Acquired Brain Injury: Stroke

Objective #1

1. Describe the functional organization of the nervous system using appropriate terminology.

Nervous System Divisions (2)

1) Central Nervous System (CNS)

• contains brain & spinal cord

• lacks regenerative properties!!

  • w strokes/TBI: neurons cannot regenerate!!!

2) Peripheral Nervous System (PNS)

• cranial + spinal nerves

Divisions of the CNS (4)

tiered structure throughout!!!

1) Cerebrum:

a) bilateral cerebral hemispheres

b) diencephalon

2) Brain stem (origin of SC):

a) midbrain

b) pons

c) medulla oblongata

3) cerebellum

4) spinal cord

Neurons: structure + communication

• cell body (soma): contain’s cell nucleus + majority of organelles

• dendrites: extend from soma and receive input from other neurons via synapsis

• axon: single process that emerges from axon hillock

  • sends output impulse to other cells

synaptic communication:

• synapses allow for unidirectional communication b/w neurons

• electrical signal converted into —> chemical signal

• release various neurotransmitters to excite/inhibit post-synaptic cell

Functional Organization of CNS

organized w/ bilateral symmetry

• cereBRUM: crossed representation —> contralateral functions

• cereBELLUM, brain stem, SC —> primarily ipsilateral

multiple specific tracts originate or terminate within various cortexes:

• efferent/motor maps: motor homunculus

• somatosensory maps: sensory homunculus

• retinotopic: occipital lobe

• topographic: right parietal cortex

Objective #2

2. Identify the primary cerebrovascular vessels (ACA, MCA, PCA) and the role of the Circle of Willis.

Vascular Supply

Internal carotids + vertebral arteries ascend to skull + converge to form:

Circle of Willis!!!

• arterial circle formed around pituitary stalk/gland

• provides collateral circulatory pathway in cerebral circulation

Great Cerebral Vessels

major terminal branches of INTERNAL CAROTID:

• Anterior cerebral artery (ACA)

• Middle cerebral artery (MCA)

major branches of VERTEBRAL ARTERIES:

• posterior cerebral arteries (PCA)

• basilar artery

thrombi forming or traveling to ANY of these WILL cause ischemia (stroke)!

Acquired Brain Injury

An injury to the brain that is neither genetic nor congenital

• vascular insults: strokes

• TBIs

• infections

• autoimmune + inflammatory conditions

Objective #3

3. Compare and contrast the impact of various types of strokes, including TIA, ischemic, and hemorrhagic. 

Types of Stroke (2)

stroke: sudden onset neurological impairment due to vascular insult

Ischemic:

• blockage due to a thrombosis or embolus —> blood flow blocked + unable to reach target tissues

• hypoperfusion due to reduced circulation or small vessel disease

Hemorrhagic:

• rupture of an aneurysm or vessel within brain tissue or surrounding space

  • exposes neural tissue to blood + its products

    • failure of blood brain barrier = cascading sequence of destructive events

Ischemia Types

Stroke:

• sudden onset

• focal involvement of the CNS

• vascular cause

• lack of rapid resolution

Transient Ischemic Attack (TIA):

• lasts about 5-15 minutes

• ischemic event where symptoms resolve rapidly (b/c of spontaneous resolution of cause)

  • Ex: embolus becomes dislodged restoring blood flow

• 24 hours is a commonly used boundary b/w TIA and stroke

Ischemic Strokes (2)

follow stroke characteristics from previous flashcard (sudden onset, etc.)

Hypoxic ischemia:

• interruption of blood flow to the brain deprives cells of glucose + oxygen

• leads to ischemic death of brain tissue of all cell types, resulting in chronic lesions (infarction)

  • irrecoverable + produce scarring within CNS

Vascular Ischemia:

• blood flow is obstructed by a thrombus or embolus, preventing delivery of oxygen and glucose

• tissue death will occur within minutes to hours (irreversible)

Objective #4

4. Differentiate the functional impact of various stroke syndromes, including ACA, MCA, and PCA territories.

Anterior Cerebral Artery (ACA) Infarction

territory impacting the MEDIAL aspect of the frontal and parietal lobes

• frontal lobe —> limbic system —> personality changes + disinhibited, impulsive behaviors

  • secondary motor area —> apraxia = impaired motor planning

• MEDIAL portions of motor + sensory cortexes —> contralateral to injury —> weakness on one side of body (hemiparesis)

will produce contralateral hemiparesis + sensory loss of the leg, apraxia + personality changes!!

Middle Cerebral Artery (MCA) infarction

territory impacting the lateral aspect of the frontal, parietal + temporal lobes (trunk, UE, face)

• will produce contralateral hemiparesis + sensory loss of the arm, apraxia

• if dominant hemisphere is involved, aphasia may occur —> inability to produce speech

• if non-dominant hemisphere is involved, neglect of environment may occur

  • profound multi-sensory lack of awareness

    • not respond to visual, auditory or tactile stimuli on non-dominant side

note: dominant hemi. is usually left

Posterior Cerebral Artery (PCA) infarction

territory impacting the occipital + temporal lobes

• will produce contralateral homonymous hemianopia

  • “same-sided half blindness”

  • right lesion = no visual info from left side of environment

Objective #5

5. Describe the clinical manifestations of hemorrhagic strokes (ICH and SAH).

Hemorrhagic Stroke: Intracranial hemorrhage (ICH)

• primarily a result of chronic HTN + underlying vascular disorders

• metabolic effects of blood disturb the function of surrounding brain tissue, as well as produce focal edema

  • release of blood into tissues of cerebrum

Hemorrhagic Stroke: ICH — secondary effects

sequence of ICH injury:

1. hematoma ruptures white matter tracts; expands for up to 24 hours

2. cerebral edema develops as product of inflammation (rupture of BBB) in surrounding tissue for up to 2 weeks

3. edema produces mass effect —> shifts cerebral tissues + collapsing arterial vessels

Hemorrhagic Stroke: Subarachnoid hemorrhage (SAH)

• starts w/ BAD headache

• caused by rupture to vessels within the subarachnoid space

• cerebral dysfunction occurs b/c of increased intracranial pressure + from toxic effects of subarachnoid blood

• vasospasm is a complication

  • can impede blood flow + provoke ischemic stroke

  • vasospasm = spastic contraction of smooth muscle lining

Cerebral Aneurysm (can lead to SAH)

• focal dilatation of the vessel wall; thin walled + at risk for rupture

• major cerebral vessels lie in the subarachnoid space —> rupture results in SAH

• some aneurysm may occur within neural tissues themselves

Objective #6

6. Describe basic medical and surgical management for the various types of strokes.

Hemorrhagic Stroke Medical/Surgical Management

• surgical clipping: open or endovascular removal of aneurysm (pictured)

• cerebellar/lobal hemorrhage: decompression + evacuation

  • for subA + intracranial hemorrhages

• deep hemorrhage: no surgical options, only medical management

Ischemic Stroke Medical/Surgical Management

*time = brain loss!!!*

prevention through anti-platelet therapies + management of artherosclerotic disease

• intravenous thrombolysis

  • IV administration of recombinant tissue plasminogen activator (rTPA) —> anticoagulant to break apart clots

  • must be administered within 4.5 hours of onset of symptoms to reduce disability + mortality

• clot retrieval (pictured)

  • thrombectomy w/ stent or coil retrievers

  • may be used in conjuction with rTPA

Ischemic Stroke Medical/Surgical Management (cont.)

• carotid endarterectomy (pictured)

  • surgical removal of thrombus from a stenotic carotid artery in neck

• decompressive craniectomy (stroke w/ significant edema)

  • used to prevent cerebral herniation after large hemispheric strokes

    • reduce intracranial pressure —> resecting portion of skull beneath skin flap to accommodate cerebral edema