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Chapter 14
Level of Consciousness
 “ the
most critical clinical index of
nervous system function, with
changes indicating either
improvement or deterioration of
the individual’s condition”
 Table 14-3 Levels of Altered Consciousness
Alterations in Cognitive Networks
 Full consciousness: awareness of self and the
environment
 Arousal: state of awakeness
Mediated by the reticular activating system
 Content of Thought: all cognitive functions
 Awareness of self, environment and affective
states (moods)

Alterations in Arousal
 Causes Table 14-1 & 14-2
 Structural
Divided by location above or below
tentorial plate
 Metabolic
 Psychogenic

Alterations in Arousal
 Pathological processes
 Infectious, vascular, neoplastic,
traumatic, congenital, degenerative,
polygenic
 Metabolic

Hypoxia, electrolyte disturbances,
hypoglycemia, drugs and toxins
Alterations in Arousal
“range from slight drowsiness to coma”
 Coma – produced by either
 Bilateral cerebral hemisphere damage or
suppression
 Brain stem* lesions or metabolic derangement that
damages and suppresses the reticular activating
system
*midbrain, medulla, pons (Figure 12-5)
Alterations in Arousal
• Clinical manifestations : critical for evaluation
“extent of brain dysfunction”
“index for identifying ↑ or ↓ CNS function”
1) Level of consciousness
2) Pattern of breathing
- Post hyperventilation apnea (PHVA)
- Cheyne–Stokes respiration (CSR)
3) Pupillary changes (size and reactivity)
4) Oculomotor response (position and
reflexes)
5) Motor response (skeletal muscle)
President Lincoln April 14, 1865
Pathway of the bullet
Clinical Manifestations
Clinical Manifestations
Clinical Manifestations
Decorticate & Decerebrate
Brain Death
“never recover nor maintain internal
homeostasis”
 Total Brain Death – criteria (5):
(cerebrum, brain stem & cerebellum)
 Completion of all appropriate and
therapeutic procedures
 Unresponsive coma (absence of motor
and reflex responses)
 No spontaneous respirations (apnea)
Brain death – criteria
 No ocular responses
 Isoelectric EEG: 6 to 12 hours without
hypothermia/depressant drugs
Cerebral Death
“death exclusive of brain stem and
cerebellum”
 No behavioral or environmental responses
 Brain continues to maintain internal
homeostasis
 Survivors
 Coma
 Vegetative state (“wakeful unconscious state”)
 Minimal conscious state
Locked-in syndrome
Seizures
 “Sudden, transient alteration of brain function
caused by an abrupt explosive disorderly
discharge of cerebral neurons”
 Alteration in brain function (transient)
 Altered level of arousal
 Convulsion – seizure with tonic-clonic movement
 Epilepsy – seizures recur without treatment (5 to
10/1000)
Conditions - Seizures
 Cerebral lesions
 Biochemical disorders
 Cerebral trauma
 Epilepsy
Seizures
 Partial (focal/local)
 Simple, complex, secondary, generalized
 Generalized (bilateral/symmetric)
 Unclassified
Seizures
 Epileptogenic focus
 Group of neurons that appear to be
hypersensitive to sudden depolarization
 Hyperthermia, hypoxia, hypoglycemia,
hyponatremia, sensory stimulation and certain
sleep phases
 Aura – partial seizure precedes generalized
 Prodroma – early manifestation – hours to days
before
Seizures
 Tonic – contraction
 Excitation spreads to subcortical, thalamic and
brain stem areas
 Loss of consciousness
 Clonic – relaxation
 Inhibitory neurons of cortex, anterior thalamus
and basal ganglia
Alterations in Awareness
 Memory
 Retrograde amnesia – past memories
 Antegrade amnesia – new memories
 Temporary or permanent (severe head injury or
Alzheimer disease)
 Executive attention deficits
Inability to maintain sustained attention
 Inability to set goals
 Working memory deficit
Table 14-6 Clinical manifestations

Memories:amygdala
thalamus
hippocampus
prefrontal cortex
Data Processing Deficits
 Agnosia – failure to recognize the form and
nature of an object: CVA
 Tactile, visual, auditory
 Dysphasia – inability to arrange words in
logical order: CVA (middle cerebral artery-L
cerebral hemisphere)
 Expressive – cannot find words, difficulty writing
(Broca’s area)
 Receptive – language is meaningless (inappropriate
words, neologisms) – Wernicke
Data Processing Deficits
 Dementia*
 Progressive failure of cerebral functions that is not
caused by an impaired level of consciousness
 ↓ orienting, memory language and executive
attention networks
 Table 14-13 Comparison of Delirium & Dementia
Dementia
 Degeneration of neurons
 Compression-space occupying lesion
 Atherosclerosis
 Genes-Alzheimer & Huntington diseases
 CNS infection –HIV, Creutzfeldt-Jakob
“nerve cell
damage and brain atrophy”
Alzheimer Disease (AD)
 Familial onset
 Early-onset-chromo mutations # 21 (very rare)
 Late onset-90% cases ? Chromo #19*
 Theories
 Mutation for encoding amyloid precursor protein
 Alteration in apolipoprotein E*
 Loss of neurotransmitter of choline
Alzheimer Disease (AD)
 Neurofibrillary tangles
 Senile plaques
 Clinical manifestations
 Forgetfulness, emotional upset, disorientation,
confusion, lack of concentration, decline in abstraction,
problem solving and judgment
 Diagnosis – R/O other causes
Burden of Alzheimer’s Disease
 5.4 million Americans
16 million by 2050
 6th leading cause of death:#prevented, cured, slowed
 >/= 65y/o average survival: 4-8 yrs, may up to 20yrs
 Caregivers burden: 60% emotional stress
: 30%depressed
 Cost 2011: $183 billion
$1 trillion by 2050
 J.Alzheimer’s Assoc. March 2011
Know the Signs
 Memory loss that disrupts daily life
 Trouble planning or solving problems
 Difficulty completing tasks
 Confusion with time or place
 Trouble understanding images and spatial
relationships
 New problems with speaking or writing words
 Misplacing things and inability to retrace steps
 Decreased or poor judgment
Know the Signs
 Social withdrawal
 Change in mood or personality
 Review Table 14-14
Cerebral Hemodynamics
 CBF – blood flow
 CPP – perfusion pressure
 CBV – blood volume
 Cerebral oxygenation – “
critical factor”
Injury States
 ↓ cerebral perfusion
 Normal perfusion but ↑ intracranial pressure
(ICP)
 ↑ cerebral blood volume
SO: “must maintain CPP and control ICP”
Increased Intracranial Pressure
(IICP)
 ↑ intracranial content, edema, excess CSF or
hemorrhage
 Normal 5 to 15 mmHg
 Stages 1-4 (Figure 14-10)
 Stage 1 vasoconstriction and external compression
of venous system - ↓ ICP (autoregulation)
 Stage 2
General
 Autoregulation -
blood vessel diameter
to maintain a constant blood flow is lost with ↑
ICP
 ↑ vasoconstriction to elevate BP > ICP
a) ↓O2 ↑CO2 → deterioration
b) small pupils, neurologic hyperventilation, widened
pulse pressure and ↓HR
 Local vasodilation 2° to ↑ CO2 →↑ BV →↑↑ ICP
→ approaches SBP - ↓ perfusion with severe
hypoxia/acidosis
 IICP – not evenly distributed throughout the
cranial vault
Cerebral Edema
• Increase in the fluid (intracellular or extracellular)
within the brain (↑ volume)
• Results: trauma, infection,
hemorrhage, tumor,
ischemia, infarct or hypoxia
1) Vasogenic: BBB is disrupted - ↑ plasma protein to
extracellular space - ↑ ICP
2) Cytotoxic: toxic factors → failure NA-K+ transport
system: K+ out, H2O in
3) Ischemic (infarction): vasogenic and cytotoxic → cell
necrosis → lysosomes → BBB↑
4) Interstitial (hydrocephalus): ↑ volume about ventricles
Hydrocephalus (Types Table
14-16)
 Excess fluid within the cranial vault,
subarachnoid space or both
 Caused by interference in CSF flow
 ↓ reaborption
 ↑ fluid production
 Obstruction
 Infancy through adulthood
Spinal Shock
“complete cessation of spinal cord function below
the lesion”
• Complete flaccid paralysis
• Absence of reflexes
• Marked disturbance of bowel and bladder function
• Days to weeks
– Return of spinal reflexes
→ hyperactive
→ spasticity, rigidity
Michael J Fox
Parkinson Disease
 After age 40 – peak onset 58 – 62 years
 107 to 187 per 100,000
 Severe degeneration of the basal ganglia involving
dopaminergic nigrostriatal pathway
 Dopamine: inhibitory neurotransmitter
 Acetylcholine: stimulatory neurotransmitter
IMBALANCE of” neurotransmitters motor
modulation”
Ach________________Dopamine
Parkinson Disease
Parkinson Disease
 Clinical manifestations
 Tremor at rest
 Rigidity (muscle stiffness)
 Bradykinesia (poverty of movement)
 Postural disturbance
 Dysarthria (uttering of words)
 Dysphagia (difficulty swallowing)
 Progressive dementia
Parkinson Disease