Disorders of the Neurologic System

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1

CPP is

cerebral perfusion pressure and is the pressure required to get oxygenated blood to the brain to perfuse

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2

Changes in blood flow (hypo/hypertension or blockage) can lead to low or too-high CCP which can lead can lead to

cerebral edema,

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3

ICP is

Intracranial pressure is the addition of arterial/venous blood flow, CSF pressure, and Brain tissue.

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4

The main culprit in causing IICP

& the loss of balance between ICP & CPP is cerebral edema

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5

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.

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6

Cerebral edema & IICP

almost always go “hand in hand”

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7

Changes in ICP can be caused by

Head injury, Brain tumor, Brain attack, infection, acid-base imbalance, meningitis, and hypoxemia from respiratory disorders

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8

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.

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9

Etiologies of Brain attacks are

atherosclerosis of cerebral arteries, brain aneurysm, heart problems that leads to decreased cardiac output.

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10

Risk factors of brain attack are

atherosclerosis, HTN, older age, DIABETTES, family history, and lifestyle choices

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11

Negative effects of a stroke

cerebral edema & IICP

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12

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

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13

Thrombotic stroke

occurs from a clot or plaque that blocks off the artery in which it has developed & causes ischemia distally

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14

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

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15

causes of thrombotic & embolic events:

A-fib, valve issues, air emboli, atherosclerosis, and intracranial artery plaque

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16

TIA=

Trans ischemic Brain attack

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17

Speacial part of TIA

Temporary, no neurological problems, but it is a massive waring sign that a real stoke is coming.

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18

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.

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Causes of hemorrhagic stroke

weak arterial wall, bleeding into a tumor, coagulation disorders, congenital vascular disorders, aneurysms, and pressure of hypertension.

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20

The three areas of a Brain attack are

Brain stem, Cerebellum, and Right or left hemisphere

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Assessing a stroke

  1. assess patient’s autonomic status (includes LOC-- level of consciousness and mental)

  2. Assess sensorimotor system

    1. Assess sensorimotor above the shoulder

    2. Assess sensorimotor below the shoulder

  3. Assess reflexes

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22

Level of consciousness includes

oriented, alert, following commands, normal speech, and conversing appropriately

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23

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.

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24

Sensorimotor

a term that encompasses the fact that movement & sensation are intricately related.

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25

Normal sensorimotor is

Normal sensation, muscle tone, and movement Symmetric, AKA the same bilaterally

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26

CN VII

Facial nerve (controls facial movement and expression) (Contralateral)

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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.

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CN II

Optic nerve

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29

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.

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CN III

Oculomotor nerve

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31

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.

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32

Visual defects in the two left halves of BOTH eyes is

homonymous hemianopia.

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33

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.

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34

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

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35

Spinothalamic tracts

ascending (sensory) tracts that carry sensations of pain, temperature, crude and light from body to brain.

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36

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

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37

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

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38

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.

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39

Normal Central reflexes are

cough, swallow, gag,

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40

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.

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41

Positive Babinski”

means that stroking plantar surface of foot makes the big toe flex “upgoing toe” NORMAL UNTIL AFTER TWO YEARS OLD

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42

S&S autonomic of Brain stem stroke

coma or near comatose state, heart rate and blood pressure changes, breathing pattern changes

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43

Cheyne-Stokes

apnea then breathing pattern changes

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44

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.

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45

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

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46

Cerebellar BA S&S

Loss of coordination, vertigo, nystagmus, nausea and vomiting, problems with coordination and balance, and vertebral –basilar artery occlusion

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47

dysphasia

impairment in the production of speech resulting from brain disease or damage.

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48

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.

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49

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.

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50

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)

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51

spatiality

where you are in space, & where things are around you

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52

Typical S&S of Hemorrhagic strokes

intense headaches, neck pain, light intolerance, nausea and vomiting, and higher mortality rate with hemorrhagic strokes

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53

To monitor and control cerebral edema

HOB (head of bed) up at least 30 degrees

Diuretics

ICP monitor

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54

How to prevent the further increase in ICP

O2

BP management (not too high or low)

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55

Treatment of hemorrhagic strokes

may need surgical intervention for certain types of hemorrhagic strokes

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56

Treatment of ischemic strokes

Thrombolytic drugs first within 3-4.5 hours first then Heparin, then send home on Coumadin

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57

Familial Alzheimer’s (FAD)

Inheritance-linked – can be early onset or late

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58

non-hereditary (AKA sporadic)

late onset—70% of cases

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59

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.

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60

Cause 2 of Alzhimers’s is

microtubules of neurons in the brain become distorted and twisted and form a neurofibrillary tangle.

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61

Cause 3 of Alzhimers’s is

the amyloid plaques and the neurofibrillary tangle combine to disrupt normal nerve impulses in the brain.

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62

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

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63

Normal basal ganglia function is based on

balance of 2 neurotransmitters—dopamine & acetylcholine

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64

EPS partly controls

fine motor skilss

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65

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

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66

Parkinson’s is summarized by

tips the scales of balance towards cholinergic, excitatory activity --not actually more acetylcholine, but more effect.)

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67

Increased cholinergic effect gives

S&S related to hypertonia (rigidity) & dyskinesia

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68

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.

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69

dysphagia

difficulty swallowing

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70

Hypertonia manifestations

overall rigidity, often noticed in the face—mask-like face

“Cog-wheel rigidity” of forearm

Dysarthria (difficulty forming words)

Dysphagia

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71

Parkinsonisms

any dysfunction of the extrapyramidal system but with any disease process or drug that disorders function of basal ganglia

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72

Basal ganglion gait” AKA “Parkinsonian gait”

stooped, shuffling posture; decreased arm swing

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73

Treatment for Parkinson’s

give medication containing dopamine (anticholinergic)

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74

Multiple sclerosis

T cells attack myelin sheath leading to demyelination causing sporadically blocked or altered nerve conduction

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75

Multiple sclerosis causes the nerve impulses 10 to be

times slower than normal myelinated ones

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76

Paresthesia

unusual sensory sensation such as numbness, shooting

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77

Ataxia

staggering gait

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78

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

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79

dysarthria

difficulty speaking due to actual jaw muscle weakness);

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80

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.

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81

Treatment for Migraines

NSAIDS and Imitrex (prodrome)

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82

Prodrome of Migraines

aura =perception of a strange light, an unpleasant smell or confusing

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83

Migraines S&S

headache itself, which is often unilateral and accompanied by N,V, photophobia, phonophobia

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84

Seizures are

sudden, explosive, disorderly charge of neurons—sudden, transient alteration in brain function

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85

S&S of seizures

ALWAYS unconscious; movement is tonic colonic -- alternating rigidity & contraction of muscles

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86

Ictus=

convulsions

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87

Seizures can be caused by

congenital seizure disorder (epilepsy) or to an acute problem in the brain, such as a head injury or stroke

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Post-ictal=

state following the end of a seizure

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89

partial seizures

begin locally and can have varied level of unconsciousness

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90

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

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91

Meningitis is

infection & inflammation of meninges

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92

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.

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93

Viral/aseptic meningitis

almost never causes sepsis.

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94

Bacterial Meningitis caused by

meningococcus & pneumococcus

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95

S&S of bacterial meningitis

edema of meninges, photophobia, headache, irritability, restlessness, decreased LOC , nausea & vomiting (Increased ICP)

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96

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

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97

Other S&S of bacterial meningitis

fever, leukocytosis shows up in CBC, sometimes petechiae and purpura in meningococcal

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98

Gold standard of meningitis CSF check is

High WBC, Higher than normal protein count, blood, lower blood glucose

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99

Myasthenia gravis is

anything that increases cholinesterase can cause muscle weakness b. one of most common neuromuscular junction disorders

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100

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

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