The Nervous System Part III - Chapter 14

The Autonomic Nervous System - automatic or involuntary motor control - visceral control, cardiac, glands, etc.

- Two Divisions A. Sympathetic B. Parasympathetic

Sympathetic = FIGHT OR FLIGHT = THORACOLUMBAR Division of ANS

- Anatomy

(1) arises from thoracic + lumbar regions of spine

(2) preganglionic/presynaptic neuron begins in CNS i.e. dendrites & soma in Spinal

cord

(3) preganglionic neurotransmitter = Acetylcholine

(4) preganglionic axons are SHORT - stop close to Vertebral Column

- synapses are in the Sympathetic Chain Ganglia

- Ganglion - contain synapses + dendrites & soma of postganglionic

(postsynaptic) neurons

- Synapse - where two neurons meet (axon of 1 meets dendrites of another)

(5) postganglionic axon long and terminates in effector (target) organ

(6) postganglionic neurotransmitter = Norepinephrine (sometimes epinephrine or

dopamine or serotonin)

Thus the neurotransmitters that typify the Sympathetic NS are from the 2nd neuron

How to STOP actions of Adrenergic NT's

1. NT diffuses away

2. Re-uptake into Synaptic Vesicles - prozac inhibits this for the NT serotonin

3. Enzymes - degrade or destroy the NT's

a. Catechol-O-Methyl Transferase - breaks down Norepi in surrounding tissues

b. Monoamine Oxidase - breaks down Norepi that is re-taken by synaptic vesicles

Receptors = Adrenergic or catecholinergic Receptors pg 536 in 8th edition

- Adrenergic Neurotransmitters: Norepinephrine, Epinephrine, Dopamine,

Serotonin

a. Alpha 1 - causes vasoconstriction in peripheral arterioles so >>> bp

b. Alpha 2 - causes decreased release of Norepinephrine (classic negative feedback

loop)

c. Beta 1 - causes an increase in heart rate and increase in strength of cardiac

muscle contraction

d. Beta 2 - causes relaxation of smooth muscle

1. Bronchodilation - relaxing smooth muscles of upper respiratory tract - allows

you to breath easier

2. Vasodialation - relaxing smooth muscles of arterioles - causes drop in bp

- notice: Norepi bound to alpha 1 causes vasoconstriction, but bound to beta 2

causes vasodilation...its all about the receptor

Parasympathetic = CRANIOSACRAL Division of ANS

- Anatomy

(1) arises from the cranial & sacral regions of spine

(2) the preganglionic neuron begins in CNS i.e. dendrites & soma Pons/Medulla or

sacral Spinal cord (same as Symp)

(3) the preganglionic neurotransmitter = Acetylcholine

(4) the preganglionic axons are LONG - stop close to or in Effector (target) organs

(5) postganglionic short - often entirely w/in wall of effector (target) organ

(6) postganglionic neurotransmitter = Acetylcholine - Thus the neurotransmitters

that typify the Parasympathetic NS are from the 2nd neuron

Acetylcholinesterase destroys acetylcholine to stop its effect

Receptors = Cholinergic Receptors pg 536 in 8th edition

- Cholinergic Neurotransmitter: Acetylcholine

1. Nicotinic - found on the dendrites of all postganglionic neurons, both sym &

parasym system

- also found on neuromuscular junction - remember the ACh receptors?

2. Muscarinic - found on glands, organs, etc. ie. heart

Salivary glands

Eye

Skin*

Heart

Lungs

Liver and gall- bladder

Genitals

Pancreas

Eye

Lungs

Bladder

Liver and gall- bladder

Pancreas

Stomach

Cervical

Sympathetic ganglia

Cranial

Lumbar

Thoracic

Genitals

Heart

Salivary glands

Stomach

Bladder

Adrenal gland

Parasympathetic Sympathetic

Sacral

Brain stem

L1

T1

Figure 14.3

Keep in mind: Sympathetic = Fight or flight...what should happen under "fighting" physiology

- parasympathetic is often (not always) the opposite

Location Sympathetic effect Parasympathetic effect

Pupil Dilation Constriction

Lens distance focus close in focus

Tears None Increase

Sweat Increase None

arrector pili contract (goose bumps) None

heart rate increase Decrease

SOC Increase Decrease

skin capillaries Vasoconstriction Vasodilation

sk muscle vessels Vasodilation None

visceral vessels Vasoconstriction None

Coronary vessels Vasodilate None

Sphincters contract relax

GI motility Decrease Increase

air ways dilate constrict

Urinary Bladder none constrict

Glycogen breakdown ==> glucose Synthesis

Erection None Stimulate

Glands None Secretion

Orgasm Stimulate None

* SOC = strength of contraction for cardiac muscle

Multiple Sclerosis

- symptoms come and go, many patients die within 7-32 years of onset of symptoms

- begins w/ visual problems (double vision, blindness, pupillary reactions)

- speech, tremors

- autoimmune - the immune system makes antibodies against myelin sheath

- demyelinating disease

Tay Sachs - seen in people from Eastern Mediterranean especially Jewish

- diagnosed 1-2 years old and often die 3-4 years old

- too much of a glycolipid (Ganglioside = GM2) esp in myelin sheath which destroys

brain

- gene for enzyme in lysosome is mutated so cannot digest Ganglioside

- blindness, reduced coordination, dementia, death

Amyotrophic Lateral Sclerosis (ALS) (Lou Gehrig D)

- degeneration of motor neurons and atrophy of the muscles they supply

- progressive weakness w/ difficulty in speaking, swallowing

- sensory and intellect remains intact

- astrocytes unable to absorb the NT glutamate which becomes toxic to ns

- Stephen Hawkins - paralyzed - world renowned physicist w/ major theories

applied to astronomy - Einstein of our day

Neural Tube Closure Defects (NTDs)

- often caused by dietary Folic Acid deficiency and diagnosed by a rise in

Alpha Fetal Protein (AFP)

- the neural tube should close by day 25-27 of embryonic gestation

- Anencephaly - Anterior NTD - failure of the forebrain (the entire cerebral cortex) to

develop

- most embryos/fetuses spontaneously abort (miscarry) very early, rarely

develop to term

- often the calvaria remains open

- Posterior NTDs = Spina Bifida

1. Spina Bifida Occulta (hidden) - a tuft of hair over the lumbar region - child has

better prognosis

2. Meningocele - meningeal (dural) herniation w/out spinal cord involvement -

- worse prognosis that #1, however, better than #3

3. Myelomeningocele - dura + spinal cord + spinal nerves herniate - worse

prognosis

Meningitis inflammation/infection of the meninges

- caused by: bacteria, viruses, fungi, parasites, toxins

- spinal tap often cloudy increase proteins, reduced sugar

- severe irritation of SC, cranial nerves, brain

- severe headache, nuchal rigidity, projectile vomiting, confusion, fever, decreased

responsiveness, increase in ICP (intracranial pressure)

Poliomyelites enterovirus that often causes gastroenteritis

- virus enters peripheral nerves, moves up the axon to reside in the ventral horn of the

spinal cord, therefore patient loses motor control

- continued muscular atrophy respiratory arrest causes death

Rabies - virus transmitted by bite of infected animal vector: dog, bat, raccoon

- almost always fatal if enters CNS

- severe cerebral edema

- symptoms manifest between 1-3 months after bite from infected animal

- malaise, headache, fever w/ paresthesias around wound = diagnostic

- extreme CNS excitability: slightest touch becomes painful, slightest

sound or movement can cause massive muscular contractions/convulsions

- eventually, flaccid paralysis, coma, respiratory arrest

Cytomegalovirus - especially dangerous for fetus and immunosuppressed

- necrotizing periventricular infections w/ severe brain destruction

- causes microcephaly

Shingles = Herpes Zoster Varicella

- caused by the Chickenpox virus

- virus travels up axon to hide, quietly in the soma of a spinal nerve

- decades later the virus activates causing a mild rash to acutely sever

blistered eruptions in the skin

Spongiform Encephalopathy = Creutzfeldt-Jakob Disease

- caused by a Prion - a normal protein that changes shape and becomes pathogenic

- protein transmitted by eating the brains or muscles of infected animals

- Mad Cow Disease a form seen in cattle

- transmitted by infected sheep brains that were added to cattle feed

- causes rapid progressive dementia

- Kuru - form of this disease seen in the Fore tribe of Papua, New Guinea.

- according to tribal custom, the women of the tribe would eat the brains of

deceased tribal members. Before this practice was stopped, Kuru was the

cause of 90% of the tribal women.

New cases have since stopped showing up.

Neurodegenerative Diseases

1. Parkinsons Disease (PD)

- progressive loss of motor function

- severe dementia & loss of brain tissue

- reduced dopamine in substantia nigra

- Dopamine = inhibitory NT, its loss causes involuntary contraction = Tremors

- cannot cross blood-brain-barrier so use L-dopa to treat (isomer of

dopamine)

- L-dopa relieves symptoms but does not slow progression & damages heart

and liver

2. Alzheimers Disease (AD)

- begins around age of 50

- patient often asks same question over and over, confusion increases

- 100,000 / yr in US die

- Beta Amyloid protein ==> Plaque deposited on and around neurons of cerebrum &

hippocampus (memory centers)

- Neurofibrillary Tangles - discovered by Alois Alzheimer in 1907

- severe dementia & loss of brain tissue

Huntingtons Disease (PD) = Huntingtons Chorea

- symptoms show up at 20-50 years old

- Chorea = spastic loss of motor control

- autosomal dominant form of genetic transmission - on chromosome 4

- continued loss of motor function w/ severe dementia & loss of brain tissue

Trauma of the NS

- Concussion - loss of consciousness due to head injury - usually complete recovery

- rotational impact (left hook) worse than straight on hits

- Contusion - blunt trauma causes bruising or crushing injury w/out rupture of the pia

mater

Vascular-Related Pathologies

- Hematomas - increase in Intracranial Pressure (ICP) which is acutely life-threatening

- compression of vessels - stops bleeding, however also compresses other blood

supplies to brain

- Hypertensive Encephalopathy - due to malignant hypertension or pre-eclampsia

(hypertension during pregnancy) - causes aneurysms which may rupture

- Epidural Hematoma - just outside of dura

- most (85%) arterial - hemorrhage is under relatively high pressure

- 1-2% of major head injuries often due to skull fractures

- Sub-Dural hematoma - veins between dural sinuses (e.g. Superior Sagittal) & veins

of brain are torn

- venous so slower build-up of ICP & herniation

- occur in 10-20% patients w/ traumatic brain injury

- brain is loose w/in dura - inertial damage when skull suddenly stops on impact yet

brain continues far enough to tear the above veins

- Subarachnoid Hematoma - usu due to ruptured aneurysms

- Intracerebral hematoma - seen in 2-3% head injuries

- most caused by hypertension or penetrating missiles (bone fragments, bullets, etc.)

Herniation of brain - caused by ICP

- brainstem through the foramen magnum

- cerebrum into lower chambers of the cranial vault

- patient may regain consciousness only to lose it again eventually enter coma

Hydrocephalus

- choroid plexuses continue to produce cerebrospinofluid, however, arachnoid

granulations do not remove it

- as ventricles enlarge they displace & destroy the normal brain tissue

- in some older cases, entire brain displaced

- shunt placed to re-route CSF to thoracic cavity & reduce pressure

Vascular-Related Pathologies

- Stroke = Cerebrovascular Accident (CVA)

- most common neurologic disorder

- 3rd leading cause of death in US

- cause cerebral infarction

1. Thrombolytic Stroke - Lesion caused by a blood clot originating w/in brain

2. Transient Ischemic Attack - TIA - mini-stroke due to intermittent vascular

occlusion or spasm

- neurological problems gone w/in 24 hrs

3. Embolic Stroke

- obstructions caused by an embolus (foreign body traveling in vessel)

- Thrombolytic Embolysm - embolus is a thrombus (blood clot) from heart, aorta,

carotids, thorax

- less common emboli: fat (from long bone fractures), air, etc.

4. Hemorrhagic Stroke = Intracerebral hematoma - most due to hypertension

END OF SEMESTERs NOTES :)