NEUROLOGICAL
EMERGENCIES
Amy Gutman MD
prehospitalmd@gmail.com
OVERVIEW
 In the next 2 hours:
 Anatomy & Physiology
 Focused Assessment & Examination
 Differential Diagnosis
 Management & Critical Thinking
 What we will not cover in the next 2 hours:
 Trauma patients with neurological findings
 Psychiatric emergencies
TERMINOLOGY
 Neurology (Greek): “ Vεῦρον” (neuron), “λογία” (study); medical
specialty studying diagnosis & treatment
of nervous system disorders
 Neuron:
Single nerve cell
 Neurotransmitter: Chemicals allowing impulses to travel
between neurons
 Ipsi / Unilateral:
Same-sided, one sided
 Contralateral:
Opposite-sided
 Paralysis:
Complete loss of function
 Paresis:
Limited function
 Anesthesia:
Complete loss of sensation
 Paresthesias:
Abnormal sensation
 Lesion:
Focus for neurological abnormality
ANATOMY & PHYSIOLOGY - CNS
 Neurons & Neurotransmitters
 Protective Structures
 Brain
 Spinal Cord
NEURONS &
NEUROTRANSMITTERS
 Billions of neurons allow body
functions via neurotransmitters
 Neurotransmitters are excitatory
or inhibitory
 Excitatory: acetylcholine, norepinephrine
 Inhibitory: dopamine, serotonin, GABA
 Each neurotransmitter directly or indirectly
influences specific type(s) of neuron
NEURONS &
NEUROTRANSMITTERS
 Nerve impulse travels from n euron
through axon to terminal & synaptic knob
 Synaptic knob communicates with dendrite of neighbor neuron
via neurovesicles that store & release neurotransmitters into
synapse
 If stimulated in a “lock & key” manner, the next neuron picks
up & continues the impulse
 Seizures: continuous release / stimulation of impulses = spasm
 Botulism: neurotransmitters bound so no impulses = flaccidity
CNS PHARMACOLOGY
 Depressants
 Increase GABA (inhibitory neurotransmitter), decreasing
nervous system activity
 Barbiturates, Benzodiazepines
 If combined other depressants can be fatal
 Abrupt discontinuation leads to withdrawal & seizures
 Stimulants
 Increase norepinephrine, dopamine to increase nervous system
& catecholamine response
 Dexromethorphan, methylphenidate, cocaine
CNS PROTECTIVE STRUCTURE - SKULL
CNS PROTECTIVE
STRUCTURES –
VERTEBRAE (SPINE)
CNS PROTECTIVE STRUCTURES MENINGES
CNS - BRAIN
Frontal Lobe
 Thinking, planning
 Executive functions
 Motor execution
Parietal Lobe
 Somatosensory
perception
 Integration of visual &
somatospatial
information
Temporal Lobe
 Language function
 Auditory perception
 Memory
 Emotion
Occipital Lobe
 Visual perception &
processing
CNS - BRAIN
CNS – VASCULAR SUPPLY
CNS – SPINAL NERVES &
DERMATOMES
CERVICAL DERMATOMES
“C 3 4 5 keeps the diaphragm alive”
ROOT
C3
C4
C5
C6
C7
C8
T1
MOTOR
Diaphragm, Trap
Diaphragm
Bicep & deltoid
Bicep
Tricep
Finger flexors
Hand intrinsics
SENSORY
Lower neck
Clavicle
Below clavicle
Thumb, forearm
Index, middle fingers
Pinky
Medial Arm
CRANIAL NERVES
1
2
3
4
5
6
7
8
9
 10
 11
 12
Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducens
Facial
Vestibulocochlear
Glossopharyngeal
Vagus
Spinal Accessory
Hypoglossal
 "On Old Olympus's
Towering Tops, A FineVested German Viewed
Some Hops"
 "Oh, Oh, Oh, To Touch
And Feel, A Good
Velvet, Spot in Heaven"
 Motor (M), sensory (S),
or both (B)
 "Some Say Money Matters
But My Brother Says Big
Brains Matter Most"
ANATOMY &
PHYSIOLOGY - PNS
Autonomic Nervous System
 Sympathetic: “Fight or Flight”
 Parasympathetic: “Feed or breed”, “Rest & Repair”
 Clinically: “Point & Shoot”
Peripheral Nerves
 43 pairs of nerves originate from CNS to form PNS
 12 pairs of cranial nerves from brain
 31 pairs of spinal nerves from spinal cord
ANATOMY & PHYSIOLOGY - PNS
PREHOSPITAL
ASSESSMENT
THE BIG PICTURE
Altered Mental Status
Focal Neurological
Complaints
“Sick” vs “Not Sick”
CHIEF COMPLAINT
 Exact quotes – words are clues
 “The room is spinning” vs “I feel like
I’m spinning”
 “My vision is blurred” vs “I have
double vision”
 Obtain from pt, witnesses, family
while beginning assessment &
management
 CC, HPI & exam should focus on
neurological aspects, without
overlooking non-neurological
processes causing AMS or deficits
HISTORY OF PRESENT ILLNESS
 Allergies
 Medications
 PMH
 Sz, trauma, HA, HTN, DM,
infections, tumors
 Cardiac, renal, hepatic,
neuro, psychiatric
diseases
 Last oral intake
 Events leading up to event
 Environmental clues
 Indoors or outdoors?
 Any unusual odors?
 Suicide notes?
 Provokes / Progression /
Palliation
 Quality
 Region/radiation
 Severity
 Time of onset
 Family/Social history
NEUROLOGICAL EXAM - ASSESSMENT
 Level of consciousness
 Memory & amnesia
 AVPU / GCS
Focal neurological exam
Af fect/mood
Speech
Behavior & posture
Cognition
Mood, Thought, Perception,
Judgment, Memory & Attention
 Grooming & personal hygiene
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GLASGOW COMA SCALE (3-15)
 Eye
4
3
2
1
Opening
= Spontaneous
= To Voice
= To Pain
= None
 Verbal
 5 = Oriented
4 =
3 =
2 =
 1=
Confused
Inappropriate words
Inappropriate sounds
None
 Motor
 6 = Obeys commands
 5 = Localizes pain
 4 = Withdraws to pain
 3 = Decorticate
 2 = Decerebrate
 1 = None
The number is less important
than the category & what you
do with it!
NEUROLOGICAL EXAM - SPEECH
 Speech and language
 “Hear them talk, watch them talk, & look at their eyes; that’s 90% of the
brain” (Henry, 2004)
 Normal speech inflected, clear, fluent, articulate, varies in volume
 Language
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Dysphonia: Inability to make laryngeal sounds
Dysprosody: Inflection, pronunciation, pitch or rhythm (cerebellum)
Dysarthria: Difficulty making individual sounds (motor integration)
Aphasia: absence of speech
Dysphasia: word finding difficulty (cortex)
Expressive aphasia: understands but cannot speak (frontal Broca’s)
Receptive aphasia: words clear, content scrambled (parietal Wernicke’s)
Apraxia: difficulty in both forming & phonating
VITAL SIGNS
 BP:
 Hypotension
 Hypertension
 Cushing’s Triad:
 Hypertension
 Bradycardia
 Bradypnea
 Respirations
 Hyperventilation
 Hypoventilation
 Cheyne-Stokes: crescendodecrescendo then apnea
 Ataxic: irregular rate & depth
 Apneustic: inspiratory pause
 Temperature:
 Infection
 Hemorrhage
 Seizure (cause or effect)
 Heat stroke
 Metabolic
PHYSICAL EXAM
 Head
 Skull: trauma; infants – bulging membranes
 Mouth: odors, bites to lateral tongue
 Neck
 Meningismus
 Skin
 Trauma, rash, IVDA, temperature
 Lungs, Cardiac, Abdomen
 Systemic illnesses and secondary effects of CNS insults
 Extremities
 Trauma, deformity, pulses
NEUROLOGICAL EXAM - EYES
 Pupil size, symmetry, reactivity
 Miosis
 Mydriasis
 Extraocular movements
 Resting eye position
 Deviation
 Nystagmus / direction
 Conjugate movement
NEUROLOGICAL EXAM –
MOTOR & SENSORY
 Cranial ner ves
 Reflexes
 Cerebellar
 Gait
 Finger pointing
 Psychiatric
 Posturing
 Any asymmetr y
 Seizure activity
 Look at eyes
Test glucose & you have the Miami / LA Stroke Scale
DIFFERENTIAL
DIAGNOSIS /
NEUROLOGICAL
EMERGENCIES
THE BIG PICTURE
Altered Mental Status
Focal Neurological
Complaints
“Sick” vs “Not Sick”
CAUSES OF AMS
 AEIOU TIPS
A
E
I
O
U
T
I
P
S
Alcohol / Drugs / Toxins
Endocrine, Exocrine, Electrolyte
Insulin
Opiates, OD
Uremia
Trauma, Temperature
Infection
Psychiatric disorder
Seizure , Stroke, Shock, Space occupying lesion
AMS PEARLS
 History often initially more important than exam
 What is MOST important question with a neuro deficit or AMS?
 Physical Exam Keys
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Odors
Respiration
Eyes
Trauma?
IVDA?
 Serial GCS
 If <8, INTUBATE!
ALCOHOL / DRUGS / TOXINS
 Drunk + ground = head & C spine injur y until proven otherwise
 Multiple toxidromes & drug reactions cause AMS or focal deficits
 Common:



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Organophosphates
CO
Sympathomimetics / withdrawal
Opiates / Withdrawal
Hypoglycemic agents
Cardiac agents
Psych Meds (TCAs, SSRIs)
 Another day, another lecture!
TEMPERATURE
 Hypothermia: AMS / coma <32.0 C
 Hyperthermia: AMS / coma >42.0C
 Environmental
 Sepsis
 Drug reaction
 Neuroleptic malignant syndrome
EXOCRINE / ENDOCRINE / ELECTROLY TE
 Most Common
 Hypo / hyperglycemia
 Hypo / hyperkalemia
 Hyponatremia
 Thyroid storm
 Cause vs effect
 AMS
 Seizures
 Syncope
 Often related to
arrhythmias
STROKE –EPIDEMIOLOGY
 Disability af fects 75% sur vivor s
 #1 cause adult disability in the US & Europe
 #3 cause death worldwide after CAD & cancer
 10% deaths worldwide
 US Management costs $43 billion annually
 Incidence increases exponentially >30 yr s
 Etiology varies by age
 95% of strokes occur in people >45 yo
 75% of strokes occur in people >65 yo
 Rule of two thirds
 2/3 all strokes ischemic
 2/3 of those thrombotic
STROKE - GENDER DIFFERENCES
 Men 1 .25 x more likely to suf fer strokes than women
 However, 60% of deaths from stroke occur in women
 Since women live longer than men, they are older on average
when they have their strokes & therefore more of ten killed
 Some risk factors for stroke apply only to women:




Pregnancy
Childbirth
Menopause
HRT
STROKE - RISK FACTORS
 Advanced age
 Previous stroke or TIA
 Diabetes
 High cholesterol
 Cigarette smoking
 Atrial fibrillation
 HRT
 Migraines
 Thrombophilia
 Patent foramen ovale
 HTN
 Most important & modifiable
STROKE - MIMICS
 Seizure
 Infection
 Hypoglycemia
 Syncope
 Brain abscess or tumor
 Drug Overdose
 Head Trauma
 Vascular Lesions
 HTN Encephalopathy
 Migraine
STROKE PATHOPHYSIOLOGY - ISCHEMIC
 Thrombotic
 Slow, progressive onset
 Causes:
 Atherosclerosis (#1 cause)
 Infective
 Inflammatory (vasculitis)
 Hypercoaguable states
 Embolic
 Abrupt onset
 Maximal deficit may improve
over time as embolus breaks
 Causes
 Mural thrombus (#1 )
 Aortic plaques
 Endocarditis
 Long bone injuries
 Dysbarism
STROKE SYNDROMES - TIA / RIND
 Altered neuro status that
resolves completely <24hrs
(TIA) or <72hrs (RIND)
 30% will have a major stroke
event within 3 years
 Treat as CVA
STROKE PATHOPHYSIOLOGY –
HEMORRHAGIC
 Spontaneous rupture leads to subarachnoid hemorrhage
 HTN
 Congenital abnormality (AV malformation, berry aneurysm)
 Blood dyscrasia / anticoagulants
 Infection
 Neoplasm
 Classic Presentation: 35-65 yo M with h/o HTN with undiagnosed
berr y aneur ysm
 Abrupt onset of “worst headache of life”
 Nuchal rigidity, photophobia, vomiting, retinal hemorrhages
 Atypical: hemorrhagic transformation of embolic stroke
STROKE PATHOPHYSIOLOGY SYSTEMIC HYPOPERFUSION
 Reduction of blood flow to all
parts of the body
 Causes:
 Pump failure: cardiac arrest,
arrhythmias
 Reduced cardiac output: MI, PE,
hemorrhage, shock
 Hypoxemia
 Entire brain affected,
especially penumbra /
"watershed"
STROKE SYNDROMES – CEREBRAL
BLOOD FLOW
 Anterior Circulation:
 80% cerebral blood flow
 Originates from carotids
 Supplies fronto-parietal,
anterior temporal, optic nerve
 Posterior Circulation:
 20% cerebral blood flow
 Originates from
vertebrobasilar arteries
 Supplies thalamus,
brainstem, occipital cortex,
cerebellum, upper cord, ears
 Circle of Willis:
 Connects ant & post
circulations
STROKE - SYMPTOMS
 Generally Unilateral
 Stroke site on opposite side than clinical ssx
 LOC, HA, & vomiting more common in hemorrhagic than
ischemic (higher ICP)
 Cerebral Cortex:
 Occipital:
 Temporal:
 Parietal:
 Frontal:
Visual field defect
Memory deficits
Hemineglect , aphasia
Disorganized thinking, confusion,
hypersexuality
SYMPTOMS
 Brainstem / Cranial Nerves:
 Altered smell, taste, hearing, or vision
 Ptosis, diplopia, pupil reactivity
 Decreased gag, tongue movement,
facial sensation & muscle weakness
 Balance problems & nystagmus
 Altered breathing & pulse
 Cerebellum
 Altered coordination
 Vertigo or disequilibrium
TIME IS BRAIN
 From the time a patient first experiences
ssx there is a 3* hr window to administer tPA
 That window includes:
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Recognition of symptoms
Call to 911 & activation of EMS
EMS response, assessment, management & transport
ED assessment & CT scan to rule out hemorrhagic stroke
Stroke team activation & screening for TPA
 11% increase in measureable (+) symptom improvement
 TPA only given to 1-2% of stroke patients
*Debatable & Changing
STROKE MANAGEMENT –
THROMBOLYTIC CHECKLIST
Answer to ALL must be YES:
Answer to ALL MUST be NO:
 >18yo
 Acute ischemic stroke
causing a measurable nonimproving neurologic deficit
 NO clinical suspicion for SAH
 Time of onset to treatment is
<180 mins
 CT proven hemorrhage
 Active internal bleeding <21
days
 B leeding diasthesis:
 Plts<100,000
 Heparin <48 hrs w/high PTT
 Warfarin use with high PT
 P rior surger y or ischemic CVA
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<3 mos
M ajor surger y <14 days
AMI, arterial stick/LP <7 days
P rior ICH, AVM, tumor,
aneur ysm or seizure + stroke
SBP >185mmHg or DBP
>110Hg
No septic emboli
STROKE - MANAGEMENT
 ABCs + Glucose
 Protect penumbra
 Keep SBP >90mmHg
 Keep CPP >60mmHg
 Hypothermia
 Oxygenate
 HOB 30 degrees (reverse T-berg if C spine in question)
 Frequent repeat neuro checks!! Reassess GCS!
*CPP = MAP - ICP
SEIZURES - EPIDEMIOLOGY
 1 – 2% general population
 Primary / Idiopathic
 Onset ages 10-20
 Often “outgrow” their medications
 Secondary precipitated by “something”
 Intracranial: trauma, mass, abcess, infarction
 Trauma, mass, abscess, infarct
 Extracranial: toxins, metabolic, HTN, eclampsia
SEIZURE – CLASSIFICATION
 Grand Mal:
 Aura, tonic-clonic, LOC, apnea, incontinence, post-ictal
 Petit Mal
 Absence
 Myoclonic
 Simple Partial Seizures
 Involve one body area
 Can progress to generalized seizure
 Complex Partial Seizures
 Characterized by auras
 Typically 1–2 minutes in length
 Loss of contact with surroundings
ECLAMPSIA
 Any pregnant patient who seizes, regardless of prior history
 Of ten secondary to undertreated / undiagnosed pre -eclampsia
 Medical emergency for both mother & child
 Management:
 IV, O2, Monitor
 Left lateral recumbent position
 Rapid Transport
 Magnesium sulfate
MAGNESIUM SULFATE
 Pregnancy -induced HTN, pre-eclampsia, eclampsia
 Decreases CNS activity & release of ACH
 Vasodilator (decreases systemic BP, improves
placental blood flow)
 Side Ef fects
 Muscle weakness
 Respiratory depression
 Hypotension & slowed cardiac conduction/AV blocks
 Antidote
 Calcium gluconate
SEIZURE - MANAGEMENT
 ABCs + C spine + Glucose + Pregnancy
 IV, O2, Monitor
 HPI
 Timeframe?
 Prior history?
 Pregnancy?
 DM?
 Trauma?
 Infection?
 Serial neuro exams
SEIZURE - STATUS EPILEPTICUS
 Seizure >5 mins OR 2 seizures between which there
is incomplete recovery of consciousness
 Management:
 ABCs
 IV, O2, Monitor
 Benzodiazepines
 Treat other causes:
 Glucose
 Magnesium
 Pyridoxine (B6)
SYNCOPE
 Acute & temporary loss of consciousness
 Pre-syncope:
 No LOC
 Pt often states “I thought I was going to pass out”
 Syncope is a symptom, not a diagnosis
 DDX:
 Cardiovascular: a rrhythmias, valve stenosis, hypotension
 Noncardiovascular: m etabolic, neurological, psychiatric
 Idiopathic
 Pearls:
 Extended unconsciousness is NOT syncope
 All drunks have head & C spine injuries if unconscious + fall
SYNCOPE MANAGEMENT
 ABCs & support ventilations
 Maintain airway
 IV, O2, Monitor, Glucose
 Look for other causative / contributive factors
 Heat stroke
 MI
 CVA
 CHI
 Dehydration
SEIZURE VS SYNCOPE
INFECTIOUS - MENINGITIS
 US Incidence
 1.5 per 100,000
 Rare in young pts (Hflu & pneumovax vaccines)*
 CDC: median age 39 years; in 1986, it was 15 months
 Mortality/Morbidity
 Depends on pathogen, age, general physical state &
severity of acute illness
 Pneumococcal mortality 21%, morbidity 15%
 Mortality 90% if severe neurologic impairment at time
of presentation even with immediate medical treatment
*PLEASE immunize your kids!
INFECTIOUS - MENINGITIS
 Bacterial
 Rapid onset of symptoms
 Fever, HA, photophobia, meningismus, AMS
 Etiology varies by age / exposure / PMH
 Neisseria meningitis associated with diffuse, purpuric rash
 Aseptic/ Viral/ Lymphocytic
 Gradual onset over 1-7 days
 Less virulent
 Atypical
 PMH / HPI critical as onset insidious
 TB(#1)
 Fungal: coccidiomycosis / crytococcus
INFECTIOUS - ENCEPHALITIS
 Brain inflammation
 Cases self-limited unless virulent
strain/immunocompromised
 Presents similarly to meningitis
 Viral / tick-borne etiology most common
 West Nile
 Herpes Simplex (HSV)
 Varicella Zoster (VZV)
 Arboviruses
 Eastern Equine viruses
 St. Louis Encephalitis
INFECTIOUS –
CORNYBACTERIUM DIPTHERIA
 Acutely ill patient + fever in a dPT deficient patient
 Bleeding membranous pharyngitis
 Exotoxin causes multi-organ system failure
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Myocarditis/AV Block
Nephritis
Hepatitis
Neuritis with bulbar / peripheral paralysis
 Ptosis, strabismus, loss of DTRs
 Management
 ABCs, intubation, volume resuscitation
 IN ED: PCN, emycin, horse serum antitoxin, pressors
INFECTIOUS –
CLOSTRIDIUM BOTULINUM
 Triad: diplopia, ophthalmoplegia,
ptosis
 Descending neurologial deficits
causing respiratory paralysis
 Normal mentation / sensation
 Infant FTT / “floppy baby”
 Raw honey contains C. botulinum
 Management:
 ABCs, intubation
 In ED: trivalent serum antitoxin
INFECTIOUS –
CLOSTRIDIUM TETANI
 Trismus, Tetany, Twitching,
Tightness
 Risus sardonicus
 Sympathetic overstimulation
 Tachycardia, hyperpyrexia,
diaphoresis
 Management:
 ABCs, intubation
 In ED: Human Tetanus
Immunoglobulin (HTIG), dT toxoid,
metronidazole
INFECTIOUS – GUILLAIN-BARRE
SYNDROME
 Most common acute polyneuropathy
 2/3s have preceding URI or
gastroenteritis
 Generalized paresthesias then
ascending paralysis
 Miller-Fischer variant: ataxia,
areflexia, and ophthalmoplegia
 1976 swine flu tainted vaccine caused
25 deaths from GBS & the foundation
for current anti-vaccine sentiment
 Management:
 ABCs, intubation
INFLAMMATORY BELL’S PALSY
 Facial nerve paralysis af fecting entire
unilateral face
 In supranuclear lesions like a cortical stroke (UMN defect), the upper
1/3 of the face spared while lower 2/3 paralyzed
 Orbicularis, frontalis & corrugator muscles innervated bilaterally,
which explains facial paralysis pattern
 Eye closure on af fected side impaired
 Bell Phenomenon: on attempting to close eye, the eye on the affected
side rolls upward & inward
 Ramsay -Hunt: zoster vesicles along ear canal, pinna, mouth
HEADACHE
 Migraine (w/ wo aura)*
 Cluster
 Traumatic
 Inflammatory
 History:
 Worst HA?
 Onset?
 Fever / AMS?
 Trauma?
 Prior history?
 Management:
 IV, O2, antiemetics
 Cool, dark environment
 Abortive therapy
 Believe it or not,
narcotics actually make
headaches worse
physiologically
*Pet peeve
HEADACHE - MIGRAINE
 Though to be related to neurogenic inflammation &
abnormalities of serotonergic transmission*
 HA either preceded by a visual aura or motor disturbance
 N/V, photophobia, sound sensitivity
 Provocation factors:
 Menstruation
 Sleep/food deprivation
 Physical activity
 Foods
 Contraceptive estrogens
*i.e. neurologists really have no freakin’ clue why they occur
HEADACHES - OTHER
 Cluster:
 Resemble CVAs
 Unilateral & persistent
 Thought to be a form of seizures by some neurologists
 Temporal Arteritis
 Temporal artery inflammation (branch of external carotid)
 Unilateral HA with temporal artery tenderness &
decreased vision in middle-aged white females
 Rapid initiation of steroids will save patients vision
 Be concerned with any HA plus fever, confusion,
nausea, vomiting or rash
PERIPHERAL VERTIGO
 Common Causes:
 Labrynthitis
 Cerumen Impaction
 OM / OE
 URI
 Meniere’s Disease: tinnitus, hearing loss, vertigo
 History:
 Acute onset of severe dizziness, N/V
 Positional worsening of symptoms
 Often recent URI or prior vertiginous episodes
 Exam:
 Fatigable horizontal nystagmus
 URI SSX
CENTRAL VERTIGO
 10-15% cases of ver tigo
 Causes:
 Brainstem ischemia or
infarction
 Cerebellar hemorrhage
 Vertebralbasilar insufficiency
 MS
 Brainstem /cerebellar lesions
 SSX:
 Disequilibrium
 N/V
 Nonfatigable nystagmus
 Focal findings:
 Ptosis
 Facial palsy
 Dysarthria
 Cerebellar findings
 Ataxia
 Vertigo Management
 IV, O2, Monitor
 Antiemetics
 Cannot be differentiated
from a posterior circulation
CVA in the field
 Always treat as if a CVA
“WEAK & DIZZY”
 Underlying disease with extensive differential diagnosis
 Often the presenting symptom of CVA, MI, sepsis
 Pay attention to “weak & dizzy” with:




Nystagmus
Nausea/vomiting
Focal neuro deficits
AMS
 Management:
 I, O2, Monitor, Glucose, EKG
OTHER NEUROLOGICAL DISORDERS
 Alzheimer’s Dementia
 Most frequent cause of dementia in the elderly
 Brain atrophy due to cerebral cortex neuron death
 Muscular Dystrophy
 Characterized by progressive ascending muscle weakness
 Multiple Sclerosis
 Unpredictable
 Resulting from deterioration of myelin sheath
 Dystonias
 Often related to psychiatric medications
OTHER NEUROLOGICAL DISORDERS
 Parkinson’s Disease
 Tremor, rigidity, bradykinesia, postural instability
 Amytrophic Lateral Sclerosis
 Myoclonus
 Spina Bifida
 Poliomyelitis
 Chronic Alcoholism
 Wernicke’s Syndrome
 Korsakoff’s Psychosis
GENERAL NEUROLOGICAL EMERGENCIES
MANAGEMENT PRINCIPLES
 ABC + Glucose
 Ensure patent airway maintaining C-spine
 Limited airway protection may lead to vomiting / aspiration
 IV, O2, Monitor
 Serial examinations
 Rapid recognition of underlying neurological emergencies
 “Sick” vs “Not Sick”
 Pre-notification
 Time is brain!
SUMMARY
 Anatomy and Physiology
 Pathophysiology
 General Assessment Findings
 Differential Diagnosis
 Management of Nervous
System Emergencies
QUESTIONS?
P R E H OSP ITALMD@ G MA IL.C OM