216B neurology 1

brain

2% of body weight

15% of CO per minute

20% of all oxygen

the brain does not

store O2

store nutrition

recover nervous tissue injury (no centrioles = no management)

what is plasticity

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

younger = more likely

Brian survival without O2:

10 seconds, apoptosis in 4-6 minuets

consciousness

depends on cerebral cortex function and reticular formation

RAS: reticular activating system

brain stem

wakefulness

activates higher centres of cerebral cortex

lower RAS = lower awareness/ wakefulness eg. sleep

low RAS acitivity d/t pathology

altered LOC

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

decreased O2 =

(sequelae)

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

leads to irrégulière. reps; apnea

assessments for RAS activity

LOC - GCS

brain injury

Caused by a pathology, plus the pathological sequelae

pathology sequelae (brain Injury)

* CVA, infection, tumor, trauma…

example of sequelae (brain injury)

ischemia, cerebral edema, metabolic acidosis, increased ICP

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

brain death

no motor responses, no brain stem reflexes, apnea

\*\*some exceptions; ex. Cervical vertebra injury

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

minimally conscious state

if some awareness

brain stem reflexes

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

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

effects of hypoxia

**agitation**, decreased LOC, seizures

* depends on severity and suddenness of onset

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)

global ischemia

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

compounding issues of global ischemia

cerebral edema

electrolyte imbalances (Na, K, Ca)

electrolyte dysfunction

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

electrolyte dysfunction (neurotransmitters)

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

watershed infacts

heightened focal damage to lowered flow regions

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

reperfusion injury

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

* repercussion injury compounds original injury

blood flow to brain every minute:

600-700 mL

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 @

effects of High ICP

obstructs fluid flow and displaces/ injures brain cells

* content compartments compensate to maintain homeostasis → bigger injury

S&S of high ICP

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

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

cranial cavity contents surrounded by rigid skull:

80% brain tissue

10% blood

10% CSF

Monroe- kellie hypothesis

reduction of venous blood flow/ reduction on CSF content

compensation for high ICP

indications of a brain injury

bleed

ischemia

inflammation/ infection

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.

clinical focus for increased ICP

NVS, assess deficits (area related)

tx to prevent further injuries

vasogenic cerebral edema

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

cytotoxic cerebral edema

increased intracellular fluid shift:

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

= high ICP

vasogenic + cytotoxic CE

complex injury → hemorage + ischemia

CE TX

underlying cause; decrease further injury

ischemic CVA

thrombus/embolus

80%

hypoxia → ischemia → injury to affected are

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

CVA deficits

area related- affected cerebral artery

MCA most common: upper lips and face

broca’s area = speech

CVA complications

the adequacy of the collateral circulation

presence of cerebral edema and increased ICP

F.A.S.T

face - drooping?

Arms - raise both?

Speech - slurred or jumbled?

time - call 911

TIA treatment

anticoagulants + antiplatlets

drugs: apixaban, dabigatran, ASA (81mg)

ischemic CVA TX

thrombolytics < 3 hours since onset

thrombectomy

CVA TX

antiplatlets and anticoagulats

\+tx HTN/ dyslipidemia…

dysarthria

weak muscle control/ slurred speech

aphasia

impairment of language/ speaking

speaking and comprehension

apraxia

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

agnosia

inability to recognize and identify objects/ persons

hemorrhagic CVA risks

less common, more fatal

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

CVA hemorrhages S&S

headache, vomiting, affected area S&S

sudden onset

hemorrhagic CVA sequelae

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

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

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

AVM S&S

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

TX for AVM

• if ruptures: as per hemmoragic CVA

• radiation (gama knife), embolization, surgical excision

aneurysm

buldge in vessel wall

aneurysm locations

cerebral: subarachnoid hemorrhage (80% circle of willis)

Aortic Abdominal

thoracic

aneurysm risk factors

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

aneurysm TX

rupture: hem. CVA TX

unruptured: clipping, coiling, flow dispersion

aortic aneurysm

age is a factor; elastin not synthesized in elderly

if ruptures: systemic bleeds

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

hematomas/ hemorrhages

intracerebral: within cerebral lobes

described by location

hematoma causes

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

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

epidural hematoma

btw dura and skull

commonly caused by skull fracture

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

subdural hematoma sequalae

increased ICP, coma necrosis

tx for hematoma

decrease ICP, evacuate

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

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

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)

infection (CNS)

spread via blood stream or direct entry

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

encephalitis

infection in Brian parenchyma

Myelitis

infection in spinal cord

encephalomyelitis

infection in brain and spinal cord

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)

meningitis common pathogens

• Streptococcus pneumoniae (pneumococcus) - vaccine

• Haemophilus influenzae - vaccine

• Niseria meningitidis (meningococcus) - vaccine

• Listeria monocytogenes

• Group B streptococcus (etiology: newborns)

meningitis mortality

strep. pneumonia (highest 34%)

neuro. deficits (50%)

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)

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)

meningitis TX

immediate brand spectrum ABX and potent anti-inflammatories

* 3rd gen cephalosporins; penicillins; vancomycin
* glucocorticosteroids eg. dexamethasone

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

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

Brain tumour sequelae

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

DX for tumors

MRI, EEG

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)

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

seizures

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

idiopathic seizures

genetic origin, cause unknown - epilepsy

eg. alteration in ion channel transport

idiopathic seizures TX

long term anti-epileptic meds

symptomatic seizures

due to a brain injury

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

symptomatic seizures TX

short-term anti-epileptic meds; treat underlying cause

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)

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’

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

seizure Dx

Eeg

MRI

seizure TX

benazodiazepiens

barbiturates

anti-convulsants

status epilepticus

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

requires immediate TX

status epilepticus TX

benzodiazepines IV

diazepam/ lorazepam