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Neurology for finals > High yield exam cram > Flashcards

High yield exam cram Flashcards

1
Q

Name the cells that produce myelin in
A) CNS
B) PNS

A

CNS = oligodendrocytes
PNS = Schwann cells

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2
Q

Where in the brain is
A) Broca’s area
B) Wernicke’s area

A

Broca’s area = frontal lobe

Wernicke’s area = Posterior superior temporal lobe

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3
Q

What is the function of
A) Broca’s area
B) Wernicke’s area

Also describe the aphasia of each region if they become damaged

A

A) Broca’s = production of speech – (damage causes non-fluent aphasia with word finding difficulties)

B) Wernicke’s = processing & understanding speech – (damage causes fluent aphasia, talks nonsense

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4
Q

Which regions of the brain are responsible for
A) Visual processing
B) Auditory processing

A

A) Visual = parietal lobe
B) Auditory = Temporal lobe

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5
Q

where are the cell bodies of motor nerves found?

A

Ventral horn

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6
Q

where are the cell bodies of sensory nerves found?

A

Dorsal horn

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7
Q

Explain the pathway of an upper and lower motor neurone (from CNS to muscle)

A

brain and brainstem -> ventral horn of the spinal cord (changes from upper to lower motor neurone here) -> peripheral muscles

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8
Q

Describe the action of a parasympathetic neuromuscular junction

A

Ach ->
nicotinic receptor on postganglionic neuron ->
Ach ->
muscarinic receptor on target organ

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9
Q

Describe the action of a sympathetic neuromuscular junction

A

Ach ->
nicotinic receptor on post ganglionic neuron ->
norepinephrine ->
adrenergic receptors on target organ

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10
Q

Describe the findings in an upper motor neurone lesion

A

UPPER (everything is UP) – lesion is in brain or spinal cord (above level of ventral horn)
- Hyperreflexia
- Upgoing plantars
- Increased tone

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11
Q

Where is an upper motor neurone lesion?

A

lesion is in brain or spinal cord (above level of ventral horn)

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12
Q

Where is a lower motor neurone lesion?

A

Lesion is in peripheral nerves (below level of anterior horn)

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13
Q

Describe the findings in a lower motor neurone lesion

A

LOWER (everything is down) –
- Reduced/absent reflexes
- Down going plantars/no response
- Reduced tone
- Muscle atrophy/fasciculations

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14
Q

What function are the following spinal tracts responsible for

  1. The Corticospinal/ pyramidal tract
  2. The Posterior/ dorsal column
  3. The Lateral spinothalamic tract
A
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15
Q

Describe the neurological findings in brown squared syndrome

A

Ipsilateral loss of fine touch, vibration, proprioception & motor

Contralateral Loss of pain & temp

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16
Q

What causes brown squared syndrome?

A

Damage to half of the spinal cord

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17
Q

Which type of fibres pick up proprioception

A

A-alpha (myelinated)

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18
Q

Which type of fibres pick up ‘touch’

A

A-Beta (myelinated)

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19
Q

Which type of fibres pick up sharp pain?

A

Unmyelinated C fibres (small and slow)

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20
Q

Which type of fibres pick up dull pain?

A

Myelinated A-delta fibres (myelinated and fast)

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21
Q

What is the definition of allodynia?

A

pain experienced with a sensory input that does not normally cause pain

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22
Q

Explain the difference between chronic primary pain and chronic secondary pain and the way that they should be managed

A

Chronic primary pain = no underlying cause – DO NOT START PATIENTS ON PAIN MEDS (but u can start antidepressants)

Chronic secondary pain = underlying cause. Medications targeted to the underlying cause are fine

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23
Q

State the type of medication each of the following are:

Amitriptyline

Duloxetine

Gabapentin and pregabalin

A
  • Amitriptyline = tricyclic antidepressant
  • Duloxetine = SNRI antidepressant
  • Gabapentin & Pregabalin = anticonvulsant
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24
Q

How is a breakthrough dose of morphine calculated?

A

Breakthrough dose = 1/6th of daily morphine dose

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25
Q

How is oral codeine/tramadol converted to oral morphine?

A

divide by 10

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26
Q

How is oral morphine dosing converted to subcutaneous morphine?

A

divide by 2

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27
Q

What is normal intracranial pressure?

A

7-15mm

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28
Q

What is Cushing’s triad?

A

bradycardia, hypertension and irregular breathing

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29
Q

How is Cerebral perfusion pressure calculated?

A

Cerebral perfusion pressure (CPP) = Difference between mean arterial pressure (MAP) -intracranial pressure (ICP)

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30
Q

What are the functions of the following structures in relation to memory:

  1. Hippocampus
  2. Cortex
  3. Thalamus
  4. Limbic system
A
  1. Hippocampus (forms memories)
  2. Cortex (stores memories)
  3. Thalamus (Searches and accesses memories)
  4. Limbic system (adds emotion significance to events which helps in the formation of memory)
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31
Q

What is meant by integrate memory loss?

A

inability to form new memories

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32
Q

What is meant by retrograde memory loss?

A

inability to access old memories

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33
Q

What are the 4 main wave patterns seen on EEG?

A

Beta
Alpha
Theta
Delta

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34
Q

Explain the appearance of each wave and when you might see it

A
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35
Q

Describe the 4 stages of sleep and what waveform is seen in each

A

Stage 1- dozing. High amplitude, low frequency, slow theta waves.

Stage 2- regular sleep. Sleep spindles

Stage 3- deep sleep. High amplitude, very slow (2Hz) delta waves interspersed with short episodes of faster waves. Declining spindle activity

Stage 4- Very deep sleep. Delta waves

REM- low amplitude, high frequency (similar to the awake state)

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36
Q

When in the sleep cycle do sleep walking, sleep talking and night terrors occur?

A

Stage 4 (very deep sleep)

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37
Q

When in the sleep cycle do dreams and nightmares occur?

A

REM

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38
Q

When in the sleep cycle does REM occur?

A

Once the body reaches stage 4 sleep, the body then moves back up through stage 3 and stage 2 before entering REM sleep.

lasts 5-30 mins every 90 mins

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39
Q

Which stage in the sleep cycle do narcoleptics fall straight into?

A

REM

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40
Q

What is meningitis?

A

Infection/inflammation of the meninges

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41
Q

What is encephalitis?

A

Infection/inflammation of the brain

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42
Q

What is myelitis?

A

Infection/inflammation of the spinal cord

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43
Q

What is the most common bacterial cause of meningitis?

A

Neisseria Meningititis

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44
Q

What is the most common viral cause of meningitis?

A

Enteroviruses e.g. coxsackie

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45
Q

In which type of infection (bacterial/viral/fungal) would you see a fibrin web in the lumbar puncture?

A

Fungal

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46
Q

What glucose measurement would you expect in the CSF of a person infected with:
A) Bacteria
B) Virus
C) Fungus

A

A) Bacteria = <2.2 (low)
B) Virus = normal
C) Fungus = 1.6-2.5 (low)

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47
Q

What is the initial empirical treatment of meningitis in babies <3m?

A

IV cefotaxime + amox

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48
Q

What is the initial empirical treatment of meningitis in those aged 3M-50Y

A

IV cefataxime

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49
Q

What is the initial empirical treatment of meningitis in those >50Y?

A

IV cefotaxime + Amox

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50
Q

What is the initial empirical treatment of meningitis in those with meningococcal meningitis?

A

IV benzylpenicillin or cefotaxime

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51
Q

What is the initial empirical treatment of meningitis in those with meningitis caused by listeria?

A

IV amox + gent

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52
Q

What is the most common cause of encephalitis?

A

Herpes simplex

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53
Q

What are the 2 antibodies associated with autoimmune encephalitis?

A

Anti-VGKC and Anti-NMDA

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54
Q

What is the most common cause of brain abscess?

A

Strep

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55
Q

What are the 3 steps to manage rabies immediately post-exposure?

A

Wash wound

Give active rabies immunization

Give human rabies immunoglobulin (passive immunisation) if high risk

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56
Q

What is the preventative treatment for tetanus?

A

Inactivated tetanus vaccine

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57
Q

What is the treatment for tetanus after an exposure?

A

Penicillin

Immunoglobulin for high risk wounds/patients

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58
Q

What is the treatment for botulism?

A

Anti-toxin (A,B,E)

Penicillin / Metronidazole (prolonged treatment)

Radical wound debridement

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59
Q

What kind of organism causes Creutzfeldt-Jakob?

A

Prion

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60
Q

How is Creutzfeldt-Jakob diagnosed?

A

MRI, EEG, CSF

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61
Q

What is the treatment for Creutzfeldt-Jakob?

A

There is no treatment

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62
Q

What are the three main features of Wernicke’s encephalopathy?

A

nystagmus
Opthalmaplegia
Ataxia

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63
Q

What are the features of Korsakoff’s encephalopathy?

A

Wernicke’s (nystagmus, opthalmaplegia, ataxia) +

Amnesia

Confabulation

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64
Q

What is confabulation?

A

gaps in memory are unconsciously filled with fabricated, misinterpreted, or distorted information

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65
Q

Describe the physical manifestations of a tonic clonic seizure

A

Rigid and shaking

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66
Q

Describe the physical manifestations of a tonic seizure

A

Stiffening

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67
Q

Describe the physical manifestations of an atonic seizure

A

Drop attacks

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68
Q

Describe the physical manifestations of a myoclonic seizure

A

Jump or jolt

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69
Q

Describe the physical manifestations of an absent seizure

A

Staring into space

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70
Q

Describe the physical manifestations of a partial/focal seizure

A

Rising feeling in stomach
Funny taste/ smell
Deja vu
Lip smacking
Repetitive picking at clothing

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71
Q

Where in the brain does a focal/partial seizure occur?

A

Temporal lobe

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72
Q

Describe the physical manifestations of an infantile spasm

A

Cyclical, repetitive full body spasming and relaxing

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73
Q

What is another name for infantile spasms?

A

West syndrome

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74
Q

Is the prognosis of west syndrome good or bad?

A

Bad

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75
Q

What are the treatments for tonic clonic, tonic and atonic seizures?

A

Men/women not able to get pregnant: Sodium valproate

Women able to get pregnant: Lamotrigine

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76
Q

What is the treatment for myoclonic seizures?

A

Men/women not able to get pregnant: Sodium valproate

Women able to get pregnant: Levetiracetam

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77
Q

What is the treatment for absent seizures?

A

Ethosuximide

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78
Q

What is the treatment for partial/ focal seizures?

A

Lamotragine

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79
Q

What is the treatment for west syndrome?

A

ACTH and Vibagatrin

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80
Q

What is ‘status epileptics’?

A

seizure lasting >5 minutes or repeated seizures without regaining consciousness in between

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81
Q

What are the rules regarding driving after a first seizure with NORMAL investigations

A

Group 1 vehicles after 6 months

Group 2 (HGV) vehicles after 5 years

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82
Q

What are the rules regarding driving if you have a diagnosis of epilepsy?

A

Have been seizure free for one year

Have an established pattern of seizures only during sleep for at least 1 year

If awake seizures as well as sleep seizures, established pattern of only sleep seizures for three years

Should not drive during medication withdrawal and for 6 months thereafter

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83
Q

What is the definition of a primary headache vs a secondary headache?

A

Primary headache = no underlying medical cause. Caused by sensitisation of normal pain pathways

Secondary headache = underlying medical cause (e.g. meningitis)

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84
Q

What causes a postural headache?

A

Low pressure (e.g. CSF leak)

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85
Q

Describe the management of a tension headache (acute & preventative)

A

Acute: Paracetamol & NSAIDs

Preventative: Tricyclic antidepressants (amitriptyline)

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86
Q

Describe the management of a cluster headache (acute & preventative)

A

Acute: Nasal triptans, high flow oxygen,

Preventative: Verapamil

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87
Q

Describe the management of a migraine (acute & preventative)

A

Acute: NSAIDs, paracetamol, Triptans, anti-emetics

Preventative: trigger management, propranolol

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88
Q

Describe the management of a medication overuse headache

A

Withdraw medications

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89
Q

Describe the management of a sub arachnoid haemorrhage (diagnosis and management)

A

Diagnosis: CT Head as soon as possible
Lumbar Puncture > 12 hours after headache onset

Management: Clipping/coiling of aneurysms
Nimodipine (Ca2+ channel blocker for vasospasm)

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90
Q

Describe the management of raised ICP

A

Bed rest, fluids, analgesia, caffeine

Epidural blood patch (stiffens the meninges and helps symptoms)

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91
Q

Describe the management of a hormonal headache

A

Triptans and NSAIDs

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92
Q

Describe the management of giant cell arteritis (diagnosis and treatment)

A

Diagnosis: ESR & biopsy

Management: High dose prednisolone

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93
Q

Describe the management of trigeminal neuralgia

A

Management: carbamazepine

94
Q

What is the mechanism of action of triptans?

A

5-HT receptor agonists

95
Q

What scoring system can be use in A&E to assess the likelihood of a stroke?

A

ROSIER score in A&E (>1 = stroke likely)

96
Q

What is the defining feature of a TIA?

A

<24hrs of symptoms

97
Q

Describe the acute management of a TIA (5)

A

Exclude hypoglycaemia

Aspirin 300mg and

Referral to a specialist within 24 hours

Diffusion weighted MRI

Carotid doppler & ECG

98
Q

Describe the acute management of ischaemic stroke

A

Exclude hypoglycaemia

CT Head

Thrombolysis: within 4.5 hours of stroke onset – Alteplase

Thrombectomy: within 24 hours of symptom onset in proximal anterior or posterior circulation strokes only (give thrombolysis alongside if <4.5 hrs)

99
Q

What is the acceptable ‘door to needle’ time in a stroke?

A

30 mins

100
Q

Describe the secondary prevention that patients who have suffered a stroke or a TIA should receive

A

Diet, exercise, stop smoking

Clopidogrel

Atorvastatin

BP and diabetes control

Warfarin (for AF) if applicable

Carotid endarterectomy if applicable

101
Q

Describe the acute management of Intracerebral haemorrhage (haemorragic stroke)

A

CT Head

Blood pressure control

Reversal of anticoagulants (if relevant)

ICP control (Burr holes or craniotomy)

102
Q

Describe the secondary prevention of Intracerebral haemorrhage (haemorragic stroke)

A

Manage hypertension

AVOID STATINS (unless benefit outweighs risk)

103
Q

Describe the acute management of sub arachnoid haemorrhage

A

<6 hours = CT head (look for hyper-attenuation)
>12 hours = Lumbar puncture

Nimodipine to stop vasospasm

Blood pressure management (achieve >140mmHg)

Endovascular coiling

104
Q

Describe the secondary prevention of sub arachnoid haemorrhage

A

BP control

Risk factor management

105
Q

What is the function of the frontal lobe?

A

High level cognitive functions

Memory

Motor cortex (precentral gyrus)

106
Q

What artery supplies the frontal Cortex?

A

Anterior cerebral artery

107
Q

In which area of the brain can Broca’s area be found?

A

Frontal cortex

108
Q

What is the function of the parietal cortex?

A

Sensory cortex (touch, pressure and position- post central gyrus)
Self and spatial Awareness

109
Q

Which artery supplies the parietal cortex?

A

Middle cerebral

110
Q

what is the function of the occipital cortex?

A

Vision

111
Q

Which artery supplies the occipital cortex?

A

Posterior communicating

112
Q

Explain the blood supply of the motor and sensory cortexes

A

shared blood supply from anterior and middle communicating arteries.

Limb/facial weakness will be dependent on which artery is blocked and is distributed according to the image below.

113
Q

What is a watershed region?

A

areas which lie between two areas with different arterial supplies

114
Q

A stroke on which side of the brain will cause neglect and inability to recognise faces?

A

Right Hemisphere

115
Q

Which vessel is blocked in a Total Anterior Circulation Stroke?

A

Carotid artery or middle cerebral artery

116
Q

What are the criteria for a Total Anterior Circulation Stroke?

A

ALL 3

  1. Unilateral weakness (with or without a sensory deficit) of the face, arm and leg
  2. Loss of vision on one side (homonymous hemianopia)
  3. Loss of awareness on one side (stroke on the non-dominant side of the brain causes you to totally ignore one side of the body) OR Dysphagia (stroke on the dominant side of the brain)
117
Q

Which vessel is blocked in a partial Anterior Circulation Stroke?

A

one of the branches of the middle cerebral artery

118
Q

What are the criteria for a partial Anterior Circulation Stroke?

A

2 out of 3 of the TACS criteria

119
Q

Which vessel is blocked in a lacunar stroke?

A

blockage in a small artery in the brainstem, basal ganglia or subcortical area

120
Q

What are the criteria for a Lacunar Stroke?

A

ONE of the following;

Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis (weakness and uncontrolled movements on the same side of the body

121
Q

Which vessel is blocked in a posterior circulation stroke?

A

a blockage in any of the posterior arteries

122
Q

What are the criteria for a posterior circulation stroke?

A

a combination of symptoms including;
* Loss of balance/coordination
* Vertigo
* Double vision
* Dysarthria
* Visual loss

123
Q

What does a basilar artery stroke cause?

A

Locked in syndrome

124
Q

What is the name given to bruising over the mastoid?

A

Battles sign

125
Q

What is battles sign indicative of?

A

a fracture in the petrous temporal bone which is leaking blood

126
Q

What are the classical signs of shaken baby syndrome?

A

brain swelling
subdural haematoma
traumatic axonal injury
contusion tears.

127
Q

For a subdural bleed, describe:

  1. Shape on CT scan
  2. Blood vessels affected
  3. Usual mechanism of injury
  4. Usual demographic affected
A
  1. crescent
  2. Sheared bridging veins
  3. Fall
  4. Elderly and alcoholic
128
Q

For an extradural bleed, describe:

  1. Shape on CT scan
  2. Blood vessels affected
  3. Usual mechanism of injury
  4. How patients present
A
  1. Lemon
  2. Middle meningeal artery
  3. Blow to pterion region
  4. Lucid period then sudden collapse
129
Q

What is Traumatic Diffuse Axonal Injury?

A

Injury to neurons caused by tearing in the white matter.

130
Q

What causes Traumatic Diffuse Axonal Injury?

A

extensive brain movement (e.g, somebody being kicked in the head, falling from height, or road traffic accidents)

131
Q

How is a diagnosis of Traumatic Diffuse Axonal Injury made?

A

Microscopically

132
Q

What will happen to the patient immediately after Traumatic Diffuse Axonal Injury has occurred?

A

Immediately unconscious

133
Q

What should doctors be suspicious of if a patient has a sudden change in personality/behaviour?

A

Frontal lobe tumour

134
Q

What is the most malignant type of brain tumour?

A

Astrocytoma (e.g. glioblastoma)

135
Q

what condition should be thought of in a patient with bilateral vestibular schwannomas?

A

neurofibromatosis II

136
Q

Name 4 cancers that metastasise to the brain

A
  • Breast
  • Kidney
  • Lung
  • Skin
137
Q

On which chromosome is the mutation that causes neurofibromatosis type 1?

A

Chromosome 17

138
Q

What is the mode of inheritance in neurofibromatosis I?

A

Autosomal dominant

139
Q

What does the gene involved in neurofibromatosis I usually code for?

A

neurofibromin (tumour suppressor)

140
Q

What are the clinical signs and symptoms of neurofibromatosis I?

A

CRABBING
* Café au lait spots
* Relative with the condition
* Axillary or inguinal freckling
* Bony dysplasia (often Bowing of legs)
* Iris hamartomas
* Neurofibromas
* Glioma of optic pathways

141
Q

On which chromosome is the mutation that causes neurofibromatosis type 2?

A

Chromosome 22

142
Q

What is the mode of inheritance in neurofibromatosis 2?

A

Autosomal dominant

143
Q

What does the gene involved in neurofibromatosis 2 usually code for?

A

merlin (tumour suppressor)

144
Q

What is tuberous sclerosis?

A

Genetic condition in which benign tissue growths called hartomas grow and can affect multiple systems

145
Q

What is the inheritance pattern of tuberous sclerosis?

A

Autosomal dominant

146
Q

describe some of the findings a patient with tuberous sclerosis may exhibit

A

Ash leaf spots
shagreen patches
angiofibroma’s
ungual fibromas
café-au-lait spots
isolated white spots of hair/eyebrow/eyelashes/beard

147
Q

What causes MS?

A

Autoimmune destruction of oligodendrocytes

148
Q

What ocular signs and symptoms may be seen in a patient with MS?

A

Optic neuritis =
- Central scotoma
- Impaired colour vision
- Relative afferent pupillary defect

149
Q

How is an episode of optic neuritis treated?

A

High dose steroids

150
Q

Name the 4 different ‘types’ of MS

A
  • Clinically isolated syndrome (first episode)
  • Relaxing remitting
  • primary progressive
  • Secondary progressive (started relaxing remitting then became progressive)
151
Q

Describe how MS is diagnosed

A

More than one episode/relapse in different parts of the nervous system with time between them.

Lumbar puncture

MRI

152
Q

What CSF findings would you expect in MS?

A
  • Oligoclonal (inflammatory) bands
  • normal glucose and protein
  • low white cell count
153
Q

How are relapses of MS managed?

A

Methylprednisolone

154
Q

What is the pathology of MND?

A

Degeneration of the nerve itself (not a demyelinating disease!)

155
Q

What is the average life expectancy in MND?

A

18M-2Y

156
Q

What is the most common type of MND?

A

ALS

157
Q

Which nerves does ALS start in?

A

Peripheral

158
Q

Name the type of MND that affects the muscles of talking and swallowing

A

Progressive bulbar palsy

159
Q

What is the classic finding in the tongue of a patient with progressive bulbar palsy?

A

Walnut tongue

160
Q

How is ALS diagnoses?

A

Diagnosis of exclusion

161
Q

Which nerves are affected in MND, upper or lower?

A

MIX!

162
Q

Name the drug that can be given to MND patients to slow the progression of the disease

A

Riluzole

163
Q

Which imaging modality is the best for detecting spinal pathology?

A

MRI

164
Q

In mixed vitamin B12 / folate deficiency, which one should be replaced first and why?

A
  • Replace vitamin B12 before folate to avoid subacute degeneration of the spinals cord
165
Q

What is Syringomyelia?

A

fluid in the spinal cord

166
Q

How does syringiomyelia present?

A

causes cape, bilateral distribution of symptoms

167
Q

What symptoms does autoimmune myositis cause?

A

acute or subacute weak & painful muscles

168
Q

How is autoimmune myositis managed?

A

Immunosupressants

169
Q

What is the difference between polymyositis and dermatomyositis?

A

Polymyositis =muscle inflammation

Dermatomyositis= skin and muscle inflammation

170
Q

Which antibodies are associated with:

Polymyositis

Dermatomyositis

?

A

Polymyositis = Anti-PM/Scl autoantibodies

Dermatomyositis = Anti-TIF1-γ antibody

171
Q

What causes myasthenia gravis?

A

Autoimmune - antibodies attack ACh receptors

172
Q

What other pathology is associated with myasthenia gravis?

A

Thymoma

173
Q

What is the classic clinic sign in myasthenia gravis?

A

Fatiguable muscles

174
Q

How is myasthenia gravis diagnosed?

A
  • Antibody tests (AChR)
  • CT/MRI of thymus gland
  • Edrophonium test
175
Q

How is myasthenia gravis treated?

A
  • Immunoglobulins/plasma exchange drugs
  • Steroids (suppress the immune system)
  • Pyridostigmine blocks the cholinesterase enzyme and stops breakdown of acetylcholine
176
Q

What is a myasthenic crisis?

A

An acute worsening of symptoms often triggered by another illness

177
Q

How is a myasthenic crisis managed?

A

IV immunoglobulins and plasmapheresis

178
Q

What is lambert eaton syndrome?

A

Autoimmune production of antibodies against voltage gated calcium channels

179
Q

What condition is Lambert-Eaton Syndrome usually secondary to?

A

paraneoplastic syndrome (SCLC)

180
Q

How can Lambert-Eaton Syndrome be differentiated from myasthenia gravis?

A

LES = Muscle weakness improves with use (opposite of myasthenia gravis)

181
Q

What causes Guillan-Barré syndrome?

A

Molecular mimicry; Campylobacter jejuni has antigens that look like proteins on peripheral neurons

182
Q

Describe the disease pattern in Guillan-Barré syndrome

A

Acute, symmetrical, ascending weakness

183
Q

How should Guillan-Barré syndrome be managed?

A

IV immunoglobulins

184
Q

What is Charcot-marie tooth?

A

Genetic condition causing Myelin or axon dysfunction

185
Q

What is the inheritance pattern of Charcot-marie tooth?

A

Autosomal dominant

186
Q

Describe the signs and symptoms of charcot-marie tooth

A

muscle wasting (inverted champagne bottle legs)
weakness
reduced tendon reflexes
peripheral neuropathy
high foot arches

187
Q

What are the causes of peripheral sensory loss (peripheral neuropathy)

A

A: Alcohol
B: B12 deficiency
C: Cancer & CKD
D: Diabetes & Drugs (amiodarone)
E: Every vasculitis

188
Q

What helps to differentiate bells palsy from a stroke?

A

Bells palsy= forehead frozen
Stroke = forehead spared

189
Q

How should bells palsy be managed

A

Pred if within 72 hours of symptoms.
Refer urgently if symptoms persist >3 weeks with no improvement

190
Q

What causes Horner’s syndrome?

A

apical lung tumour compressing the sympathetic nerves supplying the face

191
Q

What is the classic symptom triad of Horner’s syndrome?

A

Ptosis, miosis, Anhydrosis

192
Q

What are the classic symptoms of a 3rd nerve palsy?

A

Down, out & ptosis

193
Q

What do patients with a trochlear nerve palsy struggle to do?

A

Struggle to go down stairs

194
Q

What happens to the uvula if a patient has a vagus nerve palsy?

A
  • Uvula deviates towards normal side
195
Q

What happens to the tongue if there is a hypoglossal nerve palsy?

A

Deviates to abnormal side

196
Q

What causes bulbar palsy?

A

LOWER motor neuron lesions affecting CN IX-XII

197
Q

What are the clinical findings in bulbar palsy

A
  • A wasted, fasciculating tongue
  • Dysarthria
  • Dysphonia
  • Dysphagia
198
Q

What causes pseudo bulbar palsy?

A

UPPER motor neuron lesions affecting CN IX-XII

199
Q

What are the clinical findings associated with pseudo bulbar palsy?

A
  • Dysarthria (Disordered articulation & slurring of speech
  • Dysphonia (A problem with the volume of their speech)
  • Dysphagia (Difficulty swallowing)
  • A spastic, immobile tongue
  • A brisk jaw jerk
  • A brisk gag reflex
200
Q

What is the difference between bulbar palsy and pseudo bulbar palsy?

A

Bulbar = Caused by LOWER motor neuron lesions affecting CN IX-XII

Psuedobulbar = caused by UPPER motor neuron lesions affecting CN IX-XII

201
Q

What colour should normal CSF be?

A

Clear/colourless

202
Q

What is a normal specific gravity for CSF?

A

1.007

203
Q

What is a normal pH for CSF?

A

7.33-7.35

204
Q

Describe the flow of CSF

A

lateral ventricles ->
foramen of munro ->
third ventricle ->
cerebral aqueduct ->
fourth ventricle ->
Foramen of Luschka (lateral) or the Foramen of Megendie (medial) ->
circulate around the brain and spinal cord ->
Absorbed by arachnoid villi (granulations) that extend into the dural venous sinuses

205
Q

What is spina bifida occulta?

A

Patch of hair and dimple - small gap in the spine, but no opening or sac on the back

206
Q

What is spina bifida with a meningiocoele?

A

protruding bubble containing CSF

207
Q

What is spina bifida with a Myelomeningiocoele

A

protruding bubble containing CSF and spinal nerves

208
Q

Name the three types of delirium

A
  • Hypoactive
  • Hyperactive
  • Mixed
209
Q

Name 4 treatable causes of dementia

A
  • Vitamin B12 Deficiency
  • Thyroid Disease
  • HIV & Syphilis
210
Q

What causes Alzheimer’s?

A

β-amyloid plaques and neurofibrillary tangles

211
Q

What drugs can be given to help manage Alzheimer’s?

A

Cholinesterase inhibitors (e.g. Donepezil, rivastigmine) - maintains acetylcholine which compensates for the loss of receptors

NMDA antagonist (memantine)
Cells in Alzheimer make too much glutamate (toxic), memantine blocks effects of glutamate

212
Q

What is frontotemproal dementia also known as?

A

Picks disease

213
Q

What causes frontotemporal dementia?

A

Tau pathology

214
Q

What are the key features in frontotemporal dementia?

A

early change in personality / behaviour

215
Q

How is frontotemporal dementia managed?

A

Supportive- no treatment available

216
Q

What causes Lewy body dementia?

A

Lewy bodies (accumulations of α synuclein in the brain)

217
Q

What are the key features of Lewy body dementia?

A

Fluctuation in symptoms
Visual hallucinations
Parkinsonisms

218
Q

What is the key feature in vascular dementia?

A

Stepwise decline

219
Q

describe the genetics behind Huntington’s disease

A

CAG trinucleotide repeat in HTT gene on chromosome 4

220
Q

What is meant by anticipation?

A

over generations the CAG repeat expands resulting in earlier onset and more severe disease

221
Q

Describe the pathophysiology of Parkinson disease

A

Reduction of dopamine in the Substantia Nigra (part of basal ganglia)

222
Q

Describe the clinical signs of parkinsons

A

Asymmetrical Stiffness
slow movements
change in posture
tremor (4-6 hertz)

223
Q

How is parkinson’s diagnosed?

A

Clinical diagnosis but can be graded with functional imaging

224
Q

Describe the 4 main classes of parkinson’s medication and briefly explain how they work

A

Levodopa – synthetic dopamine

COMT inhibitors (entacapone) - slows breakdown of levodopa (levodopa and COMT are given together)

Dopamine agonists (Bromocriptine, cabergoline) – Less effective than levodopa. Used to delay use of levodopa or used in tandem to facilitate a lower dose.

MAO-B inhibitors (selegiline) – Blocks the enzyme that breaks down dopamine

225
Q

How many hertz is a benign essential tremor?

A

6-12

226
Q

Is benign essential tremor symmetrical or asymmetrical?

A

Symmetrical

227
Q

is benign essential tremor better or worse with voluntary movement?

A

Better

228
Q

What happens to benign essential tremor when the patient is asleep or has been drinking alochol

A

it improves

229
Q

What medications can be given to help manage benign essential tremor?

A

propranolol or primidone

230
Q

What are the causes of Horner’s syndrome?

A
231
Q
A

Neurology for finals (1 decks)

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