216B neurology 1

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Nursing

2nd

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116 Terms

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brain
2% of body weight

15% of CO per minute

20% of all oxygen
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the brain does not
store O2

store nutrition

recover nervous tissue injury (no centrioles = no management)
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what is plasticity
the brain’s way of compensating; enhance functionality in other areas

younger = more likely
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Brian survival without O2:
10 seconds, apoptosis in 4-6 minuets
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consciousness
depends on cerebral cortex function and reticular formation
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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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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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assessments for RAS activity
LOC - GCS
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brain injury
Caused by a pathology, plus the pathological sequelae
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pathology sequelae (brain Injury)
* CVA, infection, tumor, trauma…
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example of sequelae (brain injury)
ischemia, cerebral edema, metabolic acidosis, increased ICP
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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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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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minimally conscious state
if some awareness
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brain stem reflexes
gag, cough, doll’s eyes reflex (occulocephalic)
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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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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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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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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 @
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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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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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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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TIA treatment
anticoagulants + antiplatlets

drugs: apixaban, dabigatran, ASA (81mg)
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ischemic CVA TX
thrombolytics < 3 hours since onset

thrombectomy
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CVA TX
antiplatlets and anticoagulats

\+tx HTN/ dyslipidemia…
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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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agnosia
inability to recognize and identify objects/ persons
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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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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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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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aneurysm
buldge in vessel wall
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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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hematomas/ hemorrhages
intracerebral: within cerebral lobes

described by location
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hematoma causes
ruptures cerebral aneurysm, ruptured AVM, hemorrhagic CVA, head injury bleed

\+associated w comorbidities: clotting dysfunctions ( hemophilia, anticoagulants)
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epidural hematoma
btw dura and skull

commonly caused by skull fracture
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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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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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infection (CNS)
spread via blood stream or direct entry

eg. fracture, procedure/surgery, other infected sites (sinuses and otitis media)
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encephalitis
infection in Brian parenchyma
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Myelitis
infection in spinal cord
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encephalomyelitis
infection in brain and spinal cord
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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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meningitis mortality
strep. pneumonia (highest 34%)

neuro. deficits (50%)
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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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meningitis TX
immediate brand spectrum ABX and potent anti-inflammatories

* 3rd gen cephalosporins; penicillins; vancomycin
* glucocorticosteroids eg. dexamethasone
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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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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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DX for tumors
MRI, EEG
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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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seizures
spontaneous, abnormally synchronous electrical discharges from neurons in the cerebral cortex
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idiopathic seizures
genetic origin, cause unknown - epilepsy

eg. alteration in ion channel transport
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idiopathic seizures TX
long term anti-epileptic meds
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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