Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurology and special senses (Y4) > 5- Neurology (Emergencies: Raised intracranial pressure, haemorrhage, brain tumour) > Flashcards

5- Neurology (Emergencies: Raised intracranial pressure, haemorrhage, brain tumour) Flashcards

1
Q

normal intracranial pressure

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ways of measure pressure in the cranium

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Monroe Kellie doctrine

A

= sum of volumes of brain, CSF and intracranial blood is constant
- Skull is a rigid box
- If one of these components is lost e.g. a bleed or tumour (SOL) , other components of this volume will need to reduce to make sure the sum of volume stays constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

intracranial elastance curve

A
  • As intracranial volume increases initially ICP stays the same due to compensatory mechanisms
  • After mechanisms exhausted the ICP will increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 components which creat intracranial pressure

A

blood
CSF
brain

RICP=
too much blood
too much CSF
too much brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

blood

A

Need constant blood supply to supply neurones and brain tissue. Incredibly sensitive to low oxygen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cerebral perfusion pressure

A

Cerebral perfusion pressure (CCP)
Represents cerebral blood flow.

  • If ICP increased, perfusion of the brain decreases (without cerebral autoregulation)- BV will vasodilate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cerebral autoregulation

A
  • If MAP increases then CPP increases, triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
  • If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow (vasodilatation)  will result in having to increase MAP- therefore hypertension
  • If CPP <50 mmHg then cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
  • ICP can be maintained at a constant level as an intracranial mass expands, up to a certain point beyond which ICP will rise at a very rapid (exponential) rate
  • Damage to the brain can impair or even abolish cerebral autoregulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CSF production and management

A
  • CSF produced by the choroid plexus into the lateral ventricles -> 3rd -> 4th ventricles
  • Around 500mls produced each day
  • Homeostasis, protection, buoyancy and waste clearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

types of brain herniation

A
  • If herniating, usually high pressure inside
  • Types of herniation
    o Subfalcine herniation (commonest)
    o Tonsillar herniation (aka coning)
    o Uncal herniation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pathophysiology of RICP

A
  • Too much blood
  • Too much CSF
  • Too much brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

presentation of RICP

A
  • Headaches
    o At night time, waking and bending over
  • Nausea + vomiting
  • Visual disturbances e.g. double vision
  • Drop of >2 in GCS
    o Confusion
    o Seizures
    o Amnesia
  • Papilledema
  • Focal neurological signs
    o E.g. CN3 palsy – papillary dilatation
    o Bilateral abducens nerve palsy
  • Abnormal posturing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cushings triad

A

hypertension
bradycardia
irregular breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

too much blood can be due to

A
  • Too much blood within cerebral vessels (rare)
  • Too much blood outside the cerebral vessels (haemorrhage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Too much blood within cerebral vessels (rare)

A
  • Raised arterial pressure- malignant hypertension
  • Raised venous pressure- SVC obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Too much blood outside the cerebral vessels (haemorrhage)

A

o Extradural
o Subdural
o Subarachnoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Malignant (accelerated) hypertension

A
  • Systolic >180mmHg or Diastolic >120mmHg
  • Usually renal cause in children

Signs of target organ damage

  • Retinal haemorrhages
  • Encephalopathy
  • Left ventricular hypertrophy
  • Reduced renal function

Urgent referral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Superior vena cava (SVC) obstruction

A
  • Reduction in venous return from head & neck & upper limbs
  • Most common cause is malignancy e.g. Non-Hodgkin’s in children
  • Oncology Emergency

Presentation
- Local oedema of the face and upper limbs
- Dilated veins in the arm and neck and anterior chest wall
- SoB
- Difficulty swallowing
- After lifting arms the signs will get worse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

intracranial haemorrhage background

A

Extradural bleeds

Subdural bleeds

Subarachnoid haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk factors intracranial haemorrhage

A
  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke progressing to haemorrhage
  • Brain tumours
  • Anticoagulants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Investigations/ assessment for intracranial haemorrhage

A
  • Glasgow coma scale
  • Imaging
    o CT
    o MRI
    o Angiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Principles of management of intracranial haemorrhage

A
  • Immediate non- contrast CT head to establish the diagnosis
  • Check FBC and clotting
  • Admit to a specialist stroke unit
  • Discuss with a specialist neurosurgical centre to consider surgical treatment
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

location. of extradural/epidural bleeds

A
  • Occurs between the skull and dura mater
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

extradural/epidural bleeds pathophysiology

A

Rupture of the middle meningeal artery in temporo-parietal region e.g. associated with fracture of temporal bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Extradural/ epidural CT findings

A
  • Bi-convex (lemon) shape and limited by cranial sutures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

extradural typical history

A
  • Young patient with TBI that has ongoing headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

extradural presentation

A
  • Prolonged headache after injury
    - LOC and then lucid interval- Liam Neeson wife
    o Period of improved neurological symptoms and consciousness followed by rapid decline over hours as the haematoma get large enough to compress structures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

subdural bleeds location

A
  • Outermost layer of meningeal layer (dura mater and arachnoid mater)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

subdural pathophysiology

A
  • Torn bridging veins
    o Spontaneous in elderly or Alcoholic due to atrophy of brain
    o Trauma

Subdural - venous (lower pressure)
Extradural- arterial (more dangerous because higher pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Subdural CT findings

A
  • Crescent shape and not limited by cranial sutures)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

location of subarachnoid haemorrhage

A
  • Bleeding into the subarachnoid space where CSF is located
  • Between pia mater and arachnoid membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

subarachnoid haemorrhage background

A
  • A type of stroke 6%
  • Causes
  • Can occur in trauma
  • Usually spontaneous
  • High mortality and morbidity
33
Q

subarachnoid haemorrhage risk factors

A
  • More likely in females(1.6:1)
  • More likely in black, Finnish and Japanese populations
  • Average age of onset is 50-55 yrs
  • Smoking, HTN, alcohol, cocaine
  • Fx
34
Q

subarachnoid associated with

A

Associations
- Cocaine
- SCC
- Marfans or Ehlers Danlos
- Autosomal dominant polycystic kidney disease

35
Q

pathophysiology of subarachnoid

A
  • Ruptured cerebral aneurysm
  • berry aneurysm
36
Q

presentation of subarachnoid

A

Headache(48%) – thunderclap
* Sudden onset
* Often occurs during strenuous activity e.g. wright lifting or sex

Other features
* Neck stiffness – irritation of meninges
* Dizziness
* Diplopia
* Neurological:
* Visual loss (anterior communicating artery aneurysm)
* Weakness
* Seizure
* LoC

37
Q

investigations subarachnoid

A

First line: CT
* Hyper attenuation in subarach space due to blood

Lumbar puncture
* Only if CT head is negative
* RBC raised in CSF and Xanthochromia (yellow colour of CSF due to bilirubin)

Angiography (CT or MRI) – locate bleed

38
Q

too much CSF also known as

A

hydrocephalus

39
Q

Hydrocephalus
Background

A
  • CSF build up abnormally in the brain and spinal cord
  • Due to over-production or problems draining or absorbing CSF
40
Q

Pathophysiology hydrocephalus

A
  • Congenital
  • Acquired
  • Non-communicating vs communicating
41
Q

congenital hydrocephalus background

A
  • Present at birth
  • Genetic and non-genetic factors e.g. mutation in L1CAM gene linked to aqueductal stenosis
42
Q

Pathophysiology congenital hydrocephalus

A
  • Most common cause is aqueductal stenosis ->Insuff drainage of CSF
  • Cerebral aqueduct which connect third and fourth ventricle is stenosed
43
Q

Presentation of hydrocephalus

A
  • Enlargement of head circumference- sutures not fused – occipito-frontal circumference
     Bulging from anterior fontanelles
     Poor feeding and vomiting
     Poor tone
     Sleepiness
  • Downward gaze
  • Delay in neurological development
44
Q

Management of hydrocephalus

A
  • VP shunt- ventricles- peritoneum
  • VA shunt- ventricles- atria
45
Q

Normal CSF Physiology

A

There are four ventricles in the brain: two lateral ventricles, the third and the fourth ventricles. The ventricles containing CSF. The CSF provides a cushion for the brain tissue. CSF is created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles. CSF is absorbed into the venous system by the arachnoid granulations.

46
Q

Acquired causes of hydrocephalus

A
  • Intraventricular haematoma
  • Tumour
  • Infection
  • Trauma
47
Q

too much CSF is either caused by

A

Obstruction (non communicating)

Too much CSF produced (communicating)

48
Q

Too much CSF- Obstructive

A

(non-communicating)
A blockage to the flow of CSF

49
Q

Too much CSF- Communicating hydrocephalus

A
  • Overproduction of CSF or
  • Reduced absorption of CSF
  • Examples of cause
     Choroid plexus papilloma
     Infection and inflammation leading to scarring at subarachnoid space
50
Q

Ventriculoperitoneal Shunt

A

Placing a VP shunt that drains CSF from the ventricles into another body cavity is the mainstay of treatment for hydrocephalus. Usually the peritoneal cavity is used to drain CSF, as there is plenty of space and it is easily reabsorbed. The surgeon places a small tube (catheter) through a small hole in the skull at the back of the head and into one of the ventricles. A valve on the end of this tube is placed subcutaneously, and a catheter on the other side of the valve runs under the skin into the peritoneal cavity. The valve helps to regulate the amount of CSF that drains from the ventricles.

VP Shunt Complications
* Infection
* Blockage
* Excessive drainage
* Intraventricular haemorrhage during shunt related surgery
* Outgrowing them (they typically need replacing around every 2 years as the child grows

51
Q

causes of too much brain

A
  • cerebral oedema (swelling of the brain)
  • Brain tumour (metastatic or primary, meningiomas)
  • Cerebral abscess
52
Q

too much brainestablishing a diagnosis

A
53
Q

management of too much brain basics

A
54
Q

cerebral abscess

A
  • Localised pus formation with capsulation within brain parenchyma
  • Causes: spread of infection (direct (mastoiditis) vs distance), trauma or unknown
55
Q

space occupying lesion presentation depends on

A
  • Seizure
  • RICP headache
    o Vomiting
    o Papilledema
  • Focal neurology and gait disturbance
  • Neuropsychiatric effects
    o Personality
    o Mental state
    o Memory and cognition
  • Endocrine abnormalities (pituitary)
  • Incidental finding e.g. after minor head injury
56
Q

imaging for query SoL

A
  • CT non contrast
  • MRI usually done with contrast
    o Contrast helps make vascularity more prominent, helpful if tumour or infection suspected
    o Have to have working kidneys
  • Diffusion weighted MRI
  • Specialist MRI e.g. MR spectroscopy or MR perfusion
57
Q

differential diagnosis for SoL

A
  • Vascular
    o Haemorrhage
    o Infarct
    o Vascular malformation
    o Aneurysm
  • Infective
    o Abscess
  • Neoplastic
    o Metastasis
    o Primary brain tumours
  • Cyst
  • Inflammatory
    o MS
    o Granulomatous disease
58
Q

describing mass on head imaging

A
  • Patient and imaging technique used
  • Intra or extra-axial
  • Shape
  • Location
    o Supra or infratentorial
    o Lobes/ part of brain involved
  • Density OR intensity
    o Hypo/hyperdense used with CT
    o Hypo/hyperintense used with MRI
  • Border
    o How defined
    o Oedema
  • Contrast enhancement
    o Homogenous/heterogenous
    o Rim enhancement
  • Mass effect
    o Effacement of sulci : ipsilateral / contralateral
    o Midline shift
    o Ventricle compression
    o Basal cisterns: obliterated/patent
  • Hydrocephalus
59
Q
A
  • CT head without contrast
  • Intraaxial (within brain parenchyme) large irregularly shaped lesion
  • Within the front right frontal temporal lobe
  • Hypodense compared to surrounding brain
  • Well defined border
  • A degree of midline shift and contralateral hydrocephalus
  • Diagnosis- > infarct (hypodense area typically of infarct with the distribution of the right MCA)
60
Q
A
  • MRI head
  • Intraaxial
  • Cyclical lesion near the foramen of Monroe
  • Hyperintense and well circumscribed
  • No mass effect
  • No hydrocephalus
  • Diagnosis -> colloid cyst
61
Q
A
  • MRI head T1 weighted image with contrast
  • An extraaxial (outside the brain e.g. meninges) lesion arising from the left temporal convexity
  • Irregular in shape and hyperintense
  • Well circumscribed borded
  • Enhanced homogenously with contrast
  • Mass effect, however no hydrocephalus
  • Diagnosis -> meningioma
62
Q
A
  • CT with contrast
  • Intraaxial circular lesion within the left frontal lobe
  • Hypodense
  • Well circumscribed contrast enhancing border
  • Mass effect due to sulcular effacement ipsilaterally
  • Cant comment on hydrocephalus as no ventricles visible
  • Diagnosis -> abscess
63
Q
A
  • CT head without contrast
  • Intraaxial lesion which is deep to the right frontal temporal lobes and extends into the ventricular system
  • Well circumscribed
  • Hyperdense throughout
  • Mass effect as evidenced by ipsilateral sulcal effacement and midline shift
  • Associated hydrocephalus
  • Hyperdense signals in the occipital ventricles indicating areas of haemorrhage
  • Diagnosis -> Intraparenchymal haemorrhage
64
Q

Brain tumours
Background

A
  • Abnormal growths within the brain
  • Various types
65
Q

Causes of brain tumours

A

Risk factors
- Meningiomas -> benign
- Gliomas-> highly malignant
- Pituitary tumours
- Acoustic neuroma
- Metastasis
o Lung
o Breast
o Renal cell carcinoma
o Melanoma

66
Q

presentation of brain tumour

A

Presentation

  • Often asymptomatic when small
  • Focal neurological symptoms depending on location of lesion
  • RICP
    o Headache
     Constant
     Nocturnal
     Worse on wakening
     Worse on coughing, straining or bending forward
     Vomiting
    o Papilledema (fundoscopy)
    o Visual field defects
    o Altered mental state
    o Seizures
    o Unilateral ptosis
    o Third and sixth nerve palsies
67
Q

Management of brain tumours general

A

There is massive variation in brain tumours from completely benign to extremely malignant. Surgery is dependent on the grade and behaviour of the brain tumour.
Management options include:
* Palliative care
* Chemotherapy
* Radiotherapy
* Surgery

68
Q

Treatment of Pituitary Tumours

A
  • Trans-sphenoidal surgery
  • Radiotherapy
  • Bromocriptine to block prolactin-secreting tumours
  • Somatostatin analogues (e.g. ocreotide) to block growth hormone-secreting tumours
69
Q

Gliomas

A

Gliomas are tumours of the glial cells in the brain or spinal cord. There are three types to remember (listed from most to least malignant):

  • Astrocytoma (glioblastoma multiforme is the most common)
  • Oligodendroglioma
  • Ependymoma
    Gliomas are graded from 1-4. Grade 1 are most benign (possibly curable with surgery). Grade 4 are the most malignant (glioblastomas).
70
Q

Meningiomas

A

Meningiomas are tumours growing from the cells of the meninges in the brain and spinal cord. They are usually benign, however they take up space and this mass effect can lead to raised intracranial pressure and neurological symptoms.

71
Q

Pituitary Tumours

A

Pituitary tumours tend to be benign. If they grow large enough they can press on the optic chiasm causing a specific visual field defect called a bitemporal hemianopia. This causes loss of the outer half of the visual fields in both eyes. They have the potential to cause hormone deficiencies (hypopituitarism) or to release excessive hormones leading to:
* Acromegaly
* Hyperprolactinaemia
* Cushing’s disease
* Thyrotoxicosis

72
Q

Acoustic neuromas

A

are tumours of the Schwann cells surrounding the auditory nerve that innervates the inner ear. They occur around the “cerebellopontine angle” and are sometimes referred to as cerebellopontine angle tumours. They are slow-growing but eventually grow large enough to produce symptoms and become dangerous.
Acoustic neuromas are usually unilateral. Bilateral acoustic neuromas are associated with neurofibromatosis type 2.
Classic symptoms of an acoustic neuroma are:
* Hearing loss
* Tinnitus
* Balance problems

They can also be associated with a facial nerve palsy

73
Q

function of the frontal lobe

A

voluntary motor, behaviour, personality, reasoning, speaking

74
Q

function of the temporal love

A

memory hearing understaning language

75
Q

parietal love

A

sensation, spatial awareness and processing, reading

76
Q

occipital

A

vision, colour perception, recognising faces and object

77
Q

cerebellum

A

balance, coordination of voluntary movement

78
Q

brainstem

A

autonomic function
breathing, consciousness, blood pressure, heart rate, and sleep

79
Q

brainstem

A

autonomic function
breathing, consciousness, blood pressure, heart rate, and sleep

Neurology and special senses (Y4) (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions