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Transcript
CNS Disorders
EMS Professions
Temple College
Pathophysiology of CNS
Emergencies

Structural Changes


Often due to Trauma but not always
Circulatory Changes


Alterations of ICP


Response to insult
Toxic Metabolic states


Inadequate Perfusion
Alteration to blood chemistry or introduction of toxins
Psychiatric ‘mimicking’
ICP Review

CBF is a factor of CPP & CVR



CPP = MAP - ICP



If CPP , then CBF 
If CVR , then CBF most likely 
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



Breathing




Open, clear, maintain
If trauma or + history, control C-spine
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

 Yes
or No
 How?
R = Respiratory Pattern

Depth


Unusually deep or shallow?
Pattern

Regular or Unusual pattern
Can
you identify the pattern?
M = Motor Function

Paralysis?


Muscle tone?


Where? What is it like?
Posturing?


Rigid or Flaccid
Movement?


Where?
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





Asymmetrical
deficits
Unequal pupils
Afebrile
History of trauma,
structural
abnormality
Often a rapid onset

Metabolic





Symmetrical deficits
Equal pupils
(? altered function)
? Fever
History of metabolic
disorder or illness
Rapid onset less
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
 Epilepsy
 Insulin
 Overdose
 Uremia (Metabolic
causes)

Trauma
 Infection
 Psychogenic
 Stroke/Syncope

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
fibrillation
 Cigarette smoking
 Diabetes Mellitus  Sickle cell disease
 Polycythemia
 Heart disease
 Hypercoagulability
 Hyperlipidemia
 Birth control pill use
 Cardiovascular
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
Grade II
Grade III
Grade IV
Grade V
Asymptomatic or mild headache and mild
nuchal rigidity
Moderate to severe headache, nuchal
rigidity, cranial nerve dysfunction but no
other deficits
Drowsiness, confusion, mild focal deficits
Stupor, moderate to severe hemiparesis,
possibly early decerebrate rigidity,
vegetative response
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”)



Have patient close eyes and hold arms out (“Arm Drift”)



Normal: Both sides of face move equally well
Abnormal: One side does not move as well as other
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



Associated Altered LOC or Seizure?
Onset/Precipitating factors?
Initial symptoms and progression?




Assessment
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
 associated
with urination, usually in patients
who have consumed EtOH and compounded
by increased vagal stimulation
Syncope

Assessment

History of the event
 Often
preceded 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
 Clear
airway 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


Absence (petit mal)
Partial



Convulsions
Simple partial
Complex partial
Hysterical
Seizure Etiology
CVA
 Hypoxia
 Infection/Fever
 Drug/alcohol
withdrawal
 Poisoning/OD
 Thyrotoxicosis

Head trauma
 Hypoglycemia
 Brain neoplasms
 Psychiatric
disorders
 Eclampsia
 Hypocalcemia

Seizures Etiology
Most epileptic seizures
are idiopathic in origin
Generalized Seizures

Petit Mal
Absence Sz
 Children
 No LOC


Grand mal
aka Convulsions
 Common
 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

Localized clonic
activity
 Abnormal sensory
symptoms
 Usually no LOC
 May progress

 Jacksonian
(Seizure)
March
Complex
Change in
behavior
 Preceded by aura
 Repetitive motor
behavior
 No recall
 May progress

Partial Seizures

Simple partial seizures
(No loss of consciousness)

Focal motor seizures
 Local
clonic 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
 Postictal
phase
 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 noncompliance
 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
 Lg
Bore, 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




“New” Therapy


Diazepam
Lorazepam
Phenobarbital
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
 clear
airway 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

Prior behavior?
Similar

leading up to this point
past episodes
Medications & PMHx
Assessment & Management
of AMS
Primary Assessment

Onset



Level of Consciousness



Mechanism (Kinematics)
Preceding S/S
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

Cardiovascular stabilization
 Avoid

hypotension/shock
Interruption of cerebral injury
 Fix

hypoxia
the root cause problem
Protection from further harm
 Avoid
secondary brain injury
Other Neurologic
Conditions
Headache

Common complaint




Characteristics




Many persons experience regularly
~ 1/3 due to migraine HA
May be associated with significant pathology
Sudden vs Constant vs Recurring
Generalized vs Localized
Mild to Moderate to Severe Intensity of Pain
Cause is often unknown
Headache

Vascular

Migraines
 Last
minutes 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