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Clinical Neurology Flashcards

1
Q

what immune cells are abundant in the subarachnoid space in pyogenic meningitis?

A

neutrophils

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2
Q

what is encephalitis?

A

inflammation of the brain

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3
Q

what is meningitis?

A

inflammation of the meninges

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4
Q

what is meningoencephalitis?

A

inflammation of the brain and meninges

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5
Q

what is myelitis?

A

inflammation of the spinal cord

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6
Q

what time of year is viral meningitis most common?

A

late summer/autumn

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7
Q

how could you diagnose suspected viral meningitis?

A

viral stool culture
throat swab
CSF PCR

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8
Q

what is the treatment for viral meningitis?

A

generally self limiting

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9
Q

what is the most common type of virus to cause viral meningitis?

A

enteroviruses

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10
Q

what is the treatment for viral encephalitis caused by herpex simplex?

A

IV high dose aciclovir

within 6 hours of admission

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11
Q

what is the treatment for viral encephalitis?

A

IV high dose aciclovir

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12
Q

what is meningismus?

A

a triad of photophobia, headache and neck stiffness

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13
Q

why does meningismus occur?

A

caused by irritation of the meninges

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14
Q

what are the 3 main investigations you would do for suspected viral encephalitis?

A

lumbar puncture
electroencephalogram
MRI

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15
Q

what pre-emptive treatment should you start for suspected viral encephalitis? (even before investigations)

A

IV aciclovir

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16
Q

what are the 3 most common bacterial causes of meningitis in neonates?

A

listeria
group B strep
E. coli

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17
Q

what is the most common bacterial cause of meningitis in children?

A

Haemophilus influena

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18
Q

what is the most common bacterial cause of meningitis in 10-21 year olds?

A

meningococcal

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19
Q

what are the most common bacterial causes of meningitis in the 21+ age group?

A

pneumococcal (top)

meningococcal

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20
Q

what are the most common bacterial causes of meningitis in the the elderly?

A

pneumococcal (top)

listeria

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21
Q

what are the most common causes of bacterial meningitis in immunocompromised patients?

A

listeria
pneumococcal
meningococcal
gram negative rods

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22
Q

what are the most common causes of bacterial meningitis in patients with neurosurgery or opened head trauma?

A

staph

gram negative rods

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23
Q

what is the most common cause of bacterial meningitis in patients with a fracture of the cribriform plate?

A

pneumococcal

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24
Q

what are the most common causes of bacterial meningitis in patients with a basilar skull fracutre?

A

pneumococcal
haemophilus influenza
group A strep

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25
Q

what are the most common causes of bacterial meningitis in patients with a CSF shunt?

A

staph
gram negative rods
P. acnes

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26
Q

what are the 3 main potential origins of the bacteria causing meningitis?

A
  1. nasopharyngeal colonisation
  2. direct spread (ie parameningeal foci or skull fracture)
  3. remote foci of infection
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27
Q

what cause of meningitis occurs specifically in patients with AIDS?

A

cryptococcus neoformans (fungal)

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28
Q

how does bacteria from the nasopharynx gain access to the brain?

A

via bloodstream

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29
Q

what bacteria causes meningococcal meningitis?

A

neisseria meningitis

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30
Q

what causes the symptoms of meningococcal meningitis?

A

endotoxin from the bacteria

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31
Q

what is the most common cause of meningitis in children under 4 years old?

A

H. influenzae B

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32
Q

how many types of haemophilus influenza are there?

A

6

A-F

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33
Q

what type of vaccine is available against haemophilus influenza B?

A

conjugated vaccine

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34
Q

what bacterial causes pneumococcal pneumonia?

A

Strep. pneumoniae

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35
Q

what kind of bacteria is listeria?

A

gram positive bacilli

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36
Q

what is the antibiotic of choice for listeria meningitis?

A

IV ampicillin/amoxicillin

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37
Q

what are the 3 main clinical signs of bacterial meningitis?

A

fever
stiff neck
alteration on consciousness

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38
Q

what is CSF pleocytosis?

A

increased cell count in the CSF

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39
Q

what is CSF leukocytosis?

A

increased white blood cell count in the CSF

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40
Q

what are the 4 investigations you should do for suspected bacterial meningitis?

A

blood cultures
throat swab
blood EDTA for PCR
lumbar puncture

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41
Q

what cells are found in the CSF in viral, bacterial and TB causes of meningitis?

A

viral and TB- lymphocytes

bacterial- polymorphs

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42
Q

will you be able to find a gram stain in the CSF in viral, bacterial and TB causes of meningitis?

A

viral- no
bacterial- yes
TB- yes or no

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43
Q

will you be able to find a bacterial antigen in the CSF in viral, bacterial and TB meningitis?

A

viral- no
bacterial- yes
TB- yes or no

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44
Q

what is the protein within the CSF like in viral, bacterial and TB meningitis?

A

viral- normal or slightly high
bacterial- high
TB- high or very high

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45
Q

what is the glucose within the CSF like in viral, bacterial and TB meningitis?

A

viral- normal
bacterial- less than 70% of blood glucose
TB- less than 60% of blood glucose

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46
Q

describe the CSF of ‘aseptic meningitis’?

A

low number of WBC
minimally elevated protein
normal glucose

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47
Q

what imaging should be performed on all patients with suspected bacterial meningitis with papilloedema or focal neurological signs?

A

CT scan

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48
Q

what are the 6 criteria to undergo a CT prior to lumbar puncture?

A
  • immunocompromised
  • history of CNS disease
  • new onset seizure
  • papilloedema
  • abnormal level of consciousness
  • focal neurological deficit
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49
Q

when is a lumbar puncture not indicated for a patient with suspected bacterial meningitis?

A
  • clear contraindication

- confident clinical diagnosis of meningococcal infection with a typical meningococcal rash

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50
Q

what is the empiric antibiotic therapy for suspected bacterial meningitis?

A
  • IV ceftriaxone

- add IV ampicillin/amoxicillin if listeria suspected

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51
Q

what is the empiric antibiotic therapy for suspected bacterial meningitis in a patient with a penicillin allergy?

A
  • IV chloamphenicol and IV vancomycin

- IV co-trimoxazole alone if listeria suspected

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52
Q

in addition to antibiotics, what other medication should you give to all patients with suspected bacterial meningitis?

A

IV corticosteroids

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53
Q

what are the contraindications to giving steroids in suspected bacterial meningitis?

A

post-surgical meningitis
severe immunocompromise
meningococcal or septic shock
patients who are hypersensitive to steroids

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54
Q

what are the 3 options for contact prophylaxis for bacterial meningitis?

A

rifampicin
or ciprofloxacin (not in children)
or ceftraixone

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55
Q

what is the pathological hallmark of parkinsons disease?

A

dopaminergic neuron loss in the substantia nigra of the basal ganglia and Lewy body pathology

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56
Q

what are the 4 main classes of movement disorders?

A

pyramidal/UMN features
hyperkinetic
hypokinetic
ataxia

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57
Q

where within the brain is the injury if there are pyramidal/UMN features?

A

corticospinal/pyramidal tract

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58
Q

where within the brain is the injury if there are hyperkinetic features?

A

basal ganglia (extrapyramidal)

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59
Q

where within the brain is the injury if there are hypokinetic features?

A

basal ganglia (extrapyramidal)

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60
Q

where within the brain is the injury if there is ataxia?

A

cerebellum

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61
Q

what are the 3 main features of parkinsonian syndrome?

A
  • rigidity
  • bradykinesia/akinesia
  • resting tremor
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62
Q

what is dystonia?

A

prolonged muscle spasms and abnormal postures

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63
Q

what is chorea?

A

movements flowing irregularly fro one body segment to another- looks like dancing

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64
Q

what is ballismus?

A

chorea but the movements have a larger amplitude

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65
Q

what are the broad 2 subtypes of parkinsons disease?

A

tremor dominant PD

non-tremor dominant PD

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66
Q

compare tremor dominant and non-tremor dominant PD in terms of motor symptoms?

A

tremor dominant PD has a relative absence of other motor symptoms
non-tremor dominant has other motor symptoms

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67
Q

compare tremor dominant and non-tremor dominant PD in terms of rate of progression and functional disability?

A

tremor dominant PD has a slower rate of progression and less functional disability

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68
Q

what special sense can be affected in parkinsons disease?

A

smell

-hyposmia or anosmia

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69
Q

what sleep disorder can occur in parkinsons disease?

A

rapid eye movement sleep behaviour

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70
Q

what investigation is needed to diagnose rapid eye movement sleep behaviour?

A

overnight polysomnography with electromyogram

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71
Q

what is the requirement for the diagnosis of parkinsonian syndrome?

A

muscular rigidity
4-6Hz resting tremor
postural instability (not caused by primary visual, vestibular, cerebellar or proprioceptive dysfunction)

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72
Q

what are lewy bodies?

A

misfolded alpha-synuclein, which aggregate

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73
Q

what is the greatest risk factor for parkinsons disease?

A

age

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74
Q

what is the classic type of rigidity seen in parkinsons?

A

cogwheel rigidity

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75
Q

what can happen to the voice of a patient with parkinsons?

A

hypophonia

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76
Q

what can happen to the handwriting of a patient with parkinsons?

A

progressively smaller handwriting

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77
Q

during active movement what happens to a parkinsons tremor?

A

goes away

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78
Q

what is the difference between rigidity and spasticity?

A

spasticity is velocity dependent

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79
Q

describe the gait of a patient with parkinsons?

A

slow, short shuffling steps

slow turns

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80
Q

what is asthenia?

A

abnormal weakness or lack of energy

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81
Q

what are the 3 investigations for parkinsons disease?

A
  • structural brain imaging
  • possibly dopamine functional imaging
  • levodopa challenge
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82
Q

compare an essential tremor to a parkinsons tremor?

A

essential tremor is symmetrical, postural or kinetic with a higher frequency

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83
Q

how does an essential tremor respond to alcohol?

A

goes away

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84
Q

what is the core triad of features which make up multi system atrophy?

A

dysautonomia
cerebellar features
parkinsonism

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85
Q

what is the most common cause of degenerative parkinsonism?

A

multi-system atrophy

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86
Q

when is the onset of fragile X-tremor ataxia syndrome?

A

late onset, above 50 y/o

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87
Q

how do you calculate the cerebral perfusion pressure?

A

mean arterial pressure - intracranial pressure

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88
Q

after head injury what should you aim to keep the cerebral perfusion pressure?

A

above 60mmHg

ie MAP needs to be above 80mHg and ICP needs to be below 20mmHg

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89
Q

what is the normal adult intracranial pressure?

A

9-11 mmHg

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90
Q

what physical finding can be seen in an anterior cranial fossa fracture?

A

panda eyes

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91
Q

what physical finding can be seen in a middle cranial fossa fracture?

A

battle sign over mastoid area

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92
Q

what is the name for the cerebellum herniating through the foramen magnum?

A

tonsillar herniation

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93
Q

what can happen to the pupil when the ICP increases enough to compress the third cranial nerve?

A

dilated pupil

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94
Q

what is the lowest GCS you can get?

A

3

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95
Q

what is the highest GCS you can get?

A

15

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96
Q

how do you elicit pain to calculate the GCS?

A

press on medial eyebrow or supraorbital nerve

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97
Q

when calculating the GCS, if the patient flexes to pain, what can you assume is working?

A

basal ganglia

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98
Q

when calculating the GCS if the patient extends to pain, where is the damage?

A

midbrain

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99
Q

what 3 things must be true for the definition of a coma?

A

patient does not open eyes
patient does not obey comands
patient does not speak

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100
Q

what is the GCS of a patient in a coma?

A

8 or less

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101
Q

in trauma, when should you request a CT scan?

A

1) skull fracture

2) not orientated (GCS

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102
Q

what is the normal pO2?

A

13-15kPa

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103
Q

what is the normal pCO2?

A

4-4.5kPa

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104
Q

what osmotic drug can be given to reduce ICP?

A

mannitol or hypertonic saline

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105
Q

what are the 3 main late effects of head injury?

A

epilepsy
CSF leak (nose, middle ear)
cognitive problems

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106
Q

if there is CSF leak into the middle ear, what type of hearing loss might occur?

A

conductive hearing loss

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107
Q

what are the 4 primary brain tumours which commonly metastasise to the brain?

A

breast
lung
melanoma
kidney

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108
Q

what grade of astrocytoma is a glioblastoma?

A

glioblastoma equal astrocytoma grade IV

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109
Q

what is another name for tonsillar herniation through the foramen magnum onto the brain stem?

A

coning

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110
Q

what causes tonsillar herniation or coning?

A

increased intracranial pressure

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111
Q

why must you avoid taking a lumbar puncture in patients with increased intracranial pressure?

A

reduces the pressure below the brainstem -might cause herniation

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112
Q

the loss of what particular nerves causes failure of breathing after a tonsillar herniation/coning?

A

loss of C3,4,5 - diaphragm

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113
Q

what is the most common tumour in the cerebellum of a child?

A

medulloblastoma

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114
Q

why might hydrocephalus occur due to reduces CSF absorption?

A

scarring of arachnoid granulations secondary to inflammation (meningitis etc)

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115
Q

what is hydrocephalus?

A

increased intracranial pressure due to build up of CSF

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116
Q

what is the difference between missile and non-missile head injury?

A

missile- penetrating foreign object

non-missile- non-penetrating

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117
Q

why is it important to determine whether the missile head injury was low or high velocity?

A

with high velocity injuries there is also a pressure wave which radiates out causing damage in a further radius

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118
Q

what causes injury in a non-missile head injury?

A

sudden acceleration or deceleration of the head causing brain to move within the cranial cavity

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119
Q

what is a coup injury and what is a contracoup injury?

A

coup injury- at point of impact

contracoup injury- diametrically opposite point of impact

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120
Q

which is more serious- coup or contracoup injury?

A

contracup injury

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121
Q

in the timeline of a head injury, when does diffuse axonal injury occur?

A

at moment of injury

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122
Q

what scale represents the extent of diffuse axonal injury?

A

glasgow coma scale

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123
Q

what protein accumulates in diffuse axonal injury?

A

amyloid precursor protein

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124
Q

what are the 5 main causes for diffuse axonal injury?

A 
trauma
raised ICP
hypoxia
progression of dementia
progression of inflammatory disease
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125
Q

what can you do to prevent extensive diffuse axonal injury following traumatic head injury?

A

medically induce a coma

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126
Q

what artery is usually involved in a traumatic extradural haematoma?

A

middle meningeal artery

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127
Q

what is a traumatic extradural haematoma usually associated with?

A

fracture of temporal or parietal bone

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128
Q

in an extradural haematoma, what kind of herniation can occur?

A

subfalcine herniation

under falx cerebri

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129
Q

what is the normal ICP value?

A

5-13 mmHg

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130
Q

what is a tentorial herniation?

A

where the medial aspect of temporal lobes herniate over the tentorium cerebelli

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131
Q

what cranial nerve is particularly susceptible to tentorial herniation?

A

CN III

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132
Q

what is a transcalvarium herniation?

A

when brain herniates through any defect in the dura and skull

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133
Q

what are the 4 main clinical signs of rasied intracranial pressure?

A

papilloedema
nausea and vomiting
headache
neck stiffness

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134
Q

why do patients with a brain tumour often have a headache in the morning which gets better of the course of the day?

A

CO2 retention in the night causes brain to increase in size and so pushes against meninges, throughout the day the CO2 is blown off and so size of brain decreases

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135
Q

what patient group is most susceptible to brain abscesses?

A

IVDUs

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136
Q

what is the cause of vasogenic cerebral oedema?

A

defect in blood brain barrier

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137
Q

what is the most common type of cerebral oedema?

A

cytotoxic oedema

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138
Q

what is the cause of cytotoxic cerebral oedema?

A

ischaemia

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139
Q

what is the cause of hydrostatic cerebral oedema?

A

hypertension within cerebral blood vessels

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140
Q

what is the cause of interstitial cerebral oedema?

A

acute obstructive hydrocephalus

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141
Q

what is the cause of hypo-osmotic cerebral oedema?

A

large reduction in serum osmolality

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142
Q

what type of oedema is seen in hypertensive encephalopathy?

A

hydrostatic cerebral oedema

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143
Q

which part of the temporal bone does the middle meningeal artery course under?

A

squamous part of temporal bone

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144
Q

nontreated, nonfatal subdural haematomas are demarcated from the underlying brain by what?

A

neomembrane

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145
Q

what blood vessels cause subdural haemorrhages- arteries or veins?

A

veins (bridging veins that extend from brain into subdural space)

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146
Q

why is there progressive focal neurological signs/symptoms in a chronic subdural haemorrhage?

A

because venous blood leaks out slowly eventually building up pressure

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147
Q

what is he most common cause of bradykinesia?

A

parkinsons disease

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148
Q

if dementia procedes the motor symptoms of parkinsons disease or is present within the first year, what is the disease termed instead?

A

dementia with Lewy bodies

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149
Q

what is multiple sclerosis?

A

an inflammatory demyelinating disorder of the central nervous system

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150
Q

what are the 4 types of MS?

A
  1. relapsing and remitting
  2. secondary progressive
  3. progressive relapsing
  4. primary progressive
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151
Q

what happens to tone in pyramidal dysfunction?

A

increased tone

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152
Q

in pyramidal dysfunction do muscles become rigid or spastic?

A

spastic

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153
Q

in pyramidal dysfunction, are the flexors or extensors weak in the upper limbs?

A

extensors

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154
Q

in pyramidal dysfunction, are the flexors or extensors weak in the lower limbs?

A

flexors

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155
Q

what is dysarthria?

A

unclear articulation of speech

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156
Q

where is the problem in internuclear ophthalmoplegia?

A

medial longitudinal fasciculus

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157
Q

in internuclear ophthalmoplegia, is there a failure of abduction of adduction?

A

adduction

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158
Q

in internuclear ophthalmoplegia, is there nystagmus in the abducting or adducting eye?

A

abduction eye

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159
Q

what is the main symptoms of internuclear ophthalmoplegia?

A

diplopia

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160
Q

what 3 things can be used for fatigue/sleepiness in MS?

A

amantadine
modafinil (if sleepy)
hyperbaric oxygen

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161
Q

what is the name of the criteria for diagnosing MS?

A

McDonald criteria

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162
Q

what may be found in the CSF of a patient with MS?

A

oligoclonal bands

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163
Q

what is the treatment for an acute exacerbation of MS if mild?

A

symptomatic treatment

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164
Q

what is the treatment for an acute exacerbation of MS if moderate?

A

PO steroids

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165
Q

what is the treatment for an acute exacerbation of MS if severe?

A

IV steroids/ admit

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166
Q

what are the treatment options for spasticity in MS?

A

physiotherapy
oral baclofen or tizanidine
botulinum toxin
intrathecal baclofen/phenol

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167
Q

what are the treatment options for sensory symptoms in MS?

A 
anti-convulsant eg gabapentin
anti-depressant eg amitriptyline
tens machine
acupuncture
lignocaine infusion
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168
Q

what can be used for detrusor hypersensitivity in MS?

A

anticholinergic eg oxybutynin

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169
Q

what type of MS does relapsing and remitting MS usually turn into?

A

secondary progressive MS

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170
Q

what are the first line disease modifying agents for MS?

A

interferon beta
copaxone
tecedria

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171
Q

what is the first line agent for relapsing and remitting MS?

A

tecfidera

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172
Q

what is the main side effect of tecfidera?

A

bowel disturbance

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173
Q

what are the second line disease modifying agents for MS?

A

monocloncal sntibody

fingolimod

174
Q

what are the major side effects of fingolimod?

A

cardiac problems

175
Q

what severe side effect is associated with tysabri? (a drug use in severe relapsing and remitting MS)

A

progressive multifocal leukoencephalopathy

176
Q

what is muscle tone like in REM sleep?

A

low muscle tone

177
Q

do you tend to dream in REM or non-REM sleep?

178
Q

what is the length of a normal circadian rhythm?

179
Q

what is seasonal affective disorder?

A

when people have normal mental health throughout most of the year but experience depressive symptoms at the same time each year, usually winter

180
Q

what is the most common REM parsomnia?

A

Rapid eye movement Behaviour Disorder (RBD)

181
Q

what happens in RBD? (rapid eye movement behaviour disorder)

A

atonia is absent so sleeper can act out dreams, often violently and injuring themselves and bed partner

182
Q

are sleep terrors a REM or non-REM parasomnia?

A

non-REM parasomnia

183
Q

are restless legs or periodic limb movement syndrome REM or non-REM parasomnias?

A

non-REM parasomnias

184
Q

what is sleep paralysis?

A

a phenomenon where the brain holds the body in paralysis but we are returning to conscious

185
Q

what is a common vision which accompanies sleep paralysis?

A

an old hag at the edge of the bed

186
Q

what is narcolepsy?

A

a neurological disorder with a decreased ability to regulate sleep cycles

187
Q

what are the 5 main symptoms of narcolepsy?

A 
excessive daytime sleepiness
cataplexy
sleep paralysis
REM behavioural disorder
hypnagogic hallucinations
188
Q

what is cataplexy?

A

loss of muscle tone giving appearance of fainting, though patient is completely conscious

189
Q

what is cataplexy usually brought on by?

A

strong emotion

190
Q

what is the name for hallucinations which occur before you go to sleep? (abnormal)

A

hypnagogic hallucinations

191
Q

what is the name for hallucinations which occur as you wake up? (normal)

A

hypnapompic hallucinations

192
Q

what 3 investigations can help with diagnosing narcolepsy?

A
  • overnight sleep study
  • multiple sleep latency test
  • lumbar puncture
193
Q

what can be seen on lumbar puncture of a patient with narcolepsy?

A

low levels of hypocretin (a neuropeptide which regulates wakefulness)

194
Q

what is a multiple sleep latency test?

A

measures time elapsed from the start of a daytime nap to first signs of sleep (sleep latency)

195
Q

what are the 2 classes of insomnia?

A

reactive

psychophysiological

196
Q

why does reactive insomnia occur?

A

during a time of stress/anxiety

197
Q

why does psychophysiological occur?

A

loss of ability to fall asleep easily- beds are no longer associated with only sleep

198
Q

what is the most common subtype of motor neurone disease?

A

amylotrophic lateral sclerosis (ALS)

199
Q

is increased tone an upper or lower motor sign?

200
Q

is weakness an upper or lower motor sign?

201
Q

is babinski’s sign an upper or lower motor sign?

202
Q

is a spastic gait an upper or lower motor sign?

203
Q

is hyperreflexia an upper or lower motor sign?

204
Q

are fasciculations an upper or lower motor sign?

205
Q

are absent or reduced deep tendon reflexes an upper or lower motor sign?

206
Q

does amylotrophic lateral sclerosis have upper and motor lower neurone features?

A

both upper and lower motor neurone features

207
Q

does primary lateral sclerosis have upper and lower motor lower neurone features?

A

upper motor neurone features

no lower

208
Q

does progressive muscular atrophy have upper and lower motor neurone features?

A

lower motor neurone features

upper motor neurone feautres can be sublinical

209
Q

does ALS-frontotemporal dementia have upper and lower motor neurone features?

A

both upper and lower motor neurone features

210
Q

what is the prognosis for amylotrophic lateral sclerosis and ALS-frontotemporal dementia

211
Q

what is the prognosis for primary lateral sclerosis (a subtype of MND)?

212
Q

what is the prognosis of progressive musclar atrophy (a subtype of MND)?

213
Q

what pattern of atrophy is typically seen in ALS?

A

split hand syndrome

wasting of thenar muscle group, relative preservation of hypothenar muscle group

214
Q

what is the hoffmann reflex?

is this normal?

A

tapping of the distal phalynx of the 3/4th finger, causing the distal phalynx of the thumb to flex (can be normal)

215
Q

what is the snout reflex?

A

tapping the midline of closed lips, causing lips to purse (abnormal)

216
Q

what is pseudobulbar affect?

A

uncontrollable episodes of crying/laughing in response to something which should not cause that much emotion
may be mood-incongruent

217
Q

is pseudobulbar affect an upper or lower motor sign?

218
Q

what bacteria produces botulinum toxin?

A

clostridium botulinum

219
Q

how does botulinum toxin cause muscle weakness?

A

breaksdown proteins involved in vesicle formation, so reduces neurotranmitter release

220
Q

what is lambert eaton myasthenic syndrome?

A

autoantibodies to voltage gated calcium channels on presynaptic membrane, reduced neurotransmitter release

221
Q

what underling cancer is strongly associated with lambert eaton myasthenic syndrome?

A

small cell carcinoma

222
Q

what is the most comon disorder of the neuromuscular junction?

A

myasthenia gravis

223
Q

what is myasthenia gravis?

A

autoantibodies to acetyl choline receptors on the post-synaptic membrane, leads to reduced functioning of receptors causing muscle weakness and fatigue

224
Q

75% of patients with myasthenia gravis have what underlying condition?

A

thymus hyperplasia or thymoma

225
Q

at what age do women an men tend to get myasthenia gravis?

A

F- 20-30 years old

M- 50-70 years old

226
Q

the weakness in myasthenia gravis tends to fluctuate, as the day progresses does it generally get better or worse?

227
Q

what are the 3 most common weakness presentations of myasthenia gravis?

A

extraocular weakness
facial weakness
bulbar weakness
(fatiguable weakness)

228
Q

in myasthenia gravis, is weakness usually proximal or distal?

229
Q

what are the treatment options for myasthenia gravis?

A

acetylcholinesterase inhibitor
thmectomy
steroids/azathioprine
plasma exchange/immunoglobuline (n emergency)

230
Q

why do people with myasthenia gravis tend to die?

A
  • respiratory failure and aspiration pneumonia

- side effects of immunosuppression

231
Q

what is myotonia?

A

failure of muscle relaxation after use

232
Q

what disease has progressive weakness with characteristic thumb sparing?

A

inclusion body myositis

233
Q

what is the rhabdomyolysis triad?

A

myalgia
muscle weakness
myoglobinuria

234
Q

what are the 2 main complications of rhabdomyolysis?

A

acute renal failure

disseminated intravascular coagulation

235
Q

what is the treatment of polymyositis/dermatomyositis?

236
Q

what is the most common extra-axial brain tumour?

A

meningioma

237
Q

what are the 4 most common symptoms of a brain tumour in an adult?

A

progressive neurological deficit
motor weakness
headache
seizures

238
Q

what is the onset of a headache caused by a brain tumour?

A

slow onset

239
Q

what usually exacerbates a headache caused by a brain tumour?

A

worse in the morning
coughing
leaning forward

240
Q

what is cushings triad and what is it in response to?

A

increase blood pressure, decreased heart rate, irregular breathing

in response to very high IC{

241
Q

who tends to get grade 1 astrocytic tumors?

242
Q

where do children tend to get grade 1 astrocytic tumours?

A

in the cerebellum

243
Q

what is the treatment of choice for a grade 1 astrocytoma?

A

surgery (Curative)

244
Q

are grade 1 astrocytomas benign or malignant?

245
Q

if there is a grade 1 astrocytoma of the optic nerve, what diagnosis should be considered?

A

neurofibromatosis

246
Q

why are grade 2 astrocytomas considered to be malignant even though they are technically low grade?

A

because they become grade 3 and 4 tumours with time

247
Q

compare grade 1 and grade 2 tumours in terms of enhancement on contrast?

A

grade 1 enhance, grade 2 dont tend to

248
Q

what is the treatment of a grade 2 astrocytoma?

A

surgery +/- radiation/chemotherapy

249
Q

what is a glioblastoma?

A

grade 4 astrocytoma

250
Q

why do you still do surgery in cases of grade 3 and 4 astrocytomas even though it is non-curative?

A

to improve quality of life

251
Q

where do oligodendroglial tumours tend to occur?

A

frontal lobes

252
Q

what is the main presentation of oligodendroglial tumours?

A

seizures (due to calcification)

253
Q

what is the treatment for oligodendroglial tumours?

A

surgery + chemo/radiotherapy

254
Q

what condition should you think of if a patient has multiple meningiomas?

A

neurofibromatosis 2

255
Q

what are the 4 types of meningiomas? (classified by location)

A

parasagittal
convexity]sphenoid
intraventricular

256
Q

if a meningioma is found incidentally why may you choose to do nothing about it?

A

most are benign and very slow growing

257
Q

when is angiography of a brain tumour indicated?

A

if embolisation is planned

258
Q

what is the name of a benign peripheral nerve sheath tumours?

A

shwannomas

259
Q

what is the name of a malignant peripheral nerve sheath tumour?

A

malignant peripheral nevre sheath tumour

260
Q

what does bilateral vestibular schwannomas indicate?

261
Q

what are the 3 major symptoms of vestibular schwannomas?

A

hearing loss
tinnitus
balance problems

262
Q

what are the 4 major post-op complications of surgery on a vestibular schwannoma?

A

facial nerve palsy
corneal reflex
nystagmus
abnormal eye movement

263
Q

if a patient wakes up in the morning with a headache that gets better as the day goes on what should you be thinking of?

A

raised ICP

264
Q

if a patients headache is worse when they lie down what should you be thinking of?

A

raised ICP

265
Q

what are the 5 main red flags of a headache?

A

new onset over 55 years old
known/prev malignancy
early morning headache
eacerbation by valsalva (eg coughing, sneezing etc)

266
Q

are migraines usualy colourful or colourless?

267
Q

if a visual disturbance is bright, what should you be thinking about instead of a migraine?

A

occipital lobe seizure

268
Q

what is more common- migraine with or without aura?

A

without aura

269
Q

what is the criteria for diagnosing a migraines?

A

at least 5 attacks lasting from 4 -72 hours
2 from: moderate/severe, unilateral, throbbing pain, worse on movement
1 from: autonomic features, photophobia, phonophobia

270
Q

what is the pathophysiology of a migraine?

A

depolarisation somewhere in the cortex excites the trigeminal nerve causing it to release substances
-these dcause dilation of cranial blood vessels causing pain
(trigeminal vascular headache)

271
Q

how long does an aura in association with migraine last?

A

20-60 mins, usually before the headache

272
Q

what is the most common type of aura?

273
Q

what is the symptomatic treatment of migraines?

A
  1. NSAIDs
    +/- antiemetic
  2. triptans
274
Q

when should you give prophylaxis for migraines?

A

if there are more than 3 attackes per month or migrains are very severe

275
Q

how long must you trial a prophylaxis drug for migraines for?

A

4 months to see benefit

276
Q

what drugs are used for migrain prophylaxis?

A 
propanolol
topiramate
amitriptyline
gapapentin
pizotifen
sodium valproate
277
Q

what are the side effects of topieramate?

A

weight loss
paraesthesia
impaired concentration

278
Q

what lifestyle advice should you give someone with migraines?

A 
diet- avoid triggers, healthyh balanced diet
hydration
decrease caffeine
decrease stress
regular exercise
279
Q

what are trigeminal autonomic cephalgias?

A

primary headaches characterised by unilateral trigeminal distribution pain with ipsilateral autonomic features

280
Q

what are the 4 main types of trigeinal autonomic cephalgias?

A

cluster
paroxsymal hemicrania
hemicrania continua
SUNCT

281
Q

what is a cluster headache?

A

severe unilateral headache that lasts 45-90 mins, up to 8 times per day
cluster bout may last up to a few months

282
Q

what is the treatment for a cluster headaches?

A

high flow ozygen for 20 mins
subcut sumatriptan
steroids (reduce over 2 weeks)
verapamil (prophylaxis)

283
Q

what is the differnece between paroxysmal hemicranias and cluster headaches?

A

paroxysmal hemicranias are shorter in duration and more frequent

284
Q

compare age and sex of patients who get paroxysmal hemicranias and cluster headaches?

A

paroxysmal hemicranias-50-60s (F more then M)

30-40s (M more than F)

285
Q

what is a SUNCT headache?

A 
Short lived (less than 2 minutes)
Unilateral
Neuralgiaform headache
Conjunctival injections
Tearing
286
Q

what is the treatment for paroxysmal hemicranias?

A

indomethicin

287
Q

what is the treatment for SUNCT headaches?

A

lamotrigine

gabapentin

288
Q

what investigation can be done for those with new onset ipsilateral cranial autonomic features?

A

MRI brain and MR angiogram

289
Q

who tends to get trigeminal neuralgias?

A

over 60 years old

F more than M

290
Q

what triggers trigeminal neuralgias?

A

touching face (usually V2/3 area)

291
Q

what is the character of trigeminal neuralgia pain?

A

severe stabbing unilateral pain

292
Q

how long does the pain of trigeminal neuralgia last?

A

1- 90 seconds but can occur up to 100 times per day (occurs in bouts before remission)

293
Q

what is the treatment for trigeminal neuralgia?

A

carbamazepine, gabapentin, pheytoin, baclofen

surgery (rare): ablation or decompression

294
Q

what is the major difference between trigeminal autonomic cephalgias and trigeminal neuralgias?

A

trigeminal neuralgias dont have autonomic features

295
Q

what tends to happen to the limbs and head in an epileptic fit?

A

posturing of limbs

head turning

296
Q

what is a tonic clonic seizure?

A 
first tonic (stiff) phase
then clonic (jerky) phase
297
Q

what are corpopedal spasms?

A

severly painful muscle cramps of hands and feet

298
Q

why should you always do an ECG on a patient presenting with a new seizure?

A

might not be a seizure, could have a cardiac cause for collapse

299
Q

why would you choose to get a CT scan of a patient presenting acutely with a new seizure?

A
  • clinical or radiological skull fracture
  • deteriorating GCS
  • GCS not 15 after 14 hours
  • head injury with seizure
  • focal signs
  • suggestion of other intracranial pathology
300
Q

what are the 4 uses of an electroencephalogram? (EEG)

A
  • classification of epilepsy
  • confirmation of non-epileptic attacks
  • surgical evaluation
  • confirmation of non-convulsive status
301
Q

how long should you stop driving if you have a seizure? (not epilepsy, first fit)

A

car- 6 months

HGV- 5 years

302
Q

how long should you stop driving if you have an epileptic seizure?

A

car- 1 years (3 years if you also get fits during sleep)

HGV- 10 years

303
Q

what decreases the risk of SUDEP in an epileptic patient?

A

taking medication
bed partner
mild epilepsy

304
Q

what is an epileptic seizure?

A

abnormal synchronisation of neuronal activity

305
Q

do older people or young people tend to have focal epilepsy?

A

older people

306
Q

do older people or young people tend to have generalised epilepsy?

A

young people

307
Q

can generalised epilepsy cause focal or generalised seizures?

A

generalised

308
Q

can focal epilepsy cause focal or generalised seizures?

A

focal and generalised seizures

309
Q

what is the difference between a simplex= and complex seizure?

A

simple- no loss of consciousness

complex- loss of consciousness

310
Q

what is the treatment of choice for primary generalised epilepsy?

A

sodium valproate

lamotrigine in women of childbearing age

311
Q

what kind of epilepsy is juvenile myoclonic epilepsy?

A

primary generalised epilepsy

312
Q

what time of day does juvenile myoclonic epilepsy tend to have symptoms?

313
Q

what are the main 2 risk factors for seizures in generalised myoclonic epilepsy?

A

flashing lights

sleep deprivaion

314
Q

what is the treatment of choice for focal onset epilepsy?

A

carbamazepine

or lamotrigine

315
Q

what kind of epilepsy is complex partial seizures with hippocampal sclerosis?

A

focal epilepsy

316
Q

why does complex partial seizures with hippocampal sclerosis occur?

A

brain doesnt fold properly during development, hippocampus is affected

317
Q

when would you add on anti-convulsant drugs in epilepsy?

A

tried 3 anti-epileptic drugs, not suitable for surgery

318
Q

what anti-epileptic drugs affect women’s contraception?

A

hepatic-enzyme inducing drugs (eg carbamazepine)

319
Q

describe how womens contraception is altered by hepatic-enyzme inducing drugs?

A
  • OCP efficacy altered
  • progesterone only pill doenst work
  • progesterone implant doesnt work
  • depot progesterone needs more frequent dosing
  • morning after pill needs increased dose
320
Q

what does the oral contraceptive pill do to lamotrigine?

A

reduces lamotrigines efficacy

321
Q

why should sodium valproate not be given to women of childbearing age?

A

teratogenic

322
Q

where do berry aneurysms/saccular aneurysms occur?

A

circle of willis (tend to be where vessels branch)

323
Q

what is the name of the headache which happens just before you orgasm?

A

benign coital cephalgia

324
Q

what is a traumatic tap on LP?

A

when you get blood in the needle from piercing arteries while doing a LP

325
Q

what artery do you use to do cerebral angiography?

A

femoral artery

326
Q

what is the gold standard for locating the artery which has caused subarachnoid haemorrhage?

A

cerebral angiography

327
Q

what is the mainstay of treatment of an aneurysm that has previously caused a subarachnoid haemorrhage?

A

endovascular treatment

328
Q

how long does it take for delayed ischaemia from a subarachnoid haemorrhage?

329
Q

what drugs is used post-subarachnoid haemrrhages to stop vasospasm?

A

nimodipine (calcium channel blcker)

330
Q

why is nimodipine given for 3 weeks after a subarachnoid haemorrhage?

A

to reduce vasospasm to reduce delayed ischaemia

331
Q

if the headache from a subarahcnoid has not got better after a few days, what complication should you be thinking of?

A

hydrocephalus

332
Q

what salt imbalance can occur as a complication of subarachnoid haemorrhage?

A

hyponatramia

333
Q

why can hyponatraemia occur as a complication of subarachnoid haemorrhage?

A

SIADH

cerebral salt wasting

334
Q

what is the treatment of hyponatraemia due to subarachnoid haemorrhage? (how is this differnet to the normal treatment)

A

supplement sodium intake
fludrocortison
DO NOT FLUID RESTRICT
(usually you would fluid restrict)

335
Q

why do you not fluid restrict to treat the hyponatraemia that can occur due to subarachnoid haemorrhage?

A

can encourage vasospasm

336
Q

what investigation usually give the diagnosis of subarachnoid haemorrhage?

A

CT brain

if not, then lumbar puncture if safe

337
Q

what are the most common causes of intracerebral haemorrhage?

A

hypertension (50%)
aneurysm
AVM

338
Q

what is the name for the microaneurysms that arise on small arteries within the brain that are secondary to hypertension and can lead to intracerebral haemorrhage?

A

charcot-bouchard microaneurysms

339
Q

is the majority of the corticospinal tract crossed or uncrossed?

340
Q

where does the majority of the corticospinal tract decussate?

A

medullary level

341
Q

is the spinothalamic tract crossed or uncrossed?

342
Q

where does the spinothalamic tract decussate?

A

spinal level

343
Q

if there is a spinal cord lesion affecting the corticospinal tract, will it cause ipsilateral or contralateral symptoms?

A

ipsilateral

344
Q

if there is a spinal cord lesion affecting the spinothalamic tract, will it cause ipsilateral or contralateral symptoms?

A

contralateral

345
Q

are the dorsal column tracts crossed or uncrossed?

346
Q

where do the dorsal columns decussate?

A

medullary level

347
Q

if there is a spinal cord lesion affecting the dorsal columns, will it cause ipsilateral or contralateral symptoms?

A

ipsilateral

348
Q

what sensation does the spinothalamic tract deal with?

A

pain and temperature

349
Q

what sensation do the dorsal columns deal with?

A

fine touch, proprioception, vibration

350
Q

what is the most common cause of acute spinal cord compression?

A

metastatic disease of the spine leading to collapse

351
Q

what is spondylosis?

A

degeneration of the intervertebral discs ofthe spine- vey painful

352
Q

what are the 4 main causes of acute spinal cord compression?

A

tumours
trauma
infection
spontaneous haemorrhage

353
Q

what are the 3 main causes of chronic spinal cord compression?

A

degenerative disease- spondylosis
tumours
rheumatoid arthritis

354
Q

what joints in the spine does rheumatoid arthritis affect?

A

the synovial facet joints

355
Q

what kind of spinal cord injury can give you brown-sequard syndrome?

A

cord hemisection

356
Q

what are the symptoms of brown-seqard syndrome?

A

below level of injury

  • ipsilateral motor loss
  • ipsilateral dorsal column loss (fine touch, proprioception, vibration)
  • contralateral spinothalamic loss (pain and temp)
357
Q

what causes central cord syndrome?

A

hyperflexion or extension injury to an already stenotic neck

358
Q

where does the limb weakness occur in central cord syndrome?

A

predominantly distal upper limb weakness

lower limb power preserves

359
Q

where does the sensory loss occur in central cord syndrome?

A

‘cape like’ spinothalamic sensory loss (pain and temp)

dorsal columns preserves (vibration, fine touch and proprioception)

360
Q

compare acute and chronic spinal cord compression in terms of spinal shock?

A

acute compression- spinal shock

chronic compression- no spinal shock

361
Q

in chronic spinal cord compression, do LMN or UMN signs tend to predominate?

A

upper motor neuron signs

362
Q

what are the two classes of intradural tumour within the spine?

A

extramedullary (eg meningioma, schwannoma)

intramedullay (eg astrocytoma, ependymoma)

363
Q

if a tumour that is within the spine is extradural, what kind of tumour is it most likely to be?

A

metastatic

364
Q

why is dexamethasone given to patients with tumours (primary or mets) causing spinal compression?

A

reduces swelling in spinal cord

365
Q

what is the treatment for an infection causing acute spinal compression?

A

antimicrobial therapy
surgical drainage
stabilisation

366
Q

what is the treatment for a haemorrhage causing acute spinal compression?

A 
reverse anticoagulation (ie give clotting factors like vit K)
surgical decompression
367
Q

what is the treatment for degenerative disease causing spinal cord compression?

A

decompression +/- stabilisation

368
Q

where is the location of the cause of a somatosensory aura?

A

parietal lobe (somatosensory cortex on postcentral gyrus)

369
Q

where is the location of the cause of a visual aura?

A

occipital lobe (visual cortex)

370
Q

what are the 3 types of functional attacks?

A
  1. attacks with prominent motor activity
  2. episodes of collapse with no movement
  3. abreactive attacks (Fear, hyperventilationetc)
371
Q

what is the usual duration of a functional attack?

372
Q

what is status epilepticus?

A

recurrent epileptic seizures lasting more than 30 mins (no full recovery of consciousness between seizures)

373
Q

what are the 3 kinds of status epilepticus?

A
  • generalised convulsive status epilepticus
  • non convulsive status (altered state)
  • epilepsia partialis continua
374
Q

what metabolic disorders can cause status epilepticus?

A

hyponatraemia, pyridoxine deficiency

375
Q

treating an absent seizure with what drug can cause status epilepticus?

A

carbemazapine

376
Q

what is the drug treatment of status epilepticus for immediate control?

A

lorazepam IV
if delay gaining IV access-
diazepam PR
(give 50ml 50% glucose if any suggestion of hypoglycaemia, give IV thiamine if any suggestion of alcoholism)

if persisting transfer to ITU and control with general anaesthesia

377
Q

compare the difference in symptoms for a large sensory fibre and small sensory fibre peripheral neuropathy?

A

large: numbness, paraesthesia, unsteadiness
small: pain, dysasthesia

378
Q

compare the difference in reflexes for a large sensory fibre and small sensory fibre peripheral neuropathy?

A

large: absent reflexes
small: present reflexes

379
Q

what is pseudoathetosis?

A

abnormal writhing movements, usually of the fingers

380
Q

what causes pseudoathetosis?

A

loss of proprioception

381
Q

where is the nerve injured in a radiculopathy?

A

nerve root

382
Q

where is the nerve injured in a plexopathy?

A

nerve plexus

383
Q

what is the initial pattern of sensory loss or weakness in peripheral neuropathy?

A

glove and stocking

384
Q

what is guillain barre syndrome?

A

progressively demyelinating condition with progressive paraplegia that occurs over days and lasts up to 4 weeks
sensory symptoms (such as pain) proceed weakness
-association: post infectious

385
Q

why do people with guillain barre syndrome die?

A

autonomic failure- arrhythmias

386
Q

what is the treatment of guillain barre syndrome?

A

immunoglobulin infusion

plasma exchange

387
Q

what causes the neuropathy in hereditary sensory motor neuropathy?

A

demyelination

388
Q

what are the 3 main causes of chronic autonomic neuropathy?

A

diabetes
amyloidosis
hereditary autonomic neuropathy

389
Q

what are the 2 main causes of acute autonomic neuropathy?

A

guillian barre syndrome

porphyria

390
Q

what are the SMART goals for neurological rehab?

A 
specific
motivating
achievable
rational/relevant
time-defined
391
Q

where within the brain is the problem if the movement disorder presents with pyramidal/upper motor neurone features? (such as pyramidal weakness, spasticity)

A

corticospinal tract

392
Q

where within the brain is the problem if the movement disorder presents with hyperkinetic features? (such as dystonia, tics, myoclonus, chorea)

A

basal ganglia

393
Q

where within the brain is the problem if the movement disorder presents with hypokinetic features? (such as rigidity, bradykinesia)

A

basal ganglia

394
Q

where within the brain is the problem if the movement disorder presents with ataxia?

A

cerebellum

395
Q

are increased deep tendon reflexes likely to be caused by an upper motor or lower motor problem?

A

upper motor

396
Q

are decreased deep tendon reflexes likely to be caused by an upper motor or lower motor problem?

A

lower motor

397
Q

are increased pathological reflexes likely to be caused by an upper motor or lower motor problem?

A

upper motor

398
Q

is increased muscle tone likely to be caused by an upper motor or lower motor problem?

A

upper motor

399
Q

is decreased muscle tone likely to be caused by an upper motor or lower motor problem?

A

lower motor

400
Q

is increased muscle bulk likely to be caused by an upper motor or lower motor problem?

A

upper motor

401
Q

is wasting of muscle bulk likely to be caused by an upper motor or lower motor problem?

A

lower motor

402
Q

are fasiculations likely to be caused by an upper motor or lower motor problem?

A

lower motor

403
Q

where anatomically is the location of the disease if there is fatiguable weakness?

A

neuromuscular junctions

404
Q

what is the pattern of weakness that occurs with a parasagittal frontal lobe lesion?

A

paraparesis

405
Q

what is the pattern of weakness that occurs with a cervical spinal cord UMN lesion?

A

pyramidal weakness of arms and legs

406
Q

what is the pattern of weakness that occurs with a thoracolumbar spinal cord UMN lesion?

A

pyramidal weakness of legs

407
Q

is polio a disease of upper or lower motor neurones?

408
Q

what is mononeuritis multiplex?

A

an asymmetrical neuropathy of multiple nerves

409
Q

what muscle, named nerve and nerve root causes shoulder abduction? (after 30 degrees)

A

deltoid
axillary nerve
C5

410
Q

what muscle, named nerve and nerve root causes elbow extension?

A

triceps
radial nerve
C7

411
Q

what muscle within the forearm, named nerve and nerve root causes finger extension?

A

extensor digitorum
posterior interossus nerve (radial)
C7

412
Q

what muscle, named nerve and nerve root causes index finger abduction?

A

1st dorsal interosseus
ulnar nerve
T1

413
Q

what muscle (main muscle), named nerve and nerve root cause hip flexion?

A

iliopsoas
femoral nerve
L1,2

414
Q

what muscles, named nerve and nerve root cause knee flexion?

A

hamstrings
sciatic nerve
S1

415
Q

what named nerve and nerve root causes ankle dorsiflexion?

A

common peroneal nerve

L4,5

416
Q

what muscle, named nerve and nerve root causes great toe dorsiflexion?

A

extensor hallucis longus
common peroneal nerve
L5

417
Q

what nerve roots supply the ankle reflex?

418
Q

what nerve roots supply the knee reflex?

419
Q

what nerve roots supply the biceps reflex?

420
Q

what nerve roots supply the triceps reflex?

421
Q

if there is a problem with the peroneal nerve, what tendon reflex is absent?

422
Q

describe the cerebellar gait?

A

broad-based and unsteady

423
Q

what is the DANISH mneumonic for remembering cerebellar tests?

A 
Dysdiadochokinesis
Ataxia
Nystagmus
Intention Tremor
Speech
Hypotonia
424
Q

what is dysdiadochokinesis?

A

clumsy fast alternating movements

425
Q

how do you test for an intention tremor?

A

finger-nose test

heel-shin test

426
Q

what is hypomimia?

A

reduced facial expression

427
Q

what is hypophonia?

A

soft speech

428
Q

compare the visual field defect with temporal and parietal lobe lesions?

A

parietal- inferior homonymous quadrantanopia

temporal- superior homonymous quadrantanopia

429
Q

what is levodopa broken down into once in the brain?

430
Q

what type of drug can be used for tremor in parkinsons disease?

A

anticholinergics

431
Q

why are COMT inhibitors sometimes given in addition to levodopa in parkinsons disease?

A

inhibits enxyme which breaks down levodopa

432
Q

does parkinsons disease tend to be symmetrical or asymmetrical?

A

asymmetrical

Neurology (3 decks)

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