Chapter 15 - Alteration In Cognitive Systems, Cerebral Hemodynamics And Motor Function Flashcards
(180 cards)
1
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Cogntivie behavioural functional competence =
A
Integrated processes of cognitive, sensory and motor systems
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Systems get manifested through motor network =
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Behaviours that are appropriate to human activity
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Full consciousness
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State of awareness of oneself and appropriate responses to envuroennt
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Two components of consciousness
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Arousal (awake) and awareness (thought)
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Structural alterations are divided according to their
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Location of dysfunction
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Supratentorial disorders
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Produce changes in arousal
-above tentorium cerebelli
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Infratentorial disorders
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Produce decline in arousal by dysfunction of reticular activating system or brain stem
-below tentorium cerebelli
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Metabolic alterations
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Disorders procuring a decline in arousal by alterations in delivery of energy substrates
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Five patterns of neurological functions critical to evaluation process
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- Level of consciousness
- Pattern of breathing
- Pupillary reaction
- Oculomotor response
- Motor response
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Msot critical index of nervous system function
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Level of consciousness
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Level of consciousness
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Changes = improvement or deterioration
-person alert/orientated to oneself, place, others, and time
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Level of consciousness: from normal state level it diminishes to
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Confusion —> disorientation —> coma
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Pattern of breathing: normal breathing =
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Rhythmic pattern
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Pattern of breathing: when consciousness diminishes =
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Breathing repsonds to changes in PaCO2 levels
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Cheyne stokes
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Altered periods of tachypnea and apnea directly related to PaCO2
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Apneusis
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Prolonged inspiratory time and a pause before expiration
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Ataxic breathing
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Complete irregularity of breathing with increasing periods of apnea
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Pupillary reaction indicates..
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Indicate presence or level of brain stem dysfunction
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Brain stem area controlling arousal is adjacent
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To area controlling pupils
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Pupillary reaction in ischemia
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Dilated or fixed pupils
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Pupillary reaction in hypothermia/opiates
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Cause pinpoint pupils
22
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Oculomotor response :
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Resting, spontaneous and reflexive eye movements change at various levels of brain dysfunction
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Oculomotor response : normal response
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Eyes move together to side opposite from turn of head
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Oculomotor response : abnormal response
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Eyes do not turn together
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Oculomotor response : absent response
Eyes move in direction of head movement
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Oculomotor response : caloric ice water test
Ice water injected into ear canal
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Oculomotor response : caloric ice water test: normal response
Eyes turn together to side of head where ice injected
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Oculomotor response : caloric ice water test : abnormal response
Eyes do not move together
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Oculomotor response : caloric ice water test : absent response
No eye movement
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Motor responses determine
Brain dysfunction and indicates most severely damaged side of brain
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Motor response: pattern of response may be
1. Purposeful
2. Inappropriate or generalized movement
3. Not present
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Motor signs indicating loss of cortical inhibition =
Decreased consciousness
-associated with performance of primitive reflexes and rigidity
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Paratonia
Rigidity
-involuntary resistance during passive movement
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Vomiting, yawing and hiccups
Complicated reflex like motor responses integrated in brain stem
-dysfunction of medulla oblong = compulsive and receptive production of these responses
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Coma Outcomes depend on
Cause, damage, and duration of coma
-some individuals never retain consciousness and experience neurological death
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Brain death
-total brain death
Brain damaged—> irreversible —> cannot maintain homeostasis
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NDD
Neurological determination of death
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Canadian criteria for NDD
1. Unresponsive coma
2. No brain stem function
3. No spontaneous respiration
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Canadian criteria for NDD
1. Unresponsive coma
2. No brain stem function
3. No spontaneous respiration
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Cerebral death
Irreversible coma
-death of cerebral hemispheres (except for brain stem and cerebellum = remains homeostasis)
-permanent brain damage -> never responds in significant way
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Persistent vegetative state
Complete unawareness of self or environment
-no speak or cerebral function
-sleep wake cycles present
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MSC or minimally conscious state
Follow simple commands, manipulate object and give yes or no responses
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Locked in syndrome
Complete paralysis of voluntary muscles except eye movement
-thought and arousal = fully conscious
-blinking is communication
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Awareness if mediated by
Executive attention networks (EAN)
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EAN networks
Selective attention, memory
-abstract reasoning, planning, decision making judgement and self control
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Selective attention
Ability to select specific information and focus on related specific task
-visual and auditory
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Executive attention deficits: initial detection
Person fails to stay alert and orientate to stimuli
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Executive attention deficits: mild deficit
Grooming and social graces are lacking
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Executive attention deficits: severe deficit
Motionless, lack of response, doesn’t react with surroundings
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Characteristics of executive attention deficits
Inability to maintain sustained attention
-inability to set goals and recognize when goal is achieved
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Amnesia
Loss of memory
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Retrograde amnesia vs anterograde amnesia
RETROGRADE- difficulty retrieving past memories
ANTEROGRADE- inability to form new memories
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Data processing deficits
Problems associated with recognizing and processing sensory information
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Agnosia
Defect of pattern recognition, form and nature of objects
-only one sense is affected
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Agnosia is associated with
Cerebrovascular accidents to specific brain areas
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Example of Agnosia
Unable to identify a safety pin by touching it but able to name it when looking at it
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Dysphasia
Impairment of comprehension or production of language
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Expressive dysphasia
Broca dysphasia
-loss of ability to produce spoken or written language
-verbally competent
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Receptive dysphasia
Wernicke dysphasia
-inability to understand written or spoken language
-speech is fluent but has no meaning
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Pathology of dysphasia
Occlusion of middle cerebral artery
-which is one of three major arteries supplying blood to brain
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Acute confusional states and delirium
Transient disorders of awareness and may have a sudden or gradual onset
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Causes of Acute confusional states and delirium
Drug intoxication, alcohol withdrawal, post anesthesia, electrolyte imbalance
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Pathophysiology of Acute confusional states and delirium
Disruption of reticular system, thalamus, cortex and limbic system
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Delirium most commonly occurs in
Critical care units over 2-3 days
-disruption of acetylcholine and dopamine
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Delirium
Hyperactive acute confusional state
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Excited delirium syndrome
Hyperkinetic can lead to sudden death
-rapid breathing, high pain tolerance, superhuman strength
“Agitated delirium”
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Manifestations of Acute confusional states and delirium
Terrifying dreams, hallucination, gross alternation of perception
-cannot sleep
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Evaluation for Acute confusional states and delirium
CAM-ICU or confusion assessment method for intensive care unit
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Dementia
Deterioration/progressive failure of many cerebral functions
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Cause of dementia
Cerebral neuron degeneration, atherosclerosis and genetics
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Dementia manifestations
-no cure exists
-maximizing remaining capacities
-help family to understand
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What is the Leading cause of severe cognitive dysfunction in older aldutls
Alzheimer’s (exact cause unknown)
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Three forms of Alzheimer’s
1. Non hereditary
2. Early onset familial
3. Early onset AD
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Non hereditary sporadic
-late onset 70 to 90 percent
-most common form
-no specific genetic association
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Early onset familial AD
Linked to chromosomal 21 mutations
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Early onset AD
Very rare
-linked to chromosomal 19 mutations
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Pathology of AD
Accumulation of toxic fragments of amyloid plagues
-loss of acetylcholine in forebrain cholingeric neurons causing death
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Pathology of AD
Accumulation of toxic fragments of amyloid plagues
-loss of acetylcholine in forebrain cholingeric neurons causing death
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Amyloid plagues
Aggregates of midfolded proteins
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After death of neurons in AD, what occurs
Tau proteins from neuroofibrillary tangles within the neuron, increasing neural death
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Where are neruofibrillary tangles concentrated
In cerebral cortex
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AD brain atrophy occurs via
Widening of sulcus (grooves) and shrinking gyrus (folds on outermost of brain)
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First symptom of AD
Memory loss and impaired learning
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Continuation of symptoms in AD
Language, reasoning, social behaviour, dyspraxia
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Dyspraxia
Loss of movement and coordination
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Pathophysiological changes can occur ___ before dementia syndrome
Decades
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Second most common form of dementia
Frontotemporal dementia otherwise known as pick disease
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Frontotemporal dementia (3)
Umbrella term for affecting frontal and temporal regions of brain
-mutation of tau encoding genes
-genetic, onset within <60 yoa
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First symptom of Frontotemporal dementia
Apathy, poor judgment and reasoning, break laws
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Seizures represent
Manifestation of disease, not a specific disease entity
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Seizure
Sudden disruption in brain electrical function caused by abnormal discharge of cortical neurons
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Epilepsy
Recurrence of seizures where no known cause for seizures can be found
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Convulsion
Jerky, contact relax movements associated with seizures
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Probable causes of seizures in YA
Alcohol, drug withdrawl, brain tumour, perinatal insults
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Probable causes of seizures in OA
Alcohol, drug withdrawl, metabolic disorders, CNS degeneration
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Focus
Brain site where seizure originates
-epileptogenic zone
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Epileptogenic focus
Neurons are hypersensitive and activates by numerous stimuli
-fire more frequently and w greater amplitude
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How can focus be determined during a seizure
Activated SPECT
-detecting blood flow changes in brain
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Tonic phase
Muscle contraction with inc muscle tone
-loss of consciousness
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Clonoc phase
Alternating contraction and relaxation of muscles
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Clonic phase begins when
Inhibitory neurons in thalamus and basal ganglia react to cortical excitation
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Clonic phase: seizure discharge is interrupted =
Intermittent contractions that diminish and finally cease
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Inc in # of seizures =
Inc in brain damage
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Seizure cessation is due to
Epileptogenic neurons being exhausted
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What happens when the brain has reduced oxygen
Switches to anaerobic metabolism and an accumulation of lactic acid
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Normal intracranial pressure
1-15 mmHg
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ICP results from increase in
Intracranial content
-tumour, deems, hemorrhage
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Inc content =
Something must be removed
-displacement of cerebral spinal fluid
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Continued high ICP =
Alterations cerebral blood volume and blood flow
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Four stages of ICP leads to
Death
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ICP stage one
Cranial vasoconstriction and systemic adjustment result in a decrease in ICP
-no detectable symptoms
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ICP stage 2
ICP exceeds compensatory mechanisms
-pressure affects neuron oxygenation
-confusion, restlessness, lethargy
-pupil + breathing normal
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Stage 2: surgical intervention is
Best here
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Auto regulation
Mechanism to alter diameter of intracranial blood vessels to maintain constant blood flow during changes in ICP
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Stage 3
-auto regulation is lost, approaches arterial pressure
-pupils: small, sluggish
-widening of pp
-loss of peripheral vision/blindness, tinnitus
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Stage 3
-auto regulation is lost, approaches arterial pressure
-pupils: small, sluggish
-widening of pp
-loss of peripheral vision/blindness, tinnitus
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Stage 3: surgical intervention is
Needed here
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ICP stage 4
Brain tissue shifts (herniates = inc ICP)
-reduction in blood supply
-pupils: bilateral dilation+fixation
-Cheyenne stokes
-progress to coma
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Surgical intervention in stage 4
Futile here, death occurs
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Most important type of cerebral edema
Vasogenic edema
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Brain edema
Lateral ventricles compressed
-gyri are flattened
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Causes of vasogenic edema
Increased capillary permeability, disruption of BBB
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Vasogenic edema
Plasma proteins and fluid leak into cranial ECF
-accumulates in white matter = separation of myelinated fibres
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Manifestation of vasogenic edema
Consciousness disturbances and increases in ICP
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Vasogenic edema resolution
Slow diffusion
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Cytotoxic edema
Toxic factors affects neural glial and endotherlial cells causing loss of active transport mechanisms
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Cytotoxic edema: loss of K+ and gain large amounts of Na+ causing…
Change in intracellular osmolarity and cells swell
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Interstitial edema
Movement of cerebral spinal fluid from ventricles into interstitial space
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Result of interstitial edema
Fluid volume increases around ventricles = inc pressure within white matters = disappearance of myelination
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Result of interstitial edema
Fluid volume increases around ventricles = inc pressure within white matters = disappearance of myelin at ion
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Hydrocephalus
Excess CSF in ventricles or subarachnoid space
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Cause of hydrocephalus
Inc CSF production, obstruction in ventricles, defective reabsorption of CSF fluid into systemic blood
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Communicating hydrocephalus
Infancy through adulthood
-impaired absorption of CSF from subarachnoid space
Usually due to infection
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Non communicating hydrocephalus
Adults
-obstruction of CSF between ventricles
Cause: congenital (present since birth)
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The word communicating refers to the fact that CSF can
Still flow between ventricles
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Obstruction of CSF flow =
Inc pressure and dilation of ventricles
-atrophy of cerebral cortex and degeneration of white matter
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Manifestation of acute HC
Rapidly developing ICP
-deep coma
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Manifestation of acute HC
Rapidly developing ICP
-deep coma
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Manifestation of normal pressure HC
Dilation of ventricles w/o inc pressure
-slow development
-decline in memory
-triad symptom progression
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TX HC
shunt procedure
-ventricular bypass into normal intracranial channels where fluid is absorbed
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___ is one of three most common neurosurgical procedures
Shunting
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Normal muscle tone is
Having slight resistant to passive movement
-resistant is smooth consistent and even
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Hypotonia
Dec muscle tone
-tire easily, have difficulty rising from sitting position
-muacsle mass atrophy, flabby and flat
-hyper flexible joints
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Hypertonia
Inc muscle tone
-increased resistance
-enlargement, firm muscles and muscle spams
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Two major causes for alterations in muscle movement
1. Dopamine (too little or too much)
2. Neurological disorders (excessive or insufficient movement)
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Two major causes for alterations in muscle movement
1. Dopamine (too little or too much)
2. Neurological disorders (excessive or insufficient movement)
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Hyperkinesia
Excessive, purposeless movement
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Paroxysmal dyskinesias
Involuntary movements that occur as spasms
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Tardive dyskinesias
Involunatary movement of face lips tongue and extremities
-antipsychotic medication
-rapid receptive stereotypical movements (chewing or tongue protrusions)
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Common example of tardive dyskinesias
Tourette syndrome
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Ballism
Muscle disorder with wild flinging movement of limbs
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Huntingtons disease (chorea)
hyperkinesia
-involves basal ganglia and cerebral cortex
25-45 yoa
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Manifestations of HD
Face and arms (eventually whole body)
-slow thinking, euphoria and depression
-involuntary fragmented movements
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Pathophysiology of huntingtons disease
Autosomal dominant trait
-mutant in chromosome 4 = abnormally long protein due to CAG trinucleotide
-alters aa = protein toxic to neurons
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Age of disease onset =
Number of recreated amino acids chains
-increased chains = inc toxicity of protein = earlier age of onset
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Hyperkinesia
Loss of voluntary moment despite preserved consciousness
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Akinesia
Lack of spontaneous movement (facial expressions) or associated movements (arm swinging while talking)
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Bradykinesia
Slowing of performed movements
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Parkinson’s disease
Complex motor disorder accomplished by systemic non motor and neurological symptoms
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Primary PD
Begins after 40 yoa with inc incidence after 60 yoa
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Primary PD
Begins after 40 yoa with inc incidence after 60 yoa
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What is the leading cause of neurological disability in people over 60 yoa
Primary PD
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Secondary PD
Parkinson’s caused by disorder other than PD
-head trauma, infections, toxins, medication intoxication
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What is the most common cause of secondary PD
Medicication intoxication
-reversible
165
Medication intoxication PD is caused by
-neuroleptics (antispychotics, hallucinations, delusions)
-antiemetics
-anti hypertensives
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Pathophysiology of PD
Several gene mutations
-basal ganglia dysfunction due to msifolded proteins
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Result of PD
Loss of dopamine producing neurons in substantial nigra
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PD: loss of
Dopamine and excess production of cholinergic = symptoms of muscle tremors and rigidity
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Dopamine vs cholinergic
D- inhibitory
C- excitatory
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What are the tell tale symptoms of abnormal movement in Parkinson’s
Muscle tremors and rigidity
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Classic manifestations of PD
Resting tremor, rigidity, bradykinesia, dysarthria
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Dysaerthria
Loss of control of muscles you speak with
-slurring of speech
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Early symptom of PD
Loss of smell
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Disorders of equilibrium in PD
PD can’t make appropriate postural adjustments to tilting
-falls like a post
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Lou Gehrig’s disease
Degeneration of both lower and upper motor neurons
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Upper ALS
-Dec in large motor neurons in CNS
-motor neuron death = demyelination and glia proliferations, sclerosis
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Upper Lou gherig
-Dec in large motor neurons in CNS
-motor neuron death = demyelination and glia proliferations, sclerosis
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Lower lou gherig
Enervation of motor units
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Manifestations of lou gehrig
Muscle weakness in arms and legs, that progresses to speaking and swallowing
-no mental or sensory symptoms
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TX for lou gherig
Medication rilutek extends time before ventilator assistance is required
