C J Long
Overview of Topics
Traumatic Brain Injury
AIDS-related Neurological Disorders
Multiple Sclerosis (MS)
Depression & Mania
- Discuss methods for determining severity of traumatic brain injury.
- Describe brain changes associated with dementia.
- Explain the brain changes associated with Parkinson's disease and explain why L-Dopa works in some and surgery works in others.
- Describe apraxic disorders.
Traumatic Brain Injury
(See Introduction to Neuropsychology
Cerebrovascular Disorders - vascular abnormalities
a. Account for about ½ of adult neurological problems.
b. Result may be occlusion or rupture of vessel
c. CVA - Cerebrovascular accident - (stroke)
(1) Result is to deprive brain area of blood (ischemia) resulting in cell death. d. AVM - arteriovenous malformation - a congenital disorder of abnormal vessel growth.
(2) Sudden onset.
(1) This group of vessels shunts blood away from the rest of the brain.
Tumors - Neoplasms
Primary effect is pressure around region of tumor.
The majority of tumors results from abnormal growth of supporting cells, not neurons.
CNS Infections (encephalitis)
Viral (many different types)
AIDS-Related Neurological Disorders
- HIV - human immunodeficiency virus - weakens the immune system but person may remain asymptomatic for years.
- There may be no decline in cognitive functioning.
- AIDS - refers to more advanced stage of the disease (with decline in cognitive function)
Multiple Sclerosis (MS) - a demyelinating disease.
MS results from destruction of myelin in areas of the brain which disrupts neuronal functioning.
- Electrophysiological abnormality in brain function (seizures).
- Epilepsy is a syndrome not a disease.
- Generalized seizures - no localized onset
- The EEG is abnormal on either side of the head.
- Grand mal seizures - convulsion followed by coma.
- Petit mal - sudden loss of consciousness (absence attack).
- Complex partial seizures - more focal seizures with changes in cognitive functioning.
- Progressive pathological decline in cognitive function.
- Alzheimer's Disease (AD) - degeneration of the cholinergic innervation of the forebrain by neurons in the nucleus basalis.
Usually appears in the 50's - 60's.
- 20% of hospitalized psychiatric patients have AD.
- Begins by memory loss, then confusion; finally near total cognitive dysfunction.
- Associated with cerebral atrophy resulting from cell death and/or dendritic shrinkage.
- Characterized by senile plaques (deformation of terminal endings & protein in extracellular space.
- Also neurofibrillary tangles - pathological webs of neurofilaments within the neuron.
- Changes most pronounced in frontal lobes and hippocampus. (AD appears to cause deterioration of input and output of the hippocampus, thus isolating it from the rest of the brain.)
Depression & Mania (affective disorders)
- Most common - accounting for 50% of psychiatric admissions and 10% of hospital admissions.
- Depression can be associated with significant cognitive dysfunction (pseudo-dementia).
- Elevated and euphoric mood.
- Cycling depression and mania.
- Genetic Factors: 1% likelihood of bipolar disorder but 10-25% in individuals with relatives with disorder. (70% in identical twins if one is effected).
- Two neurotransmitters are involved: (norepinephrine & serotonin).
- Norepinephrine - mainly produced by raphe nuclei in brain stem.
- Serotonin - mainly produced by locus ceruleus in brain stem. (see section on sleep)
- Reserpine - elicits depression-like symptoms by depleting catecholamines suggesting that depression may result from depletion of biogenic amines.
- Monamine oxidase inhibitors block an enzyme [monoamine (MAO)] that breaks down norepinephrine, dopamine, and serotonin and relieves depression.
- Trycyclic antidepressants relieve depression by blocking reuptake of monoamines.
- All of the above contribute to the biochemical basis of depression.
Biochemical Factors in Mania:
- Lithium - a form of salt which serves to normalize mania and depression in bipolar disorders.
- Alters the sodium and potassium levels within the body.
- Also affects brain catecholamines by increasing reuptake of norepinephine.
- Loss of contact with reality characterized by hallucinations and/or delusions.
- Strong genetic factors (with 50% probability if both parents are affected).
- Little know as to the neurochemical basis.
- Dopamine hypothesis - schizophrenics thought to have either an overactive or hypersensitive central dopamine system.
- Drugs that block dopamine receptors have anti-psychotic effects.
- Symptoms made worse by drugs that increase brain dopamine levels.
- Autoimmune system disease attacks the acetylcholine receptors at neuromuscular junctions
- Progressive weakness and rapid fatigue of striated muscles
- Gets weaker with progressive use
- With fewer receptors, the remaining need maximum acetylcholine to move muscle
- Normal muscles deplete acetylcholine with use (deficit is not due to supply)
- Marked motor weakness.
- Treated by drugs that suppress immune system
- Also with drugs that inhibit acetylcholinesterase
- Extrapyramidal disorder
- Most common in elderly
- Main Cause: depletion of dopamine axons in substantia nigra, caudate and putamen
- Does not run in families
- Reduced blood flow
- Exposure to certain drugs
- History of encephalitis or viral infections.
- Possibility of toxic disease
- Body converts MPTP to MPP+ - toxic to substantia nigra
- MPTP binds to melatonin and destroys
- MPTP may be present in environment (paraquat?)
- Slow movements
- Initiation problems
- Muscle rigidity
- Tremors (tremors seen in some or rigidity in others)
- Intellectual impairment
- Depressed mood
- Treatment: L-DOPA - drug replaces missing dopamine.
- A precursor to dopamine
- L-DOPA converted to dopamine in brain
- Side effects - nausea, restlessness, sleep problems, hallucinations and delusions. Also stereotyped, repetitive movements.
- Additional drugs may control side effects.
- New Therapies
- Monamine oxidase B converts MPTP to MPP+
- Deprenyl - inhibitor of monamine oxidase B; slows onset
- Results from damage to caudate and putamen
- Genetic - controlled by autosomal dominant gene
- Gene will transmit to about 1/2 of children of afflicted parent
- Presymptomatic test is available to determine if at risk. This test only works if chromosomes of a number of relatives are investigated.
- Begin as fatal twitch, later tremors.
- Walking, speech and voluntary movements slow - later impossible.
- Other symptoms: depression, impaired memory, anxiety, hallucinations and delusions, poor judgment, alcohol and drug abuse
- Onset 30 to 50 - with death within 15 years
- Cortical damage
- Damage may disconnect language areas from motor area
- Might lose connection to pyramidal but retain extrapyramidal
- Difficulty in organizing movements purposively
- May continue to be able involuntarily
Terms to know
|traumatic brain injury
||grand mal seizures
|petit mal seizures
||complex partial seizures