Neuro-Cortical Function Flashcards
Manifestations/Mechanisms of Brain injury
- Brain is protected from external forces by the rigid skull and fluid
- Metabolic stability is maintained by regulatory mechanisms (blood brain barrier) and autoregulatory mechanisms.
- Brain injury is manifested by changes in the LOC and alterations in cognitive/motor/sensory function.
- Focal brain injury causes neurologic deficits that may or may not alter consciousness.
- Global brain injury result in altered LOC ranging from inattention to stupor or coma.
- Cerebral hemispheres are most susceptible to damage.
- See Table 16-1, p. 413 Level of Brain injury and Key Clinical Signs
The brain stem reticular formation and reticular activating system (RAS)
- Ascending sensory tracts.
- Give rise to fibers synapsing in the nonspecific nuclei of the thalamus.
- Influence widespread areas of the cerebral cortex and limbic system.
- The RAS constitutes the central core of the brain stem. See Fig. 16-1, p. 413 The brain stem reticular formation and reticular activating system (RAS).
Other manifestations of deteriorating brain function
- Pupillary reflexes and eye movements: Pupils become nonreactive and dilated as brain function deteriorates.
- See Fig 16-2, p. 415 The doll’s head eye response demonstrates the always-present vestibular static reflexes without forebrain interference or suppression.
- Abnormal flexion and extension posturing: As coma progresses, noxious stimuli can initiate rigidity and abnormal (decorticate and decerebrate) postures if motor tracts are interrupted at specific levels. See Fig. 16-3, p. 415.
- Respiratory response: Yawning, sighing are early signs with progression to Cheyne-Stokes breathing.
- Cheyne-Stokes, breathing can be very deep and rapid (hyperpnea), followed by periods of slow shallow breaths, or interrupted by episodes of apnea, in which an individual stops breathing altogether for a period.
- It often occurs in cycles lasting between 30 seconds and two minutes.
- With progression of injury continuing to midbrain, respirations change to central neurogenic hyperventilation (respirations > 40 bpm) d/t uninhibited stimulation of the inspiratory/expiratory centers.
- With medulla involvement, respirations become ataxic.
- Apnea may be due to lack of responsiveness to carbon dioxide stimulation.
- Brain Death: Irreversible loss of function of the brain, including the brain stem.
Mechanisms of Brain Injury
Hypoxia and ischemic injury:
• ATP supplies brain with energy.
• Hypoxia = deprivation of oxygen with maintained blood flow
• Ischemia = reduced or interrupted blood flow.
Cerebral ischemia can be focal (as in a stroke) or global (as in cardiac arrest)
• Focal ischemia = only a region of the brain is under perfused. Collateral circulation provides blood flow to uninvolved areas.
• Global ischemia = blood flow to entire brain is compromised.
• Inadequate blood flow to meet metabolic needs of the brain.
• Unconsciousness occurs in seconds.
• See Fig. 16-4, p. 417 Consequences of global ischemia. A global insult induces lesions that reflect the vascular architecture (watershed infarcts, laminar necrosis) and the sensitivity of individual neuronal systems (pyramidal cells of the Sommer section, Purkinje cells).
Excitotoxic Brain Injury
• Triggered by excessive activity of excitatory neurotransmitters and the receptor-mediated effects.
• Range from acute insults such as stroke to disorders such as Huntington disease.
• Glutamate is principal excitatory neurotransmitter in the brain.
• Prolonged ischemia = glutamate transport mechanisms become immobilized, causing extracellular glutamate to accumulate which leads to a process called the calcium cascade See Fig. 16-5, p. 418.
Increase Intracranial Pressure
- Three compartments contained within the rigid confines of the skull—the brain tissue and interstitial fluid (80%), the blood (10%), and the cerebrospinal fluid (10%).
- Each of these contributes to the volume of ICP which is normally maintained between 0—15 mmHg (left ventricle). The volumes of each of these components can vary slightly without causing marked changes in ICP because these will compensate for each other.
- This is called the Monroe-Kellie hypothesis/doctrine.
- Tissue volume is relatively restricted in its ability to undergo change.
- CSF and blood volume can compensate for changes in ICP.
- Initially, increases in ICP are buffered by a translocation of CSF to the spinal subarachnoid space and increased CSF reabsorption.
- The blood compartment is limited by the small amount in the cerebral circulation, most of which is contained in the low-pressure venous system.
- As the volume buffering capacity of this compartment become exhausted, venous pressure increases and cerebral blood volume and ICP rises.
- Impact of increases in blood, brain tissue or CSF volumes on ICP varies and depends on the amount of increase, effectiveness of compensatory mechanisms, and compliance of brain tissue.
Compliance is the brain’s ability to maintain ICP during changes in intracranial volume.
- The shape of the curve demonstrates the effect on ICP of adding volume to the intracranial cavity. From points A to B, the compensatory mechanisms are adequate, compliance is high, and the ICP remains relatively constant as volume is added to the intracranial cavity. At point B, the ICP is relatively normal, but the compensatory mechanisms have reached their limits, compliance is decreased, and ICP begins to rise with each change in volume. From points C to D, the compensatory mechanisms have been exceeded, and ICP rises significantly with each increase in volume as compliance is lost. ICP, intracranial pressure.
- Cerebral perfusion pressure (CPP) = pressure required to perfuse brain cells
- CPP = MABP (mean arterial blood pressure) – ICP (intracranial pressure) normal 70-100 mm Hg
- CPP can fluctuate with a change in either MABP or ICP
General and progressive manifestations of IICP
• Decreased level of consciousness – (Table 16-2)
• Glasgow coma scale (Table 16-3) index of severity: correlates with prognosis
• Headache
• Motor and reflex changes
• Changes in pupils
o Pupil reflexes: become non-reactive and dilated
o Eye movement: oculomotor responses (Fig. 16-2): Doll’s Eye; Caloric ice water Hemodynamic changes Increased BP, decreased HR, decreased RR (Cushing’s Triad)
• Respiratory changes
• Abnormal posturing (Fig. 16-3)
• Decorticate (flexor)
• Decerebrate (extensor)
Traumatic Brain Injury (TBI): structural damage to the head
• Etiology: leading causes MVC, bicycle crash, battlefield trauma, sports injuries, falls, assaults
• Mechanism of trauma:
o Acceleration
o Deceleration
o Angular rotation – rotational movement of hemispheres around the fixed brain stem
o Penetrating trauma
o Shearing injuries
• Closed vs. open
o Basilar skull fracture
o Periorbital ecchymosis
Battle sign
Blood or CSF drainage
• Primary injury: immediate response to the initial injury (See Fig. 16-9, p. 423)
• Focal lesions: affecting one area:
o Contusion: brain bruising or tearing of brain tissue from direct force, depressed skull fracture, closed acceleration/deceleration injury
o Hemorrhage (Fig. 16-10, p. 424): results from vascular injury or bleeding
Epidural hematoma – bleeding between the dura mater and skull-See Fig. 16-12, p.425; 85% involve an arterial bleed
Subdural hematoma – bleeding between the dura mater and brain See Fig. 16-11, p.425. Usually, venous, acute, chronic, elderly/alcoholics
Intracerebral hematoma – bleeding within the brain
• Manifestations of focal lesions:
• Diffuse lesions: affecting more than one area of the brain
o Concussion: transient neurogenic dysfunction caused by mechanical force to the brain
o Manifestations: May or may not be a brief loss of consciousness, Confusion, possibly amnesia, retrograde (time preceding the injury), anterograde (period following the injury)
o post-concussion syndrome:
• Diffuse axonal injuries (DAI): shearing of fragile axons by acceleration-deceleration forces at the time of injury
o Severity is determined by amount of strain and shearing
o Mild severe
• Secondary injury: complications resulting from the initial injury
• Brain swelling/Cerebral edema
o Vasogenic edema: increased cerebral capillary permeability
o Cytoxic edema: increased cerebral intracellular fluid
• Infection
• Manifestations of diffuse brain injury will be consistent with manifestations of
