Chapter 61
Level of Concsiouness
Headache
Intercranial Pressure
Seizure
Level of Conscoiuness
• Can be any spot on a spectrum from normal to
coma
• Full Conscoiuness would be orineted x’s 4
– Person, place, time, and sitution
– Coma
– Akinetic Mutism
– Vegetative State
– Locked-in Syndrome
Level of Consciousness
• PATHOPHYS
– LOC is not a disease in an of itself but instead a
symptom of another condition
• Manifestations
– Rememeber the GCS
• Diagnostics
– Full neurological assessment
– Labs (cbc,cmp,NH3, LFT, Ca++, urine)
– Test (MRI, EEG, CT)
Increased Intracranial Pressure
• Normal level is 0-15
• Monro- Kellie Hypothesis
– the sum of volumes of brain, CSF, and intracranial
blood is constant (Morki, 2001)
– If one expands or decreases then the other need
to compensate
Morki, B. (2001). The Monro-Kellie Hypothesis.
Neurology. 56(12).
Pathophysiology
of ^ ICP
• Commonly associated with head trauma but
also seen with tumors, metabolic acidosis,
edema and herniation.
• Decreased blood flow
– Cell death +/- ischemia causes system pressure
rises
• This can produce a slow bounding pulse with
respiratory irregulatories
Pathophysiology
• Cerebral Edema
– Abnormal association of water and fluid in the
intra and extra areas with an associated an
increased volume of Hisse
– Autoregulation occur as blood vessels constrict
and diliate to keep the blood flow
• Cerebral response to increase ICP
– CPP= MAP-ICP
– Normal CPP= 70-100 mmHg
Cerebral response to ICP
• Steady perfusion continues with ICP <40 &
SBP 50-150
• CPP<50 = irreversible neuro damage
• If CPP=ICP No cerebral circulation
Ceberbral Response
Cushing Response
• Widening pulse pressure
• Increased SBP
• Decreased heart rate
• Considered a late sign but
still may be treated
Cushing Triad
• Decreased Heart Rate
• Increased SBP
• Decreased Respiration
Clinical Manifestations
• #1 sign of increased intercranail pressure is
changes in LOC
• Any sudden changes in the neuro status is
significant
• As ICP increases becomes stuporous, only
reactioning to only loud painful stimulus
Posturing
Assessment of ICP
• CT, SPECT, cerebral angiography
• LP’s are contrindicated if the person is
believed to have increased intracrainal
pressure
Seizure Disorder
Abnormal motor sensory autonomic, or or pysch
disorder
Due to excessive discharge of neurons
Can have 2 classifications
partial(simple/complex)
general
SEE BOX ON PAGE 1881
Epilepsies
• Known as a reoccuring seizure
• May be primary or secondary
• Pathophysiology
– Neuron discharge by electrochemical energy to
perfer a task
– When they are supossed to stop they continue to
firing the impluse which lead to a seizure
Eplisies
Clinincal Manifestations
• Depends on what neurons
are firing
• Could be a small twitch that
doesn’t stop or could
include decrease level of
consciousness
Assess & Diagnosis
• Detailed Health History
• Family History
• Physical and Neuro Status
• MRI/EEG- localizes the area
better; they may also need
to do telemtry EEG
• In the elderly epilpsey can
present as an CVA
• Status Epilipticus
Headache
• Most common neuro problem
• May be primary but for unknown reasons
• 3 types
– Migrane
– Tension
– Cluster
– Arteritis
Pathophysiology
• S&S of a migrane result from dysfunction of the
brain stem pathways that modulate sensory input
• Caused usually by vasodilation
• May have many different triggers
• Tension-usually associated with stress
• Cluster-?????
• Arteritis-migrane response when complex are
deposits in the blood vessels walls
Migrane manifestions
Migrane Manifestation
•
•
•
•
Prodrome
Aura
Headache
Recovery
Cluster
• Unliateral small and frequent
• May 1-8 x’s/day
• Last 15 min- 3hr
Tension
• Constant steady pressure
feeling state @ temple,
front of head, or back of
neck
Arteritis
• Very general start malise,
fatigue, wt loss, fever, may
swollen tender
Assess & Diagnostics
• Detailed history
• Must be very detailed
• Need to determine if the cause is something