5- Neurology (Emergencies: Raised intracranial pressure, haemorrhage, brain tumour) Flashcards
normal intracranial pressure
ways of measure pressure in the cranium
Monroe Kellie doctrine
= 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
intracranial elastance curve
- As intracranial volume increases initially ICP stays the same due to compensatory mechanisms
- After mechanisms exhausted the ICP will increase
3 components which creat intracranial pressure
blood
CSF
brain
RICP=
too much blood
too much CSF
too much brain
blood
Need constant blood supply to supply neurones and brain tissue. Incredibly sensitive to low oxygen.
cerebral perfusion pressure
Cerebral perfusion pressure (CCP)
Represents cerebral blood flow.
- If ICP increased, perfusion of the brain decreases (without cerebral autoregulation)- BV will vasodilate
Cerebral autoregulation
- 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
CSF production and management
- CSF produced by the choroid plexus into the lateral ventricles -> 3rd -> 4th ventricles
- Around 500mls produced each day
- Homeostasis, protection, buoyancy and waste clearance
types of brain herniation
- If herniating, usually high pressure inside
- Types of herniation
o Subfalcine herniation (commonest)
o Tonsillar herniation (aka coning)
o Uncal herniation
pathophysiology of RICP
- Too much blood
- Too much CSF
- Too much brain
presentation of RICP
- 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
cushings triad
hypertension
bradycardia
irregular breathing
too much blood can be due to
- Too much blood within cerebral vessels (rare)
- Too much blood outside the cerebral vessels (haemorrhage)
Too much blood within cerebral vessels (rare)
- Raised arterial pressure- malignant hypertension
- Raised venous pressure- SVC obstruction
Too much blood outside the cerebral vessels (haemorrhage)
o Extradural
o Subdural
o Subarachnoid
Malignant (accelerated) hypertension
- 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
Superior vena cava (SVC) obstruction
- 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
intracranial haemorrhage background
Extradural bleeds
Subdural bleeds
Subarachnoid haemorrhage
Risk factors intracranial haemorrhage
- Head injury
- Hypertension
- Aneurysms
- Ischaemic stroke progressing to haemorrhage
- Brain tumours
- Anticoagulants
Investigations/ assessment for intracranial haemorrhage
- Glasgow coma scale
- Imaging
o CT
o MRI
o Angiography
Principles of management of intracranial haemorrhage
- 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
location. of extradural/epidural bleeds
- Occurs between the skull and dura mater
extradural/epidural bleeds pathophysiology
Rupture of the middle meningeal artery in temporo-parietal region e.g. associated with fracture of temporal bone
Extradural/ epidural CT findings
- Bi-convex (lemon) shape and limited by cranial sutures
extradural typical history
- Young patient with TBI that has ongoing headache
extradural presentation
- 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
subdural bleeds location
- Outermost layer of meningeal layer (dura mater and arachnoid mater)
subdural pathophysiology
- 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)
Subdural CT findings
- Crescent shape and not limited by cranial sutures)
location of subarachnoid haemorrhage
- Bleeding into the subarachnoid space where CSF is located
- Between pia mater and arachnoid membrane
subarachnoid haemorrhage background
- A type of stroke 6%
- Causes
- Can occur in trauma
- Usually spontaneous
- High mortality and morbidity
subarachnoid haemorrhage risk factors
- 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
subarachnoid associated with
Associations
- Cocaine
- SCC
- Marfans or Ehlers Danlos
- Autosomal dominant polycystic kidney disease
pathophysiology of subarachnoid
- Ruptured cerebral aneurysm
- berry aneurysm
presentation of subarachnoid
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
investigations subarachnoid
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
too much CSF also known as
hydrocephalus
Hydrocephalus
Background
- CSF build up abnormally in the brain and spinal cord
- Due to over-production or problems draining or absorbing CSF
Pathophysiology hydrocephalus
- Congenital
- Acquired
- Non-communicating vs communicating
congenital hydrocephalus background
- Present at birth
- Genetic and non-genetic factors e.g. mutation in L1CAM gene linked to aqueductal stenosis
Pathophysiology congenital hydrocephalus
- Most common cause is aqueductal stenosis ->Insuff drainage of CSF
- Cerebral aqueduct which connect third and fourth ventricle is stenosed
Presentation of hydrocephalus
- 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
Management of hydrocephalus
- VP shunt- ventricles- peritoneum
- VA shunt- ventricles- atria
Normal CSF Physiology
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.
Acquired causes of hydrocephalus
- Intraventricular haematoma
- Tumour
- Infection
- Trauma
too much CSF is either caused by
Obstruction (non communicating)
Too much CSF produced (communicating)
Too much CSF- Obstructive
(non-communicating)
A blockage to the flow of CSF
Too much CSF- Communicating hydrocephalus
- Overproduction of CSF or
- Reduced absorption of CSF
- Examples of cause
Choroid plexus papilloma
Infection and inflammation leading to scarring at subarachnoid space
Ventriculoperitoneal Shunt
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
causes of too much brain
- cerebral oedema (swelling of the brain)
- Brain tumour (metastatic or primary, meningiomas)
- Cerebral abscess
too much brainestablishing a diagnosis
management of too much brain basics
cerebral abscess
- Localised pus formation with capsulation within brain parenchyma
- Causes: spread of infection (direct (mastoiditis) vs distance), trauma or unknown
space occupying lesion presentation depends on
- 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
imaging for query SoL
- 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
differential diagnosis for SoL
- 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
describing mass on head imaging
- 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
- 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)
- MRI head
- Intraaxial
- Cyclical lesion near the foramen of Monroe
- Hyperintense and well circumscribed
- No mass effect
- No hydrocephalus
- Diagnosis -> colloid cyst
- 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
- 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
- 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
Brain tumours
Background
- Abnormal growths within the brain
- Various types
Causes of brain tumours
Risk factors
- Meningiomas -> benign
- Gliomas-> highly malignant
- Pituitary tumours
- Acoustic neuroma
- Metastasis
o Lung
o Breast
o Renal cell carcinoma
o Melanoma
presentation of brain tumour
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
Management of brain tumours general
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
Treatment of Pituitary Tumours
- Trans-sphenoidal surgery
- Radiotherapy
- Bromocriptine to block prolactin-secreting tumours
- Somatostatin analogues (e.g. ocreotide) to block growth hormone-secreting tumours
Gliomas
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).
Meningiomas
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.
Pituitary Tumours
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
Acoustic neuromas
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
function of the frontal lobe
voluntary motor, behaviour, personality, reasoning, speaking
function of the temporal love
memory hearing understaning language
parietal love
sensation, spatial awareness and processing, reading
occipital
vision, colour perception, recognising faces and object
cerebellum
balance, coordination of voluntary movement
brainstem
autonomic function
breathing, consciousness, blood pressure, heart rate, and sleep
brainstem
autonomic function
breathing, consciousness, blood pressure, heart rate, and sleep
