Download Neurological Disorders Expert Questions

Neurological Disorders expert questions
Altered mental state - Coma
DIS Ex
Coma is a state of reduced alertness and responsiveness from which the patient cannot be aroused.
The Glasgow Coma Scale is a widely used clinical scoring system for alterations in consciousness. Advantages
are a simple scoring system and assessment of separate verbal, motor, and eye-opening functions.
Disadvantages include lack of acknowledgement of hemiparesis or other focal motor signs and lack of testing
of higher cognitive functions.
Differential Diagnosis of Coma
Coma from Causes Affecting the Brain Diffusely
Encephalopathies
Hypoxic encephalopathy
Metabolic encephalopathy
Hypoglycemia
Hyperosmolar state (e.g., hyperglycemia)
Electrolyte abnormalities (e.g., hyper- or hyponatremia, hypercalcemia)
Organ system failure
Hepatic encephalopathy
Uremia/renal failure
Endocrine (e.g., Addison, hypothyroid, etc)
Hypoxia
CO2 narcosis
Hypertensive encephalopathy
Toxins
Drug reactions (e.g., neuroleptic malignant syndrome)
Environmental causes—hypothermia, hyperthermia
Deficiency state—Wernicke encephalopathy
Sepsis
Coma from Primary CNS Disease or Trauma
Direct CNS trauma
Vascular disease
Intraparenchymal hemorrhage (hemispheric, basal ganglia, brainstem, cerebellar)
Subarachnoid hemorrhage
Infarction
Hemispheric, brainstem
CNS infections
Neoplasms
Seizures
Nonconvulsive status epilepticus
Postictal state
History
Certain points in history may be especially useful
 The circumstances and rapidity with which neurologic symptoms developed;
 The antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziness, double vision,
or vomiting);
 The use of medications, illicit drugs, or alcohol; and
 Chronic liver, kidney, lung, heart, or other medical disease.
Direct interrogation of family and observers on the scene is an important part of initial evaluation. Ambulance
officers often provide the most important clues.
General physical examination
 Vitals including temperature should be measured quickly
o Fever s/o sepsis, systemic infection or hypothalamic failure
o Very high temperatures with neurological signs and seizures s/o heat related illness
o Hypothermia – alcoholic, barbiturate, sedative intoxication, peripheral circulatory failure or
hypothyroidism
o Tachypnea – systemic acidosis or pneumonia
o Abnormal respiratory patterns – brainstem disorders
o Marked hypertension – hypertensive encephalopathy or Cushing’s response to raised ICP
o Hypotension – alcohol or barbiturate intoxication, hemorrhage, MI, sepsis, profound
hypothyroidism or Addisonian crisis
 Funduscopic examination –
o Subhyaloid hemorrhages – SAH
o Exudates, hemorrhages, vessel changes, papilledema – hypertensive encephalopathy
o Papilledema – increased ICH
 Skin petechiae – TTP, meningococcemia, bleeding disorder causing ICH
Neurologic examination
 Position in bed –
o presence or absence of movements
o Focal weakness or flaccidity
 Abnormal movements –
o Twitching movements – seizures
o Multifocal myoclonus – metabolic disorder e.g. uremia, anoxia or drug intoxication (SS) –
asterixis
 Abnormal posturing
o Decorticate – flexion of the elbows and wrists and supination of the arm – bilateral damage
beyond the midbrain
o Decerebrate – extension of elbows and wrists with pronation of arms – damage to motor
tracts in midbrain or caudal diencephalon
 Level of arousal
 Brainstem reflexes
o Pupillary responses to light
o Spontaneous and elicited eye movements
o Corneal responses and
o Respiratory patterns
Presence of these responses usually means a lesion above the brainstem most probably the
hemispheres.
 Pupillary signs – to suggest cranial nerve damage and response to naloxone in case of pinpoint pupils
 Ocular movements
o The eyes look toward a hemispheral lesion and away from a brainstem lesion
o Oculocephalic reflexes – integrity of brainstem
Laboratory studies and Imaging
Bedside
 BSL – hypo- or hyper-glycemic
 Arterial blood gases – helpful in patients with lung disease and acid-base disorders
Laboratory
 EUC- electrolyte abnormalities, serum osmolarity, renal function
 Ammonia – hepatic encephalopathy

Toxicologic analysis
o Ethanol level - > 43mmol/L (0.2g/dl) impaired activity, >65mmol/L (0.3g/dl) stupor in
nonhabituated patients, >0.4g/dl in chronic alcoholics
o Drug levels where applicable e.g. lithium, carbamazepine, valproate etc.
Radiologic studies
 CXR – pneumonia or aspiration
 CT brain – structural lesions of brain. Lesions in coma that may be missed on a CT include
o Bilateral hemisphere infarction
o Acute brainstem infarction
o Encephalitis/ meningitis
o Mechanical shearing of axons in head trauma
o Sagittal sinus thrombosis
o Subdural hematomas isodense with adjacent brain tissue
Other investigations
 EEG – rarely diagnostic but useful in metabolic and drug induced states; also in clinically
unrecognised seizures in HSV encephalitis or Prion disease
 Lumbar puncture – in diagnosis of meningitis/ encephalitis and sometime SAH.
Cerebrovascular disease patterns in coma
 Basal ganglia and thalamic hemmorhage – acute onset of vomiting, headache, hemiplegia and
characteristic eye signs
 Pontine hemorrhage – sudden onset, pinpoint pupils, loss of reflex eye movements, ocular bobbing,
posturing, hyperventilation and excessive sweating
 Cerebellar hemorrhage – occipital headache, vomiting, gaze paresis and inability to stand
 Basilar artery thrombosis – neurologi prodrome or warning spells, diplopia, dysarthria, vomiting, eye
movement and corneal response abnormalities and asymmetric limb paresis
 Subarachnoid hemmorhage – precipitous coma after headache and vomiting
 Common hemispheric strokes – do not directly cause coma, except when edema surrounding large
infarct act as a mass
Coma – general management
The immediate goal in a comatose patient is prevention of further nervous system damage.
 Correct 6Hs rapidly
o Hypotension
o Hypoglycaemia
o Hypercalcemia
o Hypoxia
o Hypercapnia
o Hyperthermia
 Airway protection – if there is apnea, upper airway obstruction, hypoventilation or emesis, or risk of
aspiration
 IV access – naloxone or dextrose as indicated, thiamine with glucose in c/o malnourished patients
 Thrombolytic therapy – for basilar thrombosis with brainstem ischemia once hemmorhage excluded
 Antibiotic therapy in case of meningitis or sepsis early
Status epilepticus
DIS Ex
In the past, status epilepticus was defined as either continuous seizure activity for 30 min or more, or two or
more seizures that occur without full recovery of consciousness between the attacks.
It remains unclear how long a seizure can continue before permanent neurologic sequelae ensue. Although this
question has never been satisfactorily answered, it does appear that the longer seizures are allowed to continue,
the more likely that permanent CNS injury will result. Thus treatment should be initiated as soon as possible in
all patients with continuous seizure activity lasting more than 10 min. The longer the seizure is allowed to
continue, the more difficult it will be to control.
Causes of Secondary Seizures
Trauma (recent or remote)
Intracranial hemorrhage (subdural, epidural, subarachnoid, intraparenchymal)
Structural abnormalities
Vascular lesion (aneurysm, arteriovenous malformation)
Mass lesions (primary or metastatic neoplasms)
Degenerative diseases
Congenital abnormalities
Infection (meningitis, encephalitis, abscess)
Metabolic disturbances
Hypo- or hyperglycemia
Hypo- or hypernatremia
Hyperosmolar states
Uremia
Hepatic failure
Hypocalcemia, hypomagnesemia (rare)
Toxins and drugs (many)
Cocaine, lidocaine
Antidepressants
Theophylline
Alcohol withdrawal
Drug withdrawal
Eclampsia of pregnancy (may occur up to 8 weeks postpartum)
Hypertensive encephalopathy
Anoxic-ischemic injury (cardiac arrest, severe hypoxemia)
Treatment
The goal of treatment of status epilepticus is seizure control within 30 minutes of presentation.
Morbidity is due to hypoxemia, hyperthermia, circulatory collapse and eventual neuronal injury.
Headache and facial pain
Headache represents up to 4% of all ED visits. Most ED patients have benign primary headache syndromes, but
approximately 3 – 4% may have serious or secondary pathology.
Etiology and Classification
History

Headache pattern – important features include first severe headache, worst ever headache, steady
worsening headache over several days or significant differences from prior headaches.
 Onset - sudden onset headache especially when occurring with exertion is an independent predictor of
IC pathology – especially 25% of these patients will have SAH.
 Headache location – nonspecific and diagnosis should not be based on this. Occipitonuchal headache
location in ED patients is an independent predictor if IC pathology (PPV 16%). It is also the most
common location of headache for SAH.
 Associated symptoms – h/o syncope, altered LOC, confusion, neck pain or stiffness, persistent visual
disturbance, fever or seizure.
 Other history – medications (nitrates, MAOIs, anticoagulants), h/o trauma, toxic exposure.
 Past history – past headaches and investigations, Comorbid conditions such as malignancy, HIV,
coagulopathy or hypertension.
 Family history – migraine headaches may have positive family history. h/o SAH in first and second
degree relatives.
Physical examination
 Fever – infection e.g. meningitis, sinusitis
 Marked hypertension – hypertensive urgency or emergency
 Sinus palpation for tenderness
 Temporal artery palpation for tenderness or reduced pulsation
 Dental and TMJ examination
 Eye examination to rule out acute glaucoma, visual field defects or iritis
 Fundoscopy – s/o papilledema or subhyaloid hemmorhages in SAH
 Focused neurological examination mandatory
 Look for signs of meningeal irritation
Special aspects
 Women – migraine more common, ask for menstrual history, OCP use, pregnancy and menopause
 Pregnancy – always consider preeclampsia, migraine improves in 60-70% patients in pregnancy
 Older age – new onset in patient >50years usually have secondary cause
 HIV/AIDS – high risk for IC SOL and pathologic infections
Historical Features Suggesting Secondary Headache
Acute onset
Worst ever
Posttraumatic
Awakens from sleep
With fever
Aggravated by: sneezing, coughing, Valsalva, lying down
Morning vomiting
Altered mental status
Change in behavior
Change in pattern
Toxic exposure
Positive family history for migraines or subarachnoid hemorrhage
Investigation
Data collected from history and physical examination allows for risk stratification of patients presenting with
headache in to groups needing emergent, urgent or outpatient care.
Once the information is collated they may be divided into categories.
Indications for emergent neuroimaging
 Presence of new focal neurologic deficits
 Acute sudden onset of headache
 HIV positive patients with a new headache
 Patients >50 years with a new headache
ACEP Headache Categories
Headache Category
I.
Examples
Critical secondary causes requiring emergent identification Subarachnoid hemorrhage, meningitis, brain
and treatment
tumor with raised ICP
II. Critical secondary causes not necessarily requiring
emergent identification or treatment
Brain tumor without raised ICP
III. Generally benign and reversible secondary causes
Sinusitis, hypertension, post–lumbar puncture
headache
IV. Primary headache syndromes
Migraine, tension type, or cluster
Diagnostic adjuncts
 CT brain
o Usually non-contrast CT brain conducted.
o Use of contrast associated with 10% risk of minor reactions and 0.1% risk for severe reactions.
o If IC SOL highly suspected, contrast study may be conducted
o Negative CT scan does not exclude SAH
 Lumbar puncture
o Indicated when meningitis suspected or when CT negative in highly suspected SAH
o Contraindications – suspicion of raised ICP
o Raised ICP can be excluded by the combination of (all three present)
 Absence of papilledema
 Normal LOC and

Normal neurologic examination
o If these conditions are met, then a CT scan is not required prior to LP, especially if the CT scan
is likely to be delayed.
 MRI brain
o Cost and restricted availability limits utility in emergency situations
o More sensitive in evaluating brain injuries, difuse axonal injuries, parenchymal contusions,
isodense SDH and most tumors
Subarachnoid Hemorrhage
Of all sudden, severe headaches presenting to ED with a normal neurologic examination, 12 % have SAH.
SAH occurs in young people, with a median age of 50 years. Mortality rates from SAH are high, 50% die within
6 months.
Clinical features
 Almost half patients with SAH have no clinical findings at presentation – no neurodeficit, normal vitals,
normal LOC and no neck stiffness
 Headaches most commonly severe and of sudden onset, but may be subtle. Location of headache
usually occipitonuchal with many atypical presentations e.g. neck pain
 Resolution of pain even without treatment does not exclude the diagnosis
 Radiation of pain down the cervical spine suggests tracking of SAH down the spinal canal
Hunt and Hess Classification of Subarachnoid Hemorrhage
Classification Symptoms
Grade I
Asymptomatic or minimal headache and mild nuchal rigidity
Grade II
Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial-nerve
palsy
Grade III
Drowsiness, confusion, or mild focal deficit
Grade IV
Stupor, moderate to severe hemiparesis, possible early decerebrate rigidity, vegetative
disturbance
Grade V
Deep coma, decerebrate rigidity, moribund appearance
Diagnosis
CT scan brain
 Sensitivity of newer generation CT scans is about 93% within 24hrs of onset of symptoms and higher if
within 12hrs
 No study to date has shown CT conclusively ruling out SAH at even 12hrs.
 Sensitivity of CTB falls to just over 80% at 24hrs and then rapidly declines.
 Latest guidelines still mandate LP after negative CTB
Lumbar puncture
 LP performed 12hrs or longer after onset of headache and spectrophotometry conducted to look for
xanthochromia is nearly 100% sensitive for u to 2 weeks following a bleed.
 Xanthochromia checked visually may result in 50% false negative rates.
 LP may be delayed for 12hrs after onset of symptoms while awaiting development of xanthochromia
 Traumatic taps and xanthochromia on LP, all warrant CNS vascular imaging
Treatment
Rebleeding and vasospasm are major complications in SAH
 Risk of rebleeding is highest in first 24hrs
 In patients with raised BP, lowering systolic BP to 160mmhg and/or maintaining a MAP of 110mmhg
is associated with lower risk of rebleeding and a decreased mortality rate
 Maintain BP at prehemorrhage levels if known
 Cerebral ischemia caused by vasospasm occurs from 2 days to 3 weeks after aneurysm rupture.
 Nimodipine PO 60mg q6h, reduces the incidence and severity of vasospasm and should be given to all
patients with SAH
 In patients unable to tolerate orally, nimodipine infusion should be instituted
Seizures and persistent vomiting can cause elevations in systemic and ICP.
 Prophylactic phenytoin loading is recommended.
 Nausea and vomiting treated promptly with antiemetics
 Analgesia appropriately managed
For candidates with good neurologic condition (Hunt and Hess grades 1 to 3)
 Early angiography and surgical intervention recommended
 Alternative approaches for appropriate aneurysms include endovascular obliteration through use of
intraluminal platinum coils or detachable balloon embolisation.
Bacterial Meningitis
In cases of bacterial meningitis, the two most critical actions in the emergency department are to suspect it and to
begin empirical treatment promptly.
Epidemiology
 Attack rates are age-specific ranging from 400/100000 in neonates to 1-2/100000 in adults
 2/3rd cases are in children
 Long term complications such as cognitive defects, epilepsy, hydrocephalus and hearing loss affect
25% of survivors
 Prior to 1985 – H.influenzae (45%), S. pneumoniae (18%) and N. meningitidis (14%)
 But now after universal Hib vaccination programs, S.pneumoniae and N. meningitidis predominate
Pathophysiology
Encapsulated organisms from host airway → invade, survive and disseminate through bloodstream → gain
access to subarachnoid space → subcapsular constituents trigger inflammatory cascades in host → clinical
picture of fever, meningismus and eventually altered mental status.
Clinical features
Signs and symptoms
 25% cases s/s are classical with little diagnostic challenge
 Rapidly developing fever, headache, stiff neck, photophobia and altered mental status
 Seizures occur in 25% of patients
 Features may be non-specific in the very young and the very old.
 History regarding living conditions, trauma, immunocompetence, immunization and antibiotic use
should be sought
 Brudzinski sign – flexion of hips and knees in response to passive neck flexion
 Kernig sign – contraction of hamstrings in response to knee extension while hip is flexed
 Examination of skin to seek for purpuric rash
 Cutaneous stigmata e.g. petechiae, splinter hemorrhages and pustular lesions should be aspirated and
gram stained and cultured
 Paranasal sinues percussed and ENT examined for evidence of primary infection
 Funduscopy to assess for papilledema
 Neurologic examination – seek evidence of focal neurologic deficit e.g. disordered eye movements,
visual field defects, facial asymmetry and hemiparesis
Diagnosis
 Lumbar puncture is the only confirmatory investigation which can diagnose or rule out meningitis
 LP should be carried out as soon as it is deemed safely possible; its timing should not impede the early
administration of empirical antibiotics
 Blood cultures yield responsible organisms in only 50% of cases
 LP should be considered before neuroimaging in these cases
o Age <60 yrs
o Immunocompetent
o No h/o CNS disease
o No recent seizure <1 week
o Normal sensorium and cognition
o No papilledema
o No focal neurologic deficit
 Coagulopathy is considered as a relative contraindication. Infusion of clotting factors may be
considered in haemophiliac patient. Infusion of platelets may be considered in case of severe
thrombocytopenia, but no safe level for platelets has been ever investigatively proven.
 CSF analysis should be done for cell counts, gram stain, culture, CSF glucose and protein levels at the
least.
 Additional tests which may be required in suspected cases include:
o Viral cultures in viral meningitis
o Tests for Borrelia antibodies in c/o Lyme disease
o India ink or serum cryptococcal antigen in immunocompromised patients
o AFB stain for mycobacteria in c/o suspected tuberculous meningitis
o Agglutination tests for bacterial antigens in c/o partially treated cases – e.g. S. Pneumoniae, H.
Influenza, group B streptococci and N.meningitidis.


LP may be negative in early bacterial meningitis and repeated LP may be conducted if there is strong
clinical suspicion despite initial negative LP results
LP is contraindicated if there is infection in overlying skin
Lumbar puncture findings
Parameter
Normal
Opening
< 170mm
pressure
WBC
<5 mononuclear
% PMN
0
Glucose
>2.2mmol/dL
Protein
<50mg/dL
Gram stain
Cytology
-
Bacterial
>300mm
Viral
200mm
Neoplastic
200mm
Fungal
300mm
>1000/µL
>80%
<2.2mmol/dL
>200mg/dL
+
-
<1000/µL
1-50%
>2.2mmol/dL
<200mg/dL
-
<500/µL
1-50%
<2.2mmol/dL
>200mg/dL
-
<500/µL
1-50%
<2.2mmol/dL
>200mg/dL
+
Treatment
Ideal management has several goals. These include:
 Rapid administration of a bactericidal antibiotic that gains rapid entry into the subarachnoid space
 In some cases, use of anti-inflammatory agent to suppress the normal inflammatory processes, which
are amplified by antibiotic-induced bacteriolysis
 Counter the adverse effects of increased ICP and vasculopathy, which may lead to brain ischemia
Empirical antibiotic therapy
Patient category
Potential pathogens
Empirical therapy
Age
18 – 50 years
S. Pneumoniae, N. Meningitides
Ceftriaxone 2g IV q12h +
Vancomycin or Rifampicin
>50 years
S. pneumoniae, N. Meninigitidis, L. Ceftriaxone 2g IV q12h +
Monocytogenes, aerobic GN bacilli ampicillin 2g IV q4h + vancomycin
or Rifampicin
Special circumstances
CSF leak with h/o closed head
S. pneumoniae, H. Influenzae, GBS Ceftriaxone 2g IV q12h
trauma
Recent penetrating head injury,
S. aureus, S. Epidermidis,
Vancomycin 25mg/kg IV load then
neurosurgery or VP shunt
diphtheroids, aerobic GN bacilli
19mg/kg by nomogram plus
ceftazidime 2g IV q8h
Immunocompromised host
S. Pneumoniae, N. Meningitides, L. Vancomycin as above + ampicillin
Monocytogenes, aerobic GN bacilli 2g IV q4h + ceftazidime 2g IV q8h
Any patient
Herpes simplex virus suspected
Add Acyclovir 10mg/kg IV q8h
Steroids in meningitis
 Number of anti-inflammatory drug have been shown to improve outcomes in experimental meningitis,
but only glucocorticoids and specifically dexamethasone have been tested in clinical trials
 Dexamathasone given to adults with bacterial meningitis (10mg IV 15min before antibiotic therapy,
then 6hrly for 4 days) appears to decrease morbidity and mortality due to S. Pneumoniae but not N.
Meningitides
Supportive management
 Surveillance and correction of complications
o Seizures – phenytoin loading
o Hyponatremia
o Hydrocephalus and
o CVA
 General treatment measures – maintain normal blood volume
 Avoid hypotonic fluids
 Monitor sodium levels closely to detect SIADH or cerebral salt wasting
 Correct hyperpyrexia
 Correct coagulopathies with specific replacement therapy
 For marked cerebral edema, as noted by CT findings
o Head elevation
o Hyperventilation to PaCO2 of 25-30 mmhg
o Mannitol
o Measure ICP and MAP to monitor CPP
Chemoprophylaxis
Chemoprophylaxis for meningitis or other infections caused by N. Meningitides and H. Influenzae type b is
offered to close contacts of the index case. Among close contacts there will be a person or persons
asymptomatically carrying the organism which caused the index infection. Chemoprophylaxis aims to eradicate
asymptomatic carriage in the network of contacts to prevent further spread to susceptible members in the group.
N. meningitides
1. Ceftriaxone 250mg IM as single dose (preferred option during pregnancy) OR
2. Ciprofloxacin (adult >12yrs of age) 500mg orally as a single dose (preferred in women on OCP) OR
3. Rifampicin 600mg (neonate 5mg/kg, child 10mg/kg) orally BD for 2 days (preferred in children)
H.influenzae type b
1. Rifampicin 600mg (neonate 10mg/kg, child 20mg/kg up to 600mg) orally daily for 4 days OR
2. Ceftriaxone 1g (child 25mg/kg up to 1g) IM daily for 2 days (limited data)
3. Where index case is <2yrs of age, commence full course of Hib vaccination ASAP after recovery,
regardless of previous immunization.
4. Unvaccinated contacts <5yrs should be immunized ASAP.
Cerebrovascular Accidents
Cerebrovascular disease comprises disorders in which there is disturbance of blood supply to the brain. Stroke is
the most important manifestation of cerebrovascular disease. A stroke occurs when an artery supplying blood to
a part of the brain suddenly becomes blocked (ischemic stroke – 85%) or bleeds (hemorrhagic stroke – 15%).
Stroke poses a significant burden on patients and their families as well as on the health system and aged care
services. Each year about 40000-48000 stroke events occur in Australia and was the cause of nearly 7% of all
deaths.
Etiologic Classification
 Ischemic stroke
o Thrombosis
 Atherosclerotic disease
 Vasculitis
 Dissection
 Polycythemia
 Hypercoagulable states
 Infectious diseases – HIV, syphilis, TB, aspergillosis and trichinosis
o Embolism
 Cardiac sources
 Valvular vegetations
 Mural thrombi (AF,AMI or dysrhythmias)
 Paradoxical emboli (ASD, VSD)
 Cardiac tumors
 Artery-to-artery emboli
 Fat emboli
 Particulate emboli from IV drug injection
 Air emboli
 Septic emboli
o Systemic hypoperfusion
 Cardiac failure – diffuse injury in watershed areas at periphery of cerebral vascular
supply territories
 Hemorrhagic stroke
o Intracerebral hemorrhage
o Subarachnoid hemorrhage
 Berry aneurysm rupture
 Rupture of AVM
o Bleeding diatheses
 Anticoagulant use
 Thrombolytic use
o Vascular malformations
o Cocaine use
Anatomy of brain blood supply
 Vascular supply of brain divided into anterior and posterior circulations
 Anterior circulation –
o Common carotid arteries divide into right and left internal and external carotid arteries at the
level of the mandible
o ICA course intracranilly in cavernous sinus along sella turcica giving ut first branch the
ophthalmic artery – supplying optic nerve and retina
o ICA terminates by branching into anterior and middle cerebral arteries at the circle of Willis.
o Anterior circulation supplies blood to optic nerve, retina and frontopareital and anterotemporal
lobes of the brain
 Posterior circulation –
o Derived from two vertebral arteries that ascend through the transverse processes of the cervical
vertebrae
o Vertebral arteries enter cranium through foramen magnum, supplying cerebellum vis the
posteroinferior cerebellar arteries.
o

Vertebral arteries join to form the basilar artery, which branches to form the posterior cerebral
arteries
o Posterior circulation supplies the brainstem, cerebellum, thalamus, auditory and vestibular
functions of the ear, medial temporal lobes and the visual occipital cortex
The anterior and posterior circulations join at the circle of Willis, potentially allowing collateral flow.
The amount of collateral flow determines the extent of neurological deficit a complete carotid occlusion
on one side can cause.
Pathophysiology of stroke
Ischemic stroke
 Neurons are very sensitive to changes in cerebral blood flow and die within minutes of complete
cessation of blood flow
 Despite complete occlusion, some collateral supply usually persists
 In the region of the stroke, cells vary from irreversibly injured neurons in the centre to reversibly
injured neurons in the periphery (the penumbra)
 Degree and duration of occlusion determines the viability of the cells in the penumbra
 The earlier reperfusion occurs, the greater the chance of survival – basis for IV and intra-arterial
thrombolytic therapy and use of neuroprotective agents
Hemorrhagic stroke
 ICP rises following vascular rupture with a corresponding short-term decrease in global perfusion
 ICP and CPP gradually improve, but do not return to baseline
 Marked reduction in perfusion occurs around the area of hemorrhage probably due to local compression
 Blood breakdown products from ICH also mediate vasoconstriction into wider area of brain, remote
from the location of bleed.
Clinical features
History
 H/o HT, CAD and DM all suggestive of underlying atherosclerotic disease and suggest thrombosis
 H/o AF, valvular replacement or recent MI all suggest embolism
 Question regarding recent TIAs, similar transient neurological symptoms prior to the stroke s/o
thrombosis whereas multiple TIAs in different distributions s/o embolism
 Sudden onset of symptoms usually s/o embolic or hemorrhagic stroke
 Associated symptoms of headache, vomiting or recent trauma should be sought and recorded
 Recent h/o neck injury, MVA, chiropractic manipulation or sports related injury s/o carotid or vertebral
artery dissection
 h/o straining or coughing s/o ruptured aneurysm
Physical examination
General examination
 temperature – s/o infection or secondary to aspiration
 skin examined for signs of
o emboli – Janeway lesions and Osler nodes
o bleeding disorder – ecchymosis or petechiae
 funduscopic examination –
o papilledema to r/o mass lesion, cerebral vein thrombosis or hypertensive crisis
o pre-retinal hemorrhage – SAH
o evidence of hypertensive retinopathy
 cardiovascular examination to look for AF, CCF or valvular disease
Neurologic examination
Basic neurologic assessment can be broken down into six major areas:
1. level of consciousness – simple questions TSP, simple commands
2. visual assessment – visual fields and extraocular movements
3. motor function – upper limb check for pronator drift, lower limb: lift legs of bed for 5s, gait assessment
4. sensation and neglect – pinprick testing, identifying numbers on plams, double simultaneous extinction;
neglect also checked by asking patient to draw a box or house
5. cerebellar function – giat, finger-to-nose and/or heel-to-shin testing
6. cranial nerves – each nerve individually assessed
Stroke syndromes
Transient ischemic attack
 TIA is a neurologic deficit that resolves within 24h (although most resolve within 30m) and is most
commonly associated with thrombotic strokes
 Many clinical TIAs may be associated with CT findings of infarction
 10% of patients with TIA may return to ED with a stroke within 90 days, with half of these in just 2
days.
Ischemic stroke syndromes
Artery involved
Clinical features
(syndrome)
Anterior cerebral artery
 Contralateral leg weakness > arm weakness
infarction
 Mild cortical sensory deficits
 May preserve speech or motor actions and respond slowly
Middle cerebral artery
 Contralateral weakness and numbness
infarction
 Affecting face and arm > leg
 Aphasia (receptive, expressive or both) if dominant hemisphere involved
 In right handed patients and 80% of left handed patients, left hemisphere
is dominant
 Inattention, neglect or extinction on double-simultaneous stimulation –
non-dominant hemisphere involvement
 Constructional apraxia – inability to draw objects
 May be dysarthric but not aphasic
 Homonymous hemianopia and gaze preference to side of infarct may be
present
Posterior cerebral artery
 May be unaware of deficit until tested
infarction
 Motor involvement minimal and visual cortex abnormalities may go
unrecognized
 Light-touch and pinprick sensations may be significantly reduced
Vertebrobasilar
 Dizziness, vertigo, diplopia, dysphagia, cranial nerve palsies
syndrome
 Bilateral limb weakness singly or in combination
 Hallmark is crossed neurologic deficit i.e. ipsilateral CN deficits with
contralateral motor weakness
Lateral medullary
 Specific posterior circulation stroke involving vertebrobasilar arteries
(Wallenburg) syndrome
and/or posterior inferior cerebellar artery
 Ipsilateral loss of facial pain and temperature
 Contralateral loss of same senses over the body
 Gait and limb ataxia
 Partial ipsilateral CN lesions of V, IX, X, and XI in varying combinations
 Ipsilateral Horner syndrome may be present
Basilar artery occlusion
 Severe quadriplegia, coma and the locked-in syndrome
 Lesions in pontine tectum – complete motor paralysis except for upward
gaze
Cerebellar infarction
 Present following ‘drop attack’ with sudden onset of inability to walk or
stand
 Often accompanied by vertigo, headache, nausea, vomiting and neck pain
 CN abnormalities often present
Lacunar infarction
 Pure motor or sensory deficits caused by infarction of small penetrating
arteries
 Commonly associated with HT
 Lesions primarily in the pons and basal ganglia
Management of adult stroke – Australian guidelines
Pre-hospital care
 Ambulance services, health care professionals and general public should receive education concerning
the importance of early recognition of stroke, emphasising stroke is a medical emergency
 Stroke patients should be given a high priority grouping by ambulance services
 Ambulance services should be trained in the use of validated pre-hospital stroke screening tools
 Ambulance services should preferentially transfer suspected stroke patients to a hospital with stroke
unit care, where feasible.
Early assessment and diagnosis
Assessment of TIA
 All patients with suspected TIA should have a full assessment of stroke risk at initial point of health
care contact
 Following investigations should be undertaken routinely for all patients with suspected TIA:
o FBC, EUC
o Cholesterol level
o Glucose level and
o ECG
 Patients classified as high risk should have an urgent CTB (<24hrs)
 Carotid duplex ultrasound undertaken urgently in patients with carotid territory symptoms
 Patients classified as low risk should have a CTB and carotid ultrasound as soon as possible (48-72hrs)
Triage in ED
 Diagnosis should be reviewed by a clinician experienced in the evaluation of stroke
 Emergency department staff should use validated stroke screen tool to assist in rapid accurate
assessment
 Local protocols should be developed jointly by staff from prehospital services, ED and stroke unit to
expedite early transport, referral and access to imaging.
Imaging
 All patients with suspected stroke should have an urgent CTB or MRB (<24hrs)
 A repeat CT or MRI should be considered if clinical condition deteriorates
 All patients with carotid territory symptoms should have urgent carotid duplex study to consider carotid
revascularization
Investigations
 Following investigations to be conducted routinely in all patients with stroke
o FBC, EUC
o ECG
o ESR and/or CRP
o Fasting lipids and
o Glucose
 Selected patients may require further additional investigations
o Angiography
o CXR
o Syphilis serology
o Vasculitis screen and
o Prothrombotic screen
Acute medical and surgical management
Ischemic stroke and TIA
 Thrombolysis
o IV rt-PA in acute ischemic stroke should be undertaken in patients satisfying inclusion and
exclusion criteria
o
IV rt-PA should only be given under authority of specialist physician with expert knowledge
of stroke management, experience in use of IV thrombolytic therapy.
o Thrombolysis should only be undertaken in a hospital setting with appropriate infrastructure
o De-identified data from all patients treated with thrombolysis should be recorded in a central
register to allow monitoring, review, comparison and benchmarking of key outcome measures
over time
 Antithrombotic therapy
o Aspirin (150-300mg) should be given ASAP after onset of stroke symptoms (<48hrs) if
CT/MRI excludes hemorrhage
o Routine use of anticoagulation (IV heparin) in unselected patients with TIA/ ischemic stroke is
not recommended
 Blood pressure lowering therapy
o If BP is extremely high, institute or increase anti-HT therapy with close monitoring only by
10-20%
o Pre-existing anti-HT therapy should be continued (PO or NG) provided there is no significant
hypotension or contraindication
 Surgery for ischemic stroke
o Selected patients (18-60 yrs of age) with significant MCA infarction should be urgently
referred to neurosurgical team for consideration of hemi-craniectomy
o Insufficient evidence at this stage to recommend intracranial endovascular surgery
Intracerebral hemorrage
 Hemostatic drug rFVIIa is experimental and only used in clinical trial settings
 Routine surgery for supratentorial ICH is not recommended except
o Stereotactic surgery for deep ICH
o Craniotomy ofr superficial hematoma
 Surgical evacuation for cerebellar hemisphere hematomas >3cm may be undertaken
 In ICH patients with hypertension the MAP should be maintained below 130mmhg.
General stroke care
Physiological monitoring - regular
 Regular vital signs (P, BP, T, O2 sat)
 GCS and focal neurological deficits
 BSL
Oxygen therapy
 For hypoxic patients
Glycemic control
 Diabetic patients should have BSL closely monitored
 Intensive, early maintenance of euglycemia is currently not recommended
 Hypoglycaemia is to be avoided
Neuroprotective agents
 Only used in clinical trial settings
ABCD tool for risk stratification of TIA patients
A → age > 60 years (1point)
B → blood pressure > 140/90mmhg (1point)
C → clinical features: unilateral weakness (2points), speech impairment without weakness (1point)
D → duration: >60mins (2points), 10-59mins (1point) and
D → diabetes (1point)
ABCD >4 → high risk – admitted to stroke unit to facilitate rapid assessment and treatment
ABCD <4 → low risk – managed in community by GP, private specialist or TIA clinic where available
Thrombolysis criteria
Patient selection criteria
Indications
1. Onset of ischemic stroke within the preceding 3 hours
2. Measurable and clinically significant deficit on NIHS scale examination
3. Patient’s CT does not show hemorrhage or non-vascular cause for symptoms
4. Patient’s age >18 years
Absolute contraindications
1. Uncertainty about time of onset e.g. waking up from sleep
2. Coma or sever obtundation with fixed eye deviation and complete hemiplegia
3. Only minor stroke deficit which is rapidly improving
4. Seizure at onset of stroke
5. Hypertension: systolic BP ≥185mmhg or diastolic BP ≥110mmhg on repeated measures
6. Clinical presentation s/o SAH despite normal CT
7. Presumed septic embolus
8. Patient receiving heparin within the last 48hrs and has elevated APTT or known h/o bleeding disorder
9. INR >1.5
10. Platelet count < 100000/µL
11. Serum glucose < 2.8 mmol/L or >22.0 mmol/L
Relative contraindications – use with caution, weight benefit risk ratio
1. Severe neurological impairment, NIHSS score >22
2. Age > 80years
3. CT evidence of extensive MCA territory infarction
4. Stroke or serious head trauma in past 3 months
5. Major surgery within past 14 days
6. Known h/o ICH, SAH, AM or intracranial neoplasm
7. Suspected recent MI <30 days
8. Recent biopsy or surgery of parenchymal organ with risk of unmanageable bleeding e.g. liver
9. Recent trauma with internal injuries or ulcerated wounds
10. GIT or urinary tract hemorrhage within last 30 days
11. Arterial puncture at noncompressible site within last 7 days
12. Concomitant serious, advance or terminal illness