216B neurology 1

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Nursing

2nd

116 Terms

1

brain

2% of body weight

15% of CO per minute

20% of all oxygen

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2

the brain does not

store O2

store nutrition

recover nervous tissue injury (no centrioles = no management)

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3

what is plasticity

the brain’s way of compensating; enhance functionality in other areas

younger = more likely

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4

Brian survival without O2:

10 seconds, apoptosis in 4-6 minuets

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5

consciousness

depends on cerebral cortex function and reticular formation

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6

RAS: reticular activating system

brain stem

wakefulness

activates higher centres of cerebral cortex

lower RAS = lower awareness/ wakefulness eg. sleep

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low RAS acitivity d/t pathology

altered LOC

eg. decreased perfusion, altered metabolic state (ex. met. acidosis)

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8

decreased O2 =

(sequelae)

decreased function of brainstem’s repo centers and decreased sensitivity to increased CO2

leads to irrégulière. reps; apnea

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9

assessments for RAS activity

LOC - GCS

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10

brain injury

Caused by a pathology, plus the pathological sequelae

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11

pathology sequelae (brain Injury)

  • CVA, infection, tumor, trauma…

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12

example of sequelae (brain injury)

ischemia, cerebral edema, metabolic acidosis, increased ICP

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13

brain injury- higher severity =

more pronounces neuro dysfunction

focal (ex. loss of earring caused by tumour in occipital lobe)

or

global deficit ( antlers consciousness, stupor, coma, alt. VS, declining autorégulation)

eg. loss of protective reflexes- blinking urination, defecation

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14

brain death

no motor responses, no brain stem reflexes, apnea

**some exceptions; ex. Cervical vertebra injury

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vegetative state

is not brain dead

damage to grey and white matter

maintenance of brain stem reflexes; sleep-wake cycle; hypothalamic reg (ex. body temp)

no awareness of self/ surroundings

inability to interact/ produce responses

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16

minimally conscious state

if some awareness

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brain stem reflexes

gag, cough, doll’s eyes reflex (occulocephalic)

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18

hypoxia

deficient delivery of O2 to the tissue

often result of hypoxemia (anemia/ toxicity)

RBCS/ affinity of toxic substances → CBC?

decreased O2 supply to all brain tissue

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19

effects of hypoxia

agitation, decreased LOC, seizures

  • depends on severity and suddenness of onset

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ischemia

lack of O2/ removal of waste within a tissue

focal: CVA - speech affected

global: effects all brain tissue (metabolic acidosis/ ketoacidosis) / loss of OC (severe arrhythmia/ MI)

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global ischemia

no nutreoint and O2 delivery → depletion of resources within 5 minutes → Brian injury

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22

compounding issues of global ischemia

cerebral edema

electrolyte imbalances (Na, K, Ca)

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electrolyte dysfunction

excess intracellular calcium → calcium cascade; protein breakdown, DNA injury, free radical formation, lipid peroxidation, mitochondrial injury = cell death

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electrolyte dysfunction (neurotransmitters)

abnormal neurotransmitter secretion/ recycling → accumulation of neurotransmitters or depletion of neurotransmitters

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watershed infacts

heightened focal damage to lowered flow regions

→ more injuries to areas seen as non-important (ex. hippocampus)

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reperfusion injury

injury due to belated reperfusion caused by inflammatory mediators/ toxic by-products/ catecholamines/ nitric oxide

  • repercussion injury compounds original injury

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27

blood flow to brain every minute:

600-700 mL

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CPP

pressure gradient between internal carotid artery and subarachnoid veins

tells us what pressure is required to perfuse the brain

min CPP = 45mmhg profound (ischemia @ <40)

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29

effects of High ICP

obstructs fluid flow and displaces/ injures brain cells

  • content compartments compensate to maintain homeostasis → bigger injury

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S&S of high ICP

Cushing’s triad, wide PP, bradycardia, irrégulière. respiration

max impact→ ‘Brian herniation’ pressure displacement of brain tissue

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cranial cavity contents surrounded by rigid skull:

80% brain tissue

10% blood

10% CSF

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Monroe- kellie hypothesis

reduction of venous blood flow/ reduction on CSF content

compensation for high ICP

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indications of a brain injury

bleed

ischemia

inflammation/ infection

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common causes of increased ICP

CVA

hematomas- epidural, subdural, intracerebral

head injury, concussion

infection

brain tumour

= risk of cerebral edema → increased ICP

will be compensated but monro-kellie hyp.

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clinical focus for increased ICP

NVS, assess deficits (area related)

tx to prevent further injuries

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vasogenic cerebral edema

BBB compromise: head injury, hematoma (bruise), hemorrhage (active bleed), CNS infection (meninges)→ inflammation→ increased permeation= high ICP

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cytotoxic cerebral edema

increased intracellular fluid shift:

hypo osmotic states/ electrolyte imbalance; ischemia leading to electrolyte imbalance → H2O shift into cells

= high ICP

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vasogenic + cytotoxic CE

complex injury → hemorage + ischemia

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CE TX

underlying cause; decrease further injury

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40

ischemic CVA

thrombus/embolus

80%

hypoxia → ischemia → injury to affected are

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TIA ‘transient ischemic attacts

‘angina’ of the brain (a warning of CVA risk)

transient episodes

start CVA prevention tx

‘mini stroke’- artery is temporarily blocked

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42

CVA deficits

area related- affected cerebral artery

MCA most common: upper lips and face

broca’s area = speech

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CVA complications

the adequacy of the collateral circulation

presence of cerebral edema and increased ICP

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F.A.S.T

face - drooping?

Arms - raise both?

Speech - slurred or jumbled?

time - call 911

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45

TIA treatment

anticoagulants + antiplatlets

drugs: apixaban, dabigatran, ASA (81mg)

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ischemic CVA TX

thrombolytics < 3 hours since onset

thrombectomy <24 hours since onset

carotid endarectomy or angioplasty

  • auscultate for bruits

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CVA TX

antiplatlets and anticoagulats

+tx HTN/ dyslipidemia…

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48

dysarthria

weak muscle control/ slurred speech

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aphasia

impairment of language/ speaking

speaking and comprehension

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apraxia

moving the muscles needed int he correct order and sequence (post. parietal cortex)

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51

agnosia

inability to recognize and identify objects/ persons

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52

hemorrhagic CVA risks

less common, more fatal

HTN, meds, age, arterial deficits (atriovenous malformation, aneurysms), bleeding disorders

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CVA hemorrhages S&S

headache, vomiting, affected area S&S

sudden onset

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54

hemorrhagic CVA sequelae

hemorrhage, ischemia, ICP increased, edema, necrosis, death

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hemorrhagic CVA ER TX

stabalize (intubate/O2, sedate e.g. reverse anticoag.)

osmotic diuretics mannitol/ hypertonic NS 3%NaCl

optimise perfusion (eh. HTN TX)

surgical evacuation

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56

AVM: atriovenous malformation

congenital defect in structural formation of cerebral vessels

bundle arteries + veins lacking in capillary networks and normal wall structure

high pressure art. flow enters thinner venous vessels rapildly, causing a rupture/ hemmorage

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AVM S&S

AVM network steals blood flow from surrounding area → ischemia = slow onset neuro deficits, headaches, seizures…

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TX for AVM

  • if ruptures: as per hemmoragic CVA

  • radiation (gama knife), embolization, surgical excision

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59

aneurysm

buldge in vessel wall

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60

aneurysm locations

cerebral: subarachnoid hemorrhage (80% circle of willis)

Aortic Abdominal

thoracic

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aneurysm risk factors

atherosclerosis, HTN, malformed vessels (congenital thin intima or media), age

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aneurysm TX

rupture: hem. CVA TX

unruptured: clipping, coiling, flow dispersion

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aortic aneurysm

age is a factor; elastin not synthesized in elderly

if ruptures: systemic bleeds

  • tx: fluids (isotonic; NS/LR), surgery

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64

hematomas/ hemorrhages

intracerebral: within cerebral lobes

described by location

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65

hematoma causes

ruptures cerebral aneurysm, ruptured AVM, hemorrhagic CVA, head injury bleed

+associated w comorbidities: clotting dysfunctions ( hemophilia, anticoagulants)

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66

epidural hematoma

btw dura and skull

commonly caused by skull fracture

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67

subdural hematoma

btw dura and subdural space

commonly caused by acel/decel injuries→ venous tearing

acute: sudden onset - high M&M d/t high ICP

subacute: slow onset - same danger

chronic: d/t brain atrophy = shrinking = tearing of veins = very slow onset

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subdural hematoma sequalae

increased ICP, coma necrosis

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tx for hematoma

decrease ICP, evacuate

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70

concussion

a traumatic brain injury, induced by traumatic biochemical forces

  • eg. direct impact; acceleration- deceleration forces (accidents, sports, falls, physical abuse)

mild-moderate brain injury (inflammation rather than a bleed)

additive effects - repetition makes it worse

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concussion S&S

headache, amnesia, confusion, heightened sensitivities, nausea, irritability, insomnia, poor concentration/memory

  • level of symptom is relevant to degree of injury eg. amnesia of event vs preceding to the event

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concussion TX

low stimulation, slow return to normal ADL/ activities, prevent second impact, if symptoms are severe TX focuses on receiving cerebral edema and ICP (slow and steady)

post concussion syndrome (>3months)

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73

infection (CNS)

spread via blood stream or direct entry

eg. fracture, procedure/surgery, other infected sites (sinuses and otitis media)

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74

encephalitis

infection in Brian parenchyma

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75

Myelitis

infection in spinal cord

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76

encephalomyelitis

infection in brain and spinal cord

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77

meningitis

inflammation of Pia matter arachnoid, subarachnoid space (CSF space)

  • spread throughout due to infected CSF and flow within CSF

  • purulent (bacterial) and lymphocytic (viral)

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meningitis common pathogens

  • Streptococcus pneumoniae (pneumococcus) - vaccine

  • Haemophilus influenzae - vaccine

  • Niseria meningitidis (meningococcus) - vaccine

  • Listeria monocytogenes

  • Group B streptococcus (etiology: newborns)

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79

meningitis mortality

strep. pneumonia (highest 34%)

neuro. deficits (50%)

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80

meningitis pathology sequelae

severe inflammation→BBB compromised→inflammation causes further capillary leaking, cerebral edema vascular congestion, cellular death; meningeal thickening→meningeal adhesions = vascular congestion and decreased CSF outflow (hydrocephalus)

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meningitis S&S

fever, headache, stiff neck (nuchal rigidity), N&V, aches, CN deficits, seizures, brudzinski sign (flexion of neck→ flexion of hip+knee); petechia rash (sing of sepsis caused by meningitis)

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82

meningitis TX

immediate brand spectrum ABX and potent anti-inflammatories

  • 3rd gen cephalosporins; penicillins; vancomycin

    • glucocorticosteroids eg. dexamethasone

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83

Brain tumours

neoplasms (abnormal cellular proliferation) which can metastasize

  • primary (originate in CNS)

  • metastatic (originated in other tissues: lung, breast)-40%

low-grade and high-grade tumor

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84

Brian tumor S&S

focal disturbances ( the affected region)

global CNS effects if increased vol. causes a CNS sequelae

general: headache, N&V, focal changes (eg visual), LOC changes, seizures

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Brain tumour sequelae

cerebral edema, increased ICP, brain compression, blood and CSF flow disturbances

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86

DX for tumors

MRI, EEG

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87

tx for tumors

depends on tumour origin, stage, size and location depender

  • surgery - excision of tumour

  • radiation - gamma knife

  • chemo eg. alkalizing agents (DNA damage)

    • temozomide (TMZ

    • s/e: quickly replication eukaryotic cells (hairless, GI upset, bone marrow suppression, low BC counts)

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TX overview

  • preserve brain function

  • treat causse (eg. abs, cerebral stunting, tPA, hematoma evac)

  • treat high ICP/ cerebral edema (hypertonic, osmotic diuretics, drainage of CSF (temp.))

  • maintain VS

  • preserve function

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89

seizures

spontaneous, abnormally synchronous electrical discharges from neurons in the cerebral cortex

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90

idiopathic seizures

genetic origin, cause unknown - epilepsy

eg. alteration in ion channel transport

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91

idiopathic seizures TX

long term anti-epileptic meds

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92

symptomatic seizures

due to a brain injury

  • results in altered action potential/ neurotransmitter balance/ electrolyte balance

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symptomatic seizures TX

short-term anti-epileptic meds; treat underlying cause

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3 main classes of seizures

  • focal: specific groups of neutrons in one hemisphere

  • generalized: both hemispheres involved (eg. absence seizures, tonic-clinic seizures)

  • unknown: neither categories (eg. febrile seizures)

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seizures S&S

specific to seizure type

  • loss of consciousness - common

  • aura/ partial seizure (maybe)

  • some w automatisms - repeating behaviour

  • may be in two or one hemisphere

  • may progress to other seizures (focal→ generalized)

    • ‘evolving seizures’

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life threatening seizure symptoms

  • tonic convulsions: constriction of muscles (airway)

  • loss of consciousness: impairs respiratory rate/ depth

  • convulsions cause falls/ flailing- prevention

  • stem of ANS cause sever VS changes

    • tachycardia, HTN, reflex hypotension, hyperventilation

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seizure Dx

Eeg

MRI

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seizure TX

benazodiazepiens

barbiturates

anti-convulsants

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status epilepticus

seizure can process to an unstoppable state→ life threatening (ER)

requires immediate TX

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status epilepticus TX

benzodiazepines IV

diazepam/ lorazepam

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