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187 Cards in this Set
- Front
- Back
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Two Basic Components of Nervous System
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Central Nervous System (CNS) & Peripheral Nervous System (PNS)
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Central Nervous System (CNS)
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Consists of brain and spinal cord
Protected by skull and vertebral column Functions: Computational and control |
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Peripheral Nervous System (PNS)
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Consists of all nervous tissue outside CNS
Found outside skull and vertebral column Function: relays somatic and visceral sensory (afferent) input to CNS for processing and transmitting motor (efferent) output from the CNS effector organs throughout body Divided into sensory and motor divisions Motor division is comprised of: autonomic/visceral nervous system ( SNS, PSNS, and Enteric) and somatic nervous system |
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The Brain: Divided into three regions
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Forebrain, Midbrain, Hindbrain
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Forebrain
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Largest part of the brain
Contains: Cerebrum (divided into right and left hemispheres), Basal Ganglia (large masses of gray matter) Diencephalon (which includes the thalamus, hypothalamus and pineal gland) Limbic System |
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Forebrain Lobes
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The surface of each hemisphere is divided into six lobes by major grooves (sulci or fissure): Frontal, parietal, occipital, temporal, limbic, and central lobes
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Frontal Lobe
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Controls voluntary motor activity. Involved in executive functions (anticipation, goal selection, planning, self-monitoring), motivation, emotion, selection & control of socially relevant behavior.
Contains Broca’s area. Frontal lobe injuries can result in lack of concentration/ motivation/problem solving, have motor deficits |
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Broca’s area
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A region of the brain concerned with the production of speech, located in the cortex of the dominant frontal lobe.
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Parietal Lobe
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Somatosensory: Receives & processes all sensory data from various parts of the body (e.g., olfactory, auditory, visual, pain, touch)
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Occipital Lobe
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Visual receptive & association area
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Temporal Lobe
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Auditory center
Contains Wernicke’s area (reception and interpretation of speech) Also involved in balance, taste and smell |
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Wernicke’s area
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reception and interpretation of speech (Also involved in balance, taste and smell)
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Limbic Lobe
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These structures of limbic system include the limbic lobe, amygdala, fornix, hippocampus, olfactory cortex, and portions of the thalamus.
Emotions: Controls affect in conjunction with prefrontal cortex Emotion-related behavior: Mediates behavior patterns that determine survival (mating, aggression, fear, affection, nutrition) Memory: Control the transfer of information from short-term memory to long-term memory Olfaction: Perception of smell Impairment such as Lesions (e.g., in hippocampus can cause impairment in short-term memory) |
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Basal Ganglia
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The basal ganglia include the striatum (caudate nucleus, putamen), globus pallidus, subthalamic nuclei, and substantia nigra.
Processing area that links cerebral cortices to thalamic nuclei so it can initiate, coordinate, & carry out smooth motor movements and supportive posture during highly skilled movements (ex: walking) Connects: sensory info about muscle conditions cortical info about desired motor activity and cerebellar info about timing and coordination |
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Diencephalon
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Pathway between cortex and spinal cord. Controls involuntary functions. Actually located in the forebrain between the cerebral hemispheres and brain stem
Thalamus: Relay station for sensory information (perception of sensations occur here but need cortical level to interpret sensory info) Hypothalamus: Maintenance of homeostasis, behavior patterns |
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Thalamus
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Relay station for sensory information (perception of sensations occur here but need cortical level to interpret sensory info)
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Hypothalamus
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Maintenance of homeostasis, behavior patterns
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Brain Stem
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Midbrain (CN III exists here)
Hindbrain: pons and medulla oblongata |
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Midbrain
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In brain stem (CN III exists here)
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Hindbrain
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In brain stem
pons (2 respiratory control centers –pneumotaxic and apneustic) medulla oblongata: Reticular activating system (controls sleep-wake cycle and consciousness) |
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pons
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2 respiratory control centers –pneumotaxic and apneustic
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medulla oblongata
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Reticular activating system (controls sleep-wake cycle and consciousness)
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The four principal anatomic areas of the brain
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cerebrum, Diencephalon, brain stem, cerebellum
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CBF
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Cerebral Blood Flow
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Adequate CBF is maintained to the normal brain by...
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cerebral arterial blood vessels either dilating or constricting automatically in response to usual fluctuations in mean arterial blood pressure
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MAP
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Mean Atrial Pressure
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Normal Mean Arterial Blood Pressure (MAP) is...
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50 -150 mm Hg. (Fluctuations below or above this range cause autoregulation to fail, and therefore, result in ischemia or cerebral edema respectively)
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If MAP is < 50mmHg...
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then vessel already maximally dilated; ischemia occurs
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If MAP is > 150mmHg...
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then vessel already maximally constricted; cerebral edema occurs
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Chemical regulation of cerebral blood flow
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(Cerebral blood vessels respond to metabolic factors such as oxygen, carbon dioxide, and pH)
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Oxygen tension (PaO2 < 50)
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causes vasodilation
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If PaCO2 decreases...
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vasoconstriction
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If PaCO2 increases...
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vasodilation
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H+: Acidosis...
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vasodilation
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H+: Alkalosis...
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vasoconstriction
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ICP
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Intracranial Pressure
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ICP (Intracranial Pressure)
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The pressure exerted in the intracranial cavity by its contents
(Three contents: Brain matter, blood, CSF; The cranial cavity is filled with 80% brain tissue, 10% blood and 10% CSF in the rigid confines of a nonexpandable skull) |
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ICP (Intracranial Pressure) Contents
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Three contents: Brain matter, blood, CSF
The cranial cavity is filled with 80% brain tissue, 10% blood and 10% CSF in the rigid confines of a nonexpandable skull |
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Normal ICP (Intracranial Pressure)
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is 0-15 mm Hg
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Monro-Kellie Hypothesis
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Under normal conditions, a reciprocal relationship exists among the three intracranial volumes. Since the skull cannot expand, an increase in one of these volumes must be balanced with a decrease in one or both of the other components.
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If increased brain tissue...
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decrease blood volume or CSF
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Causes for increased components: Increased tissue volume
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Tumor, edema, bleeding into brain
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Causes for increased components: Increased blood volume
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Vasodilation, obstruction to venous outflow
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Causes for increased components: Increased CSF
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Excess production or obstruction to circulation of CSF
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CPP
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Cerebral perfusion pressure
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CPP (Cerebral perfusion pressure)
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Represents the difference between the Mean Arterial Blood Pressure (MAP) and the Intracranial Pressure (ICP)
CPP=MAP-ICP |
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CPP=
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MAP-ICP
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Normal CPP (Cerebral perfusion pressure)
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brain needs 60-80 mmHg of perfusion pressure
Death to brain cells begins at 50mmHg At 40mmHg cerebral tissues become acidotic causing more cell death |
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Death to brain cells begins at...
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50mmHg
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cerebral tissues become acidotic causing more cell death at...
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40mmHg
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Etiology: Increased Brain Tissue Volume
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Hemorrhage
Cerebral edema (vasogenic, cytoxoc, ischemic) |
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Etiology: Increased CSF
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Hydrocephalus
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Etiology: Increased Blood Volume
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High PaCO2 or loss of autoregulation
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Increased ICP : Increased Brain Tissue Volume: Cerebral Edema (Brain swelling)
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Three types of cerebral edema:
Vasogenic Cytogenic Ischemic |
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Vasogenic Cerebral Edema (Pathophysiology)
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tumors, ischemia, infections, or impaired BBB (Blood Brain Barrier) --> increased permeability to plasma proteins --> leak of proteins into extracellular space --> pulls water with it and increases extracellular fluid around brain cells --> edema
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Cytotoxic Cerebral Edema (Pathophysiology)
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(all cellular contents swell)
hypo-osmatic states (water intoxication or ischemia) --> failure of Na/K pump --> accumulate Na in cell --> water follows --> edema and necrosis |
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Ischemic Cerebral Edema (Pathophysiology)
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(combination of vasogenic and cytotoxic edema)
ischema --> production of O2 free radicals --> damage blood brain barrier --> protein leaks into extracellular space |
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Increased ICP because of increased CSF Volume is a result of...
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Hydrocephalus
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Hydrocephalus
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Progressive enlargement of ventricular system due to abnormal increase in CSF volume
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Hydrocephalus (Etiology)
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Overproduction of CSF
Impaired reabsorption of CSF Obstruction of CSF flow in ventricular system |
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Hydrocephalus (Pathophysiology)
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Enlargement of cerebral hemispheres --> dilation of ventricular system beyond point of obstruction --> effacement of sulci on brain surface & reduced white matter volume
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Hydrocephalus (Clinical manifestations)
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Inutero: separation of cranial sutures
Adults & children: s/s of increased ICP (headache, vomiting); herniation |
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Increased ICP (Pathophysiology)
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increased ICP --> as ICP increases, CPP decreases --> cerebral blood flow decreases causing tissue hypoxia --> acidosis and increase in CO2 levels --> causes cerebral vasodilation and edema --> further increased ICP
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Stages of increased ICP
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Stage I: 1st decrease CSF, then vasoconstriction if ICP remains elevated. “Compensated” to normal ICP range
Stage II: If ICP remains increased intracranial hypertension occurs Stage III: All compensatory mechanisms exhausted and now decompensation begins rapidly Stage IV: Brain tissue herniates from the compartment of greater pressure to one of lesser pressure |
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Stage I of increased ICP
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1st decrease CSF, then vasoconstriction if ICP remains elevated. (“Compensated” to normal ICP range)
s/s: subtle, may have confusion, drowsiness all related to slight ischemia |
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Stage II of increased ICP
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If ICP remains increased, intracranial hypertension occurs
To maintain perfusion of brain tissue, increase of SBP (systolic blood pressure) (ex. CPP=MAP-ICP; if ICP 30, what does the MAP required to maintain CPP at least 60?) s/s: Decreased LOC (level of consciousness), cheyne stokes (an abnormal pattern of breathing characterized by breathing becoming shallower until it stops for a while and then breathing starts again and rapidly crescendos to a peak before decaying away again; waxing/waning) or central neurogenic hypervent. resp., pupils sluggish and dilated, cushings triad (increased BP, widened pulse pressure, slowing HR) |
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Stage III of increased ICP
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All compensatory mechanisms exhausted and now decompensation begins rapidly; Increased ICP and accumulation of CO2 cause vasodilation.
As ICP approaches MAP, CPP falls and tissue hypoxia and acidosis occur (ex. CPP=MAP-ICP; if MAP60 and ICP 50 what is CPP?) |
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Stage IV of increased ICP
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Brain tissue herniates from the compartment of greater pressure to one of lesser pressure. This causes further decreases in blood supply and further hypoxia and ischemia to occur.
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if ICP 30, what does the MAP required to maintain CPP at least 60?
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CPP=MAP-ICP; 90mm/Hg
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Cushing's Triad
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increased BP, widened pulse pressure, slowing HR
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if MAP 60 and ICP 50 what is CPP?
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CPP=MAP-ICP; 10mm/Hg
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Herniation syndromes
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Displacement of brain tissue under the tough folds of falx cerebri or tentorium cerebelli
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Herniation syndromes (Types)
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A). Supratentorial Herniations
I). Cingulate Herniation II). Transtentorial Herniations 1). Central syndrome 2). Uncal syndrome B). Infratentorial Herniation |
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Supratentorial Herniations
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Herniations in area located above the tentorium cerebelli; contains the cerebrum
(ex: Cingulate Herniation, Transtentorial Herniations) |
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Cingulate Herniation
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Frontal lobe & cingulate gyrus compressesd under falx cerebri; horizontal displacement of a cerebral hemisphere due to an expanding lesion that forces the cingulate gyrus under the falx cerebri, compressing the internal cerebral vein and the contralateral hemisphere
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Transtentorial Herniation
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A bulge of brain tissue out of the cranium through the tentorial notch, caused by increased intracranial pressure.
(ex: Central syndrome, Uncal syndrome) |
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Central syndrome
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Downward shift through tentorial notch
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Central syndrome (S/S)
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decreased LOC, cheyne stokes, fixed pupils, decerebrate posturing
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cheyne stokes
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an abnormal pattern of breathing characterized by breathing becoming shallower until it stops for a while and then breathing starts again and rapidly crescendos to a peak before decaying away again; waxing/waning
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Uncal Syndrome
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Shifts from the middle fossa through tentorial notch compressing 3rd cranial nerve
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Uncal Syndrome (S/s)
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decreased LOC, loss pupil reflex, cheyne stokes, decerebrate posturing
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Cranial Nerve III
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Controls most of the eye's movement, constriction of the pupil, and maintains an open eyelid
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Infratentorial Herniation
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Brain structures below the tentorium cerebelli shift downward through foramen magnum; Can cause death
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Infratentorial Herniation (S/s)
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Decreased LOC, abnormal response, stiff arched neck;
Can cause death |
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Increased ICP and Herniation (S/s)
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Changes in LOC: Decreased blood flow affected RAS/Cortex
V/s: Cushing’s triad (decreased BPM, widening pulse pressure, and decreased hear rate) Ocular signs: Compression on CNIII causing dilation of pupils Decreased motor function: Decorticate and decerebrate Headache/vomiting |
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reticular activating system (RAS)
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the network in the reticular formation that serves an alerting or arousal function
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Primary/Direct Head Injury
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damage is caused by impact.
Categorized as open or closed; according to location of injury (focal, polar, diffuse); or according to mechanism of injury (concussion, contusion) |
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Primary/Direct Head Injury: Closed
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When head strikes object or object strikes head. Dura mater intact.
Coup/focal injury: Injury at site of impact Contrecoup: Rebound effect and injury at opposite site of impact Diffuse axonal injury (DAI) Concussions, contusions, intracranial hematomas |
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Coup/Focal injury
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Injury at site of impact
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Contrecoup
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Rebound effect and injury at opposite site of impact
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Diffuse axonal injury (DAI)
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the shearing (tearing) of the brain's long connecting nerve fibers (axons) that can occur with severe brain injury.
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Primary/Direct Head Injury: Open
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Break in dura and contents exposed to environment
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Effects of the initial trauma: Primary injury
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Contusions, Concussions, Hematomas
Focal or Diffuse injury (Mild, Moderate, Severe) |
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Concussion
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“Mild head injury"
LOC for 5 min or less with retrograde amnesia (forgetting things that occurred before the injury) S/s : headache, N/v, dizziness, Postconcussive syndrome: mild S/s such as headache, irritability, insomnia, and poor concentration and memory may persist for months |
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Contusions
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“moderate head injury”
Damage to brain tissue Many small hemorrhages & some swelling of brain tissue LOC; also hemiparesis (hemiparesis), aphasia, cranial nerve palsy occurs Some damage present (necrosis, laceration, bruising) |
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Hemiparesis
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weakness on one side of the body
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Aphasia
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Loss of ability to understand or express speech, caused by brain damage
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Cranial Nerve Palsy
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Palsy (full or partial paralysis) of the third, fourth or sixth cranial nerves can result in difficulty moving the eye with such symptoms as eyes that don't point in the same direction, reduced depth perception, double vision, ptosis, vision loss, a dilated pupil that doesn't respond to light, etc.
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Hematoma Types
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Laceration of brain tissue
Epidural Subdural (Acute, Subacute, Chronic) |
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Epidural Hematoma (S/s and Pathology)
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Laceration of brain tissue; Accumulation of blood between inner bones of skull and the dura
Cause: Tear of middle meningeal artery Classic S/s: head injury --> brief period of consciousness --> lucid period in which consciousness is regained --> rapid progression to unconsciousness |
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Subdural Hematoma (S/s and Pathology)
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Laceration of brain tissue; Collection blood between dura and arachnoid or into the CSF-filled subarachnoid space (i.e., subarachnoid hematoma)
Cause: Tear in small bridge veins that connect veins on surface of cortex to the dural sinuses Types: Acute (Develops rapidly due to tear of large vein), Subacute (Develops slowly over days due to blood clot lysing and drawing fluid into space), Chronic (Develops weeks after injury; seen in elderly) |
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Acute Subdural Hematoma
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Develops rapidly due to tear of large vein
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Subacute Subdural Hematoma
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Develops slowly over days due to blood clot lysing and drawing fluid into space
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Chronic Subdural Hematoma
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Develops weeks after injury; seen in elderly
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Primary injury: Focal
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is specific observable damage
(Mild, Moderate, Severe) |
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Primary injury: Diffuse
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diffuse axonal injury (DAI): due to "shaking effect” of acceleration/deceleration injuries --> shearing of axons --> axonal damage
(Mild, Moderate, Severe) |
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Primary injury: Focal or Diffuse: Mild
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Coma 6-24h (residual cognitive, sensorimotor, and psychological defects)
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Primary injury: Focal or Diffuse: Moderate
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Coma>24h Recovery incomplete
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Primary injury: Focal or Diffuse: Severe
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Vegetative state “primary brainstem injury”
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Open Head Trauma Types
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Linear fracture, Basilar skull (or basal skull) fracture, Depressed skull fracture
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Open Head Trauma: Linear fracture
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Thin line on x-ray
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Open Head Trauma: Basilar skull (or basal skull) fracture
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Bones of frontal and temporal lobe
Dura mater torn and brain tissue lacerated (Perfect pathway for infection) S/s: Leak of CSF from ear or nose, Battle's sign (bruising behind ears) |
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Open Head Trauma: Depressed skull fracture
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Compound fracture (An injury in which a broken bone pierces the skin, causing a risk of infection)
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Battle's sign
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bruising behind ears
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Secondary Head Injury
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damage results from subsequent brain swelling, infection, or cerebral hypoxia
Primary injury triggers: Ischemia, Increased ICP, Altered vascular regulation, Edema (cytotoxic anad vasogenic) Skull fracture leading threat of infections Concomitant trauma: injuries to other body systems (e.g., chest injury) |
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Concomitant trauma
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Head Injury's injuries to other body systems (e.g., chest injury)
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Blood flow must be maintained at...
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750 to 900 mL/ min or 15% of the resting cardiac output
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Regulation of Cerebral Blood Flow is controlled by
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autoregulatory mechanisms or local mechanisms, sympathetic nervous system
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If cerebral blood flow is totally interrupted for 30 seconds...
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Neurological metabolism altered
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If cerebral blood flow is totally interrupted for 2 minutes...
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Metabolism stops
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If cerebral blood flow is totally interrupted for 5 minutes...
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Cellular death occurs
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Cerebrovascular Accident (Brain Attack)
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The sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function.
Incidence: >700,000 people in the US each year with 20% dying with in 1st year after stroke One of the top 3 causes of morbidity & mortality in US Direct and indirect costs $41 billion annually Types: Ischemic (87%): Transient ischemic attack (TIA) Thrombotic Cardiogenic Embolic Lacunar infarct Hemorrhagic (13%) |
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Risk Factors for Stroke: Hemorrhagic
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HTN (greatest risk)
Advanced age Aneurysm Arteriovenous malformation Head injury Blood dyscrasis (e.g., hypercoagulopathies) Cocaine |
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Risk Factors for Stroke: Ischemic
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HTN, atherosclerosis (thrombotic), Diabetes Mellitus, heart disease such as atrial fibrillation (embolic), obesity, hyperlipidemia, sickle cell disease
Age, gender, race Family history, previous stroke, sedentary lifestyle, smoking, alcohol & drug abuse, hormone replacement therapy, oral contraceptives, dehydration |
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Ischemic Stroke: Transient Ischemic Attack (TIA)
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"ministroke”
Focal cerebral neurologic deficits lasting < 1 hr 200,000-500,000 TIAs are diagnosed annually in US Causes: Atherosclerotic disease of cerebral vessels and emboli May precede a stroke, risk greatest in 1st month following TIA |
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Ischemic Stroke: Transient Ischemic Attack (TIA) (S/s)
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Depend on cerebral vessel involved, but often numbness and mild weakness of contralateral body structures:
Middle cerebral artery (forearm, hand & mouth) Left hemisphere (brief global aphasia) Left PCA (posterior cerebral artery) (transient visual disturbance) Brief unconsciousness and headache |
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Ischemic Stroke: Transient Ischemic Attack (TIA): Middle cerebral artery (S/s)
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forearm, hand & mouth weakness
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Ischemic Stroke: Transient Ischemic Attack (TIA): Left hemisphere (S/s)
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brief global aphasia
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Ischemic Stroke: Transient Ischemic Attack (TIA): Left PCA (posterior cerebral artery) (S/s)
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transient visual disturbance
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Ischemic Stroke: Thrombotic Stroke
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Large vessel stroke
20% of ischemic strokes Decreased blood flow due to atherosclerotic blood vessels --> thrombi --> ischemia Form in either arteries supplying the brain or in intracranial vessels Risk factors: Arteriosclerosis, HTN, smoking, elevated cholesterol, Diabetes Mellitus, hypercoagulopathies (think of risk factors for cardiac disease) |
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Ischemic Stroke: Thrombotic stroke (Pathophysiology)
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plaque or clot formation --> occlusion of artery (commonly in internal carotid, vertebral, and basilar vertebral artery) --> ischemia --> S/s dependent on specific artery affected (generally include: loss of conciousness, motor impairment (contralateral), sensory deficits, agnosias, visual disturbances, aphasia, hemineglect syndrome, spatial-perceptual deficits)
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Ischemic Stroke: Lacunar infarct
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Small vessel stroke; <15 mm wide
25% of ischemic strokes Occur in deep, noncortical parts of the brain/brainstem Occlusion of smaller branches of cerebral arteries Causes: Hypertension, embolism, smalll intracerbral hemorrhages, vasospasm |
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Ischemic Stroke: Lacunar infarct (S/s)
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S/s: No cortical deficits (no aphasia), but produce “lacunar syndromes”- pure motor hemiplegia (Paralysis of one side of the body), dysarthria (Difficult or unclear articulation of speech that is otherwise linguistically normal)
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Ischemic Stroke: Cardiogenic Embolic Stroke (S/s)
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20% of ischemic strokes
Risk factors: Heart disease (e.g., Atrial fibrillation, endocarditis, valvular prostheses, disorders of aorta, carotids, fat and air emboli) Cause: Arterial occlusion caused by fragments that break from thrombus formed outside the brain Occlusion of cerebral blood vessel Sudden onset, often at bifurcations of smaller vessels (most frequent site-middle cerebral artery) Causes ischemia and S/s seen in thrombotic stroke S/s dependent on specific artery affected (generally include: loss of conciousness, motor impairment (contralateral), sensory deficits, agnosias, visual disturbances, aphasia, hemineglect syndrome, spatial-perceptual deficits) |
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Hemorrhagic Strokes
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8-18% of all strokes
Risk factors: HTN, ruptured aneurysms, AV malformations, trauma, erosion of vessels by tumors Rupture of vessel wall leading to bleeding into the brain tissue Causes increased ICP due to increased contents and volume in brain which causes displacement of brain tissue and compression of structures (mass effect) --> ischemia Also irritation from blood causes inflammatory response --> vasodilation and increased cerebral edema further increasing ICP and ischemia S/s: fever, headache, hemiparesis (Abnormal posturing is an involuntary flexion or extension of the arms and legs/weakness), dysphagia, visual disturbances, nausea/vomiting, death If bleeding into subarachnoid space see neck stiffness, photophobia (Extreme sensitivity to light), kernig’s sign (flex leg & then extend --> pain in hamstrings) and brudzinski’s sign (flex head onto chest --> flexion of knees) |
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kernig’s sign
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flex leg & then extend --> pain in hamstrings
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Hemorrhagic Stroke (Pathophysiology)
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Ischemia --> brain cells do not store glucose or oxygen and cannot perform anaerobic metabolism --> necrosis of cells lead to edema --> edema further compromises and increases ICP --> around site of necrosis is area of ischemia which may be salvaged
OR Ischemia --> secondary injury to cells due to glutamate over stimulation causing influx of Ca --> destruction of cell membranes, release of O2 free radicals which perpetuates the cell destruction |
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Secondary injury (Pathophysiology)
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ischemia and hypoxia --> massive release of glutimate leading to glutimate over stimulation --> increased Na and H2O influx, increased Ca into cell and K+ out leads to increased need for ATP to pump ions out --> anaerodic metabolism, acidosis, and cell death
OR ischemia and hypoxia --> breakdown of cell membranes, arachidonic acid and formation of O2 free radicals --> free radicals bind to other cell membranes causing rupture --> cell death leads to more free radical and more cell death |
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Manifestations of Secondary Injury
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reflect location of injury
Neuromotor deficits: Motor neurons destroyed causing loss of movements (akinesia). Remember, that motor pathways cross at medulla so if stroke in Right hemisphere paralysis is of Left side (Initially hyporeflexic and then progress to hyperreflexia) Dysphagia: Impaired swallowing (CN 5,7,9) Aphasia: Receptive: If in Wernickes area (temporal lobe) can’t interpret (lacks auditory association) Expressive: Affects Broca’s area-motor area for speech (located in frontal lobe) Dysarthria: Difficulty pronouncing words. Different than aphasia because due to weakness of lips, tongue, and larynx muscles Spatial perceptual (parietal lobe) Agnosia: Difficulty in interpreting visual, tactile or other sensory info. Unilateral neglect: Neglect of affected side Visual field defects: Occur because visual pathways pass through hemispheres Homonymous hemianopia: Loss of a portion of the visual field May manifest as loss of 1/2 visual field, loss of vision in one eye, or partial lesions in both eyes. Nsg: Arrange objects in unaffected visual field and then teach pt to scan and consciously look to the affected side. Safety measures Kinesthesia: Loss of sensation Emotional lability and thought changes |
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Akinesia
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loss of movements
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Dysphagia
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Impaired swallowing
(CN 5,7,9) |
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Receptive Aphasia
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Affects Wernickes area (temporal lobe)
can’t interpret (lacks auditory association) |
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Expressive Aphasia
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Affects Broca’s area-motor area for speech
(located in frontal lobe) |
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akinesia
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Neuromotor deficits where motor neurons destroyed causing loss of movements
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Dysarthria
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Difficulty pronouncing words. (Different than aphasia because due to weakness of lips, tongue, and larynx muscles).
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Homonymous hemianopia
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Visual field defects that may manifest as loss of 1/2 visual field, loss of vision in one eye, or partial lesions in both eyes.
Nsg: Arrange objects in unaffected visual field and then teach pt to scan and consciously look to the affected side. Safety measures |
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Agnosia
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Difficulty in interpreting visual, tactile or other sensory info.
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Kinesthesia
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Loss of sensation
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Stroke Management
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Diagnostics: H&P, neuro exam, CT, MRI, arteriography, PET(brain cell metabolism)
Thrombolytic treatment: TPA must be done within the first 3 hrs after stroke Complication: Bleeding Anticoagulants and antiplatelets Control cerebral edema (diuretics and hyperventilation) |
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Meningitis
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(An infection of the CNS)
Infection of meninges that may be caused by bacteria, viruses, & fungi Risk factors: Low socioeconomic status, Chronic disease (diabetes, alcoholism), Immunocompromised (AIDS), Complicated labor (neonatal), Age, Neonates and elderly Majority occur in preschool age children Over 95% of pediatric cases < 3 yrs of age Recent UR tract colonization by or infection with an organism that has a propensity for causing meningitis and a focus of infection contiguous with the CNS Communication of subarachnoid space with skin or mucosal surfaces |
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Bacterial meningitis
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Infection of pia mater & arachnoid & of fluid in subarachnoid space
Access route: Systemic or bloodstream infection or direct extension into subarachnoid space Accompanied by bacteria & abnormally high numbers of WBCs in CSF |
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Aseptic meningitis
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Meningeal inflammation without a readily identifiable pathogen
Caused by variety of infectious agents (most are viruses) |
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Fungal meningitis
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Chronic, less common
Occurs in persons with impaired immune responses or alterations in normal body flora |
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TB meningitis
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on rise (esp with AIDS)
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Meningitis (Pathophysiology)
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Bacterial invasion (Usual sequence of events) --> Bacteria colonize upper respiratory mucosa --> Enter systemic circulation --> Enter CNS (most common agents are neisseria meningitis, streptococcus pneumoniae in adults) enter via choroid plexis (In children, the most common is haemophilus influenzae) --> proliferate in subarchnoid space --> Then set off the inflammatory response --> Subarachnoid space essentially devoid of defense mechanisms which allow bacteria to multiply --> Inflammatory response mediated by prostaglandins and cytokines --> Results in increased blood brain barrier permeability, thrombosis of vessels within subarachnoid space, and CSF outflow resistance (inflamation exudates thicken the csf obstructing normal flow) --> Results in increased ICP
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Meningitis (S/s)
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Neonates: (Very subtle symptoms) 50% afebrile, Irritability, poor feeding, lethargy and diarrhea
Older children and adults: Headache, malaise, photophobia, fever, neck stiffness, nausea/vomiting Signs of meningeal irritation: Headache, photophobia, Neck stiffness (On active or passive extension sign), Brudzinski sign (Spontaneous flexion knees and hips when passively flex neck), Kernig’s sign (Posterior thigh pain when extension of knee with hip held in flexion) Neurologic signs: Seizures, altered mental status, neuro deficits Other findings: Petechial rash |
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Brudzinski sign
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Flexion of the hips and knees in response to passive flexion of the neck; signals meningeal irritation.
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Kernig’s sign
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Posterior thigh pain when extension of knee with hip held in flexion; signals meningeal irritation.
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Petechial rash
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is the appearance of red or purple discolorations on the skin that do not blanch on applying pressure
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Meningitis Labs
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Lumbar puncture:
Low glucose often <40mg/dl Elevated protein Increased WBCs CSF culture is gold standard for diagnosis Peripheral WBC with diff, blood cultures |
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Seizures
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(Chronic Neurologic Disorder)
A transient, finite paroxysmal abnormal neuronal discharge that interrupts brain function and results in sudden change in behavior, sensory perception, and motor activity Provoked seizures and Unprovoked seizures Incidence: 1st episode occurs before age 20. After age 20, often caused by a structural change (e.g., trauma, tumor, or stroke) |
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Provoked Seizures (Etiology)
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(acquired/secondary/acute seizures)
Neoplastic disease: Brain tumors Trauma: Physical (Head trauma), Chemical (Exposure to toxins: heavy metal, withdrawal from alcohol or sedative hypnotic drugs, drug abuse such as cocaine) Vascular diseases: Hypoxia, CVA Infectious diseases of the CNS: Meningitis, encephalitis Sensory stimuli: Fever, fatigue, stress, sensory stimuli: flashing lights, loud noises Metabolic or nutritional disorders: Fluid & electrolyte imbalances (hypoglycemia, hyponatremia, water intoxication) |
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Unprovoked seizures (Etiology)
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(primary or idiopathic)
Genetic factors: Congenital abnormalities of the CNS, perinatal brain injury. Sensory stimuli serve as predisposing factors |
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Types of seizures:
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Partial: last about 1 min (simple, complex, secondarily generalized)
Generalized: (Absence (petit mal), Tonic Clonic, Myoclonic, Atonic) Status epilepticus, Prodromal Period, Aura |
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Partial Seizures
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last about 1 min
involve neurons on 1 side of brain focal onset: hand, mouth twitches originate from cortical brain tissue (superficial) types: simple, complex, secondarily generalized |
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Simple Partial Seizures
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(without LOC) sensory, motor or both
Sensory: ex tingling, crawling sensation Motor: contralateral side |
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Complex Partial Seizures
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(with LOC) temporal lobe. Begin in localized area but progresses to involve both hemispheres.
aimless wandering, stares straight ahead, lip smaking, automatic hand movement |
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Secondarily Generalized Partial Seizures
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rapidly moves from partial to generalized (often have aura)
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Generalized Seizures
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(Absence (petit mal), Tonic Clonic, Myoclonic, Atonic)
Involve neurons in both cerebral hemispheres Do not have focal onset Usually originate from subcortical or deeper brain foci (thalamus, basal ganglia, brain stem) Impaired or loss of consciousness always occurs due to spread of electrical activity to thalamus and reticular activating system |
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Absence (petit mal) Generalized Seizures
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usually seen in children; rarely occurs beyond adolescence
Manifests as brief staring spell last few seconds If untreated, may occur up to 100X/day Can be precipitated by flashing lights, hyperventilation, S/s: Brief loss of consciousness, blinking, lip smacking |
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Tonic Clonic (Grand mal) Generalized Seizures
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Usually lasts <5 minutes
Involve sudden unconsciousness followed by muscle rigidity (tonic phase) Tonic: Muscle contraction or tension (spasm) with extension of extremities, respirations are arrested, bladder and bowel incontinence Clonic: Relaxing of muscle, following by rhythmic contractions (alt contraction and relaxation) Eyes roll back, salivate, diaphoretic/Inducing heavy perspiration |
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Seizures (Pathophysiology)
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hypersensitive neuron in cerebral cortex is stimulated by any of the following: hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation --> cells fire in increasing frequency and amplitude until threshold is reached --> inhibitory neurons slow the firing, cause interrupting seizure (tonic clonic)
OR hypersensitive neuron in cerebral cortex is stimulated by any of the following: hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation --> cells fire in increasing frequency and amplitude until threshold is reached --> impulse spreads to nearby neurons and over entire brain --> muscles contract and loss of consciousness, stiffening of body, tempor, apnea, biting tongue, cyanosis, jaws fixed, hands clenched, in continent --> end of seizure causes depressed CNS action, post ictal state: sleepy, confused |
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Status Epilepticus (Seizures)
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seizures that do not stop spontaneously or occur in succession with out recovery
Occurs in some seizure disorders Potentially life-threatening Seizure activity increases need for ATP by 250% and cerebral O2 consumption by 60% and can lead to brain tissue injury and destruction |
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Prodromal Period (Seizures)
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Precedes some seizures, may last minutes or hours
Vague change occurs in emotional reactivity or affective responses (Depression or anxiety) Other phenomena: headache, lethargy |
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Aura (Seizures)
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Brief sensory experience
Seen with partial seizures Feeling of weakness, dizziness, numbness, “funny feeling”, or odor immediately preceding a seizure |
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Spinal Cord Injury (SCI) (Pathophysiology)
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damage to the neural elements of the spinal cord
Trauma which causes fracture/dislocation --> fragmentation of bone/displacement of bone, disc or ligaments --> which compromise blood flow to cord, or cord can be compressed or transected, or neural tissue overstretched Mainly occurs in persons aged 16-30 Most common cause is trauma due to motor vehicle accidents followed by falls, violence (gunshot wounds), & recreational sporting activites Also can be due to tumors, osteoporosis, congenital abnormalities (e.g., spinal bifida), ischemia & infarction, and bone disease with pathologic fracture of vertebrae Mortality rates are higher the first after injury; death usually due to renal failure, sepsis, resp failure |
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Spinal Cord Injury (SCI) Mechanisms
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flextion injury, extension injury, flextion-rotatoin injury, compression injury
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Mechanisms of initial Spinal Cord Injury (SCI)
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Cord compression due to bone displacement, interruption of blood supply, traction (pulling) on the cord (E.g., diving injury)
Transection or tearing due to penetrating injuries |
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Primary Spinal Cord Injury (SCI) (Pathophysiology)
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injury which causes edema and microscopic hemorrhages at the site of the injury --> edema at site of injury and 2 segments above and below injury --> decrease microcirculation to cord causing necrosis and destruction to axon sheath --> cord swelling increases degree of dysfunction --> loss of normal activity of spinal cord function below level of injury
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Secondary Spinal Cord Injury (SCI) (Pathophysiology)
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additional events further compromise cord leading to increased necrosis --> release of vasoactive suvstances from the wound (inflammation), vessel trauma leading to ischemia, release of proteolytic enzymes --> vasospasm, increased vascular permibility, decreased blood flow, delayed swelling causing further necrosis
OR additional events further compromise cord leading to increased necrosis --> decreased extracellular Ca with increased intracellular Ca --> net effect causes ischemia and cord necrosis --> can be reversed by high dose steroids in 1st 6 hours |
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Spinal Cord Injury (SCI) (S/s)
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Loss of normal activity of the spinal cord below level of injury
Spinal shock: Loss of reflexes below level of injury which lasts 7 to 20 days then return of reflexes. Flaccid paralysis, loss of sensation, bowel and bladder control, poor venous circulation (due to peripheral Vasodilation from loss of sympathetic innervation) Motor and sensory impairment/loss depends on level of injury and degree of injury: Tetraplegia/quadriplegia (Paralysis all 4 extremities seen with injury above C6), If injury above C4 then loss of respitory muscle function occurs (injury can be fatal), Paraplegia (Injury to thoracic, lumbar, or sacral vertebrae; Paralysis 2 lower extremities occurs) |
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Types of SCI: Incomplete injuries
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Central cord syndrome
Anterior cord syndrome |
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Central cord syndrome
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Most common in cervical cord region. Damage is to central part of the cord
Weakness and sensory loss in both upper and lower extremities (greater deficit in upper) |
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Anterior cord syndrome
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Seen with flexion injuries
Motor paralysis and loss of pain and temp below level of injury. However, sensation, touch and vibration intact |
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Spinal Cord Injury Complications
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Autonomic hyperreflexia (autonomic dysflexia)
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Autonomic hyperreflexia (autonomic dysflexia)
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Seen in injuries above 6th thoracic vertebrae and after spinal shock subsides
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Autonomic hyperreflexia/autonomic dysflexia (Pathophysiology and S/s)
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stimulus (distended bladder, bowel skin pain receptors) --> triggers reflexive arteriolar spasm --> increased blood pressure --> baroreceptors sense hypertension and parasympathetic response triggered to decrease heart rate and vasodilate --> impulse to vasodilate cannot reach below injury, but can decrease heart rate --> S/s: can vasodilate above injury (flushed, sweating, headache, blurred vision), constricted below (cool, clammy), decreased heart rate (30-40 bpm)
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