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CPP is
cerebral perfusion pressure and is the pressure required to get oxygenated blood to the brain to perfuse
Changes in blood flow (hypo/hypertension or blockage) can lead to low or too-high CCP which can lead can lead to
cerebral edema,
ICP is
Intracranial pressure is the addition of arterial/venous blood flow, CSF pressure, and Brain tissue.
The main culprit in causing IICP
& the loss of balance between ICP & CPP is cerebral edema
Cerebral edema is
ischemia from a blockage of an artery in the brain or going to the brain leads to cells becoming hypoxic swelling and increased vascular permeability leading to increased ICP and decreased CPP and further brain ischemia.
Cerebral edema & IICP
almost always go “hand in hand”
Changes in ICP can be caused by
Head injury, Brain tumor, Brain attack, infection, acid-base imbalance, meningitis, and hypoxemia from respiratory disorders
Brain attack is
the process of any interruption of the normal blood supply to a part of the brain or the entire brain, resulting in damaged brain tissue.
Etiologies of Brain attacks are
atherosclerosis of cerebral arteries, brain aneurysm, heart problems that leads to decreased cardiac output.
Risk factors of brain attack are
atherosclerosis, HTN, older age, DIABETTES, family history, and lifestyle choices
Negative effects of a stroke
cerebral edema & IICP
Patho of ischemic brain attack is
diminished perfusion to brain tissue leads to cellular ischemia which may lead to infarction then inflammatory process leads to swelling, cerebral edema then increased ICP and further decrease in perfusion
Thrombotic stroke
occurs from a clot or plaque that blocks off the artery in which it has developed & causes ischemia distally
Embolic stroke
when fragments that break from an arterial thrombus break off & travel “downstream” until they “get stuck” in a smaller artery and cause ischemia to brain distally
causes of thrombotic & embolic events:
A-fib, valve issues, air emboli, atherosclerosis, and intracranial artery plaque
TIA=
Trans ischemic Brain attack
Speacial part of TIA
Temporary, no neurological problems, but it is a massive waring sign that a real stoke is coming.
Patho of Hemorrhagic stroke
blood leaks out into the cerebral tissue, then irritates the tissue, then inflammatory process, then swelling, cerebral edema and increased ICP then cellular ischemia, injury, and/ or infarction of the surrounding area.
Causes of hemorrhagic stroke
weak arterial wall, bleeding into a tumor, coagulation disorders, congenital vascular disorders, aneurysms, and pressure of hypertension.
The three areas of a Brain attack are
Brain stem, Cerebellum, and Right or left hemisphere
Assessing a stroke
assess patient’s autonomic status (includes LOC-- level of consciousness and mental)
Assess sensorimotor system
Assess sensorimotor above the shoulder
Assess sensorimotor below the shoulder
Assess reflexes
Level of consciousness includes
oriented, alert, following commands, normal speech, and conversing appropriately
Abnormal LOC is
not being alert, not following commands, not oriented, speech might be garbled, confusion behavioral changes, and dysfunctional mental status through conversational efforts.
Sensorimotor
a term that encompasses the fact that movement & sensation are intricately related.
Normal sensorimotor is
Normal sensation, muscle tone, and movement Symmetric, AKA the same bilaterally
CN VII
Facial nerve (controls facial movement and expression) (Contralateral)
Example of CN 7 BA
If there is focal cerebral edema around the right CN VII, that allows a smile, you would expect to see facial drooping on the left side of the mouth.
CN II
Optic nerve
Example of CN 2 BA
If there is focal cerebral edema around the right CN II, that transmits visual images to the brain, you would expect visual defects in the two left halves of BOTH eyes.
CN III
Oculomotor nerve
Example of CN 3 BA
Bilateral loss of the pupillary light response - both pupils either fixed and dilated or fixed and pinpoint - indicates a lesion in the brain stem.
Visual defects in the two left halves of BOTH eyes is
homonymous hemianopia.
corticospinal tract or pyramidal tract
descending (motor) tracts and bundles of long axons that originate in the cell bodies of certain certain areas of the motor cortex.
Decussate
anatomically, these axons cross over, or from their point of origin in the cerebral cortex to the opposite side of the body at the junction between the spinal cord and brain stem
Spinothalamic tracts
ascending (sensory) tracts that carry sensations of pain, temperature, crude and light from body to brain.
The spinothalamic
crosses over but in a different area so if there is a focal lesion related to corticospinal or spinothalamic tracts in the brain, expect to see asymmetric sensorimotor changes
The pathologic BA changes will usually be
unilateral but on the contralateral side of the body because of decussation abnormal findings on the opposite side of the lesion in the brain
Example of asymmetric sensorimotor changes
a patient with a tumor on the right side of the brain would have decreased strength & sensation of arms and legs on the contralateral, or left side of the body.
Normal Central reflexes are
cough, swallow, gag,
Normal Peripheral Reflexes are
expected degree of response, which is equal bilaterally (therefore symmetric), and reflects good connections in the reflex arc of the spine and also normal interpretation in the brain.
Positive Babinski”
means that stroking plantar surface of foot makes the big toe flex “upgoing toe” NORMAL UNTIL AFTER TWO YEARS OLD
S&S autonomic of Brain stem stroke
coma or near comatose state, heart rate and blood pressure changes, breathing pattern changes
Cheyne-Stokes
apnea then breathing pattern changes
S&S sensorimotor of Brain stem stroke
pupils fixed and dilated/pinpoint, HR problems, decerebrate & decorticate posturing, often comatose and strength would be weaker bilaterally & often symmetrically.
S&S reflex of Brain stem stroke
sneezing, coughing, gagging, & swallowing are diminished or lost, and are reflexes weaker, usually symmetrically, and sometimes there is bilateral positive Babinski’s
Cerebellar BA S&S
Loss of coordination, vertigo, nystagmus, nausea and vomiting, problems with coordination and balance, and vertebral –basilar artery occlusion
dysphasia
impairment in the production of speech resulting from brain disease or damage.
aphasia
trouble with speaking, understanding speech, or reading or writing as a result of damage to the part of the brain that is responsible for language processing or understanding.
The left hemisphere of brain:
comprehend, integrate, and express language ability to do math, organize, reason, and analyze, is the seat of insight (including insight to his/her disease), creativity, face recognition, musical ability, etc.
left-sided neglect
a tendency to completely ignore the environment on the left side. (pt won’t perceive that there is anything on the left side of a plate of food or that there is a nurse standing on his left)
spatiality
where you are in space, & where things are around you
Typical S&S of Hemorrhagic strokes
intense headaches, neck pain, light intolerance, nausea and vomiting, and higher mortality rate with hemorrhagic strokes
To monitor and control cerebral edema
HOB (head of bed) up at least 30 degrees
Diuretics
ICP monitor
How to prevent the further increase in ICP
O2
BP management (not too high or low)
Treatment of hemorrhagic strokes
may need surgical intervention for certain types of hemorrhagic strokes
Treatment of ischemic strokes
Thrombolytic drugs first within 3-4.5 hours first then Heparin, then send home on Coumadin
Familial Alzheimer’s (FAD)
Inheritance-linked – can be early onset or late
non-hereditary (AKA sporadic)
late onset—70% of cases
Cause of Alzhimers’s is
unknown but it is thought that there is a mutation that improperly encodes a normal protein called amyloid. The abnormal amyloid forms plaque-like material called senile plaques.
Cause 2 of Alzhimers’s is
microtubules of neurons in the brain become distorted and twisted and form a neurofibrillary tangle.
Cause 3 of Alzhimers’s is
the amyloid plaques and the neurofibrillary tangle combine to disrupt normal nerve impulses in the brain.
Dementia
a type of forgetfulness that is different from normal absentmindedness; emotional upset, behavioral changes, and if posterior frontal lobe is involved, there are also motor changes such as rigidity, and postural & gait changes
Normal basal ganglia function is based on
balance of 2 neurotransmitters—dopamine & acetylcholine
EPS partly controls
fine motor skilss
Parkinson’s is a basal ganglia
dysfunction disease caused by unknown source, but suspected to be genetic, viral, or environmental toxin-induced depletion in dopamine
Parkinson’s is summarized by
tips the scales of balance towards cholinergic, excitatory activity --not actually more acetylcholine, but more effect.)
Increased cholinergic effect gives
S&S related to hypertonia (rigidity) & dyskinesia
Dyskenesia manifestations
involuntary facial & trunk movements, pattern of alternating movements between thumb & forefinger described as “pill-rolling”, inability to make appropriate posture adjustment when tipping or falling.
dysphagia
difficulty swallowing
Hypertonia manifestations
overall rigidity, often noticed in the face—mask-like face
“Cog-wheel rigidity” of forearm
Dysarthria (difficulty forming words)
Dysphagia
Parkinsonisms
any dysfunction of the extrapyramidal system but with any disease process or drug that disorders function of basal ganglia
Basal ganglion gait” AKA “Parkinsonian gait”
stooped, shuffling posture; decreased arm swing
Treatment for Parkinson’s
give medication containing dopamine (anticholinergic)
Multiple sclerosis
T cells attack myelin sheath leading to demyelination causing sporadically blocked or altered nerve conduction
Multiple sclerosis causes the nerve impulses 10 to be
times slower than normal myelinated ones
Paresthesia
unusual sensory sensation such as numbness, shooting
Ataxia
staggering gait
S&S of Multiple sclerosis
usually asymmetric, periods of exacerbations and remissions, weakness of certain muscles, paranesthesia, ataxia, bladder control problems, double vison, and dysarthria
dysarthria
difficulty speaking due to actual jaw muscle weakness);
Migraines Patho
trigger causes an alteration in the production of neurotransmitter chemicals that activate the inflammatory response resulting in vasodilation, increased capillary permeability and a pulsating one-sided throbbing headache.
Treatment for Migraines
NSAIDS and Imitrex (prodrome)
Prodrome of Migraines
aura =perception of a strange light, an unpleasant smell or confusing
Migraines S&S
headache itself, which is often unilateral and accompanied by N,V, photophobia, phonophobia
Seizures are
sudden, explosive, disorderly charge of neurons—sudden, transient alteration in brain function
S&S of seizures
ALWAYS unconscious; movement is tonic colonic -- alternating rigidity & contraction of muscles
Ictus=
convulsions
Seizures can be caused by
congenital seizure disorder (epilepsy) or to an acute problem in the brain, such as a head injury or stroke
Post-ictal=
state following the end of a seizure
partial seizures
begin locally and can have varied level of unconsciousness
Grand mal seizures aka general seizures and causes
all over the place is systemic and can be precipitated by brain irritation due to cerebral edema
Meningitis is
infection & inflammation of meninges
Meningitis patho
microbe enters highly vascular nasopharyngeal area & crosses into blood then blood system takes it to the meninges via the blood-vessel-rich choroid plexus then the inflammatory process begins that eventually results in increased vascular permeability and edema.
Viral/aseptic meningitis
almost never causes sepsis.
Bacterial Meningitis caused by
meningococcus & pneumococcus
S&S of bacterial meningitis
edema of meninges, photophobia, headache, irritability, restlessness, decreased LOC , nausea & vomiting (Increased ICP)
S&S of edema of meninges surrounding spinal cord
neck stiffness, also known as nuchal rigidity. positive Brudzinski’s and /or Kernig’s signs— maneuvers that demonstrate any kind of meningeal irritation
Other S&S of bacterial meningitis
fever, leukocytosis shows up in CBC, sometimes petechiae and purpura in meningococcal
Gold standard of meningitis CSF check is
High WBC, Higher than normal protein count, blood, lower blood glucose
Myasthenia gravis is
anything that increases cholinesterase can cause muscle weakness b. one of most common neuromuscular junction disorders
Myasthenia gravis patho
chronic autoimmune disease sometimes associated with thymic tumor or other changes in thymus and/Or antibodies produced by the body's own immune system block, alter, or destroy the receptors for acetylcholine