
  2. To speech
  3. To pain
  4. None
234
Q

What causes lateral medullary syndrome (wallenberg’s)

A

-Occlusion of the posterior inferior cerebellar artery

235
Q

What cause neuroleptic malignant syndrome

A

-Occurs in patients taking antipsychotic medications

236
Q

How does neuroleptic malignant syndrome present `

A

Within hrs/days of starting an antipsychotic
Pyrexia/hyperthermia
Muscle rigidity
Autonomic instability : hypotension & tachycardia
Agitate delirium with confusion

237
Q

What might be seen on the bloods in neuroleptic malignant syndrome

A

-Raised creatinine kinase + raised urea = AKI
-Leukocytosis
-AKI secondary due to rhabdomyolysis

238
Q

Urinary incontinence
Dementia and bradyphrenia
Gait abnormality similar to parkinson’s (e.g. shuffling or broad-based)

A

Normal pressure hydrocephalus
Treated with a shunt or acetazolamide (carbonic anhydrase inhibitor)

239
Q

Give 4 metabolic abnormalities that occur in refeeding syndrome

A

Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance

240
Q

Give 3 causes of a peripheral neuropathy causing predominantly motor loss

A

-GBS
-Lead poisoning
-Charcot marie tooth

241
Q

Give 4 causes of a peripheral neuropathy causing predominantly sensory loss

A

A : alcohol
B : B12 deficiency
C : cancer and CKD
D : DM and drugs *
E : every vasculitis

242
Q

Give 4 features that favour pseudoseizures over true seizures

A

Pelvic thrusting
Crying after seizures
Don’t occur when alone
gradual onset

243
Q

Give 2 features that factors true seizures

A

Tongue biting
Raised serum prolactin

244
Q

Give 5 causes of raised ICP

A

Idiopathic
Traumatic
Infection - meningitis
Tumour
Hydrocephalus

245
Q

How is raised ICP managed

A

-Simple management : elevate head of bed to 30 degrees
-IV mannitol : osmotic diuretic
Controlled hyperventilation
Removal of CSF

246
Q

Give the reflexes and the nerve root

A

Ankle : S1-S2
Knee : L3-L4
Biceps : C5-C6
Triceps : C7-C8

247
Q

2 year old
Preceding viral illness
Encephalopathy : confusion, seizures, oedema, coma
Fatty infiltration of the liver, kidneys and pancreas
Hypoglycaemia

A

Reye’s syndrome

248
Q

Eye deviated down and out
Ptosis

A

Third nerve palsy

249
Q

Explain the homonymous quadrantanopias

A

PITS
-> Parietal lobe - inferior
-> Temporal lobe - superior

250
Q

Cause of bitemporal hemianopia

A

-Lesion of optic chiasm, often pituitary tumour

251
Q

Cause of homonymous hemianopia causing incongruous defects

A

Lesion of optic tract
Left homonymous hemianopia = lesion of right optic tract

252
Q

Cause of homonymous hemianopia with incongruous defects

A

-Lesion of optic radiation or occipital cortex
-Macula sparing : occipital cortex

253
Q
  • Left sided CN III palsy - ptosis and fixed dilation pupil pointing down and out
  • Right sided arm, hip and knee weakness
  • Right sided hyperreflexia
A

-Weber’s syndrome - midbrain stroke - ipsilateral CN III palsy and contralateral hemiparesis
-Left posterior cerebral artery

254
Q

Contralateral homonymous hemianopia
Macular sparing
Visual agnosia

A

Posterior cerebral artery

255
Q

Teenager
Hypersomnolence
Sleep paralysis
Vivid hallucinations on going to sleep or waking up

A

Narcolepsy
Ix : multiple sleep latency EEG
Tx : daytime stimulant (e.g. modafinil) and nighttime sodium oxybate

256
Q

Bell’s palsy hasn’t resolved in 3 mnths, what should be done?

A

Refer urgently to ENT or a neurologist

257
Q

sensation loss : fine touch, proprioception, vibration

A

Dorsal column

258
Q

What is used to measure disability or dependence in activities of daily living in stroke patients

A

Barthel index

259
Q

Which of the following features is typically spared in this condition :

Breathing difficulties
Emotional lability
Opthalmoplegia
Slurred speech
Swallowing difficulty

A

Opthalmoplegia

260
Q

Peropheral ‘finger-nose ataxia’

A

Cerebellar hemisphere lesion

261
Q

Gait ataxia

A

Cerebellar vermis lesion

262
Q

Lamotrigine : mechanism of action, adverse effects

A

sodium channel blocker
stevens-johnsons syndrome

263
Q
  • onset ~ 65
  • Postural inastability and falls
  • atypical parkinson syndrome : tau
  • Cognitive impairment
  • Impairment of vertical gaze
A

progressive supranuclear palsy

264
Q

Give 3 ascending tracts of the CNS

A

DCML
Spinothalamic
Spinocerebllar

265
Q

What in formation does the DCML transport

A

vibration, proprioception and fine touch from from the body to the brain

266
Q

what information does the anterior spinothalamic tract carry

A

crude touch and pressure

267
Q

what information does the lateral spinothalamic tract carry

A

pain and temperature

268
Q

what information does the spinocerebellar tract carry

A

proprioceptive signals : info about muscle stretch and the rate of muscle stretch

269
Q

what information do descending tracts carry in the CNS

A

Motor info

270
Q

what are upper motor neurones

A

Carry motor info from the brain and brainstem to the ventral horn of the spinal cord

271
Q

what are lower motor neurones

A

They carry motor info from the spinal cord to peripheral muscles

272
Q

what are pyramidal tracts

A

Descending tracts
They pass through the pyramids of the medulla oblongata
Voluntary, conscious control of body and face muscles
Corticospinal : cortex to body
Corticobulbar : cortex to bulb

273
Q

Explain the pathway of the corticospinal tract

A

-Info from pimary motor cortex, premotor cortex coverage to for internal capsule
-The CST then passess through the pons and caudal medulla where it divides
-Lateral CST : decussates in pyramid of medulla
-Anterior CST : stays ipsilateral
-Tracts descend into the spinal cord, terminating at ventral horn where they synapse with LMN to peripheral muscle

274
Q

what are extrapyramidal tracts

A

Originate in brainstem, don’t pass through pyramids
Unconscious, reflexive movement of muscle to control balance, locomotion, posture and tone
4 types : reticulospinal, vestibulospinal, rubrospinal and tectospinal

275
Q

impaired adduction of the eye on the side of the lesion
horizontal nystagmus of abducting eye on contralateral side

A

internuclear opthalmoplegia : caused by MS or vascular disease
and is due to lesion in medial longitudinal fasciculus (MLF)

276
Q

give a common presentation of tuberous sclerosis

A

child presenting with epilepsy found to have skin features of tuberous sclerosis

277
Q

which limbs are more affected in an anterior cerebral artery stroke

A

Lower limbs

278
Q

Which limbs are more affected in a middle cerebral artery stroke

A

Upper + associated aphasia

279
Q

what is the best imaging for a TIA

A

Diffusion-weighted MRI

280
Q

Wrist drop is associated with damage to what nerve and what kind of injury

A
  • Radial nerve
  • Fracture of the shaft of the humerus
  • Or compression of nerve against humerus after sleeping on arm.
281
Q

Damage to what cranial nerve will cause an absent of corneal reflex : no blinking or tearing on application of cotton wool

A

CNI

282
Q

-Headache worse when upright, better on lying down
-PMH : marfan’s

A

-Spontaneous intracranial hypotension
-Headahce cause by CSF leak -> MRI with gadolinium shows pachymeningeal enhancement

283
Q

what GCS would suggest need for intubation

A

<8

284
Q

what is given 1st line for spasticity in MS

A

Baclofen and gabapentin

285
Q

what is a common cause of bilateral foot drop

A

-Peripheral neuropathy
-Presents with ‘high-stepping’ gait

286
Q

During trauma, fluid draining from the nose or ear is tested for what to determine if it is CSF

A

Glucose
Beta-2-transferrin is gold standard

287
Q

what type of medications are levodopa and other antiparkinsons medications ?

A

‘critical’ medications
They must always be given on time and not stopped on acute admission

288
Q

give 3 drugs that ca cause SJS

A

CARBAMAZEPINE
Lamotrigine
Allopurinol

289
Q

-Painful third nerve palsy -> down and out eye with painful eye movement
-Headache and blurred vision
-Dilated pupil unresponsive to light

A

Posterior communicating artery aneurysm

290
Q

what is becker muscular dystrophy

A

Less severe form of muscular dystrophy
develops after the age of 10
pseudohypertrophy and + GOWER’S SIGN

291
Q

give 6 drugs that can cause idiopathic intracranial hypertensions

A

COMAAR

C : ciclosporin
O : oral contraceptives
M : mineralocorticoids
A : amiodarone
A : antibiotics
R : retinoic acid

292
Q

what is seen on neuroimaging in normal pressure hydrocephalus

A

Ventriculomegaly with relative preservation of cortical sulci

293
Q

Initial signs of degenerative cervical myelopathy

A

Neck pain
Stiffness
Reduced range of motion

294
Q

Progressive signs of degnerative cervical myelopathy

A

-Shooting pains from neck, down the spine
-Weakness in arms and hands
-Numbness and tingling in arms and hands
-Clumsiness and poor coordination
-Difficulty handling small objects (pens, coins, phone)
-Balance issues

295
Q

common exam question for degnerative cervical myelopathy

A

lower limb stiffness and imbalance
previous misdiagnosis of carpal tunnel (unresponsive to treatment)

296
Q

define myelopathy

A

-Injury to the spinal cord due to severe compression
-Can be due to trauma, congenital stenosis, degenerative disease or disc herniation.

297
Q

How would a posterior inferior cerebellar artery stroke (wallenberg/lateralk medullary syndrome) present

A

-Ipsilateral : facial pain and temp loss
-Contralateral : limb/torso pain and temp loss
-ATAXIA, NYSTAGMUS

298
Q

How would an anterior inferior cerebella artery stroke present (lateral pontine syndrome)

A

Ipsilateral facial paralysis and deafness
Other symptoms similar to wallenbergs

299
Q

how does HSE present and what is seen on CT

A

-Prodrome : fever, headahce and malaise
-Acute encephalopathy : focal neurological deficits, seizures, confusion and behavioural changes
-Bilateral temporal lobe changes

300
Q

Subacute

A

Bilateral
Fine touch
vibration

301
Q

Syirngomyelia

A

motor
loss of pain and temp

302
Q
  • Severe unilateral headache
  • Scalp tenderness
  • Jaw claudication
  • Amaurosis fugax
A

Temporal / giant cell arteritis

303
Q

what is strongly associated with GCA

A
  • Polymyalgia rheumatica
304
Q

how is GCA diagnosed

A
  • Raised ESR
  • Multinucleated giant cells on temporal artery biopsy
305
Q

How is GCA managed

A
  • 60mg pred is visual / jaw sx
  • 40mg pred if not
306
Q

TIA : most common cause, imaging, management

A
  • AF
  • Diffusion-weight MRI
  • 300mg aspirin
  • Can’t drive for 4 weeks
307
Q

what secondary prevention is used in a TIA

A
  • 75mg clopidogrel
  • 80mg statin
  • Carotid endarecetomy if >70% stenosis
308
Q

First line tx for alzheimer’s

A
  • Donepezil (AChE inhibitor)
  • Memantine if severe (NMDA antagonists)
309
Q

what antidepressants can worsen cognition in alzheimer’s

A

TCA’s

310
Q

Cauda Equina : cause

A
  • Causes : trauma, infection, herniation of lumbar disc
311
Q

Cauda Equina : presentation (5)

A
  • Bilateral sciatica
  • Bowel/bladder dysfunction
  • Saddle parastesia
  • Lower limb weakness/sensory deficit
  • Sexual dysfunction
312
Q

What is thoracic outlet syndrome and how might it present

A
  • Compression of brachial plexus, subclavian artery or subclavian vein at site of thoracic outlet
  • Young woman with dropping shoulders and long neck
313
Q

3 possible presentations and thoracic outlet syndrome

A
  1. Brachial plexus : pain;ess muscle wasting of the hand, numbness and tingling
  2. Subclavian artery : painful claudication of arm leading to ulceration and gangrene
  3. Subclavian vein : painful diffuse arm swelling and distended veins
314
Q

Injury following fall onto outstretch wrist

A
  • Median nerve injury : inability to extend wrist or abduct thumb
315
Q
  • Ex : female, hx of MH disorder
  • Px : pelvic thrusting, gradual onset, emotional and upset after seizure
  • Ix : no abnormal EEG activity
A

functional seizure / NEAD

316
Q

Unilateral vision loss, pain, red eye, N&V

A

Glaucoma

317
Q

constantly adducted eye

A

CN VI palsy

318
Q

Ptosis, Miosis, Anhidrosis

A

Horner’s syndrome : damage to sympathetic nervous system

319
Q

give 4 central lesion causes of horner’s

A

4 S’s : anhidrosis of arm, trunk and face
- Stroke
- MS
- Swelling (tumours)
- Syringomyelia

320
Q

give 4 pre-ganglionic causes of horner’s

A

4 T - arise from spinal cord in chest, causes anhidrosis of face

  • T : Tumour (Pancoast)
  • T : Trauma
  • T : Thyroidectomy
  • T : Top rib
321
Q

Give 4 post ganglionic causes of horner’s

A

4 C’s : travel to the head alongside internal carotid, do not cause anhidrosis

  • C : Carotid aneurysm
  • C : Carotid artery dissection
  • C : cavernous sinus thrombosis
  • C : cluster headache
322
Q

test for horners

A
  • Cocaine eye drop : no change in pupil
323
Q
  • Px : ‘please look to the left’ : one eye completely fails to adduct, the other shows nystagmus while abducting
A

Internuclear opthalmoplegia

324
Q

what causes internuclear opthalmoplegia and what can it be a common sign of

A
  • Lesion of medial longitudinal fasciculus
  • MS
325
Q

give 6 RF for retinal detachment

A
  • Male
  • > 40
  • Prev ocular surgery
  • Fx
  • Retinal detachment in other eye
326
Q

How does retinal detachment present

A
  • Painless vision loss
  • Flashing lights
  • Floaters
  • ‘Cobwebs in periphery’
  • Curtain over part of eye
327
Q

how is retinal detachment Ix and Tx

A
  • Ix : RAPD, altered red reflex, reduced acuity, visual field defects
  • Tx : surgical repair
328
Q

how does a central retinal artery occlusion present

A
  • sudden painless loss of vision (seconds), cherry red spot in macula, pale optic disc, RAPD
329
Q

what causes a retinal artery occlusion. amndhow is it treated

A
  • clot from internal carotid into opthalmic artery
  • Tx : ocular massage, IV mannitol, urokinase injection
330
Q

what is cushing’s triad

A
  • widening pulse pressure, braducardia, irregular breathing
  • sign of raised ICP
331
Q

If large enough what will pituitary tumours cause

A

bilateral hemianopia by pressing on optic chiasm

332
Q

what tumours commonly metastasise to the brain

A
  • lung
  • breast
  • renal cell carcinoma
  • melanoma
333
Q

charcots neurological triad

A

Triad of sx associated with MS

  1. Dysarthria
  2. Nystagmus
  3. Intention tremor
334
Q

what regular medications are used in MS

A
  1. Dimethyl fumarate (mild)
  2. Alemtuzumab + natalizumab
  3. Immunosupression (betaferon)
335
Q

how does sodium valporate work, 3 key SE

A
  • Increases GABA activity
  1. Weight gain
  2. P450 enzyme inhibitor
  3. Teratogenic
336
Q

how does carbamazepine work, 3 key SE

A
  • Binds to sodium channels, increase refractory period
  1. P450 enzyme inhibitor
  2. Inappropriate ADH secretion
  3. Visual disturbance (diplopia)
337
Q

How does lamotrigine work, key SE

A
  • sodium channel blocker
  1. SJS
338
Q

How can you elicit the myasthenic snarl

A

Count to 50 , then smile

339
Q

what can be used to help spasms in MS

A
  • Baclofen

3a (45 decks)

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