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Neurology Systems > Week 4 > Flashcards

Week 4 Flashcards

1
Q

how are headaches classified? and give examples for each

A

primary (no underlying medical cause):
- tension type headache
- migraine
- cluster headache

secondary (has an identifiable structural or biochemical cause):
- tumour
- meningitis
- vascular disorders
- systemic infection
- head injury
- drug-induced

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2
Q

what is the most common cause of a primary headache?

A

migraine

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3
Q

pathophysiology of primary headache

A
  • sensitisation of normal pain pathways
  • involves brainstem and cortical structures and trigeminovascular system
  • calcitonin gene related peptide is a key transmitter
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4
Q

what is the management for a primary headache?

A

consider:
- modifiable lifestyle triggers > especially important in migraine
- abortive treatment
- transitional treatment > more important in cluster headache
- preventative treatment

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5
Q

primary headache investigation

A
  • look for an underlying secondary cause triggering off a primary headache disorder.
  • for most patients, investigation is not required.
  • MRI is more sensitive than CT, but is more likely to show incidental findings.
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6
Q

secondary headache investigation

A
  • specific investigations can help to confirm diagnosis and guide treatment
  • e.g. CT and CT angiogram in subarachnoid haemorrhage
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7
Q

describe a tension headache

A

mild, bilateral headache which is often pressing or tightening in quality, has no significant associated features and is not aggravated by routine physical activity

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8
Q

what is the treatment for a tension type headache?

A
  • acute: paracetamol, NSAIDs
  • preventative: tricyclic antidepressants (amitryptyline)
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9
Q

what symptoms occur during attacks of migraine?

A
  • headache
  • nasuea, photophobia, phonophobia
  • functional disability
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10
Q

what is a migraine?

A

Migraine is a neurologic chronic disorder with episodic manifestation (CDEM), characterized by recurrent and reversible attacks of pain and associated symptoms such as headache.

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11
Q

describe aura in the context of migraine

A
  • transient neurological systems resulting from cortical or brainstem dysfunction > cortical spreading depression.
  • slow evolution of symptoms: moves from 1 area to the next e.g. vision > sensory > speech
  • most common type of aura is visual aura
  • duration 16-60 minutes
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12
Q

what is considered a chronic migraine?

A

headache on >/= 15 days per month of which >/= 8 days have to be migraine, for more than 3 months.

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13
Q

describe a medication overuse headache

A
  • headache present on >/= 15 days/month which has developed or worsened whilst taking regular symptomatic medication.
  • use of triptans, ergots, opiods and combination analgesic > 10 days/month
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14
Q

what are some modifiable lifestyle triggers in migraine?

A
  • normal life events trigger or are associated with attacks in those predisposed to migraine.
  • sleep disturbance
  • dehydration
  • diet
  • hunger
  • environmental stimuli
  • stress
  • changes in oestrogen level in women
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15
Q

what is the treatment for an acute migraine?

A
  • aspirin or NSAIDs
  • triptans
  • limit to 10 days per month (2 days per week) to avoid the development of medication overuse headache.
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16
Q

what is the prophylactic treatment for migraine?

A
  • propanolol, candesartan
  • anti-epileptics: topiramate, valproate
  • tricyclic antidepressants: amitriptyline, nortriptyline
  • flunarizine
  • botox
  • CGRP monoclonal antibodies
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17
Q

does migraine without aura get better or worse with pregnancy?

A

better

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18
Q

what is the treatment for migraine during pregnancy?

A
  • acute: paracetamol, NSAID (1st two trimesters), triptans
  • preventative: propanolol or amitryptyline
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19
Q

describe neuralgia

A
  • an intense burning or stabbing pain
  • usually brief but may be severe
  • pain extends along the course of the affected nerve
  • usually caused by irritation of or damage to a nerve
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20
Q

cranail neuralgias are caused by irritation of nerves that mediate the sensation in the head, name these

A
  • trigeminal
  • glossopharyngeal and vagus
  • nervus intermedius (branch of facial nerve)
  • occipital
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21
Q

trigeminal neuralgia definition

A

Trigeminal neuralgia, also known as tic douloureux, is a chronic pain condition characterized by severe, sudden, and brief bouts of shooting or stabbing pain that follow the distribution of one or more divisions of the trigeminal nerve, affecting the patient’s facial region.

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22
Q

what is the duration of each stab in trigeminal neuralgia?

A

5-10 seconds

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23
Q

what are some cutaneous triggers of trigeminal neuralgia?

A
  • wind, cold
  • touch
  • chewing
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24
Q

what are common and uncommon causes of trigeminal neuralgia?

A

common:
- vascular compression of the trigeminal nerve

uncommon:
- MS
- intracranial arteriovenous malformation
- intracranail tumour
- brainstem lesions

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25
Q

what is the medical treatment of trigeminal neuralgia?

A
  • carbamazepine
  • oxcarbazepine
  • lamotrigine
  • pregabalin/gapapentin/lacosamide
  • phenytoin can be used for severe exacerbations
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26
Q

what is the surgical treatment for trigeminal neuralgia?

A
  • glycerol ganglion injection
  • stereotactic radiosurgery
  • microvascular decompression
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27
Q

what are some cranial autonomic symptoms that can be caused by trigeminal autonomic cephalagias?

A
  • conjunctival infection/lacrimation
  • nasal congestion/rhinorrhoea
  • eyelid oedema
  • forehead and facial sweating
  • miosis/ptsosis (Horner’s syndrome)
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28
Q

what are key distinguishing features of cluster headaches?

A
  • recurrent unilateral periorbital pain of sudden onset
  • associated symptoms: watery and bloodshot eye, lacrimation, rhinorrhoea, miosis, ptosis, lid swelling, and facial flushing
  • headache duration of 15 minutes to 3 hours, occuring once or twice daily over 4-12 weeks, followed by a pain-free period of several months
  • striking circadian rhythmicity; attacks occur at same time each day, bouts occur at same time each year
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29
Q

management of cluster headaches

A
  • avoiding triggers
  • prophylaxis with verapamil, topiramate, lithium etc.
  • acute: 100% oxygen via a non-rebreathable mask and a subcutaneous or nasal triptan.
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30
Q

what is transitional treatment for cluster headaches?

A
  • oral prednisolone taper
  • greater occipital nerve block
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31
Q

features of paroxysmal hemicrania

A
  • pain: unilateral and mainly orbital and temporal
  • excruciatingly severe pain
  • duration 2-30 mins
  • in 10%, attacks may be precipitated by bending or rotating the head
  • 2-40 attacks per day
  • absolute response to indometacin
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32
Q

features of hemicrania continua

A
  • strictly unilateral continuous headache
  • episodic (lasting weeks-months) or chronic (unremitting)
  • moderately-severe continous background headache
  • superimposed exacerbations of more severe pain lasting 20 mins to several days
  • mainly orbital and temporal
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33
Q

features of SUNCT/SUNA

A
  • unilateral orbital, supraorbital or temporal pain
  • stabbing or pulsating pain with 10-240 seconds duration
  • attack frequency from 3-200/day with no refractory period
  • accompanied by conjunctival injection and lacrimation
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34
Q

medical treatment for SUNCT/SUNA

A

Lamotrigine
Topiramate
Oxcarbazepine
Carbamazepine
Duloxetine
Pregabalin / Gabapentin

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35
Q

transitional treatment for SUNCT/SUNA

A

greater occipital nerve block

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36
Q

surgical treatment for SUNCT/SUNA

A
  • occipital nerve stimulation
  • deep brain stimulation
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37
Q

which presentations of headache are more likely to have a sinister cause? (though most headaches are not sinister)

A
  • head injury
  • first or worst
  • sudden (thunderclap) onset
  • new daily persistent headache
  • change in headache pattern or type
  • returning patient
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38
Q

describe thunderclap headaches

A
  • high intensity headached reaching maximum intensity in less than 1 minute
  • majority peak instantaneously
  • whole head (worst occipitally)
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39
Q

what must be excluded in thunderclap headaches?

A

subarachnoid haemorrhage

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40
Q

subarachnoid haemorrhage investigations

A

CT then CT angiogram
lumbar puncture when CT not definitive

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41
Q

management of subarachnoid haemorrhage

A
  • nimodipine to prevent vasospasm
  • treat complications
  • HHH therapy > hydration, hyperoxia, hypertension
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42
Q

what are features of intracranial hypotension?

A
  • spontaneous or post lumbar puncture
  • postural headache: headache develops or worsens soon after assuming an upright posture and lessens or resolves shortly after lying down, due to ‘brain sink’
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43
Q

what is the treatment for intracranial hypotension?

A
  • bed rest, fluids, analgesia, caffeine
  • i.v. caffeine
  • epidural blood patch
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44
Q

what are key distinguishing features of giant cell arteritis?

A
  • associtation with temporary monocular blindness
  • temporal tenderness
  • jaw claudiaction
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45
Q

what are useful iomarkers in giant cell arteritis?

A
  • elevated erythrocyte sedimentation rate ESR (blood test) usually >50, often much higher, rarely normal
  • raised CRP and platelet count
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46
Q

treatment for giant cell arteritis?

A

high dose prednisolone

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47
Q

what are common types of primary brain tumour?

A
  • neuroepithelial tissue: glioma (glioblastoma multiforme)
  • meninges: meningioma
  • pituitary: adenoma
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48
Q

what are the commonest tumours that spread to the brain (secondary)?

A
  • renal cell carcinoma
  • lung carcinoma
  • breast carcinoma
  • malignant melanoma
  • GI tract
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49
Q

what % of patients with cancer will get cerebral metastases?

A

15-30%

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50
Q

what cells are gliomas derived from and what is their function?

A
  • astrocytes > structural and nutritional support to nerve cells.
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51
Q

give features of grade IV glioma

A
  • most common
  • most aggressive
  • glioblastoma multiforme (GBM)
  • spread by tracking through white mater and CSF pathway
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52
Q

what are characteristics of meningiomas?

A
  • slow-growing
  • extra-axial
  • usually benign
  • arise from arachnoid mater
  • frequently occur along falx, covexity or sphenoid bone
  • usually cured if completely removed
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53
Q

most common type of pituitary tumour?

A

adenoma

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54
Q

what can a pituitary adenoma cause?

A
  • visual disturbance > compression of optic chiasm
  • hormone imbalance
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55
Q

clinical presentation of brain tumour

A
  • raised ICP
  • focal neurological deficit
  • epileptic fits
  • CSF obstruction
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56
Q

raised ICP symptoms

A
  • headache (typically morning)
  • nausea/vomiting
  • visual disturbance (diplopia, blurred vision)
  • somnolence
  • cognitive impairment
  • altered conciousness
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57
Q

signs of raised ICP

A
  • papilloedema
  • 6th nerve palsy
  • cognitive impairment
  • altered conciousness
  • third nerve palsy
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58
Q

investigations for brain tumours

A

adequate cerebral imaging:
- CT
- MRI
- PET
- (angiography)

if suspecting metastasis:
- CT chest/abdo/pelvis
- mammography
- biopsy skin lesions/lymph nodes

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59
Q

glioblastoma multiforme magaement options

A
  • complete surgical excision impossible > biopsy or debulk only
  • steroids
  • anticonvulsants
  • radiotherapy
  • chemotherapy > temazolamide
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60
Q

management options for brain tumour metastasis

A
  • steroids
  • anticonvulsants
  • radiotherapy > whole brain, steriotatic
  • surgery
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61
Q

prognosis of meningioma

A

commonly cured by surgery
may require anticonvulsants

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62
Q

prognosis of astrocytomas

A

low grade - long-life expectancy
high grade/GBM - average 1 year survival

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63
Q

why should a lumbar puncture NOT be performed when there are signs and symptoms to suggest an intracranial mass lession?

A
  • could cause meningitis
  • could cause a herniation syndrome and the patient could die
  • could cause an air embolism
  • might make headache worse
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64
Q

what is a primary insult caused by head injury?

A

focal and/or diffuse brain trauma

65
Q

what are secondary insults that can be caused by a brain injury?

A
  • hypotension
  • hypoxia
  • infection
  • haematoma
66
Q

how is the initial assessment of a head injury performed?

A
  • concious level assessed using Glasgow Coma Scale.
  • scored out of 15 (GCS 15 fully conscious).
  • correlates with severity of head inury: 13-15 > mild injury, 9-12 > moderate injury, 3-8 > severe injury.
67
Q

describe a linear skull fracture

A
  • commonly temporo-parietal from blow or fall onto side or top of head and may continue onto the skull base, ‘hinge’ fracture.
68
Q

describe a depressed skull fracture

A
  • focal impact which may push fragments inwards to damage the meninges, blood vessels and the brain; risk of meningitis and post-traumatic epilepsy.
69
Q

what type of skull fracture causes a fragmented skull?

A

comminuted (mosaic)

70
Q

describe a ring fracture

A

fracture line encircling the foramen magnum caused by a fall from height, usually landing on the feet, but sometimes the head, leading to the skull base and cervical spine being forced together.

71
Q

describe a ‘contre-coup’ fracture

A

fracturing of the orbital plates (anterior fossa) caused by a fall onto the back of the head.

72
Q

how can a raised ICP without intervention cause death?

A

compression of the brainstem due to herniation of the cerebellar tonsils into the foramen magnum

73
Q

what type of motion can cause subdural haemorrhage?

A

any motion which causes rotational or ‘shearing’ forces can cause the veins to be stretched and torn due to the relative movement between the brain and the dura
- e.g. hyperextension

74
Q

what is the most common cause of subarachnoid haemorrhage?

A

natural disease - rupture of a cerebral artery (‘berry’) aneurysm

75
Q

describe a ‘Coup’ brain contusion

A

occurs when a head is struck with a heavy blow- the contusion is found directly under the site of impact

76
Q

describe a Contre-coup brain contusion

A
  • caused by a moving head striking a fixed object or unyielding surface - contusions are found diamterically oppsite the site of head impact, e.g. a fall onto the back of the head would result in contusions on the frontal and temporal poles and on the undersurface of the frontal lobes.
77
Q

what is a normal ICP?

A

5-15cm of water

78
Q

what ICP is abnormal?

A

sustained increase beyond 20cm of water is pathological

79
Q

describe the Monro-Kellie hypothesis

A
  • intracranial volume is fixed due to a non-compliant skull.
  • contents are non-compressible.
  • change in volume of contents or addition of new space occupying lesion increases pressure unless compensated by reduction of other content.
80
Q

give an example of the Monro Kellie hypothesis

A
  • e.g. large extradural hematoma
    Compensation by brain:
  • reduction of venous blood
  • displacement of CSF towards spine
  • reduction CSF volume

brain has minimal compliance so if these cannot compensate for the increase in volume then ICP rises exponentially

81
Q

pathology of raised ICP (what pathological processes occur due to ICP)

A
  • localised shift of brain across various compartments.
  • focal or global reduction of blood flow.
  • focal or global ischaemia.
  • reduced energy production.
  • pump failure on cell membrane.
  • cellular dysfunction.
  • interstitial microenvironment changes (toxic metabolites)
  • membrane damage and cell death
82
Q

what is normal cerebral blood flow?

A

50ml/100g/min or 700ml/min
- white matter > 20ml/100g/min
- grey matter > 70ml/100g/min

83
Q

what is the cerebral perfusion pressure (CPP)?

A

difference between mean arterial pressure (MAP) and intracranial pressure (ICP)

84
Q

what is cerebro-vascular resistance (CVR)?

A

resistance offered by cerebral vasculature to flowing blood

85
Q

describe autoregulation of cerebral blood flow (CBF)

A
  • ability of brain to maintain constant blood flow over a wide range of pressures
  • brain also has the ability to increase blood flow to specific regions in brain when these are active e.g. temporal lobe during speech
86
Q

what factors does cerebral blood flow (CBF) depend on?

A
  • mean arterial pressure (driving blood into intra-cranial cavity)
  • intracranial pressure (creates a gradient against incoming blood)
  • vascular resistance (low resistance higher flow or vice versa)
  • autoregulatory mechanisms of the brain
87
Q

Describe how autoregulation influences secondary insult following an intracranial
event

A

Injured brain loses its ability to autoregulate hence hypotension, hypertension, hypoxia or raised ICP can lead to significant secondary insult

88
Q

what is the 2nd leading cause of death worldwide?

A

stroke

89
Q

how many stroke deaths occur each year?

A

5 million

90
Q

what % of strokes occur in people >65 (UK)

A

75%

91
Q

how many patients die within 1 year of a stroke (UK)?

A

1/3

92
Q

stroke definition

A

is the sudden onset of focal or global neurological symptoms caused by ischemia or hemorrhage and lasting more than 24 hours.

93
Q

what % of strokes are ischaemic and what % are haemorrhagic?

A

85% ischaemic
15% haemorrhagic

94
Q

what is a transient ischaemic attack?

A

is the sudden onset of focal or global neurological symptoms caused by ischemia that resolve within 24 hours. May precede a stroke.

95
Q

what are causes of ischaemic stroke?

A
  • Large artery atherosclerosis (e.g. Carotid) 35%
  • Cardioembolic (e.g. atrial fibrillation) 25%
  • Small artery occlusion (Lacune) 25%
  • Undetermined/Cryptogenic 10-15%
  • Rare causes (<5%) Arterial dissection, Venous sinus thrombosis
96
Q

what are causes of haemorrhagic stroke?

A
  • Primary intracerebral hemorrhage (70%)
  • Secondary hemorrhage: Subarachnoid hemorrhage, Arteriovenous malformation (30%)
97
Q

what are non-modifiable risk factors in stroke?

A
  • previous stroke
  • age
  • male
  • family history
98
Q

what are modifiable risk factors of stroke?

A
  • hypertension
  • smoking
  • diabetes mellitus
  • hyperlipidaemia
  • heavy alcohol use
  • obesity
  • atrial fibrillation
  • oral contraceptives.
  • malignancy
  • thrombophilia etc.
99
Q

how does hypertension increase the risk of stroke?

A

Chronic hypertension exacerbates atheroma and increases involvement of smaller distal arteries.

100
Q

diabetes mellitus increases the incidence of strokes by?

A

3x

101
Q

anticoagulants such as warfarin and DOACs reduce the risk of ischaemic stroke by?

A

2/3rds

102
Q

what is the arterial supply to the anterior part of the brain?
(most of cerebral hemispheres, cortical deep white matter)

A

2x internal carotid arteries:
- 2x anterior cerebral artery (ACA)
- 2x middle cerebral artery (MCA)

103
Q

what is the arterial supply to the posterior part of the brain?
(brainstem, cerebellum and occipital lobes)

A

2 vertebral arteries > 1 basilar:
- 3 pairs of cerebellar arteries
- 2 posterior cerebral arteries (PCA)

104
Q

list the functions of the frontal lobe

A
  • High level cognitive functions ie. abstraction, concentration, reasoning
  • Memory
  • Control of voluntary eye movement
  • Motor control of speech (dominant hemisphere)
  • Motor cortex
  • Urinary continence
  • Emotion and personality
105
Q

list the functions of the parietal lobe

A
  • Sensory cortex
  • Sensation (identify modalities of touch, pressure, position)
  • Awareness of parts of the body
  • Spatial orientation and visuospatial information (non dominant hemisphere)
  • Ability to perform learned motor tasks (dominant)
106
Q

list the functions of the temporal lobe

A
  • Primary auditory receptive area
  • Comprehension of speech (dominant) – Wernicke’s
  • Visual, auditory and olfactory perception
  • Important role in learning, memory and emotional affect
107
Q

list the functions of the occipital lobe

A
  • primary visual cortex
  • visual perception
  • involuntary smooth eye movement
108
Q

what are the different types of stroke (OCSP stroke classification)?

A
  • total anterior circulation stroke (TACS)
  • partial anterior circulation stroke (PACS)
  • lacunar stroke (LACS)
  • posterior circulation stroke (POCS)
109
Q

OCSP classification of a lacunar stroke (LACS)

A
  • small vessel affected
  • anterior
  • may have weakness (>/= 2/3 face arm leg) and numbness (>/= 2/3 face arm leg)
110
Q

OCSP classification of partial anterior circulation stroke (PACS)

A
  • large/partial vessel affected
  • anterior
  • may have weakness (>/= 2/3 face arm leg) and numbness (>/= 2/3 face arm leg)
  • will have 1 of either hemianopia or dysphasia (LHS) or neglect (RHS)
111
Q

OCSP classification of TACS

A
  • large/total vessels affected
  • anterior
  • may have weakness (>/= 2/3 face arm leg) and numbness (>/= 2/3 face arm leg)
  • must have hemianopia and 1 of either dysphasia (LHS) or neglect (RHS)
112
Q

OCSP classification of posterior circulation stroke (POCS)

A
  • large or small vessels affected
  • posterior
  • may have weakness (>/= 2/3 face arm leg) and numbness (>/= 2/3 face arm leg)
  • may have hemianopia, dysphasia or neglect
  • must have brainsyem +/- cerebellar signs
113
Q

what can a stroke in the right hemisphere cause?

A
  • left hemiplegia (paralysis)
  • homonymous hemianopia e.g. cant see left side of visual field in both eyes
  • neglect syndromes (agnosias): visual agnosia, sensory agnosia, anosagnosia (denial of hemiplegia), prosopagnosia (failure to recognise faces)
114
Q

what are symptoms of a TACS?
(blockage of main artery to one hemisphere)

A
  • complete hemiparesis/numbness
  • loss of vision on one half of visual field (hemianopia)
  • loss of awareness on one side (non-dominant) or dysphasia (dominant)
115
Q

TACS is often due to the blockage of which arteries?

A

carotid or middle cerebral artery

116
Q

what are symptoms of PACS?
(branch of main artery affected)

A

2 of 3 TACS criteria:
- complete hemiparesis/numbness
- loss of vision on one half of visual field (hemianopia)
- loss of awareness on one side (non-dominant) or dysphasia (dominant)

OR

one higher cortical deficit:
- loss of awareness on one side (non-dominant) or dysphasia (dominant)

OR
- monoparesis (partial loss of voluntary motor function in a single limb)

117
Q

symptoms of a lacunar stroke (LACS)?
(small ‘perforating’ artery affected)

A

weakness/numbness of:
- face + arm + leg
- or face + arm
- or arm + leg

  • may have dysarthria
  • ataxic hemiparesis
  • NO effect on higher function e.g. no dysphasia, innattention or hemianopia
118
Q

what are symptoms of POCS?
(any posterior artery affected)

A

combination of symptoms including:
- loss of balance/coordination
- vertigo
- double vision
- dysarthria
- visual loss (hemianopia)

119
Q

what is the 1 year mortality and recurrence rate of TACS?

A

60% and 6%

120
Q

what is the 1 year mortality and recurrence rate of PACS?

A

16% and 17% (high early)

121
Q

what is the 1 year mortality and recurrence rate of LACS?

A

11% and 9% (constant)

122
Q

what is the 1 year mortality and recurrence rate of POCS?

A

19% and 20%

123
Q

what are investigations for stroke performed in all/most patients?

A
  • Routine blood tests (FBC, glucose, lipids, ESR…)
  • CT or MRI head scan (infarct vs. hemorrhage)
  • ECG + Holter (?AF, LVH)
  • Carotid doppler ultrasound (?stenosis)
124
Q

what are investigations for stroke performed in some patients?

A
  • Echocardiogram (valves, ASD, VSD, PFO)
  • Cerebral angiogram/venogram (vasculitis?)
  • Hyper-coaguable blood screen
125
Q

what are some secondary preventative measures for stroke?

A
  • anti-hypertensives
  • anti-platelets
  • lipid-lowering agents
  • warfarin for AF
  • carotid endarterectomy
126
Q

acute management of ischaemic stroke

A
  • CT head to exclude haemorrhage
  • admission to a specialist stroke centre.
  • thrombolysis with tissue plasminogen activator (TPA) such as alteplase** WITHIN 4.5 hours of symptoms onset** and with no contraindications to thrombolysis
  • thrombectomy within 24 hours of symptom onset.
  • aspirin 300mg daily for two weeks (after haemorrhage is excluded with CT).
127
Q

what is a coma?

A

“ A state of unrousable psychological unresponsiveness in which the subjects lie with eyes closed and show no psychologically understandable response to external stimulus or inner need”

128
Q

what does conciousness depend on?

A
  1. arousal (reticular activating system)
  2. awareness of environment (cerebral hemispheres)
129
Q

what are causes of a low Glasgow coma score (GCS)?

A

toxic metabolic states:
- hypoxia/hypercapnia/sepsis/hypotension
- drug intoxication/renal or liver failure
- hypoglycaemia, ketoacidosis

  • seizures
  • damage to reticular activating system
  • causes of raised ICP: tumour, stroke, EDH, SDH, SAH, hydrocephalus
130
Q

what is a persistent vegetative state?

A
  • a state in which the brain stem recovers to a considerable extent but there is no evidence of recovery of cortical function.
  • there is arousal and wakefulness but the patient does not regain awareness or purposeful behaviour of any kind.
131
Q

describe ‘locked-in’ syndrome

A
  • the patient has total paralysis below the level of the third nerve nuclei and, although able to open, elevate and depress the eyes, has no horizontal eye movements and no other voluntary eye movements.
  • the diagnosis depends on recognising that the patient can open their eyes voluntarily and signal numerically by eye closure.
132
Q

describe resuscitation of a coma patient

A
  • ABC
  • blood samples: glucose, biochemistry, haematology, blood gas, toxicology.
  • establish baseline blood pressure, pulse, temperature, IV access and stabilise the neck.
  • examine for evidence of meningitis - treat on suspicion.
133
Q

three components of neurological assessment of coma

A
  • glasgow coma scale GCS
  • brainstem function
  • motor function & reflexes
134
Q

glasgow coma scale

A

The Glasgow Coma Scale should be determined to grade the severity of the impairment in consciousness:
- Eye response (out of 4.: 4 open spontaneously, 3 open to voice, 2 open to pain, 1 do not open.
- Verbal response (out of 5): 5 oriented, 4 confused, 3 inappropriate words, 2 incomprehensible sounds, 1 no sounds.
- Motor response (out of 6): 6 obeys command, 5 localises to pain, 4 withdraws to pain, 3 abnormal flexion to pain, 2 extension to pain, 1 no movement.

135
Q

When does the GCS regard a patient as being in a comatose state?

A

Eye opening - 2 or less
Verbal response - 2 or less
Motor response - 4 or less

GCS of 8 or less

136
Q

how is brainstem function assessed in coma

A
  • by testing cranial nerve function.
137
Q

how is motor function assessed in coma?

A
  • motor response
  • muscle tone
  • tendon reflexes
  • seizures
138
Q

how is a coma without focal or lateralising signs and without meningism investigated?

A
  • toxicology screen including alcohol level
  • measure blood sugar and electrolytes
  • assess hepatic and renal function
  • acid-base assessment and blood gases
  • measure blood pressure
  • consider CO poisoning
139
Q

how is a coma without focal or lateralising signs but with meningism investigated?

A
  • CT head scan
  • lumbar puncture: appearance, cell count, glucose level, capsular antigen tests.
140
Q

how is a coma with focal brainstem or lateralising cerebral signs investigated?

A

CT or MRI obligatory
- if CT/MRI not diagnostic, investigate as for other causes of coma e.g. including metabolic screen, lumbar puncture, EEG.

141
Q

what are causes of a coma without focal brainstem or lateralising cerebral signs and without meningism?

A

toxic
metabolic
systemic e.g. infection
epilepsy

142
Q

what are causes of coma without focal brainstem or lateralising cerebral signs but with meningism?

A

subarachnoid haemorrhage
meningitis
encephalitis

143
Q

what are causes of coma with focal brainstem or lateralising cerebral signs?

A

focal cerebral e.g. tumour, infarct, haemorrhage, abscess

144
Q

prediction of outcome in coma

A

Overall, only 15% of patients in non-traumatic coma for more than 6 hours will make a good or moderate recovery, the other 85% will die, remain vegetative or reach a state of severe disability in which they remain dependent

145
Q

describe the continuing care of patients in a coma

A
  • Maintenance of vital functions
  • Care of skin, avoidance of pressure sores
  • Attention to bladder and bowel function
  • Control of seizures
  • Prophylaxis of DVT, peptic ulceration
  • Prevention of contractures
  • Consider the “Locked - in” Syndrome
146
Q

Head injury can lead to focal neurological signs/Epilepsy due to

A
  • Diffuse axonal injury
  • Contusion
  • Intracerebral haematoma
  • Extra-cerebral haematoma
  • Extra-dural haematoma
  • Sub-dural haematoma
147
Q

describe the management of a head injury

A
  • stabilise cervical spine
  • ABC
  • if GCS is 8 or less > intubation + ventilation
  • treat raised ICP
  • cranial imaging - may need decompressive surgery or removal of haematoma
  • neurological observation
148
Q

how is raised ICP treated?

A
  • surgery to relieve pressure > haematoma, ventricular shunt.
  • osmotic agents e.g. mannitol
  • nurse with head at 30-45% (venous return)
  • reduce pain
  • maintain good PO2, reduce PO2
  • reduce metabolism (reduce temperature, barbiturates)
149
Q

what are characteristics of radiculopathy?

A
  • pain in single dermatome
  • dermatomal sensory disturbance
  • weakness in myotome
  • loss of reflex
150
Q

what are long tract signs that occur due to myelopathy?

A
  • clonus
  • upgoing plantars
  • increased tone
  • Hoffman sign
  • brisk reflexes
  • proprioception impairment: Romberg’s test, tandem walking
151
Q

what does the GCS score assess medically? (not concious level, think more of the actual brain mechanisms that allow conciousness)

A

cerebral perfusion level

152
Q

what a pathology that can cause unreactive pupils when assessing an unconscious patient?

A

herniation of brain contents

153
Q

what part of the frontal lobe mediates (Restraint) empathic, civil and socially appropriate behaviour?

A

orbitofrontal cortex

154
Q

On a CT head of a 50 year old patient a tumour is identified in the cerebellum. Which signs might you elicit on examination of this patient? DANISH-P

A
  • Dysdiadochokinesia
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Slurred speech
  • Hypotonia
  • Past pointing (dysmetria)
155
Q

what is the most common primary brain tumour in adults?

A

glioblastoma multiforme

156
Q

what are gliomas?

A

tumours of the glial cells in the brain or spinal cord
- most common types: GMB, oligodendroglioma, ependymoma

157
Q

what is the most common malignant primary brain tumour in children?

A

medullablastoma

158
Q

what is the most common primary brain tumour in children?

A

pilocytic-astrocytoma (benign)

Neurology Systems (14 decks)

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