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Year 3 > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a glioma?

A

A Neuroepithelial tumour usually seen within the hemispheres though can be anywhere in CNS
2 main types; astrocytomas and oligodendrogliomas

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2
Q

Why are tumours of neuronal cells only present in childhood?

A

Fully differentiated neurons can’t multiply or give rise to neoplasms so tumours have to occur before completion of differentiation

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3
Q

What is a medulloblastoma?

A

Childhood brain tumour arising from the cerebellum

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4
Q

What is a neurofibroma?

A

Tumours deriving from endoneurium which is a layer of connective tissue around the myelin sheath of each nerve in the PNS

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5
Q

Personality changes and disinhibition would indicate a tumour located where?

A

Frontal lobe

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6
Q

Describe the sensory (ascending) tracts in the Dorsal Horn

A

Responsible for fine touch, vibration and proprioception
Ipsilateral (decussates in medulla)
Fasciculus cuneatus (lateral) responsible for T6 and above
Fasciculus gracilis responsible for below T6

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7
Q

Describe the anterolateral part of the sensory tract?

A

Anterior spinothalamic responsible for crude touch and pressure
Lateral spinothalamic responsible for pain and temperature
Contralateral (decussates in spinal cord)

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8
Q

Describe the pyramidal tracts of the motor (descending) pathway

A

Anterior corticospinal and lateral corticospinal tracts are responsible for voluntary movement of the limbs
Anterior is ipsilateral and lateral is contralateral

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9
Q

Which tracts are known as the extrapyramidal motor tracts?

A

All coordinate INvoluntary movements

Tectospinal = head and neck movements in response to visual stimuli
Vestibulospinal tract = posture and balance
Rubrospinal = fine motor control
Reticulospinal = medial for contraction and increases tone, lateral inhibits contraction and decreases tone

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10
Q

What does DANISH stand for?

A

Dysdiadokinesia = impairment of rapid alternating movements
Ataxia = broad gait
Nystagmus
Intention Tremor
Scanning dysarthria = slow or poorly articulated speech
Hypotonia

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11
Q

Headache red flags

A

Worse in morning
Wakes you up
Worse when coughing or leaning forward
Associated with vomiting

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12
Q

Gold standard test for the brain tumour

A

MRI

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13
Q

Describe a subfalcine herniation

A

Asymmetrical expansion of a hemisphere causes compression of the cingulate gyrus under the falx cerebri
Can cause compression of the anterior cerebral artery branches
Symptoms = weakness in contralateral leg

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14
Q

Describe a tentorial herniation

A

Medial part of the temporal lobe hernaites over the tentorium cerebelli
Causes compression of ipsilater 3rd cranial nerve -> pupil dilation, reduced eye movements

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15
Q

Describe tonsillar hernation

A

Displacement of the cerebellar tonsils through the foramen magnum
Compresses brainstem so compromises the respiratory centre in the medulla -> life threatening

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16
Q

Describe transcalvarial herniation

A

Swollen brain herniated through any defect in the dura and skull

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17
Q

What’s the main cause of a subarachnoid haemorrhage?

A

A ruptured berry aneurysm

These are formed from a congenital weakness of the elastic tissue in the artery wall

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18
Q

Symptoms of a subarachnoid haemorrhage?

A

Sudden onset of a thunderclap headache - worst, occipital, during strenuous activity “hit on back of head”
Nausea and vomiting
Neck stiffness and photophobia if meningeal irritation

3rd nerve palsy if aneurysm is on posterior communicating artery

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19
Q

Investigation if you suspect a brain haemorrhage

A

Unenhanced CT

If inconclusive then a lumbar puncture looking for blood

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20
Q

Treatment for a subarachnoid haemorrhage

A

Bed rest and support
Control any hypertension
Nimodipine (Ca channel blocker) prevents vasospams which can cause ischaemia

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21
Q

How would you treat a brain aneurysm?

A

Endovascular treatment placing platinum coils via a catheter into the aneurysm to promote thrombosis and ablation of the aneurysm
Direct surgical clipping may be needed

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22
Q

Causes of a subdural haemorrhage

A 
Acute = trauma ruptures the bridging veins
Chronic = brain atrophy causes bridging veins to be stretched
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23
Q

Symptoms of a subdural haemorrhage

A

Altered state of consciousness following trauma or a fall

Chronic = headaches, confusion, urinary incontinence, weakness, seizures…

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24
Q

What does a subdural haemorrhage look like on a CT scan?

A

Semilunar shape

Midline shift

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25
Q

Management of a subdural haemorrhage

A

No immediate treatment as they often resolve on their own
Must involve neurosurgery
Serial imaging
Can be drained surgically

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26
Q

What is the pterion?

A

Thinnest part of the skull

Join of the temporal, parietal, frontal and sphenoid bones

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27
Q

Causes of an extra dural haemorrhage

A

Trauma causes shearing stress that separates the bone and the dura
Most commonly trauma to the pterion which damages the middle meningeal artery

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28
Q

Symptoms of an extra dural haemorrhage

A

Head trauma that causes a brief loss of consciousness, then lucidness then further deterioration
Headache
Contralateral hemiparesis - damage to stalks that attach cerebrum to brain stem and contain ascending and descending tracts
Ipsilateral pupil dilation - temporal lobe can herniate and compress oculomotor nerve

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29
Q

Management of an extra dural haemorrhage

A

If expanding, immediate neurosurgical treatment

If small and patients are neurologically intact then conservative treatment

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30
Q

What produces the myelin sheath?

A

In CNS, oligodendrocytes

In PNS, Schwann cells

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31
Q

How many spinal nerves are there?

A 
31 pairs
C1-8
T1-12
L1-5
S1-5
Co1
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32
Q

Which dermatome is the nipple in?

A

T4

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33
Q

Which dermatome is the umbilicus

A

T10

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34
Q

At what level does the spinal cord end?

A

L1-2

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35
Q

Where should a lumbar puncture be inserted?

A

Between L3-4

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36
Q

Myoclonus

A

Quick involuntary muscle jerk
E.g. hiccups, hypnic jerk when falling asleep
Brief activation of muscles

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37
Q

Dystonia

A

Sustained or intermittent muscle contractions that cause abnormal movements
Often initiated or worsened by voluntary action
Associated with overflow muscle activation

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38
Q

Chorea

A

Brief, irregular movements that move flit and flow from one body part to another
Patients often appear restless or fidgety

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39
Q

Tics

A

‘Un” voluntary repetitive movements or vocalisations

Suppressible for a short period of time but this causes a lot of anxiety

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40
Q

Pathology of Parkinsons Disease

A

Loss of dopaminergic neurons in the substantia nigra

Surviving cells contains Lewy bodies

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41
Q

Early signs of Parkinsons Disease

A 
Anosmia
Depression and anxiety
Sleep disorder
Urinary urgency and constipation
Hypotension
Restless leg syndrome
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42
Q

Motor problems associated with Parkinson’s Disease

A 
Akinesia
Tremor (pin-rolling)
Rigidity
Stooped posture
Shuffling gait with reduced arm movements
Speech and swallowing difficulties
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43
Q

Investigations for Parkinsons Disease

A

Dopamine Transporter Imaging using SPECT or PET

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44
Q

Management of Parkinson’s Disease

A

1st Line for those with motor symptoms = Levodopa
= converted to dopamine in the brain - need more over time, on-off problems
No motor symtoms = L Dopa, dopamine agonists or MAO inhibitors

45
Q

What is Parkinsonism?

A

Any conditions that causes TRAP (extrapyramidal) symptoms = Tremor, Rigidity, Akinesia, Postural disturbances
Can be caused by anything affecting the nigrostriatal dopamine pathway e.g. antipsychotics (block D2 receptors)

46
Q

What is MS?

A

Multiple Sclerosis
T-cell mediated inflammatory disorder causing multiple plaques of demyelination throughout the brain and spinal cord (CNS only) occurring sporadically over years

47
Q

Investigations for MS

A

MRI = areas of demyelination

Lumbar puncture = oligoclonal bands in CSF with no corresponding bands in the serum

48
Q

Management of MS

A

Symptoms - physiotherapy or baclofen for pyramidal dysfunction. Gabapentin for neuropathic pain
Acute - oral or IV steroids
Disease modifying - Tecfidera (oral), interferons, glutamir acetate (injection)

49
Q

What is myaesthenia gravis?

A

Auto-immune disorder of the NMJ

Antibodies to ACh receptors -> signals don’t get through

50
Q

Symptoms of myaesthenia gravis

A

Weakness that gets worse throughout day - fatigability. Particularly, extraocular, facial and bulbar weakness
Drooping eyelids
Double vision that comes and goes

Can cause a respiratory crisis cos of weak muscles of respiration

51
Q

Investigations for myaesthenia gravis

A

Anti-AChR antibodies

Anti-MuSK antibodies

52
Q

Management of myaesthenia gravis

A

Acute - acetylcholinesterase inhibitors, IVig
Steriods then move to steroid-sparing e.g. azathioprine

AVOID GENTAMICIN

53
Q

What is Guillan-Barre Syndrome?

A

Acute demyelination disorder that usually occurs after infection with campylobacter or CMV
Causes ascending weakness

54
Q

Symptoms of Guillan-Barre Syndrome

A

Post infection
Weakness and sensory loss
Loss of tendon reflexes

55
Q

Investigation and treatment of Guillan-Barre syndrome

A

Confirm with nerve conduction studies

IVIg given within first 2 weeks can reduce severity and duration of paralysis

56
Q

Pathogenesis of Huntington’s Disease

A

Autosomal dominant with age-dependent penetrance (Anticipation)
Extra CAG repeats (>20) so increased glutamines on the protein -> neurotoxic. Unstable during meiosis so it gets worse each time its passed down and appears earlier
Loss of basal ganglia which causes flattening of ventricles
Caudate nucleus is atrophic
Loss of cells in cerebral cortex

57
Q

Presentation of Huntington’s disease

A

Fidgetiness, difficulty concentrating, clumsiness
Chorea, inability to walk
Difficulty speaking and swallowing
Patients usually die 10-20 years after 1st onset of symptoms

58
Q

What is Duchenne Muscular Dystrophy?

A

X-linked recessive disorder (1/3 spontaneous) causing progressive muscle wasting and weakness
The mutation is in the dystrophin gene which codes for dystrophin proteins that connect actin filaments to cell membrane and ECM.
-> progressive loss of muscle cells -> muscle wasting and weakness

59
Q

Presentation of DMD

A 
Developmental delay (boy not walking by 18 months)
Gower’s sign = put hands down to push themselves up
Toe walking - calf hypertrophy
Exaggerated lumbar lordosis
60
Q

Investigations for DMD

A

Screen looking for raised creatinine kinase

Genetic testing to confirm

61
Q

Management for DMD

A

No curative treatment - usually disabled by 10, die in 20s
Steroids may delay progression
Physiotherapy

62
Q

What is Spinal Muscular Atrophy?

A

Autosomal Recessive disorder that causes loss of anterior horn cells in spinal cord
Usually a deficiency in SMN1 gene which causes motor neuron loss

63
Q

Presentation of Spinal Muscular Atrophy

A

Floppy and weak baby - hypotonia and muscle weakness

Respiratory failure is resp. Muscles are affected

64
Q

Management of Spinal Muscular Atrophy

A

Treatment using similar SMN2 gene which prevents essential exon7 being spliced out
Prevents progression but doesn’t stop whats already happened

65
Q

Most common causes of meningitis

A 
Streptococcus pneumonia
Neisseria Miningitidis (meningococcus)
66
Q

Describe Streptococcus Pneumonia with regards to meningitis

A 
Most common type of meningitis
Alpa Haemolytic
Gram positive cocci in chains
High risk of developing with diabetes, cochlear implants or skull fractures
There is a vaccine
67
Q

Describe Neisseria Meningitidis with regards to meningitis

A

Gram negative cocci in pairs
Symptoms due to endotoxin
More common in young children and adults
12 capsular groups and theres a vaccine for ACWY

68
Q

Treatment for Bacterial Meningitis

A

Ceftriaxone IV 2g bd (chloramphenicol is penicillin allergy) and Dexamethasone
If listeria suspected (anyone >60 or immunocompromised) add amoxicillin

69
Q

Most common cause of encephalitis in UK

A

Herpes Simplex Virus

70
Q

Presentation of encephalitis

A

Personality and behavioural changes
Confusion, reduced consciousness, coma
Speech disturbance
Seizures

71
Q

Treatment for Encephalitis

A

Suspected HSV or VZV then acyclovir IV immediately

Long-term complications are common including memory impairment, personality change, epilepsy

72
Q

Absense seizure

A

Loss of awareness and vacant facial expression <10secs
Maybe slight eye flutterings but no motor symptoms
Patient may be unaware

73
Q

Myoclonic Seizure

A

Jerk movements

74
Q

Tonic seizure

A

Stiffening of the body. No jerking

75
Q

Atonic seizure

A

Sudden collapse with loss of muscle tone and consciousness

76
Q

Tonic clonic seizure

A

Tonic stiffening followed by clonic jerking phase
Possible incontinence after convulsions
Slow return to consciousness followed by drowsiness, confusion and headaches

77
Q

Management of Epilepsy

A

1st line for tonic clonic, tonic or atonic seizures = Sodium Valproate (or lamotrigine)
1st line for myoclonic = Sodium Valporate (or levetiracetam)

Sodium Valporate is teratogenic so avoid in women of child-bearing age
Many AEDs can make contraceptives ineffective

78
Q

In spinal cord, where is the white and grey matter?

A

Grey matter is in the middle with anterior and dorsal horns

White matter around the outside containing the ascending and descending tracts

79
Q

Describe nigrostriatal dopamine pathway

A

Pars compacta in substantia nigra of the midbrain
Controls movement
More dopamine = more movement

80
Q

Describe mesocorticolimbic dopamine pathway

A

Travels from VTA of midbrain to prefrontal cortex then to nucleus accumbens
Controls mood/reward
More dopamine = higher mood

81
Q

Describe tuberoinfundibular dopamine pathway

A

From hypothalamus to pituitary
Controls prolactin release
More dopamine = less prolactin

82
Q

What foramina does CN I pass through?

A

Olfactory

Cribiform plate

83
Q

What foramina does CN II pass through?

A

Optic Nerve

Optic Canal

84
Q

What foramina does CN III pass through?

A

Oculomotor Nerve

Superior Orbital Fissure

85
Q

What foramina does CN IV pass through?

A

Trochlear

Superior Orbital Fissure

86
Q

What foramina does CN V pass through?

A

Trigeminal
V1 = SOF
V2 = Foramen rotundum
V3 = Foramen ovale

87
Q

Wht foramina does CN VI pass through?

A

Abducens

Superior orbital fissure

88
Q

What foramina does CN VII pass through?

A

Facial Nerve

Internal auditory meatus then stylomastoid foramen

89
Q

What foramina does CN VIII pass through?

A

Vestibulocochlear

Internal auditory meatus

90
Q

What foramina does CN IX pass through?

A

Glossopharyngeal

Jugular Foramen

91
Q

What foramina does CN X pass through?

A

Vagus Nerve

Jugular Foramen

92
Q

What foramina does CN XI pass through?

A

Accessory Nerve

Jugular foramen

93
Q

What foramina does CN XII pass through?

A

Hypoglossal

Hypoglossal Canal

94
Q

Describe what CN III does and signs of a CN III palsy

A

Eye movements (MR, SR, IR, IO), pupil constriction, accomodation, eyelid opening

Palsy = Ptosis, ‘down and out’ eye, dilated, fixed pupil

95
Q

Describe what CN IV does and signs of a palsy

A

Superior oblique eye movement

Palsy = down and in gaze, vertical diplopia

96
Q

Describe what CN VI does and signs of a palsy

A

Lateral rectus eye movement

Palsy = Eye cant move outwards, horizontal diplopia

97
Q

If there is a CN X palsy, which way will the uvula deviate?

A

Away from the site of the lesion

98
Q

If there is a CN XII palsy, which way will the tongue deviate?

A

Towards the side of the lesion

99
Q

Which cranial nerve nuclei are located in the medulla oblongata?

A 
9, 10, 11 and 12
Glossopharyngeal
Vagus
Accessory
Hypoglossal
100
Q

Which cranial nerve nuclei are located in the posterior part of the pons?

A 
5, 6, 7 and 8
Trigeminal
Abducens
Facial
Vestibulocochlear
101
Q

Which cranial nerve nuclei are located in the central part of midbrain?

A

3 and 4
Oculomotor
Trochlear

102
Q

Which blood vessel lies deep to the pterion?

A

Middle meningeal artery

103
Q

Biceps reflex, which nerve?

A

C5 (6)

104
Q

Triceps reflex, which nerve?

A

C7

105
Q

Supinator/brachioradialis reflex, which nerve?

A

C6

106
Q

Patellar reflex, which nerve?

A

L4

107
Q

Ankle reflex, which nerve?

A

S1

108
Q

Describe neurofibromatosis

A

Type 1 and 2. 1 is more common (90%)
Autosomal dominant
Chromosome 17 (type 1), 22 is type 2
Neurofibromas, cafe-au-lait spots and freckling, learning disability

109
Q

Treatment for status ellipticus

A

IV lorazepam
IM midazolam (can also do buccal or nasal)
Can add phenytoin IV
If not working, can add phenobarbitone

Year 3 (10 decks)

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