Ch.16 Flashcards
(46 cards)
1
Q
ALTERATIONS IN COGNITIVE
SYSTEMS
A
Consciousness
* State of awareness of oneself and the environment
* Arousal
* State of awakeness
2
Q
ALTERATIONS IN AROUSAL
A
- Structural
- Divided by location
above or below
tentorial plate
- Divided by location
- Metabolic
- Psychogenic
- Coma is produced by either:
- Bilateral hemisphere damage or suppression
- Brain stem lesions or metabolic derangement that
damages or suppresses the reticular activating system
3
Q
ALTERATIONS IN AROUSAL Clinical manifestations
A
- Level of consciousness changes
- Pattern of breathing
- Posthyperventilation apnea (PHVA)
- Cheyne-Stokes respirations (CSR)
- Pupillary changes
- Oculomotor responses
- Motor responses
- Vomiting, yawning, hiccups
4
Q
BRAIN DEATH (TOTAL BRAIN
DEATH)
A
- Body can no longer maintain internal homeostasis
- Brain death criteria:
- Completion of all appropriate and therapeutic procedures
- Unresponsive coma (absence of motor and reflex
responses) - No spontaneous respirations (apnea)
- No ocular responses
- Isoelectric EEG
- Persistence 6 to 12 hours after onset
5
Q
CEREBRAL DEATH
A
- Cerebral death (irreversible coma) is death of the cerebral hemispheres exclusive of the brain stem and cerebellum
- No behavioral or environmental responses
- The brain can continue to maintain internal
homeostasis - Survivors of cerebral death:
- Remain in coma
- Emerge into a persistent vegetative state
- Progress into a minimal conscious state (MCS)
- Locked-in syndrome
6
Q
ALTERATIONS IN AWARENESS
A
Selective attention:
* Ability to select from available, competing environmental
and internal stimuli
* Sensory inattentiveness
* Extinction
* Neglect syndrome
* Selective attention deficit
* Memory
* Amnesia
* Retrograde amnesia
* Anterograde amnesia
* Executive attention deficits
* ADHD
* Image processing
7
Q
SEIZURES
A
- Syndrome versus disease
- Sudden, transient alteration of brain function caused by an abrupt explosive, disorderly
discharge of cerebral neurons - Motor, sensory, autonomic, or psychic signs
- Convulsion
- Tonic-clonic (jerky, contract-relax) movements associated
with some seizures
- Tonic-clonic (jerky, contract-relax) movements associated
- Epilepsy: a seizure activity with no underlying
cause
8
Q
SEIZURES Etiologic Factors
A
- Cerebral lesions
- Biochemical disorders
- Cerebral trauma
- Epilepsy
9
Q
SEIZURE types
A
- Partial seizures
- Simple (without impairment of consciousness)
- Complex (with impairment of consciousness)
- Secondary generalized (partial onset evolving to
generalized tonic-clonic seizures)
- Generalized seizures
- Absence
- Myoclonic
- Clonic
- tonic-clonic
- atonic
- Unclassified epileptic seizure
10
Q
SEIZURES types con.
A
Aura
* A partial seizure experienced as a peculiar sensation preceding onset of generalized seizure that may take the form of gustatory, visual, or auditory experience or a feeling of dizziness, numbness,
or just “a funny feeling”
Prodroma
* Early clinical manifestations, such as malaise, headache, or sense of depression, that may occur hours to a few days before onset of a seizure
Tonic phase
* State of muscle contraction
Clonic phase
* State of alternating contraction and relaxation of muscles
Postictal phase
* Time period immediately following cessation of seizure activity
11
Q
DATA PROCESSING DEFICITS
A
- Agnosia
- Dysphasia
- Aphasia
12
Q
Agnosia
A
Tactile, visual, auditory, etc.
13
Q
Dysphasia
A
- Expressive dysphasia
- Nonfluent; cannot find words, difficulty writing
- Occlusion of one or several branches of left middle cerebral
artery supplying inferior frontal gyrus
*Receptive dysphasia - Fluent; can produce verbal language but it is meaningless, with inappropriate words, similar sounds or meaning substituted for correct words
- Occlusion of inferior division of left middle cerebral artery
- Transcortical dysphasia
- Ability to repeat and to recite. Speech is fluent but the words make no sense. The individual cannot read or write and has impaired comprehension.
- Occlusion of left middle cerebral artery of left internal carotid
artery
14
Q
Aphasia
A
Inability to communicate (more severe form of dysphasia)
15
Q
ACUTE CONFUSIONAL STATES (ACS)
A
- Transient disorders of awareness that result from
cerebral dysfunction- Secondary to drug intoxication, metabolic disorder, or nervous
system disease - Delirium
- Secondary to drug intoxication, metabolic disorder, or nervous
16
Q
Delirium
A
- Hyperkinetic-acute state of brain dysfunction associated with right upper middle temporal gyrus or left temporal occipital junction disruption and several neurotransmitters are involved
- Difficulty in concentrating, restlessness, irritability, insomnia, tremulousness, and poor appetites. Completely inattentive and perceptions are grossly altered in full state.
- Hypokinetic-More likely to be associated with right sided frontal basal ganglion disruption
- Associated with under activity, (fevers or metabolic disorders), or under the influence of depressants. Decrease mental function, specifically alertness, attention span, accurate perception, interpretation of the environment and reaction to the
environment. Forgetfulness is prominent and the individual
dozes frequently.
17
Q
DEMENTIA
A
- Progressive failure of cerebral functions that is not
caused by an impaired level of consciousness - Losses:
– Orientation
– Memory
– Language
– Judgment
– Decision making
18
Q
ALZHEIMER DISEASE (AD)
A
- Familial, early and late onset
- Nonhereditary (sporadic, late onset)
Theories: - Mutation for encoding amyloid precursor protein
- Alteration in apolipoprotein E
- Loss of neurotransmitter stimulation of choline
acetyltransferase - Neurofibrillary tangles
- Senile plaques
- Diagnosis is made by
ruling out other causes of
dementia
19
Q
ALZHEIMER DISEASE (AD) Clinical Manifestations
A
– Forgetfulness
– Emotional upset
– Disorientation
– Confusion
– Lack of concentration
– Decline in abstraction,
problem solving, and
judgment
20
Q
CEREBRAL HEMODYNAMICS
A
- CBF-Cerebral blood flow
- The brain is normally maintained at ta rate that matches local metabolic needs of the brain
- CPP-Cerebral perfusion pressure (70-90mm hg)
is the pressure required to perfuse the cells of the
brain - CBV-Cerebral blood volume is the amount of blood in the intracranial vault at a give time
- Cerebral oxygenation-is the critical factor and is measured by oxygen saturation in the internal jugular vein
21
Q
INCREASED INTRACRANIAL
PRESSURE (IICP)
A
- Normal 1to 15 mm Hg
- Caused by an increase in intracranial content
– Tumor growth, edema, excessive CSF, or hemorrhage
Stage 1 - Attempt to further decrease IICP
Stage 2 - Continued expansion of intracranial content. May see episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes
Stage 3 - Brain tissues being to experience hypoxia and hypercapnia, condition rapidly deteriorates.
Stage 4 - Brain tissue shifts (herniates) form the compartment of greater pressure to a compartment of lesser pressure. Causing further ischemia and hypoxia in the herniating tissues.
22
Q
CEREBRAL EDEMA
A
- Increase in the fluid (intracellular or extracellular)
within the brain - Types:
- Vasogenic
- Cytotoxic
- Interstitial
23
Q
Vasogenic
A
- The blood brain barrier is disrupted and plasma proteins leak into the extracellular spaces, drawing water to them and increasing the water content of the brain parenchyma.
- Starts in area of injury an spreads
24
Q
Cytotoxic
A
- Toxic factors directly affect the cellular elements of the brain
parenchyma, causing failure of the active transport systems - Cells lose potassium and gain larger amounts of sodium. Water follows by osmosis and the cells swell
25
Interstitial
Seen with noncommunicating hydrocephalus. Caused by
transependymal movement of CSF from the ventricles in the
extracellular spaces of the brain tissues. Brain fluid volume
increases around the ventricles
26
HYDROCEPHALUS
* Excess fluid within the cranial vault, subarachnoid space, or both
* Caused by interference in CSF flow
* Decreased reabsorption
* Increased fluid production
* Obstruction within the ventricular system
27
Noncommunicating hydrocephalus
* Internal
* Intraventricular
* Obstruction iwthin the ventricular system
* More common in children
28
Communicating (extraventricular) hydrocephalus
* Defective resorption of CSF
* More common in adults
29
Acute hydrocephalus
* Develop in a couple of hours in a person who has sustained
head injury
30
Normal-pressure hydrocephalus
* Dilation of the ventricles without increased pressure develops slowly with the individual or family noting declining memory and cognitive function.
* Symptoms of an unsteady, broad-based gait with a history of falling; incontinences; and dementia
31
ALTERATIONS IN NEUROMUSCULAR
FUNCTION
* Muscle tone
* Hypotonia
* Decreased muscle tone
* Hypertonia
* Increased muscle tone
* Spasticity
* Gegenhalten (paratonia)
* attempting to move the limb of a person with paratonia will result in that person involuntarily resisting the movement.
* Dystonia
* Rigidity
32
ALTERATIONS IN MOVEMENT
Paresis and paralysis
* Upper motor neuron syndromes:
* Hemiparesis or hemiplegia
* Diplegia
* Paraparesis or paraplegia
* Quadriparesis or quadriplegia
* Pyramidal motor syndromes
* Spinal shock
Lower motor neuron syndromes:
* Flaccid paresis or flaccid paralysis
* Hyporeflexia or areflexia
* Fibrillation
* Hyperkinesia
* Paroxysmal dyskinesias
* Tardive dyskinesia
* Huntington disease
* Hypokinesia
33
LOWER MOTOR NEURON SYNDROMES
Amyotrophies:
* Paralytic poliomyelitis
* Nuclear palsies
* Guillain-Barré syndrome
* Progressive spinal muscular atrophy
* Progressive bulbar palsy
* Bulbar palsy
34
Hyperkinesia
* Excessive movement
* Chorea, wandering, tremor at rest, postural tremor, etc.
35
Huntington disease
* Also known as chorea
* Autosomal dominant hereditary degenerative disorder
* Severe degeneration of the basal ganglia (caudate
nucleus) and frontal cerebral atrophy
* Depletion of gamma aminobutyric acid (GABA)
36
Hypokinesia
* Decreased movement
* Akinesia
* Bradykinesia
* Loss of associated movement
37
PARKINSON DISEASE
* Severe degeneration of the
basal ganglia (corpus
striatum) involving the
dopaminergic nigrostriatal
pathway
* Parkinsonian tremor, rigidity,
bradykinesia
* Postural disturbances
* Autonomic and neuroendocrine symptoms
* Cognitive-affective symptoms
* Secondary parkinsonism
38
DISORDERS OF POSTURE (STANCE)
* Dystonia
* Dystonic postures and
movements
* Decorticate posture
* Decerebrate posture
* Basal ganglion posture
* Senile posture
39
DISORDERS OF GAIT
* Spastic gait
* Scissors gait
* Cerebellar gait (ataxic)
* Basal ganglion gait
* Senile gait (pseudoparkinsonian gait)
40
DISORDERS OF EXPRESSION
* Hypermimesis
* Hypomimesis
* Dyspraxias and apraxias
41
Hypermimesis
Manifests as pathologic laughter or crying, laughter is
associated with right hemisphere injury and crying is
associated with left hemisphere injury
42
Hypomimesis
Manifests as the loss of emotional language (aprosody)
and is associated with right hemisphere damage
43
Dyspraxias and apraxias
Difficulty in performing tasks requiring motor skills
including speaking, writing, using tools or utensils,
playing sports, following instructions, and focusing
44
EXTRAPYRAMIDAL MOTOR
SYNDROMES
* Basal ganglia motor syndromes
* Cerebellar motor syndromes
45
Basal ganglia motor syndromes
* An imbalance of dopaminergic and cholinergic activity in
the corpus striatum.
* Excess cholinergic activity produces akinesia and
hypertonia.
* Excess of dopaminergic activity produces hyperkinesia
and hypotonia
* Example Parkinson and Huntington
46
Cerebellar motor syndromes
* Associated with ataxia and other symptoms affecting
coordinated movement
* Primarily influence the same side of the body, so that
damage to the right cerebellum generally causes symptoms on the right side of the body
