Physiological Psychology Chapter 10

Brain Damage and Neuroplasticity

A tumor (neoplasm) is

A group of cells growing independently of the rest of the body

Encapsulated

Surrounded by capsule

Infiltrating

Spreading beyond its origin area

Benign

Non-cancerous, does not spread to surrounding tissue

Malignant

Cancerous growth that can spread

Meningiomas take up _% of brain tumors

20%

Meningiomas

Encapsulated, between the meninges, only affects brain function through pressure on surrounding tissue

Infiltrating Tumors

Often Malignant, grows through surrounding brain tissue

Gliomas

Frequent type of malignant brain tumor that originates from glial cells

Metastatic Tumors

Cells carried to the brain via the bloodstream from other parts of the body, often begins as lung cancers, recovery is unlikely if cancer has spread

Stroke

Cerebrovascular disorder of sudden onset caused by cerebral hemorrhage or cerebral ischemia

Infarct

Area of dead or dying tissue produced by stroke

Infracts is often surrounded by

Penumbra (tissue that may recover or die off)

Cerebral Hemorrhage

Bleeding in the brain due to a ruptured blood vessel, often caused by bursting aneurysms

Aneurysms

Balloon-like dilations in artery walls; either congenital, caused by vascular toxins, or infections

Cerebral Ischemia

Disruption of blood supply to the brain

3 main causes of cerebral ischemia

Thrombosis: formation of thrombus (blockage)

Embolism: an embolus (traveling thrombus) gets lodged in a smaller vessel

Arteriosclerosis: Blood vessel walls thicken and narrow often due to fat deposits, leading to blockage

Ischemic Brain Damage

Damage develops over time often visible a day or two after episode, areas like the hippocampus are more susceptible

Ischemia-Induced Release of Glutamate

Mechanism is believed to be an excessive release of glutamate that occurs when blood vessels are blocked

In Ischemia-Induced release of glutamate glutamate bonds to

NMDA receptors that open up and let in too much Ca2 and Na+ ions into neurons

Cerebral Ischemia stroke treatment options

NMDA-Receptor Antagonists, Tissue Plasminogen Activator, Endovascular Therapy

NMDA-Receptor Antagonists

Effective but require immediate post-stroke administration

Tissue Plasminogen Activator

Breaks down blood clots, effective if administered within hours of stroke

Endovascular Therapy

Surgical removal of a thrombus or embolus

Contusion

Bleeding from the brain in absence of a lacerations, results in hematomas

Contusions are caused by

The brain hitting the skull

Subdural Hematoma

Blood accumulation in the subdural space, distorting neural tissue

Hematoma

A bruise or collection of clotted blood

mTBI (concussions)

When consciousness is disturbed after a head blow without structural damage evidence; effects can be long term and can accumulate over time

Chronic Traumatic Encephalopathy (CTE)

Dementia and cerebral scarring from multiple mTBIs

Infections occur when

Microorganisms make their way into the CNS, leading to encephalitis (brain inflammation)

Bacterial infections can cause

Cerebral abscesses (pus pockets) and meningitis (meninges inflammation)

Syphilis, a bacterial infection, can lead to

General paresis, characterized by mental illness and dementia

Viral infections

Some viruses have a particular affinity for the nervous system (rabies)

Hydrophobia

Fear of water that is a symptom of rabies

Heavy metal toxicity

Metals like mercury or lead can accumulate in the brain, causing toxic psychosis

Crackpot

Toxic psychosis from using cracked tea pots with a lead core

Drug-induced Neurotoxicity

Sometimes drugs used to treat a disease can have neurotoxic effects

Tardive Dyskinesia (TD)

A disorder produced by prolonged exposure to certain antipsychotic medications

Endogenous Neurotoxins

The body can produce harmful substances causing neurotoxic effects (antibodies attacking the nervous system stress hormones like cortisol)

Some genetic disorders are accidents of

Cell division (down syndrom)

Apoptosis

Self destruct program that is slower and cleaner; adaptive

Necrosis

Self destruct program that is quick and causes inflammation

Epilepsy

Seizures that recur spontaneously

Seizures with __ are easier to detect

Convulsions (motor changes)

Causes of seizures

Head trauma, tumors, genetics, GABA dysfunction, neurotoxins, viruses

Seizures

Pathological Firing that disrupts normal brain functioning

Epileptic Auras

Individuals may experience unique changes just before a seizure

Two categories that seizures are characterized into

Focal and Generalized

Focal Seizures

Occur in a specific area of the brain, often don’t cause total loss of consciousness

Simple seizures

Typically involve a single type of sensory or motor symptom

Complex Seizures

Often originate in temporal lobes (temporal lobe epilepsy); repetitive, seemingly normal actions; everything become significant

Parkinson’s Disease occurs in _% of population over age 65

1-2%

Symptoms of Parkinson’s disease

Stiffness, temor, mask-like face, loss of smell, sleep disturbance, depression

Parkinson’s disease causes

No single cause identified, linked to degeneration in substantia nigra and reduced dopamine, presence of lewy bodies (clumps of alpha synuclein protein in neurons)

Treatments to Parkinson’s disease

L-doba (metabolic precursor to dopamine), Deep brain stimulation (electrical stimulation of brain areas, can alleviate symptoms but does not stop or slow progression)

Huntington’s disease

Rare progressive motor disorder with severe dementia

Huntington’s disease is incurable and death typically occurs about __ years after symptom onset

20 years

All individuals carrying the huntington gene,

Develop the disorder, and half of their offspring inherit it

Huntington’s disease is caused by

A mutated dominant gene called huntingtin that results in build up of huntingtin protein which becomes toxic and causes cell death

Multiple Sclerosis

Progressive disease attacking CNS myelin sheaths; autoimmune disorder that results in neuron damage

Symptoms of Multiple Sclerosis

Sensory, visual, motor problems

Treatments for Multiple Sclerosis

Immunomodulatory drugs offer marginal benefits, but not many others

Alzheimer’s disease is the most common cause of

Dementia (10% of people over 65)

3 stages of progression in Alzheimer’s

1. Preclinical stage- pathological brain changes without noticeable symptoms

2. Prodromal stage- Mild cognitive impairment indicating progression

3. Dementia stage- Progressive memory decline, personality changes

Defining neuropathological characteristics of alzheimer’s disease

• Neurofibrillary Tangles- tau protein tangles in cytoplasm

• Amyloid Plaques- clumps of beta-amyloid protein and degenerating neurons

• Neuron Loss- especially in medial temporal lobe structures

Neural Degeneration

Occurs in brain development and disease; laboratory studies often induce degeneration through axotomy (cutting axons)

Types of Neural Degeneration

• Anterograde Degeneration- from the cut to synaptic terminals

• Retrograde Degeneration- from the cut back to the cell body

• Transneuronal Degeneration- spreads from damaged neurons to connected neurons via synapses

Neural Regeneration sometimes is in the PNS, but almost never in the

CNS

Neural regeneration begins from

Proximal stump

If myelin sheath is not there, neural regeneration

Regrowth is difficult

Schwann cells in the PNS

Myelinate PNS axons, clear debris and scar tissue from degeneration

Oligodendroglia in the CNS

Myelinate CNS axons, do not clear debris or stimulate/guide regeneration

In the CNS, astrocytes form

A glial scar post-injury, creating a physical barrier to axon regrowth

Collateral Sprouting

Occurs when axons degenerate, adjacent healthy axons grow new branches to synapse at sites left by degenerating axons

Neural Reorganization

The brain can reorganize in response to injury, often focused on sensory and motor cortices

When a neuron loses part of retina,

Moves over to process a different part

Two mechanisms of neural reorganization

1. Strengthening Existing Connections

2. Establishing of New Connections

Cognitive reserve

High education and intelligence levels help patients develop alternative strategies for task accomplishment

Large factors in why people can or cannot recover from damage

Extent of damage and age of person

Use it or lose it

When neurons aren’t being used, they start to do other things

Treating spinal injury

Standing over treadmill, making a person move

benefits of cognitive and physical exercise

Activity reduces the risk of neurological disorders

Treatment for Phantom Limbs

Mirror Box Therapy