39 terms



Terms in this set (...)

Lou Gehrig's Disease (Amyotrophic Lateral Sclerosis)
-Neurologically degenerative, rapidly progressive and fatal
-Weakness and wasting of muscles that are under voluntary control
-No accompanying sensory or cognitive changes
-Muscle atrophy results from motor neuron degeneration and sclerosis of the corticospinal tract in the lateral column of the spinal cord
Amyotrophy = without muscle nutrition or progressive muscle wasting/atrophy
-Death results in 2 to 5 years after onset of the manifestations
Usually due to respiratory failure
-Most common motor neuron disease in the US
-20,000 in US have ALS at one time with approximately 5,000 new cases diagnosed each year
-90-95% of cases occur randomly without associated risk factors
-5-10% of cases occur in what is termed familial ALS
-Most people diagnosed between 40-60 years of age
ALS cont
-Incidence is higher in men in the earlier ages
Incidence becomes equal with women after menopause
-Most health problems needing intervention r/t swallowing, managing secretions, communication, respiration
-During early stages, surviving motor neurons sprout new branches to reinnervate affected muscle fibers
Initially have weakness to muscles in body, then progresses to flaccid and/or spastic paralysis
-When more than ½ motor neurons affected, reinnervation fails and weakness is evidenced
Traumatic Brain Injury Assessment
Level of Consciousness
Pattern of Breathing
Size & Reactivity of pupils
Eye position and reflex response
Skeletal muscle motor responses
Abnormal Posturing
-Hemispheric damage above the midmbrain
-Severe damage to diencephalon or midbrain
Symptoms of Brain Injury
-Highly variable
-Depends on area of brain injured
-Depends on extent of injury
-Coup/Countercoup injury
Coup = impact against object (head strikes a wall)
Countercoup = impact within skull (head rebounds from wall)
-Depends on type of injury
Focal = specific and grossly observable lesions
Diffuse = results from a "shaking" effect that produces strains and distortions in the brain; damage seen with a microscope
Spinal Cord Injuries
-Forces of trauma compress tissues, pull or exert tension on tissues, or shear tissues and affect the spinal cord
-Bones, ligaments, and joints of vertebral column may be damaged
Fracture, dislocation, or both
-Damage to the motor neuron
-Herniated intervertebral discs
-Partial or Complete severing of spinal cord
Much of injury can be due to cord ischemia
NEVER MOVE without stabilizing
Spinal cord injuries all have potential to result in....
Despite etiology, all have potential to result in
Loss of voluntary control
Flaccid paralysis
Decreased muscle tone
Muscle atrophy
Absent or decreased reflexes
Long term loss depends on....
Long term loss depends on
Level of injury and
Extent of transection
C2 - ventilator dependent; quadriplegic
C4 - move head, mouth, shoulders, diaphragm
C6 - weak hands, drive with hand controls
T1 - normal upper body; paraplegic
-The brain's capacity for recovery from injury is far greater than previously thought.
-The brain has the ability to reorganize (i.e., neuroplasticity) after disease or injury
This phenomenon can be facilitated through activity-dependent processes including environmental enrichment, forced-use, complex skills training, and exercise.
-Most of our understanding of this activity-dependent plasticity is derived from studies of brain injury related to stroke and spinal cord injury.
-Dr. Pettinato's suggested reading: "The Brain that Changes Itself" by Norman Doidge
-Happen in response to injury
----Brain not anchored to skull - floating
----Sudden changes in motion can tear blood vessels
-Can happen in response to aneurysm or artery bursting as last stage of chronic HTN
-The skull is an enclosed compartment
-----Bleeds shift and distort brain
-----Bleeds may herniate brain tissue (push it out of its normal space)
-----Bleeds may compress blood vessels, leading to ischemia
Bleeds cont
-Within brain: Hemorrhagic Stroke
Generally arterial aneurysms bursting
Between skull and dura
Between the dura and the pia matter
-Subarachnoid and intracerebral
Between pia mater and the brain (into CSF) or brain tissue
Venous or arterial
Bleed S &S
-Severe headache
-Change in level of consciousness
Confused, Delirious, Lethargic, Obtunded (dulled), Stuperous, Comatose
-Glascow Coma Scale
Eye opening, Verbal response, Motor response
-Brain stem function
Pupillary response, corneal reflex
-Sudden, explosive, disorderly discharge of brain neurons
-Produces a brief disruption of electrical function of the brain and alters brain function
Affects motor, sensory, autonomic, psychic systems
Affects level of consciousness
-May result in convulsive movement
Jerky, contract-relax (tonic-clonic) movement
Seizure caused by...
--Caused by sudden changes (paroxysmal depolarization) in the membrane potential of neurons
--Plasma membrane thought to be more permeable making them more sensitive
--Seizure Threshold may be lower in others; can trigger a seizure with
Hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory information, emotional/physical stress, fatigue, lack of sleep
CVA (Stroke)
--20% hemorrhagic
50% mortality, high morbidity
--80% ischemic
Thromboemboli from heart in A. fib. or fat on valves
Thrombotic (blood clot formation)
EARLY Treatment is cruicial
Must treat < 3 hrs of CVA onset with fibrinolytic
-Most frequent cause of disability in elderly
-One of top 5 causes of death in elderly
-1/3 die at time, 1/3 significant deficit, 1/3 functional recovery
Much recovery occurs early but can continue for a long time
Signs of stroke
Signs of stroke
-Numbness or weakness on one side of body
-Confusion, trouble speaking or understanding
-Visual disturbances
-Dizziness, trouble walking
-Severe headache (hemorrhagic stroke)
Cerebral Blood Flow
Basilar/vertebral: feeds cerebellum and brain stem
-Lack of flow affects gait, speech, swallowing, vision
Anterior cerebral: feeds frontal lobes
-Lack of flow causes contralateral motor sensory loss, impaired cognition, incontinence, aphasia (left side stroke)
Middle Cerebral: middle of brain
-Lack of flow causes contralateral motor/sensory loss, aphasia, altered consciousness, neglect syndrome
Disruption of flow to this area most fatal
Posterior Cerebral: occipital and temporal
-Lack of flow causes vision and memory loss
Right vs. Left
Contralateral hemiplegia related to cortical strokes
If right hemisphere affected:
-Spatial, perceptual abilities
-Judgment (loss of judgment with no awareness)
-Memory (short-term memory loss)
-Mood (indifference, impulsive)
Right vs. Left CONT
If left hemisphere affected:
-Altered speech and understanding of it
-Aphasia (inability to communicate) - expressive, receptive
-Patient has slow cautious behavior style, step-by-step and continuous instruction to complete tasks
-Patient has difficulty learning new information
-Patient has depression
CVA (Stroke) Risk factors
Risk factors:
Atrial fibrillation*
African American
High cholesterol*
Sedentary lifestyle*
prior stroke or transient ischemic attack (TIA)
* = Modifiable
Prevention also with platelet inhibitors (aspirin, Plavix, Ticlid, Aggrenox) or anticoagulants (warfarin [Coumadin])
Infections Altering Neuro Function:Meningitis
Infection in subarachnoid space
Often bacterial
Recovery depends on prompt treatment
Symptoms: headache, fever, stiff neck, cerebral dysfunction
Infections Altering Neuro Function: Encephalitis
Inflammation of the brain
Often viral
Difficult to diagnose, treatment supportive unless etiology is herpes, then acyclovir use
Infections Altering Neuro Function: Brain Abscess
Brain Abscess
Mostly bacterial, necrotizing
Infections from neighboring structures (teeth, sinuses, ears) or penetrating wounds
Cognitive Functions Assessed in Delirium and Dementia:
Memory (Short and Long Term)
Executive Functioning
Spatial Orientation/Recognition
Delirium vs. Dementia
--Abrupt onset
--Typically physiologic cause
--Typically reversible, IF treated
--Fluctuating course
--Altered levels of consciousness
--Progressive failure of cerebral functions
--Irreversible confused states
--Decline in intellectual ability
Pathology of Alzheimer's Disease (AD)
There are 3 consistent neuropathological hallmarks:
Amyloid-rich senile plaques
Neurofibrillary tangles
Neuronal degeneration
These changes eventually lead to clinical symptoms, but they begin years before the onset of symptoms
Early symptoms of AD
--AD begins slowly
At first the only symptom may be mild forgetfulness (can be confused with age-related memory change).
Most people with mild forgetfulness do not have AD.
--In the early stage of AD, people may have trouble remembering recent events, activities, or the names of familiar people or things.
--They may not be able to solve simple math problems. Such difficulties may be a bother, but usually they are not serious enough to cause alarm.
Middle to Late Stages of AD
--Symptoms are more easily noticed and become serious enough to cause people with AD or their family members to seek medical help.
Forgetfulness begins to interfere with daily activities.
--Middle Stages: may forget how to do simple tasks (brush teeth, comb hair); can no longer think clearly; can fail to recognize familiar people and places.
--They begin to have problems speaking, understanding, reading, or writing.
--Later Stages: may become anxious or aggressive, or wander away from home; eventually need total care
--No treatment can stop AD. Medications may help prevent some symptoms from becoming worse or slow the progression of AD for a limited time.
--Early and middle stages of the disease:
tacrine (Cognex)
donepezil (Aricept)
rivastigmine (Exelon)
galantamine (Razadyne, previously known as Reminyl)
--Moderate to severe AD:
memantine (Namenda)
Is limited in its effects
AD managment
-Some medicines may help minimize behavioral symptoms of AD
-Medications all have side-effects; therefore, behavioral, environmental, and social strategies are primary.
-Treating troublesome behavioral symptoms often makes patients more comfortable and makes their care easier for caregivers.
Parkinson's Disease (PD)
Parkinson's disease (PD) belongs to a group of conditions called motor system disorders
Are the result of the loss of dopamine-producing brain cells
he four primary symptoms of PD...
The four primary symptoms of PD are:
--Tremor (trembling in hands, arms, legs, jaw, and face)
--Rigidity (stiffness of the limbs and trunk)
--Bradykinesia (slowness of movement)
--Postural instability (impaired balance and coordination)
As symptoms worsen patients may have difficulty walking, talking, or completing other simple tasks.
PD cont
---Usually affects people over the age of 50
---Early symptoms of PD are subtle and occur gradually.
In some people the disease progresses more quickly than in others
--Other symptoms:
Depression and other emotional changes
Difficulty in swallowing, chewing, and speaking
Urinary problems or constipation
Skin problems
Sleep disruptions.
--There are no blood or laboratory tests available to diagnose PD.
--At present, there is no cure for PD.
--Some medications provide relief from the symptoms:
----levodopa combined with carbidopa
Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain.
Nerve cells can use levodopa to make dopamine and replenish the brain's dwindling supply.
---Other drugs mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine.
bromocriptine, pergolide, pramipexole, and ropinirole,
---An antiviral drug, amantadine, also appears to reduce symptoms.
--Appropriate if the disease doesn't respond to drugs.
--Deep brain stimulation (DBS)
Electrodes are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed
A part of the brain called the globus pallidus is overactive; this is destryoed by creating a scar.
Reduces the brain activity to globus pallidus, which may help relieve movement symptoms such as tremor and stiffness (rigidity).
Multiple Sclerosis (MS)
--Degeneration of previously normal myelin with relative preservation of axons
--Onset between ages 20-40
Peak age of 30
--Male/Female ratio 1:2
--May occur when a previous viral insult to the nervous system has occurred in a genetically susceptible individual
--Autoimmune process
Interaction of systemic immune system with the CNS
Degeneration of myelin with inflammatory edema occurs
--CD4 T-Cells cross the blood-brain barrier, followed by chemotaxis and infiltration of monocytes and macrophages
--T-cells become autoreactive to a single myelin protein
--Stress seems to trigger the onset of symptoms or worsen symptoms
-----Paresthesias (numbness, tingling)
-----Strange sensation of tightness, banding, itching, constriction
-----Imbalance, ataxia (lack of coordination)
-----Visual changes (blurring, double vision)