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