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Amy Gutman MD NEUROLOGICAL EMERGENCIES.

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1 Amy Gutman MD NEUROLOGICAL EMERGENCIES

2  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 OVERVIEW

3  Neurology (Greek):“Vε ῦ ρον” (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 TERMINOLOGY

4  Neurons & Neurotransmitters  Protective Structures  Brain  Spinal Cord ANATOMY & PHYSIOLOGY - CNS

5  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

6  Nerve impulse travels from neuron 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 NEURONS & NEUROTRANSMITTERS

7  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 PHARMACOLOGY

8 CNS PROTECTIVE STRUCTURE - SKULL

9 CNS PROTECTIVE STRUCTURES – VERTEBRAE (SPINE)

10 CNS PROTECTIVE STRUCTURES - MENINGES

11  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

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13 CNS – VASCULAR SUPPLY

14 CNS – SPINAL NERVES & DERMATOMES

15 ROOT MOTOR SENSORY C3 Diaphragm, Trap Lower neck C4 Diaphragm Clavicle C5 Bicep & deltoid Below clavicle C6 Bicep Thumb, forearm C7 Tricep Index, middle fingers C8 Finger flexors Pinky T1 Hand intrinsics Medial Arm CERVICAL DERMATOMES “C keeps the diaphragm alive”

16  1Olfactory  2Optic  3Oculomotor  4Trochlear  5 Trigeminal  6Abducens  7Facial  8 Vestibulocochlear  9Glossopharyngeal  10 Vagus  11Spinal Accessory  12 Hypoglossal  "On Old Olympus's Towering Tops, A Fine- Vested 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" CRANIAL NERVES

17  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

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19 PREHOSPITAL ASSESSMENT

20 Altered Mental StatusFocal Neurological Complaints THE BIG PICTURE “Sick” vs “Not Sick”

21  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 CHIEF COMPLAINT

22  Provokes / Progression / Palliation  Quality  Region/radiation  Severity  Time of onset  Family/Social history  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? HISTORY OF PRESENT ILLNESS

23  Level of consciousness  Memory & amnesia  AVPU / GCS  Focal neurological exam  Affect/mood  Speech  Behavior & posture  Cognition  Mood, Thought, Perception, Judgment, Memory & Attention  Grooming & personal hygiene NEUROLOGICAL EXAM - ASSESSMENT

24  Eye Opening  4 = Spontaneous  3 = To Voice  2 = To Pain  1 = None  Verbal  5 = Oriented  4 = Confused  3 = Inappropriate words  2 = Inappropriate sounds  1= None  Motor  6 = Obeys commands  5 = Localizes pain  4 = Withdraws to pain  3 = Decorticate  2 = Decerebrate  1 = None GLASGOW COMA SCALE (3-15) The number is less important than the category & what you do with it!

25  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  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 NEUROLOGICAL EXAM - SPEECH

26  BP:  Hypotension  Hypertension  Cushing’s Triad:  Hypertension  Bradycardia  Bradypnea  Respirations  Hyperventilation  Hypoventilation  Cheyne-Stokes: crescendo- decrescendo then apnea  Ataxic: irregular rate & depth  Apneustic: inspiratory pause  Temperature:  Infection  Hemorrhage  Seizure (cause or effect)  Heat stroke  Metabolic VITAL SIGNS

27  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 PHYSICAL EXAM

28  Pupil size, symmetry, reactivity  Miosis  Mydriasis  Extraocular movements  Resting eye position  Deviation  Nystagmus / direction  Conjugate movement NEUROLOGICAL EXAM - EYES

29  Cranial nerves  Reflexes  Cerebellar  Gait  Finger pointing  Psychiatric  Posturing  Any asymmetry  Seizure activity  Look at eyes NEUROLOGICAL EXAM – MOTOR & SENSORY

30 Test glucose & you have the Miami / LA Stroke Scale

31 DIFFERENTIAL DIAGNOSIS / NEUROLOGICAL EMERGENCIES

32 Altered Mental StatusFocal Neurological Complaints THE BIG PICTURE “Sick” vs “Not Sick”

33  AEIOU TIPS  A Alcohol / Drugs / Toxins  E Endocrine, Exocrine, Electrolyte  I Insulin  O Opiates, OD  U Uremia  T Trauma, Temperature  I Infection  P Psychiatric disorder  S Seizure, Stroke, Shock, Space occupying lesion CAUSES OF AMS

34  History often initially more important than exam  What is MOST important question with a neuro deficit or AMS?  Physical Exam Keys  Odors  Respiration  Eyes  Trauma?  IVDA?  Serial GCS  If <8, INTUBATE! AMS PEARLS

35  Drunk + ground = head & C spine injury until proven otherwise  Multiple toxidromes & drug reactions cause AMS or focal deficits  Common:  Organophosphates  CO  Sympathomimetics / withdrawal  Opiates / Withdrawal  Hypoglycemic agents  Cardiac agents  Psych Meds (TCAs, SSRIs)  Another day, another lecture! ALCOHOL / DRUGS / TOXINS

36  Hypothermia: AMS / coma <32.0 C  Hyperthermia: AMS / coma >42.0C  Environmental  Sepsis  Drug reaction  Neuroleptic malignant syndrome TEMPERATURE

37  Most Common  Hypo / hyperglycemia  Hypo / hyperkalemia  Hyponatremia  Thyroid storm  Cause vs effect  AMS  Seizures  Syncope  Often related to arrhythmias EXOCRINE / ENDOCRINE / ELECTROLYTE

38 STROKE –EPIDEMIOLOGY  Disability affects 75% survivors  #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 yrs  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

39 STROKE - GENDER DIFFERENCES  Men 1.25 x more likely to suffer 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 often killed  Some risk factors for stroke apply only to women:  Pregnancy  Childbirth  Menopause  HRT

40 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

41 STROKE - MIMICS  Seizure  Infection  Hypoglycemia  Syncope  Brain abscess or tumor  Drug Overdose  Head Trauma  Vascular Lesions  HTN Encephalopathy  Migraine

42  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 PATHOPHYSIOLOGY - ISCHEMIC

43  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 SYNDROMES - TIA / RIND

44  Spontaneous rupture leads to subarachnoid hemorrhage  HTN  Congenital abnormality (AV malformation, berry aneurysm)  Blood dyscrasia / anticoagulants  Infection  Neoplasm  Classic Presentation: yo M with h/o HTN with undiagnosed berry aneurysm  Abrupt onset of “worst headache of life”  Nuchal rigidity, photophobia, vomiting, retinal hemorrhages  Atypical: hemorrhagic transformation of embolic stroke STROKE PATHOPHYSIOLOGY – HEMORRHAGIC

45 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"

46  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 SYNDROMES – CEREBRAL BLOOD FLOW

47 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: Visual field defect  Temporal: Memory deficits  Parietal: Hemineglect, aphasia  Frontal: Disorganized thinking, confusion, hypersexuality

48 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

49 TIME IS BRAIN  From the time a patient first experiences ssx there is a 3* hr window to administer tPA  That window includes:  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

50 Answer to ALL must be YES:  >18yo  Acute ischemic stroke causing a measurable non- improving neurologic deficit  NO clinical suspicion for SAH  Time of onset to treatment is <180 mins Answer to ALL MUST be NO:  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 surgery or ischemic CVA <3 mos  M ajor surgery <14 days  AMI, arterial stick/LP <7 days  P rior ICH, AVM, tumor, aneurysm or seizure + stroke  SBP >185mmHg or DBP >110Hg  No septic emboli STROKE MANAGEMENT – THROMBOLYTIC CHECKLIST

51  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! STROKE - MANAGEMENT *CPP = MAP - ICP

52  1 – 2% general population  Primary / Idiopathic  Onset ages  Often “outgrow” their medications  Secondary precipitated by “something”  Intracranial: trauma, mass, abcess, infarction  Trauma, mass, abscess, infarct  Extracranial: toxins, metabolic, HTN, eclampsia SEIZURES - EPIDEMIOLOGY

53  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 SEIZURE – CLASSIFICATION

54 ECLAMPSIA  Any pregnant patient who seizes, regardless of prior history  Often secondary to undertreated / undiagnosed pre-eclampsia  Medical emergency for both mother & child  Management:  IV, O2, Monitor  Left lateral recumbent position  Rapid Transport  Magnesium sulfate

55 MAGNESIUM SULFATE  Pregnancy-induced HTN, pre-eclampsia, eclampsia  Decreases CNS activity & release of ACH  Vasodilator (decreases systemic BP, improves placental blood flow)  Side Effects  Muscle weakness  Respiratory depression  Hypotension & slowed cardiac conduction/AV blocks  Antidote  Calcium gluconate

56  ABCs + C spine + Glucose + Pregnancy  IV, O2, Monitor  HPI  Timeframe?  Prior history?  Pregnancy?  DM?  Trauma?  Infection?  Serial neuro exams SEIZURE - MANAGEMENT

57  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) SEIZURE - STATUS EPILEPTICUS

58  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

59  ABCs & support ventilations  Maintain airway  IV, O2, Monitor, Glucose  Look for other causative / contributive factors  Heat stroke  MI  CVA  CHI  Dehydration SYNCOPE MANAGEMENT

60 SEIZURE VS SYNCOPE

61  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 INFECTIOUS - MENINGITIS *PLEASE immunize your kids!

62  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 - MENINGITIS

63  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 - ENCEPHALITIS

64  Acutely ill patient + fever in a dPT deficient patient  Bleeding membranous pharyngitis  Exotoxin causes multi-organ system failure  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 – CORNYBACTERIUM DIPTHERIA

65  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 BOTULINUM

66  Trismus, Tetany, Twitching, Tightness  Risus sardonicus  Sympathetic overstimulation  Tachycardia, hyperpyrexia, diaphoresis  Management:  ABCs, intubation  In ED: Human Tetanus Immunoglobulin (HTIG), dT toxoid, metronidazole INFECTIOUS – CLOSTRIDIUM TETANI

67  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 INFECTIOUS – GUILLAIN-BARRE SYNDROME

68  Facial nerve paralysis affecting 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 affected 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 INFLAMMATORY - BELL’S PALSY

69  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 HEADACHE *Pet peeve

70  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 HEADACHE - MIGRAINE *i.e. neurologists really have no freakin’ clue why they occur

71  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 HEADACHES - OTHER

72  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 PERIPHERAL VERTIGO

73  10-15% cases of vertigo  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 CENTRAL VERTIGO

74  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 “WEAK & DIZZY”

75  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

76  Parkinson’s Disease  Tremor, rigidity, bradykinesia, postural instability  Amytrophic Lateral Sclerosis  Myoclonus  Spina Bifida  Poliomyelitis  Chronic Alcoholism  Wernicke’s Syndrome  Korsakoff’s Psychosis OTHER NEUROLOGICAL DISORDERS

77  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! GENERAL NEUROLOGICAL EMERGENCIES MANAGEMENT PRINCIPLES

78  Anatomy and Physiology  Pathophysiology  General Assessment Findings  Differential Diagnosis  Management of Nervous System Emergencies SUMMARY

79 QUESTIONS?


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