The Limbic System

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The Limbic System
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The Limbic System

• Connected to many higher and lower brain regions.
• Closely connected to the hypothalamus.
• Psychosomatic illnesses
• Connects to the prefrontal cortex.
• Connects emotion and logic and understanding.

• Hippocampus and amygdala involved in converting
  short term memories into long term ones.

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Reticular Formation

• Central core of the medulla, pons, and midbrain.
• Reticular nuclei connect to the hypothalamus,
  thalamus, cerebellum, and spinal cord.
• Governs arousal.

• Reticular Activating Systemkeeps the cortex
  attentive.
• Repetitive impulses are damped.
• Novel ones are attended to.
• LSD interferes with the dampening of unimportant
  stimuli.

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Reticular Formation

• Inhibited by sleep centers in the hypothalamus.
• Depressed by alcohol, tranquilizers, and other
  drugs.
• Damage to this area may cause one to go into a
  coma.

• Also helps to control course movements of the
  limbs.

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Brain Protection

• Meninges
• 3 Layers
• Cover and protect the CNS.
• Protect blood vessels and enclose venous sinuses.
• Contain cerebrospinal fluid.
• Form partitions within the skull.

• Dura MaterMost externaltoughest.
• Outer layer is attached to the skull. Forms the
  true external covering of the brain.
• Arachnoid Matermiddle menix. Loose covering.
  Subarachnoid space---contains major blood
  vessels.
• Pia Materclings tightly to the brain.

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Assorted Brain Information

• Meningitis
• Bacterial or viral
• Encephalitis
• Cerebrospinal Fluid
• Floats brain.
• Decreases weight.
• Hydrocephalus

• Blood brain barrier
• Made of continuous endothelium of the capillary
  wall.
• Thick basal lamina surrounding the capillaries.
• Astrocytes that cling to the capillaries.
• Tight junctions
• Selectively permeable
• Nonpolar substances enter easily.

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Brain Disorders and Injuries

• Alzheimers Disease
• 5-15 of those over 65.
• 50 of those over 85
• Acetylcholine shortage in associative areas of
  the cortex and in the hippocampus.
• Amyloid.
• Genetic component.
• Autoimmune
• Immunization with Beta amyloid

• Parkinsons DiseaseDegeneration of the dopamine
  releasing neurons in the substantia nigra.
• Basal nuclei become overactive.
• L-dopa---Awakenings
• Fetal tissue transplants

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Brain Disorders and Injuries

• Huntingtons Disease
• Autosomal Dominant Disorder
• Degeneration of the basal nuclei and the cerebral
  cortex.
• Chorea
• Too much dopamine.
• Fatal within 15 years of onset.

• Concussion
• Contusiontissue destruction.
• Subdural or subarachnoid hemorrhage
• Strokes3rd leading cause of death in the US.
  Ischemia. Blood clots.
• Cerebral hemorrhage
• Transient ischemic attacks.
• Glutamate
• Neuronal death

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Rabies

• After uptake into peripheral nerves, rabies virus
  is transported to the central nervous system
  (CNS) via retrograde axoplasmic flow. Typically
  this occurs via sensory and motor nerves at the
  initial site of infection. The incubation period
  (see figure, number 4) is the time from exposure
  to onset of clinical signs of disease. The
  incubation period may vary from a few days to
  several years, but is typically 1 to 3 months.
  Dissemination of virus within the CNS is rapid,
  and includes early involvement of limbic system
  neurons (see Figure, number 5). Active cerebral
  infection is followed by passive centrifugal
  spread of virus to peripheral nerves. The
  amplification of infection within the CNS occurs
  through cycles of viral replication and
  cell-to-cell transfer of progeny virus.
  Centrifugal spread of virus may lead to the
  invasion of highly innervated sites of various
  tissues, including the salivary glands. During
  this period of cerebral infection, the classic
  behavioral changes associated with rabies develop

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Rabies

• The first symptoms of rabies may be nonspecific
  flu-like signs malaise, fever, or headache,
  which may last for days. There may be discomfort
  or paresthesia at the site of exposure (bite),
  progressing within days to symptoms of cerebral
  dysfunction, anxiety, confusion, agitation,
  progressing to delirium, abnormal behavior,
  hallucinations, and insomnia. The acute period of
  disease typically ends after 2 to 10 days (6).
  Once clinical signs of rabies appear, the disease
  is nearly always fatal, and treatment is
  typically supportive. Disease prevention is
  entirely prophylactic and includes both passive
  antibody (immune globulin) and vaccine.
  Non-lethal exceptions are extremely rare. To date
  only six documented cases of human survival from
  clinical rabies have been reported and each
  included a history of either pre- or postexposure
  prophylaxis.

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Rabies

• Pathology of rabies infection is typically
  defined by encephalitis and myelitis.
  Perivascular infiltration with lymphocytes,
  polymorphonuclear leukocytes, and plasma cells
  can occur throughout the entire CNS. Rabies
  infection frequently causes cytoplasmic
  eosinophilic inclusion bodies (Negri bodies) in
  neuronal cells, especially pyramidal cells of the
  hippocampus and Purkinje cells of the cerebellum.
  These inclusions have been identified as areas of
  active viral replication by the identification of
  rabies viral antigen.

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Tourettes Syndrome

• What causes Tourettes?
• Research is ongoing, but it is believed that an
  abnormal metabolism of the neurotransmitters
  dopamine and serotonin are involved with the
  disorder. It is genetically transmitted parents
  having a 50 chance of passing the gene on to
  their children. Girls with the gene have a 70
  chance of displaying symptoms, boys with the gene
  have a 99 chance of displaying symptoms.

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Tourettes Syndrome

• Symptoms of Tourettes.
• Both multiple motor and one or more vocal tics
  present at some time, although not necessarily
  simultaneously The occurrence of tics many
  times a day (usually in bouts) nearly every day
  or intermittently throughout the span of more
  than one year Periodic changes in the number,
  frequency, type and location of the tics, and in
  the waxing and waning of their severity. Symptoms
  can sometimes disappear for weeks or months at a
  time Onset before the age of 18. Coprolalia.