Author Question: Riku is a 19-year-old college student. One morning, after a long night of studying, Riku woke up and ... (Read 78 times)

jjjetplane · **on:** Jun 25, 2018

Riku is a 19-year-old college student. One morning, after a long night of studying, Riku woke up and made himself a hot cup of coffee and toast.

Much to his surprise, when he brought the cup to his mouth to drink, the coffee spilt onto the table. Riku went to the bathroom mirror and noticed the left side of his face seemed to droop. He quickly got dressed and ran to the medical clinic on the college campus. As he ran, his left eye began to feel scratchy and dry, but he could not blink in response. The physician at the clinic listened to Riku's story and then did a careful cranial nerve examination. She concluded that Riku had Bell palsy, an inflammatory condition of the facial nerve most likely caused by a virus.

What are an afferent neuron and efferent neuron? What are efferent components of the facial nerve and their actions?

Under certain circumstances, axons in the peripheral nervous system can regenerate after sustaining damage. Why is axonal regeneration in the central nervous system much less likely?

At a healthy myoneural junction, acetylcholine is responsible for stimulating muscle activity. What mechanisms are in place to prevent the continuous stimulation of a muscle fiber after the neurotransmitter is released from the presynaptic membrane?

Question 2

Ramandeep is an active 23-year-old. She works as a part-time nurse during the day and is studying for a postgraduate certificate in the evening.

Ramandeep started to wear a bite plate at night after she began to experience jaw pain and headaches. Sometimes the pain radiated to her ear, and she would apply a hot water bottle to it to ease the discomfort. It was not until her husband mentioned to her that he heard her grinding her teeth at night while she was sleeping. She knew then that her headaches might be from temporomandibular joint syndrome, and she went to her dentist to confirm her thoughts. In addition to the bite plate, the dentist also recommended she should continue with the application of heat, use NSAIDs when needed, and incorporate regular relaxation exercises throughout her stressful days.

What effect does heat have on nociceptors so that it makes a good nonpharmacologic treatment for pain?

Heat and cold treatment are both hypothesized to have an effect on the release of endogenous opioids. What are these chemicals, and why are they hypothesized to be beneficial in the body?

Using your knowledge of physiology, how do NSAID analgesics function in the management of pain?

macybarnes · **Reply #1 on:** Jun 25, 2018

Answer to Question 1

An afferent neuron passes sensory input to the central nervous system and enters the central nervous system by the dorsal root. An efferent neuron is responsible for carrying motor output away from the central nervous system and is located in the ventral root. The efferent output supplied by the facial nerve consists of general visceral and pharyngeal components. The general visceral component is involved with the reflexive activity of the nasopharynx. It is also involved with mucous secretion in the nasopharynx, lacrimation, and salivation in the sublingual and submandibular glands. The pharyngeal efferent path supplies motor innervation to the facial muscles and to the stapedius muscle.

The axons of peripheral nerves are surrounded by myelin and covered by endoneurium. This loose connective tissue creates a directional tube to the target organ. If the endoneurium is intact after axonal injury, the axonal bud is able to grow within the endoneurial tube to its former destination. In the central nervous system, endoneurial tissue is absent. Axonal regeneration is therefore limited in this part of the nervous system.

The actions of a chemical synapse are controlled, in part, by the efficient removal of neurotransmitter after it has been released from the synaptic terminals. Three methods to inactivate neurotransmitters are in place. One involves the reuptake of the chemical into the presynaptic membrane for reuse. Another process involves the deactivation of the neurotransmitter by enzymes in the synaptic cleft. (In this situation, the enzyme is acetylcholinesteras e.) The third method involves the simple diffusion of the neurotransmitter into the surrounding intercellular fluid so that it becomes dilute and ineffective on postsynaptic membranes.

Answer to Question 2

The application of heat causes local vasodilation and therefore reduces tissue ischemia. By improving circulation, heat also speeds the removal of inflammatory mediators and metabolites. Finally, heat reduces local swelling. Collectively, the reduction of ischemia, chemical irritants, and local swelling all decrease nociceptive stimulation and therefore the sensation of pain.

Endogenous opioids appear to act as neurotransmitters. Their exact function is not known, but there is speculation they block the calcium channels found in primary afferent neurons and the neurons of the dorsal root and trigeminal ganglia. The transmission of pain impulses is inhibited by their action because the blocking of calcium channels halt neurotransmitter release at the synaptic bulbs. Current research is addressing the possible effect opioids also have on sodium and potassium channels in the modulation of pain signals.

NSAIDs inhibit cyclooxygenase (COX) enzymes, which act to mediate the production of prostaglandins in the body. Prostaglandins (in particular, E2) sensitize nociceptors to chemical mediators and therefore catalyze pain sensations. NSAIDs decrease the sensitivity of blood vessels to chemical mediators and reverse the vasodilatation seen as part of the inflammatory process. They also inhibit the release of inflammatory mediators from granulocytes. NSAIDs therefore have a powerful affect on limiting inflammatory processes and decreasing the sensation of pain.