Brain Damage & Neuroplasticity

tumor

mass of rapidly dividing cells that can damage surrounding tissue

meningioma

benign tumor of the meninges, 20% of tumors found in the brain

encapsulated tumor

tumors that grow within their own membrane, easy to identify in CT scan

benign tumor

tumors that are surgically removable with little risk of further growth in the body

infiltrating tumor

grows diffusely through surrounding tissue

malignant tumor

A cancerous tumor that is invasive enough to impair the functions of one or more organs, difficult to remove or destroy

Gliomas

Brain tumors that develop from glial cells, infiltrating, rapidly growing, & common

metastatic tumors

grow from infiltrating cells that are carried to the brain by the bloodstream

acoustic neuromas

tumors that grow on nerves or tracts (tracts are bundles of axons in the CNS)

CNS & PNS

the mammalian PNS can regenerate but the CNS is very limited

cerebrovascular accident (CVA)

a.k.a. "Stroke". Lack of blood supply to the brain causing brain damage

cerebral hemmorhage

a type of stroke that occurs when an artery located in the cerebrum, the main part of the brain, bursts

cerebral ischemia

a disruption of the blood supply to an area of the brain

neuronal death

the death of some neurons that surround newly formed synaptic connections among other neurons; also called programmed cell death

glutamate toxicity

-Cellular ion pumps begin to fail

-Calcium ion influx results in release of glutamate, excitatory neurotransmitter

-Glutamate opens Na+ and Ca++ channels

-Ca++ influx activates degradative enzymes, causing further cell death

pharmacological treatment for stroke

anti coagulants to dissolve blood clots & help circulation, tissue plasminogen (tPA) only effective if given within the first 3 hours

Epilepsy

chronic brain disorder characterized by recurrent seizure activity

Later interventions for Strokes

block neurodegeneration, enhance neural growth factors, exercise and sensory stimulation

Facial (partial) seizures

start at a focus, remain localized

simple seizure

no loss of consciousness, usually sensory and/or motor

complex seizure

loss of consciousness, often involving temporal lobes, automatisms, no memory of seizure activity

Generalized seizures

seizures that involve the entire brain

grand mal seizure

type of severe seizure with tonic-clonic convulsion

petit mal seizure

milder form of seizure lasting only a few seconds and does not include convulsive movements; also known as absence seizures

Traumatic Brain Injury (TBI)

A traumatic insult to the brain capable of producing physical, intellectual, emotional, social, and vocational changes.

Apoptosis

programmed cell death, occurs in cells that are dysfunctional, more adaptive than necrosis, nucleus is impacted in early process

Necrosis

neuron dies passively due to injury, can cause inflammation, nucleus is impacted late in process

amyotrophic lateral sclerosis (ALS)

degenerative disorder of motor neurons in the spinal cord and brainstem

Wernicke-Korsakoff syndrome

Organic brain syndrome resulting from prolonged heavy alcohol use, involving confusion, unintelligible speech, and loss of motor coordination. It may be caused by a deficiency of thiamine, a vitamin metabolized poorly by heavy drinkers.

Parkinson's disease

A disorder of the central nervous system that affects movement, often including tremors.

Parkinson's disease symptoms

hand tremors, moves in slow motion, poor balance, and doesn't speak often

Parkinsons Disease pathology

Degenerating substantia nigra (SN) in midbrain causes decreased amounts of dopamine in midbrain

Lewy bodies present in degenerating SN

Onset typically after 45

Parkinsons disease treatment

L-Dopa & other dopamine agonists, MAO-B inhibitors, deep brain stimulation (subthalamic nucleus), and tissue grafts into striatum

Huntington's Disease

A human genetic disease caused by a dominant allele; characterized by uncontrollable body movements and degeneration of the nervous system; usually fatal 10 to 20 years after the onset of symptoms.

Huntington's disease treatments

No cure, Reserpine, Tetrabenazine - inhibit DA release, decreasing dyskinesia

Haloperidol - DA antagonist, decreases dyskinesia

Huntington's disease pathology

deterioration of the striatum, especially GABA neurons, hereditary, fatal disease, linked to trinucleotide repeat in the huntingtin gene on chromosome 4

multiple sclerosis (MS)

destruction of the myelin sheath on neurons in the CNS and its replacement by plaques of sclerotic (hard) tissue

Multiple Sclerosis Symptoms

-Weakness, numbness, tingling in a limb

-Optic neuritis (amaoursis fugax)

-Double vision

-Loss of balance

-Urinary frequency/urgency

-Ataxia (lack of voluntary movements)

-Hyper-reflexia

-Fatigue

-Hoffman sign (flicking middle finger causes thumb flexion)

-Lhermittes sign (shock sensation down spine on neck flexion)

Multiple Sclerosis Treatment

no cure, some experimental drugs can slow progression

Alzheimer's disease

a progressive and irreversible brain disorder characterized by gradual deterioration of memory, reasoning, language, and, finally, physical functioning

Alzheimer's Disease Symptoms

memory loss, loss of recognition, mood swings, and trouble problem solving simple equations

Alzheimer's Disease Prevalence

10% for ages 65+, 50% for ages 85+.

Alzheimer's Disease Treatment

physical activity, socialization, medication to slow progression, no cure, AChE inhibitors and NMDA receptor antagonists

Kindling Model of Epilepsy

Repeated electrical stimulation to the brain (kindling) Epileptic episode

Post-kindling, stimulation elicits convulsions

Observed in mice, rats, and primates

Observed in many brain regions

Neuroplastic changes are permanent

Kindled subjects will respond several months later

Transgenic mouse model of Alzheimer's

genetically alter mice so that they produce more of amyloid

MPTP neurotoxicity model of Parkinson's disease

accidental tragedy led to useful animal model, Deprenyl blocks MPTP toxicity, given to early PD patients and delays progression of disease

PNS regeneration

CAN regenerate with help of Schwann Cells, begins from proximal stump, regrowth through intact myelin sheath (w/o myelin sheath regrowth is inaccurate or incomplete)

CNS regeneration

Oligodendrocytes release factors that actively block regeneration, collateral sprouting may account for recovery of function

Mechanisms of Reorganization

(1) strengthening of existing connections through release from inhibition (2) establishment of new connection by collateral sprouting

collateral sprouting

the process by which axons of some healthy neurons adjacent to damaged cells grow new branches

Anterograde degeneration

of the distal segment, the segment of a cut axon from the cut to the synaptic terminals

Retrograde degeneration

of the proximal segment, the segment of a cut axon from the cut back to the cell body

transneuronal degeneration

spreads from damaged neurons to neurons that are linked to them by synapses

Schwann Cells

myelinate PNS axons, clear the debris and scar tissue resulting from neuronal degeneration

Oligodendroglia

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