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INSTANT PDF DOWNLOAD. NU 545 Unit 2 Study Guide. Focused summary of key concepts, lecture highlights, and exam-relevant material. Structured to reinforce understanding, identify weak areas, and prepare confidently. Perfect for efficient last-minute review. NU 545 unit 2, NU 545 study guide, Nursing unit 2 exam, NU 545 practice questions, NU 545 2026, NU 545 test bank, NU 545 rationales, Nursing study guide, NU 545 exam review, NU 545 practice test, NU 545 Q&A, NU 545 nursing, Unit 2 study guide, NU 545 foundations, NU 545 review, NU 545 preparation
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Study Guide Unit 2
CHAPTER 15
(eBook key search term: “limited to myelinated fibers” ) Mature neurons do not divide and injury in the CNS causes permanent loss of damaged neurons. Crushed nerves recover better than cut nerves. Peripheral nerves can repair themselves through axonal reaction Local changes occur when the axon is severed
Functional areas of the cerebral cortex (midsagittal view)
(prosencephalon) Telencephalon Frontal Lobe Prefrontal area Goal-oriented behavior,^ short term memory, concentration ,^ elaboration of thought , and inhibition on limbic area (emotional region of the brain) Premotor area (Brodmann area 6)
Programs motor movement (contains cell bodies that form part of the basal ganglia system - extrapyramidal system); controls eye movement (Brodmann area 8; middle frontal gyrus) Primary motor area (Brodmann area 4)
Primary voluntary motor = somatotopic organization (Homunculus = little man); Cerebral cortex central impulses control the opposite side of the body = contralateral control Broca speech area (Brodmann area 44, 45) **most important in the left hemisphere
Motor aspect of speech ; speech and language processing area; dysfunction (damage from CVA) may result in inability to form words expressive aphasia or dysphasia
Parietal Lobe Somatic sensory input (Brodmann areas 3, 1, 2)
Provides communication between motor and sensory areas; storage, analysis, and interpretation of stimuli Temporal Lobe Primary auditory cortex (Brodmann area 41) Wernicke area (Brodmann area 22)
Sensory speech area; responsible for reception and interpretation of speech (superior temporal gyrus) ; dysfunction / damage may result in receptive aphasia or dysphasia Secondary function of balance Memory consolidation and smell Occipital Lobe Primary visual cortex (Brodmann area 17)
Receives input from the retinas
Remainder of lobe Visual association (Brodmann areas 18, 19) Corpus Callosum Bundle of myelinated fibers that connects the two cerebral hemispheres (conveying contralateral projection) which is essential in coordinating activities between hemispheres Limbic System Located between the telencephalon and diencephalon and surrounding the corpus callosum
Mediates emotion and long-term memory through connections in the prefrontal cortex
Controls vital functions and visceral activities Closely associated with the limbic system
Thalamus Largest component of the diencephalon; surrounds the third ventricle
Major center for afferent (SENSORY) impulses to the cerebral cortex Cortical processing = interpretation of sensations Relay center for information from the basal ganglia and cerebellum to appropriate motor area Hypothalamus Forms ventral part Main functions: (a) Maintains constant internal environment; (b) implements behavioral patterns Visceral and somatic responses Affectual responses Hormone synthesis (endocrine function) Sympathetic / Parasympathetic control (autonomic nervous system function) Body temperature regulation Feeding responses Regulation of physical expression of emotions Sexual behavior Pleasure-punishment centers Level of arousal or wakefulness Subthalamus Lateral to hypothalamus Important basal ganglia center for motor activities
Reticular Formation (Brainstem)
Prefrontal area (F) Broca speech area (F) Wernicke area (F)
Regulates vital reflexes (cardiovascular function and respiration)
Essential for maintaining wakefulness.
Goal-oriented behavior (i.e. ability to concentrate)
Short-term or recall memory
Elaboration of thought
Inhibition on the limbic (emotional) areas of the CNS.
Motor aspects of speech (usually on left hemisphere);
Damage to this area (ex. CVA) results in inability to form words, called expressive aphasia or dysphasia****.
Reception and interpretation of speech (superior temporal gyrus)
Damage to this area results in difficulty understanding words or written language, called receptive aphasia or dysphasia.
Limbic system (F) Hypothalamus (F) Cerebellum (H) Temporal Lobe (F) Primitive behavioral responses
Visceral reaction to emotion
Feeding behaviors
Biologic rhythms
Sense of smell
Expression of affect (emotional and behavioral states)
Consolidation of memory
Maintenance of a constant internal environment
Implementation of behavioral patterns
Integrative centers control function of the ANS
Regulation of body temperature
Regulation of endocrine system
Regulation of emotional expression.
Conscious and unconscious muscle synergy
Maintaining balance and posture
Damage to the cerebellum is characterized by ipsilateral (same side) loss of equilibrium, balance, and motor coordination
Secondary function of balance
(eBook key search term: “cognitive cerebral function) The neural systems essential to cognitive function are: a. Attentional systems that provide arousal and maintenance of attention over time b. Memory and language systems by which information is communicated c. Affective or emotive systems that mediate mood, emotion, and intentions.
Cognitive cerebral functions require a functioning reticular activating system regulates aspects of attention, information processing, and maintains consciousness.
Awareness (content of thought) encompasses all cognitive functions (including awareness of self, environment, and affective states – moods) Awareness is mediated by the core networks (selective attention and memory) under the guidance of executive attention networks (the networks that involve abstract reasoning, planning, decision making, judgment, error correct, and self-control) Each attentional function is not localized in a single brain area but is a network of interconnected brain circuits.
Prefrontal cortex is involved in cognitive functions such as planning and evaluating outcomes, and consequences for actions The prefrontal area mediates several cognitive functions (executive attention functions – planning, problem solving, goal-setting) o It is responsible for goal-oriented behavior (i.e., ability to concentrate), short-term or recall memory, and elaboration of thought and inhibition on the limbic (emotional areas of the CNS)
(eBook key search term: “ lower portion of Brodmann area 8” and “from midbrain and exit”) Six extrinsic eye muscles (attached to the outer surface of each eye) allow gross eye movements and permit the eyes to follow a moving object. These muscles arise from the common tendinous ring in the orbit, the eye cavity, and attach to the eyeball. The six muscles are: lateral, medial, inferior and superior rectus muscles, and the inferior and superior oblique muscles. The muscles, when contracting, cause movement of the eyeball, by pulling the eyeball towards the muscle.
The frontal eye fields (the lower portion of Brodmann area 8 ), which are involved in controlling eye movements , are in the middle frontal gyrus.
The superior colliculi of the midbrain are involved with voluntary and involuntary visual motor movements (e.g. the ability of the eyes to track moving objects in the visual field). Abnormal ocular movements occur because of oculomotor, trochlear, or abducens cranial nerve dysfunction (e.g., strabismus, nystagmus, and paralysis of individual extraocular muscles)
o Oculomotor: fibers emerge from midbrain (oculomotor nucleus) o Trochlear: fibers emerge from posterior midbrain (trochlear nucleus) o Abducens: fibers leave inferior pons (abducens nucleus)
The occipital lobe lies caudal to the parietooccipital sulci and superior to the cerebellum. The primary visual cortex (Brodmann area 17) is in this region and receives input from the retinas. Much of the remainder of this lobe is involved in visual association (Brodmann areas 18, 19).
(eBook key search term: “ nigra which synthesizes”) The midbrain is primarily a relay center for some motor and sensory tracts, as well as a center for auditory and visual reflexes, temperature control, sleep-wake cycles, arousal, and attention. Damage to the midbrain can result in a wide variety of movement disorders , difficulty with vision and hearing , and trouble with memory.
1. Corpora Quadrigemina (Tectum – roof of the midbrain): a. Disorders of selective attention related to visual orienting behavior are produced by disease that involves portions of the midbrain i. Superior colliculi: responsible for involuntary and voluntary visual motor movements (i.e. ability to track moving objects in the visual field); disease manifests as slowness in orienting attention ii. Inferior colliculi: responsible for movement affecting the auditory system (i.e. positioning head to improve hearing); relay center along the auditory pathway 2. Tegmentum (floor of the midbrain): a. Red nucleus: receives ascending sensory information from the cerebellum minor motor pathway (rubrospinal tract) cervical spinal cord b. Substantia nigra (inferior portion of the basal ganglia): synthesizes dopamine (neurotransmitter and precursor of norepinephrine); dysfunction of this structure is associated with Parkinson’s Disease, drug addiction, schizophrenia, Huntington’s disease, and multi-system atrophy c. Cerebral peduncles (anterior midbrain): made up of efferent fibers of the corticospinal, corticobulbar, and corticopontocerebellar tracts (tracts that link the cortex to the brainstem). d. Cerebral aqueduct (Aqueduct of Sylvius): carries CSF between 3rd / 4th ventricle obstruction hydrocephalus
Because the midbrain houses the hypothalamus, it also plays a major role in automatic body functions. Other notable structures include: Nuclei of the third and fourth cranial nerves (pupils) mid-position pupils CNS damage or disease affecting lower midbrain Central reflex hyperpnea (brainstem breathing pattern) Severe damage to midbrain/upper pons decerebrate (abnormal posturing – internal rotation with hyperpronation of forearms) Damage to tegmentum near hypothalamus and third ventricle akinetic mutism (neither to move [akinesia] nor speak [mutism])
Syndromes associated with midbrain pathology include the Weber, Claude, Benedikt, Nothnagel, and Parinaud syndromes Parkinsonism is a neurologic condition characterized by tremors, rigidity, hypokinesia , and postural instability because of degeneration of the corpus striatum or substantia nigra.
(eBook key search term: “ CSF is a clear”) CSF is a clear, colorless fluid like blood plasma and interstitial fluid. Intracranial and spinal cord structures float in the CSF and are thereby partially protected from jolts and blows , and the buoyant properties of CSF also prevent the brain from tugging on meninges, nerve roots, and blood vessels.
(eBook key search term: “ the arachnoid villi protrude”) Protrude from the arachnoid space, through the dura mater, and lie within the blood flow of the venous sinuses. The villi function as one-way valves, directing CSF outflow into the blood but preventing blood into the subarachnoid space.
(eBook key search term: “ choroid plexuses in the lateral”) The choroid plexus (rich network of blood vessels supplied arising from the pia mater) function to produce cerebrospinal fluids (CSF) Lies in close contact with ventricular ependymal cells Tight junctions of the choroid blood vessel providing a limiting barrier between the CSF and blood that functions similarly to the Blood-Brain Barrier CSF does not accumulate and is reabsorbed by means of a pressure gradient between the arachnoid villi and the cerebral venous sinuses. – it is reabsorbed into the venous circulation through the arachnoid villi , primarily located superior to the falx cerebri in the superior sagittal sinus. Thus, CSF is derived from the blood, and after circulating throughout the CNS, it returns to the blood.
(eBook key search term: “ blood supply to the brain”)
CHAPTER 16
(eBook key search term: “ GCT integrates”) Gate control theory (GCT) integrates and builds upon features of other theories (specificity theory, pattern theory, etc.) to explain the complex multidimensional aspects of pain perception and pain modulation.
Pain transmission is modulated by a balance of impulses conducted to the spinal cord where cells in the substantia gelatinosa function as a “gate” – spinal gate that regulates pain transmission to higher centers in the CNS Nociceptive transmission (mechanical, thermal, and chemical) opening of the gate transmit the perception of pain o Large myelinated A-delta fibers and small, unmyelinated C fibers terminate on interneurons in the substantia gelatinosa (laminae in the dorsal horn of the spinal cord) Non-nociceptive stimulation (from touch sensors in the skin; rubbing a painful area) closure or partial close of the spinal gates decreased pain perception: o Larger A-beta fibers
(eBook key search term: “ lightly myelinated medium ”)
Nociceptors ( primary order neurons) are free nerve endings in the afferent PNS that selectively respond to different chemical, mechanical and thermal stimuli. When stimulated they cause nociceptive pain. Nociceptors are categorized according to the stimulus to which they respond and by the properties of the axons associated with them. Nociception has four phases: transduction, transmission, perception, and modulation. A-delta fibers are lightly myelinated, medium-sized fibers that are stimulated by severe mechanical deformation or by mechanical deformation and/or extremes of temperature. o Transmit sharp, well-localized “fast” pain sensations o Cause reflex withdraw of affected body part from the stimulus BEFORE a pain sensation is perceived (i.e. pulling a hand away from a hot stove) Unmyelinated C fibers are smaller, unmyelinated polymodal fibers; stimulated by mechanical, thermal, and chemical nociceptors o Slowly transmit dull, aching, or burning sensations that are poorly localized and longer lasting A-beta fibers are large myelinated fibers o Transmit touch and vibration sensations o Do NOT normally transmit pain but play a role in pain modulation
(eBook key search term: “ coming into the gate ”)
Nociceptors are free nerve endings in the afferent peripheral nervous system that selectively respond to different chemical, mechanical, and thermal stimuli.
A-delta and C fibers comprise the primary, first-order sensory afferents coming into the gate at the dorsal horn of the spinal cord. o A-delta fibers: lightly myelinated, medium-sized fibers that are stimulated by severe mechanical deformation (mechanonociceptors) or by mechanical deformation and/or extremes of temperature (mechanothermal nociceptors). Rapidly transmit sharp, well-localized “fast” pain sensations. Responsible for causing reflex withdrawal of the affected body part from the stimulus before a pain sensation is perceived. Unmyelinated C fibers: polymodal; stimulated by mechanical, thermal, and chemical nociceptors. o Slowly transmit dull, aching, or burning sensations that are poorly localized and longer lasting.
Pain transmission is the conduction of pain impulses along the A-delta and C fibers into the dorsal horn of the spinal cord and brainstem, thalamus, and cortex. Note: A-beta fibers are large, myelinated fibers that transmit touch and vibration sensations; they do not normally transmit pain but play a role in pain modulation.
(eBook key search term: “ conscious awareness of pain ”) Define Pain perception: the conscious awareness of pain that occurs primarily in the reticular and limbic systems and the cerebral cortex. Three systems interact to produce the perception of pain and individual responses to pain:
(eBook key search term: “ pain threshold is the point ”) Pain threshold: the point at which a stimulus is perceived as pain and it does not vary significantly among people or in the same person over time Intense pain at one location may increase threshold in another location – perceptual dominance – therefore, pain at one site may mask other painful areas Generally DECREASED with repeated exposure to pain
Pain tolerance: the duration of time or the intensity of pain that an individual will endure before initiating overt pain responses Generally decreased by person’s cultural perceptions, expectations, role behaviors, physical and mental health, gender, age, fatigue, anger, boredom, apprehension, and sleep deprivation. Tolerance may be INCREASED by alcohol consumption, persistent use of pain medication, hypnosis, warmth, distracting activities, and strong beliefs or faith
(eBook key search term: “ GABA and glycine ”) Define: family of morphine-like neuropeptides that inhibit transmission of pain impulses in the spinal cord, brain, and periphery
Their receptors play a role in various CNS, GI system, immune system, and other organ system disorders.
There are 4 types of opioid neuropeptides (substances that act as neurotransmitters by binding to one or more G-protein-coupled opioid receptors):
(eBook key search term: “ it begins suddenly ”)
Epinephrine causes vasoconstriction (improves thermal regulation), stimulates glycolysis, and increases metabolic rate, thus increasing body heat. Heat is distributed by the circulatory system.
(eBook key search term: “ produce heat through two ”) In human, body temperature is maintained around 37C (98.6F) and rarely exceeds 41C. The normal range is 36.2C to 37.7C. Temperature regulation (thermoregulation) is mediated by the hypothalamus; peripheral thermoreceptors in the skin and abdominal organs (unmyelinated C fibers and thinly myelinated A-delta fibers) and central thermoreceptors in the spinal cord and trigeminal ganglia provide the hypothalamus with information about skin and core temperatures. HEAT PRODUCTION HEAT LOSS a. Chemical reactions of metabolism: the chemical reactions that occur during ingestion and metabolism of food and those required to maintain the body at rest (basal metabolism) require energy and produce heat. These processes occur in the body core (primarily the liver) and are in part responsible for the maintenance of core temperature.
b. Skeletal muscle contraction: produces heat through two mechanisms (both which are controlled by the posterior hypothalamus and occur in response to cold ): i. Gradual increase in muscle tone. ii. Production of muscle oscillations – shivering; which does not occur in neonates)
c. Chemical thermogenesis : also called nonshivering or adrenergic thermogenesis; results from release of epinephrine and norepinephrine a rapid, transient increase in heat production by raising the body’s basal metabolic rate. i. Occurs in brown adipose tissue (rich with mitochondria and blood vessels) and is essential for nonshivering thermogenesis.
a. Radiation: heat loss through electromagnetic waves ; these waves emanate from surfaces with temperatures higher than the surrounding air temperature. (temperature of the skin is higher than that of air, the skin and the body lose heat to the air) b. Conduction: heat loss by direct molecule-to-molecule transfer from one surface to another , with warmer surfaces losing heat to cooler surfaces. (skin loses heat through direct contact with cooler air, water, or another surface) c. Convection: the transfer of heat through currents of gases or liquids and occurs passively as warmer air at the surface of the body rises away from the body and is replaced by colder air i. Process may be aided by fans or wind combined effect of conduction and convection by wind is conventionally measured as the wind-chill factor. d. Vasodilation: peripheral vasodilation increases heat loss by diverting core-warmed blood to the surface of the body. As the core-warmed blood passes through the periphery, heat is transferred by conduction to the skin surface and from the skin to the surrounding environment. i. Occurs in response to autonomic stimulation under the control of the hypothalamus. e. Decreased muscle tone: to decrease heat production, muscle tone may be moderately reduced and voluntary muscle activity curtailed; this may explain in part the “washed-out” feeling associated with high temperatures and warm weather. f. Evaporation: evaporation of body water from the surface of the skin and the linings of the mucous membranes is a major source of heat reduction****. Insensible water loss accounts for about 600ml of water loss per day. Sweating may result in 2.2L of fluid lost per hour. Electrolytes are also lost. Large volume loss through sweating may result in decreased plasma volume, decreased BP, weakness, & fainting. Heat loss by sweating/evaporation is affected by: i. Sympathetic neural activity. ii. Favorable temperature difference between the body and the environment. iii. Humidity: when high, sweat does not evaporate and instead remains on the skin or drips, when low, evaporates quickly. g. Increased pulmonary ventilation: exchanging air with the environment through the normal pulmonary ventilation provides some heat loss, although it is minimal in humans. This normal process occurs faster at higher body temperatures through and increase in ventilator rates; thus, hyperventilation is associated with hyperthermia. h. Voluntary mechanisms: in response to high body temperatures, people physically “stretch out,” thereby increasing the body surface area available for heat loss. They also “take it easy,” thereby decreasing skeletal muscle work,
and they “dress for warm weather” in garments that reflect heat and promote convection, conduction, and evaporation (light-colored, loose-fitting clothes). i. Heat adaptation: the body of an individual who goes from a cooler to a much warmer climate undergoes a period of adjustment, a process that takes several days to several weeks.
(eBook key search term: “ heat exhaustion or collapse ”) HEAT EXHAUSTION / COLLAPSE HEAT STROKE Most common heat related injury; result of prolonged high core or environmental temperatures. High temperatures cause the appropriate hypothalamic response of profound vasodilation and profuse sweating (prolonged period) produce dehydration, decreased plasma volumes hypotension, decreased cardio output, and tachycardia
S/S: Individual feels weak, dizzy, nauseated, and faint. Ceasing activity = decreases muscle work decreased heat production and lying down redistributes vascular volume. Should be encouraged to drink warm fluids to replace fluid lost through sweating.
Rectal temp > 41C or 106F; a potentially lethal result of breakdown in control of an overstressed thermoregulatory center.
Causes/Patho: overexposure to environmental heat or impaired physiologic mechanisms for heat loss sweat cools the person starting with the face and forehead, and fanning the face enhances this mechanism brain cannot tolerate temperatures greater than 40.5C (104.9F) cardiovascular and thermoregulatory system stops functioning body’s heat loss mechanisms fail sweating ceases (skin becomes dry and flushed; irritability, confusion, stuporous, comatose with possible visual disturbances)
Continued progression high core temperatures and vascular collapse cerebral edema, degeneration of the CNS, swollen dendrities, renal tubular necrosis, hepatic failure with delirium, multi-system organ failure
Coma or death results unless immediate, effective treatment is initiated
Treatment: remove from warm environment, use cooling blankets or cool water bath, or ice packs on head, neck, axillae, and groin area. *Care must be taken to prevent too rapid cooling of the surface, which causes peripheral vasoconstriction and prevents core cooling.
Children more susceptible to heat stroke than adults because: They produce more metabolic heat when exercising. They have greater surface area to body mass ratio. Their sweating capacity is less.
(eBook key search term: “ sleep is an active ”) Sleep is an active, multiphase, complex brain process that provides restorative functions and promotes memory consolidation. Normal sleep has two phases that can be documented by EEG: a. Rapid eye movement (REM) sleep b. Non-REM (NREM) or slow-wave sleep
Sleep cycle (NREM and REM sleep alternate – each cycle lasting for approximately 9-100 minutes)
REM SLEEP NREM SLEEP Etiology: controlled by the pontine and reticular formation; vivid dreaming ; also known as paradoxic sleep because the EEG
Etiology: initiated by the withdrawal of neurotransmitters from the reticular formation and by the inhibition of arousal mechanisms in
(eBook key search term: “ cause and extent of brain damage ”) Outcomes depend on the cause (etiology) and extent of brain damage and duration of coma (time since onset). a. The Glasgow Coma Scale (GCS) is used to assess severity of brain injury. The hallmark of a severe TBI is LOC for 6 hours of more. Age and admission GCS score are important diagnostic factors in TBI. b. TBI classification using the GCS are: i. Mild TBI with GCS score of 13 to 15 (associated with mild concussion) ii. Moderate TBI with GCS score of 9 to 12 (associated with structural injury such as hemorrhage or contusion) iii. Severe TBI with GCS score of 3 to 8 (associated with cognitive and/or physical disability or death. GLASSGOW COMA SCORE (GCS) SCORE BEST EYE RESPONSE (4) BEST VERBAL RESPONSE (5)
BEST MOTOR REPONSE (6)
1 No eye opening No verbal response No motor response 2 Eye opening to pain Incomprehensible sounds Extension to pain 3 Eye opening to verbal command Inappropriate words Flexion to pain 4 Eyes open spontaneously Confused Withdrawing from pain 5 -- Oriented Localizing pain 6 -- -- Obeys commands The Glasgow Coma Score (GCS) is scored between 3 and 15, with 3 being the worst and 15 the best. It is composed of the sum of three parameters: Best Eye Response, Best Verbal Response, and Best Motor Response (Mild Brain ate Brain Injury, 9 to 12; Severe Brain Injury, 8 or less)
(eBook key search term: “ most critical clinical index ”) Level of consciousness is the most critical clinical index of nervous system function or dysfunction. Changes can indicate either improvement or deterioration of the individual’s condition and state of awareness. A person who is alert and oriented to self, others, place, and time functioning at the highest level of consciousness (implies full use of all the person’s cognitive capacities) From this normal alert state, LOCs diminish in stages from confusion to coma
(eBook key search term: “ vomiting, yawning, and hiccups ”) Vomiting, yawning, and hiccups are complex reflex motor responses that are integrated by neural mechanisms in the lower brainstem. Most CNS disorders produce nausea and vomiting. These responses may be produced by: Compression or diseases involving tissues of the medulla oblongata (e.g., infection, neoplasm, infarct, or other more benign stimuli to the vagal nerve). Direct involvement of the central neural mechanism (e.g., pyloric obstruction) – usually vomiting occurs without nausea. Injuries that involve the vestibular nuclei or its immediate projections , particularly when double vision is present (diplopia). Injuries that impinge directly on the floor of the fourth ventricle. Injuries that produce brainstem compression secondary to increased ICP.
(eBook key search term: “ brain death (total brain death) ” and “complete unawareness”) a. Brain death (or total brain death ): occurs when irreversible brain damage is so extensive that the brain has no potential for recovery and no longer can maintain the body’s internal homeostasis. State laws define brain death as irreversible cessation of function of the entire brain, including the brainstem and cerebellum. This is to be distinguished from cerebral brain death , which is the death of the cerebral hemispheres exclusive of the brainstem and cerebellum. i. Clinical criteria for brain death:
1. Completion of all appropriate and therapeutic procedures with no possibility of brain function recovery. 2. Unresponsive coma (absence of motor and reflex movements). 3. No spontaneous respiration ( apnea ) – a PaCO2 that rises above 60mmhg without breathing efforts, providing evidence of a nonfunctioning respiratory center ( apnea challenge ). 4. No brainstem function (ocular responses to head turning or caloric stimulation; dilated fixed pupils; no gag or corneal reflex). 5. Isoelectric (flat) EEG ( electrocerebral silence ) for 6-12 hours for patients who are not hypothermic and have not ingested depressant drugs 6. Persistence of these signs for an appropriate observation period b. Persistent vegetative state (PVS): complete unawareness of the self or surrounding environment and complete loss of cognitive function (unresponsive wakefulness syndrome) i. Diagnostic criteria for PVS: 1. Periods of eye opening (spontaneous or following stimulation). 2. Potential for subcortical responses to external stimuli, including generalized physiologic responses to pain, such as posturing, tachycardia, diaphoresis, and subcortical motor responses, such as grasp reflex. 3. Return of vegetative autonomic functions, including sleep-wake cycles and normalization of respiratory and digestive system functions. 4. Occasional roving eye movements without concomitant visual tracking ability. 5. There may possibly be random hand, extremity, or head movements. The individual can maintain BP and breathing without support. Brainstem reflexes are intact, but cerebral functions are lost. No discrete localizing motor responses are present, and the individual does not speak any comprehensive words or follow commands. 6. Recovery unlikely if persist longer than 12 months
Evaluation: diagnosis is made by ruling out other causes. Definitive diagnosis can only be made by autopsy. Clinical history (including mental status exams, clock drawing, and geriatric depression scale), CSF analysis, brain imaging of structure, blood flow and metabolism; and the course of the illness is used to assess progression of AD. Genetic susceptibility tests for PSEN1, PSEN2, and APP are used to screen for early-onset AD Treatment: there are no disease modifying therapies, and treatment is directed at using devices to compensate for the impaired cognitive function (memory aids, maintaining unimpaired cognitive functions; and maintaining or improving the general state of hygiene, nutrition, and health Cholinesterase inhibitors (used in mild-moderate cases of AD) NMDA receptor antagonist blocks glutamate activity and may slow the progression of disease in moderate-severe AD Anti-myeloid drugs are in clinical trials
(eBook key search term: “ seizures are classified” and “ seizures associated with fever”) SEIZURE STATUS EPILEPTICUS Seizure:^ a sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons.
Types of Seizures (see Table 17.17)
S/S: LOC, apnea, hypoxia, acidosis, and lactate accumulation with resulting brain tissue injury and destruction (overall medical concerns for seizures)
Status epilepticus : In adults, it is a state of continuous seizures lasting more than 5 minutes OR Rapidly recurring seizures before the person has fully regained consciousness from the preceding seizure OR A single seizure lasting more than 30 minutes. Cause: often results from abrupt discontinuation of antiseizure medications but also may occur in untreated or inadequately treated persons with seizure disorders.
****This situation is a medical emergency because of the resulting cerebral hypoxia** , as well as the risk of aspiration , intellectual disability, dementia, and even death.
Long-term Complications: neuronal death, neuronal injury, and alteration of neuronal networks. Patho: a group of neurons may exhibit a paroxysmal depolarization shift and function as an epileptogenic focus These neurons are hyperexcitable (more easily activated by hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation, and certain sleep phases) Epileptogenic neurons fire more frequently and with greater amplitude
When the intensity reaches a threshold point, cortical excitation spreads e xcitation of the subcortical, thalamic, and brainstem areas: Tonic phase (muscle contraction with increased muscle tone) = loss of consciousness
When inhibitory neurons in the cortex, anterior thalamus, and basal ganglia react to the cortical excitation seizure discharge is interrupted: Clonic phase (alternating contraction and relaxation of muscles) = intermittent; gradually decrease and finally cease epileptogenic neurons are exhausted
During seizure activity – cerebral blood flow , oxygen consumption (60% greater than normal) rapidly depleting O2 and glucose lactate accumulates in brain tissue (severe seizure continues) progressive brain injury and irreversible damage
**If seizure focus in the brain is active for a prolonged period a mirror focus may develop in contralateral normal tissue seizure activity (particularly with focal epilepsy - i.e., temporal or frontal lobe)
Etiology: a seizure disorder is a manifestation of disease, NOT a specific disease. Onset of seizures may point to the present of: an ongoing primary neurological disease (including cerebral lesions, biochemical disorders, cerebral trauma, and epilepsy) OR conditions such as metabolic defects , congenital malformations , genetic predisposition , perinatal injury, postnatal trauma, myoclonic syndromes , infection, brain tumor, and vascular disease OR hypoglycemia , fatigue, emotional or physical stress, fever, hyponatremia , constipation, blinking lights , use of stimulant drugs , loud noises, certain odors, and withdrawal from drugs/alcohol.
Phases of seizures: Two types of symptoms signal the preictal phase of a generalized tonic-clonic seizure:
Treatment: Correct or control cause (#1) – if not possible… o Anti-seizure medications (goal: complete suppression of seizure activity without intolerable side effects or drug resistance) Dietary treatments Ketogenic diet or modified Atkins diet (<20g carbs/daily) Surgical interventions – people with drug-resistant epilepsy Vagus nerve stimulator (reduces seizure frequency in persons with drug-resistant focal seizures)
BENIGN FEBRILE SEIZURES -seizures associated with fever in the absence of central nervous system infection - “Simple febrile seizures” – occur in 2%-5% of children (most common childhood seizure; pathogenesis is unknown) Susceptibility Factors: age, degree and rate of temperature elevation, and nature of the particular fever-inducing illness
Common in children younger than 5 to 6 years of age; brief (less than a few minutes generalized convulsions associated with high fever; important to exclude meningitis as cause of seizures; usually do not develop epilepsy
Characteristics:
Treatment: phenobarbital use is recommended
(eBook key search term: “ intracranial hypertension” and “ increased intracranial pressure”)
