Traumatic Brain Injury

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.
(2) Sudden onset.
d. AVM - arteriovenous malformation - a congenital disorder of abnormal vessel growth.

(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)
Bacterial
Fungal
Other

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.

Epilepsy

• 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.

Dementia

• 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)

Depression

• Most common - accounting for 50% of psychiatric admissions and 10% of hospital admissions.
  
• Depression can be associated with significant cognitive dysfunction (pseudo-dementia).

Mania

• Elevated and euphoric mood.

Bipolar disorder

• 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).

Biochemical Factors:

• 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.

Schizophrenia:

• 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.

Myasthenia Gravis

• Autoimmune system disease attacks the acetylcholine receptors at neuromuscular junctions

• Symptoms
  • 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.

• Treatment
  • Treated by drugs that suppress immune system
  • Also with drugs that inhibit acetylcholinesterase

Parkinson's Disease

• Extrapyramidal disorder
• Most common in elderly

• Causes
  • 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?)

• Symptoms
  • 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

Huntington's Disease

• Causes
  • 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.

• Symptoms
  • 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

Apraxia

• Causes
  • Cortical damage
  • Damage may disconnect language areas from motor area
  • Might lose connection to pyramidal but retain extrapyramidal

• Symptoms
  • Difficulty in organizing movements purposively
  • May continue to be able involuntarily

Terms to know