Neurology Flashcards
indications for a lumbar puncture
Diagnosis of meningitis/encephalitis
Diagnosis of SAH - If clinically suspected but no abnormalities on CT
Measurement of CSF pressure (Idiopathic intracranial hypertension)
Therapeutic removal of CSF (Idiopathic intracranial hypertension)
Intrathecal drug administration
Diagnosis of miscellaneous conditions (behcets, MS, neurosyphillis)
where do you do an LP
L4/L5 space
csf finding in MS
Moderately raised protein levels - <1g/L
Up to 50 lymphocytes/mm3
Oligoclonal IgG bands on electrophoresis
complications of LP
Post LP headache
Occurs in 30%, onset within 24 hours with resolution over 2 weeks
Classically a constant bilateral dull ache
Worse when upright, as due to intracranial hypertension
Treat with analgesics +/- blood patch (Re-injection of a patients own blood to form a clot)
Dry-tap
Usually due to poor technique
Infection
Damage to spinal nerves
Causes weakness/paresthesia
Coning of cerebellar tonsils
contraindications for LP
Suspicion of mass in the brain/spinal cord/raised ICP
This can lead to coning of the cerebellar tonsils
Any unconscious patient must have a CT prior to LP
Overlying/local infection
Congenital lesions in the area
Meningomyelocele
Problems with haemostasis
Platelets <40
Clotting abnormalities
Anticoagulation
Haemodynamic instability
what does xanthochromia in the CSF indicate
bleeding in the brain
contraindications for an MRI
Electrically, magnetically or mechanically activated implants
Pacemakers, cochlear implants, drug infusion pumps
Implants containing ferrous material
Aneurysm clips
Surgical staples
Bullets, shrapnel, metal
Screen patients with XR if they have a history of metal foreign bodies in the eye
Some implants are now MRI safe
acute management of a head injury
Ensure C-spine is secured
A-E resus
A: some level of intubation usually required
Record GCS prior to intubation
B: chest injuries often co-exist and lead to an additional secondary brian injury from hypoxia
C: shock occurs in polytrauma patients – ensure cross match is done ASAP
Record GCS
Brief history if conscious
Neurological exam
Check for signs of deterioration
Most important - Changing pupillary responsiveness
As ICP rises there is initially a progressive dilation on the side of the lesion, with sluggish response to light
If bilateral it is a pre-terminal sign
Falling pulse/rising BP
Cushings reflex: late sign
Manage appropriately if signs of rising ICP
Appropriate imaging
CT head if indicated
C spine radiography if indicated
Always indiated if there is a TBI with LOC
Prevent secondary insults
Hypoxia
Hypercapnia leads to cerebral vasodilation –
increasing cerebral blood volume and raising ICP
Raied ICP patients may be hyperventilated in ICU
Hypoxaemia also leads to cerebral vasodilation, as well as causing profuse lactic acidosis which damaged cerebral neurones – not breathing for 4 minutes starts to cause irreversible brain damage
Hypovolaemia
MABP between 60-160 mmHg is autoregulated
Following a head injury this autoregulation goes and therefore cerebral perfusion relies on SBP
As such , this resus is vital to regulate SBP and therefore brain perfusion
Hypoglycaemia
GCS 15 and haemodynamically stable = patients can be discharged
Period of unconciousness after a head trauma = head Xr required before discharge
Discharge with a head injury warning card
If intoxicated they need to be admitted as its hard to differentiate between intoxication and brain injury
indications for CT head within 1 hour during a head injury
GCS <13 at the time, or <15 2 hours after the injury
Focal neurological deficit
Signs of increasing ICP: Headache Blurred vision Vomiting Decreased awakeness Seizure Weakness Anergy
Suspected skull #
Post-traumatic seizure
Vomiting >1 times
indications for a CT head within 8 hours after a head injury
Anticoagulated patients
LOC + >65/Dangerous mechanism of injury (fall from a height)/Retrograde amnesia >30 mins/Inability to recall events before injury
when should you admit a patient following a TBI
If imaging show pathology
If GCS <15
If this is the case monitor them every 30 minutes
Continuous worrying signs
Tx status epilepticus
A-E
100% oxygen
Oral/nasal airway
IV access
Bloods Glucose Calcium Magnesium FBC U+E LFT clotting
CXR to rule out aspiration
Take urine sample if possible
ABG
Set up ECG
if >5 mins
IV lorazepam
4mg bolus repeated after 5 mins if no response
Finger prick glucose
If hypoglycaemia 50ml 50% glucose IV
Any suspicion of alcoholism
IV pabrinex – 2 ampoules over 10 mins
In females of childbearing age do a pregnancy test
If seizure activity persists despite 8mg of lorazepam
IV phenytoin 15mg/kg slow infusion (50mg/min)with ECG monitoring
EEG monitoring useful if unsure about nature of status
> 10 mins = call ICU
They may intubate under thiopentone (GA)
Tx neuromuscular ventilatory compromise
CALL FOR HELP – CRIT CARE
Ensure airway is safe
Sit up, O2 monitoring, HR and saturations (90-92)
Suctioning If secretions
NBM
Blood gases
IV access
CXR for ?infection
Further investigation for critical care and neurology
characteristic finding on CT with extradural haematoma
lentiform lesion
midline shift
ventricle compression
Tx extradural haematoma
Urgent neurosurgical referral
Burr hole to release pressure
Prognosis very good if this is performed early
Very minor it may be managed conservatively with regular monitoring
in base of the skull fractures what are given if there is a csf leakage
prophylactic antibiotics
Tx for base of skull fractures
urgent neurosurgical referral
Tx for acute hydrocephalus
Only definitive management is surgery so medical management exists to delay that
Azetazolamide +/- furosemide
Azetazolamide is a carbonic anhydrase inhibitor and is usually used in glaucoma to prevent the production of intraocular fluid, but in this case it reduces the amount of CSF produced
Surgical management
Ventriculoatrial, or ventriculo-peritoneal shunting for progressive symptoms
Valves open at certain pressures to allow release of CSF
Neurosurgical removal of tumours if necessary
Endoscopic 3rd ventriculostomy is an alternative procedure for obstructive hydrocephalus
Hole is made in 3rd ventricle so the CSF can bypass the cerebeal aquaduct (most common site of malformation) and drain into the interpeduncular cistern
GCS components
Motor
1 – no response
2 – extensor response to pain
3 – flexor response to pain
4 – withdraws from pain, pulls limb away
5 – localises to pain, responds towards painful stimuli
6 - Obeys commands
Voice
1 – no speech
2 – incomprehensible muffled speech
3 – inappropriate speech, understandable but no conversational effort
4 – confused orientation, answers questions with some confusion
5 – oriented
Eyes
1 – no eye opening
2 – eyes open in response to pain
3 – eyes opening in response to speech
4 – eyes open spontaneously
how is GCS score roughly stratified
13-15 = mild injury
9-12 = moderate injury
<9 = severe injury
what is cheyne-stokes breathing and what does it indicate
rapid breathing following by apnoea
coning
what does a unilaterally enlarged pupil indicate in the context of a semi concious patient
raised ICP
what does a bilaterally enlarged fixed pupil indicate in the context of a semi-concious patient
Deep coma
Brainstem death
what does a bilateral pinprick indicate in the context of a semi-concious patient
opiate overdose
pontine lesions causing sympathetic interruption
what are some important points in the history of a ?stroke
Exact time of onset
Speed of symptom onset
Body parts affected
Seizure?
Previous history of stroke?
Diabetic?
Tumours?
AF/MI?
On anticoagulants?
Drugs/smoking/alcohol?
how should you examine a ?stroke patient
GCS
NHISS
National institute of health stroke scale
Combines several parts of a clerking exam into a single scale evaluating possible location, thrombolysis benefit and severity stratification
CVS Murmurs (endocarditis) Signs of dissection BP HR
Respiratory
SpO2
RR
Crackles?
Neuro
LMN/UMN
CNS
Cerebellar
indications for urgent (<1 hour) brain CT in ?stroke
If considering thrombolysis
If bleeding risk
If decreased consciousness
Neck stiffness
Tx of confirmed embolic stroke
A-E management
Withold antiplatelet therapy until haemorrhage excluded
If ischaemic stroke confirmed administer 300mg aspirin
If <4.5 hours including at least 30 minutes of symptoms start thrombolysis
Thrombolysis
First check for contraindications (see table below)
Must have lab results back (clotting + platelets)
0.9mg/kg alteplase as per clinical pathway in hospital
10% bolus over 1 minute, remainder over 60minutes
post thrombolysis Tx for strokes
SALT
Swallow assessment within 2 hours – also helps with communication
Physiotherapy Relieves spasticity Prevents contractures Baclofen may be used to relieve spasticity Early mobilisation is vital
Occupational therapy
Limb splinting, ward groups
Nursing Implement SSKIN bundle Early nutrition required if NBM LMWH anticoagulation started on day 3 post-ischaemic stroke Ensure TED stockings are being worn
post thrombolysis Tx for strokes
SALT
Swallow assessment within 2 hours – also helps with communication
Physiotherapy Relieves spasticity Prevents contractures Baclofen may be used to relieve spasticity Early mobilisation is vital
Occupational therapy
Limb splinting, ward groups
Nursing Implement SSKIN bundle Early nutrition required if NBM LMWH anticoagulation started on day 3 post-ischaemic stroke Ensure TED stockings are being worn
post discharge stroke management
Lifestyle Cardioprotective diet Stop smoking Reduce drinking Exercise more
Antihypertensive therapy
Most importantly
Start 2 weeks post stroke if there is elevated BP
BP should be lowered slowly as autoregulation is likely impaired
Antiplatelet therapy
Aspirin 300mg daily for 2 weeks
Clopidogrel 75mg therafter
Statin
Offer 48 hours post stroke independent of cholesterol levels
Manage comorbidities
Strict diabetes management
Control AF well
Carotid USS will also be undertaken
post-stroke complications
Malignant MCA syndrome (Rapid neurological deterioration due to cerebral oedema associated with MCA infarcts)
DVT/PE
Aspiration + hydrostatic pneumonia
Pressure sores
Depression
Seizures
Incontinence
Post-stroke pain
Worsens outcomes
Multifactorial in nature
Often requires pain team input
Tx of Malignant MCA syndrome
NICE recommends empirical treatment in any patient <60 with a CT/MRI showing an infarct of at least 50% in the MCA with decreasing GCS
Treatment = rapid decompressive hemicraniectomy
what factors make a patient ‘high risk’ for stroke post TIA
TIA when anticoagulated
Multiple TIAs (especially in a short period of time)
ABCDD score >3
Age
>60 is 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
Tx for patients that have had a TIA and have been determined high risk for stroke
Statin
300mg aspirin
Unless currently taking low dose aspirin
Arrange referral to a specialist clinic in 24 hours
Advice patients not to drive until seen by specialist
Tx for patients that have had a TIA and have been determined low risk for stroke
Statin
300mg aspirin
Unless currently taking low dose aspirin
Arrange referral to a specialist clinic within a week
Advice patients not to drive until seen by specialist
what is required to diagnose a venous sinus thrombosis
MRI angiography
Tx of haemorrhagic stroke
Antiplatelets/anticoagulation CONTRAINDICATED
Reverse anticoagulation
Lower BP to <140/90 in 1 hour
IV labetolol
Neurosurgical intervention may be required
If GCS is falling and there is evidence of coning
complications of subarachnoid haemorrhage
Death
30% die immediately
Rebleed
Aneurysms - Inital bleed may be fatal but with sufficient vasospasm a clot may form
This usually holds for 3-4 days before rebleeding
AVMs
Generally rebleed within a few years rather than days
Hydrocephalus
Due to fibrosis of CSF pathways from the insult
Cerebral vasospams
May be severe leading to delayed vascular damage
investigation of ?SAH
Bloods FBC U+E LFT ESR Clotting G+S
CT Initial investigation of choice Usually seen within 48 hours Quantity of blood should be estimated for prognosis AVM usually visible on CT
LP - if CT normal
Should be done >12 hours after symptom onset
CSF will become xanthochromic (yellow from bilirubin) – visual inspection is sufficient for diagnosis
CT/MRI Angio - for surgery
Tx for SAH
4 weeks bed rest
Hypertension control
Nimodipene – reduces vasospasm, reduces mortality
Give to all if BP allows
IV fluids – may also prevent further vasospasm
Analgesia, anti emetics
Stool-softners to prevent straining
Discuss with neurosurgery
10-20% will rebleed within a few weeks
Aneurysms will usually be coiled by interventional radiology due to imminent risk of rebleed
Some will require neurosurgical clipping
AVMs usually rebleed within years rather than days but are generally dealt with at the time of presentation
Coiling by IR more common but gamma knife therapy may also be done
11% of patients develop hydrocephalus and require a shunt
what is the sign of an acute subdural hematoma on CT head
crescent shape pool of blood with midline shift and ventricle occlusion
management of acute subdural haematoma
craniotomy
what are the signs of a chronic subdural hematoma on CT head
blood becomes dark and assumed a more lentiform shape (like extradural)
Tx tension headache
If episodic (<15d/month) Paracetamol Aspirin NSAIDS Advice not to overuse the medication
If medication is used more than twice a week consider preventative treatment
Low dose amitryptaline
75mg initally, titrated upwards if there is a partial response
Chronic tension headache is more difficult to treat
Reassurance, relaxation techniques and addressing underlying stressors are important
Medication overuse headaches and clinical depression should be excluded and/or treated
