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Neurology > Clinical stuff > Flashcards

Clinical stuff Flashcards

1
Q

What are the 5 causes of blackouts?

A
  1. No blood
  2. Blood no good
  3. Brainstem
  4. Cerebral
  5. Psychological
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2
Q

What are the causes of “no blood” black outs?

A

Vasovagal syncope

Postural Hypotension

Hyperventilation

Cardiac Dysrhythmia

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3
Q

What are the causes of “blood no good” blackouts?

A

Hypoxia

Hypoglycaemia

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4
Q

What is Vasovagal Syncope?

A

Fainting

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5
Q

What causes Vasovagal snycope?

A

Vagal activity increaces will symapthetic activity decreses

As a result the heart slows and blood pools in the peripheries.

Cardiac output decreases resulting in inadequate perfusion to the brain.

The patient then collapses, venous return improves and cardiac output goes back to normal

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6
Q

What is postural hypotension?

A

Patient feels dizzy upon standing, blacks out and collapses

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7
Q

Why does postural hypotension occour?

A

Decreased symapthetic activity affecting the heart and peripheral circulation

Normal cardio-acceleration and peripheral vasoconstriction in response to standing does not occour.

Cardiac output is no sufficiant resulting in loss of consciousness

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8
Q

What is usually the cause of postural hypotension?

A

Decreased sympathetic activity due to anti-hypertensive drugs

occasionally due to a physical lesion of the sympathetic pathways

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9
Q

What kind of person experiances postural hypotension

A

middle aged or elderly

Parkinson’s disease

Peripheral neuropathy

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10
Q

What happens during hyperventilation?

A

Patients overbeath and wash out CO2 from their blood.

Arterial hypocapnia is a potent cerebral vasocontrictive stimulus.

Inadequate perfusion to the brain resulting in loss of consciousness

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11
Q

How can you prevent hyperventialtion?

A

Rebreathing into a paper bag.

Stops hypocapnia as you are rebreathing air which has more CO2 in it

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12
Q

What signs and symptoms are suggestive of cardiac dysrhytmia being the cause of blackouts?

A
  • Older patient
  • attacks unrelated to posture
  • Hx of Ischaemic heart disease
  • Palpatations
    • Dizziness and colour change prior to collapse
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13
Q

What are Vertebro-basilar transient iscaemic attacks?

A

Thrombo-embolic material from the heart of proximal large arteries occlude arteries supllying the brainstem.

Cause ischemia of the brainstem tissue untill they are dislodged

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14
Q

what are the symptoms of Vertebro-basilar transient ischaemic attack?

A

Lasting about 8 minutes

Vertigo

Visual field defects (diplopia, hemianopia)

Auditory phenomena (sudden sensorineural hearing loss)

Facial numbness or paresthesias

Dysphagia, dysarthria, hoarseness

Syncope (drop attacks)

Hemisensory extremity symptoms (eg, contralateral to facial component

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15
Q

What factors make Vertebro-basilar transient ischaemic attacks more likely in a patient?

A

Older patient

know arteriopathic history

Presence of a source of emboli - MI, atrial fibrilation, neck bruits etc

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16
Q

What is a “hysterical attack”

A

Some patients attract attention to themselves, at a conscious or unconscious level by having blackouts.

Attacks consist of apparent loss of conciousness with falling and sometimes simulated convulsive movements.

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17
Q

What is narcolepsy?

A

episodes of sleep of unatural duration and stength occouring at unsual times.

Sufferers may also experiance

  • Cataplexy
  • Sleep paralysis
    • Hypnogogic Hallucintions
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18
Q

What is transient global amensia?

A

For a few hours the patient acts normally but afterwards they cant remember anything that happened

usually ony happens a couple times in a patients life

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19
Q

What are the layers of the meinges?

A

Dura mater

Arachnoid mater

Pia mater

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20
Q

What causes Viral Meningitis?

A

Enteroviruses like ECHO virus

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21
Q

How do you diagnose viral meningitis?

A

Viral stool culture

Throat swab

CSF PCR

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22
Q

How do you treat viral meningitis?

A

Supportive - Self limiting

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23
Q

What is the most common cause of community aquired bacterial meningitis in children?

A

H. influenza

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24
Q

What is the most common cause of community acquired bacterial meningitis in ages 10-21?

A

Neisseria meningitidis

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25
Q

What is the most common cause of community acquired bacterial meningitis in adults

A

streptococcus pneumoniae

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26
Q

What is a major risk factor for streptococcus pneumoniae meningitis?

A

Fracture of the cribiform plate

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27
Q

What type of meningitis does “ decreased cell mediated immunity” increase the risk for?

A

Listeria monocytogenes

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28
Q

What type of meningitis does head trauma or neurosurgery put you at higher risk off?

A

S. aureus

S. epidermidis

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29
Q

What type of meningitis does a basilar skull fracture put you at higher risk of?

A

S.pneumoniae

H. influenzae

beta-hemolytic strep group A

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30
Q

What causes meningococcal meningitis?

A

Neisseria meningitis

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31
Q

How does Neisseria meningitis cause symptoms?

A

Endotoxins

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32
Q

Who gets memingococcal meningitis?

A

Young children

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33
Q

What is characterisitic of Tuberculous Meningitis?

A

Reactivaion:- Elderly

Previous TB on CXR

Non specific ill health

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34
Q

How do you treat Tuberculous Meningitis?

A

Isoniazid + rifampicin

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35
Q

What is cryptococcal meningitis?

A

Fungal meningitis presenting mainly in HIV disease

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36
Q

What is Chorea?

A

Fragments of movements flowing irregulary from one body segment to the next

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37
Q

What is ballismus?

A

Extreme chorea

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38
Q

What are the two broad subtypes of parkinson’s disease?

A

Tremor dominant Parkinson’s Disease

Non-tremor dominant Parkinson’s Disease

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39
Q

What sub type of parkinsons disease is associated with a slower rate of progression and less functional disability

A

Tremor-dominant subtype

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40
Q

What are the non-motor features of parkinson’s disease?

A

Olfactory dysfunction

cognitive impairment

psychiatric symptoms

sleep disorders

autonomic dysfunction

pain

fatigue

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41
Q

What is the classic disease progression of parkinson’s disease?

A

Diagnosed made with motor symptoms but non motor symptoms have been around for a while

Initally motor features are well controlled

at 17 years 80% report gait freezing and falls while 50% report choking

At 20 years 83% have dementia

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42
Q

What does the disease progression graph look like for Parkinson’s disease

A
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43
Q

What are the pathological hall marks of parkinsons disease?

A

Loss of dopaminergic neurons within the substania nigra and lewy body pathology

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44
Q

What are Lewy bodies?

A

Build ups of insoluble misfolded alpha-synuclien

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45
Q

Does having parents with parkinson disease increase your risk of parkinson’s disease?

A

Yes

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46
Q

What mutations are the most common causes of parkinsons disesae?

A

LRRK2

Parkin

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47
Q

What is the most common cause of meningitis in children under the age of 4 ?

A

H. influenzae

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48
Q

How do you treat parkinson’s disease ?

A

Increase dopamine in the brain

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49
Q

What are the adverse side affects of dopamine treatment in parkinsons?

A

Impulse control disorders made worse

Hallucinations - Carefull in the elderly

Nausea

Oedema

Daytime somnolence

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50
Q

What are the long term complications of dopaminergic therapy in parkinson’s disease?

A

Motor flucations:- on time/off time

Dyskinesia and chorea (corrolates with levodopa conc)

Hallucinations

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51
Q

What are the motor symptoms of parkinsonisim?

A

Bradykinesia

Rest tremor

Rigidity

Postural and gait impariment

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52
Q

What is typical with Vascular Parkinsonism?

A

Predominantly affects lower limbs

Poor levodopa response

Resting tremor uncommon

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53
Q

What is Duchenne muscular dystrophy?

A

X linked genetic disease resulting in progressive muscle weakness

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54
Q

What is huntington disease?

A

Progressive neurodegenerative disorder

onsent between 30-50 yrs

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55
Q

How is huntington disease inherited ?

A

Autosomal Dominant

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56
Q

What is the most common cause of dementia?

A

Alzheimer’s disease (50-70%)

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57
Q

What are the 5 things measured in the cerebral spinal fluid when ivestigating meningitis?

A

WBC count

Neutrophils

Protein

Glucose

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58
Q

What would you expect the WBC count to be in the CSF during bacterial meningitis?

A

WBC count >2000

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59
Q

What would you expect the neutophil count to be in the CSF of expected bacterial meningitis?

A

Neutrophils >1180

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60
Q

What would you expect of the protein content in the CSF of expected bacterial meningitis?

A

Protein >220 mg/dl

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61
Q

What would you expect the glucose level to be in the CSF of expected bacterial meningitis?

A

Glucose <34mg/dl

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62
Q

What CSF findings are 99% perdictive of bacerial meningitis?

A

WBC >2000

Neutrophils >1180

Protein >220mg/dl

Glucose <34 mg/dl

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63
Q

What should you do when a patient is addmitted to hospital with acute adult bacterial meningitis

A
  • Take blood for culture and coagulation screen
  • Take throat swab
  • Swab any skin lesions
  • Start “intial therapy before pathogens are identified” treatment
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64
Q

What types of patients which acute adult bacterial meningitis need a CT prior to lumbar puncture?

A
  • Immunocompromised patients
  • History of CNS disease
  • New onset of seizure
  • Papilloedema
  • Abnormal levels of consciousness
    • Focal neurological deficit
      *
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65
Q

What is the empiracal antibiotic for acute adult bacterial meningitis?

A

IV ceftriaxone 2g bd

if listeria is suspected add

Amoxicillin 2g qds

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66
Q

What is the empiric antibiotic for acute adult bacterial meningitis for someone with a penicillin allergy?

A

Chloramphenicol IV 25 mg/kg every 6hrs

plus

Vancomycin IV 500 mg every 6 hours

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67
Q

Whats the deal with steriods and bacterial meningitis?

A

Give to all patients suspected of bacterial meningitis before or with the first dose of antibiotics and then every 6 hours

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68
Q

When are the only times you wouldnt give steriods in adult acute baterial meningitis ?

A
  • Post surgical meningitis
  • Severe immunocompromise
  • septic shock
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69
Q

What must you remeber to do when you have a paient with meningitis?

A

Call Public Health

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70
Q

Explain the concept of Cerebral Perfusion Pressre?

A

Cerebral perfusion pressure = mean arterial pressure — intracranial pressure

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71
Q

What are the ideal CPP = MAP — ICP pressures that you want to keep

A

Cerebral perfussion pressure = Mean arterial pressure — Intracranial pressure

>60mmHg = >80mmHg — < 20mmHg

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72
Q

What is normal adult Intercrainial Pressure?

A

9-11mmHg

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73
Q

How can you spot an anteior cranial fossa fracture?

A

Panda eyes

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74
Q

How can you spot a middle crania fossa fracture?

A

“battle sign”

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75
Q

What kills patients with head injuries?

A

Hypoxia

Hypotension

Raised Intracranial Pressure

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76
Q

When should you request a CT scan of the head in patients with head trauma?

A

Any patient with :

  • Skull fracture
  • GCS <15
  • Focal neurological signs
    • Taking anti-coagulants
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77
Q

What are the types of traumatic intracranial bleeding from outside to inside?

A

Extradural haematoma

Subural haematoma

Traumatic subarachnoid haemorrhage

Intracerebral contusion

Intracerebral haematoma

Intraventricular haemorrhage

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78
Q

Why is sedation useful in the management of head injuries?

A

Reduces cerebral metabolic rate

Reduces cerebral blood flow

Reduces ICP

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79
Q

What is the most common cause of spontaneous subarachnoid haemorrhage?

A

Ruptured aneursym

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80
Q

What is a saccular aneurysms?

A

True aneurysms with involvement of all layers of the vessle

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81
Q

What is classic in Lower motor neurone disorders?

A
  • Weak
  • Low tone
    • Fasiculations
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82
Q

What causes botulism?

A

Clostridium botulinum - PWID

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83
Q

How does botulinum toxin work?

A

Cleaves presynaptic protiens involved in vesicle formation and block vesicle docking

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84
Q

What is Lambert Eaton Myasthenic Syndrome?

A

Antibodies to presynaptic calcium channels leading to less vesicle release.

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85
Q

What is strongly associated with Lambert Eaton Myasthenic Syndrome?

A

Small cell carcinoma

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86
Q

What is the most common disorder of the neuromuscular junction?

A

Myasthenia Gravis

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87
Q

What is Myasthenia Gravis?

A

Autoimmune antibodies to acetyl choline receptors

Reduced number of functioning receptors leads to muscle weakness and fatiguability

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88
Q

When do you first start to experiance symptoms in myasthenia gravis?

A

When ACh receptors are reduced to 30% of normal

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89
Q

When are the two peaks of indcidence in myasthenia gravis?

A

Females: 30 - 40

Males: 60 - 80

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90
Q

What are the common clincial features of myasthenia gravis?

A

Weakness typically fluctuating

Extraocular weakness, facial and bulbar weakness

proximal limb weakness

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91
Q

How do you treat myasthenia gravis?

A

Immunomodulating

Steriods/azathioprine

emergency treatment wih plasma exchange or immunoglobulin

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92
Q

How does myasthenia gravis cause death?

A

Respiratory failure (diaphram)

and

Aspiration pneumonia

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93
Q

What are fasiculations?

A

Visible, fast, fine and spontaneous muscle twitch

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94
Q

What is myotonia?

A

Failure of muscle channel relaxation after use

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95
Q

What does myalgia mean?

A

Muscle weakness

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96
Q

What cause myotonia?

A

Problem with the cholride channel

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97
Q

What is Rhabdomyolysis?

A

“Dissolution of muscle”

Damage to skeletal muscle causes leakage of large quantities of toxic intracellular contents into the plasma

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98
Q

What is multiple sclerosis?

A

An inflammatory demyelinating disorder of the central nervous system

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99
Q

When do people with multiple sclerosis usually present?

A

30s and 40s

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100
Q

What are the 6 clincial features of Multiple Sclerosis?

A

Pyramidal dysfunction

Optic neuritis

Sensory Symptoms

Lr Urinary tract dysfunction

Cerebellar and brain stem features

Cognitive impairment

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101
Q

What does pyramidal dysfunction in MS cause?

A

Increased tone

Spasticity

Weakness

Extensors of upper limbs

Flexors of lower limbs

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102
Q

What is Optic neuritis?

A

Painful visual loss lasting 1-2 weeks

common in Multiple Sclerosis

103
Q

What causes Diplopia in MS?

A

Abducens nerve palsy

104
Q

What causes facial weakness in multiple sclerosis?

A

Facial nerve

105
Q

What is internuclear ophthalmoplegia?

A

Medial longitudinal fasciculus resulting in distortion of binocular vision due to failure of adduction

106
Q

What urinary symptoms do people with multiple sclerosis get?

A

Frequency

nocturia

urgency

urge incontinence

retention

107
Q

What is required to diagnose MS?

A

At least 2 episodes suggestive of demyelination

dissemination in time and place

108
Q

What should be on your differential diagnosis list for multiple sclerosis?

A

Vasculitis

Granulomatous disorder

vascular disease

structural lesion

infection

metabolic disorder

109
Q

What are the three principes to treating multiple sclerosis?

A
  1. Acute exacerbations
  2. Symptomatic treatment
    1. Disease modifying therapy
      1.
110
Q

How do you treat a mild , moderate and severe acute exacerbation of multiple sclerosis?

A

Mild - symptomatic treatment

Moderate - Oral steriods

Severe - IV steriods

111
Q

What are the treatment options for spasticity in multiple sclerosis?

A

Physio

Oral medication - Baclofen and tizanidine

Botulinum toxin

Intrathecal baclofen

112
Q

What does intrathecal mean?

A

Via the CSF

113
Q

How can you manage the sensory symptoms of Multiple sclerosis?

A

Anti-convulsant

Anti-depressant

Tens machine

Acupunture

Lignocaine infusion

114
Q

What anti-convulsant is appropriate in multiple sclerosis?

A

Gabapentin

115
Q

What antidepressant drug is usefull in multiple sclerosis?

A

Amitriptyline

116
Q

What three problems do people with multiple sclerosis get with regards to their bladder?

A

Increased tone at bladder neck

Detruser hypersensitivity

Detruser sphyncteric dyssenergia

117
Q

What is detruser sphyncteric dyssenergia?

A

Dyscoordination of the detruser muscles and external sphincter muscles

118
Q

How do you treat unrinary tract dysfunction in multiple sclerosis?

A
  • Bladder drill / diary
  • anti-cholinergics - oxybutynin
  • Desmopressin
    • Catherterisation
      *
119
Q

How do you treat fatigue in patients with Multiple sclerosis?

A

Amantadine

or if sleepy Modafinil

120
Q

What is the first line disease modifying therapy in multiple sclerosis

A

Interferon beta

Glitiramer acetate

Tecfedira

121
Q

What are there second line disease modifying drugs for multiple sclerosis

A

Monoclonal antibody

Fingolimod

122
Q

What is the third line therapy for multiple sclerosis?

A

Mitoxantrone

123
Q

What are interferon Beta and Copaxone?

A

Injectable disease modifying drugs for multiple sclerosis (first line)

124
Q

What effect does interferon Beta and Copaxone on multiple sclerosis?

A

Decrease relapse rate by 1/3

Decrease severity of relapses by 50%

has an effect on disability

125
Q

What is Tecfidera ?

A

Oral agent used in multiple sclerosis

126
Q

What affect does Tecfidera have on Multiple Sclerosis?

A

44 % reduction in relapse rate

127
Q

How does Fingolimod work in the treatment of multiple sclerosis?

A

Sphingosine-1-phosphate modulator

128
Q

What affect does Fingolimond have on multiple sclerosis?

A

>50% reduction in relapse rate

129
Q

What are the features of a large motor fibre nerve damage?

Symptoms

Power

Sensation

Reflexes

A

Symptoms - Weakness, unsteadiness, wasting

Power- reduced

Sensation - normal

Reflexes - Absent

130
Q

What are the features of a large sensory fibre nerve damage?

Symptoms

Power

Sensation

Reflexes

A

Symptoms - Numbness, paraesthesia, unsteadiness

Power - Normal

Sensation - Vibration and joint posistion sense

Reflexes - Absent

131
Q

What are the symptoms of small fibre nerve damage?

Symptoms

Power

Sensation

Reflexes

A

Symptoms - Pain, Dyesthesia

Power - Normal

Sensation - Pin prick and termperature reduced

Reflexes - Present

132
Q

What are the features of autonomic nerve damage?

Symptoms

Power

Sensation

Reflexes

A

Symptoms - Dizziness, Impotence and nausea

Power - Normal

Sensation - Normal

Reflexes - Present

133
Q

What does Radiculopathy mean?

A

Problem with the anterior or posterioir rami

134
Q

How would you describe this pattern of loss?

A

Glove and stocking

135
Q

What is an acute cause of Demyelinating neuropathy?

A

Guillaine Barre Syndrome

136
Q

What is characterisitc of Guillain-Barre Syndrome?

A

Progressive paraplegia over days up to 4 weeks

137
Q

What are the sequence of events during an exacerbation of Guillian-Barre Syndrome?

A

Sensory symptoms

Parapelgia, weakness and pain

138
Q

What are the 6 broad families of axonal neuropathies?

A

Idiopathic

Vaculitic

Paraneoplastic

Infections

Drugs/toxins

Metabolic

139
Q

What infections can cause axonal neuropathies?

A

HIV

Syphillis

Lyme

Hepatitis B/C

140
Q

What drugs/toxins can cause Axonal Neuropathies?

A

Alcohol

Amiodarone

Phenytoin

Chemotherapy

141
Q

What are the metabolic causes of Axonal Neuropathies?

A

Diabetes

B12 folate deficiencies

Hypothyroidism

Chronic Uremia

Porphyria

142
Q

What are the (a) chronic and (b) acute causes of autonomic neuropathy?

A

Chronic - Diabetes, Amyloidosis, Hereditary

Acute - GBS, Porphyria

143
Q

How can you treat Vasculitic axonal peropheral neuropathy?

A

Pulsed IV methylprednisolone + cyclophosphamide

144
Q

Do cases on Peripheral lecture

A

DO IT

145
Q

What is characterisitc of Non REM sleep?

A

Partial muscle relaxation

Reduced cardiac output

Snychronised rythmic EEG

Non-narrative dreams

146
Q

What is characterisitc of REM sleep?

A

Mostly at the end of the night

EEG shows fast activity similar to being awake

Atonic muscles

Cerebral blood flow increased

Impaired thermal regulation

Narrative dreaming

147
Q

How do you investigate narcolepsy?

A

Overnight polysomnography

148
Q

What can you measure in the CSF to help with a diagnosis of Narcolepsy?

A

CSF hypocretin

149
Q

What CSF hypocretin level is suggestive of narcolepsy?

A

less than 110pg/ml

150
Q

What is nociceptive pain?

A

An appropriate physiological response to painful stimuli via an intact nervous system

151
Q

What is neuropathic pain?

A

An inappropriate response caused by dysfunction in the nervous system

152
Q

What does allodynia mean?

A

Pain from stimulus that is not normally painful

153
Q

What does hyperalgesia mean?

A

More pain than expected from a painful stimulus

154
Q

How do topical analgesics affect pain?

A

Reduce pain impusles transmitted by A-Delta-fibres and C-fibres

155
Q

How do brain tumours commonly present?

A

Progerssive neurolgical deficit 70%

Motor weakness 50%

headache 50%

sexiures 25%

156
Q

What is classical for a headache caused by a brain tumour ?

A

Worse in the morning

Wakes them up when they are asleep

Worse with coughing and leaning forward

157
Q

Learn this

A
158
Q

What are the four grades of Astrocytic tumors?

A

I Pilocytic

II Low grade astrocytoma

III Anaplastic astrocytoma

IV Glioblastoma

159
Q

What is a Grade 1 astrocytoma?

A

Truly benign low growing legion

160
Q

Who gets grade 1 astrocytomas?

A

Children and young adults

161
Q

How do you treat grade 1 astrocytomas?

A

Surgery - Curative

162
Q

What is this ?

A

Pilocytic Astrocytoma grade 1

163
Q

Where do people normally get “low Grade” astrocytomas?

A

Temporal Lobe

Posterior Frontal lobe

Anterior Parietal lobe

164
Q

How do low grade astrocytomas nomrally present ?

A

Seizures

165
Q

What are the treatment options for grade II astrocytomas?

A

No treatment

Raidation

Chemotherapy

Combined Radiation and Chemotherapy

Plus or minus surgery

166
Q

What factors suggest a poor prognosis in Grade II astrocyomas?

A
  • Age >45
  • Low performance score
  • tumor >6cm
  • Tumour crossing midline
    • Incomplete resection
      *
167
Q

What is Glioblastoma Multiform?

A

Stage 3 / 4 astrocytoma

Most common primary tumor

median survival < 1yr

168
Q

What is an Anaplastic astrocytoma?

A

Grade III/IV malignant astrocytoma

Median survival 2 years

169
Q

How do you treat grade 3 and 4 astrocytomas?

A

Surgery - not curative but can help symptoms

Post operative radiotherapy

170
Q

Where do people get olidodendroglial tumors and at what age?

A

Frontal lobes

Adults 25-45 yrs old

171
Q

How do people with Oligodendroglial tumors present ?

A

With seizures

172
Q

How do you treat Oligodendroglial tumors ?

A

Chemothrapy + surgery

173
Q

What is the median surivial for Oligodendroglial tumors?

A

10 years

174
Q

What are the brain tumor red flags for adults and children?

A

Adults

Headaches that wake you +/- vomiting

New neurological deficit incl seizures

Children

Tiptoeing, ataxia and vomiting

175
Q

What are the red flags for headaches?

A
  • New onset headache over aged 55
  • Known/previous malignancy
  • Immuno-suppressed
  • Early morning headache
  • Exacerbated by valsalva
176
Q

What exaerbating symptoms should you ask about in headaches

A

Posture

Valsalva

177
Q

How do you diagnose a migraine?

A

Pain that is 2 Of:

  • Moderate/severe
  • Unilateral
  • Throbing
  • Worst on movement

And 1 of:

  • Photophobia
    • Phonophobia
178
Q

What is the pathophysiology of Migraines?

A

Stress triggers changes in the brain releasing serotonin

Blood vessels constrict and dilate

Chemicals including substance P irritate the nerves and blood vessels

179
Q

What is an Aura when refering to a migraine?

A

Fully reversible visual, sensory , motor or language symptom

180
Q

What are common triggers for migraines ?

A

Sleep

Dietary

Stress

Hormonal

Physical exertion

Headache diary can help identify triggers

181
Q

How do you treat a migraine?

A

Aspirin

Naproxen

Ibuporfen

ASAP ( sooner the better)

182
Q

What are Triptans?

A

5HT agonist used to treat migraines

Take at the start of the headache

Sublingual

183
Q

Whats the problem with triptans?

A

Not sure if they are really that great and they are pretty expensive

184
Q

When would you consider prophylaxic treatment for migraines ?

A

More than 3 attacks per month

Very severe attacks

185
Q

What can be used as prophylaxis for migraines?

A

Propanolol

Topiramate

186
Q

What prophylatic affect does propanolol have on migraines?

A

Reduces frequency by 60-80%

187
Q

What are the contraindications for propanolol?

A

Contraindicated in asthma and heart failure

188
Q

What is the downside to using Topiramate as a prohylaxis for migraines

A

It takes a while to start working

Many side effects:- weight loss, paraesthesia, impaired concentration enzyme inducer

189
Q

What are trigeminal autonomic cephalgias?

A

Group of primary headache disorders characterised by unilateral trigeminal distribution pain that occurs with prominent ipsilateral cranial autonomic features.

190
Q

Give examples of Ipsilateral cranial autonomic features

A

Ptosis
Miosis

Nasal stuffiness

Nausea/vomiting

Tearing

Eye lid oedema

191
Q

What are the 4 types of trigeminal autonomic cephalgias?

A

Cluster

Paroxsymal hemicrania

Hemicrania continua

SUNCT

192
Q

Who gets cluster headaches?

A

People in their 30s and 40s

193
Q

When do people usually get cluster headaches?

A

Around sleep time

194
Q

What are the features of cluster headaches

How long do they last and how frequent are they

A

Severe unilateral headache

Lasting 45-90 mins

1-8 time a day for weeks to months

195
Q

How do you treat cluster headaches?

A

High flow Oxygen for 20 mins

Sub cut sumatriptan 6mg

Steroids reducing course over 2 weeks

196
Q

What can be used as a prophylaxis for Cluster headaches?

A

Verapamil

197
Q

Who gets paroxysmal hemicrania?

A

Elderly 50s-60s

198
Q

What are the features of paroxysmal hemicrania?

How long does it last?

How frequent ?

A

Severe unilateral headache with unilateral autonomic features

10-30 mins

1-40 times a day

199
Q

How do you treat paroxysmal hemicrania?

A

Responds well Indomethicin

200
Q

What are the main differences between Paroxysmal Hemicrania and cluster headaches?

A

Paroxysmal Hemmicranias have a shorter duration and are more frequent than cluster headaches

They also respond really well to Indomethicin

201
Q

What does SNUCT stand for?

A

S - short lied (15-120 seconds)

U - unilateral

N - neuralgiaform headache

C - conjunctival injections

T - tearing

202
Q

How do you treat SUNCT?

A

Lamotrigine

or

Gabapentin

203
Q

What investigations would you do for someone with new onset unilateral cranial autonomic features?

A

MRI brain

MR angiogram

204
Q

Who gets trigeminal neuralgia?

A

Older people >60

Woman

205
Q

What triggers trigeminal neuralgia ?

A

Touch - usually V2/3

206
Q

What are the features of trigeminal neuralgia?

Duration ?

Frequency?

A

Severe stabbing unilateral pain

1-90seconds

10 - 100 times a day

few weeks to months before remission

207
Q

how do you treat trigeminal neuralgia?

A

Carbamazepine

Gabapentin

Phenytoin

Baclofen

Surgical - Abalation vs decompression

208
Q

When is a CT scan appropriate in someone who presents with falls/seziures ?

A
  • Suspected skull fracture
  • Deterioratting GCS
  • Focal signs
  • Head injury with seizure
    • Failure to be GCS 15/15 4hrs after arrival
209
Q

If it is your 1st seziure how long must you wait before you can drive again?

A

6 months

210
Q

If you have epilepsy how long must you wait before driving again?

A

1 year

or

3 years during sleep

211
Q

What conditions are commonly confused with eplilepsy ?

(i.e should be on your differential diagnosis list)

A

Syncope

Non-epilepti attack disorder

Panic attacks/Hyperventilation

Sleep phenomena

212
Q

What is Epilepsy?

A

A tendency to recurrent, usually spontaneous eplieptic seizures

213
Q

What is a an eplieptic seizure?

A

Abnormal synchronisation of neuronal activity

Usually excitaory with high frequency action potentials

214
Q

What are the 7 types of eplileptic seizures?

A

Partial

Simple

Complex

Generalised

Absence

Myoclonic

Atonic

Tonic

Tonic Clonic

215
Q

When does primary generalized epilepsy usually present ?

A

Childhood or early teens

216
Q

How do you treat primary generalized epilepsy?

A

Sodium Valproate

or

Lamotrigine

217
Q

What is important to remember about Sodium Valproate?

A

Its teratogenic

218
Q

What is focal onsent epilepsy?

A

Epilepsy with an underlying stuctural cause

219
Q

How do you treat Focal onset epilepsy?

A

Carbamazepine

Iamotrigine

220
Q

What are the symptoms of Focal onset epilepsy?

A

Complex partial seizures with hippocampal sclerosis

221
Q

How effective are Anti-epiletic drugs (AEDs)

A

55% seizure free on monotherapy

222
Q

What can be used as an anticonvulsant during an acute seizure?

A

Phenytoin

223
Q

What are the two best anti-convulsant?

A

Lamotrigine

Levetiracetam

224
Q

What is important to remeber about anti-convulsants?

A

Interfere with the oral contraceptive pill

225
Q

What are the the three types of spontaneous intracranial haemorrhage?

A

Subarachnoid haemorrhage

Intracerebral haemorrhage

Intraventricular haemorrhage

226
Q

What is a subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space

227
Q

What is the mortality of subarachnoid haemorrhages?

A

45% at 1 month

228
Q

How does a subarachnoid heamorrhage present?

A

Sudden onset:

  • Severe headache
  • Collapse
  • Vomiting
  • Neck pain
    • Photophobia
229
Q

What is a good investigation for looking for brian aneurisims?

A

Cerebral Angiography

230
Q

What is the risk of a subarachnoid heamorrage re-bleeding at

(a) 2 weeks
(b) 6 months

A

2 weeks - 20%

6 months - 50%

231
Q

After someone has a subarachnoid heamorrage what 3 things do you have to look out for ?

A

Delayed Ischaemia

Hydrocephalus

Hyponaturaemia

232
Q

How do you treat delayed ischaemia ?

A

Nimodipine

233
Q

How do you treat hydrocephalus?

A

CSF draingage

234
Q

What is an intracerebral haemorrhage?

A

Bleeding into the brain parenchyma

235
Q

What is the most common cause of Intracerebral haemorrhages?

A

Hypertension - 50%

236
Q

How do intracerebral haemorrhages present?

A

Headache

Focal neurological deficit

Decreased conscious level

237
Q

How do you treat intracerebral haemorrahge?

A

Surgical evacuation of haematoma

238
Q

What is a Intraventricular haemorrhage and how does it happen?

A

Bleeding into a ventricle

Occurs with rupture of a subarachnoid or intracerebral bleed into a ventricle

239
Q

What are the clincial features of a upper motor neurone lesion?

A

Increased tone

Hyper reflexia

Muscle wasting

No fasiculation

240
Q

What are the clinical features of a lower motor neurone lesion?

A

Decreased tone

Muscle wasting

Fasciculation

Diminished reflexes

241
Q

What do the spinothalamic tracts do?

A

Pain

temperature

crude touch

242
Q

Do the spinothalamic trats govern the ipsilateral or contralateral side of the body?

A

Contralateral

243
Q

What do the Dorsal columns of the spinal cord do?

A

Fine touch

Proprioception

Vibration

244
Q

What is motor neuron disease?

A

untreatable and rapidly progressive neurodegenerative condition

245
Q

How does motor neurone disease progress?

A

Starts focal and then spreads continously untill generalzed paresis

246
Q

What is the average survival time of Motor Neuron disease?

A

3 years

247
Q

Is motor neuron disease familial or sporadic?

A

10% familial , 90% sporadic

248
Q

What is Amyotrophic lateral sclerosis?

A

It is the most common subtype of motor neuron disease

249
Q

What is the most common age range for motor neuron disease?

A

50-75 year

250
Q

Where does Motor Neuron Disease usually start?

A

Normally extremeties ( mostly upper)

251
Q

What things must you warm someone with parkisnons about when they are first starting on Levodopa?

A

Impulse control disorders made worse

Sleepiness

Psychotic symptoms

252
Q

What is the frist lime pharmacological treatment for alzehmiers ?

A

Acetlylholinesterase inhibitors

Donepezil

Galantamine

Rivastigmine

253
Q

What is the second line pharmacological treatment for alzehimers?

A

Memantine

NMDA antagois

Neurology (8 decks)

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