Approach to Neurological

Emergencies
(plus a CRASH course in
neuroanatomical localisation)
Approach to the neurological examination

• ‘Where is the lesion?’

• ‘How have findings evolved over time?’
– Correct diagnosis rests largely on anatomic localisation,
and rate of onset and time course of illness
• Eg differential diagnosis of sudden and acute visual loss
differs from that of insidious gradual onset visual loss
– Abrupt usually indicates vascular; subacute infectious
or inflammatory; insidious neoplastic (or other)
– Localisation should be clear after your history! If not,
take a better history.
 Neurological examination
1. Assess mental status (LOC/attention)
2. Language testing (includes 6 parts: fluency, comprehension, naming, repetition,
reading, writing)
– Aphasic patients usually have difficulties reading/writing.
[NB as aphasic patients often labelled as ‘confused’]
3. Assess cranial nerves II – XII
4. Do motor examination (tone, power, look for atrophy/fasciculations)
5. Check coordination (finger-nose, heel-shin, rapid alternating movts)
6. Test reflexes, both deep tendon and plantar
7. Check sensations, both primary (light touch, pinprick, temperature, vibration,
position sense) and cortical (graphesthesia, stereognosis, and double simultaneous
stimulation) sensory modalities
– Sensory testing often least reliable part of exam
8. Assess gait and stance, including Romberg’s test and tandem walking
– Don’t overlook this in an emergency evaluation (if possible to do)
 Neuroanatomical Localisation
• Start with motor:
– Upper (central) motor neuron or Lower
(peripheral) motor neuron lesion?
 Upper motor neuron lesion
• Hallmark of UMN lesions hyperreflexia with or
without increased muscle tone
• Localise to:

• BRAIN • SPINAL CORD

1. Cortical brain (frontal, temporal,
parietal, occipital lobes) 1. Cervicomedullary
2. Subcortical brain structures (corona junction
radiata, internal capsule, basal
ganglia, thalamus) 2. Cervical
3. Brainstem (medulla, pons, midbrain) 3. Thoracic
4. Cerebellum
4. Lumbosacral
 Lower motor neuron lesion
• Hallmark of LMN lesions decreased muscle tone
with flaccidity and hyporeflexia
• Localise to:
1. Anterior horn cells
2. Nerve root(s)
3. Plexus
4. Peripheral Nerve
5. Neuromuscular junction
6. Muscle
 Pearls or Top Tips
• A lesion of the left hemisphere which does not
affect language function more likely to be
subcortical
• Presence of cortical sensory deficits points to
cortical, most likely parietal, lesion
• Weakness arising from cortical lesions often
involves face and arm > leg (ie incomplete
hemiparesis); subcortical lesions (int capsule/basal
gangla) tend to cause complete hemiparesis
 Lobes of the brain

Subcortical
structures
 Brainstem lesions
• Hallmark of brainstem lesions = involvement of
cranial nerves + crossed findings e.g. CN
abnormalities contralateral to hemiparesis
• CN abnormalities (other than 7th) plus long tract
signs
• Sudden change in level of consciousness (LOC)
with pupillary abnormalities and involuntary limb
movements = bilateral thalamic and brainstem
involvement (top of the basilar syndrome)
 midbrain

• Diplopia, weakness/ataxia

• Impaired upward gaze

• CN III or IV palsy
• Contralateral hemiparesis or ataxia
 pons

• Speech & swallowing difficulties, weakness, sensory changes, diplopia

• Contralateral hemiparesis or sensory
• Dysarthria loss
• Ipsilateral facial (CN VII) • Nystagmus
• CN VI palsy • Ataxia
• Horner’s syndrome • Quadriplegia with bilateral lesions
• Impaired horizontal gaze affecting the basis pontis (‘locked-in’)
 medulla

• Dizziness, vertigo, difficulty swallowing,

hiccups, nausea, vomiting, and unsteadiness
• Horner’s syndrome • Ipsilateral sensory loss (face and body)
• CN IX, X, XII • Hemiplegia may be seen with medial
lesions (rare)
• Ataxia
 cerebellum
• Unsteadiness, dizziness, nausea, vomiting

• Ipsilateral ataxia of the limbs

• Gait ataxia
• Ipsilateral CN VI-like palsy (rare)
• Nystagmus
• Dysarthria
 Spinal cord lesions
• Hallmark is hyperreflexia, distal weakness, bowel
and bladder dysfunction, and the presence of a
sensory level
• Quadriparesis or paraparesis without facial
weakness points to a SC lesion

[However, high cervical (C2-4) and foramen magnum

lesions may result in facial numbness, ipsilateral
Horner’s, ipsilateral weakness of tongue and trapezius]
• Anterior cord
• Central cord (usually cervical)
• Posterior cord
• Conus medullaris/cauda equinae
• Anterior cord Symptoms weakness, sensory changes, bladder/bowel
fxn changes
• Central cord (usually cervical)
Upper (mainly) motor neuron weakness, spinothalamic
sensory loss (sparing posterior columns), sphincter
• Posterior cord dysfxn
• Conus medullaris/cauda equinae
• Anterior cord Symptoms weakness, sensory changes
• Central cord (usually
Paraparesiscervical)
with lower motor neuron weakness in arms
(+-fasciculations, atrophy), sensory loss in a ‘shawl’ or
• Posterior cord ‘cape’ distbn
• Conus medullaris/cauda equinae
• Anterior cord
• Central cord (usually cervical)
• Symptoms sensory changes, esp ‘band-like’ changes
Posterior cord Loss of vibration and joint position sensation
• Conus medullaris/cauda equinae
• Anterior cord
• Central cord (usually cervical)
• Posterior cord
• Conus medullaris/cauda equinae
Symptoms sacral sensory changes, buttock/back pain,
change in bladder/bowel function
Saddle sensory loss, sphincter dysfunction, weakness
ranging from absent->mild foot drop(L5/S1)-
>paraparesis
 Lower motor neuron lesion
• Hallmark of LMN lesions decreased muscle tone
with flaccidity and hyporeflexia
• Localise to:
1. Anterior horn cells
2. Nerve root(s)
3. Plexus
4. Peripheral Nerve
5. Neuromuscular junction
6. Muscle
 Lower motor neuron lesion
• Hallmark of LMN lesions decreased muscle tone
with flaccidity and hyporeflexia
• Localise to:
Flaccid weakness, wasting, fasciculations, NO sensory loss
1. Anterior horn cells
2. Nerve root(s)
3. Plexus
4. Peripheral Nerve
5. Neuromuscular junction
6. Muscle
 Lower motor neuron lesion
• Hallmark of LMN lesions decreased muscle tone
with flaccidity and hyporeflexia
• Localise to:
1. Anterior horn cells
Pain! Signs confined to a single limb usually
2. Nerve root(s) Weakness, sensory loss (radicular/plexus pattern),
Hyporeflexia
3. Plexus
4. Peripheral Nerve
5. Neuromuscular junction
6. Muscle
 Lower motor neuron lesion
• Hallmark of LMN lesions decreased muscle tone
with flaccidity and hyporeflexia
• Localise to:
1. Anterior horn cells
2. Nerve root(s)
3. Plexus Focal weakness (often distal in polyneuropathy)
Sensory loss almost always present!
4. Peripheral Nerve Hyporeflexia
5. Neuromuscular junction
6. Muscle
 Lower motor neuron lesion
• Hallmark of LMN lesions decreased muscle tone
with flaccidity and hyporeflexia
• Localise to:
1. Anterior horn cells
2. Nerve root(s)
3. Plexus
4. Peripheral Nerve Weakness on repetitive testing
(‘fatiguable weakness’)
5. Neuromuscular junction NO sensory loss
6. Muscle Normal reflexes (easily obtained)
 Lower motor neuron lesion
• Hallmark of LMN lesions decreased muscle tone
with flaccidity and hyporeflexia
• Localise to:
1. Anterior horn cells
2. Nerve root(s)
3. Plexus
4. Peripheral Nerve
5. Neuromuscular junction
Weakness esp difficulty getting out of a
6. Muscle car/chair or climbing stairs, muscle
ache/cramps, proximal distbn, SYMMETRICAL
NO sensory loss, Normal reflexes
Approach to Neurological
Emergencies

Dr Kathleen Bateman
Neurology Division
What do these people have in common?
 Stroke
• Diagnosis/management of stroke dealt with
separately (Prof Bryer)
• Ischaemic stroke = most common neurological reason
for emergency room visits
• ‘Time is brain’
• If less than 4.5 hours since onset of symptoms:
– Brain CT scan urgently to exclude a bleed
– Check glucose
– Consider IV rtPA thrombolysis according to national stroke
guidelines
 Transient Ischaemic Attack
• Definition:
– ‘Transient episode of neurological dysfunction, caused by focal
brain, (spinal cord) or retinal ischaemia, without acute
infarction’
• Diagnosis should be considered only if the transient
neurologic event is potentially from a specific
cerebrovascular territory!
• Emergency because TIAs portend strokes
• Risk is high in short term:
– 10% risk of stroke in first 90 days
– 4% risk of stroke within first 24 hours
ABCD2 score for Stroke Risk Assessment after TIA

Age ≥60? 1

BP ≥140/90 mmHg at initial evaluation 1

Clinical features: unilateral weakness 2

Clinical features: speech disturbance without weakness 1

Diabetes Mellitus 1

Duration of Symptoms 10-59 minutes 1

Duration of Symptoms >60 minutes 2

TIA investigation and management
• ABCD2 score:
– 0-3 points: Low risk
• 2 day stroke risk 1%, 7 day stroke risk 1.2%, 90 day stroke risk 3.1%
– ≥3 high risk
• All patients need urgent investigation:
– Carotid dopplers (?high grade stenosis amenable to CEA)
– ECG (?Atrial fibrillation)
• Consider Holter ECG and echo in selected patients (eg history
palpitations, cardiac symptoms/signs)
• Therapy:
– Anticoagulation if in AF
– Antiplatelet therapy (aspirin/aspirin+dipyridamole/clopidogrel)
– Appropriate secondary prevention (ACEI, statin)
 Epileptic seizures

• Epileptic seizure = paroxysmal burst of abnormal and excessively

synchronised neuronal activity causing a clinical neurologic deficit
with signs/symptoms acc to the area of brain involved

• Usually has abrupt, clear onset and a less discrete (but detectable)
ending
• May have an ‘aura’ (stereotyped sensation while awareness intact)
• May be followed by postictal state with lethargy/confusion
• May be unprovoked
• May be provoked by medication use/withdrawal, sleep deprivation,
trauma, stroke, metabolic derangement, or toxins
 Status epilepticus
• 40% of cases occur in people with epilepsy
• Definition of SE:
> 30 minutes of continuous or intermittent seizure
activity
• However, 5 minutes of continuous seizures or
discrete seizures with incomplete recovery
should prompt treatment for impending SE
• Most GTC sz last about 1 min
 Status epilepticus
• Three risk factors independently predict SE mortality:
– Older age
– Longer duration of SE
– Aetiology of SE (cerebral anoxia)
• Aim to terminate seizures asap (<20min)
• Becomes harder to terminate SE the longer it has been present
– 80% patients respond within 30 min of onset
– >60% patients FAIL to respond after 2hrs of SE (to 1st line drugs)
• Mortality is high! 26% in adults <60 yrs, 39% in >60 yrs
• Mortality risk for SE lasting > 1 hour is 10 X higher than SE < 1
hour! (32% vs 2.7%)
 Basic Management of Generalised Convulsive Status
Epilepticus (GCSE)
• ABC
– assess airway, breathing, give oxygen, consider intubation
– Cardiac monitor, pulse oximetry, IV access, fluid resuscitation
• Fingerprick glucose
– If low, give 100mg thiamine IV & 50ml 50% DW
• Look for traumatic injuries, remove clothes, get history from
paramedics/family/other
• Blood/urine samples
• ECG
• Urgent brain imaging (once patient stable)
• Consider potential causes
– Lp to exclude infection
• Do these steps in parallel with pharmacological treatment…
 Pharmacological Management of GCSE
Notes:
Lorazepam 0.05 - 0.1mg / kg IVI @ 2mg/ min •Lorazepam is the preferred benzodiazepine (BZD) for IV use as it
and
has a much longer anti-seizure effect (12-24 hrs) than diazepam
Phenytoin 18mg / kg IVI @ 50mg / min
(15-30 min)
•Midazolam is preferred BZD for IM use
Phenytoin 10mg / kg IVI @ 50mg / min •Rectal diazepam can be given where no IV access or IM
midazolam contraindicated/unavailable
•The brain concentration of phenytoin is maximal at the end of the
Phenobarb 18mg / kg or Valproate 15mg / kg infusion. Therefore, if there is ongoing seizure activity at the end of
IVI @ 50mg / min over 5 minutes the infusion, proceed to the next step and do not wait to observe
for a possible delayed effect.
•If adverse effects are observed during infusion of phenytoin
Phenobarb 10mg / kg Valproate 15mg / kg (cardiac) or phenobarb (cardiac or respiratory), the infusion rate
IVI @ 50mg / min over 5 minutes should be decreased
•Once seizure activity has been aborted, serum concentrations of
the AEDs should be maintained by appropriate oral doses
• Admission to ICU
•If seizure activity is aborted by the 2nd dose of valproate only, a
• Intubation and ventilation
continuous infusion of valproate at 1mg /kg / min can be
• Continuous EEG monitoring
considered to decrease the likelihood of recurrence.
• General anaesthesia with:
Midazolam
•0.2mg/kg bolus @ < 4mg / min
•Infusion 0.1-0.4mg/kg/h until no convulsive activity and burst-suppression on EEG
or Notes:
Propofol •Drugs of choice = midazolam or propofol
•2mg/kg bolus over 2-5 minutes •Thiopentone can cause
•Infusion 2-10mg/kg/h until no convulsive activity and burst-suppression on EEG • Severe hypotension
or • Delay in post-infusion recovery
Thiopentone •Thiopentone probably most potent of the 3 drugs,
•100-200mg bolus over 20 sec therefore can be used when midazolam or propofol fails
•50mg boluses every 2-3 minutes until no convulsive activity and burst-suppression
on EEG Seizure Examples of EEG patterns
•Infusion 3-5mg/kg/h

Notes:
•The outcome of generalized status epilepticus (SE) is inversely related to the
duration of SE. Generalized SE should therefore be managed as a medical Burst-suppression
emergency
•Focal motor SE (“epilepsia partialis continua”) is not an emergency and should
not be treated with intravenous AEDs. The aim is to abort seizure activity over
hours by means of oral AEDs and not minutes as is the case with generalized SE.
Courtesy F.Henning, using International Guidelines, 2009)
 GCSE vs NCSE
• Convulsive vs non-convulsive SE
• Convulsive obvious
• NCSE hard to detect clinically (need EEG to confirm)
– Patient may have confusion or fluctuating awareness or unresponsiveness/coma
– Sometimes subtle face/limb twitching or nystagmoid eye movts
• Common presentations in EU:
– Continuation of generalised convulsion or GCSE
– Confused/poorly responsive patient with earlier epilepsy
• Think about NCSE in any pt with a generalised sz whose mental status
doesn’t improve in 20min, or normalise in 60 min after sz
– Do urgent EEG (only way to confirm NCSE)
– Suspect if clear clinical improvement occurs quickly after IV BZD
– Needs specialist care in ICU as management complex
 What neurological emergency is this?

• Video
 Altered Mental Status

• Sudden alteration in mental status can be divided into

• Delirium (aka encephalopathy)
– Often fluctuating confusion, inattention, distractibility,
alteration of arousal, and global cognitive dysfunction
• Coma
– Unconsciousness with impairment of awareness and
wakefulness
– ‘State of profound unresponsiveness in which patient lies
motionless, with eyes closed, and cannot be aroused even
by painful stimuli’
 Altered Mental Status

• Assessment difficult because

– Large number of causes
– Limited time available for diagnosis

‘Time is brain’!

• May be mild to deep

– For objective measure use Glasgow Coma scale
 Altered Mental Status

• Assessment difficult because

– Large number of causes
– Limited time available for diagnosis

‘Time is brain’!

• May be mild to deep

– For objective measure use Glasgow Coma scale
 Altered Mental Status

• Localisation?
• Causes?
 Altered Mental Status
Bilateral hemispheral
• Localisation?
dysfunction vs structural cause
• Causes?

Structural lesions
– Mostly cause focal/lateralising
neurological signs
– have abnormal brain imaging

BUT absence of focal signs doesn’t exclude structural

damage e.g. meningitis/encephalitis, acute hydrocephalus,
anoxic-ischaemic encephalopathy post resuscitation
 Causes of Altered Mental Status

1. Drugs/toxins
2. Infections
3. Metabolic & Endocrine & Nutritional
4. Trauma
5. Hypoxia
6. Seizures
7. Vascular
8. Other…incl range of focal brain lesions
 Causes of Altered Mental Status

1. Drugs/toxins Carbon monoxide

Cyanide
Systemic sepsis or CNS infection e.g.
2. Infections Ethanol, atypical alcohols
meningitis/encephalitis
Hypoglycaemia, DKA, HONK
Anticholinergic drugs, cholinergic drugs
Acute
With or adrenal
without failure (Addison’s)
secondary haemorrhage or
(o-phos)
3. Metabolic & Endocrinecontusion & Barbiturates,
Myxoedema
Both
Sedatives (BZD,
Nutritional
acute hypoxiachloral
and hypoxic-
UraemiaStatus epilepticus
hydrate) ischaemic injury – convulsive/non-
4. Trauma Liver failure
convulsive
Opioids (inclIschaemic
heroin) strokes
Thiamine deficiency (Wernicke’s)
Intracerebral haemorrhage esp cerebellar
Sympathomimetics (amphetamines,
5. Hypoxia Hyponatraemia
Subarachnoid haemorrhage
cocaine, theophylline)
Hypercalcaemia
PsychedelicsCerebral venous sinus
(LSD, mescaline, PCP)thrombosis
6. Seizures Profound acid-base imbalance
Hypertensive
Antidepressants encephalopathy
(TCAs, MAOI)
Over rapid correction of Na (CPM)
Neuroleptics (butyrophenones,
7. Vascular Porphyria
phenothiazines)
lithium
8. Other…incl range of focal brain lesions
 Remember mimics!

• Exclude conditions mimicking coma

– Locked-in syndrome (check for blinking and
vertical eye movements)
– Generalised muscle paralysis
– Catatonia
– Extreme abulia
– Psychogenic unresponsiveness
 Helpful clinical clues to look for on history
and examination
1. Look for signs of focal brain injury or herniation
– Anisocoria, pupillary light reflex, papilloedema
– Forced deviation of eyes (horizontal/vertical)
– Absence of corneal, oculocephalic, oculocaloric reflexes
– Asymmetrical motor response to pain

2. Look for signs of meningeal irritation

 Helpful clinical clues to look for on history
and examination
3. Look for abnormal movements
– subtle rhythmic movements (nystagmoid jerks or
facial/finger repetitive movements): NCSE
– Myoclonus: metabolic/NCSE/post anoxic
– Tremors: hyperthyroidism/intoxication or alcohol/drug
withdrawal

4. Look for signs of systemic illness on general

examination
- signs of trauma, fever, skin rash, breath odour
 Basic management of unconscious patient
• ABC
– assess airway, breathing, give oxygen, consider intubation
– Cardiac monitor, pulse oximetry, IV access, fluid resuscitation
• Fingerprick glucose
– If low, give 100mg thiamine IV & 50ml 50% DW
• Look for traumatic injuries, remove clothes, get history from
paramedics/family/other
• Blood/urine samples
• ECG
• Urgent brain imaging (once patient stable)
• Consider potential causes
– Lp to exclude infection/SAH
– EEG to detect NCSE
• Focus first on conditions requiring specific treatment
 Investigations
• Brain imaging
– CT scan initially, MRI may be
helpful if CTB normal, MRV
• Blood tests may include – Urine toxicology screen
– Glucose – Drug levels
– Arterial blood gas – Serum alcohol (maybe)
– Electrolytes, renal fxn – Septic screen
– LFTs, ammonia – Thyroid function
– FBC, coag screen – Cortisol
– Urine keto acids
 Investigations

• Cerebrospinal fluid
– Perform urgently if unexplained fever or
meningism, and no contraindications

In suspected meningitis,
• Electroencephalogram CI to LP:
• Marked coma (GCS <10/15)
• New focal neuro deficit (eg
hemiparesis)
• Papilloedema
• Unexplained seizures
• Presence of VPS
*

*Isolated CN palsies not a CI to LP but caution advised with co-

existent reduced LOC
Note non-neurological CI to LP include severe coagulopathy or
cardioresp compromise or local sepsis over LP site
 Treatment & Prognosis
• Specific management related to cause
• Daily clinical examination best prognostic tool
• Confounding factors must be avoided (eg sedatives)
• Underlying cause most important determinant of outcome
• Outcome poorest among patients with anoxic-ischaemic coma
 Specific management:
Meningitis/encephalitis
• Give first dose of antibiotics immediately
– If possible, do blood culture and/or lumbar puncture (LP) immediately
before administration of the first dose of antibiotics
– Neither procedure must significantly delay ab

• Treat empirically with

– Ceftriaxone 80-100mg/kg (maximum 2g 12 hourly) IV (IM/IO if no IV access)
– Penicillin allergy is not a contraindication to ceftriaxone in acute meningitis
• Only omit ceftriaxone if there has been documented ceftriaxone anaphylaxis,
– Use Chloramphenicol 25mg/kg (maximum 500mg) i.v instead, if available.

• T/F to hospital immediately, detailing all treatment in referral letter!

 Specific management:
Meningitis/encephalitis
1. CSF and blood tests required in all cases:
– CSF differential cell count, glucose, total protein, Gram stain, bacterial culture and sensitivity
– Opening CSF pressure
– Serum glucose
– Peripheral white cell count and differential
– Blood culture
– Serum procalcitonin (C-reactive protein if unavailable)
– HIV test
2. Other diagnostic tests that should be performed for specific indications:
– CSF HSV PCR - fulfils case definition for encephalitis
– CSF CMV PCR - HIV-infected, CD4 <100 cells/mm 3 with encephalomyelitis
– CSF measles PCR - during a measles outbreak or suggestive clinical features
– CSF CLAT - HIV-infected and >5 years of age (see below)
– CSF mycobacterial culture / GeneXpert MTB-RIF- uncertain length of history or other reason to
suspect TB meningitis (take large volume 6ml)
– Serum and CSF testing for syphilis according to protocol of local laboratory
 Specific management:
Meningitis/encephalitis
• Read Bacterial Meningitis National Guidelines
(in press)
– Further in-hospital management detailed

• Encephalitis:
– fever + altered mental status, especially if seizures
– Consider empiric acyclovir pending CSF HSV PCR
result
 Case description
• GFJ pt
 Thunderclap headache (abrupt onset)

• 11 -25% of thunderclap headaches will be due

to SAH Landtblom 2002; Linn 1994

• Edlow 2003: reasons for missing a SAH?

1. failure to appreciate the clinical presentation
2. failure to understand the limitations of CT
imaging
3. Failure to perform/correctly interpret CSF
 Thunderclap headache
• Take an accurate history!
– Headache most maximal within seconds, a few
within 5 minutes, usually severe (‘first and worst’)
– this will identify who has had a true acute onset
headache, but it will not distinguish accurately
betw primary/secondary headaches
– SAH associated features: nausea, vomiting, pyrexia,
photophobia, meningism, visual disturbances,
transient LOC, coma, seizures, focal neuro signs
 Thunderclap headache
• All pts with thunderclap headache need an urgent CTB
– Note that CTB can never completely exclude a SAH, & its
sensitivity falls rapidly >48hrs

• All pts with normal CTB need a CSF examination

– When not a SAH, still a fairly high chance of other pathology

• Neurology/neurosurgical consult
– Consider further imaging with CT angiogram in certain
cases, especially if delayed presentation >48 hours
Causes of acute onset headaches
 Red flags in headaches
• Sudden onset of headache (thunderclap)*
• Onset of headache over 50 years of age*
• Significant change in the characteristics/frequency/severity of prior
headaches
• Headache that changes with posture or precipitated by valsalva/physical
exertion
• New onset headache with an underlying medical disorder (e.g. cancer, HIV)
• Headache subsequent to head trauma
• Signs or symptoms of systemic illness (e.g. fever, chills, weight loss, neck
stiffness, jaw claudication)
• Focal neurological signs or symptoms*
• Papilloedema*

1. US Headache Consortium. Evidence-based guidelines in the primary care setting:

neuroimaging in patients with nonacute headache.American Family Physician, 2000 (online). Available at
http://www.aafp.org/afp (Evidence based guidelines)
2. SIGN guidelines, November 2008
• List of ‘red flags’ in headache not based on
good data
– These features are mostly based on small
retrospective studies and do not have sufficient
sensitivity or specificity to rule out intracranial
pathology (Silberstein, 1992)
• 28 studies, 22 retrospective, 6 prospective unblinded
 Red flags
• Only a minority of patients with headaches
with ‘red flags’ will have a detectable
secondary cause…

..but consensus is they should probably be imaged

by CT brain (with/without contrast)
• Sudden onset severe unilateral headache

Urgent CT angiography or
DSA

Referral to neurosurgery
 Summary
• Highlighted aspects of recognition +/- immediate
management of common neurological emergencies
– Stroke
– Status epilepticus
– Unconscious patient
– Meningitis/encephalitis
– Abrupt onset headaches (SAH)
– Acute CN III palsies
• By no means comprehensive!
• Final case video..