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Year 3 - Neurology (DP) > Neurological Dysfunction > Flashcards

Neurological Dysfunction Flashcards

1
Q

What risk factors at birth can contribute to developing epilepsy?

A

Intrauterine infections (Rubella, Toxoplasmosis)
Maternal drug abuse
Perinatal trauma and anoxia

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2
Q

What antibiotics can increase the risk of seizures?

A

Penicillins
Cephalosporins
Quinolones

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3
Q

When would a CT be carried out in the context of a seizure?

A 
Clinical/Radiological skull fracture
Deteriorating GCS
Focal signs
Head injury
Failure to have a GCS of 15 four hours after arrival
Suggestion of other pathology
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4
Q

What investigation is mandatory on admission with a seizure?

A

ECG

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5
Q

How is an EEG useful in epilepsy?

A

Classification
Confirmation of non-epileptic attack
Surgical evaluation
Confirmation of non-convulsive state

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6
Q

What is the prevalence of seizures?

A

2-5%

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7
Q

What is the prevalence of epilepsy?

A

0.5%

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8
Q

After your first seizure, what are the DVLA rules for driving?

A

Cannot drive a car for 6 months during which you must be seizure-free
Cannot drive a HGV/PCV for 5 years during which you must be seizure-free

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9
Q

If diagnosed with epilepsy (>=2 seizures), what are the DVLA rules for driving?

A

No car driving until seizure-free for 1 year

HGV/PCV drivers must be seizure-free for 10 years OFF medication

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10
Q

During what, if a seizure occurs, might there be no DVLA penalty?

A

Sleep

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11
Q

What are some common epilepsy mimics?

A 
Syncope
Non-epileptic attack disorder:
- Pseudoseizures
- Psychogenic non-epileptic attacks
Panic/Hyperventilation
Sleep phenomenon
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12
Q

What are epileptic seizures?

A 
Abnormal synchronisation of neuronal activity:
- Usually excitatory
- High frequency APs
Interruption of normal brain activity:
- Focal OR
- Generalised
Usually brief (seconds - minutes)
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13
Q

What is the incidence of epilepsy?

A

50-80/100,000

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14
Q

In what populations is epilepsy most common?

A

Infants

Elderly

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15
Q

What is the overall mortality for epilepsy?

A

1/400 per year

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16
Q

What is the overall mortality for severe epilepsy in young adults?

A

1/100

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17
Q

What are the types are generalised seizures?

A 
Absence
Myoclonic
Atonic
Tonic
Tonic-clonic
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18
Q

What is a simple partial seizure?

A

Focal site of origin

WITHOUT impaired consciousness

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19
Q

What is a complex partial seizures?

A

Focal site of origin

WITH impaired consciousness

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20
Q

What predisposition do most generalised epilepsies have?

A

Genetic

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21
Q

When are generalised epilepsies most common?

A

Childhood

Adolescence

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22
Q

What is the EEG appearance of a generalised epilepsy?

A

Generalised spike-wave abnormalities

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23
Q

What is the first line treatment for primary generalised seizures?

A

Sodium valproate

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24
Q

What is the first line treatment for primary generalised seizures in pregnancy?

A

Lamotrigine

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25
Q

Early morning jerks, generalised seizures. Triggered by sleep deprivation and ‘flashing light’s in a 12 year old boy?

A

Juvenile myoclonic epilepsy (Janz syndrome)

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26
Q

What is the first line treatment for partial seizures?

A

Carbamazepine

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27
Q

What is the first line treatment for partial seizures in pregnancy?

A

Lamotrigine

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28
Q

What is a common type of frequent partial seizures?

A

Complex partial seizures with hippocampal sclerosis

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29
Q

What drugs inhibit presynaptic voltage-gated sodium channels?

A

Carbamazepine
Lamotrigine
Phenytoin
Topiramate

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30
Q

What drugs inhibit presynaptic voltage-gated potassium channels?

A

Retigabine

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31
Q

What drugs inhibit presynaptic voltage-gated calcium channels?

A

Pregabalin and Gabapentin (N-type channels)

Ethosuximide (T-type channels)

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32
Q

What drug inhibit synaptic vesicle glycoprotein 2A (SV2A)?

A

Levetiracetam

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33
Q

What drugs increase the postsynaptic GABAa receptor activity?

A

Benzodiazepines
Barbituates
Felbamate
Topiramate

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34
Q

How does sodium valproate work?

A

Increases GABA synthesis

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35
Q

How does Tiagabine work?

A

Inhibits the GABA transport (which removes GABA from synapse)

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36
Q

How does Vigabatrin work?

A

Inhibits GABA transaminase (which degrades GABA)

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37
Q

When is phenytoin used in seizures? Why?

A

Acute management only

Rapid loading possible

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38
Q

What is a side effect of phenytoin?

A

Enzyme inducer

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39
Q

What are the side effects of sodium valproate?

A

Weight gain
Teratogenesis
Hair loss
Fatigue

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40
Q

What effect can carbamazepine have on primary generalised seizures?

A

Can make them worse

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41
Q

What is a Jacksonian March?

A

A sign of a focal seizure

Starts in a distal body part and spreads proximally

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42
Q

What is a down-side to lamotrigine?

A

Takes a long time to titrate up

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43
Q

Why is levetiracetam good?

A

Few interactions

Usually well tolerated

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44
Q

What is a side effect of levetiracetam?

A

Mood swings

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45
Q

What are some side effects of Topiramate?

A

Sedation
Dysphasia
Weight loss

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46
Q

If the first line therapies for partial/focal seizures do not work, what can be offered?

A

Oxycarbazine
Levetiracetam
Topiramate
Sodium valproate

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47
Q

What are the first line drugs for generalised absence seizures?

A

Sodium valproate
OR
Ethosuximide

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48
Q

What are the second line drugs for generalised absence seizures?

A

Topiramate
OR
Levetiracetam

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49
Q

What are the first line drugs for generalised myoclonic seizures?

A 
Sodium valproate
OR
Levetiracetam
OR
Clonazepam
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50
Q

What are the second line drugs for generalised myoclonic seizures?

A

Lamotrigine
Or
Topiramate

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51
Q

What is the first line drug for atonic/tonic/tonic-clonic generalised seizures?

A

Sodium valproate

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52
Q

What are the second line drugs for atonic/tonic/tonic-clonic generalised seizures?

A 
Levetiracetam
OR
Topiramate
OR
Lamotrigine
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53
Q

How many patients are seizure free on monotherapy?

A

55%

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54
Q

How many additional patients are seizure free on polytherapy?

A

10%

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55
Q

Why should non-pregnant women be wary of taking anti-epileptics?

A

Some are enzyme-inducers (carbamazepine, phenytoin, topiramate)
Affect efficacy of COC

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56
Q

What shouldn’t women use for contraception when taking anti-epileptics and why?

A

POP

Implants

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57
Q

What contraceptive requires more frequent dosing if also taking an AED?

A

Depot progestogen

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58
Q

What effect does taking AEDs have on emergency contraception?

A

Ineffective

Dose needs increased

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59
Q

During pregnancy, what doses of folic acid does a pregnant woman need to take if on an AED? What is the normal dose?

A

5mg per day

usually 400mcg

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60
Q

After how long is a person deemed to be in status epilepticus?

A

5 minutes

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61
Q

What are the types of status epilepticus?

A 
Generalised Convulsive Status Epilepticus
Non-convulsive states:
- Conscious
- In an 'altered' state
Epilepsia Partialis Continua:
- Continual focal seizures
- Consciousness preserved
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62
Q

What severe metabolic disorders can trigger status epilepticus?

A

Hyponatraemia

Pyridoxine deficiency

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63
Q

Why can status epilepticus cause lasting damage?

A

Excess cerebral energy demand

Poor substrate delivery

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64
Q

What can status epilepticus result in?

A

Respiratory insufficiency and hypoxia
Hypotension
Hyperthermia
Rhabdomyolysis

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65
Q

How do we treat hypoglycaemia in status epilepticus?

A

50ml of 50% IV glucose

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66
Q

What anticonvulsants can be given after 5 minutes of seizures activity (ie patient is in status epilepticus) in hospital?

A 
Lorazepam 4mg IV (first line)
OR
Midazolam 10mg buccally/intranasally
OR
Diazepam 10mg IV/PR
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67
Q

What anticonvulsants can be given in primary care in status epilepticus?

A

Midazolam 10mg buccally/intranasally
OR
Diazepam 10mg PR

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68
Q

How often and when can benzodiazepines be repeated in status epilepticus?

A

Repeated ONCE after 5 minutes

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69
Q

If benzodiazepines fail to control status epilepticus, what drugs can be given within 30 minutes of onset of seizures?

A

Phenytoin 18mg/kg IV at 50mg/min:
- ECG monitoring is ESSENTIAL
OR (if no ECG/Phenytoin) available
Sodium valproate 20-30mg/kg IV at 40mg/min

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70
Q

If status epilepticus persists beyond 60 minutes of onset, how is it treated?

A

Admit to ITU

Administer general anaesthesia (Thiopentane or Propofol)

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71
Q

If the patient is malnourised or alcohol abuse is suspected, what else can be prescribed during status epilepticus?

A

IV Thiamine 250mg over 30mins

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72
Q

What is the incidence of spontaneous subarachnoid haemorrhage?

A

6/100,000 (per year)

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73
Q

How does a subarachnoid haemorrhage present?

A 
Sudden onset severe headache
Collapse
Vomiting
Neck pain
Photophobia
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74
Q

What are some differentials for the thunderclap headache in subarachnoid haemorrhage?

A

Migraine

Benign coital cephalagia

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75
Q

What focal deficit signs might be seen in subarachnoid haemorrhage?

A

Dysphasia
Hemiparesis
CN iii palsy

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76
Q

What might be seen on fundoscopy in subarachnoid haemorrhage?

A

Retina/Vitreous haemorrhage

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77
Q

When is an LP safe in the context of a subarachnoid haemorrhage?

A

If no neurological deficit AND If no papilloedema
OR
With a normal CT

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78
Q

What does CSF look like in subarachnoid haemorrhage and in what time frame?

A

Bloodstained or Xanthochromic

6-48 hours after haemorrhage

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79
Q

What technique is used for cerebral angiography? Via what artery?

A

Seldinger technique via femoral artery

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80
Q

When might cerebral angiography miss an aneurysm?

A

Vasospasm

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81
Q

What are some complications of a subarachnoid haemorrhage?

A 
Re-bleeding
Delayed ischaemia
Hydrocephalus
Hyponatraemia
Seizures
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82
Q

What is the re-bleed risk in the first 14 days following a subarachnoid haemorrhage?

A

20%

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83
Q

What is the re-bleed risk in the first 6 months following a subarachnoid haemorrhage?

A

50%

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84
Q

When do Delayed Ischaemic Neurological Deficits occur following a subarachnoid haemorrhage and how do they present?

A

3-12 days later

Altered conscious level or focal deficit

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85
Q

What causes a Delayed Ischaemic Neurological Deficit?

A

Vasospasm

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86
Q

How can a Delayed Ischaemic Neurological Deficit be prevented? How does it work?

A

Nimodipine:

- Prevents vasospasm and ischaemic

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87
Q

What is ‘Triple H’ therapy and what does it treat/prevent?

A 
Induced:
- Hypertension
- Hypervolaemia
- Haemodilution
Treats vasospasm and prevents DIND
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88
Q

How does hydrocephalus present?

A

Increasing headache

Altered conscious level

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89
Q

How can hydrocephalus be treated?

A

CSF drainage:

  • LP
  • External ventricular shunt
  • Ventricular-peritoneal shunt
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90
Q

Why do we not fluid restrict in hyponatraemia following subarachnoid haemorrhage?

A

It is often just transient

91
Q

How can hyponatraemia following subarachnoid haemorrhage be treated?

A

Fludrocortisone

92
Q

What are 50% of intracerebral haemorrhages secondary to?

A

Hypertension:

  • ‘Charcot-Bouchard’ microaneurysms of small perforating vessels
  • Basal ganglia haemorrhage
93
Q

What are 30% of intracerebral haemorrhages secondary to?

A

Aneurysm OR

AVM

94
Q

How does an intracerebral haemorrhage present?

A

Headache
Focal neurological deficit
Reduced consciousness

95
Q

What investigations are important in intracerebral haemorrhage?

A

CT (urgent if reduced consciousness)

Angiography (if suspected aneurysm/AVM)

96
Q

How is an intracerebral haemorrhage treated?

A

Surgical evaluation +/- treatment of underlying cause

97
Q

What factors contribute to a poor prognosis in intracerebral haemorrhage?

A

Large basal ganglia/thalamic clot with:

  • Major focal deficit OR
  • Deep coma
98
Q

Where are most AVMs located?

A

Within the brain parenchyma

99
Q

How can AVMs present?

A

Seizures

Headache

100
Q

What is Steal syndrome?

A

Ischaemic syndrome

Resulting from a vascular assist device (eg. AV fistula)

101
Q

How is an AVM treated?

A

Surgery
Endovascular embolisation
Stereotactic radiotherapy
Conservative

102
Q

Where do LMNs run from?

A

Ventral horn (of spinal cord) to muscle

103
Q

What are the signs of an UMN lesion?

A

Increased tone
Minimal muscle wasting
NO fasciculations
Hyperreflexia

104
Q

What are the signs of a LMN lesion?

A

Reduced tone
Muscle wasting
Fasciculations
Diminised reflexes

105
Q

What can cause chronic spinal cord compression?

A

Degenerative disease (spondylosis)
Tumours
Rheumatoid arthritis

106
Q

How do chronic compressions present?

A

Similar to acute compressions except UMN signs predominate

107
Q

A patient presents initially with a flaccid, areflexic paralysis. There is some return of reflexes 2 days later. 2 weeks later, increased tone and hyperreflexia are noted.

A

Cord transection - “Spinal shock”

108
Q

A patient presents with right sided loss of motor function from the umbilicus down. There is a loss of proprioception, vibration and touch sensations from the umbilicus downwards on the right side. From the pubic symphysis downwards, there is a loss of pain and temperature sensation on the left side. What is this condition and where has the lesion occur?

A

Brown-Sequard syndrome:

- Right sided cord hemisection at T10 level

109
Q

A 68 year old patient experiences a hyperestension injury to his neck. There is noticeable upper limb weakness. There is loss of pain and temperature sensation in both of the upper limbs, and across the chest and upper back. On examination, power is preserved in the lower limbs and proprioception, fine touch and vibration is preserved in both upper and lower limbs. There is evidence of urinary retention. He has a past medical history of osteoarthritis in his cervical and lumbar spine. What is this condition? Why are the upper limb motor functions affect more? Why are proprioception, vibration and fine touch sensations normal?

A

Central cord syndrome:

  • Neurones supplying upper limb are more central in the lateral corticospinal tract
  • Dorsal column is left intact
110
Q

How can lung/breast/kidney/prostate cancers result in spinal cord compression?

A

Metastasis to extradural space

111
Q

What intradural extramedullary tumours can cause spinal cord compression?

A

Meningioma

Schwannoma

112
Q

What intradural intramedullary tumours can cause spinal cord compression?

A

Astrocytoma

Ependyoma

113
Q

What infections can cause epidural abscesses resulting in spinal cord compression?

A

Bloodborne Staph.

TB

114
Q

How do we manage spinal trauma?

A 
Immobilise
Investigate:
- Xray/CT
- MRI
Methylprednisolone:
- Bolus
- 24 hour infusion
Surgical decompression and traction/ex-fix
115
Q

What are dissociative seizures, non-epileptic attack disorder, pseudoseizures, psychogenic non-epileptic seizures and hysterical seizures all types of?

A

Functional attacks

116
Q

What are non-epileptic seizure attacks related to?

A

Traumatic events
Physical/Sexual abuse
Other stress
Anxiety/Depression

117
Q

How can a functional attack be diagnosed?

A

History
Linguistic analysis
Outpatient EEG (+ video with provocation)
Longterm video EEG monitoring

118
Q

Where do somatosensory auras arise from?

A 
Somatosensory cortex (parietal lobe)
Occasionally insular lobe
119
Q

Where do visual auras arise from?

A

Occipital lobe

Occasionally temporal lobe

120
Q

Where do auditory auras arise from?

A

Auditory cortex (temporal lobe)

121
Q

What are vertiginous auras? Where do they arise from?

A

Vertigo-attacks

Arise from temporoparietal lobe (near visual and auditory association areas)

122
Q

Where do autonomic auras arise from?

A

Temporal lobe:

  • Insula
  • Amygdala
123
Q

How is a functional attack defined?

A
  1. Attacks with prominent motor activity
  2. Episodes of collapse with no movement
  3. Abreactive attacks
    - Fear
    - Gasping
    - Hyperventilation
124
Q

How long do function attacks last?

A

10-20 minutes (prolonged compared to epileptic seizures)

125
Q

What are the signs of peripheral autonomic neuropathy?

A

Postural hypotension
Impotence
Nausea and vomiting

126
Q

What are the signs of peripheral small fibre neuropathy?

A

Pain dysaesthesia

127
Q

What are the signs of peripheral large sensory fibre neuropathy?

A

Numbness
Paraesthesia
Unsteadiness

128
Q

What are the signs of peripheral large motor fibre neuropathy?

A

Weakness
Unsteadiness
Wasting

129
Q

What is pseudoathetosis?

A

Abnormal writing (usually of the fingers) due to loss of proprioception (seen in large sensory fibre neuropathy)

130
Q

How does Mononeuritis Multiplex present?

A

Simultaneous/Sequential neuropathy (sensory and motor deficits) of non-contiguous nerve trunks

131
Q

What is Mononeuritis Multiplex associated with?

A 
Diabetes
GPA
EGPA
Rheumatoid arthritis
SLE
Sarcoidosis...
132
Q

A patient experiences some weakness that she initially described as starting in her feet and ankles. Over time this spread up to her knees at which she also started to experience some weakness in her hands. There was also some loss of sensation in the same distribution. What is this condition? What is the name of the distribution?

A

Length-Dependant Peripheral Neuropathy

‘Glove and stocking’ distribution

133
Q

What is a plexopathy?

A

Disorders typically affecting the brachial (C5-T1) and/or lumbosacral plexuses (T12-L4 and L4-S3/4)

134
Q

What is a radiculopathy?

A

Disorders affecting the nerve roots

135
Q

What are some differential diagnoses of radiculopathies?

A

Carpal tunnel (median nerve) vs C8 radiculopathy

136
Q

What do nerve conduction studies show in axonal loss?

A

Reduced amplitude

Normal velocity and latency

137
Q

What do nerve conduction studies show in demyelination?

A

Slowed velocity
Prolonged latency
Normal/Slightly reduced amplitude

138
Q

What are some acute demyelinating neuropathies? How long do they develop over?

A

Guillaine-Barre Syndrome
Acute Inflammatory Demyelinating Polyradiculopathy
Days-Weeks

139
Q

What are some chronic demyelinating neuropathies?

A

Chronic Inflammatory Demyelinating Polyneuropathy

Hereditary Sensory Motor Neuropathy (ie. Charcot-Marie-Tooth Disease)

140
Q

What is the incidence of Guillaine-Barre Syndrome?

A

1-2/100,000 per year

141
Q

How does Guillaine-Barre Syndrome present?

A

Progressive paraplegia over days - 4 weeks
Sensory symptoms precede weakness
Pain

142
Q

When do symptoms of Guillaine-Barre Syndrome peak?

A

10-14 days

143
Q

What is Guillaine-Barre Syndrome associated with?

A

GI infection (Campylobacter)

144
Q

How do Guillaine-Barre Syndrome patients die?

A

ANS failure resulting in cardiac arrhythmias

145
Q

How is Guillaine-Barre Syndrome treated?

A

Ig infusion and/or
Plasma exchange
(Minimal role for steroids)

146
Q

What are the variants of hereditary neuropathies?

A

Pure motor/sensory
Sensorimotor
Small fibre (ie. Congenital Insensitivity to Pain +/- Anhydrosis)

147
Q

What is the most common mutation in hereditary neuropathies?

A

CMT1a

148
Q

What can cause an ANA/ENA positive vasculitis axonal neuropathy?

A

Rheumatoid arthritis

Sjogrens

149
Q

What cancers can result in paraneoplastic syndromes with axonal neuropathy features?

A

Myeloma
Ab mediated:
- Breast cancer
- SCLS

150
Q

What infections can result in an axonal neuropathy?

A

HIV
Syphilis
Lyme
Hepatitis B/C

151
Q

What drugs can result in an axonal neuropathy?

A 
Alcohol
Amiodarone
Phenytoin
Chemotherapy:
- Cisplatin
- Vincristine
152
Q

What metabolic conditions are associated with axonal neuropathies?

A 
Diabetes
B12/Folate deficiency
Hypothyroidism
Chronic uraemia
Porphyria
153
Q

What conditions can result in chronic autonomic neuropathy?

A

Diabetes (gastroparesis)
Amyloidosis
Hereditary

154
Q

What conditions can result in acute autonomic neuropathy?

A

Guillan-Barre

Porphyrias

155
Q

How is a vasculitic axonal neuropathy treated?

A

Pulsed IV:

  • Methylprednisolone AND
  • Cyclophosphamide
156
Q

How is a demyelinating peripheral neuropathy treated?

A

IV Ig (pooled from donors)
Steroids
Azathioprine, Mycophenalate, Cyclophosphamide

157
Q

What are pyramidal/UMN features?

A

Pyramidal weakness:
- Upper limb extensors weaker than flexors
- Lower limb flexors weaker than extensors
Spasticity

158
Q

Where do extrapyramidal symptoms arise?

A

Basal ganglia

159
Q

What are signs of cerebellar disease (ataxia)?

A

Lack of voluntary coordination
Gait abnormality
Disdiadochokinesia

160
Q

How does an UMN lesion affect deep tendon, superficial and pathological reflexes?

A

Deep tendon - Increased
Superficial - Reduced
Pathological - Increased

161
Q

What general signs are seen in muscle disease?

A

Wasting (usually proximal)
Reduced tone
Reduced/Absent deep tendon reflexes

162
Q

What do fasciculations, babinski reflex and wasting indicate?

A

LMN lesion

163
Q

What general signs are seen in NMJ disease?

A

Fatiguable weakness
Normal/Reduced tone
Normal tendon reflexes
No sensory symptoms

164
Q

What pattern of sensory loss is seen in UMN lesions?

A

Central

165
Q

What can cause an UMN lesion?

A

Stroke
Space occupying lesion
Spinal cord injury

166
Q

What UMN sign a does parasagittal frontal lobe lesion cause?

A

Paraparesis (partial paralysis of lower limbs)

167
Q

What can cause a LMN lesion?

A

MND
Spinal muscular atrophy
Lead poisoning
Poliomyelitis

168
Q

What is the muscle, nerve and nerve root responsible for shoulder abduction?

A

Deltoid
Axillary
C5

169
Q

What is the muscle, nerve and nerve root responsible for elbow extension?

A

Triceps
Radial
C7

170
Q

What is the muscle, nerve and nerve root responsible for finger extension?

A

Extensor digitorum
Posterior interosseus (radial)
C7

171
Q

What is the muscle, nerve and nerve root responsible for index finger abduction?

A

1st dorsal interosseus
Ulnar
T1

172
Q

What is the muscle, nerve and nerve root responsible for hip flexion?

A

Iliopsoas
Femoral
L1/L2

173
Q

What is the muscle, nerve and nerve root responsible for knee flexion?

A

Hamstrings
Sciatic
S1

174
Q

What is the muscle, nerve and nerve root responsible for ankle dorsiflexion?

A

Peroneals
Common fibular and sciatic
L4/L5

175
Q

What is the muscle, nerve and nerve root responsible for great toe dorsiflexion?

A

Extensor hallucis longus

Common fibular L5

176
Q

What does a hemianaesthesia suggest?

A

Contralateral cerebral lesion

177
Q

If there are no other signs in a hemianaesthesia, what should we suspect?

A

Non-organic cause

178
Q

What signs does “dissociated sensory loss” mean?

A

Lost spinothalamic function (pain and temp.)

Preserved dorsal column function

179
Q

What does dissociated sensory loss suggest? What can cause this?

A

Hemicord damage:

  • Anterior spinal artery syndrome
  • Brown-Sequard syndrome
  • Syringomyelia
180
Q

How would a cerebellar gait be described?

A

Broad-based

Unsteady

181
Q

How can an intention tremor or ataxia be assessed in cerebellar disease?

A

Finger-nose test

Knee-heel test

182
Q

What is disdiadochokinesis?

A

Clumsy, fast, alternating movements

183
Q

What are some possible addition features of cerebellar disease?

A

Nystagmus

Dysarthria

184
Q

What is the pattern of extrapyramidal symptoms in Parkinson’s Disease?

A

Usually asymmetrical

185
Q

What is the pattern of extrapyramidal symptoms in drug-induced or atypical Parkinson’s?

A

Symmetrical

186
Q

What lobe is responsible for executive functions, self-criticism and trying again?

A

Frontal

187
Q

What lobe is responsible for responding to primitive stimuli?

A

Orbitofrontal cortex

188
Q

What does orbitofrontal cortex damage cause?

A

Disinhibition

189
Q

What is the function of the dorsolateral prefrontal cortex?

A

Response to external stimuli and executing work responsibilities

190
Q

What parts of the brain are responsible for motivation? Damage can cause abulia (lack of will) and akinetic mutism.

A

Cingulate gyrus and dorsomedial frontal lobe

191
Q

What sort of gait is seen in frontal lobe dysfunction?

A

Magnetic gait (feet carried up and forward)

192
Q

What kind of aphasia can be seen in frontal lobe dysfunction?

A

Expressive/Broca’s

193
Q

What is agnosia? Damage to what lobe can result in this?

A

Inability to interpret sensations and recognise things

Temporal

194
Q

What type of aphasia is seen in temporal lobe damage?

A

Receptive/Wernicke’s

195
Q

What visual field defects are seen in temporal lobe damage? Is the defect contralateral/ipsilateral? What part of the optic pathway is affected?

A

Congruous upper homonymous quadranantopia
Contralateral
Meyer’s loop

196
Q

Why can auditory dysfunction arise in temporal lobe damage?

A

Heschel’s gyrus (Temporal transvers gyrus):

- Hearing represented bilaterally

197
Q

What are signs/symptoms of a temporal lobe seizure?

A 
Deja-vu
Jamais-vu
Amnesia
Auditory/Visual/Gustatory/olfactory/sensory hallucinations
Emotional lability
198
Q

What visual defect is seen in parietal lobe damage? Is the defect contralateral/ipsilateral? What part of the optic pathway is affected?

A

Congruous lower homonymous quadrantanopia
Contralateral
Superior optic radiations (Baum’s loop)

199
Q

This is a disease of the dominant angular gyrus (part of the inferior parietal lobe). It presents with:

  • Dysgraphia
  • Left-right disorientation
  • Finger agnosia
  • Acalculia
A

Gertmann’s Syndrome

200
Q

What does damage to the non-dominant angular gyrus of the parietal lobe cause?

A

Inattention

201
Q

What happens to levodopa when taken?

A

Crosses BBB

Converted to dopamine in the brain

202
Q

How can peripheral breakdown of levodopa be prevented?

A

Carbidopa

203
Q

What can levodopa be broken down by in the brain? What drugs can prevent this?

A

Catechol-O-Methyltransferase (COMT)
COMT inhibitors:
- Entacapone
- Tolcapone

204
Q

What receptors do dopamine agonist work on?

A

Act on D2-type receptors

205
Q

What are some examples of dopamine agonists?

A

Pramipexole
Ropinirole
Bromocriptin

206
Q

What anticholinergics can reduce the tremor in Parkinson’s?

A

Trihexyphenidyl

Diphenhydramine

207
Q

Why are anticholinergics typically avoided in Parkinson’s?

A

Can cause severe side effects:

  • Delirium
  • Drowsiness, vertigo, headache
  • Dry mouth
  • Mydriasis +/- Photophobia
208
Q

What effect can amantadine have in Parkinson’s?

A

Many alleviate levodopa-related dyskinesias
Mild attenuation of:
- Tremor
- Dystonia

209
Q

In Parkinson’s, failure to respond to high does levodopa is a strong indicator for what?

A

Non-idiopathic Parkinson’s

210
Q

Visual compromise (optic neuritis, nystagmus, diplopia), stiffness and weakness are presenting features of what?

A

MS

211
Q

Oligoclonal bands in CSF

A

MS

212
Q

What effect does fever have in MS?

A

Can worsen symptoms

213
Q

What MND has pure UMN features?

A

Primary Lateral Sclerosis

214
Q

What is it important to ask about in assessing MND?

A 
Cramps
Fasciculations
Foot drop
FHx
Behavioural changes
215
Q

Fasciculations (including the tongue) and wasting in muscle groups outside a single myotome are what sort of signs?

A

LMN

216
Q

Increased tone, clonus, loss of dexterity, brisk reflexes (preserved in wasted/fasciculating muscles) and Babinski reflex are what sort of signs in MND?

A

UMN

217
Q

What is an MRI used for in stroke?

A

To identify:

  • Old lesions
  • Non-vascular lesions
218
Q

What is a diffusion-weighted MRI used for in stroke?

A

To identify new ischaemic lesions (hyperintense)

219
Q

What is a T2 sequence MRI used for in stroke?

A

Identify bleeds and microbleeds

220
Q

What are time-of-flight MRI sequences used for in stroke?

A

To identify occlusions of extra- and intracranial arteries

221
Q

What are perfusion-weighted MRI sequences useful for in stroke?

A

Identify areas at risk of iscaemia

222
Q

What do CT hyperintesities in stroke indicate?

A

Bleed

223
Q

What are early CT signs of a stroke?

A

Loss of lentiform nucleus
Poor grey-white matter differentiation
Loss of insular ribbpn

Year 3 - Neurology (DP) (5 decks)

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