Exam 4 Flashcards
1
Q
Full Consciousness
A
Cognitive cerebral function, fully aroused, fully aware
A state of awareness of both oneself and the environment and a set of responses to that environment.
- The fully conscious person responds to external stimuli with many responses
- Any decreased state of this awareness and responses is a decrease in consciousness
2
Q
Consciousness involves
A
- Arousal
- Awareness
3
Q
Arousal
A
an individual’s state of awakeness (mediated by the reticular activating system: RAS)
Can vary in an individual from day to night as someone’s level of awakeness.
4
Q
Vegetative State
A
NO cerebral function, but crude awakened state
A crude awakening state characterized by loss of cerebral function
- its like “being in a fog” - you’re not able to fully respond to what’s happening; some can hear you but they cannot respond
- this is maintained by the reticular activating system and the brain stem
5
Q
Vegetative State maintained by
A
Reticular activating system and brain stem.
6
Q
Types of alterations in arousal (3)
A
- Structural
- Metabolic
- Psychogenic
7
Q
Structural Alterations in Arousal types and causes
A
Can be above or below tentorial plate.
Causes include:
- infections
- Vascular
- Neoplasms
- Traumatic (brain bleeds)
- Congenital
- Degenerative
- Polygenic
8
Q
Awareness
A
Content of thought. Encompasses all cognitive functions.
9
Q
Reticular Activating System
A
Mediates arousal/maintains consciousness.
Responsible for regulating aspects of attention and information processing.
When someone looses cerebral function, the RAS has to work harder to maintain a level of consciousness. RAS and brainstem will compensate by maintaining a vegetative state.
10
Q
Manifestations of a structural alteration of arousal
A
Depend on if the problem is above or below the tentorial plate. (don’t have to differentiate)
11
Q
Metabolic alterations in arousal causes
A
Causes include:
- Hypoxia
- Electrolite disturbances
- Hypoglycemia (low blood sugar)
- Drugs
- Endogenous (from within) and exogenous (injested) toxins.
12
Q
Psychogenic alterations in arousal
A
Unresponsiveness that might be present in some psychiatric disorders.
Different than metabolic and structural alterations, because the person is actually awake. They “choose” not to respond to the environment.
13
Q
Evaluation points of neurologic function (5)
A
- Level of Consciousness
- Patterns of breathing
- Pupillary reaction
- Oculormotor responses
- Motor responses
14
Q
Level of Consciousness (evaluation of neurologic function)
A
The most critical index of nervous system function. A Change in level of consciousness (LOC) can indicate either improvement or deterioration of the individual’s condition.
Alert and oriented x4 refers to person, place, time, and situation. If a person is aware of all of these things then they are considered to be functioning at the highest level of consciousness.
From the highest state it can decrease to confusion and even coma.
15
Q
Patterns of breathing (eval of neuro function)
A
Helps evaluate the level of brain dysfunction and coma.
- Rate
- Rhythm
- Pattern
16
Q
Cheyne-Stokes Respirations:
A
abnormal pattern of ventilation that have alternating periods of Tachypnea (elevated resp. rate) and Apnea (lack thereof). Commonly see Cheyne-Stokes in very depressed levels of Consciousness.
17
Q
Pupillary reactions (eval of neuro function)
A
Can indicate the level and presence of brainstem dysfunction because brainstem areas that control arousal are adjacent to areas that control pupils.
Pupillary reactions can be a variety of changes, so we must take a look at what is causing it; example is Drugs
18
Q
Causes of fixed pupils
A
- Severe ischemia
- Hypoxia
- Hypothermia
19
Q
Oculomotor responses (eval of neuro function)
A
-Resting
-Spontaneous
-Reflexive
:eye movements that can change at various levels of brain dysfunction in comatose individuals.
If a person is in a metabolic induced coma, they may retain reflective eye movements even when other signs of brainstem damage are present.
20
Q
Motor Responses (eval of neuro function)
A
help evaluate the level of brain dysfunction and determine the most severely damaged side of the brain.
Ex. If someone has a stroke and the right side of their body is not functioning properly, then we know it is the left side of the brain that is most damaged. ( see page 351 to see DOLL’S EYES PHENOMENON )
21
Q
Patterns of motor responses
A
- Purposeful movements
- Inappropriate movements
- No motor movements
22
Q
Motor responses associated with decreased consciousness
A
- Rigidity
- Reflex grasping
- reflux sucking
- snout reflex
- palmo-mental reflex
23
Q
Posturing types
A
Occur with neurologic dysfunction
- Decorticate
- Decerebrate
24
Q
Decorticate Posturing
A
(raptor arms)
- Flexion of arms, wrists and fingers
- Adduction in upper extremities
- Extension, internal rotation and plantar flexion in lower extremities
25
Decerebrate Posturing
(Straight arms)
- All four extremities in rigid extension
- Hyperpronation of forearms
- Plantar extension of feet
26
Types of neurologic death
Two forms of neurologic death that result from severe pathologic conditions and are associated with irreversible coma.
- Cerebral Death
- Brain Death
27
Brain death
Occurs when the brain is damaged so completely that it can never recover and cannot maintain the body’s internal homeostasis.
- Cessation of function of the entire brain including brain stem and cerebellum.
- Must be on life support because the brain doesn’t sustain life.
Brain death has occurred when there is no evidence of brain function for an extended period of time (flat EEG for 6-12 hours) and resulted from structural or known metabolic disease, not drugs, alcohol, or hypothermia.
28
Cerebral Death
Irreversible coma.
Death of the cerebral hemispheres exclusive of the brainstem and cerebellum. Internal homeostasis may be maintained (ie body temperature, cardio, etc.)
Damage is permanent, and the individual is forever unable to respond behaviorally in any significant way to the environment.
29
Alterations in awareness
- Selective Attention Deficit
- Executive Attention Deficit
- Alterations in Image Processing
- Sensory Inattentiveness
- Deficiencies in Memory
30
Selective Attention Deficit
This rarely occurs as an isolated event, it is usually associated or caused by other deficits including seizures, contusions, hematomas, strokes, gliomas, alzheimers, tumors, and dementia.
It refers to the ability to select certain information and focus on it for processing and can be temporary, permanent, or progressive depending on its cause.
31
Manifestations of selective attention deficit
- Cannot focus attention
- Decreased eye head, and body movements toward stimuli
- History of falls, injuries (safety issue.)
32
Memory
The ability of the brain to store and retrieve information
33
Amnesia
Loss of memory
34
Types of amnesia
- Retrograde
| - Anterograde
35
Retrograde amnesia
Loss of the past memories, both personal and factual history like events. New memories can still be formed and retained.
S & S vary according to the side of the brain the damage was done on. Either way, memory problems that others report as formerly known information.
Left Side Trauma:Inability to retrieve past personal history, unaware of recent current events.
Right Side Trauma:Inability to remember past persons, places, objects, music, etc:
36
Manifestations of retrograde amnesia
vary according to the side of the brain the damage was done on. Either way, memory problems that others report as formerly known information.
- Left Side Trauma:Inability to retrieve past personal history, unaware of recent current events.
- Right Side Trauma:Inability to remember past persons, places, objects, music, etc:
37
Anterograde Amnesia
The past information is retained, the person is unable to remember any new personal or factual information (post trauma).
38
Manifestations of anterograde amnesia
Vary according to the side of the brain the damage was done on but overall a person would be confused, disoriented, inability to listen, remember new information. They would show signs of behavioral changes.
- Left Side Trauma: Impaired language and semantic memory. Disorientation to time, situation, place, name, and persons.
- Right Side Trauma: Impaired episodic memory (personal history), emotional memory, disorientation (self, person, and place).
39
Executive Attention Deficits
e.g. ADHD
Inability to maintain sustained attention in order to set goals and recognize when an an object will help them meet a goal. It also manifests with a working memory deficit so the person is not able to remember instructions or information needed to complete a task or guide behavior.
It can be temporary, progressive, or permanent depending on the trauma/cause.
40
Alterations in Image Processing
The inability to form concepts, categorize, assign meaning, and make generalizations using sensory data. It can be temporary or permanent depending on the trauma/cause. They show the inability to reason and think abstractly, very concrete reasoning is demonstrated, might be delusional.
41
Sensory Inattentiveness
AKA “Neglect Syndrome”
Inability to recognize sensory input from the dysfunctional side/part of body. An example includes a person who had a stroke with loss of function in right arm, they can't perceive sensation, eventually the brain stops recognizing the limb all together.
42
Seizure
Results from a sudden, explosive disorderly discharge of cerebral neurons.
This can involve, motor, sensory, autonomic and psychic clinical manifestations and temporarily altered arousal.
They may not involve all of these manifestations.
43
Convulsions
The jerky contract-relax movement associated with some seizures
44
Epilepsy
Seizure activity for which no underlying correctable cause for the seizure can be found.
45
Causes of seizures
- Hypoglycemia
- Exhaustion
- Stress
- Stimulant drugs
- Environmental stimuli such as blinking lights, odors, and changes in temps.
46
Classifications of seizures (3)
- Partial
- Generalized
- Unclassified
47
Partial seizures
Begin locally.
Three types:
- Simple
- Complex
- Secondarily generalized
48
Simple partial seizure
do NOT include loss of consciousness but may have sensory, motor, psychic our autonomic signs.
49
Complex partial seizure
includes impairment of consciousness, may be precipitated by simple partial seizure.
50
Secondary generalized partial seizure
Partial onset but evolve to generalized tonic-clonic seizure
51
Generalized seizures
Bilaterally symmetric and so not have a local onset. (Grand-Mal seizure)
- Absence
- Myoclonic
- Clonic
- Tonic
- Tonic-clonic
- Atonic
52
Phases of generalized seizures
1. Aura: Partial seizure immediately preceding the onset of a generalized tonic-clonic seizure.
2. Prodroma: Early manifestations occurring hours to days before a seizure - warning sign
3. Tonic Phase: Muscle contraction with increased muscle tone.*
4. Clonic phase: alternating contraction and relaxation of muscles*
5. Postictal phase: altered level of consciousness that can last 5-30 min.
* During seizure
53
Treatment for seizure/epilepsy
Correcting or controlling the cause and, if none is identified, give antiseizure medicine.
54
Types of data processing deficits
- Agnosia
- Dysphasia
- Acute Confusional States (ACS)
- Dementia
55
Agnosia
A defect of pattern recognition. A failure to recognize the forms and nature of objects.
-Tactile
-Visual
-Auditory
:generally only one sense is affected.
Although agnosia is associated most commonly with cerebrovascular accidents, it may arise from any pathologic process that injures specific areas of the brain.
56
Dysphasia
Impairment of comprehension or production of language with impaired:
- Communication
- Comprehension
- Use of symbols
In either written or verbal language is disturbed or lost. It is usually associated with cerebrovascular accident involving the middle cerebral artery or one of its many branches. It results from dysfunction in the left cerebral hemisphere, usually the frontotemporal region.
57
Types of dysphasia
- Expressive
- Receptive
Not as important to know:
-Transcortical (can't repeat/recite, but can understand)
58
Acute Confusional States
Transient disorders of awareness that result from cerebral dysfunction caused by drug intoxication, metabolic dosorders, nervous system disease/trauma/surgery
- Delerium
- Hypokinetic confusional state
59
Delerium
Associated with overactivity of nervous system; causes hyperconfusion
- occurs in critical care units or following surgery or withdrawal
- this will improve over time/lasts 2-3 days
60
Manifestations of delirium
- difficulty concentrating
- restlessness
- irritability
- sleep problems
- poor appetite
61
Hypokinetic confusional states
Underactivity of nervous system.
Occurs in people with fever or metabolic disorders
62
Manifestations of Hypokinetic Confusional States
- Forgetfulness
| - Sleep a lot
63
Dementia
Progressive failure of cerebral functions. Doesn't go away. Caused by neuro degeneration, compression, atherosclerosis and trauma; also associated with genetic pre-dispositions including alzheimer and Huntington disease
Decrease in:
- Orienting
- Memory
- Language
- Judgement
- Decision making
64
Alzheimer disease
one of the most common causes of severe cognitive dysfunction in older persons and the leading cause of dementia
Exact cause unknown
•Linked to three genes with mutations on chromosome 21
•Formation of neuritic plaques containing a core of amyloid-beta protein, creation of neurofibrillary tangles, and degeneration of basal forebrain cholinergic neurons with loss of acetylcholine.
65
Manifestations of Alzheimer
* Insidious, forgetfulness, and emotional upset •Becomes more forgetful over time
* Memory loss gradually increases
* Loses the ability to concentrate
* Loses the ability to problem solve
* Judgment deteriorates
* Behavioral changes
* Mood swings
66
Alterations in Cerebral hemodynamics
An injured brain reacts with structural, chemical, and pathophysiological changes that are called secondary brain injuries. Critical features of these changes include alterations in cerebral blood flow, intracranial pressure and oxygen delivery.
67
Cerebral blood flow (CBF)
Blood flow to the brain is normally maintained at a rate that matches metabolic needs of brain
68
Cerebral perfusion pressure (CPP)
70-90mm Hg; pressure required to perfuse cells of the brain
69
Cerebral Blood volume (CBV)
The amount of blood in the intercranial vault at a given time.
Can fluctuate depending on needs of brain at the time
70
Cerebral Oxygenation
Critical factor; measure by oxygen saturation in the internal jugular vein
71
Alterations in cerebral blood flow may be related to three injury states
- Inadequate cerebral perfusion (cerebral oligemia)
- Increase intercranial Pressure (with normal perfusion)
- Excessive cerebral blood volume (cerebral hyperemia)
72
Normal intracranial Pressure
1-15 mm Hg
73
Increased Intracranial Pressure (IICP)
May result from an increase in
- Intracranial content (tumor growth)
- Edema
- Excess CSF (Cerebrospinal fluid)
- Hemorrhage
- IICP necessitates an equal reduction in volume of the other cranial contents.
- The easiest thing for the brain to get rid of to make more room is remove CSF
- If removing the CSF doesn’t work, cerebral blood volume and blood flow are altered
Four stages
74
Stage 1 of Increased Intracranial Pressure (IICP)
Vasoconstriction and external compression of venous system in attempt to decrease pressure.
- Compensatory response begins
- So the Actual ICP may not change if compensatory mechanism is successful
75
Stage 2 of Increased Intracranial Pressure (IICP)
Continued expansion of intercranial content. There is an increase in ICP that may start to exceed brain’s ability to adjust
S/S- subtle & transient:
- confusion
- restlessness
- drowsiness
- pupillary
- breathing changes
76
Stage 3 of Increased Intracranial Pressure (IICP)
ICP now has an effect on arterial pressure; the brain tissues begin to experience hypoxia and the patient’s conditions begin to rapidly deteriorate.
S/S:
- widened pulse pressure
- bradycardia
- small sluggish pupils
- decrease levels of arousal
77
Stage 4 of Increased Intracranial Pressure (IICP)
Brain tissue shifts (herniates) from area of high pressure to a compartment of lesser pressure
- When it shifts, the brain tissue’s blood supply is compromised-- leads to more ischemia & hypoxia
- Small hemorrhages develop in the brain tissue as well as obstructive hydrocephalus
78
Cerebral edema
Increase in fluid content of brain tissue
Occurs after brain insult from:
- Trauma
- Infection
79
Types of cerebral edema
- Vasogenic edema*** most important
- Cytotoxic (metabolic) edema
- Interstitial edema
80
Vasogenic edema
Caused by increased permeability of the capillary endothelium of the brain after injury to vascular structures.
Edema starts at the vascular site of injury and spreads from there.
81
Manifestations from vasogenic edema
- Disturbances of level of consciousness
| - Severe increase of ICP
82
Cytotoxic edema
Caused by toxins that directly affect brain's cellular elements of the brain that transport K+ and Na+ in the brain.
Damage to cell membranes=loss of potassium/increased sodium creates swelling.
83
Interstitial edema
Seen mostly with noncommunicating hydrocephalus.
Edema caused by movement of spinal fluid.
84
Hydrocephalus
Characterized by excess fluid in the cerebral ventricles and subarachnoid space, or both.
Occurs because of interference with Cerebrospinal Fluid (CSF) flow; Increases pressure and dilation of ventricles. The increased pressure and dilation cause atrophy of the cerebral cortex and degeneration of white matter.
85
3 Kinds of Hydrocephalus
- Non-communicating
- Communicating
- Acute
- Normal
86
Non-communicating hydrocephalus
Obstruction within the ventricular system; is seen more often in children; also known as Intraventricular Hydrocephalus;
Develops gradually
87
Communicating
Refers to defective resorption of CSF from the cerebral subarachnoid space; is found more often in adults;
develops gradually
Signs and Symptoms : decrease in memory and cognitive function over time
88
Acute hydrocephalus
May develop in a couple hours in persons who have sustained head injuries. Contributes significantly to Intracranial Pressure increase.
Very Dangerous!
Sign and Symptoms: will go into a deep coma if not treated immediately
89
Alteration in muscle tone
- Hypotonia
| - Hypertonia
90
Normal muscle tone
Involves a slight resistance to passive movement. Movement is smooth, constant, and even throughout the range of motion.
91
Hypotonia
- Decreased muscle tone
- Passive movement of a muscle occurs with little to no resistance
- Joints hyperflexible
- Muscles can atrophy due to decreased use and appear flabby or fat.
Caused by cerebellar damage
92
Manifestations of hypotonia
- Tire easily or are weak
- Difficulty rising or sitting without support
- Difficulty using stairs
- Inability to stand on toes
93
Hypertonia
- Increased muscle tone
- Passive movement of a muscle occurs with resistance (more than in normal muscle tone)
- Muscles can atrophy due to decreased use or overstimulation of muscle fibers
- Muscles can also experience hypertrophy due to over-stimulation of the muscle fibers (more rare)
94
Manifestations of hypertonia
- Individuals tire easily or are weak
- Rigidity
- Difficult to move
95
Paresis
Weakness, incomplete loss of muscle power and tone. Some function, but not much.
(2 types, upper motor neuron and lower motor neuron syndromes)
96
Paralysis
Complete loss of muscle power and function, cannot overcome gravity.
(2 types, upper motor neuron and lower motor neuron)
97
Upper Motor Neuron Syndromes
Associated with spastic muscle tone, contributing to the loss of function.
98
Lower Motor Neuron
Associated with flaccid motor tone. Impairs both voluntary and involuntary movement.
99
Hemiparesis/Hemiplegia
One side is affected
100
Paraparesis/Parapalegia
Waist down
101
Quadriparesis/Quadriplegia
Affects all extremities
102
Areflexia
Loss of tendon reflexes
103
Diplegia
Loss of function corresponding to the trauma of a cerebral hemisphere injury
104
Spinal Shock
Complete loss of spinal cord function below injury
105
Huntington Disease
Also known as chorea, is a relatively rare, hereditary, degenerative hyperkinetic movement disorder diffusely involving the basal ganglia and cerebral cortex.
The onset of Huntington disease is usually between 25 and 45 years of age, when the trait may already have been passed to the person’s children.
106
Patho of Huntington Disease
It is inherited from both mothers and/or fathers who have the autosomal dominant trait with high penetrance.
- The principal pathologic feature of Huntington disease is severe degeneration of the basal ganglia, particularly the caudate nucleus.
- Basal ganglia and nigral depletion of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter, is the principal biochemical alteration in Huntington diseasel.
- It alters the integration of motor and mental function. Frontal cerebral atrophy occurs late in the disease.
107
Manifestations of Huntington Disease
Symptoms of Huntington disease progress slowly and include:
- Involuntary fragmentary movements such as chorea (irregular, uncontrolled, excessive movement)
- Athetosis (writhing movements)
- Ballism (flinging movements).
Chorea, the most common type of abnormal movement, begins in the face and arms, eventually affecting the entire body.There is a progressive dysfunction of intellectual and thought processes (dementia).
108
Treatment of Huntington Disease
The diagnosis is based on family history and clinical manifestation of the disorder.No known treatment.
109
Parkinson Disease
a commonly occurring disorder of movement. Either primary Parkinson disease or secondary parkinsonism may occur.
110
Primary Parkinson
Begins after the age of 40 years, with the incidence increasing after 60 years. It is more prevalent in males and a leading cause of neurologic disability in individuals older than 60 years.
111
Secondary Parkinson
Parkinsonism caused by disorders other than Parkinson’s disease (ie. head trauma, infection, neoplasm, atherosclerosis, toxins, drug intoxication).
112
Patho of Parkinson
The pathogenesis if primary Parkinson disease is unknown. Several genes have been identified. Epidemiologic data also suggest viral and environmental toxins as possible causes.
There is degeneration of the basal ganglia with dysfunctional or misfolded a-synuclein protein and loss of dopamine producing neurons in the substantia nigra and dorsal striatum. The resulting depletion of dopamine, an inhibitory neurotransmitter, and relative excess of cholinergic (excitatory) activity in the feedback circuit are manifested by hypertonia (tremor and rigidity) and akinesia, producing a syndrome of abnormal movement called parkinsonism.
Dementia may develop over decades with infiltration of Lewy bodies (accumulation of abnormal protein in nerve cells) and plaque formation similar to Alzheimer disease.
113
Manifestations of Parkinson
- Tremor at rest
- Rigidity
- Bradudinesia/akinesia
- Postural disturbance
- Dysarthria
- Dysphagia
114
Treatment of Parkinson
the diagnosis of Parkinson disease is based on the history and physicail examination. Treatment is symptomatic with drug therapy to decrease akinesia. Deep brain stimulation is replacing surgery to treat persons unresponsive to drug therapy. Implants of stem cells and fetal cells as well as gene therapy hold promise for future treatments.
115
Open trauma injuries
- dura matar is penetrated/ not intact
- there is exposure to environment
- less common than closed injury
- includes compound fractures and missile injuries
116
Closed trauma injuries
- involves head striking a hard surface or a rapidly moving object striking the head
- more common than open trauma
- dura mater is not penetrated/remains intact
- no exposure to outside environment
117
Coup
injury directly below site of forceful impact
118
Countrecoup
injury is on opposite side of brain from site of forceful impact
119
Local (focal) injuries
- also called focal injury
- affects one area of brain
- usually associated with an event of primary brain injury
120
Diffuse (diffuse axonal injury) injuries
- these are widespread injuries
- affect more than one area of brain - aka diffuse
- usually associated with an event of primary brain injury
121
Primary brain injuries
```
•Caused by the impact
•Involves:
-contusions
-concussions
-extradural hematomas (epidural hematoma)
-subdural hematoma
-intracerebral bleeds
```
122
Focal Brain injuries
- Specific
- Grossly observable brain lesions- cortical contusions, epidural hemorrhage, subdural hematoma, intracerebral hematoma
- Force of impact produces contusions
- Coup or contrecoup- compression of the skull at point of impact
- Contusion/ bleeding from small tears in blood vessels- forces; found in frontal lobe
123
Extradural hematomas
AKA epidural hematoma:
- Bleeding between dura mater and the skull
- 1-2% of major head injuries
124
Manifestations of extradural hematomas
-Lose consciousness at time of injury
-Become lucid for a few minutes to a few days
As the hematoma accumulates:
-Headache of increasing severity
-vomitting
-Drowsiness, confusion
-Seizures
-Hemiparesis
125
Subdural hematomas
- Bleeding between the dura mater and the brain
- 10-20% of persons with traumatic brain injury
- Acute vs. Chronic
126
Acute subdural hematomas
develop rapidly within hours and located at the top of the skull
127
Chronic subdural hematomas
develop over weeks to months & occur in elderly and alcohol abusers
128
Intracerebral hematomas
- Bleeding within the brain:
- 2-3% of persons with head injuries
- Associated with contusions
129
Manifestations of Intracerebral Hematomas
- Decreased LOC
- Contralateral hemiplegia
- ICP rises
- Temporal lobe herniation may appear
130
Open Brain trauma
- discrete (focal) injuries
- compound fractures and missile injuries
- Compound fracture: opens a communication between -cranial content and environment
131
Manifestations of open brain trauma
- Laceration of the scalp
- Tympanic membrane- sinuses
- Eye- mucous membrane are present
* Further investigate if these occur
132
Missile injuries
- Crush injury (laceration & crushing of what missile touches)
- Stretch injury (blood vessels & nerves damaged w/o direct contact – result of stretching)
- Tangential injury is to the coverings & brain (scalp & brain lacerations)
133
Causes of Missile injuries
- Skull fractures
- Laceration of meninges cerebral
- Projectiles & debris from scalp & skull injuries
- Bullets, rocks, shell fragments, knife & blunt instruments
- Hemorrhagic contusions may coalesce into large confluent intracranial hematoma.
134
Manifestations of acute subdural hematomas
Begins with:
- headache
- drowsiness
- restlessness or agitation
- slowed cognition
- confusion
As it progresses:
- loss of consciousness
- respiratory changes
- pupillary dilation
135
Manifestations of Chronic subdural hematomas
- Headache
- Tenderness over hemataoma on palpation
- progressive dementia
- generalized rigidity (paratonia)
136
Types of diffuse brain injury
- Mild concussion
- Classic concussion
- Mild diffuse axonal injury (DAI)
- Moderate DAI
- Severe DAI
137
Diffuse brain injury characteristic
Widespread. Can include an array of affects:
- Physical Paralysis, Periferal
- Difficulty swallowing
- Learning Difficulties
- Behavioral problems
- Agitation
- Impulsive
- Socially withdrawn
138
Mild concussion
- Immediate
- Transitory (manifestations won't last)
Spinal pressure increases
EEG change
No loss of consciousness
139
Classic concussion
Loss of consciousness up to 6 hours.
Reduction in reflex
140
Mild Diffuse Axonal Injury (DAI)
- 30% Posturing
- Prolonged confusion
- Restlessness
141
Moderate Diffuse Axonal Injury (Moderate DAI)
- Conciousness deteriorates-Unconcious lasting days to weeks
- Post-tramatic AMNESIA
- Often permanent deficit in memory, attention, executive fxn, etc
142
Severe Diffuse Axonal Injury (Severe DAI)
Posturing
- (+) Levels of concussion-Intercranial pressure 4-6 days after
- IMMEDIATE Autonomic Dysfunction-RESOLVES in a few weeks--MAY retain pulmonary complications
143
Post-concussive Syndrome
- Not a brain Injury
- after a Concussion
- Headache
- Anxiety
- Insomnia
- Can’t concentrate
- Fatigue- 2-3 wks
144
Three types of brain injury
- Primary
- Secondary
- Tertiary
145
Primary brain injury
Caused by the original impact or Injury.
Involves:
- Contusions
- Concussions
- Extradural Hematomas (Epidural Hematomas)
- Subdural Hematomas
- Intracerebral Bleeds (Hemorrhages)
146
Secondary brain injury
Result of both systemic and intracranial processes and is an indirect result of primary brain trauma:
- Systemic Hypotension
- Hypoxia
- Anemia
- Edema
- Inflammatory Reaction, Cascades
- Ischemia
- Increased ICP
147
Tertiary brain injury
Occurs days to months after the primary injury and is associated with Infection:
- Pneumonia
- Fever
- Infections
- Immobility.
If Tertiary Brain Injury occurs it can cause further injury than the primary Injury did.
148
Spinal injuries
Most commonly occur because of vertebral injuries. The four vertebral injuries are:
- Simple fractures-a single break
- Compressed fracture- vertebral body compressed anteriorly
- Comminuted fracture-vertebral body “bursts” into many pieces
- Dislocation- vertebrae move out of alignment
Fractures occur with both direct and indirect trauma that compress, pull, or shear the tissues and most commonly occur from motor vehicle accidents.
149
Manifestations of spinal injuries
Normal activity of the spinal cord cells at and below the level of injury ceases because of loss of the continuous tonic discharge from the brain or brain stem and inhibition of suprasegmental impulses immediately after cord injury, thus causing spinal shock.
the big take away was:
Loss of motor and sensory function depends on level of injury and type of injury
150
Hyperextension
Hyperextension of the spine can result in fracture or non-fracture injuries with spinal cord damage. Usually happens in the cervical area from acceleration force that propels the neck backwards.
151
Flexion
A flexion injury produces dislocation or fracture of vertebra, discs, and ligaments. It results from a sudden and excessive force that propels the neck forward. It also may compromise vascular structures within the spinal cord.
152
Axial Compression
The spinal cord is contused directly by shattered bone or disk material colliding into the spinal canal. It results from a force applied from the top of the head.
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Flexion-Rotation
Ruptures support ligaments and produces fractures of the vertebra. It would be like if someone twisted and broke your neck, its the combination of a shearing force with acceleration.
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Spinal shock
This is a result of spinal cord injury. Reflexes are lost completely in all segments below the lesion. It can last 7-20 days typically but can go as long as 3 months.When reflexes return this is the termination of spinal shock.
Involves: all skeletal muscles, bladder, bowel and sexual function and autonomic control.
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Autonomic Hyperreflexia (dysreflexia)
may occur after spinal shock resolves. The syndrome is associated with a massive, uncompensated cardiovascular response to stimulation of the sympathetic nervous system. The condition is life-threatening and requires immediate treatment. Individuals most likely to be affected have lesions at the T6 levels.
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Manifestations of autonomic hyperreflexia
- Paroxysmal hypertension (up to 300mm Hg, systolic)
- a pounding headache
- blurred vision
- sweating above the level of the lesion with flushing of the skin
- nasal congestion
- nausea
- piloerection caused by pilomotor spasm
- bradycardia (30 to 40 beats/min).
The symptoms may develop singly or in combination (syndrome) and often are associated with a distended bladder or rectum.
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Degenerative Disk Disease (DDD)
degeneration of vertebrae
-diminished blood supply and loss of disk proteoglycans -cause disk dehydration, alterations in disk structure and impaired function
pathologic findings: disk protrusion, spondylolysis and/or subluxation, degeneration of vertebrae and spinal stenosis
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Spondylolysis
- structural defect (degeneration or develop. defect) of spine
- involves lamina or neural arch of vertebra
- heredity plays role in development, as does DDD
S/S - lower back and limb pain
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Spondylolisthesis
- occurs when vertebra slides forward and into vertebra below it
- happens in L5-S1
- graded from 1-4 based on the % of slip that occurs
- grades 1-2 managed nonsurgically and symptomatically
- grades 3-4 usually require operative decompression, stabilization or both
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Spinal Stenosis
- narrowing of the spinal cord
- lumbar and cervical spine most often involved
S/S -
- pain
- numbness and tingling in legs
- these are chronic symptoms that appear late and must be treated with decompression surgery
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Stroke patho
Abnormality of the brain caused by a pathological process in the blood vessels
Brain abnormalities such as:
-Ischemia (death of cells) with or without infarction
-Hemorrhage
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Types of stroke
- Thrombotic
- Embolic
- Hemorrhagic
- Lacunar
- TIA’s
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Thrombotic stroke
Arise from arterial occlusions caused by thrombi formation in arteries
- Atherosclerosis
- Inflammatory disease
- Transient Ischemic Attacks (TIA’s)
- Difference between TIA’s and thrombotic stroke less important
- Brief episode of neuro dysfunction caused by focal disturbance of brain
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Embolic Stroke
Involves fragments which break from a thrombus formed outside the brain
Embolus involves small brain vessels and obstructs at a bifurcation or other point of narrowing
Atrial fibrillation, left ventricular aneurysm, recent MI, endocarditis, rheumatic valve disease
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Hemorrhagic stroke
AKA intracranial hemorrhage
Causes:
- hypertension
- ruptured aneurysms or vascular malformation
- bleeding into a tumor
- hemorrhage associated with anticoagulants, clotting disorders, & brain injuries
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Lacunar stroke
Caused by occlusion of a single deep perforating artery that supplies small blood vessels
Usually in basal ganglia, internal capsules, and pons
May have pure motor or sensory deficits
Ischemic vs. hemorrhagic
Ischemic: ischemia of brain tissues d/t vascular occlusions
Abrupt- emboli
Gradual- atheroma
Partial occlusion of narrowed vessels
Hemorrhagic: ischemia d/t brain bleeding into tissues
Ruptured aneurysms, AVM’s, tumors, coagulation disorders, trauma, cocaine, amphetamines
Hypertension
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Ischemic lacunar stroke
Ischemia of brain tissues d/t vascular occlusions
Abrupt- emboli
Gradual- atheroma
Partial occlusion of narrowed vessels
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Hemorrhagic lacunar stroke
Ischemia d/t brain bleeding into tissues
Causes:
- Ruptured aneurysms
- AVM’s
- tumors
- coagulation disorders
- trauma
- cocaine/amphetamines
- Hypertension
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Cerebral Infarction
results when an area of the brain loses its blood supply because of vascular occlusion
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Causes of Cerebral Infarction
- Abrupt vascular occlusion (embolus)
- Gradual vessel occlusion (atheroma)
- Partial occlusion of stenotic vessel
**Usually caused by Cerebral thrombi and Cerebral emboli (but also HypOtension and atherosclerosis)
Can be ischemic or hemorrhagic
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Cerebral Hemorrhage
a mass of blood is formed as bleeding continues into the brain tissue
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Causes of cerebral hemorrhage
* *Hypertension (primary cause)
- ruptured aneurysms
- arteriovenous malformations
- tumors
- coagulation disorders
- trauma
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Ischemic vs hemorrhagic cerebral infarction
Infarction is losing blood supply to the brain and Hemorrhage is bleeding into your brain.
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Types of intracranial aneurysm
- Saccular (berry) aneurysm
| - Fusiform aneurysm
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Saccular (berry) aneurysm
a localized, progressively growing sac that affects only a portion of the circumference of the arterial wall and may be the result of congenital anomalies or degeneration
- Occurs frequently
- CONGENITAL abnormalities (in arterial wall) and degenerative changes
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Fusiform aneurysm
A LARGE aneurysm that stretches to affect the entire circumference of the arterial wall.
Occur from Diffuse Arteriosclerotic changes in arteries
Most commonly in Basilar arteries or Internal Carotid Arteries
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Arteriovenous Malformation (AVM)
a tangled mass of dilated blood vessels creating abnormal channels between the arterial and venous systems. AVM’s may occur in any part of the brain and can vary in size. They occur equally in males and females; although they are usually present at birth the onset of symptoms usually occur before age 30.
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Patho of arteriovenous malformation
AVM’s have abnormal vessel structure (bcs the blood vessels are abnormally thin) which results in complex growth and remodeling patterns. People with AVM fall into a chronic nondescript headache category. One or several arteries may feed the AVM and may become torturous and dilated over time. With moderate to large AVM’s, sufficient blood is shunted into the malformation and to deprive surrounding tissue of adequate blood profusion
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Manifestations of arteriovenous malformation
o 20% of people with AVM’s have a characteristic , chronic, nondescript headache ( some experience migraine)
o 50% experience Seizures caused by compression
o 10% experience hemiparesis or other focal signs
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Subarachnoid hemorrhage
Cerebral disorder where blood escapes from a defective or injured vessel into the subarachnoid space from leak or tear. Often recur, especailly if from aneurism
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People at risk for subarachnoid hemorrhage
- Intracranial aneurysm
- Intracranial arteriovenous malformation (AVM)
- Hypertension
- Sustained head injuries
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Patho of subarachnoid hemorrhage
- Hemorrhage from leak: blood oozes into the subarachnoid space
- Hemorrhage from tear: blood under pressure is pumped into subarachnoid space. More rapid.
Both result in an increase in intracranial volume which is irritating to the neural tissues and produces an inflammatory response
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Manifestations of subarachnoid hemorrhage
-Headache
-Changes in mental status
-Changes in consciousness
-Nausea/vomiting
-Localized neurological deficits
As progression occurs:
-Positive Kernig sign (straightening the knee with the hip and knee in a flexed position produces pain in the back of the neck region)
-Positive Brudzinski sign (Passive flexion of the neck produces neck pain and increased rigidity)
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Migraine
Episodic/familial neuro disorder. It has not been clearly established however there are neuro, vascular, hormonal, and neurotransmitter components associated. Headache is the marker and can last anywhere from 4-72 hours. More common in women, ages 25-55 and frequently associated with menstruation. It can also be triggered through altered sleep patterns, missed meals, over exertion, weather change, stress, and hormonal changes.
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Risk factors for migrane
increased risk for epilepsy, depression, anxiety, cardiovascular disease, and strokes.
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Manifestations of migranes
- unilateral head pain
- throbbing pain
- worsens with activity
- nausea
- vomiting
- photophobia
- phonophobia.
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3 Phases and Manifestations of migrane
- Pre-Monitory Phase: Can occur hours to days before the Aura and migraine. The person could be irritable, tired, have an altered level of consciousness, or experience food cravings.
- Aura-Phase: Described above, could last 1 hour or longer.
- Headache Phase: Lasts 4-72 hours, intense pain, photophobia, nausea, vomiting
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Cluster Headache
A group of disorders in which headaches occur in clusters or several times per day followed by a period of remission. Trigeminal activation and pain occur but the mechanism is unclear. The pain will come and goes within a period of days. They usually occur on one side of the head and occur more frequently in med between 25 and 50 years of age. It can also be triggered through altered sleep patterns, stress, missed meals, over exertion, weather change, stress, and hormonal changes.
Manifestation: It is EXTREME pain for a short duration. It usually peaks in ten minutes and lasts about 3 hours.
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Tension-Type Headache
This is the most common type of headache, thought to be stress related. It is not aggravated by physical activity. The average age of onset is during the second decade of life. It is a mild to moderate bilateral headache. The headache occurs in episodes and lasts several hours to several days. Exact mechanisms are unknown however it involves the hypersensitivity of pain fibers from the trigeminal nerve and contraction of jaw and neck muscles.
Manifestation: Gradual onset of pain with a sensation of a tight band or pressure around the head. Localized pain and tenderness.
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Meningitis
```
inflammation of the brain or spinal cord. Caused by systemic or bloodstream infection (usually respiratory) S/S depend on type.
Types:
-Bacterial
-Viral
-Fungal
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Bacterial meningitis
Infection of CSF (cerebral spinal fluid) or bacteria in arachnoid and subarachnoid spaces. Most commonly caused by meningococcus and pneumococcus.
-Infectious signs: fever, tachycardia, chills, petechial rash. -Neurologic signs: severe photophobia, +Kergnig and +Brudzinski signs, decrease consciousness, localized neuro deficits and possible seizures. Meningeal signs: see bacteria in CSF.
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Viral meningitis
Limited to the meninges. *Hallmark S/S is high fever and severe HA.
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Fungal meningitis
chronic but much less common. Usually occurs in people with impaired immune responses. Develops insidiously and gradually.
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Encephalitis
Acute febrile illness usually of viral origin with nervous system involvement. Commonly occurs from mosquito viruses or Herpes simplex virus. S/S: fever, delirium, confusion that can progress to unconsciousness, seizures, involuntary movement, paralysis.
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MS
Relatively common acquired autoimmune inflammatory disorder involving destruction of axonal myelin in the brain and spinal cord. The onset is usually between 20 and 40 years of age and is more common in women. Men may have a more severe progressive course. The prevalence rate is affected by gene-environment interactions in susceptible individuals.
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Patho of MS
Involves an autoimmune process that develops when a previous viral insult to the nervous system as occurred in a genetically susceptible individual. Early inflammation and demyelination lead to irreversible axonal degeneration and scarring (sclerosis). MS not oly has focal inflammatory changes but also manifests diffuse injury throughout the CNS called MS lesions.
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Manifestations of MS
- paresthesias of the face
- trunks or limbs
- weakness
- visual disturbances or urinary continence
- indicating diffuse CNS involvement.
Individuals with advanced MS have cerebellar symptoms including ataxia, slurred speech, and intention tremor.
Painful sensory events, spastic paralysis and bowel and bladder incontinence are common and disabling with progressive disease.
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Amyotrophic Lateral Sclerosis
Worldwide neorodegenerative disorder that diffusely involves lower and upper motor neurons, resulting in progressive muscle weakness. Classic ALS (Lou Gehrig disease) may begin at any time from the fourth decade of life; its peak occurrence is in the early fifties. The male/female ratio is about 1.5:1, equalizing after menopause. Ten percent of persons with ALS have a fmilial form and specific genes have been identified.
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Patho of ALS
The principal pathologic feature of ALS is lower and upper motor neuron degeneration, although without inflammation.
200
Manifestations of ALS
Weakness beginning in arms and legs and progressing to atrophy and spasticity
201
Myasthenia Gravis
Acquired chronic autoimmune disease mediated by antibodies against the acetylcholine receptor (AChR) at the neuromuscular junction, and is characterized by muscle weakness and fatigability.
202
Patho of Myasthenia Gravis
results from a defect in nerve impulse transmission at the neuromuscular junction.
203
Manifestations of myasthenia gravis
- has an insidious onset with the foremost complaint of muscle fatigue and progressive weakness.
204
Types of primary brain tumors
- Astrocytomas
- Oligodendrogliomas
- Ependymomas
- Meningioma
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Astrocytomas
- most common tumor
- can occur anywhere in brain or spinal cord
- are slow growing and invasive
206
Oligodendrogliomas
- 2% of brain tumors
- commonly occurs in frontal lobes
- are avascular and encapsulated
- are slow growing and doesn’t spread
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Ependymomas
- common in children; rare in adults
- occurs in the walls of ventricles and in the spinal cord
- are more malignant; not encapsulated
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Meningioma
- 30% of brain tumors
- occurs in olfactory grooves which are located at the sphenoid bone (at base of skull)
- are slow growing and encapsulated
