Post on 12-Jan-2016
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 NetworksFull consciousness: awareness of self and
the environment
Arousal: state of awakenessMediated by the reticular activating system
Content of Thought: all cognitive functionsAwareness of self, environment and affective states (moods)
Alterations in ArousalCauses Table 14-1 & 14-2
StructuralDivided by location above or below tentorial plate
MetabolicPsychogenic
Alterations in ArousalPathological processes
Infectious, vascular, neoplastic, traumatic, congenital, degenerative, polygenic
MetabolicHypoxia, electrolyte disturbances, hypoglycemia, drugs and toxins
Alterations in Arousal“range from slight drowsiness to coma”
Coma – produced by eitherBilateral cerebral hemisphere damage or
suppressionBrain 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 consciousness2) 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 responsesIsoelectric EEG: 6 to 12 hours without hypothermia/depressant drugs
Cerebral Death “death exclusive of brain stem and
cerebellum”
No behavioral or environmental responsesBrain continues to maintain internal
homeostasisSurvivors
ComaVegetative 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 depolarizationHyperthermia, 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 – relaxationInhibitory neurons of cortex, anterior
thalamus and basal ganglia
Alterations in Awareness
MemoryRetrograde amnesia – past memoriesAntegrade amnesia – new memoriesTemporary or permanent (severe head injury or
Alzheimer disease)
Executive attention deficits Inability to maintain sustained attention Inability to set goals Working memory deficitTable 14-6 Clinical manifestations
Memories:amygdala hippocampus thalamus prefrontal cortex
Data Processing Deficits Agnosia – failure to recognize the form
and nature of an object: CVATactile, 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
DementiaDegeneration 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*
TheoriesMutation for encoding amyloid precursor proteinAlteration in apolipoprotein E*Loss of neurotransmitter of choline
acetyltransferase
Alzheimer Disease (AD)Neurofibrillary tangles
Senile plaques
Clinical manifestationsForgetfulness, emotional upset, disorientation,
confusion, lack of concentration, decline in abstraction, problem solving and judgment
Diagnosis – R/O other causes
Burden of Alzheimer’s Disease5.4 million Americans 16 million by 20506th leading cause of death:#prevented, cured, slowed>/= 65y/o average survival: 4-8 yrs, may up to 20yrsCaregivers burden: 60% emotional stress
: 30%depressedCost 2011: $183 billion $1 trillion by 2050
J.Alzheimer’s Assoc. March 2011
Know the SignsMemory loss that disrupts daily lifeTrouble planning or solving problemsDifficulty completing tasksConfusion with time or placeTrouble understanding images and spatial
relationshipsNew problems with speaking or writing wordsMisplacing things and inability to retrace
stepsDecreased or poor judgment
Know the SignsSocial 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
GeneralAutoregulation - blood vessel
diameter to maintain a constant blood flow is lost with ↑ ICP
↑ vasoconstriction to elevate BP > ICPa) ↓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 productionObstruction
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 pathwayDopamine: inhibitory neurotransmitterAcetylcholine: stimulatory neurotransmitter
IMBALANCE of” neurotransmitters motor modulation”
Ach________________Dopamine
Parkinson Disease
Parkinson Disease Clinical manifestations
Tremor at restRigidity (muscle stiffness)Bradykinesia (poverty of movement)Postural disturbanceDysarthria (uttering of words)Dysphagia (difficulty swallowing)Progressive dementia
Parkinson Disease