Untitled document (2)

Plasticity After Brain Damage

• Understanding brain resilience and recovery after damage

Introduction to Plasticity

• Origin of the term 'plasticity': Latin "plasticus", meaning "to mold"

• Concept of the brain's ability to adapt and change after damage

I. Brain Damage and Short-term Recovery

A. Causes of Brain Damage

• Illness:

  • Vascular Disorders: Stroke

  • Tumors

  • Infections:

    • Bacterial (e.g., meningitis), a severe risk for college students

    • Viral (e.g., viral meningitis)

• Injury:

  • Traumatic Head Injury:

    • Open Head Injury (e.g., bullet wound)

    • Closed Head Injury (e.g., car/bicycle accident)

  • Epilepsy

• Substance Abuse: Alcohol and chemical toxicity

• Genetic Factors:

  • Inherited degenerative diseases (e.g., Parkinson's, Huntington's Chorea)

• Unknown Origins:

  • Alzheimer's Disease and Dementing Illnesses (e.g., frontotemporal deterioration)

B. Specific Types of Damage

1. Closed Head Injury:

   • Defined as a sharp blow to the head without brain puncture

   • Causes: rotational forces (shearing, twisting)

   • Results in:

     • Contusion (tissue damage)

     • Swelling (edema)

     • Hemorrhage/blood clots

   • Most common in younger populations; often from accidents

II. The Impact of Chronic Traumatic Encephalopathy (CTE)

• A neurodegenerative disease found in individuals with multiple head injuries, especially in contact sports

• Notable case: Aaron Hernandez, diagnosed with Stage III CTE

• Larger trend: Several players (e.g., Miami Dolphins from 1972) died from CTE by January 2022

III. Understanding Strokes (CVA)

A. Types of Strokes

1. Ischemic Stroke:

   • Caused by obstruction/blood clot

   • Accounts for ~87% of strokes in the U.S.

   • Damage due to lack of oxygen and glucose

2. Hemorrhagic Stroke:

   • Caused by blood vessel rupture

   • Accounts for ~13% of strokes in the U.S.

   • Direct brain damage and complications from blood spill

B. Stroke Management

1. Thrombolytic Therapy:

   • Uses Tissue Plasminogen Activator (tPA) for ischemic strokes

   • Must be administered within 4.5 hours; not suitable for hemorrhagic strokes

2. Mechanical Thrombectomy:

   • Surgical removal of clots from arteries; applicable for ischemic strokes

3. Therapeutic Hypothermia (TH):

   • Cooling brain temperature post-stroke can improve outcomes if initiated quickly

4. Experimental Approaches:

   • Investigating glutamate receptor blockers and cannabinoids for potential neuroprotection

IV. Later Mechanisms of Recovery

A. Increased Brain Stimulation

• Diaschisis: Reduced activity of surviving neurons after damage

• Importance of stimulation from the contralateral body side

B. Regrowth of Axons

• Peripheral Nervous System: Regrowth at approx. 1 mm/day

• Central Nervous System: Limited regrowth; efficacy restricted by scar tissue and myelin's growth-inhibiting proteins

C. Axon Sprouting

• Collateral sprouts formed by undamaged axons replacing lost neuronal connections

• Outcomes can vary; beneficial or harmful effects in certain brain areas

D. Denervation Supersensitivity

• Postsynaptic cells become more sensitive to available neurotransmitters after losing connections

• Function ensures continued activity in the face of reduced neural input

E. Reorganized Sensory Representations and Phantom Limb

• Phantom Limb Phenomenon: Continuing sensation of an amputated limb

  • Possible range of sensations from tingling to pain

  • Insights from researchers like Vilayanur Ramachandran on treatment through mirror therapy

F. Learned Behavioral Adjustments

• Deafferenated limbs can still function despite loss of sensory input

• Rehabilitation emphasizes forced use of affected limbs, although challenging

Additional References

• Emphasizes insight into clinical neuropsychology as a field for those interested in brain-behavior relationships

• Encouragement for graduate study in this field, citing resources like the American Psychological Association's Division 40.

Plasticity After Brain Damage

Understanding brain resilience and recovery after damage

Introduction to Plasticity

• Origin of the term 'plasticity': Derived from the Latin "plasticus", meaning "to mold", indicating the brain's adaptability.

• Concept: Plasticity refers to the brain's capacity to adapt functionally and structurally following damage, allowing for recovery and compensation for lost functions.

I. Brain Damage and Short-term Recovery

A. Causes of Brain Damage

1. Illness:

   • Vascular Disorders:

     • Stroke: An interruption of blood supply to the brain, leading to loss of function in the affected area.

     • Tumors: Growths that may exert pressure on brain structures or disrupt normal functioning.

     • Infections:

       • Bacterial (e.g., meningitis): Highly contagious and dangerous for specific populations like college students.

       • Viral (e.g., viral meningitis): Less severe but still impactful on brain health.

2. Injury:

   • Traumatic Head Injury:

     • Open Head Injury: Injury where the skull is penetrated (e.g., bullet wound) leading to direct brain exposure to the environment.

     • Closed Head Injury: Injury without exposure (e.g., car/bicycle accident); can cause rotational forces leading to diffuse axonal injury.

   • Epilepsy: Recurrent seizures can damage brain tissues over time.

   • Substance Abuse: Long-term alcohol use and chemical toxicity can alter brain structure and function.

   • Genetic Factors:

     • Inherited degenerative diseases (e.g., Parkinson's, Huntington's Chorea): Result from genetic mutations impacting neuron health.

   • Unknown Origins:

     • Alzheimer's Disease and Dementing Illnesses: Such as frontotemporal dementia, often impacted by lifestyle and environmental factors.

B. Specific Types of Damage

• Closed Head Injury:

  • Defined as a sharp blow to the head without puncturing the skull.

  • Causes: Primarily result from rotational forces that can cause shearing and twisting of neural pathways.

  • Results:

    • Contusion: Bruising of brain tissue.

    • Swelling (edema): Accumulation of fluid causing increased intracranial pressure.

    • Hemorrhage/Blood Clots: Internal bleeding may alter brain pressure and function.

  • Most common in younger populations, often occurring in accidents.

II. The Impact of Chronic Traumatic Encephalopathy (CTE)

• Description: A neurodegenerative disease associated with repeated brain trauma, particularly prevalent in athletes of contact sports.

• Symptoms: Cognitive impairments, mood disorders, and progressive dementia.

• Notable Cases: Aaron Hernandez was diagnosed with Stage III CTE post-mortem, highlighting the disease's severity.

• Larger Trend: As of January 2022, several NFL players, including a group of Miami Dolphins from 1972, have been confirmed to have succumbed to CTE-related illness.

III. Understanding Strokes (CVA)

A. Types of Strokes

1. Ischemic Stroke:

   • Caused by obstruction or a blood clot in the arteries supplying blood to the brain.

   • Accounts for approximately 87% of strokes in the United States, leading to significant brain damage due to lack of oxygen and glucose supply.

2. Hemorrhagic Stroke:

   • Results from a rupture in a blood vessel, leading to bleeding into or around the brain.

   • Accounts for about 13% of strokes in the U.S., often resulting in immediate brain damage and secondary complications due to blood leakage.

B. Stroke Management

1. Thrombolytic Therapy:

   • Utilizes Tissue Plasminogen Activator (tPA) to dissolve blood clots in cases of ischemic strokes.

   • Must be administered within 4.5 hours of symptom onset; not advised for hemorrhagic strokes due to risk.

2. Mechanical Thrombectomy:

   • A surgical procedure to physically remove clots from occluded arteries, suitable for certain ischemic stroke patients.

3. Therapeutic Hypothermia (TH):

   • Inducing controlled cooling of the brain after a stroke can enhance outcomes if applied promptly.

4. Experimental Approaches:

   • Research is ongoing into the use of glutamate receptor blockers and cannabinoid treatments for providing neuroprotection during stroke recovery.

IV. Later Mechanisms of Recovery

A. Increased Brain Stimulation

• Diaschisis: Refers to a decrease in activity of surviving neurons post-injury; recovery can be enhanced through stimulation from the contralateral (opposite side) body.

B. Regrowth of Axons

• Peripheral Nervous System: Capable of regrowth at approximately 1 mm per day under favorable conditions.

• Central Nervous System: Limited regrowth due to presence of scar tissue and inhibitory proteins associated with myelin.

C. Axon Sprouting

• Collateral Sprouts: Formed by undamaged axons attempting to reconnect or replace lost neuronal connections; results can be variable depending on location and context.

D. Denervation Supersensitivity

• Mechanism: Postsynaptic cells may subsequently increase their sensitivity to neurotransmitters available after losing presynaptic connections; this phenomenon helps maintain activity despite reduced neural input.

E. Reorganized Sensory Representations and Phantom Limb

• Phantom Limb Phenomenon: Refers to the continuing sensation (e.g., pain or tingling) in an amputated limb due to reorganization of sensory pathways in the brain.

• Potential Treatments: Mirror therapy, as studied by researchers like Vilayanur Ramachandran, has shown promise in alleviating phantom limb sensations.

F. Learned Behavioral Adjustments

• Adaptation: Deafferented limbs (those with disrupted sensory input) can still show functionality; rehabilitation often focuses on forced use of these limbs to encourage recovery, although this can be challenging.

Additional References

• Insight into clinical neuropsychology as a burgeoning field focused on understanding brain-behavior relationships.

• Encouragement for pursuing graduate studies in neuropsychology, with resources available from the American Psychological Association's Division 40, which specializes in such research and professional practices.