Professional Documents
Culture Documents
Level of Consciousness
the
most critical clinical index of nervous system function, with changes indicating either improvement or deterioration of the individuals condition
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
Alterations in Arousal
Pathological processes
Infectious, vascular, neoplastic,
Alterations in Arousal
range from slight drowsiness to coma
suppression Brain stem* lesions or metabolic derangement that damages and suppresses the reticular activating system
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) - CheyneStokes respiration (CSR) 3) Pupillary changes (size and reactivity) 4) Oculomotor response (position and reflexes) 5) Motor response (skeletal muscle)
Clinical Manifestations
Clinical Manifestations
Clinical Manifestations
Brain Death
never recover nor maintain internal homeostasis
therapeutic procedures Unresponsive coma (absence of motor and reflex responses) No spontaneous respirations (apnea)
hypothermia/depressant drugs
Cerebral Death
death exclusive of brain stem and
cerebellum
No behavioral or environmental responses
Survivors
Coma
Vegetative state (wakeful unconscious state) Minimal conscious state
Locked-in syndrome
Seizures
Sudden, transient alteration of brain function
10/1000)
Conditions - Seizures
Cerebral lesions Biochemical disorders
Cerebral trauma
Epilepsy
Seizures
Partial (focal/local)
Seizures
Epileptogenic focus Group of neurons that appear to be
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
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
nerve cell
Theories
Mutation for encoding amyloid precursor protein Alteration in apolipoprotein E* Loss of neurotransmitter of choline
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
relationships New problems with speaking or writing words Misplacing things and inability to retrace steps Decreased or poor judgment
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
hemorrhage
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
approaches SBP - perfusion with severe hypoxia/acidosis IICP not evenly distributed throughout the cranial vault
Cerebral Edema
Increase in the fluid (intracellular or extracellular)
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
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
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