Neuro System Flashcards
Alzheimer’s Disease
Loss of memory, reasoning, judgment, and language to such an extent that it interferes with everyday life
This is also the definition of dementia
Alzheimer’s Disease (AD) is the most common form of dementia in people 65 years and older
First diagnosed in 1907 by Alois Alzheimer, by staining brain cells
Etiology of Alzheimer’s Disease
No direct cause identified Increased age Chromosomal links Several genes have been found to be associated with AD Testing is available
Pathophysiology of Alzheimer’s Disease
Disruption of
Neuron communication
Neuron metabolism
Neuron repair
Beta-amyloid plaques- insoluble deposits of proteins
Plaques dense insoluble deposits of proteins and cellular material that develop in hippocampus- the area of the brain that helps with memory
Neurofibrillary tangles- from microtubules that die
Decreased Acetylcholine- a neurotransmitter
Pathophysiology
Healthy neurons have internal microtubules that guide nutrients to the end of the axon
In AD the tubules get tangles, and the cells they support die
This leads to memory failure, personality changes, difficulty with ADL’s
Preclinical Alzheimer’s Disease
Before symptoms appear the area around the hippocampus begins to shrink
In time – likely 10-20 years- memory loss occurs
Changes are subtle and often not noticed for years
Mild Alzheimer’s Disease- Stage 1
Memory disturbances noticed by family- get lost easily
Poor judgment- walk out without shoes
Does not care about things that were previously very important
Carelessness at work or home chores
Difficulty with problem solving- paying bills
May become irritable, suspicious, agitated, apathetic, have motor difficulties
Trouble adapting to new surroundings
Do well in familiar surroundings with very rigid routines
Moderate Alzheimer’s Disease- Stage 2
Pacing, wandering especially at night
Potential for serious injury
Language disturbance- talk around issues
Spontaneous language difficult- finding words
Repeat words or phrases
Papilalia- words they spoke
Echolalia- words spoken by others
Apraxia- difficulty using everyday objects
Hyperorality- desire to put everything in mouth
Irritability- fear personal harm, theft
Occasional incontinence
Severe Alzheimer’s Disease- Stage 3-4
Plaques and tangles are widespread in brain Won’t recognize family Unable to communicate, swallow Little voluntary movement of limbs Generally rigid in flexed postures Incontinence is usual Aspiration common
Diagnosing Alzheimer’s Disease
No definitive test Exclusion of other medical problems Toxic from drugs, metabolic problems, CV disease, infection, tumor Confirmed diagnosis Dementia with 2 or more areas of cognition Slow onset Loss of normal alertness CT, MRI, PET, lab tests to rule out
Multi-infarction Dementia
Blood flow to parts of brain is blocked Occurs in steps Problem with recent memory Wandering Laughing/crying inappropriately Difficulty handling money As more vessels are blocked mental function declines
Lewy Body Dementia
Progresses more rapidly
Brain cells called Lewy Bodies appear throughout the brain
Symptoms range from Parkinson-like to AD
Bradykinesia, rigidity
Tremor, shuffling gait
Visual hallucinations may be first symptom
Nursing Care for Alzheimer’s Dementia
Good history and assessment Concentrate on ADL’s- mobility issues Family & co-worker comments Reaction to change in environment Personality changes Head injury Social isolation Paranoid, abusive language
Verbal Communication in Alzheimer’s Dementia
Tone of voice always slow and calming Watch their non-verbals Will look away, back up, increase hand gestures if they don’t understand Pacing, waving arms, hostility environmental stimuli Approach calmly with assurance Gently distract Your body and words should match Don’t use visual, auditory, tactile communication at the same time
Disturbed Though Processes
Enhance memory
Calendars, dry-erase boards, clocks
Allow them to reminisce
Long-term memory intact longer than short
Reorienting can lead to frustration and possibly acting out behavior
Repetition is always helpful to ensure retention of information- is aggravating to family
Risk for Injury
If home Disconnect electrical appliances Watch loose rugs, lighting adequate Turn hot water tank down Lock doors in different manner – near the top out of sight If in hospital Monitor closely Family at bedside helps to orient them
Urge Incontinence
Toilet in advance of need- q3 hours
Not aware of need until just before urinating
Watch for non-verbal signs of need
Holding genitals, picking at cloths, anxious wandering
Restrict fluids after supper
For bowel incontinence
Create a pattern from their usual routine
Bed pads, adult briefs
Avoid Foley catheter
Self Care
Care in early stages to protect autonomy Little reminders Step-by-step directions Allow enough time Constant encouragement
Caregiver Strain
They grieve the person they used to know
Each decline is another grief
Watch for patients who are incontinent or have overly demanding behavior
Offer suggestions for respite, home visits, adult day care, nursing home
Issues of feeding tube, DNR
Headache
Assessment- to determine type of headache Location, character of pain Duration, frequency Methods tried to treat Localized tenderness to touch Precipitating factors Familial tendencies
Tension Heache - from muscle contraction
Pain builds slowly, lasts for days, vice-like pain in head and neck
Cluster- short attacks of periorbital pain
A form of migraine
More in spring/fall, last 15 min – 3 hrs, occur 1-4 times per day, deep, boring pain, usually unilateral
Triggered by alcohol consumption
Treated with lithium, steroid dose pack (interrupts pain cycle) or O2 at 9 L per mask for 15 minutes
Migraine (Vascular)
Vasospasm or ischemia of intracranial vessels
Begin in puberty, more common in women, associated with monthly hormone changes
Last 4-72 hours, usually unilateral
Throbbing, pulsating
Photophobia, phonophobia, N&V, focal neuro symptoms- visual aura pre-headache (jagged edge of light in visual field)
Triggered by stress, missing meals, tyramine-rich food (pickles, aged cheese, red wine), nitrates (cured meats), alcohol, sleeplessness
Treatment of Migraines
Quiet, dark environment Ibuprofen, caffeine Ergotamine Tryptans sumatriptan (Imatrex) zolmitriptan (Zomig) Plus antiemetics Amytriptyline, valproate, verapamil can be used as preventative, but must be taken daily Work on decreasing stress/fatigue in daily life
Ergotamine-Drug of Choice
Unknown exact method of action
Vasoconstriction of cranial vessels
Perivascular anti-inflammation
Seritonin blocking (a neurotransmitter)
Oral, sublingual, rectal, inhaled
Can cause N&V so can be given with an antiemetic
Should not be taken with triptans due to possible prolonged vasospasm
Metabolized in liver and kidney
Ergotamine tartrate with caffeine (Cafergot, Migergot)
Prevent cerebral vessel vasodilation
Triptans
Binds at receptors in the blood vessels of the brain – vasoconstriction
Also inhibit the release of a compound that causes inflammation, so it decreases inflammation around blood vessels
Can be given orally, intranasally, or SubQ
zolmitriptan (Zomig)
sumatriptan succinate (Imitrex)
Side effects
Coronary vasospasm (not given to patients with CAD)
Chest heaviness- transient
Increased Intracranial Pressure ( ICP):
Skull is closed vault Balance between Brain tissue Blood Cerebrospinal fluid When there is increase in one the others must decrease- compensation or compliance Hemorrhage Tumor Obstruction in CSF outflow Increased CO2= vasodilation
Symptoms of Increased Intracranial Pressure
Caused by traction on cerebral blood vessels from swelling tissue, and pressure on pain-sensitive dura
Depends on location of pressure – tumor, hemorrhage
Is usually subtle, so need to observe patients closely
Increased Intracranial Pressure
Change in LOC- restlessness, irritability, confusion- know examples of confusion Decrease in Glasgow Coma Scale score Best Eye opening (1-4) Best Verbal Response (1-5) Best Motor Response (1-6) Changes in speech Pupil change Motor or sensory changes Change in HR, or rhythm Headache, N&V, blurred vision Review breathing patterns
Abnormal Breathing with ICP
Cheyne stokes- shallow-deep-shallow-apnea
Central neurogenic hyperventilation- deep & fast
Apneustic- prolonged inspiration, hold, exhale, apnea
Ataxic- completely irregular
Diagnosing increased ICP
Symptoms
Skull x-ray to see shifts
CT/MRI to see fluid, tumor, abscess
Lumbar Puncture generally not done – risk of herniation of brain stem
Pressure lowered in spinal cord and brain tries to find ways of decreasing pressure – is usually fatal
Treatment of Increased ICP
Maintain cerebral oxygenation Intubation, ventilation Keep O2 at 90-100% Steroids to reduce edema Decrease intracranial pressure Hyperventilation – remove more CO2 Osmotic diuretic Keep HOB elevated, neck in neutral position to facilitate venous drainage
Treatment of Increased ICP Continued
Maintain Cerebral perfusion
IV fluid to prevent hypotension & secondary brain injury
Vasoactive meds to or B/P
ICP monitoring – in ventricles
Control body temp, prevent chilling
Prevent seizures
Sedation
Mannitol- hyperosmotic agent- increases plasma osmolality to cause fluid to be pulled into vascular supply – and be excreted
Created osmotic gradient and pulls fluid out of cells creating diuresis
Other treatment Options
High dose barbiturates- metabolic needs of brain
Provides pain control and sedation
Requires mechanical ventilation
Neuromuscular Blocking Agents
Skeletal muscle relaxation
Pain medication and sedatives are needed too
Posturing
Decorticate – abnormal flexion due to brain damage at the cortical level
Decerebrate – abnormal extension, usually a more serious injury and worse prognosis
Bilateral flaccidity – no muscular response to stimulation – very poor prognosis
These postures may be unilateral or bilateral and are usually seen in response to pain or stimulation
Nursing Assessment of Increased ICP
Glasgow Coma scale- 3-15 ( 9 = coma)
Change in LOC- early change
Pupil response- unresponsive, unequal
On same side as brain lesion (hematoma, tumor, etc)
Brain lesion will cause pupil change on ipsilateral side
Motor/sensory deficits are usualy contralateral side
Vital signs- late changes
Dropping B/P can be very dangerous
Treating with IV fluids can further ICP
Cranial nerve assessment
Blink reflex- stroke lashes
Gag reflex
Nursing Care for Increased ICP
Altered cerebral tissue perfusion
Supine with HOB , neck in alignment
Avoid severe hip flexion - intra-abd pressure
Maintain airway, limit suctioning
Fluid balance- strict I&O
Control body temp- shivering ICP
Monitor serum glucose levels – metabolic demand
Avoid blowing nose, coughing, holding breath
Nursing Care for Increased ICP
Monitor intracranial pressure
Monitor site for signs of infection or leaking
Test CSF leak by testing for glucose
Clear nasal drainage means dural tear, so don’t suction nose- meningitis
Fluids sometimes replaced based on output
temp increased metabolic needs and ICP, avoid shivering
Traumatic Brain Injury
Insult to brain that is capable of producing physical, intellectual, emotional, social, and vocational changes
30% are fatal
Often seen with facial, abdominal of musculoskeletal injuries
Penetrating Skull Injury
Skull fracture common blunt force
Bullet/knife wound
Skull fragments can cause laceration of brain tissue, nerves, blood vessels
Hematoma common
Blunt Force Injury Without Skull Fracture
Causes tearing of tissue and blood vessels at brain area of impact
Rebound or Contrecoup
Injury at point of impact as well as at opposite side of brain
Consciousness
Complex function controlled by Reticular Activating System with feedback loops 2 criteria Wakefulness Awareness Self Environment Time
Levels of Awareness:
Confusion
alteration in thought, attention, comprehension
Delirium
drug or medical condition induced, often reversibly. Less able to focus, change in cognition
Dementia
Chronic Confusion
Disorientation
One criteria of confusion, unable to identify self, environment, time
Bacterial Meningitis
Almost any bacteria can cause this
Meningococci
Pneumoncocci
Haemophilus influenzae (h-flu)
Inflammation of the meninges – usually arachnoid and sub-arachnoid space
Skull fracture provided easy entry for bacteria
Clinical Manifestations of Meningitis
Nuchal rigidity – classic symptom Brudzinski’s sign Kernig’s sign Photophobia Fever, chills, tachycardia, headache Nausea & vomiting Petechia or hemorrhagic rash Irritability in early stages to acute illness, confusion or coma MEDICAL EMERGENCY
Kernig Sign
lay flat with hip and knee flexed at 90 degrees. The extend the lower leg. If meningeal irritation there is hamstring spasm, pain and resistance to further extension
Brudzinski Sign
lay flat, lift the head rapidly from the bed. If meningeal irritation this produces forward flexion of the hips, and flexion of the knees and ankles.
Treatment
Lumbar Puncture
Be sure there is no increased ICP- brain herniation
Elevated pressure
Elevated proteins
Decreased glucose – bacteria feeding on it
Elevated white count – immune response
Anticonvulsants
IV antibiotics help some
Blood brain barrier is interrupted by inflammation and antibiotics can help
Nursing Issues with Meningitis
Same issues as with ICP
Watch for CSF leak from nose or ears, especially with skull fracture
Tests positive for glucose
Separates out into bloody and yellow concentric rings on dressings
Epidural Hematoma
Between Dura and skull (above dura) From injury to blood vessels Usually with skull fracture Bleeding is continuous and arterial Immediately unconscious (arterial bleed) Awakens and is alert (CSF compensation) Loss of consciousness with rapid decline to coma (Compensation fails)
Subdural Hematoma
Between Dura and Arachnoid
Caused by tearing of bridging veins
Acute, subacute, chronic
Symptoms within 24-48 hrs of injury, due to venous bleeding
If conscious- severe headache
All symptoms of ICP
Chronic in alcoholics- brain atrophy, very subtle changes
Medical Managment of Brain Bleeds
Support of all organs
Ventilatory support
Management of fluid balance
Nutrition/ GI function
Initial management same for all head injuries
Sometimes evacuation of clot or blood through burr hole
Brain Death
Cessation and irreversibility of all brain functions including the brainstem
Criteria vary a bit from state to state
No evidence of cerebral or brainstem function for at least 6-24 hours
No depressant drugs or alcohol poisoning can be present
Criteria for Brain Death
Unresponsive coma, no motor or reflex movement No spontaneous respiration Pupils fixed and dilated (unresponsive) Absent ocular response to head turning Absent Dolls eye response (in coma only) No nystagmus with caloric test Flat EEG No cerebral circulation on angiogram Persistence of these symptoms for 1 hour, and for 6 hours after onset of coma
Criteria for Brain Death
Dolls eye- movement of eyes in opposite direction of head rotation- THIS IS NORMAL means brainstem is still functioning.
If eyes move in the same direction as the head is – means brainstem in dead.
