Sympathetic And Parasympathetic Nervous Systems Biology Essay

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Frontal Lobe- It is the place for our cognitive thinking. The place where our personality and maturity is developed and determined. Its main function is for our brain to organize thoughts, plan things, to give reasons, sexual urge, for our emotions, to solve problems, judging and for our motor skills.

Parietal Lobe- its main functions is to send information or messages to the different parts of our body. It's responsible for our pain and touch sensation, processing of information, for our speech and visual perception, for us to recognize things around us, for the processing of stimuli and for cognition.

Occipital Lobe- It is the smallest of all four lobes, located at the back most of the skull. It's responsible for our visual perception; this lobe is responsible more on our visual as it contain the primary visual cortex. It's responsible for our color recognition, visual reception, spatial and movement recognition.

Temporal Lobe- primarily responsible for our auditory processing. Smell and sounds recognition. It can also help us distinguish different sounds, smell and memories. It also controls our visual and hearing memory. Temporal lobe is also responsible for the formation of new ideas and sorting it.

B. How does the aging process impact the neurological system?

-Aging on brain function can be caused by some aging disorders like, stress, anxiety, depression, and stroke and sometimes by a degenerative brain disorder called Alzheimer's disease that degrades the function of the aging people. Other cause of aging on brain function is that when we get old, our brain's nerve cells tend to decrease and which it also decreases its function. And as people age, blood flow to our brain is decreased causing our brain cells to function less and that is also one of the cause of aging in our brain function.

C. Compare and contrast the sympathetic and parasympathetic nervous systems in terms of function.

Sympathetic Nervous System is the "fight or flight" respond. It diverts the blood flow away from the GI tract that causes the GI to be upset. Pupils are dilated that causes the person to have a clear vision even in a far distance of the subject. It also upset the urinary function of the body that causes less urination of a person. It also increases the heart of a person and the contractility of cardiac cells causing the bronchioles of the lungs to dilate, which is responsible for the alveolar oxygen exchange. This also stimulates the sexual orgasm of a person.

While the Parasympathetic Nervous System is the "rest and digest" respond of the body, making the systems to relax and to digest foods. The pupils are constricted that gives us a closer vision of our subject. The GI tract's peristalsis is increased causing us to defecate more often than usual, that can also lead to diarrhea. This time the heart is relaxed, it gives us a decreased in heart rate. Our sexual arousal is also stimulated.

II. A neurological article investigating pathologic changes that affect motor control and those that affect the sensory pathways.

Spinal Nerve Function in Five Volunteers Experiencing Transient Neurologic Symptoms after Lidocaine Subarachnoid Anesthesia

Abstract

The etiology of transient neurologic symptoms (TNS) after 5% lidocaine spinal anesthesia remains undetermined. Previous case reports have shown that patients acutely experiencing TNS have no abnormalities on neurologic examination or magnetic resonance imaging. The aim of our study was to determine whether volunteers with TNS would exhibit abnormalities in spinal nerve electrophysiology. Twelve volunteers with no history of back pain or neurologic disease underwent baseline electromyography (EMG), nerve conduction studies, and somatosensory-evoked potential (SSEP) testing. Then, the volunteers were administered 50 mg of 5% hyperbaric lidocaine spinal anesthesia and were placed in a low lithotomy position (legs on four pillows). The next day, all volunteers underwent follow-up EMG, nerve conduction, and SSEP testing and were questioned and examined for the presence of complications including TNS (defined as pain or dysthesia in one or both buttocks or legs occurring within 24 h of spinal anesthesia). Volunteers who had TNS underwent additional EMG testing 4-6 wk later. Five of the 12 volunteers reported TNS. No volunteer had an abnormal EMG, nerve conduction study, or SSEP at 24 h follow up, nor were there any changes in EMG studies at delayed testing in the five volunteers experiencing TNS. On statistical analysis, the right peroneal and the right tibial nerve differed significantly for all volunteers from pre- to postspinal testing. When comparing pre- and postspinal testing of the TNS and non-TNS volunteers, statistically significant changes occurred in the nerve conduction tests of the right peroneal and left tibial nerve. There was no difference in measurements of F response, H reflex latency, amplitude, or velocity for either leg. Multivariate analysis of variance showed no significant difference between TNS and non-TNS volunteers for the changes in the nine nerve conduction tests when considered together (P = 0.4). We conclude that acute TNS after lidocaine spinal anesthesia did not result in consistent abnormalities detectable by EMG, nerve conduction studies, or SSEP in five volunteers.

Abstract

Implications: Electrophysiologic testing in volunteers experiencing transient neurologic symptoms is not abnormal.

Transient neurologic symptoms (TNS) after 5% lidocaine spinal anesthesia were first reported in 1993. Since that time many case reports and clinical studies have documented the symptomatology of this syndrome. The incidence of TNS reported in prospective, randomized trials varies from 4% to 37%.

The etiology of TNS remains undetermined; however, spinal nerve injury caused by local anesthetic toxicity is a potential etiology. Laboratory evidence of neurotoxicity with 5% lidocaine, and a clinical case report of permanent neurologic injury after spinal anesthesia with 5% lidocaine, have fueled speculation that TNS represents the benign end of a spectrum of lidocaine-induced neurotoxicity. Two editorials and lectures have questioned the continued use of spinal lidocaine citing the possibility of a neurotoxic etiology of TNS. Despite this concern, patients with TNS have been reported as having subsequent normal neurologic examinations and magnetic resonance imaging. Although these findings question a nerve injury etiology for TNS, no previous study has examined the effects of subarachnoid lidocaine on spinal nerve function in patients with TNS. We designed this study to determine whether volunteers reporting symptoms of TNS would have changes in neuroelectrophysiology as detected by electromyography (EMG), nerve conduction studies, or somatosensory-evoked potentials (SSEP).

Methods

After institutional review board approval, 12 volunteers (ASA physical status I or II) consented to undergo baseline nerve conduction, EMG, and SSEP testing; a 50-mg 5% lidocaine (Astra, USA, Westborough, MA) spinal anesthesia; followed by repeat EMG, nerve conduction and SSEP testing, and a physical examination. Exclusion criteria included a history of radicular pain, back pain of any type, or neurologic disease.

Prespinal and postspinal electrophysiologic testing was performed by a blinded physician with certification in electrophysiologic diagnostic testing and consisted of bilateral peroneal and tibial F responses, bilateral H reflexes, bilateral peroneal and tibial SSEPs, and monopolar needle examination of bilateral lower extremities. Prespinal examination was performed 2 h before spinal anesthesia, and postspinal testing was performed 24 h after spinal anesthesia. Limb length and temperature were recorded and data examined for changes in F wave minimal latency, SSEP N1 or P1 values, and for abnormalities in insertional activity, motor unit potentials, and motor unit recruitment. H reflexes were recorded over 10 stimuli which had been adjusted to deliver maximal H reflex amplitude, and the minimal latency and amplitude were recorded. F waves were recorded in each trial over 15 stimuli with the minimal latency recorded. Delayed (4-6 wk postspinal) studies consisted of monopolar EMG with analysis of the same variables. Nerve conductions were performed on an EMG machine (Viking IV; Nicolet, Madison, WI) by using standard surface disk electrodes and standard filter settings for the appropriate tests. EMG was performed by using a monopolar needle electrode and a surface reference electrode.

After baseline testing, volunteers received a peripheral IV infusion with lactated Ringer's solution. Spinal anesthesia was performed with the unmedicated volunteer in the lateral decubitus position by using a 25-gauge Whitacre needle (Kendall, Mansfield, MA) with the orifice directed laterally at the L2-3 interspace. Cerebrospinal fluid (0.2 mL) was aspirated before and after the injection of 50 mg 5% hyperbaric lidocaine. Volunteers were positioned supine for 5 min and, then, placed in a modified low lithotomy position with four pillows underneath the knees. Monitoring included electrocardiography, automated blood pressure, and pulse oximetry. Block height and duration, as well as Bromage scale of motor block (zero = free movement of legs and feet, one = minimal flexion of knees with free movement of the feet, two = unable to flex knees but can move feet, and three = unable to move legs or feet), were assessed every 5 min for the first 30 min and then, every 10 min until block resolution.

All volunteers underwent repeat nerve conduction, EMG, and SSEP testing 24 h after spinal anesthesia. In addition, they completed an interview and examination in which they were specifically questioned regarding the presence of headache, backache, pain into the buttocks or legs, difficulty with ambulation, degree of activity, and supplemental pain medication. For this study, TNS were defined as pain in one or both buttocks or legs, beginning within 24 h of spinal anesthesia. Volunteers were questioned about the onset, duration, and treatment used for any symptoms. Pain was assessed with a verbal pain rating scale (0 = no pain; 10 = worst pain imaginable). Back pain without pain in the buttocks or legs was not considered to be TNS and was recorded separately. Volunteers reporting TNS were followed for 2 wk and underwent follow-up EMG and nerve conduction studies 4-6 wk after spinal anesthesia.

Differences in the incidence of TNS, back pain without radiation, and volunteer demographics were analyzed by using Pearson χ2 analysis of contingency tables and linear-by-linear association. Unpaired, two-sided t-tests were used to compare patient characteristics, baseline electrophysiologic tests, and changes (post- minus pretest results) with TNS and non-TNS volunteers. Confidence intervals for differences (95%) were based on the t-tests. Multivariate analysis of variance (MANOVA) was used to compare the ensemble of nine nerve conduction tests between TNS and non-TNS volunteers. Two-sided t-tests were used to compare the pre- and poststudy test results. Finally, the Pearson correlation coefficient was used to compare changes in test results (post- minus pretest) to volunteer characteristics, with statistical significance based on two-sided tests. Significance was defined as P < 0.05.

Results

Demographics were comparable between volunteers experiencing TNS and those not reporting TNS. There were no postdural puncture headaches. All volunteers had measurable sensory and motor block. Median block height was T4. All volunteers experienced profound motor block, (Bromage score = three). Mean detectable sensory analgesia to alcohol swab was 92 min. No volunteer required treatment for hypotension, bradycardia, or nausea.The incidence of TNS was 42% (5 of 12). There was no association between the incidence of TNS and age, weight, or sex. One volunteer did experience transient paresthesia during spinal needle placement and did not report TNS. Of the five volunteers who reported TNS, four complained of bilateral symptoms, and one reported unilateral pain. Two volunteers reported pain extending from the back into the buttocks and thighs, although the other three volunteers reported that the pain extended to the knees and below. All five volunteers reported pain in the S1 or S2 dermatomal distribution as well as low back pain. Of interest, there were two sibling pairs of volunteers, and they all reported TNS. Volunteers noted onset of symptoms 5-9 h after spinal anesthesia (mean 7 h) with a duration between 3 and 4 days (mean 91 h). The median verbal pain rating score for patients reporting TNS (scale 1-10) was 8.0 (range 4.5-8). No volunteer exhibited continued symptoms at the 2-wk follow up. Neither volunteers experiencing TNS, nor those who did not, had an abnormal EMG, nerve conduction study or SSEP at 24 h postspinal. One volunteer who did not report TNS had an unexpected baseline abnormality on the posterior tibial SSEP which was unchanged after spinal anesthesia. The five volunteers who experienced TNS had no measurable electrophysiologic abnormalities by EMG studies at delayed follow up. None of the patient characteristics and baseline test scores differed significantly between the TNS and non-TNS groups. Although the nerve conduction tests were interpreted as normal by the electrophysiologist when analyzed statistically, the right peroneal nerve and the right tibial nerve differed significantly for all of the volunteers from pre- to postspinal examination. When comparing pre- and postspinal testing of the TNS and non-TNS volunteers, statistically significant changes occurred in the nerve conduction tests of the right peroneal and left tibial nerve. In these two cases, nerve conduction in the TNS group decreased slightly and the non-TNS group increased from pre- to posttesting. Overall MANOVA analysis showed a nonsignificant difference between TNS and non-TNS groups for the changes in the nine nerve conduction tests when considered together (P = 0.4), and EMGs and SSEPs were unchanged from pre- to posttesting. The changes in test results, generally, did not have a statistically significant relationship to patient characteristics. The two exceptions were a negative correlation between the change (post- minus pretest) in nerve conduction tests of the left peroneal nerve and right tibial nerve versus height (taller volunteers had a greater decrease in these test scores, r = −0.7, −0.6, respectively, P = < 0.05).

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