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91 Cards in this Set

  • Front
  • Back
Assesses level of consciousness
Three ares: eye opening, motor response, verbal response
15 Point Scale
Glasgow Coma Scale
Most critical clinical index of nervous system function
Level of Consciousness
Put in order:
Coma, Lethargy, Obtundation, Disorientation, Confusion, Stupor
Confusion
Disorientation
Lethargy
Obtundation
Stupor
Coma
Loss of ability to think rapidly and clearly
impaired judgement and decision making
Confusion
beginning loss of consciousness;
disorientation to time followed by disorientation to time followed by disorientation to place and impaired mamory;
lost last is recognition of self
Disorientation
Limited spontaneous movement or speech;
easy arousal with normal speech or touch;
may or may not be orientated to time, place, person
Lethargy
Mild to moderate reduction in arousal (awakeness) with limited response to the environment;
falls asleep unless atimulated verbally or tactilely;
answers questions with minimum response
Obtundation
A condition of deep sleep or unresponsiveness from which theperson may be aroused or caused to open eyes only by vigorous and repeatd stimulation;
response is often withdrawal or grabbing at stimulus
Stupor
no verbal response to the external environment or to any stimuli, noxious stimuli such as deep pain or suctioning do not yield motor movement
Coma
associated with purposeful movement on stimulation
Light Coma
associated with nonpurposeful movement only on stimulation
Coma
Associated with unresponsiveness or no response to any stimulus
Deep Coma
Helps evaluate level of brain dysfunction and coma
Patterns of Breathing
(Rate, Rhythm, and Patern)
Regulated by lower brain stem in response to changes in PaCO2
Level of Consciousness
Deep breathing pattern with apnea
Cheyne-Stokes
Increased ventilatory response to CO2;
Results in hypercapnia;
Decreased ventilatory stimulus
Cheyne-Stokes
Indicates the presence and level of brain stem dysfunction;
Altered by drugs
Pupillary Changes
Resting State
Spontaneous Reaction
Reflexive Eye Movements
Varying Levels of Brain Dysfunction Effect
Grasp Reflex
Snout Reflex
Palmomental Reflex
Suck Reflex
Pathologic Reflexes
Maintainenance of abnormal posture during contractions
Increased Muscle Tone
Fasciculations(Parkinson's)
Dystonia
Tremoring Muscles
Fasciculations
Flexion of arms, wrists, and fingers with adduction in upper extremities
Extension, internal rotation, and plantar flexion in lower extremities
Damage to brain stem above the pons
Decorticate Response
All four extremities in rigid extension, with hyperpronation of forearms and plantar extension of feet
Brain stem lesion below the pons
Decerebrate Response
Which is worse and why?
~Decorticate Response
~Decerebrate Response
Decerebrate
The damage is lower on the brain the worse it is
Hypothermia
Acid-base Imbalance
Internal Homeostasis is not maintained
Symptoms of Brain Death
Body works but the brain doesn't
Normal body temperature
Acid-Base Balance
Irreversible Coma
Permanenet Brain Damage
Internal Homeostasis is intact
Cerebral Death
Completion of all appropriate and therapeutic procedures
Unresponsive Coma (no motor or reflex movements
No spontaneous respiration
No ocular responses to head turning or caloric stimulation; dilated fixed pupils
Isoelectric (flat) EEG (electrocerebral silence)
Persistence of these signs for 30 minutes to 1 hour and for 6 hours after onset of coma and apnea
Confirming test indicating absence of cerebral circulation (Optional)
Criteria for Brain Death (Box 14-1)
A sudden, explosive, disorderly discharge of cerebral neurons
Sudden transient alteration of brain dysfunction
Seizure
Any disorder that changes neuro-response
Seizure
Jerky, contract-relax (tonic-clonic) movement of muscle associated with seizures
Side effect of a seizure
Convulsion
Seizure with no underlying cause
Epilepsy
Cerebral Lesions
Biochemical Disorders
Cerebral Trauma
Epilepsy
Etiology of Seizures
Hypoglycemia
Fatigue
Emotional or physical stress
Febrile Illness
Large amounts of water ingestion
Constipation
Drugs (Stimulants; Withdrawal of antidepressants)
Hyperventilation
Environmental Stimulus (Blinking Light, Loud Noises)
Precipitating Factors of Seizures
Siezures that begin locally
Partial Seizures
Without impairment of consciousness
With motor signs
With special sensory or somatosensory symptoms
With autonomic signs or symptoms
With psychic symptoms
Simple Partial Seizure
With impairment of consciousness
Simple partial onset followed by imparied consciousness
Impaired consciousness at onset - with or without automatisms
Complex Partial Seizure
Bilaterally symmetric and without local onset
Generalized Seizures
Partial onset evolving to generalized tonic-clonic seizures
Secondarily Generalized Seizures
Absence
Myoclonic
Clonic
Tonic
Petit Mal Seizures
Tonic-Clonic
Grand Mal Seizures
Atonic
Likely to receive injury
Drop Attack
Relaxed Muscles
Myoclonic
Periods of alternating Contraction and Relaxation of muscles
No Spasms
Clonic
State of muscle contraction with excessive tone
Spasms, Rigid Muscles
Tonic
Periods of alternating contraction and relaxation where the contractions are rigid
Tonic-Clonic
No muscular activity
Atonic
Partial seizure preceding onset of generalized seizure
Gustatory, Visual, or Auditory
Dizziness, Numbness, "Funny Feeling"
Aura
Early clinical signs and symptoms
Malaise, HA, sense of depression hours or days before onset of seizure
Prodroma
Time period immediately following the cessation of seizure activity
Respiratory status returns
Can last hours or days
Postictal Phase
Loss of past memories
Retrograde Amnesia
Inability to form new memories
Anterograde Amnesia
Inability to sustain attention
Inability to set goals
Recognize object meets a goal
Working Memory Deficit (instructions, etc.)
Executive Attention Deficits
Direct destruction by ischemia and hypoxia
Indirect destruction by compression
Toxins and chemical effects
Patho of Executive Attention Deficits
Recognition failure of objects: form and nature
Tactile, visual, or auditory
Agnosia
Alzheimer's Disease
Agnosia
Impairment of comprehension or production of language
Comprehension and use of symbols (written or verbal) is lost
Difficulty speaking or comprehending
Dysphasia
Loss of comprehension or production of language
Inability to speak
Aphasia
Expressive
Receptive
Transcortical
Types of Dysphasia
Nonfluent; cannot find words
Difficulty writing
Expressive Dysphasia
Fluent; meaningless inappropriate words
Unable to monitor language for correctness
Speech may be incomprehensible
Word Salad
Receptive Dysphasia
Echolalia (repeat)
Inability to read and write
Impaired comprehension
Transcortical Dysphasia
Leading cause of severe cognitive dysfunction in older adults
Alzheimer Disease
Diagnosis of exclusion; Based on clinical findings
Autopsy - only was to truly diagnose
Diagnosis Criteria for Alzheimer's Disease
Cortical atrophy and loss of neurons, particularly parietal and temporal lobes "senila plaques"
Presence of amyloid-containing neuritic plaques and "neurofibrillary tangles"
Associated decrease level of choline acetyltransferase activity
Protein in the neurons becomes distorted and twisted, forming a neurofibrillary tangle
Patho of Alzheimer Disease
Lasts 2 - 4 years
Memory loss, subtle personality changes, disorientation time & place
Stage 1 Alzheimer Clinical Manifestations
Confusion stage
Lasts several years
Impaired cognition, restlessness, agitation, irritability
Wandering; Sundowner's Syndrome
Repetitive Behavior
Stage 2 Alzheimer Clinical Manifestations
Terminal Stage
Lasts 1-2 years
Emaciation
Inability to Communication
Bowel and Bladder Incontinence
May have seizures
Disoriented
Wasting Syndrome
Stage 3 Alzheimer Clinical Manifestations
5 to 15 mmHg
Normal Intracranial Pressure (ICP)
Tumor growth, edema, excess CSF, hemorrhage
Causes of ICP
Subtle and transient; episodic confusion, restlessness, drowsiness, slight pupillary and breathing changes
Decreased levels of arousal, widened pulse pressure, bradycardia, pupils small and sluggish
Clinical Symptoms of ICP
Brain herniation into spinal cord
Prolonged effect of ICP
Weakness
Partial paralysis with incomplete loss of muscle power
Loss of fine motor skills
Paresis
Loss of complete motor function
Patients tend to forget the affected part of the body is there
Loss of motor function
Paralysis
Weakness on one side of the body
Hemiparesis
Paralysis on one side of the body
Hemiplegia
Paralysis of both upper or lower extremities
Diplegia
Paralysis of LOWER extremities
Paraplegia
Paralysis of all four extremities
Quadriplegia
First sign/symptoms after spinal cord injury
Spinal Shock
Complete cessation of spinal cord function belowe lesion
Spinal Shock
Characterized by:
Flaccid Paralysis
Absence of Reflexes
Marked disturbances of bowel and bladder
Spinal Shock
Hemiparesis
Hemiplegia
Diplegia
Paraplegia
Quadriplegia
Upper Motor Neuron Syndromes
Loss of voluntary movement despite preserved consciousness and normal peripheral nerve and muscle function
Hypokinesia
Decreased associated and voluntary movements
Akinesia
Slowness of voluntary movements
Bradykinesia
Expressionless Face, Statue-like Posture, Absence of Speech Inflection, Absence of Spontaneous Gestures
CLinical Signs of Hypokinesia
Excessive Movements
Hyperkinesia
Dyskinesias
Paroxysmal Dyskinesias
Tardive Dyskinesias
Categories of Hyperkinesia
Abnormal involuntary movements
Dyskinesias
Abnormal involuntary movements (spasms, tremors)
Paroxysmal Dyskinesias
Involuntary movement of trunk, face, extremities
Usually caused by side effect of prolonged phenothiazine drug therapy
Tardive Dyskinesias