Alterations in Neurological and Endocrine Functions

The nervous system is a composite collection of specialized cells and neurons that coordinate to facilitate systemic function in the body. It comprises of both the central and peripheral nervous systems. Dysfunctions in any component of the nervous system may trigger a neurological disorder, which could affect the spine, the brain, or the nerves that interlink organs. There are several diseases that affect the nervous systems. Some of the more common ones include stroke and Parkinson’s disease. The endocrine system also controls the normal functioning of the body. This system comprises of chemical messengers and feedback mechanisms for hormones secreted directly into the bloodstream by internal glands to regulate the functions of distant target organs. When glands produce excessive or inadequate amounts of hormones, hormonal imbalance ensues, and endocrine diseases may result (Naveed, Ghaya, & Hameed, 2015). Various endocrine glands exist, and hence there are many endocrine disorders. However, diabetes remains to be the most prevalent endocrine disease. An understanding of the alterations in neurological and endocrine functions is imperative for the appreciation of the disease processes involving these systems. 

Types of Stroke 

Stroke is a condition affecting the arteries within or leading to the brain. There are various types of stroke and the following classification is based on etiology. 

Ischemic Stroke 

This is the most prevalent type of stroke accounting for eighty-seven percent of all the reported incidences. It can develop due to the formation of a local thrombus or due to embolism with the consequent occlusion of a cerebral artery. These causes can further be classified as atheroembolic or large artery disease, cardioembolic, lacunar, or cryptogenic (Musuka, Wilton, Traboulsi & Hill, 2015) . These precipitants vary globally in proportions by population. Thrombotic ischemic strokes preferentially occur in older persons with atherosclerosis and high blood cholesterol, or diabetes. Occasionally, symptoms of thrombotic strokes may happen unexpectedly and commonly during sleep or early in the morning. In some instances, they may occur progressively over hours or days. Embolic strokes, on the other hand, occur following a heart surgery or disease. They occur rapidly without any warning signs. A significant number of embolic strokes occur in persons with atrial fibrillation. 

Hemorrhagic Stroke 

Hemorrhagic stroke is a consequence of the rupture of a cerebral artery and accounts for about thirteen percent of cerebrovascular accidents (Ojaghihaghighi, Vahdati, Mikaeilpour & Ramouz, 2017). In addition to the starvation of the cells, the pressure buildup in the brain tissue results in irritation and inflammation which further cause brain damage. Hemorrhagic stroke can be due to intracerebral or subarachnoid hemorrhage. Intracerebral hemorrhage is typically caused by elevated blood pressure. Bleeding is sudden and rapid. No warning signs precede, and hemorrhage may result in a coma or other fatality. Subarachnoid hemorrhage is usually precipitated by an arteriovenous malformation (AVM) or an aneurysm. 

Strokes can also be classified based on the duration and evolution of symptoms: 

Transient Ischemic Attacks (TIA) 

TIA is characterized by sudden focal deficits lasting from seconds to twenty-four hours with complete recovery. They may indicate that extensive cerebral infarction or underlying cerebral hemorrhage is unlikely. The most common symptoms of TIA are aphasia and hemiparesis. They may also result in transient monocular blindness (amaurosis fugax) consequent to an occlusion in the retinal arteries (Vodopivec, Cestari & Rizzo, 2016) . Transient global amnesia lasting several hours, followed by complete recovery may also occur. This is common in persons above sixty-five years of age and may be due to posterior circulation ischemia. 

Progressive Stroke 

This is a type of stroke in which the focal neural deficits worsen after the patient initially presents with the condition. The deterioration may be due to increased cerebral edema, hemorrhagic transformation or increasing volume of infarction. 

Primary and Secondary Parkinson’s Disease 

Parkinson’s disease is one of the most common neurodegenerative disorders. It affects almost one percent of the population above sixty-five years (Rizek, Kumar and Jog, 2016) . The condition is typified by rest tremor, bradykinesia, and rigidity. It then progresses to present with postural instability. Parkinson’s disease can broadly be classified into two: primary and secondary. 

Primary Parkinson’s Disease 

This type of Parkinson's disease is the most prevalent accounting for over eighty percent of persons diagnosed with parkinsonism. It is also referred to as idiopathic parkinsonism as its cause has not yet been adequately elucidated. However, various hypotheses have been developed in an attempt to explain its pathophysiology. Nonetheless, it is generally agreed that the etiology of primary parkinsonism is due to an intricate interaction between genetics, aging, and environmental factors. Pathological studies have also shown that primary parkinsonism is associated with the degeneration of dopaminergic neurons in the nigrostriatal pathway (Caggiu et al., 2019) . The damage of substantia nigra (SN) dopaminergic neurons may also be due to oxidative stress, inflammation, apoptosis, and nitric oxide toxicity. The two hallmark features of primary parkinsonism include the depigmentation of SN dopaminergic neurons and the existence of Lewy bodies in the residual ones. The degree of nigrostriatal dopamine loss has been shown to correlate with the severity of specific motor symptoms such as bradykinesia. The loss of over seventy percent of SN dopaminergic neurons has been associated with clinically detectable parkinsonism. Accordingly, primary Parkinson’s disease may be managed through drugs such as levodopa that boost the levels of dopamine. 

Secondary Parkinson’s Disease 

Unlike primary parkinsonism whose causes are unknown, secondary Parkinson’s disease has known causes. It is also referred to as atypical parkinsonism. Although it is difficult to distinguish primary from secondary Parkinson’s disease, the latter is not appropriately responsive to dopaminergic medication. The following aspects inform secondary parkinsonism: 

Infection-induced parkinsonism (Caggiu et al., 2019) 

Vascular parkinsonism 

Progressive supranuclear palsy 

Parkinsonism due to metabolic disorders or hypoxia 

Normal-pressure hydrocephalus 

Toxin-induced parkinsonism 

Drug-induced parkinsonism 

Parkinsonism secondary to brain tumor or trauma 

Multiple system atrophy 

Pain 

Pain can be classified into the following five categories: 

Neurophysiologic pain – nociceptive and neuropathic pain. 

Neurogenic pain – constant pain and neuralgia. 

Temporal or time-related pain - acute and chronic pain 

Regional pain such as headaches and other pains, including orofacial, chest, abdominal, joint, pelvic, and lower back pain. 

Etiologic pain such as dental, ischemic, post-operative, cancer, inflammatory, and vascular pain. 

Pathways of Pain 

The cell-bodies of pain transmitting neurons are located in the dorsal root ganglia. The axons of Aδ and C fibers upon entry into the spinal cord communicate with second-order neurons that may bifurcate into ascending or descending branches in the dorsolateral tract (McCance & Huether, 2014) . Ultimately, all primary afferents end up in the substantia gelatinosa or the marginal layer of the spinal cord. Two types of interneurons are located in the dorsal horn. Excitatory interneurons transmit pain signals to other interneurons, projection cells, or motor cells for pain withdrawal reflex and other reflexes (McCance & Huether, 2014) . Inhibitory interneurons, on the other, hand moderate the transmission of nociceptive pain. From the spinal cord, pain signals are transmitted to the brain for interpretation. 

Acute and Chronic Pain 

Acute pain is a mechanism designed to protect an individual. It warns one about conditions or experiences that are immediately injurious and prompts the initiation of timely actions to relieve it (McCance & Huether, 2014) . Acute pain is characteristically transitory and typically persists for a short time, not exceeding three months. Its onset is often sudden, and relief is conferred by the withdrawal of the mediators that activate nociceptors. Persistent or chronic pain, on the other hand, usually lasts for more than three months and past the anticipated restoration time after the original outset of injury or damage (McCance & Huether, 2014) . Acute pain serves no particular purpose and is yet to be adequately understood. In many cases, chronic pain appears to be disproportionate to visible tissue injuries. 

Type II Diabetes Mellitus (T2DM) 

T2DM or non-insulin dependent diabetes has been shown to account for over 90% of all cases and mainly affects adults, usually older forty-five years (Wu, Ding, Tanaka & Zhang, 2014). As such, it is sometimes referred to as adult-onset diabetes. Nevertheless, reports indicate an increase in cases of T2DM among younger adults and children. Kahn, Cooper, and Del Prato (2014) postulate that this trend is attributable to the increasing levels of physical inactivity, obesity, and intake of energy-dense diets. There seems to be a complex interaction between genetics and the environment in the development of T2DM. Some of the risk factors for the disease include family history, physical inactivity, hypertension, obesity, and age. T2DM is typified by predominant tissue resistance to insulin. At such, the effectiveness of insulin is subtle and the body attempts to counter this ineffectiveness initially by increasing the production of the hormone to maintain the homeostasis of glucose. However, over time, the production of insulin diminishes resulting in T2DM. 

One of the manifestations of T2DM includes recurrent infections (including skin infections, carbuncles, and boils) and delayed wound healing. Hyperglycemia stimulates the growth of microbes, while the reduced perfusion that typifies T2DM impedes the healing process (McCance & Huether, 2014) . Patients with T2DM may also present with genital pruritus since glycosuria and hypoglycemia are optimal conditions for fungal growth. Candida infections thus develop resulting in pruritus especially among female patients. Persons with T2DM may present with visual changes, particularly blurred vision (McCance & Huether, 2014) . This occurs due to the fluctuation of ocular water balance due to raised blood sugar levels. 

Moreover, diabetic retinopathy may ensue resulting in the loss of vision. T2DM is additionally typified by paresthesia, which is a sign of neuropathy (McCance & Huether, 2014) . Patients may also be fatigued as a result of the metabolic changes that hinder proper nutrient utilization, consequently resulting in lethargy. 

Many organs contribute to the chronic hyperglycemia and insulin resistance associated with T2DM. These include the pancreas, liver, kidneys, adipose tissue, digestive system, brain, and muscles. Genes have also been shown to be associated with the disease process. Such genes include those that code for the function and mass of beta-cells, the molecular structures of insulin and proinsulin, receptors of insulin, gluconeogenesis, and the sensitivity of cells to insulin (McCance & Huether, 2014) . Genetic abnormalities are consequent to epigenetic alterations that take place due to influences of the environment spanning generations. The complex interaction of environmental, genetic, and epigenetic impacts culminate in the pathophysiologic mechanisms of T2DM – diminished insulin secretion by the pancreatic beta-islet cells (McCance & Huether, 2014) . While many people with risk factors for T2DM show insulin resistance, only those who are hereditarily susceptible to the dysfunction of beta-cells, and thus, a relative insulin deficiency will develop T2DM. 

References 

Caggiu, E., Arru, G., Hosseini, S., Niegowska, M., Sechi, G., Zarbo, I. and Sechi, L. (2019). Inflammation, Infectious Triggers, and Parkinson's Disease.  Frontiers in Neurology , 10. 

Kahn, S., Cooper, M., & Del Prato, S. (2014). Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future.  The Lancet ,  383 (9922), 1068-1083. doi: 10.1016/s0140-6736(13)62154-6 

McCance, K., & Huether, S. (2014).  Pathophysiology: The biologic basis for disease in adults and children  (7th ed.). St. Louis: Mosby. 

Musuka, T., Wilton, S., Traboulsi, M., & Hill, M. (2015). Diagnosis and management of acute ischemic stroke: speed is critical.  Canadian Medical Association Journal ,  187 (12), 887-893. doi: 10.1503/cmaj.140355 

Naveed, S., Ghayas, S., & Hameed, A. Hormonal imbalance and its causes in young females. Journal of Innovations in Pharmaceuticals and Biological Sciences , 2 (1), 12-16. Retrieved on October 16, 2019 from http://www.jipbs.com/VolumeArticles/FullTextPDF/38_JIPBSV2I103.pdf 

Ojaghihaghighi, S., Vahdati, S., Mikaeilpour, A., & Ramouz, A. (2017). Comparison of neurological clinical manifestation in patients with hemorrhagic and ischemic stroke.  World Journal of Emergency Medicine ,  8 (1), 34-38. doi: 10.5847/wjem.j.1920-8642.2017.01.006 

Rizek, P., Kumar, N. & Jog, M. (2016). An update on the diagnosis and treatment of Parkinson's disease. Canadian Medical Association Journal , 188(16), pp.1157-1165. 

Vodopivec, I., Cestari, D., & Rizzo, J. (2016). Management of Transient Monocular Vision Loss and Retinal Artery Occlusions.  Seminars In Ophthalmology ,  32 (1), 125-133. doi: 10.1080/08820538.2016.1228417 

Wu, Y., Ding, Y., Tanaka, Y., & Zhang, W. (2014). Risk Factors Contributing to Type 2 Diabetes and Recent Advances in the Treatment and Prevention.  International Journal of Medical Sciences ,  11 (11), 1185-1200. doi: 10.7150/ijms.10001