Headache Flashcards
Which reflex regulates MAP by adjusting cardiac output and total peripheral resistance
baroreceptor reflex
if a patient has a blood pressure of 120/80 how would you estimate their MAP
MAP = 1/3 pulse pressure + diastolic pressure
1/3 (120-80) +80
13.3 +80
93.3 mmHg
what does CPP stand for
cerebral perfusion pressure
what does ICP stand for
intracranial pressure
how is ICP measured
by inserting a pressure transducer into brain parenchyma or a catheter into the lateral ventricle
what can a fall in cerebral perfusion pressure lead to
can result in cerebral ischaemia and eventually neuronal death
how is intracranial pressure measured
by inserting a pressure transducer into the brain parenchyma or a catheter into the lateral ventricle
what does the munro Kellie doctrine state
is that the sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two.
Some examples of the blood brain barrier and diseases that can affect it
eclampsia - makes the membrane more permeable and so results in pulmonary oedema
Meningitis - makes it more permeable to toxins and some antibiotics
HIV virus - thought to cross the barrier by hiding in monocytes to cause encephalitis
equation for CPP (Cerebral perfusion pressure)
CPP = MAP - ICP MAP = 1/3 pulse pressure + diastolic
in the context of trauma what can a decrease in MAP and increase in ICP result in
a catastrophic decrease in CPP
relationship between hyper/hypocapnia and cerebral perfusion
Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and hypocapnia induces cerebral vasoconstriction and decreases CBF.
what is the cerebral metabolic rate
The cerebral metabolic rate of oxygen (CMRO2) is the rate of oxygen consumption by the brain, and is thought to be a direct index of energy homeostasis and brain health.
What is autoregulation and how does it affect cerebral blood flow and ICP?
Autoregulation of cerebral blood flow is the ability of the brain to maintain relatively constant blood flow despite changes in perfusion pressure
how does a headache occur (nerves)
The headache occurs when the 5th cranial (trigeminal) nerve is stimulated. This nerve sends impulses (including pain impulses) from the eyes, scalp, forehead, upper eyelids, mouth, and jaw to the brain.
cerebral venous thrombosis (in terms of headache)
Cerebral venous thrombosis (CVT) is an uncommon cerebrovascular disease presenting with a remarkably wide spectrum of signs and mode of onset. In all series, headache is the most frequently occurring symptom at any time, present in over 80% of cases,1 and it is also the commonest initial symptom.
what is anopsia (aka anopia)
also known as blindness, is the absence of vision due to either a structural defect of the eye(s) or the lack of the eye(s) completely.
what is a scotoma
a partial loss of vision or blind spot in an otherwise normal visual field.
what does it mean if pupils are equal and reactive to light
that shining a light into the eye causes constriction of the ipsilateral pupil (direct reflex) and of the contralateral pupil (consensual reflex)
where is CSF produced
produced by the choroid plexus mainly in the lateral ventricles of the brain
(around 500mls a day)
composition of CSF
few cells
lower protein and glucose concentrations than in plasma
Brief description of CSF fluid flow
- through foramen of munro to third ventricle
- through aqueduct of Slyvius to the fourth ventricle
- through foramina of Luschka (lateral) and foramen of Magendie (midline) into the cisterna magna behind medulla and under the cerebellum
- Cisterna magna is continuous with subarachnoid space
- CSF flows upward over the brain and is reabsorbed by arachnoid granulations into venous sinus blood
Cushioning function of the CSF
brain and CSF have almost identical specific gravity
brain floats and is cushioned by CSF
minor blows to head cause skull and brain to move simultaneously so it doesn’t get bashed against a hard surface
metabolic function of CSF
- helps ,maintain a constant environment for brain cells
- drains unwanted metabolites from venous blood
- transports hormones from one side of the brain to the other
three (basic) causes of increased ICP
- Increase in brain volume : localised space occupying lesion (tumour, abscess), generalised brain oedema (hyponatremia, hypertensive encephalopathy)
- increase in blood volume: Intracerebral, subdural bleeding, vasodilation due to hypercapnia, decreased venous draining due to thrombosis , cough, head down tilt
- increase in CSF volume: hydrocephalus, meningitis
describe idiopathic intracranial hypertension
- cause unknown
- headaches worse on coughing or sneezing
- examination is normal apart from papilloedema
- refer to neurologist
- requires CT/MRI to exclude other causes of increase ICP
- lumbar puncture to measure opening pressure
brief description of hydrocephalus
what is non communicating due to? what is communicating due to?
- accumulation of CSF resulting in an increase in ICP
- Non communicating would be due to blockage somewhere between foramen of munro and foramina of Luschka and Magendie
- communicating would be due to failure to drain via the arachnoid granulations
features indicating rising ICP
- headache due to stretch receptors and nociceptors around intracranial vessels and with the dura mater, worse in the morning
- nausea and vomiting due to pressure on vomiting centres in brain stem
- visual disturbances due to raised pressure around the optic nerve
- seizure
- decreased level of consciousness from drowsy to eventual deep coma
- abnormal posturing ( decorticate and decerebrate)
- Cushing response
- Brain death when ICP exceed CPP
what is papilloedema
Papilledema is swelling of your optic nerve, which connects the eye and brain. This swelling is a reaction to a buildup of pressure in or around your brain that may have many causes.
Describe oculomotor palsy (CNIII)
A complete third nerve palsy causes a completely closed eyelid and deviation of the eye outward and downward. The eye cannot move inward or up, and the pupil is typically enlarged and does not react normally to light.
what does uncal herniation cause/what is it
herniation of part of the temporal lobe over the tentorium cerebelli and it causes ipsilateral CN III (oculomotor) palsy and a blown pupil
warning with doing a lumbar puncture in ICP
do not perform an LP in a patient with raised ICP unless they have idiopathic intracranial pressuree
describe decorticate posturing
indicates severe brain injury
flexor response spontaneously or in response to pain
M3 on glasgow coma scale
damage to upper midbrain
an abnormal posturing in which a person is stiff with bent arms, clenched fists, and legs held out straight.
describe decerebrate posturing
indicates severe brain injury
extensor response spontaneously or in response to pain
M2 on Glasgow coma scale
damage to upper pons
describe Cushing response/ reflex
- attempts to raise MAP to increase CPP and CBF
- triggered by brainstem ischaemia due to increase in ICP
- indicates that death may be imminent unless ICP reduced
- sympathetic activation causes a rise in TPR and hence increase in MAP and systolic pressure
- In response to increase in MAP the baroreceptor reflex causes a bradycardia through increased vagal parasympathetic tone
Cushings triad (in context of a head trauma)
- Decreased heart rate
- increased systolic blood pressure
- disordered breathing pattern with pattern of alternating apnoea and sighing
-get immediate senior help from anaesthetist, intensivist and neurosurgeon to decrease ICP
what is mononuclear vision loss and where is the lesion located
Loss of vision in one eye
Lesion is in optic nerve (right after the eye)
what is bitemporal hemianopia and where is the lesion located
visual loss of half in both eyes
For example: loss of left half in left eye and right half in right eye
lesion is in the optic chiasm - where the optic nerves meet
what is contralateral hemianopia and where is the lesion located
visual loss of half in both eyes
for example: loss of half left in left eye and half left in right eye
lesion can be in the optic tract ( after optic chiasm) or optic radiations
another name for idiopathic intracranial pressure
pseudotumour cerebri
difference between intracranial and intracerebral
The former refers to all bleeding occurring within the skull, while the latter indicates bleeding within the brain parenchyma.
difference between extradural, subdural and subarachnoid
extradural is on the outside of the natural covering of the brain (‘dura mater’)
subdural is on the inner surface of the dura
subarachnoid is under the arachnoid layer
stroke vs infarct
stroke is the sudden onset neurological onset whereas an infarct is what causes the stroke
what is an incidentaloma
victim of medical imaging technology
find something even when not looking for it
Saccular (berry) aneurysm
Berry (saccular) aneurysms are the most common type of intracranial aneurysm, representing 90% of cerebral aneurysms. Generally speaking, there is a ballooning arising from a weakened area in the wall of a blood vessel in the brain.
Saccular aneurysms are rounded berrylike outpouchings that arise from arterial bifurcation points, most commonly in the circle of Willis
Charcot-Bouchard aneurysm
Charcot-Bouchard aneurysms are minute aneurysms (microaneurysms) in the brain that occur in small penetrating blood vessels with a diameter that is less than 300 micrometers. The most common vessels involved are the lenticulostriate branches (LSA) of the middle cerebral artery (MCA).
examples of a intraparenchymal haemorrhage
stroke
contusion
clinical features of an intraparenchymal haemorrhage
Non-traumatic intraparenchymal hemorrhages typically present with a history of sudden onset of stroke symptoms including a headache, nausea, vomiting, focal neurologic deficits, lethargy, weakness, slurred speech, syncope, vertigo, or changes in sensation
clinical features of subarachnoid hemorrhage
A subarachnoid hemorrhage is bleeding in the space between your brain and the surrounding membrane (subarachnoid space). The primary symptom is a sudden, severe headache. The headache is sometimes associated with nausea, vomiting and a brief loss of consciousness.
clinical features of a subdural haemotoma
Headache that doesn't go away. ... Confusion and drowsiness. Nausea and vomiting. Slurred speech and changes in vision. Dizziness, loss of balance, difficulty walking. Weakness on one side of the body.
pathophysiology of a subdural haematoma
Bleeding in a SDH occurs from tearing of the bridging veins that cross from the cortex to the dural venous sinuses, which are vulnerable to deceleration injury. This subsequently leads to accumulation of blood between the dura and arachnoid and results in a gradual rise in intracranial pressure (ICP).
looks like a crescent shape on a CT
clinical features of a Extradural haematoma
typical symptoms of EDH include headache, nausea/vomiting, confusion and reduced level of consciousness. Typical clinical signs of EDH include confusion, cranial nerve deficits, motor or sensory deficits of the limbs, hyperreflexia, spasticity, upgoing plantar reflex and Cushing’s triad
pathophysiology of extradural haematoma
As the volume of blood leaking from the damaged blood vessel into the extradural space increases, it begins to strip the outer layer of the meninges, the dura mater, away from the skull. This often leads to the lemon-shaped haematoma, which is visible on CT and MRI imaging
clinical features of concussion
headache or “pressure” in head.
Nausea or vomiting.
Balance problems or dizziness, or double or blurry vision.
Bothered by light or noise.
Feeling sluggish, hazy, foggy, or groggy.
Confusion, or concentration or memory problems.
Just not “feeling right,” or “feeling down”.
clinical features of cerebral brain thrombosis
Patients with cerebral venous thrombosis (CVT) present with a remarkably wide spectrum of signs and symptoms. Most common are headaches (> 80%), seizures (approximately 40%), hemiparesis (approximately 40%), altered consciousness (15-20%), and papilledema (20-30%) [1–3].
what causes cerebral brain thrombosis
Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome. Obesity. Low blood pressure in the brain (intracranial hypotension) Inflammatory bowel disease like Crohn’s disease or ulcerative colitis.
define meningism
irritation of the meninges
-typically causes neck stiffness, photophobia and headache
define meningitis (presents with, caused by, which one is fatal)
inflammation of the meninges
- typically presents with fever, headache and meningism
- can be caused by bacteria, virus, fungi, parasites, non infective causes
- bacterial meningitis is fatal
define encephalitis
inflammation fo the brain parenchyma
what is meningio-encephalitis
inflammation of the brain substances and parenchyma
what is a cerebral abscess
focal collection within the brain parenchyma, which can arise as a complication of a variety of infections, trauma or surgery
what are the meninges
three connective tissue membranes that ensheath the CNS
- dura mater
- arachnoid mater
- pia mater
2 functions of the meninges
- provide a support framework for the cerebral and cranial vasculature
- acting with CSF to protect CNS from mechanical damage
viral CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)
appearance - usually clear/turbid opening pressure - normal WBC - high, usually high lymphocyte glucose - high glucose protein - high microbiology - usually sterile
bacterial CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)
appearance - turbid/purulent opening pressure - normal/elevated WBC - high, mainly polymorphs glucose - low protein - high microbiology - organism on gram stain
tuberculosis CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)
appearance - turbid/viscous opening pressure - normal/elevated WBC - high, mainly lymphocytes glucose - low protein - high microbiology - positive Ziehls - Nielson stain
subarachnoid haemorrhage CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)
appearance - blood stained (yellow) opening pressure - elevated WBC - normal/slightly increased glucose - normal protein - increased microbiology - sterile
effects of meningitis
- disrupts blood brain barrier
- increases entry of water soluble antibiotics
- raised ICP
- cerebral oedema
- increased CPP
- can lead to CSF obstruction and hydrocephalus
most common causes of meningitis in the UK
Neisseria Meningitidis
Streptococcus pnuemoniae
risk factors for community acquired meningitis
- > 65 age
- splenectomy
- complement deficiency
- alcohol excess
- HIV
- diabetes mellitus
- travel to endemic areas (Africa, Mecca)
two physically demonstrable symptoms of meningitis.
Kernig sign: Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
Brudzinski’s sign: Position the patients supine and passively flex their neck. This test is positive if this manoeuvre causes reflex flexion of the hip and knee.
contraindications to a lumbar puncture
- signs suggestive of raised ICP
- shock
- extensive or spreading purpura
- after convulsions stabilised
- clotting abnormalities
- local superficial infection at site of LP
- respiratory insufficiency
signs of raised ICP
- reduced or fluctuating levels of consciousness
- relative bradycardia and hypertension
- focal neurological signs
- abnormal posture or posturing
- unequal, dilated, or poorly responsive pupils
- abnormal “dolls eye” movement
where is LP preferentially performed
L4,5 or L3,4
what do you treat suspicion of meningiococcal infection with
benzylpenicillin or ceftriaxone
at what age is a meningiococcoal infection highest
<5 years or 15-19
bacterial meningitis symptoms
- fever
- headache(typically over hours)
- rash (peticheal/blotchy)
- neck stiffness
- confusion
- vomiting
- shock
glass test
for meningitis
Press the side of a clear glass firmly against the skin.
Spots/rash may fade at first.
Keep checking.
Fever with spots/rash that do not fade under pressure is a medical emergency.
Do not wait for a rash. If someone is ill and getting worse, get medical help immediately.
what to give neonates in bacterial meningitis
cefotaxime plus amoxicillin
what to give children over 3 months in bacterial meningitis
cefotaxine or ceftriazone
what to give adults (18-60) in bacterial meningitis
cefotaxime or ceftriazone
what to give adults over 60 in bacterial meningitis
ceftotaxime or ceftriazone
PLUS
amoxicillin or ampicillin
acute complications of meningitis
septic shock
subdural empyema
seizures
cerebral venous sinus thrombosis
chronic complications of meningitis
deafness - especially in children learning difficulties behavioural problems epilepsy visual disturbances
follow up for probable or confirmed bacterial meningitis
should be followed up within 6 weeks of hospital discharge
brief description of viral meningitis
(what percentage of cases does it cause? what viruses cause it? is meningism present? symptoms?
- causes 50-80% of cases
- enterovirus and herpesvirus (herpes simplex and varicella zoster), HIV
- mild onset
- meningsm less prominent
- fever not always present
- rash in varicella zoster and genital ulcers in herpes simplex
- non specific symptoms
Herpes simplex encephalitis description
affects what lobe
what do you treat it with
neurological emergency
affects temporal lobe
treat with IV acyclovir
pathogenesis of cerebral abscesses (direct, haematogenous, other)
direct spread: ears, sinuses, dental infections (single abscesses)
haematogenous: bacteraemia associated brain abscesses (multiple abscesses)
following penetrating trauma or neurosurgery
conditions that can lead to bacteraemia associated brain abscesses (haematogenous causes)
infective endocarditis
lung abscess, empyema
pelvic infections
pulmonary aterio-venous malformations
clinical features of cerebral abscesses
headache fever confusion seizure focal neurology
how to diagnose a cerebral abscess
CT/MRI brain, aspiration/drainage of abscess and send for microscopy, culture and sensitivity (MC&S), echocardiogram
LP is contraindicated in patients with focal neurology signs/symptoms
treatment of a cerebral abscess
surgical drainage of the abscess
empirical antibiotic treatment
treatment duration (4-6 weeks)
Key infections to be aware of in HIV patients with a low CD4 count (4 things)
cryptococcal meningitis (fungal meningitis)
cerebral toxoplasmosis (causes cerebral abscesses)
tuberculosis
progressive multifocal leukoencephalopathy (destroys cells that produce myelin)
How to diagnose tuberculoma (radiograph)
discrete enhancing lesions of the brain surrounded by oedema (can be single or multiple)
how to diagnose tuberculoma (CSF)
if no evidence of raised ICP
- very high protein and normal glucose with pleocytosis
- acid fast bacilli (AFB) on Ziehl-Neelsen stain and culture
how do diagnose cerebral malaria
thick and thin blood films x 3
rapid diagnostic tests
FBC (platelets), LFTs, BM
what is acute rhinosinusitis
symptomatic inflammation of the nasal cavity and paranasal sinuses
most common cause of acute rhinosinusitis
viral infection
viral sinusitis (when does it resolve, treatment)
resolves in 7-10 days
treatment: analgesia, intranasal glucocorticoids
symptoms of acute rhinosinusitis
frontal headache and nasal symptoms PLUS at least 2 of:
- nasal blockage
- rhinorrhea/discharge
- loss of smell
- facial pressure/tenderness
three key clinical features of meningitis
fever, headache and neck stiffness
describe features of a migraine
bad headache nausea photophobia phonophobia (sound) osmophobia (odours) lasts 3-72 hours women > men
describe features of a cluster headache
severe side locked headache lasts 30-90 mins unilateral tearing unilateral red eye unilateral nasal stuffiness pain behaviour circadian circannual men more likely than women
describe features of temporal arteritis (giant cell arteritis)
age > 50 years tender scalp thick, ropey temporal arteries fever weight loss night sweats raised inflammatory markers likely to go blind steroid and biopsy asap
describe features of acute glaucoma
headache vomiting eye pain rock hard eye blurred vision mild dilated pupil get optician to measure eye pressure
features of a tension headache
most common type of primary headache
mild, featureless headache
features of analgesic headache
painkillers (particularly opiates) can transform episodic migraines into chronic featureless dull headache
avoid paracetamol or NSAIDs more than 15 days/month
avoid opiates, analgesic compounds more than 10 days/month
features of trigeminal neuralgia
Episodes of severe, shooting or jabbing pain that may feel like an electric shock. Spontaneous attacks of pain or attacks triggered by things such as touching the face, chewing, speaking or brushing teeth. Attacks of pain lasting from a few seconds to several minutes. Pain that occurs with facial spasms.
some common things headache might be due to
dehydration alcohol - hangover influenza high altitude high pressure hyponatraemia
what can you test for when you do a lumbar puncture?
opening pressure microscopy, culture and sensitivity (MC&S) viruses (PCR) protein glucose (paired serum) oligoclonal bands (paired serum) flow cytometry cytology neurodegenerative biomarkers
why would you test flow cytometry when doing a lumbar puncture
checks for haematological cancer
why would you test raised lactate when doing a lumbar puncture
for mitochondrial disease
diagnostic indications for a lumbar puncture
suspected neurological infection
suspected subarachnoid haemorrhage
suspected neuroinflammatory disease
suspected CNS malignancy
therapeutic indications for a lumbar puncture
suspected raised intracranial pressure secondary to IIH
intrathecal administration of drugs (methotrexate)
complications of a lumbar puncture
post LP headache (reduced with atraumatic / non cutting needle)
pain
bleeding (spinal haematoma)
infection
damage to surrounding structures
cerebral herniation (only in cases on raised ICP but. not IIH)
failure of procedure
anatomical landmarks for an LP
left lateral position
between L3/4 or L4/5
line between both posterior superior iliac crests
go in at a 15 degree angle (aim to hit umbilicus)
what anatomical landmarks makes the pop sound when performing an LP
ligamentum flavum
only push 1/2 cm in further to obtain CSF
in bad cases of IIH what would be done after multiple LPs
shunting
describe multiple sclerosis
- demyelinating autoimmune disease
- damage to the insulating cover of nerve cells of brain and spinal cord
- characterised by: lesions “plaques” in the CNS, inflammation, destruction of myelin sheaths of neurons
how to diagnose MS
clinical presentation alone (If 2+ relapses and signs)
clinical presentation and MRI
clinical presentation and CSF
what would you see in the CSF of someone with MS
oligoclonal bands of IgG on electrophoresis
2 most common organisms that cause meningitis
neisseria meningitidis
streptococcus pnuemoniae
why is CSF examined in a subarachnoid haemorrhage
RBC (must be high in all tubes to distinguish from trauma)
xanthochromia (presence of bilirubin)
xanthochromia and subarachnoid haemorrhage
can be seen in patients with jaundice, high CSF protein or carotene addiction
3 headaches in the context of domestic violence
tension headache
migraine
traumatic brain injury
what do you typically treat tension headaches with (generally speaking)
analgesics/ tricyclics
what do you typically treat migraines with
analgesics triptans amitriptyline topiramate propranolol candesartan
what do you typically treat cluster headaches with
sumatriptan
oxygen
verapamil
lithium
what do you typically treat trigeminal neuralgia with
carbamezapine
stepwise approach to migraine treatment
Step 1 : over the counter analgesics, NSAIDs
step 2: Triptans
Step 3: combination treatment of triptans with NSAIDs +/- antiemetic (prochlorperazine, metoclopramide)
what pathways does paracetamol work on
effects on prostaglandin production
on serotenergic, opioid, nitric oxide, and cannabinoid pathways
3 main properties of NSAIDs
analgesic
anti-inflammatory
anti - pyretic
how do NSAIDs work
they inhibit prostaglandin synthesis on COX enzymes (COX1 and COX2)
3 main classifications of NSAIDs
carboxylic acids
enolic aicd
cox II inhibitor
what are naproxen and ibuprofen examples of
NSAIDS - carboxylic acid - propanoic acid
examples of cox II inhibitor NSAIDs
celecoxib
valdecoxib
Triptan medication
what type of drug are they, what are they designed to do
5HT agonists
designed to stop headaches once they have come on for migraines and cluster headaches
prescribing triptans and monitoring use
should be taken early during a migraine but not during the aura
do not repeat if not responding to first dose
avoid using for more than 10 days a month (can lead to medication overuse headache)
four medications for prophylaxis of migraines (from lecture)
tricyclic antidepressants
topiramate
candesartan
propanolol
examples of tricyclic antidepressants
amitriptyline amoxapine imipramine trimipramine protriptyline
mechanism of tricyclic antidepressants (TCA’s) in prophylaxis of headaches
inhibit reuptake of noradrenaline and serotonin (5HT)
how does topiramate work
blocks voltage gated sodium and calcium channels
inhibits excitatory glutamate pathways
enhances effect of GABA
inhibits carbonic anhydrase activity
how does candesartan work (in relation to prophylaxis of headaches)
it is an angiotensin II receptor antagonist (ARB - antihypertensive)
inhibits vasoconstriction by blocking the stimulation of AT1 receptors in vascular smooth muscle
(inhibits excessive cerebral vasoconstriction)
analgesics and other meds given to people with tension type headaches
analgesics include - paracetamol, NSAIDs, opioids (codeine) tricyclic antidepressants (TCD)
description of a cluster headache
thunderclap headache
sharp, burning or piercing sensation on one side of the head , often felt around the eye, temple and face, tends to occur on the same side for each attack
restless and agitated during attacks because pain is so intense, usually rocking, pacing, or banging their head against the wall
acute treatment for a cluster headache
oxygen - breathing 100% o2 at minimum of 12L/min
triptans - sumitriptan (nasally or IV)
prophylaxis for cluster headaches
first line is verapamil (Ca channel blocker)
corticosteroids (inappropriate for long term use)
lithium carbonate
another name for medication overuse headache
rebound headahce
true/false
medication overuse headache only occurs in people with a history of a primary headache
true
treatment for medication overuse headache
abrupt withdrawal or tapering down of medication
when is inpatient withdrawal therapy recommended for people with medication overuse headache
patients overusing opioids, benzodiazepines, or barbituates
what drug has moderate evidence of prophylactic treating of migraines in patients with medication overuse headaches as well
topiramate
2 latest treatments for migraines
botox
monoclonal antibodies
describe what is meant. by a primary tumour CNS
originates from cell types native to the brain
describe what is meant by a secondary tumour CNS
derived from cells that have spread (metastasised) from somewhere else in the body
symptoms of brain tumours
changes in mood personality changes cognitive decline nausea projectile vomiting decreased appetite visual problems speech problems ataxia
clinical symptoms of a frontal brain tumour
personality changes behavioural or emotional changes inappropriate behaviour impaired judgement loss of vision primitive reflexes
clinical symptoms of a occipital brain tumour
visual loss
visual hallucinations
clinical symptoms of a temporal brain tumour
personality changes
auditory hallucinations
complex partial seizures
memory difficulties
clinical symptoms of a parietal brain tumour
receptive aphasia (if on left side)
spatial disorientation (if on right side)
impaired speech
lack of recognition
clinical symptoms of a brainstem tumour
behavioural and emotional changes difficulty speaking and swallowing drowsiness headache (especially in the morning) hearing loss muscle weakness on one side of the face endocrine abnormalities symptoms relating to hydrocephalus if ventricles obstructed
common sources of metastatic brain tumours
lung breast colon melanoma kidney choriocarcinoma
uncommon sources of metastatic brain tumours
prostrate
gynae
percentage of metastatic brain tumours
20% of all cancer patients
what might a ragged ring on a contrast CT mean?
glioblastoma
metastasis
what might a smooth ring on a contrast head CT mean?
abscess
what might C-shaped lesion on a contrast head CT mean
demyelination
what differentials would you have if you looked at a contrast head CT and saw a cyst with nodules
pilocytic astrocytoma
haemingioblastoma
PXA
ganglioma
what do meningiomas arise form
arise from meningoethelial cells (arachnoid cells)
can arise anywhere in CNS where there is dura/meninges
incidence of meningiomas
increases with age (most common in middle aged females)
risk factors for developing a meningioma
female sex
previous radiotherapy
genetic conditions including NF2
other oestrogen dependent tumours
common brain tumour in children
ependymoma
common intraventricular brain tumours
ependymoma medulloblastoma neurocytoma colloid cyst meningioma
common posterior fossa brain lesions
medulloblastoma
pilocystic astrocytoma
brain stem glioma
haemangoblastoma
medulloblastoma
an embryonal tumour
represents 5% intracranial tumours
two peak incidences of medulloblastomas
children and young adults (20yrs)
what grade tumour is a medulloblastoma
grade 4
how would you classify a medulloblastoma on histological appearance
classic
desmoplastic
excessive nodularity
large cell/anaplastic
most common glioma in children and young adults
pilocytic astrocytoma
preferential location for pilocytic astrocytomas
cerebellum, midline structures (thalamus, brain stem, optic chasm)
typical brain lesions in the sella location
pituitary adenoma
craniopharyngioma
what disease produces excess ACTH (adrenocorticotropic hormone.)
Cushings disease
can come from a pituitary adenoma
what disease produces excess growth hormone
acromegaly
can come from a pituitary adenoma
increased prolactin can cause? from what pathology
gynaecosmastia (an increase in the amount of breast gland tissue in boys or men, caused by an imbalance of the hormones estrogen and testosterone. Gynecomastia can affect one or both breasts, sometimes unevenly.) or galactorrhea (excessive or inappropriate production of milk.)
can be caused from a pituitary adenoma
myxopapillary ependymoma
location incidence clinical imaging histology
location: exclusively in conus, cauda equina, and film terminals of spinal cord
incidence: adults most commonly affected
clinical: present with back pain
imaging: sharply circumscribed mass which is contrast enhancing
histology: elongated fibrillary processes arranged in radial pattern around vascularised mucoid fibrovascualr cores
clinical signs of a schwannoma
often incidental but can produce signs of nerve compression - pain, CN VIII - hearing loss/tinnitus
genetic NF type I brain tumours
schwannoma
pilocytic astrocytoma
genetic NF type II brain tumours
meningiomas
what does H&E stand for
haemotoxylin and eosin stain
a histochemical stain most commonly used to demonstrate tissue structure in pathology
how can glioblastomas be diagnosed directly
via H&E stain
what is IDH and why is it important
isocitrate dehydrogenase
found in 50-80% of astrocytomas and oligodendrogliomas
main chemo medication used for brain tumours
temozolamide
