Neurological System Flashcards

Question

Describe the function of the Occipital lobe

Answer 1

Visual association

Answer 2

Primary auditory cortex Sensory speech area= reception and interpretation of speech and dysfunction (aphasia, dysphagia) memory consolidation and smell

Answer 3

Controls vital function, visceral activities, closely associated with Limbic system. Epithalamus Thalamus: Integrating center for afferent (sensory) impules to the cerebral cortex Hypothalamus: maintains a constant internal environment and implement behavioral patterns, integrative centers control ANS function, regulate body temp, endocrine function and adjust emotional expression Subthalamus: basal gangilia center for motor function

Answer 4

``` Superior (vision): Voluntary/involuntary visual movement, ability for eyes to track objects in visual field Inferior colliculi (Auditory): Positionin head to improve hearing ```

Answer 5

Cerebellum: Conscious/unconscious muscle synergy, maintains balance/posture. Damage is characterized by ipsilateral (same side) loss of equilibrium, balance and motor corrdination Pons: Transmits information from cerebellum to the brainstem between the 2 cerebellar hemispheres Medulla Oblingata: Helps control HR, RR, CP, coughing, sneezing, swallowing and vomiting

Answer 6

Connects the brain and the body Conducts somatic and autonomic reflexes Provides motor pattern control centers Modulates sensory and motor function

Answer 7

Sensory: Carries impulses for sense of SMELL EXAM: Person is asked to sniff aromatic substance and identify them

Answer 8

Sensory: carries impulses for vision EXAM: vision and vision field tested with an eye chart and by testing point at which person 1st sees an object moving into visual field. The inside of the eye is viewed with an ophthalmoscope to observe blood vessels of the eye interior

Answer 9

Motor fibers that direct eyeball; levator muscle of the eyelid, smooth muscle of the iris and cillary body and proprioception (sensory) to the brain from extraocular muscle EXAM: pupils examined for size, shape and equality. Pupillary reflex tested with penlight and ability to follow moving objects

Answer 10

Proprioceptor and motor fibers for superior oblique muscle of the eye (extraocular muscle) EXAM: tested with CN III relative to ability to follow moving objects

Answer 11

Motor/sensory for the face. Conduct sensory impulses from the mouth, nose, surface of eye and dura mater. Also contain motor fibers that stimulate chewing EXAM: Sensation of pain, touch, temp tested with safety pin and hot/cold objects. Corneal reflex tested with wisp of cotton, motor branch tested by asking subject to clench teeth, open mouth against resistence and move jaw from side to side

Answer 12

Motor fibers to lateral rectus muscle and proprioceptor fibers from same muscle to brain EXAM: tested with CN III, relative ability to move eyes laterally

Answer 13

Mixed: motor fibers to muscle of facial expression and to lacriminal/salivary glands carry sensory fibers from taste buds of anterior part of tongue EXAM: Anterior 2/3 of tongue tested for ability to taste SWEET, SALTY, SOUR and BITTER. Symmetry of face checked. Subject asked to close eyes, smile, whiste. Tearing tested with ammonia fumes

Answer 14

Sensory; vestibular branch transmits impulses for snes of equilibrium. Cochlear branch tranmits impulses for sense of hearing EXAM: hearing checked by air/bone conduction by tuning fork. Vestibular tests

Answer 15

Mixed. Motor fibers serve pharynx and salivary glands. Sensory fibers carry impulses from pharynx, posterior tongue (taste buds) and pressure receptors of caratoid arteries EXAM: gag/swallow reflex checked. Persons asked to speak and cough. Posterior 1/3 of tongue may be tested for taste

Answer 16

Sensory/motor impulses for pharynx, large part of this nerve is parasympathetic motor fibers that supply smooth muscle of abdominal organs. Receives sensory impulses for viscera EXAM: Same as CN IX, both serve muscle of throat

Answer 17

Sensory/motor fibers for sternocleidomastoid and trapezius muscle and muscle of soft palate, pharynx and larynx EXAM: Sternocleidomastoid and trapequis muscle check for strength by asking subject to rotate head and shrug shoulders against resistence

Answer 18

Motor fibers to muscle of tongue and sensory impulses from tongue to brain EXAM: ask persons to stick out tongue and any position abnormalities are noted

Answer 19

Fight or Flight Response Mobilizes energy store in time of needs *Decreased peristalsis, increased blood sugar levels, temp and blood pressure, regulates vasomotor tone

Answer 20

*Rest and digest* Functions to conserve and restore energy * Promotes rest/tranquility, decrease HR, enhances visceral function leading to digestion, controls pupil constriction and tears secretion, increase salivary secretion, contracts urinary bladder*

Answer 21

Structural changes: Decreased # of neurons, decreased brain weight/size, fibrosis and thickening of meninges, narrowed gyri and widened sulci, increased ventricles Cellular changes: decreased myelin, deposition of lipofuscin, presence of senile plaque, mulitple neurofibrillary tangles, lewy body Function changes: diminished sensory function, sleep disturbance, memory impairments

Answer 22

1. Specificity Theory: proposes that pain and touch are carried on distinct pathways that project to distinct brain centers Useful for specific injuries and acute pain (not chronic, cognitive/emotional elements) 2. Pattern Theory: proposes that any somatic sense organs respond to a dynamic range of stimulus intensities. Limited (does not account for all types of pain experiences) 3. Gate Control Theory: integrates and builds upon features of other theories to explain the complex aspects of pain perception and pain modulation. Pain transmission is modulated by a balance of impulses conducted to the spine where cells in the substantia gelatinsoa act as a gate 4. Neuromatrix Theory: Advancement of the gate control theory and proposes that the brain produces patterns of nerve impulses drawn from various inputs. This includes genetic, sensory-discrimination, affective-motivational, evaluative-cognitive experiences. Feelings of pain felt in the absense of inputs from body (phantom limb pain)

Answer 23

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of damage. Nociceptive pain: pain with normal tissue injury from KNOWN cause Somatic: fracture, thermal, trauma/ visceral: bowel obstruction Nonciceptive pain: Neuropathic pain and Central/peripheral Neurophysiologic pain: Nociceptive pain (somatic, visceral, referred), Neuropathic (central pain, peripheral pain) Neurogenic pain: Neuralgia, constant Temproal pain: acute or chronic Regional pain: Abdomen, chest, HA, low back, orofacial, pelvic, joint Etiologic pain: cancer, dental, inflammatory (infection, trauma), ischemic, vascular, postoperative

Answer 24

Persistent low back pain- poor mm tone, inactivity, mm strain, exercise Myofascial pain syndrome- mm spasm, tenderness, stiffness, as disease progresses = pain becomes generalized Chronic postoperative pain- disruption or cutting of sensory nerves Cancer pain- advanced disease, treatment, coexisting disease Deafferentation pain-damage of peripheral nerve. Burning pain triggered by various stimuli (cold, light touch or sound) Hyperesthesia- increased sensitivity and decreased pain threshold to tactile and painful stimuli Hemiagnosia-loss of ability to identify source of pain on 1 side of body. Associated with stroke Phantom limb pain Complex regional pain syndrome- associated with limb injury, surgery or fracture

Answer 25

< 3 months Clinicals symptoms: increased HR, HTN, diaphoresis, dilated pupils, and axiety Acute somatic: pain is sharp and localized on A Delta fibers. Pain is dull, aching, throbbing and poorly localized on C fibers Acute visceral: pain is poorly localized. Aching, gnawing, throbbing or intermittent cramping, N/V, hypotension, restlessness and shock Referred: pain in an area is removed or distant from its point of orgin

Answer 26

Temperature regulation. Achieved through heat production, heat conservation, and heat loss. Peripheral thermoreceptors in skin and abdominal organs Central thermoreceptors in the spinal cord and trigeminal ganglia

Answer 27

1. Radiation: loss through electromagnetic waves from surfaces with temp that is higher than surrounding air 2. Conduction: by direct transfer from one surface to another, so that warmer surface loses heat to cooler surface 3. Convection: Transfers of heat through currents of gas or liquid, exchanges warmer air at body's surface with cooler air in surrounding space (fans/wind) 4. Vasodilation: Diverts core-warmed blood to surface of body with heat transferred by conduction to skin surface and from there to surrounding environment. 5. Evaporation: Body water evaporates from surface of skin and linigng of mucus membrane. Major source of heat reduction connected with increased sweating in warmer surroundings

Answer 28

1. Chemical reactions of metabolism: ocurrs during ingestion and metabolism of food and while maintaining body at rest. occurs in body core 2. Skeletal mm contraction: gradual increase in mm tone or rapid mm oscillation (shivering). Controlled by posterior hypothalamus 3. Chemical (nonshivering) thermogenesis: epinephrine and norepinephrine are released and produce rapid, transient increase in heat production by raising basal metabolic rate. Quick, brief effect that counters heat loss through conduction or convection.

Answer 29

Febrile response or pyrexia that is temporary resetting of the hypothalamic thermostat to a higher level in reponse to pyrogenic cytokines and exogenous pyrogens. Exogenous pyrogens: pathophysiologic mechanism of fever to begin here, which is produced by pathogens Pyrogenic cytokines: produced by phagocytic cells as they destroy micoorganisms within the host

Answer 30

1. aids infectious response 2. kills many organisms 3. decrease the serum levels of iron, zinc and copper (all needed for bacterial replication) 4. promotes lysosomal breakdown and autodestruction of cells (preventing viral replication of infected cells) 5. Body switches from burning glucose to a metabolism based on lipolysis and proteolysis (depriving bacteria of a food source) 6. heat increase lymphocytic transformation and motility of polymorphonuclear neutrophils (immune response)

Answer 31

1. Hyperthermia 2. Hypothermia 3. Trauma

Answer 32

Elevation of the body temp without an increase in the hypothalamic set point. Causes derve damage, coagulation of cell proteins and death

Answer 33

Convulsions: 41c (105.8F) Death: 43C (109.4F)

Answer 34

Therapuetic: used to destroy pathologic microorganisms or tumor cells by facilitiating the hosts natural immune process or tumor blood flow Accidental: Heat cramps- treat with administration of dilute salt solution through oral/paternal routes Heat exhaustion: causes profound vasodilation and profuse sweating that leads to dehydration, decrease plasma volume, hypotension, decreased cardiac output and tachycardia. Treatment- person to stop and lie down. Rest, drink cool fluids Heat stroke: overexposure to environmental heat, impaired physiologic mechanism for heat loss. Symptoms: core temp is >40C, 104F. no sweating, rapid pulse, confusion, agitation and coma. Malignant hyperthermia: potientally lethal hypermetabolic complication of rare inherited mm disorder that is triggered by inhaled anesthetics and depolarizing mm relaxants. Most commen in children and adolescents. Treat with withdrawal of provoking agent, body cooling therapy and drugs that antagonize the ryanodine receptor. Temp may rise 1C, 1.8F every 5 minutes.

Answer 35

Core body temp < 35C (95F) Produces depression of the CNS, RR system, vasoconstriction, alterations in microcirculation and coagulation, ischemic tissue damage.

Answer 36

1. Accidental: high energy ATP are depleted. Sudden immersion in cold water or prolonged exposure to cold environments. Children and older adults at high risk d/t thermoregulatory mechanisms are immature or altered. Peripheral vasoconstriction shunts blood away from the cooler skin to the core in an efor to decrease heat loss. Produces peripheral tissue ischemia. 2. Therapeutic: ATP storage is preseserved. Used to slow metabolism and preserve ischemic tissue after brain trauma or duing brain surgery, aftrer cardiac arrest and neonatal hypoxic encephalopathy.

Answer 37

Mild: passive rewarming may be sufficient If core temp is >30C (86F): active rewarming may be required -Active rewarming = Warm water baths, warm blankets, hearting pads, warm oral fluids Core rewarming: Admin of warm IV solutions, warm gastric lavage, warm peritoneal lavage, inhaled warm gases Extreme cases: exchange transfusions, warming blood in a pump oxygenator circut, mediastinal lavage. Rewarming should proceed no faster than a few degrees per hour.

Answer 38

1. Rapid eye movement (REM) sleep | 2. Non-rapid eye movement (NREM) sleep

Answer 39

Begins about 1-2 hours after NREM starts. | paradoxical sleep, memorable dreams, loss of voluntary mm control

Answer 40

Parasympathetic acitivity increases: decreased HR, RR, BP, temp and mm tone. 3 stages: N1= light sleep. Slow eye movements. Last about 10-12 minutes N2= slow eye movement, cycle lasts about 30-60 minutes N3 = no slow eye movement. 12-23% of sleep time spent here

Answer 41

Wakefulness = brainstem and basal forebrain serotonin, norepinephrine, dopamine acetylcholine, glutamin The production of these neurotransmitters decrease with sleep Sleep = GABA, galanin NREM sleep = melanin-concentrating hormone, adenosine, prostaglandin D2, nitric oxide and cytokines REM sleep = ACh, GABA, glutamate

Answer 42

Newborns sleep 16-18 hrs per day 53% is REM sleep and 23% NREM Infant sleep cycle is about 50-60 minutes They enter REM immediately Children develop adult sleep patterns between ages 3-5 Sleep is important for growth and neurocognitive development

Answer 43

Total sleep time is decreased Longer time is needed to fall asleep, awaken more frequently through the night time in REM is decreased Causes for changes in sleep patterns: physical ailments, lack of daily routine, circadin rhythm changes, medications and lifestyle changes

Answer 44

1. Dysomnia (intrinsic and extrinsic sleep disorders and circadin rhythm disorders) 2. Parasomnia (arousal and sleep wake transition disorders and REM sleep disorders) 3. Medical/psychiatric 4. Proposed sleep disorders

Answer 45

Difficulties in initiating or maintaining sleep or excessive sleepiness.

Answer 46

1. Insomnia 2. Obstructive sleep apnea syndrome 3. Restless leg syndrome 4. Obesity Hypoventilation 5. Circadian rhythm disorder 6. Hypersomnia 7. Narcolepsy

Answer 47

Inability to fall asleep or stay asleep; accompanied by fatigue during wakefulness- may be mild, moderate or severe. Transient (lasting few days to months) Results in hyperarousal, decreased cortical GABA, increased arousal during REM sleep and dysregulation of sleep-wake cycle.

Answer 48

Unpleasant sensations (prickling, tingling, crawling) that occur at rest and are worse in the evening/night. Person feels the urge to move legs for relief. More common in women with iron deficiency. Familial tendency. *Related to diurnal variation in iron transport across the blood-brain barrier and loss of dopamine

Answer 49

Alpha-2 Delta drugs (gabapentin) Dopamine agonist Iron administration

Answer 50

Disorder of breathing during sleep, related to an upper airway obstruction associated with reduced blood oxygen saturation and hypercapnia. Most common sleep disorder

Answer 51

Obesity, males, older age, postmenopausal women

Answer 52

Using the Apnea Hypopnea Index (AHI): represents apnea (total airway closure) or hypopnea (partial airway closure) episodes per night.

Answer 53

Normal: 0-5 abnormal sleep episodes Mild: 5-15 abnormal sleep episodes Moderate: 15-29 abnormal sleep episodes Severe: >30 abnormal sleep episodes

Answer 54

Partial or total airway collapse related to pharyngeal anatomy or decreased pharyngeal dilator mm tone

Answer 55

Obstruction to airway recurring at night causes loud snoring, gasping, multiple apneic episodes that last 10 seconds or longer. Hypercapnia, low oxygen saturation that leads to polycythemia, pulmonary hypertension, HTN, right-sided CHF, dysrhythmias, cyanosis and peripheral edema

Answer 56

Continuous positive airway pressure (treatment of choice) Surgery of upper airway/jaw CHILDREN: adenotonsillar hypertrophy is cause of OASD and adenotonsillectomy is treatment of choise

Answer 57

Rapid time-zone change (jet lag) Changes in sleep schedule with an advance or delay of 3 hours or more in sleep time changes in total sleep time from day to day that desynchronizes rhythm

Answer 58

1. Impact on performance through cognitive functions (attention, learning, memory, vigilance) 2. Decreased speed of mental processing 3. Abnormal activation in the prefrontal cortex, parietal lobe, thalamus, temporal lobes shown on functional neuroimaging 4. Task performance decreases as sleep debt accumulates

Answer 59

Arousal and sleep wake transition disorders and REM sleep disorders

Answer 60

1. Sleep walking (somnambulism) 2. Night terrors 3. Confusional arousal 4. Rearranging furniture 5. Violent behanior 6, Bruxism (grinding teeth) 7. Sleep enuresis

Answer 61

1. attentional systems that provide arousal and maintenance of attention over time 2. memory and language systems by which information is communicated 3. affective or emotive systems that mediate mood, emotion, and intention.

Answer 62

1. Arousal (state of awakeness) | 2. Awareness (content of thought)

Answer 63

regulates aspects of attention and information processing and maintain consciousness. Infection, vascular alterations, neoplasms, traumatic injury, congential alterations, degenerative changes, polygenic traits and metabolic disorders can cause alterations in arousal.

Answer 64

produce changes by either diffuse or localized dysfunction. Diffuse dysfunction = caused by disease processes affecting the cerebral cortex or the underlying subcortical white matter (encephalitis). Disorders outside the brain, but within the cranial vault can also produce diffuse dysfunction (neoplasm, closed-head trauma) Localized dysfunction = directly impair function of the thalamic or hypothalamic activing systems. Primariily masses ( bleeding, infarcts, emboli, tumors)

Answer 65

Produces a decline in arousal by 1. direct destruction of the reticular activating system and its pathway (accumulation of blood/pus, demyelinating disorders) 2. The brainstem may be destroyed by direct invasion or indirect impairment of its blood supply (cerebrovascular disease) (tissue compression)

Answer 66

produce a decline by alterations in delievery of energy substrates as occurs with hypoxia, electrolyte disturbances, and hypoglycemia. metabolic disorders caused by the liver or renal failure = alterations in neuronal excitability because of failure to metabolize or elliminate drugs/toxins.

Answer 67

Uncommon, may signal general psychiatric disorders. | Despite apparent unconsciousness, person is physiolocally aware and the neurologic exam is normal

Answer 68

1. level of consciouness 2. pattern of breathing 3. pupillary reaction 4. oculomotor responses 5. motor responses

Answer 69

1. confusion- loss of ability to think rapidly and clearly; impaired judgement and decision making 2. disorientation- Beginning loss of conscniousness; disorientation to time, then place and impaired memory; lost last is recognition of self 3. lethargy- limited spontaneous movement of speech; easy arousal with normal speech/tough; may not be oriented to time, place, person 4. obtundation- mild-moderate reduction in arousal with limited response to environment; falls asleep unless stimulated. minimal response to Q 5. Stupor- a condition of deep sleep/unresponsiveness from which person can be aroused or open eyes at vigorous/repeated stimuli. response is often withdrawal or grabbing at stimulus 6. light coma- assosicated with purposeful movement on stimulation 7. coma- no verbal response to external environment to any stimulil; noxious stimuli (deep pain or suctioning) yeilds motor movement 8. deep coma- associated with unresponsiveness or no respone to any stimuli

Answer 70

1. Normal- neural center in forebrain produces a rhythimc breathing pattern. 2. Posthyperventilation- RR stop after hyperventilation has lowered the Paco2 level below normal. Rhythmic breathing returns when the Paco2 returns to normal. Location of injury: diffuse bilateral metabolic or structural diseae of cerebellum) 3. Cheyne-Stokes RR- abnormal thythm of ventilation (periodic breathing) with alternating periods of hyperventilation and apnea (crescendo-decrescendo pattern) Damaged brain has higher Paco2 levels and stimulate ventilation. Paco2 decreases below normal and breathing stops until carbon dioxide reaccumulates and repeats the cycle. Cases seen in opiate or sedative drug overdose

Answer 71

1. Central reflex hypernea- sustained deep rapid but regular patter. Decreased Paco2 and a corresponding increase in PH and increased P02 2. Apneusis- Prolonged inspiratory cramp (a pause at full inspiration). Common variant is a brief end-inspiratory pause of 2-3 seconds, alternating with an end-expiratory pause. Damage to RR control mechanism at pontine level, pontine infarction. 3. Cluster breathing- Cluster of breaths has a disordered sequence with irregular pauses between breaths. Dysfunction in lower pontine and high medullary areas 4. Ataxic breathing- completely irregular breathing occurs with random shallow and deep breaths and irregular pases. Rate is slow. Dysfunction of medulla 5. Gasping breathing pattern (agonal gasps)- A pattern of deep "all-or-none" breathing is accompanies by slow respiratory rate. Indicative of a failing medullary RR center

Answer 72

1. purposeful (defensive or withdrawal of limbs to noxious stimuli) 2. inappropriate or not purposeful (generalized motor movement, posturing, grimacing or groaning) 3. not present (unresponsive, no motor response)

Answer 73

Upper extremity flexion, lower extremity extension. Slow developing flexion of arm, wrist and fingers with abduction in upper extremity and extension, internal roation, and plantar flexion of lower extremity. Location of injury: hemispheric damage ABOVE midbrain releasing meduallry and pontine reticulospinal systems.

Answer 74

Upper/lower extremity extensor response. Hyperextension of the vertebral column with clenching teeth, extension, abduction and hyperpronation of the arms; hyperpronation of the arms and extension of lower extremities. Location of injury: Associated with severe damage involving midbrain or upper pons

Answer 75

1. Brain death | 2. Cerebral death

Answer 76

Occurs when brain damage is so extensive that it can never recover (irreversible) and cannot maintain the body's internal homeostasis. This includes irreversible cessation of function of the entire brain, including the brainstem and cerebellum.

Answer 77

1. Completion of all appropriate diagnostic and therapeutic procedures with no possibility of brain function recovery 2. Unresponsive coma (no motor or reflex movements) 3. No spontaneous respiration (apnea) 4. No brainstem function (ocular responses to head turning, dilated, fixed pupils, no gag or corneal reflex 5. Isoelectirc (flat) EEG 6. Persistence of these signs for an appropriate observation period

Answer 78

Irreversible coma. The death of the cerbral hemispheres exclusive of the brainstem and cerebellum. Brain damage is permanent, person is unable to respond behaviorally significantly to the environment. Brainstem may maintain internal homeostasis (body temp, CV functions, RR and metabolic functions) May present in a coma, persisten vegetative state, minimally conscious state.

Answer 79

All cognitive functions, including awareness to self, environment and affective state (moods)

Answer 80

Selective attention deficits, memory, nondeclarative memory (unconscious), amnesia, image processing and detection

Answer 81

Temporary, permanent or progressive. Seizure activity, parietal lobe contusions, subdural hematomas, stroke, gliomas/metatastic tumors, late Alzheimers dementia, frontotemporal dementai and psychotic disorders.

Answer 82

Failure to report, respond or orient to visual, auditory or tactile stimuli that are presented contralateral to a brain lesion. Given that this failure is not primary sensory/motor disorders. Most cases, right parietal cortex is injured and the left side of the body/space is ignored.

Answer 83

Recording, retention and retrieveal of information. 2 types of long term memory: Declarative: learning and remembrance of spisodic memories (personal hx, events and experiences) and semantic memories (facts/information) Nondeclarative (unconscious): memories for action, behavior or skill that become automatic

Answer 84

1. Drug intoxication 2. Alcohol or drug withdrawal 3. Metabolic disorders (hypoglycemia, thyroid storm) 4. Brain trauma or surgery 5. Postanestesia 6. Febrile illness or heat stroke 7. Electrolyte imbalance, dehydration 8. Heart, kidney, liver failure

Answer 85

An acquired deterioration and a progressive failure of many cerrebral function of many cerebral functions that includes impairment of intellectual processes with a decrease in orienting, memory, language, judgement and decision making. Person may exhibit alterations in behavior (agitation, wandering, aggression)

Answer 86

Infection: encephalitis, meningtitis, neurosyphilis Normal pressure hydrocephalus: Chronic subdural hematoma, nutritional deficiencies Drug intoxication: alcohol, sedatives Metabolic disorders: Thyroid abnormalities, chronic hepatic encephalopathy, cerebral vasculitis, sarcoidosis Tumors: Frontal and temporal love, pseudodementia of depression Medial side effects: Anticholinergics, antihypertensives, antihistamines

Answer 87

Neurodegenerative disorders: Alzheimers, Dementia with Lewy bodies, frontotemporal dementia, pick disease, Huntington disease, Parkinson disease Vascular disease: Vascular dementia, Multi-infarct, Amyloid angiopathy Infection: Creutzfeldt-Jakob Disease, postencephalitic dementia, dementai assosicated with HIV

Answer 88

Neuron degeneration, compression of brain tissue, atherosclerosis of cerbral vessels and brain trauma. Genetic predisposition = neurodegenerative diseases: alzhiemers, huntington and parkinson CNS infections = HIV, prions in Creutzfeldt-jakob disease lead to nerve cell degeneration and brain atrophy

Answer 89

Mental status: memory loss, disorientation to place and time, loss of facial recognition Neurobehavior: Initially normal; progressive cognitive, language, abstraction and judgement impairment Neurologic exam: Initially NORMAL

Answer 90

Mental status: Variable, frontal/executive, focal cortical, memory Neurobehavior: depression, anxiety, decreased cognitive function and memory loss neurologic exam: Myoclonus (quick, involuntary muscle jerk), rigidity, parkinsonism

Answer 91

Mental status: Initially affects concentration and attention, then memory or cognition loss but unpredictable levels of ability, attention, or alertness. Delirium prone Neurobehavior: Visual hallucination, depression, sleep disorder, delusion, transient loss of consciouness neurologic exam: Parkinsonism, changes in walking or movement may present first

Answer 92

Mental status: PPA variant, language loss with talking less and speech becoming hesitant, or loss of understanding language, which may precede memory loss, spares drawing Neurobehavior: Behavioral variant FTD, loss of empathy, apthay, increased inappropriate or decline in personal or social conduct, loss of judement and reasoning, hyperorality, euphoria, depression Neurologic exam: Caused by CBD and PSP variants

Answer 93

mental status: N/A Neurohavior: Apathy, loss of interest early, impaired cognition, judgement, and memory occur later Neurologic exam: Chorea, bradykinesia, dystonia

Answer 94

mental status: Frontal/executive, cognitive slowing, memory can be intact Neurobehavior: often but not always sudeen, usually within 3 months of a stroke, variable, apathy, falls, focal weakness, delusions, anxiety Neurologic exam: Usually motor slowing, spasticity; can be normal or may have symptom improvement with stroke recovery

Answer 95

Greatest risk: age and family HX DM, midlife HTN, hyperlipidemia, midlife obestity, smoking, depression, cognitive inactivity or low education attainment, female gender, estrogen deficit at time of menopause, physical inactivity, head trauma, elevated serum homocysteine and cholesterol levels, oxidative stress and neuroinflammation.

Answer 96

lifelong activity, presence of apoE2 and antioxidant substances, omega-3 fatty acids, estrogen replacement at time of surgical menopause, low-calorie diet, and nonsteroidal anti-inflammatory agents.

Answer 97

Early onset: autosomal dominant and linked to 3 genes with mutations on chromosome 21. Late onset: genetic- apolipoprotein E gene-allele 4 on chromosome 19: interferes with amyloid beta clearance from the brain and processed into neurotoxic fragments found in the plaques and tangles in the brain. Sporadic late onset is most common and does not have a specific genetic association. Accumulation of extracellular neuritic plaques containing a core of abnormally foled amyloid beta and tau proteins, intraneuronal neruofibrillary tangles and degeneration of basal forebrain cholinergic neurons with loss of acetylcholine. Failure to process and clear amyloid precursor protien results in accumulation of toxic fragments of amyloid beta protein that leads to formation of diffuse neuritic plaques, disruption of nerve impulse transmission and death of neurons.

Answer 98

Mild cognitive Impairment = Cognitive: mild memory loss, particularly for recent event (episodic memory) and new information (semantic memory). Functional: possibly depressed (vs apthay), mild anxiety Early stage = Cognitive: measureable short-term memory loss, difficulty planning, disorientation to location. Functional: mild IADL problems Middle stage = Cognitive: significant forgetfulness, easy to get lost, may dress inapporpriate, hallucincation. Functional: IADL dependent, some ADL problems Late stage = Cognitive: little cognitive ability, language not clear, personality change, does not recognize family members, wantering, repetitive behavior. Functional: ADL dependent, incontinent, difficulty eating. End stage = Cognitive: no significant cognitive function, loss of word speech. Functional: nonambulatory/ bedbound, unable to eat

Answer 99

Clinical hx, including mental status exam (mini-mental status exam, clock drawing, geriatric depression scale), CSF analysis, brain imaging of structure, blood flow and metabolism, and course of illness (over the span of 5 years or more) Genetic suspectibility test for PSEN1, PSEN2, APP are used to screen early-onset

Answer 100

Treatment is directed at using devices to compensate for impaired cognitive function- memory aides, maintaining unimpaired cognitive functions, and maintaining or improving general state of hygiene, nutrition and health. Cholinesterase inhibitors for mild-moderate cases N-methyl-D-aspartate receptor antagonist blocks glutamate activity and may SLOW PROGRESSION from moderate-severe

Answer 101

Cranial nerve VII (facial)

Answer 102

Etiology is unknown. Inflammatatory reaction compressing the facial nerve in the fallopian (facial) canal of the middle ear followed by demyelinating neural change. Symptoms: unilateral facial weakness and inability to smile or whistle May be caused by reactivation of herpesvirus in CN VII geniculate ganglia or an autoimmune response.

Answer 103

Score Best eye response Best verbal Response Best Motor response 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 Withdrawal from pain 5 N/A N/A Localized pain 6 N/A N/A Obeys Commands

Answer 104

Mild brain injury: 13 or higher Moderate brain injury: 9-13 Severe brain injury: 8 or less

Answer 105

Alternation in brain function or other evidence pathology caused by an external force Most common: falls for children and older adults followed by unintentional blunt trauma and motor vehicles accidents Can be classified as PRIMARY and SECONDARY PRIMARY: caused by direct impact or injury and can be focal, affecting one area of the brain or diffuse, involving more than one area of the brain SECONDARY: indirect consequence of the primary injury and includes systemic responses and a cascade of molecular and chemical events that affect the brain.

Answer 106

Caused by closed (blunt) trauma or open (penetrating) trauma

Answer 107

Posterior defects: 1. Anencephaly: The skull and much of the brain in missing. Pathologic mechanism unknown. 2. Encephalocele: A saclike herniation of vaious amount of brain and meninges protrude through a defect in the skill; requires surgery to correct 3. Meningocele: Saclike cyst of meninges filled with spinal fluid 4. Myelomeningocele: Contains neural tissue, spinal cord or nerves

Answer 108

Imbalance between the production and reabsorption of CSF Ventricular enlargement and increased intracranial pressure (dilates the ventricles and pushes or compresses brain tissue against the skull) Obstructive hydrocephalus is most common; congenital aqueductual stenosis.

Answer 109

Disorder of movement, muscle tone or posture that is caused by injury or abnormal development in the immature brain.

Answer 110

prenatal or perinatal cerebral hypoxia, hemorrhage, infection, genetic abnormalities, or low birth weight

Answer 111

Results from damage to corticospinal pathway (upper motor neurons) and is associated with increased muscle tone, persistent primitive reflexes, hyperactive deep tendon reflexes, clonus, rigidity of extremities, scoliosis and contractures.

Answer 112

caused by damage to cells in the basal ganglia, thalamus or cerebellum and includes 2 types: dyskinetic (movements are stiff, uncontrolled, abrupt and reptitive resulting in difficult fine motor coordination and purposeful movements and ataxic (gait disturbances and reflects cerebellar involvement)

Answer 113

inborn error in the metablisim of amino acids, characterized by phenylalanine hydroxylase deficiency and results in inablility of the body to conver essential amino acid phenylalanine to tyrosine. Autosomal recessive disorder characterized by mutation of phenylalanine phdroxylase gene. Elevated serum phenylalanine levels results in developmental abnormalities of the cerebral cortical layers, defective myelination and cystic degeneration of gray and white matter. TX: reduction of dietary phenylalanine, must continue for life.

Neurological System Flashcards

(137 cards)