Neurology 2 Flashcards
What is normal ICP?
0-10mmHg
What are the causes of increased ICP?
Vasogenic: increased capillary permeability
tumour, trauma, ischaemia, infection
cytotoxic: cell death
interstitial: obstructive hydrocephalus
What are the symptoms of increasing ICP?
Headache: dull persisting ache, worse on lying, present on waking, worse by coughing / straining
vomiting
seizures
irritability
What are the signs of increasing ICP?
GCS deterioration
progressive dilation of pupil on the affected side
Cushing’s reflex
Cheyne-Stokes respiration
What is the management of increasing ICP?
A-E
Elevate the head of the bed to 30-40 degrees
If intubated, hyperventilate to reduce PaCo2
(immediately decreases ICP)
Mannitol: 0.2g/kg 20% IV over 15 minutes
Clinical effect after 20 minutes
Corticosteroid - if oedema around tumour
Fluid restriction
Consider monitoring ICP - surgically implanted extradural catheter
Make diagnosis and treat
controlled hypothermia, CSF drainage and barbiturates
How would you approach a patient with ?spinal cord trauma?
A-E
MOI
Physical exam: visual inspection, palpation of vertebral column, neurological assessment
Imaging: AP/lateral C2 open mouth
CT
spine x ray
What are the indications for CT spine?
If already having head/other body CT
If X-rays are suspicious
If intubated/rapid diagnosis required
Describe the approach to the unconscious patient?
A-E
LOC - needs C-spine stabilisation: collar or sandbags and tape
neurological deterioration: urgent CT head to T4/5 should be performed
If not, x ray of c, t and l-spine
What factors might indicate radiography of c-spine?
over 65
paraesthesia in the extremities
dangerous mechanism
5 factors not cleared
What are the 5 factors that clinically Clear the C-spine?
Simple rear end RTA sitting position in ED Walking at any time delayed onset of neck pain absence of C-spine tenderness
If none present, radiography is required
If one or more - patient asked to rotate the neck 45 degrees to the left and to the right
If the patient able to do this, C-spine cleared
What bone is injured in base of skull fracture?
Temporal bone (75%) - known as posterior fossa fracture
Anterior fossa (25%): occipital, sphenoid and ethmoid bones
What are the signs of posterior fossa base of skull fractures ?
Battle’s sign: bruising over the mastoids
CSF otorrhoea
Bleeding of the ear
Conductive deafness: lasts 6-8 weeks
If lasting <3 weeks may be due to haemo-tympanum / mucosal oedema
CN palsies of V, VI and VII
Facial numbness and weakness, lateral rectus palsy
What are the signs of anterior fossa fractures?
Raccoon eyes
CSF rhinorrhoea
bleeding from the nose
Which base of skull fractures require referral to neurosurgery?
posterior fossa - need referral but often will not require intervention
anterior fossa - urgent referral
What are the complications of base of skull fractures?
Intracranial infection (relatively rare)
facial nerve palsy
ossicular chain disruption
carotid injury
How are depressed skull fractures managed?
Can be subtle on examination
Impossible to know if there is interruption of the dura without exploration
All compound depressed skull fractures are surgically explored within 12 hours
Describe motor response on GCS
motor / 6
6: obeys commands
5: localises to pain
4: withdraws from pain
3: flexor response to pain:
2: extensor response to pain
1: no response
Describe verbal response on GCS?
verbal / 5:
5: orientated
4: confused conversation: responds to questions, some disorientation
3: inappropriate speech, random speech, no conversational exchange
2: incomprehensible speech: moaning but no words
1: no speech
Describe eye response on GCS?
eye / 4
4: spontaneous eye opening
3: eye opening in response to speech
2: eye opening in response to pain
1: no eye opening
How is GCS classified in terms of injury?
13-15: mild injury
9-12: moderate injury
<9: severe injury
What are the neuro differentials for an unconscious patient?
Vascular: stroke, shock, haematoma, SAH
Infective / inflammatory: sepsis, meningitis, encephalitis, abscess
Trauma: traumatic brain injury
Autoimmune: brainstem demyelination
Metabolic: hypo/hyper: glycaemia, calcaemia, natraemia
hypo: adrenals, thyroidism
severe uraemia
Wernicke-Korsakoff
Neoplasm: cerebral tumour
How should an unconscious neuro patient be managed?
A-E + temperature breathe top to toe examination respiration: classical patterns Cheyne stokes kussmaul resp: deep and laboured
Neurological
pupils: classical signs
Ix: bloods and urine tests
imaging: head CT and MRI
LP: if CT excluded mass lesions / raised ICP
What are the classical pupil signs?
Unilateral dilated pupil: raised ICP
Bilateral fixed, dilated pupil: sign of brainstem death or deep coma
pinpoint: opiate overdose, pontine lesions interrupting the sympathetic pathway
What is a STROKE?
an acute, focal neurological deficit of cerebrovascular origin that persists >24 hours
What is a TIA?
An acute, focal neurological deficit of cerebrovascular origin that persists <1 hour without signs of cerebral infarction on MRI scanning
High risk of stroke within 4 weeks of a TIA
What is amaurosis fugax?
Sudden, transient loss of vision in one eye
Often occurs with TIAs and cane the first clinical evidence of ICA stenosis
This can also occur due to ocular disease or migraine
What are the irreversible risk factors for ischaemic stroke?
age
personal / family history
hyper-coagulable states
atrial fibrillation
What are the reversible risk factors for ischaemic stroke?
Hypertension hypercholesterolaemia diabetes smoking acohol poor diet low exercise increased weight use of oestrogen containing oral contraceptives
less commonly: endocarditis, migraine, polycythaemia, APL syndrome, vasculitis, amyloiditis
What are the risk factors for haemorrhagic stroke?
Family history Uncontrolled hypertension Vascular abnormalities (aneurysms, AVMs, HHT) Coagulopathies / anticoagulant therapy Heavy recent alcohol intake
What are the two types of stroke?
ISCHAEMIC (85%): arterial embolus from a distant side
arterial thrombosis in atheromatous carotid, vertebral or basilar artery
HAEMORRHAGIC (15%)
SAH: 5%
Intra-cerebral haemorrhage: 10%
What are the three types of cerebral ischaemia?
Regional infarction
lacunar infarction
global ischaemia
What is a regional infarction?
Thrombosis / embolus in large vessels
usually affects cortical areas
What are lacunar infarctions?
microinfarcts: caused by small vessel disease: arteriosclerosis
usually affecting sub-cortical areas e.g. basal ganglia
can be asymptomatic
What is global ischaemia?
infarcts at arterial boundary zones due to a global reduction in blood flow due to severe hypotension
‘watershed’ infarction
if severe, can cause cortical laminar necrosis where there is death of the majority of neurones 24 hours after the insult, with patient remaining in a vegetative state
‘post-arrest syndrome’
What are the three zones of cerebral ischaemic damage?
Infarct core: tissue almost certain to die
oligaemic periphery: tissue that will survive, due to collateral supply
ischaemic penumbra: tissue in between - can have either outcome
What is malignant MCA syndrome?
when large cerebral infarcts cause death by associated tissue oedema, leading to herniation ad brainstem compression
What are the clinical features of ischaemic stroke?
Contralateral limb weakness / hemiplegia facial weakness higher dysfunction visual disturbances epileptic fit (rare)
What higher dysfunction symptoms can be seen in ischaemic stroke?
Expressive aphasia Receptive aphasia Apraxia Asterognosis Agnosia Inattention
What are the 4 different types of stroke?
TACS: proximal MCA occlusion
PACS: distal MCA or ACA occlusion
LACS: occlusion of a lacunar branch of the MCA
POCS: PCA occlusion
What are the criteria for TACS?
Contralateral hemiplegia and/or sensory loss; must be at least 2 of face/arm/leg involvement
Homonymous hemianopia
Higher dysfunction: dysphasia, decreased level of consciousness, visuo-spatial neglect, asterognosis or apraxia
What are the criteria for PACS?
two out of three TACS criteria:
hemiplegia and/or sensory loss
homonymous hemianopia
higher dysfunction
Higher dysfunction alone with vision spared
What are the criteria for LACS?
Pure motor symptoms (>2/3 face, arm, leg)
Pure sensory symptoms (>2/3 face, arm, leg)
Pure sensorimotor symptoms (>2 face, arm, leg)
Ataxic hemiparesis
2 of the face/arm/legs
the lenticulate striate vessels are deep vessels, so no higher cortical functions are affected
What are the criteria for POCS?
one of
- Cranial nerve palsy AND contralateral motor/sensory deficit
- Bilateral motor or sensory deficit
- Conjugate eye movement problems such as nystagmus or double vision
- Cerebellar dysfunction
- Isolated homonymous hemianopia
Describe the prognosis for TACS
60% die after 1 year
35% are dependent only 5% independent
low recurrence risk
Describe the prognosis for PACS
15% die within a year
30% dependent 55% independent
20% recurrence 1 year
Describe the prognosis for LACS
10% die within a year
30% dependent, 60% independent
10% recurrent within a year
Describe the prognosis for POCS
20% due within a year
30% dependent
50% independent
20% recurrence within a year
History points for stroke
Exact time of onset , body parts affected, seizure at onset
PMH: previous stroke / MI , AF, DM, abscess , tumour
DH: warfarin, heparin, OCP
Social: alcohol abuse, smoking, illicit drugs
How would you examine a patient with ?stroke
A-E DONT FORGET GLUCOSE!
GCS
NHISS - national institute of health stroke scale
15-item neurologic examination stroke scale, evaluating levels of lots of different neurological deficit
CVS and heart signs
Resp: spo2, RR, crackles
Neurological: UMN/LMN, CNS, cerebellar examination
What investigations would you do for ?stroke
Bloods: FBC, U&Es, glucose + HbA1c, lipids, coagulation studies, ESR
Brain imaging - CT to exclude primary intracranial haemorrhage
MRI?
ECG
What are the indications for brain imaging within 1 hour?
if considering thrombolysis
if bleeding risk/headache at onset
if decreased consciousness
if neck stiffness
What is the aim of imaging in ?stroke
define arterial territory, exclude stroke mimics and determine haemorrhagic vs thrombo-embolic pathology
CT vs MRI for stroke?
MRI: gold standard, higher resolution imaging of arterial territories, but less commonly used due to availability
CT: rapid and commonly used, mainly to exclude haemorrhage. Early signs of infarct seen. If visible on CT, lesions will be seen by day 7
what is the acute management of stroke?
A-E
Aspirin 300mg STAT
Once haemorrhage excluded on CT, thrombolysis if within 4.5 hours (alteplase)
THrombectomy within 6 hours
Ward management: SALT, physio, OT, nursing, LMWH on day 3 post stroke
Describe the indications and dose of thrombolysis
First, check for contra-indications
must have laboratory blood results back and excluded Haemorrhage by imaging
Within 4 hours
Alteplase 0.9mg/kg as per clinical pathway within hospital
10% bolus over 1 minute, remainder over 60 minutes
Describe the roles of the MDT in the management of a stroke patient
SALT: swallow assessment within 2 hours, also help patients with communication
Physio: relieve spasticity and prevent contractures
Baclofen may be used to relieve spasticity
early mobilisation = vital
OT: limb splinting, ward groups
Nursing: SSKIN bundle, early nutrition required if NBM
How is eligibility for thrombolysis assessed in practice?
emergency cal - stroke consultant notified
quick, focussed hx ad examination, NIHSS score assess for contraindications IV access, baseline bloods Weight Catheterise
URGENT CT and thrombolyse after consultant review
How is the patient monitored following thrombolysis?
patient closely monitored over 24 hours via cardiac monitor and has specific observations completed on STOC (stroke thrombolysis observation chart).
if patient develops a severe headache, acute HTN, n+V they get an emergency CT
What therapeutic interventions should be avoided following thrombolysis?
avoid: catheterisation during infusion
avoid aspirin or heparin for 24 hours
avoid NG tube insertion for 24 hours
What is the management of stroke if thrombolysis is contra-indicated?
300mg Aspirin STAT
Manage conservatively on ward
What is the secondary prevention management of stroke?
Antihypertensive therapy:
anti platelet: 300mg aspirin od for 2 weeks and clopidogrel 75mg after
atorvastatin 80mg offer from 48 hours post-stroke regardless of cholesterol levels
identify and tackle lifestyle factors:
stop smoking and excess alcohol, regular exercise, cardio protective diet
manage other co-morbidities: good AF control / anticoagulation, good diabetes control + carotid USS
What are the driving regulations post-stroke?
normal license: must not drive for 4 weeks post-stroke
after this, they may return if clinical improvement is ok without notifying DVLA
Describe the post-stroke complications
Malignant MCA syndrome DVT / pulmonary embolism Aspiration and hydrostatic pneumonia pressure sores depression seizures incontinence post-stroke pain - worsens outcome, multi-factorial in nature (central, muscular etc) often requires pain team input
What is malignant MCA syndrome?
Rapid neurological deterioration due to the effects of cerebral oedema following middle cerebral artery territory stroke
high morbidity / mortality, occurring mainly in patients <60
What is the presentation of malignant MCA syndrome?
Increasing agitation / restlessness
reducing GCS
haemodynamic / thermal instability
signs of raised ICP
What is the management of malignant MCA syndrome?
decompressive hemicraniectomy
if CT/MRI shows an infarct of at least 50% of the MCA territory, in a patient <60 with any decrease in gcs, NICE recommend immediate referral for decompressive hemicraniectomy
What are the high risk features of a TIA?
Recurrent TIAs within a short period of time
AF or TIA whilst anticoagulated
ABCD2 score 4+
What are the ABCD2 criteria ?
AGE: >60 = 1 point
BLOOD PRESSURE: >140/90 = 1 point
CLINICAL FEATURES: unilateral weakness = 2 points
speech disturbance without weakness = 1 point
DURATION of symptoms: 60+ mins = 2 points
10-59 minutes = 1 point
DIABETES: 1 point if pre-existing
What is the management if high risk features are present?
300mg aspirin (unless contraindicated) if currently taking low-dose aspirin, continue current dose arrange referral to a specialist clinic within 24 hours advise patients not to drive until seen by specialist
Secondary prevention: Atorvastatin 80mg
If low risk, mx = the same but referral to specialist is less urgent; within 1 week
How are these patients managed in specialist clinic?
carotid artery doppler to assess for carotid artery stenosis
if >50%, carotid endarterectomy should be offered
What are the benefits of carotid endarterectomy?
reduces risk of further stroke / TIA by 75%
risk of procedure related stroke and mortality risks also
an alternative is percutaneous luminal angioplasty +/- stunting
What are the risk factors for venous sinus thrombosis?
Pro-thrombotic risk factor (85%) - OCP, pregnancy, malignancy, genetic thrombophilia
head injury
recent LP
Infection
Describe the pathology of venous sinus thrombosis?
Venous infarction leads to vascular congestion
eventually there is haemorrhagic necrosis
split into cortical and dural venous thrombosis
Describe the signs of cortical venous thrombosis?
Headache: may be thunderclap focal signs seizures fever encephalopathy
What are the signs of dural venous sinus thrombosis?
cavernous sinus thrombosis: ocular pain, worse on movement Proptosis and chemises ophthalmoplegia papilloedema fever
saggital and lateral sinus thrombosis: signs of raised ICP, headache, vomiting, fever, papilloedema, seizures
What are the investigations and findings for venous sinus thrombosis?
CT: often normal
LP: raised ICP
MRI angiography: may be required for diagnosis
SUSPECT if thunderclap headache and raised ICP with no signs of meningitis and no changes on CT
What percentage of strokes are haemorrhagic?
15%
10% intra-cerebral haemorrhage
5% SAH
What is the cause of deep intra-cerebral haemorrhage?
Rupture of micro-aneurysms and degeneration of small deep penetrating arteries
Occur in sub-cortical areas
Who gets lobar intra-cerebral haemorrhage?
occurs in normotensive individuals >60 in the cerebral cortex
can be (rarely) caused by cerebral amyloid angiopathy
What is the presentation of intra-cerebral haemorrhage?
As per haemorrhagic stroke
What ix should be done for intra-cerebral haemorrhage?
CT - haemorrhage seen immediately
MRI: very reliable after 2 hours from symptom onset
What is the management of intra-cerebral haemorrhage?
CT head immediately
FBC and clotting
ADMIT
Surgical tx discussed and ICU for ventilation
reverse anticoagulation
Lower BP to <140/90 in 1 hour: IV betalol but avoid hypotension
Neurosurgical intervention may be required: if deepening coma and coning
What is the presentation of SAH?
Thunderclap headache - develops over seconds, usually in times of transient hypertension like exercise or sex
vomiting: comes on after developing the headache
Photophobia
increasing drowsiness / coma
focal signs may point to location of lesion
What are the examination findings of SAH?
Neck stiffness
Positive Kernig’s sign: takes 6 hours to develop
Papilloedema: may be present, along with retinal haemorrhages
patient may earlier have experienced a sentinel headache due to a small warning leak from the offending aneurysm.
What are the predisposing abnormalities for SAH?
Berry aneurysm: 70%
arteriovenous malformations: 10%
no lesion found: 20%
Where do berry aneurysms form?
Circle of Willis and adjacent arteries:
Anterior communicating artery - most common
posterior communicating artery: at bifurcation from ICA
Middle cerebral artery: at the bifurcation / trifurcation
What are the risk factors for berry aneurysms?
polycystic kidney disease FH smoking HTN Ehlers-Danlos / Marfans
What are arteriovenous malformations?
congenital collection of abnormal arteries / veins
Tendency to rebleed if symptomatic once
10% will rebleed annually
can also cause epilepsy, often focal
What are the complications of SAH?
Death - 30% will die immediately
Rebleed: aneurysms - if vasospasm is sufficient, a clot can form but this rebleeds in 3-4 days
AVM: rebleed in years
Hydrocephalus: due to fibrosis in the CSF pathways
Cerebral vasospasm: can be severe, leading to delayed ischaemic change
What investigations should be done for SAH?
Bloods: FBC, U+E, LFT, ESR, clotting
CT: initial investigation of choice
LP: if CT normal - >12h after symptom onset. CSF will be xanthochromic, visual inspection enough for diagnosis
CT/MRI angiography in all patients fit for surgery
What is the management of SAH?
4 weeks bed rest - HTN control nimodipine - prevent vasospasm, reduce mortality IV fluids: prevent vasospasm analgesia, anti-emetics stool softeners to prevent straining discuss with neurology ?Surgical intervention
What neurosurgical interventions might be done for SAH?
‘coiling’ - inserting a catheter into the arterial system (taking an “endovascular approach”), placing platinum coils into the aneurysm and sealing it off from the artery.
neurosurgical clipping
What is subdural haematoma?
collection of blood in the subdural space following rupture of a vein, usually following a head injury, although can occur spontaneously
What is the cause of acute subdural haematoma?
Severe acceleration-deceleration head injury, often with co-existing brain damage
Describe the typical patient with acute subdural haematoma
young - come into hospital with a dilated pupil and no lucid interval before decreased GCS
What is the management of acute subdural haematoma?
Craniotomy and early evacuation of the Clot
often seriously ill even with early intervention
need ICU admission with intracranial pressure monitoring
What are the causes of subacute subdural haematoma?
May occur spontaneously or after minor trauma
risk factors:
elderly - cortical atrophy stretches brittle veins
alcohol abuse: clotting is reduced
other coagulopathies
What are the s/s of subacute subdural haematoma?
raised ICP signs: headache drowsiness confusion focal neurological signs
eventually stupor and coma due to coning
What imaging modality should be used for subdural haematoma?
What changes are seen?
CT
acute: classical crescenteric shape with increased density (white) conforming to the contour of the skull
may be accompanying midline shift and compression of the ventricles
Chronic subdural haematoma: blood becomes more radiolucent (dark) and assumes a lentiform shape similar to that of an extradural haematoma
What patients get extradural haematoma?
young patients following minor assault or sporting injury
blow = to Side of head, enough to cause a fracture and associated tearing of the middle meningeal artery
Blood accumulates rapidly over minutes to hours in the extradural space
What is the presentation of extradural haematoma?
brief duration of unconsciousness and then a lucid recovery period
progressive hemiparesis and stupor develops due to transtentorial coning.
Ipsilateral dilated pupil, then bilateral fixed dilated pupils
untreated –> hemiplegia and respiratory arrest
What investigations are done for extradural haematoma?
CT: characteristic lentiform shape
midline shift and compression of the ventricles as it enlarges
What is the management of extradural haematoma?
Urgent neurosurgical referral
Burr holes to release pressure
Prognosis very good if this is performed early
What are the primary headache disorders?
Tension headache
migraine
cluster headache
What are the secondary headache syndromes?
raised ICP Idiopathic intracranial hypertension hypertension meningeal irritation (SAH/meningitis) post-traumatic GCA Sinusitis Metabolic disturbance Drugs: nitrates, vasoactive agents
What are the causes of facial pain?
Trigeminal neuralgia
Postherpetic neuralgia
Atypical facial pain
What is a tension headache?
Continuous, severe pressure, felt bilaterally over the vertex, occiput and eyes
can be ‘band like’ but not pulsating
Who gets tension headaches? When do they occur?
anyone - but most common in middle aged women
every day and can persist for many months/years
What is the management of tension headaches?
Reassurance
Standard analgesics:
If episodic: paracetamol and aspirin/NSAID (warn about overuse)
If medications 2+ times/week - preventative:
low dose amitryptiline
75mg initially, and treated upwards if partial response
chronic tension headache - reassurance, relaxation and addressing underlying stressors important
What is a cluster headache?
short lived: 30-120 min episodes of sever unilateral pain, typically centred on one eye
comes on very suddenly, often waking a patient from sleep
May get red eye, eye/nose watering, ptosis, vomiting on affected side
May get an aura beforehand
When do cluster headaches come on? frequency?
May occur several times / day and are recurrent for several weeks or months before the disorder remits
What are the precipitants of cluster headache?
males > females
Alcohol = common precipitant
strong smells, exercise
What is the management of cluster headache?
exclude secondary causes and other causes of eye pain
e.g. ACAG
Subcutaneous triptan: sumatriptan 6mg
High flow oxygen
oral triptan/analgesia not effective for acute attack.
prophylactic treatment is with alcohol avoidance and verapamil, lithium or prednisolone
What are the causes / triggers of migraine?
? who knows!! onset in puberty
menstruation, OCP use, physical exercise, food (cheese, chocolate, red wine), alcohol, emotional states.
Vasodilatation after a period of vasoconstriction (aura phase) is thought to correlate with the onset of the headache.
What are the subsets of migraine?
Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine
How does a classical migraine with aura present?
Starts with a sense of ill health followed by visual aura in the field of vision opposite to the side of the succeeding headache. Sensory aura less common
THEN: throbbing headache with anorexia, nausea, vomiting and photophobia.
Headache begins locally and spreads bilaterally, aggravated by movement an can last several hours/days
What is the presentation of a migraine without aura?
Classical visual/sensory aura = absent, however patients may feel non-specifically unwell prior to onset of headache
What is the management of migraine (non-pharm)
Examine to rule out other differentials: focal neurology, raised ICP, meningism, temporal arteritis, retinal haemorrhage
headache diary: assess frequency, severity of attacks, precipitants and exacerbating/relieving factors
avoidance of external triggers
What is the pharmacological management of migraine?
In acute attack: oral NSAID or paracetamol + anti-emetic (metoclopramide)
offer oral triptan (sumatriptan 50mg) if attacks severe to take ASAP at start of attack.
don’t use opioids.
follow up - if they don’t respond to triptan, might not be migraine
What is the preventative treatment of migraine?
If >2 / month
Topiramate / propranolol first line - prop in child bearing age
amitryptiline / anti-convulsants if these aren’t successful or tolerated
How are menstrual related migraines managed?
Mefanamic acid from first day of Menses throughout menstruation, or triptans starting 2 Days before expected menses
COCP avoided in women with migraine with aura, however, contraceptive methods that prevent menstruation can be tried
slight increased stroke risk in those on COCP greater if migraine sufferers
Who is most likely to suffer with idiopathic intracranial hypertension?
young, obese women
What are the s/s of idiopathic intracranial hypertension?
Raised ICP symptoms but no mass lesion on imaging
thought to be a disorder of CSF resorption
most common presentation is visual disturbance (diplopia, obscurations and headaches)
Sometimes associated with pulsatile tinnitus and a 6th nerve palsy
bilateral papilloedema
What is the management of idiopathic intracranial HTN?
weight loss
trial of corticosteroids
surgical shunt
What is the cause of trigeminal neuralgia?
Compression/pathology (MS) of the trigeminal nerve root
What are the symptoms of trigeminal neuralgia?
Agonising sharp pain over the distribution of the facial nerve on one side, lasting only seconds, with sensory trigger
What is the management of trigeminal neuralgia?
simple analgesics ineffective;
carbamazepine offers good symptom control
Referral
What is atypical facial pain?
Episodic aching in non-anatomical distributions of head/neck
commonly associated with depression/anxiety, and may respond to anti-depressants
What is hydrocephalus?
Excessive CSF within the cranium
High CSF pressure leads to dilatation of the lateral ventricles +/- dilation of the 3rd / 4th ventricles
What are the causes of non-communicating hydrocephalus and communicating?
Non-communicating = most common type, due to blockage of the CSF pathway from the ventricles to sub-arachnoid space
Communicating hydrocephalus = due to impairment of CSF reabsorption at the arachnoid villi along the dural venous sinuses
usually precipitated by infection or SAH
Rarely, hydrocephalus can be due to excess CSF production
Who is most likely to develop hydrocephalus?
Patients with congenital malformations
e.g. stenosis of the aqueduct of sylvius
posterior fossa/brainstem tumours
post-brain insult
SAH/head injury/meningitis
What are the clinical features of hydrocephalus?
Headache vomiting papilloedema cognitive impairment ataxia bilateral pyramidal signs
What are the investigations of hydrocephalus
CT - assess signs of ventricles
MRI if suspecting malformations/tumours
What is the medical management of hydrocephalus?
Medical - reduce CSF secretion / increase absorption
(delay surgical management)
acetazolamide, alone or in combination with furosemide
What is the surgical management of hydrocephalus?
Ventriculo-atrial or ventricle-peritoneal shunting for progressive symptoms
valves open at certain pressures to release CSF
Endoscopic third ventriculostomy is an alternative procedure, appropriate for obstructive hydrocephalus
neurosurgical removal of tumours if appropriate
What is normal pressure hydrocephalus?
Syndrome of enlarged lateral ventricles, usually in the elderly, associated with a classic triad: dementia, desperate no signs of cortical atrophy on CT
Urinary incontinence
Apraxic gait
whacky wobbly weeing
Isolated CSF measurements normal, but continuous monitoring may show intermittent periods of raised pressure
What is the management of normal pressure hydrocephalus?
Some patients respond to ventriculoperitoneal shunting, only indicated if they respond to trials of lumbar drainage
