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					CNS Disorders



 EMS Professions
  Temple College
                    Pathophysiology of CNS
                              Emergencies
   Structural Changes
       Often due to Trauma but not always
       Circulatory Changes
            Inadequate Perfusion
       Alterations of ICP
            Response to insult
   Toxic Metabolic states
       Alteration to blood chemistry or introduction of toxins
   Psychiatric „mimicking‟
                                       ICP Review
   CBF is a factor of CPP & CVR
       If CPP , then CBF 
       If CVR , then CBF most likely 
   CPP = MAP - ICP
       MAP = Diastolic + 1/3 PP
       PP = SBP - DBP
   PCO2 has greatest effect on CVR
       Sympathomimetics may  CVR
                                        ICP Review
   As PCO2 , CVR 
       Therefore, if PCO2 , CVR 
       Then, as CVR  , CBF 
   Normal ICP < 15 mm Hg
   As ICP , CPP  then CBF 
   Compensation for  ICP via  MAP
       Cushing’s Reflex (Triad)
       Cushing’s triad with coma indicates possible herniation
Altered Mental Status
                                    Coma
   A decreased state of consciousness from
    which a patient cannot be aroused
   Mechanisms
     Structural lesions
     Toxic Metabolic states

     Psychiatric „mimicking‟
                              Brain injury
   Recall that Brain injury is often
    shown by:
     Altered Mental Status
     Seizures

     Localizing signs
Is unconsciousness itself an
immediate life threat?

              YES, IT IS!

 Loss of airway
 Vomiting, aspiration
Altered Mental State

Manage ABC’s
Before Investigating
Cause!
             Initial Assessment/Management
   Airway
       Open, clear, maintain
       If trauma or + history, control C-spine
   Breathing
       Presence? Adequacy (rate, tidal volume)?
       High concentration O2 on ALL patients with altered
        mental status
       Assist ventilations prn
   Circulation
       Pulses? Adequate Perfusion?
                    Investigate Cause
   DERM
     D = Depth of Coma
     E = Eyes

     R = Respiratory Pattern

     M = Motor Function
D = Depth of Coma
 What does patient respond to?
 How does he respond?




    Avoid use of non-specific terms like
      “stuporous”, “semi-conscious”,
          “lethargic”, “obtunded”
D = Depth of Coma
 AVPU
 Glasgow Scale (later)




          Describe level of
      consciousness in terms of
        reproducible findings
E = Eyes
   Pupils
       Size - mid, dilated or constricted
          measurement   - e.g. 4 mm
     Shape - round, oval, pontine
     Equality - equal in size

     Symmetry - equal in reaction/response

     Response to light
          Yesor No
          How?
R = Respiratory Pattern
   Depth
       Unusually deep or shallow?
   Pattern
       Regular or Unusual pattern
        Can   you identify the pattern?
M = Motor Function
   Paralysis?
       Where?
   Muscle tone?
       Rigid or Flaccid
   Movement?
       Where? What is it like?
   Posturing?
       How?
   Symmetrical Motor Function?
                          Physical Exam
   Vital Signs
     Shock?
     Increased ICP?

     Hypoxia/Hypercarbia

   Diagnostics
     Dysrhythmias?
     Blood glucose

     Oxygen saturation
                       Physical Exam
   Detailed (Head-to-Toe) Exam
     Injuries causing coma?
     Injuries caused by coma?

     Clues to the cause
       Probable Causes of AMS
   Not enough Oxygen
   Not enough Sugar
   Not enough blood flow to deliver oxygen, sugar
   Direct brain injury
     Structural

     Metabolic
     Differentiating AMS Causes
   Structural                   Metabolic
       Asymmetrical                 Symmetrical deficits
        deficits                     Equal pupils
       Unequal pupils                (? altered function)
       Afebrile                     ? Fever
       History of trauma,           History of metabolic
        structural                    disorder or illness
        abnormality                  Rapid onset less
       Often a rapid onset           likely
                            Management
 Maintain ABCs
 Attempt to identify cause

 Mainstays of therapy

     Oxygenation/Ventilation
     IV fluids appropriate for the patient

     D50 (if hypoglycemic)

     Narcan if possibility of opiate OD

     Flumazenil in known benzo only OD
           AEIOU TIPS
 Alcohol              Trauma
 Epilepsy             Infection

 Insulin              Psychogenic

 Overdose             Stroke/Syncope

 Uremia (Metabolic
  causes)
Cerebrovascular Accident
      AEIOU TIPS
           Cerebrovascular Accident

 Any disease process that disrupts
  blood flow to a distinct region of the
  brain
 Transient Ischemic Attack (TIA)

       S/S less than 24 hours without
        permanent neuro deficits
       Cerebrovascular Accident
 500,000/yr in US
 25% die

 Survivors often socially, financially
  devastated
 $20 billion in medical costs, lost
  wages
    Cerebrovascular Accident (CVA)
   Pathophysiology
     Thrombosis (brain itself)
     Embolus (head, neck or heart)

     Hemorrhage (within brain)

     Ischemia (systemic blood flow)
    Predisposing Factors: Modifiable

 Hypertension       Chronic atrial

 Cigarette smoking   fibrillation
 Diabetes Mellitus  Sickle cell disease

 Heart disease      Polycythemia

 Hyperlipidemia     Hypercoagulability

 Cardiovascular     Birth control pill use

  disease            Cocaine use
             Predisposing Factors:
                    Unmodifiable
 Age
 Gender

 Race

 Prior stroke

 Heredity
               CVA Mechanisms
 Ischemic stroke--80 to 85%
 Hemorrhagic stroke--15 to 20%
          CVA Origin

 Thrombus
 Embolus

 Aneurysm

 Arrhythmia

 Hypovolemia
                             Ischemic Stroke
   Blood vessel occlusion
       Thrombosis
       Embolism
          Plaque fragments from carotids
          Chronic atrial fibrillation

          Fat particles

          IV substance abuse particulates

   Systemic hypoperfusion
       Pump failure
       Hypovolemia
         Ischemic Stroke Syndromes
   Transient Ischemic Attack (TIA)
       Neurological deficits that resolve in 24 hours
        or less (most in 30 minutes)
       Commonly result from carotid artery disease
       Same symptoms as CVA
       Often warning sign of impeding CVA
       5% risk of stroke per year
          Ischemic Stroke Syndromes
   Dominant Hemisphere Infarction
       Contralateral weakness, numbness
       Contralateral blurring of vision of half the
        visual field in both eyes
       Difficulty pronouncing words (dysarthria)
       Difficulty speaking or understanding speech
        (dysphasia or aphasia)
          Ischemic Stroke Syndromes
   Nondominant Hemisphere Infarction
       Contralateral weakness, numbness
       Contralateral visual field cut
       Neglect of contralateral extremities
       Constructional apraxia (difficulty drawing
        figures like a clock face)
       Dysarthria
       Usually NOT dysphasic or aphasic
         Ischemic Stroke Syndromes
   Vertebrobasilar Syndrome
       Involves blood flow to brainstem,
        cerebellum, and visual cortex
       Dizziness, vertigo
       Diplopia
       Dysphagia
       Ataxia, bilateral limb weakness
                        Hemorrhagic Stroke
 30 to 50% 30-day
  mortality
 Younger patient
  population
 Two subtypes:

       Intracerebral, usually 2o to
        hypertension
       Subarachnoid, usually
        from berry aneurysms
Hemorrhagic Stroke Syndromes
   Intracerebral Hemorrhage
       Headache, nausea, vomiting precede deficits
       Patients commonly have decreased LOC with
        extreme hypertension
       Contralateral hemiplegia, hemianesthesia
       Possible aphasia, extremity neglect depending
        on hemisphere involved
Hemorrhagic Stroke Syndromes
   Subarachnoid Hemorrhage
Grade I     Asymptomatic or mild headache and mild
            nuchal rigidity
Grade II    Moderate to severe headache, nuchal
            rigidity, cranial nerve dysfunction but no
            other deficits
Grade III   Drowsiness, confusion, mild focal deficits

Grade IV    Stupor, moderate to severe hemiparesis,
            possibly early decerebrate rigidity,
            vegetative response
Grade V     Deep coma, decerebrate rigidity,
            moribund appearance
                    CVA Assessment
   Presentation of CVA varies with
    area(s) of brain involved and type of
    CVA
                           CVA Presentation
   Brain can show injury in only three ways:
       Decreased LOC
       Seizures
       Localizing signs
          Hemiparesis  or hemiplegia
          Dysphasia (Receptive or expressive)

          Visual disturbances

          Gait disturbances

          Inappropriate affect

          Bizarre behavior

          Incontinence
Cincinnati Prehospital Stroke Scale
   Have patient smile (“Facial Droop”)
       Normal: Both sides of face move equally well
       Abnormal: One side does not move as well as other
   Have patient close eyes and hold arms out (“Arm Drift”)
       Normal: Both arms drift same amount or do not drift
       Abnormal: One arm does not drift or one drifts down compared
        to other or can‟t move arms
   Have patient say, “You can‟t teach an old dog new
    tricks.” (“Speech”)
       Normal: Correct words, no slurring
       Abnormal: Slurs words, uses inappropriate words, or unable to
        speak
                                    Assessment
   Signs & Symptoms
       Ischemic S&S usually of slower onset
         Hemiparesis  or hemiplegia
         Numbness or decreased sensation of face or
          unilateral
         Altered LOC or coma

         Convulsions

         Visual disturbances

         Slurred or inappropriate speech

         Headache or dizziness
                                      Assessment
   Signs & Symptoms
       Cerebral Embolus with rapid onset
         Emboli  from valvular HD or Afib
         rapid onset

         Often with an identifiable cause (e.g. Afib,
          Valvular heart disease, recent long bone
          fracture)
                                   Assessment
   Signs & Symptoms
       Cerebral hemorrhage associated with
        rapid onset
         high mortality rate
         Often with severe HA (“Worst headache ever”)

         N/V

         Rapid decrease in LOC or seizure

         Coma, Cushing’s and Herniation
   History
                                         Assessment
       Associated Altered LOC or Seizure?
       Onset/Precipitating factors?
       Initial symptoms and progression?
            Dizziness, Severe HA, N/V
       Previous CVA or TIA?
       Previous neuro deficits?
       Concomitant illnesses?
          Sickle Cell Disease
          Atrial fibrillation

       Risk factors for stroke & thrombus formation?
          BCP, Smoking
          HTN, CVD
                                     Assessment
   Physical Exam
       Mental Status & Behavior
       Extremity Motor & Sensory
            Gait
       Pupils & Vision
       Cincinnati Prehospital Stroke Scale
       Evidence of Cushing‟s or Herniation
       Blood glucose level
         CVA Management


     Basic Objective
Improve cerebral blood flow
     and oxygenation
                       CVA Management
   Airway
       If no gag reflex, intubate
       Otherwise, position to ensure drainage of
        secretions
       Suction prn
   Breathing
       Oxygen via NRB
       Ventilate with BVM and O2 if rate or tidal
        volume inadequate
       Intubate if herniating
                        CVA Management
 Controlled hyperventilation if intracranial
  hemorrhage suspected with increased ICP
  and neurologic deterioration
 Indicators

       Sudden onset
       Headache
       Rapid loss of consciousness
       Seizures
       Unequal pupils
                           CVA Management
   Circulation
       Check blood glucose level
          Hypoglycemia  may mimic CVA
          Treat hypoglycemia with D50

       Establish IV Access
          Draw    blood samples
          TKO

          avoid   solutions with glucose
       Monitor ECG
          10% of CVAs are associated with cardiac event
          12 Lead ECG if suspected ischemia
                        CVA Management
 Do not assume patient cannot understand
  because they cannot talk
 Position appropriately:

       If hypertensive, semireclined (head slightly
        elevated)
       If normotensive, on affected side
       If hypotensive, supine
                           CVA Management
   Increased Blood pressure treated ONLY
    if strongly suggestive of ischemic stroke
       If systolic >220 or diastolic >120 consider
        gradual blood pressure reduction
          Labetalol

          Nitropaste

          Nitroprusside

       Controlled reduction
       Return to pre-CVA levels, NOT to “normal”
                       CVA Management
   Thrombolytic agents
       Consider for all patients with ischemic CVA
        presenting within 3 hours of onset
       Early recognition of ischemic stroke and
        administration of thrombolytics can
        prevent/limit loss of neurologic function
       Requires CT scan!!!
                             CVA Management
   Think like AMI of the Brain
       Time is tissue
   Therapy Mainstays
       Oxygenation/Ventilation
       IV Access
       Rapid assessment & differential
          Treat  associated conditions (hypoglycemia,
             hypoxia, hypotension)
       Rapid Transport to appropriate facility
            CT Scan & Thrombolytics vs. CT Scan & Neurosurgery
  Syncope
AEIOU TIPS
                                Syncope
 aka Fainting
 Pathophysiology

     Brief loss of consciousness caused by
      transient cerebral hypoxia
     May be caused by lack of glucose or
      seizure activity in the brain
                                          Syncope
   Types
       Postural
          Inadequate   blood flow to brain due to position
       Vasovagal
          Excessive vagal stimulation
          Carotid Sinus stimulation/pressure

       Cardiogenic
          Dysrhythmia,usually bradycardia
          Stokes-Adams Syndrome
                                         Syncope
   Types
       Tussive
          “coughing  spell” resulting in  intrathoracic
           pressure causing  venous return to the heart
          most often in overweight male smokers with
           chronic bronchitis
       Micturation
          associatedwith urination, usually in patients
          who have consumed EtOH and compounded
          by increased vagal stimulation
                                       Syncope
   Assessment
       History of the event
         Oftenpreceded by sensation of light-headedness
         Rapid return of consciousness is most common

       Past History
         History of vertigo
         Similar past episodes

       Many possible causes
                                            Syncope
   Management
       Manage ABCs
         Clearairway and Assist ventilations as needed
         Oxygen NRB (initially)

         Calm & Reassure

         Assess for underlying cause
              ECG
              Blood glucose
              History (present and past)
              Physical Exam
         Treatment    based on underlying cause
  Seizures
AEIOU TIPS
                                       Seizures
   Alteration in behavior/consciousness 2°
    unstable, uncoordinated electrical activity
    in the brain
       Often a result of altered membrane
        permeability
       Manifested by sudden, brief episodes of:
          altered consciousness
          altered motor activity

          altered sensory phenomena

          unusual behavior
                     Seizure Categories
   Generalized
       Tonic-Clonic (grand mal)
          AKA   Convulsions
       Absence (petit mal)
   Partial
       Simple partial
       Complex partial
   Hysterical
                    Seizure Etiology
 CVA                    Head trauma
 Hypoxia                Hypoglycemia

 Infection/Fever        Brain neoplasms

 Drug/alcohol           Psychiatric

  withdrawal              disorders
 Poisoning/OD           Eclampsia

 Thyrotoxicosis         Hypocalcemia
         Seizures Etiology

Most epileptic seizures
are idiopathic in origin
           Generalized Seizures

   Petit Mal         Grand mal
     Absence Sz        aka Convulsions
     Children          Common

     No LOC            Often w/Aura

                        Sudden LOC

                        Tonic / Clonic

                        Postictal phase

                        Status epilepticus
               Generalized Seizures
 Symmetrical
 No local onset

 Irritable focus difficult to identify

       Near simultaneous activation of entire
        cortex
       Focus may begin deep in brain and spread
        outward
              Generalized Seizures
   Tonic-Clonic Seizures (Grand Mal)
       Aura (preictal phase)
       Loss of consciousness/postural tone
       Tonic phase
       Hypertonic (tetanic) phase
       Clonic phase
       Post-ictal phase
       May experience transient neurologic
        deficits (Todd‟s paralysis)
              Generalized Seizures
   Absence Seizure (Petit Mal)
       Brief loss of awareness (10 - 30 seconds)
       Usually no loss of postural tone
       May occur 100+ times a day
       Primarily pediatric problem
       Often described as “daydreaming”, not
        paying attention
       Usually disappear as child matures
                 Partial Seizures
 Seizure begins locally
 May remain localized or spread to
  entire cortex
 Result from focal structural lesion

  in brain
                               Partial Seizures
   Simple                          Complex
     Localized clonic                Change in
      activity                         behavior
     Abnormal sensory                Preceded by aura
      symptoms                        Repetitive motor
     Usually no LOC                   behavior
     May progress                    No recall
         Jacksonian   March          May progress
         (Seizure)
                       Partial Seizures
   Simple partial seizures
    (No loss of consciousness)
       Focal motor seizures
         Localclonic activity
         May display Jacksonian march

     Sensory seizures
     Autonomic seizures
                   Partial Seizures
   Complex partial seizure (psychomotor
    or temporal lobe seizures)
      Distinctive aura

      Loss of consciousness

      Automatisms

      May be mistaken for drunks or
       psychotics
      May experience episodes of rage
       Hysterical “Seizures”
 Usually in front of audience
 Usually follow interpersonal stress

 Movements asymmetrical or purposeful

 Does not fall, hit head, bite tongue

 Incontinence rare

 Recalls things said, done during

  “seizure”
                                     Assessment
   Seizure Assessment
       Duration
         Seizure

         Postictalphase
         Typical for the patient?

       Onset
         Events   before
         HA

         Aura

         Trauma

         Vision   Disturbances
                                Assessment
   Recent History
       Trauma to the head/brain
       HA / Neck Pain
       Pregnancy
       Brain tumor
       Recent Infection/Illness
       CVA Symptoms
       Introduction of Poisons into body
                            Assessment
   Past History
       Diabetes Mellitus
       Seizure Disorder
       Tumor
       CVA
       Medications
       Recreational Drug Use
       Alcohol abuse
                              Assessment
   Physical Exam
       Evidence of trauma
       Evidence of alcohol, drug abuse
       Rash, stiff neck
       Pregnant
       CVA Signs
       Incontinence
            Status Epilepticus
 Two or more seizures without
  intervening conscious period
 Usually due to medication non-
  compliance
 Management same as for other
  Seizures just more aggressive
                Seizure Management
   Patient actively seizing
       Do NOT restrain
       Do NOT put anything in mouth
       Oxygen NRB if possible
       ECG Monitor when possible
       IV Access
          LgBore, NS
          Assess blood glucose
                  Seizure Management
   Patient actively seizing
       If hypoglycemic: Assess IV patency FIRST!!
          Dextrose 50% 12.5 - 25 grams IV push
          Consider Thiamine 100 mg slow IV push

       Diazepam, slow IV administration until
        seizure stops or until ~ 10 mg
          Usually   aimed at 2.5 mg doses, one after another
       Phenobarbital, 100 mg/min IV push to a total
        ~390 mg or seizure stops
          Barbiturate coma
          NMB & Intubation
                    Seizure Management
   Current Mainstays of Therapy for Actively Seizing
    Patient
       Diazepam
       Lorazepam
       Phenobarbital
   “New” Therapy
       Phosphenytoin
   Other Considerations
       Glucose
       MgSO4
       Paraldehyde
       Dilantin (phenytoin) 18mg/kg at 25 mg/min
                Seizure Management
   After seizure stops:
       Open -Clear- Maintain airway
       O2 via NRB
       Assist ventilations if needed
       Roll patient onto side protecting head
       Reassess ABCDs
       Assess blood glucose
       Physical Exam and History
   Most seizure deaths are due to anoxia
        Seizure Management

  If the patient is
 epileptic, do these
seizures match what
is “normal” for him?
                        Just because the
                       patient is epileptic,
                       he does NOT have
                         to be having an
                        epileptic seizure!
                Mandatory Transports
   First time seizures
   Seizure patient off medications
   Change in seizure pattern
   Associated with trauma
   Pregnant patient
   Status epilepticus
   Associated with increased body temperature
       Not always; Seldom in young children
       Has infection been diagnosed and treatment
        initiated?
Insulin: Hypo/Hyperglycemia
         AEIOU TIPS
                  Insulin
 Hypoglycemia
 Hyperglycemia
       DKA
       HHNC
                                        Insulin
   Assessment
       Medical Alert Tag/Bracelet
       Evidence of DM Medications
       Fruity breath odor
       Signs of repeated SQ injections
       Blood glucose level
       (See Endocrine for further assessment)
                                           Insulin
   Management
       Hypoglycemia
         Management     ABCs: Oxygen/IV/ECG
         Dextrose 50% (adult), 12.5 - 25 grams IV push
          via patent line
         Consider Thiamine 100 mg slow IV push

         Dextrose 25% (children), 0.5 - 1 grams IV push
          (2-4 cc/kg) via patent line
         Carbohydrate meal

         Assess for underlying cause

         Consider transport
                                             Insulin
   Management
       DKA/HHNC
         Management   ABCs: Oxygen/IV/ECG
         Ventilate/Intubate prn

         Fluid administration titrated to signs of shock
              250 cc boluses and reassess
         Consider  administration of Regular Insulin
          (consult medical control)
         Assess for underlying cause

         Transport
 Alcohol
AEIOU TIPS
                             Alcohol
        EtOH present in up to 40% of
               AMS patients

 “Dead drunk”
 Mixed overdose

 May be associated with

       Head trauma
       Hypoglycemia
                         Alcohol

Is it alcohol or
is it something
      else?
                   A patient is
                   never “Just
                     Drunk”
                                           Alcohol
   Management
       Manage ABCs
          Clear airway and ventilate as needed
          Oxygen

          IV access prn

       Assess for other causes of AMS
          ECG  Monitor
          Blood glucose level

          History of mixed poisoning or EtOH poisoning

          Physical exam

       Treat other causes
Overdose/Poisoning
  AEIOU TIPS
                Overdose/Poisoning
   Possible Overdose/Poisonings resulting
    in AMS
       Alcohol: Ethanol/Methanol
       Narcotics
       Sedative-hypnotics
       Solvent inhalation
       Stimulants
                                      Overdose
   Assessment
       Needle marks?
       Pupil responses?
       Slow respirations?
          Associated   hypotension
       Odd behavior?
       Breath odors?
       Color of oral mucosa, vomitus?
       History of Recent Drug/Poison use?
Uremia/Metabolic Causes
     AEIOU TIPS
    Uremia (Metabolic Causes)
 Uremia/Renal Failure
 Hyperthyroidism

 Hypothyroidism

 Addisonian Crisis

 Hepatic Coma/Encephalopathy
Uremia (Metabolic Causes)
   Assessment
     Med Alert?
     Patient medications?

     Physical findings?
       The Physical Exam and History (recent
        and past) are most useful
  Trauma
AEIOU TIPS
                          Trauma
 Concussion
 Cerebral contusion

 Intracranial hematoma

 Hypovolemia

 Hypoxia
                                       Trauma
   Assessment
       Physical findings?
         Evidence   of brain injury
       History of recent or remote trauma?
                  Trauma

Altered Mental Status =
      Head Injury
Until Proven Otherwise
                    Trauma

  Head injury severity
  cannot be evaluated
accurately in presence of
         shock
                                                     Trauma
   Management
       Manage ABCs
       Spinal motion restriction if indicated
       Clear airway and secure prn
       Ventilate prn
       Oxygen
       Establish IV access, NS
            Fluid to titrate BP to ~ 90 mm Hg systolic
       Assess for other causes: ECG, Blood glucose
       Transport to trauma center
Infection/Fever
 AEIOU TIPS
                  Infection
 Meningitis
 Encephalitis

 Brain abscess

 Sepsis

 Fever
                              Infection
   Assessment
     Headache?
     Fever?

     Sore throat?

     Stiff neck (nuchal rigidity)?

     Rash?

     Associated symptoms of systemic
      infection
                                           Infection
   Management
       Infection Control Measures
       Manage ABCs
          clearairway and ventilate prn
          oxygen

          IV access prn

       Consider
          acetaminophen for fever
          fluid / rehydration
Psychogenic
AEIOU TIPS
                             Psychogenic
 Hysterical faking
 Catatonia
       “psychomotor disturbances characterized by
        physical rigidity, negativism, or stupor”
       may occur in schizophrenia, mood disorders
        or organic mental disorders
                                Psychogenic
   Assessment
       Circumstances?
        Events    leading up to this point
       Prior behavior?
        Similar   past episodes
       Medications & PMHx
Assessment & Management
        of AMS
                 Primary Assessment
   Onset
       Mechanism (Kinematics)
       Preceding S/S
   Level of Consciousness
       AVPU
       GCS (later)
   Airway obstruction or compromise
       Fluid
       Unprotected airway (e.g. coma)
                Primary Assessment
   Ventilatory ability
       Adequate Ventilatory rate and depth?
       Respiratory Insufficiency 2° to  ICP? (e.g.
        irregular patterns)
   Cardiovascular compromise
       Shock /hypotension /hypovolemia
       Hypertension
              Primary Assessment
   Neuro Exam (motor & sensory)
     Posturing? Muscle Tone?
     Pupillary Reflexes?

     Extraocular Movements?

     Symmetry

   History
     Present and Recent
     Past
                   Management of AMS
   Goals:
       Airway control/ maintenance
         Avoid    hypoxia
       Cardiovascular stabilization
         Avoid    hypotension/shock
       Interruption of cerebral injury
         Fix   the root cause problem
       Protection from further harm
         Avoid    secondary brain injury
Other Neurologic
   Conditions
                                       Headache
   Common complaint
       Many persons experience regularly
       ~ 1/3 due to migraine HA
       May be associated with significant pathology
   Characteristics
       Sudden vs Constant vs Recurring
       Generalized vs Localized
       Mild to Moderate to Severe Intensity of Pain
   Cause is often unknown
                                   Headache
   Vascular
       Migraines
         Lastminutes to hours to days
         Usually very intense, throbbing pain

         Photosensitivity

         N/V

         Often unilateral

         May be preceded by aura (not common)

         Occur commonly in women
                                       Headache
   Vascular
       Cluster
          Series  of headaches
          Usually last for a few minutes or a few hours

          Sudden, intense pain

          Usually unilateral

          May be accompanied by nasal congestion,
           irritated or watery eye (same side)
          Occur commonly in men
                                 Headache
   Tension
       Most common headache
       Occur regularly
       Often awake in a.m. and worsens throughout
        the day
       Dull, ache
       Feels like pressure on neck and/or head
                                    Headache
   Organic
       Not very common
       Due to some specific cause (illness/injury) in
        the body
          Tumor

          Infection

          Meningitis

          Hypoglycemia

          etc.
                                          Headache
   Potentially Serious Pathologies
       Complaint
         “Worst  headache ever”
         “It hurts right here”

         May localize at posterior neck at base of skull
              Possible subarachnoid hemorrhage

       Concern for possible intracranial
        hemorrhage
                                 Neoplasms
 Less common neoplasm
 Risk factors

       genetic
       exposure to radiation
       tobacco use
       occupational exposure to toxins
       medications/drugs/poisons
       diet
                                 Neoplasms
   Pathophysiology
       Most often a result of metastasis from
        another cancer (malignant)
   Assessment
       focused on the detailed neuro exam
       not a diagnosis diagnosis BUT should be
        included in the differential dx
                Muscular Dystrophy
 Genetic disorder
 Results in degeneration of muscle fibers

 Types

       Duchenne
       Fascioscapulohumeral
       Limb Girdle
       Myotonic
                     Muscular Dystrophy
   Duchenne dystrophy
       most common childhood muscular
        dystrophy
       onset usually by age 6
       symmetrical weakness and wasting of
           first the pelvic and leg muscles
          then pectoral and proximal upper extremities

       progresses and results in early death
          usually   in adolescence
                      Multiple Sclerosis
   Common demyelinating disorder of the CNS
   Results in patches of sclerosis (patches) in brain
    and SC
   Occurs primarily in young adults
   Typical S/S
       visual loss, diplopia
       nystagmus
       weakness, paresthesias
       symptoms may have periods of exacerbation and
        remission
               Parkinson’s Disease
   Degenerative changes in the basal ganglia
    result in deficiency of dopamine
   Characterized by rhythmical muscular
    tremors, rigidity of movement, and droopy
    posture
   Usually occurs after 40 years of age
   Leading cause of neuro disability > 60 years
   Estimated 500,000 in US
             Central Pain Syndrome
   Known as Trigeminal Neuralgia
   paroxysmal bursts of pain in one or more
    branches of the trigeminal nerve
   Often induced by touching trigger points in or
    about the mouth
   Causes
       tumor
       some medications (phenothiazines)
                                      Bell’s Palsy
   Paresis or paralysis of the facial muscles
       usually unilateral
   Occurs in 23 of 100,000 persons
   Caused by dysfunction of the 7th cranial nerve
       cause is usually a viral infection
       other causes
          post trauma
          herpes simplex

          lyme disease

          idiopathic
                  Amyotrophic Lateral
                           Sclerosis
   Progressive motor neuron disease
   aka ALS or Lou Gehrig disease
   disease of the motor tracts of the lateral
    columns and anterior horns of the SC
       results in progressive muscular atrophy, increased
        reflexes, and spastic irritability of muscles
                                     Spina Bifida
   An embryolgic failure of fusion of one or more
    vertebral arches
       results in spinal cord exposure
       spinal cord may protrude outward
       various types based upon type of deformity
   Child requires frequent surgeries
       increased risk of latex allergies
                                Poliomyelitis
   An inflammatory process of the Spinal Cord‟s
    gray matter
   May be caused by the poliomyelitis virus
       Enters bloodstream and nervous system
       results in paralysis of the limbs
   Uncommon today in the US due to polio
    vaccine

				
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