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Neurology > 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
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2
Q

ways of measure pressure in the cranium

A
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3
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
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4
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
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5
Q

cushings triad

A

hypertension
bradycardia
irregular breathing

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6
Q

too much blood can be due to

A
  • Too much blood within cerebral vessels (rare)
  • Too much blood outside the cerebral vessels (haemorrhage)
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7
Q

Too much blood within cerebral vessels (rare)

A
  • Raised arterial pressure- malignant hypertension
  • Raised venous pressure- SVC obstruction
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8
Q

Too much blood outside the cerebral vessels (haemorrhage)

A

o Extradural
o Subdural
o Subarachnoid

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9
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

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10
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

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11
Q

intracranial haemorrhage background

A

Extradural bleeds

Subdural bleeds

Subarachnoid haemorrhage

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12
Q

Risk factors intracranial haemorrhage

A
  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke progressing to haemorrhage
  • Brain tumours
  • Anticoagulants
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13
Q

Investigations/ assessment for intracranial haemorrhage

A
  • Glasgow coma scale
  • Imaging
    o CT
    o MRI
    o Angiography
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14
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
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15
Q

location. of extradural/epidural bleeds

A
  • Occurs between the skull and dura mater
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16
Q

extradural/epidural bleeds pathophysiology

A

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

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17
Q

Extradural/ epidural CT findings

A
  • Bi-convex (lemon) shape and limited by cranial sutures
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18
Q

extradural typical history

A
  • Young patient with TBI that has ongoing headache
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19
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
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20
Q

subdural bleeds location

A
  • Outermost layer of meningeal layer (dura mater and arachnoid mater)
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21
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)

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22
Q

Subdural CT findings

A
  • Crescent shape and not limited by cranial sutures)
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23
Q

location of subarachnoid haemorrhage

A
  • Bleeding into the subarachnoid space where CSF is located
  • Between pia mater and arachnoid membrane
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24
Q

delete - subarachnoid haemorrhage background

A
  • A type of stroke 6%
  • Causes
  • Can occur in trauma
  • Usually spontaneous
  • High mortality and morbidity
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25
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
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26
Q

subarachnoid associated with

A

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

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27
Q

pathophysiology of subarachnoid

A
  • Ruptured cerebral aneurysm
  • berry aneurysm
28
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

29
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

30
Q

too much CSF also known as

A

hydrocephalus

31
Q

Pathophysiology hydrocephalus

A
  • Congenital
  • Acquired
  • Non-communicating vs communicating
32
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
33
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
34
Q

Management of hydrocephalus

A
  • VP shunt- ventricles- peritoneum
  • VA shunt- ventricles- atria
35
Q

Acquired causes of hydrocephalus

A
  • Intraventricular haematoma
  • Tumour
  • Infection
  • Trauma
36
Q

too much CSF is either caused by

A

Obstruction (non communicating)

Too much CSF produced (communicating)

37
Q

Too much CSF- Obstructive

A

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

38
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
39
Q

causes of too much brain

A
  • cerebral oedema (swelling of the brain)
  • Brain tumour (metastatic or primary, meningiomas)
  • Cerebral abscess
40
Q

too much brainestablishing a diagnosis

A
41
Q

management of too much brain basics

A
42
Q

cerebral abscess

A
  • Localised pus formation with capsulation within brain parenchyma
  • Causes: spread of infection (direct (mastoiditis) vs distance), trauma or unknown
43
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
44
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
45
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
46
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
47
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)
48
Q
A
  • MRI head
  • Intraaxial
  • Cyclical lesion near the foramen of Monroe
  • Hyperintense and well circumscribed
  • No mass effect
  • No hydrocephalus
  • Diagnosis -> colloid cyst
49
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
50
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
51
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
52
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

53
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
54
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

55
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
56
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).
57
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.

58
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

59
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

60
Q

function of the frontal lobe

A

voluntary motor, behaviour, personality, reasoning, speaking

61
Q

function of the temporal love

A

memory hearing understaning language

62
Q

parietal love

A

sensation, spatial awareness and processing, reading

63
Q

occipital

A

vision, colour perception, recognising faces and object

64
Q

cerebellum

A

balance, coordination of voluntary movement

65
Q

brainstem

A

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

Neurology (12 decks)

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