chapter 44 prt 1

Acute Disorder of Brain Function

Disorder of brain function can result from various pathological processes. Early detection and acute management are crucial to prevent mortality and reduce functional decline due to the limited space within the skull and the inability of nerve and muscle cells to regenerate.

• Brain disorders can lead to severe sequelae, such as paralysis, highlighting the importance of understanding and managing these conditions to prevent long-term disabilities.

• Acute disorders can result from trauma or systemic issues like hypoglycemia, kidney failure, or liver failure, all of which can damage the central nervous system (CNS).

Mechanisms of Brain Injury

Primary Injury

Primary injury involves direct and immediate damage to brain tissue.

• Head Trauma: Direct physical injury to brain tissue.

• Stroke: Occlusion of blood vessels leads to ischemia and potential hemorrhage.

• Brain Edema: Enlargement of brain tissue increases pressure within the skull, leading to tissue damage.

Secondary Injury

Secondary injury occurs as a consequence of the primary injury, developing over days, weeks, or months. It involves:

• Continuation of cellular damage, leading to cell death or necrosis.

Ischemia and Hypoxia

• Hypoxia: Lack of oxygen inside the cell.

• Hypoxemia: Decreased blood oxygenation. emia indicates a blood-related issue.

Ischemia can be both a primary insult and part of the secondary response.

• Lack of oxygen inhibits ATP production in mitochondria, affecting brain function due to its high metabolic rate and limited glycogen stores.

• Brain tissue can survive without oxygen for only 5-10 minutes before irreversible damage occurs.

Mechanisms of Brain Death

1. Anaerobic Metabolism:

   • Production of lactic acid lowers pH, damaging brain cells.

   • Deterioration of ion gradients, especially calcium (\text{Ca}^{2+})

     • Excessive intracellular calcium (\text{Ca}^{2+}) activates phospholipases, initiating apoptosis (programmed cell death).

2. Excitatory Amino Acids: Function of Glutamate

   • Glutamate, an excitatory neurotransmitter, is crucial for learning and memory. It works through two receptors:

     • AMPA

     • NMDA

     • Normal Function:

       • Glutamate opens AMPA channels, allowing sodium (\text{Na}^{+}) influx, which depolarizes the cell.

       • Depolarization releases calcium (\text{Ca}^{2+}), stimulating the opening of NMDA channels.

       • Calcium (\text{Ca}^{2+}) influx from the extracellular fluid (ECF) occurs.

     • Impaired Membrane Integrity:

       • Excessive glutamate release due to cell membrane damage.

       • Overload of intracellular calcium (\text{Ca}^{2+}) leading to apoptosis and free radical production.

       • Production of nitric oxide (NO), which converts to reactive nitrogen species (RNS), causing cell injury.

       • Free radicals injure cells.

     • Reuptake Mechanism Failure:

       • Glutamate reuptake mechanism fails, causing glutamate to remain bound to AMPA receptors.

Glutamate, when excessive, acts as an excitotoxin due to its toxic effects on brain tissue.

3. Reperfusion Injury:

   • Similar to myocardial infarction (MI), reperfusion of ischemic tissue leads to free radical damage.

     • Blockage resolved, blood flow restored, introducing hydroxy radicals, superoxide, and peroxide.

     • Free radicals exacerbate ischemic damage.

Neural Cell Injury Sequence

• Ischemia leading to:

  • Excessive glutamate.

  • Hypoxia.

  • Reperfusion.

• Cell Hypoxia:

  • Reduced ATP production in mitochondria.

  • Calcium (\text{Ca}^{2+}) overload intracellularly due to impaired pumping.

  • Free radical production and cell death.

• Mitochondria Sequestration of Calcium (\text{Ca}^{2+}):

  • Leads to calcium (\text{Ca}^{2+}) overload.

• Glutamate:

  • Opens NMDA channels, causing calcium (\text{Ca}^{2+}) overload.

• Reperfusion:

  • Introduces oxygen free radicals and inflammatory/immune cells, causing cell death.

Intracranial Pressure (ICP)

Normal ICP ranges from 15 mmHg or less. Elevated ICP can impair neurological function.

• Volume of Cranium Components:

  • Brain tissue.

  • Cerebrospinal fluid (CSF).

  • Blood.

• Monro-Kellie Hypothesis:

  • Compensatory responses to changes in volume within the cranium.

  • Increase in one component necessitates a decrease in others to maintain ICP.

    • Transient changes occur during sneezing, coughing, or changes in head position.

• Compensatory Mechanisms:

  • CSF reduction by shunting fluid towards the spinal canal.

  • Blood volume reduction via vasoconstriction.

• Permanent ICP Increase:

  • Requires identification of the underlying cause.

Causes of Increased ICP

1. Increased Brain Tissue Volume:

   • Tumor: Uncontrolled growth exerts pressure.

   • Hemorrhage: Blood accumulation increases pressure.

   • Infection: Inflammatory reaction and edema.

2. Edema:

   • Cytotoxic Edema:

     • Intracellular swelling due to impaired sodium-potassium pump.

     • Sodium (\text{Na}^{+}) accumulation draws water into cells.

     • Common in global ischemia.

   • Vasogenic Edema:

     • Interstitial edema due to blood vessel injury.

     • Endothelium damage leads to fluid leakage into the interstitial space.

     • Often unilateral, caused by hypertension, stroke, or ischemia.

     • Can cause midline shift, which is dangerous.

3. Increased CSF:

   • Hydrocephalus: Accumulation of CSF.

     • In children, can cause skull expansion due to flexibility.

     • Types:

       • Obstructive: Blockage in CSF circulation.

       • Non-Obstructive: Impaired CSF reabsorption.

4. Increased Blood Volume:

   • High PaCO2 and acidosis cause increased blood volume in the brain.

Clinical Manifestations of Increased ICP

• Headache, vomiting, and drowsiness.

• Blurred vision and papilledema (swelling of the optic disc).

• Decreased consciousness.

• Impaired pupillary light reflex.

• Paralysis and inability to open eyes or speak.

Brain Compression and Herniation

Increasing ICP can lead to brain compression against the skull and within the cranial compartments.

• Dura Mater:

  • Falx cerebri: Dura mater between hemispheres.

  • Tentorium cerebelli: Dura mater between cerebrum and cerebellum.

Compression can compromise blood vessels, leading to ischemia.

• Herniation:

  • Protrusion of brain tissue through openings in the dura.

  • Types:

    • Subfalcine herniation.

    • Transtentorial herniation.

    • Uncal herniation: Temporal lobe through tentorial opening.

    • Tonsillar herniation: Cerebellum through foramen magnum.

Management

• Diagnosis: CT or MRI.

• Treatment: Surgical (hemorrhage, tumor) or medical.

• Monitoring: ICP and cerebral perfusion pressure (CPP).

  • Maintain CPP above 60 mmHg to prevent ischemia.

Avoid hyperventilation and diuretics in the long term due to the risk of ischemia.

Focus on cerebral oxygenation:

• Hypothermia or hypotonic saline infusion.

• Drug-induced coma to reduce brain metabolism.

Assessment and Detection of Brain Injury

1. Level of Consciousness (LOC):

   • Consciousness: State of alertness and attentiveness to the environment.

   • Neurophysiology: Relies on reticular activating system (RAS).

   • Levels:

     • Confused: Impaired thinking, oriented in time, place and own data.

     • Delirious: Disoriented, restless, hallucinating, easily aroused.

     • Comatose: Unarousable, no motor responses to painful stimuli.

   • Glasgow Coma Scale (GCS):

     • Components: Eye opening, verbal response, motor response.

       • Eye Opening:

         • Spontaneous: 4.

         • To speech: 3.

         • To pain: 2.

         • None: 1.

       • Verbal Response:

         • Oriented: 5.

         • Confused: 4.

         • Inappropriate words: 3.

         • Sounds: 2.

         • None: 1.

       • Motor Response:

         • Obeys commands: 6.

         • Localizes pain: 5.

         • Withdraws from pain: 4.

         • Abnormal flexion (decorticate): 3.

         • Abnormal extension (decerebrate): 2.

         • None: 1.

     • Posturing:

       • Decorticate: Flexion of elbows, wrists, and fingers, extension of legs, cortex of the brain is not working properly.

       • Decerebrate: Extension of all limbs, arms internally rotated, whole cerebrum is not working.

     • Glasgow Coma Scale Interpretation:

       • Mild: 13-15.

       • Moderate: 9-12.

       • Severe: Below 8.

2. Cranial Nerve Reflexes:

   • Pupillary Reflex:

     • Optic nerve (II) afferent, oculomotor nerve (III) efferent.

     • Assesses pupil size, shape, and reactivity.

     • Meiosis: Small pupils, damage in pons.

     • Dilated and fixed pupils: Increased ICP or hypotension.

   • Oculovestibular Reflex:

     • Detects head movement.

     • Doll's Eye Test(Oculocephalic): Eyes move opposite to head movement.

     • Cold Caloric Test (Oculovestibular): Cold water in ear causes eye movement.

       • Normal reaction when eyes move toward the ear receiving the water

3. Brain Hemodynamics and Metabolism:

   • Maintain CPP above 60 mmHg.

   • Hypothermia reduces metabolism and oxygen demand.

   • Avoid fever and seizures.

Traumatic Brain Injury (TBI)

Leading cause of death and disability in the United States.

• Causes: Transportation accidents, falls, firearms, sports accidents.

• Classification: Based on location, severity, and mechanism of injury.

  • Use Glasgow Coma Scale to check level of consciousness severity
    -Mild: 13-15
    -Moderate: 9-12
    -Severe: Below 8

• Primary Injury:

  • Focal: Localized injury.

    • Motor cortex affects contralateral motor function.

    • Frontal lobe affects personality, judgement and motor skilss.

  • Polar (Coup-Contrecoup): Injury due to acceleration-deceleration movement to hitting windshield.

  • Diffuse: Widespread damage to neurons, especially axons in the white matter.

    • Often results in coma.

• Mechanisms of Injury:

  • Concussion: Mild TBI without brain tissue injury.

    • CT/MRI is normal

    • Loss of consciousness for less than 30 minutes

    • Headaches, nausea and vomiting

  • Contusion: Brain injury (laceration, bruising, necrosis) verified by CT/MRI.

  • Intracranial Hematoma: Blood pocket formation inside the brain.
    -Epidural
    -Subdural
    -Subarachnoid

Intracranial Hematomas

Collection of blood within the skull due to disrupted blood vessels.

Meninges Anatomy

• Dura Mater: Two layers (parietal and visceral). Connects arachnoid and skull.

• Arachnoid Mater

• Pia Mater

Spaces: Epidural (between skull and dura), subdural (between dura and arachnoid), subarachnoid (between arachnoid and pia).

1. Epidural Hematoma:

   • Blood collection between dura and skull, middle meningeal artery.

   • Rapid arterial bleeding with rapid onset of symptoms.

   • Lucid interval: Initial minor injury, followed by symptom-free period, then rapid deterioration. High pressure. Lose consciousness then die.

2. Subdural Hematoma:

   • Blood collection between dura and arachnoid membrane, bridging veins.

   • Slower venous bleeding.
     -Acute, within first 24 hours of injury
     -Subacute, headaches vomiting and blurred vision within first couple of days. Slow bleeding
     -Chronic
     -Consolidated Hematoma
     -High risk for rebleeding because of elder population.
     -Tissue an clots

3. Subarachnoid Hemorrhage:

   • Arterial bleeding between arachnoid and pia mater.

   • Cerebral aneurysm or arteriovenous malformation (AVM).

   • Blood mixes with CSF, increasing ICP.

   • Symptoms: Severe headache, hydrocephalus, vasospasm.

Secondary Injury

Hematoma cause ischemia and hypoxia by putting pressure on blood vessels. Causes rupture and hemorrhage on top of that.

Treatment

Stabilizing the patient (cardiopulmonary stabilization) is important
-Cushing reflex: brain ischemic response. Increased ICP, high systolic blood pressure, low pulse

-Avoid hypotermia during treatment, only mild hypotermia
Stabilize intravascular volume and normal CO2

-Elevated ICP osmotic diuretic, brain gets edematous with tissue in the brain

-Open head/skull fracture: use antibiotics to prevent meningitis or encephalitis

Clinical skull fracture test:

• Clear fluid leaving out of ear or nose= hallow test

-Raccoon eyes preorbital hematoma

-Under the ear= battle sign ( hematoma)