NUR 606 Week 9 Discussion 1: Question-Based Discussion—Team C (Neurologic Trauma/Disorders)

March 8, 2022
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NUR 606 Week 9 Discussion 1: Question-Based Discussion—Team C (Neurologic Trauma/Disorders)

NUR 606 Week 9 Discussion 1: Question-Based Discussion—Team C (Neurologic Trauma/Disorders)

1. What is a subdural hematoma? In your definition, be sure to include location, common causes, and time to development. What signs and symptoms would you expect a patient with a subdural hematoma to exhibit?
According to VanMeter & Hubert (2018), a subdural hematoma develops when blood fills the space between the dura and the arachnoid. Some common causes of subdural hematomas include falls, blows to the head, infants when violently shaken, sports injuries, and car accidents (VanMeter & Hubert, 2018). A small tear in a vein that causes blood to accumulate slowly can develop into an acute, subacute, or chronic subdural hematoma (VanMeter & Hubert, 2018). The difference between the three classifications of subdural hematomas is related to symptoms timeliness of presentation and, in the case of chronic, the level of brain atrophy observed in the patient. An acute subdural hematoma will have signs that present in approximately 24 hours, whereas a subacute subdural hematoma will have intracranial pressure changes that develop in about a week (VanMeter & Hubert, 2018). In cases of chronic subdural hematomas, they are more prevalent in elderly patients due to brain atrophy. An atrophied brain has more space and can have tears in the arachnoid, which allows for a hematoma to develop and additional cerebral spinal fluid leakage into the subdural space (hygroma), creating pressure changes (VanMeter & Hubert, 2018). Signs of a subdural hematoma include balance or walking problems, confusion, vomiting, seizures, speech problems, and loss of consciousness (Laurent et al., 2020). Symptoms can include nausea, dizziness, headache, weakness, and sleepiness (Laurent et al., 2020).
2. Spinal cord injury can occur anywhere along the spine. Is injury to the cervical spine or lumbar spine more critical? Using pathophysiology, explain why.
The most critical spinal cord injury occurs at the cervical level between C1 to C7. The cause of a cervical spinal cord injury is related to hyperextension or hyperflexion of the neck with a possible fracture (VanMeter & Hubert, 2018). When an injury occurs in the cervical region, inflammation can extend upward to the level of C3 to C5 and interfere with phrenic nerve innervation to the diaphragm affecting a patients’ respiration. According to Wang et al. (2018), a traumatic cervical spinal cord injury (CSCI) has a high complication, disability, and mortality rate with a poor prognosis. The authors identify respiratory failure as the most common lethal factor post-traumatic CSCI (Wang et al., 2018). Cervical injuries affect motor and sensory function in the arms, trunk, legs, respiration, SNS function (T1 to L2), and parasympathetic fibers (VanMeter & Hubert, 2018). A cervical injury can cause paralysis to all four extremities called tetraplegia or quadriplegia. With the injury of the cervical spine, the stimulation of the sympathetic system can result in autonomic dysreflexia, a severe complication caused by a sensory stimulus that triggers a massive sympathetic reflex response that cannot be controlled by the brain (VanMeter & Hubert, 2018). Furthermore, VanMeter & Hubert (2018) illustrate that a sensory stimulus to the sympathetic nervous system (SNS) below the level of injury can stimulate an entire chain of SNS ganglia, causing excessive vasoconstriction with a sudden increase in blood pressure, severe headache, and visual impairment. Vasoconstriction cannot be reduced through the cardiovascular control center, and the patient is at significant risk for a stroke or heart failure (VanMeter & Hubert, 2018).
Conversely, lumbar spine injuries occur at L1 to L5 and result in some loss of function or degrees of paralysis in the hips and legs and bowel and bladder control issues. A lumbar spinal cord injury can cause paraplegia and interfere with function in the lower extremities and sacral parasympathetic nerves (VanMeter & Hubert, 2018). Hence, the prognosis for a patient with a lumbar spine injury is vastly better than a patient with a cervical spinal cord injury.
3. What is the difference between communicating and noncommunicating hydrocephalus? This can occur in infants, often with no focal signs. Explain why this is.
According to VanMeter & Hubert (2018), hydrocephalus is a condition in which excess cerebral spinal fluid (CSF) accumulates within the skull and compresses the brain tissue and blood vessels. There are two types of hydrocephalus termed communicating and noncommunicating hydrocephalus. Noncommunicating hydrocephalus or obstructive hydrocephalus occurs in babies when the flow of CSF through the ventricular system is blocked (VanMeter & Hubert, 2018). This blockage occurs at the aqueduct of sylvius or the foreman magnum (VanMeter & Hubert, 2018). The cause of noncommunicating hydrocephalus is related to fetal developmental abnormalities such as stenosis or a neural tube defect and in neonates, and associated myelomeningocele or Arnold – Chiari malformation is present (VanMeter & Hubert, 2018). This type of obstruction can lead to an increase in the back pressure of fluid in the brain’s ventricles, which gradually dilate or enlarge the ventricles and compress the blood vessels and brain tissues (VanMeter & Hubert, 2018).
In communicating hydrocephalus, the absorption of CSF through the subarachnoid villi is impaired and results in increased pressure of CSF in the system (VanMeter & Hubert, 2018). In neonates, the skull can expand to some degree in the early stages of hydrocephalus to relieve the pressure. However, if the communicating hydrocephalus is not promptly identified and treated, the brain tissues can become damaged (VanMeter & Hubert, 2018).
The skull sutures of a neonate or young infant are not completely closed, allowing their heads to enlarge and fontanelles to bulge in the early stages of hydrocephalus (VanMeter & Hubert, 2018). Therefore, focal signs are often not present.
4. What is the difference between a partial and a general seizure? Give an example of each and describe what you might expect to observe from a patient experiencing each type.

General seizures have multiple foci or origins in the deep structures of cerebral hemispheres and the brain stem causing loss of consciousness (VanMeter & Hubert, 2018). Whereas partial seizures have a single or a focal origin often in the cerebral cortex and may or may not involve altered consciousness (VanMeter & Hubert, 2018).

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There are two types of generalized seizures. The first type is called an absence or petit mal seizure and is more common in children than adults beginning at age five. An absence or petit mal seizure can last for 5 to 10 seconds and can occur many times during the day. Patients experiencing a general seizure can have a brief loss of awareness and sometimes transient facial movements, such as twitches of the eyelids or lip-smacking (VanMeter & Hubert, 2018). Typically, a child can be observed staring into space for a moment and then resuming activity previously pursued with no memory of the incident (VanMeter & Hubert, 2018). The second type of general seizure is a tonic-clonic or grand mal seizure. This type of seizure may occur spontaneously or after simple seizures, and a pattern can be observed in this type of seizure that typically ends spontaneously (VanMeter & Hubert, 2018). For patients experiencing a tonic-clonic or grand mal seizure, prodromal signs can occur, such as nausea, irritability, depression, or muscle twitching hours before the seizure (VanMeter & Hubert, 2018). An aura such as a peculiar visual or auditory sensation will immediately proceed with losing consciousness and fall to the floor in many individuals (VanMeter & Hubert, 2018). This is followed by the ictal phase, where strong tonic muscle contractions result in flexion followed by extension of the limbs and rigidity of the trunk occur (VanMeter & Hubert, 2018). A cry can escape as the abdominal and thoracic muscles contract forcing air out of the lungs, and the jaw is clenched tightly, ceasing respirations (VanMeter & Hubert, 2018). This is followed by the clonic stage, in which the muscles ultimately contract and relax, resulting in a series of forceful and jerky movements that involve the entire body. Individuals typically have increased salvation; foaming at the mouth and bowel and bladder incontinence can occur (VanMeter & Hubert, 2018). When the contractions subside spontaneously, the body is observed as limp, and consciousness slowly returns. The postictal period leaves the person confused and fatigued with aching muscles, eventually falling into a deep sleep (VanMeter & Hubert, 2018).
Simple partial or focal seizures can arise from an epileptogenic focus related to a single area of damage in the cortex (VanMeter & Hubert, 2018). They are manifested by repeated motor activity such as jerking or turning the head or eye aside, jerky movements of the leg, or by a sensation such as tingling that begins in one area and may spread (VanMeter & Hubert, 2018). A person experiencing a seizure may have auditory or visual experiences such as ringing in the ears or a sensation of light (VanMeter & Hubert, 2018). Memory and consciousness remain, although awareness is reduced. An example of a Jacksonian seizure is a focal motor seizure in which clonic contractions begin in a specific area and spread progressively. An example of this is described as contractions that “march” up the arm and then to the face (VanMeter & Hubert, 2018).
5. Describe where you might expect to find plaques that cause the following early signs of multiple sclerosis: diplopia, tremors in the legs, facial weakness.
Multiple sclerosis is progressive demyelination of the neurons in the brain (VanMeter & Hubert, 2018). This disease is characterized by remissions and exacerbations with marked degeneration and is the second most common cause of disability in the United States (VanMeter & Hubert, 2018). Plaque formation following the early signs of multiple sclerosis can be found frequently beside the lateral ventricles in the brain, in the brain stem, and in the optic nerves (VanMeter & Hubert, 2018). If the cranial nerves are affected, a patient will experience diplopia, otherwise known as double vision (VanMeter & Hubert, 2018). When a plaque is formed on the corticospinal tract, a patient will experience weakness in the legs, and plaques forming on the cerebellum can cause tremors in the legs (VanMeter & Hubert, 2018). When motor nerve tracks have plaque formation, a patient will experience weakness and paralysis, including areas of the face (VanMeter & Hubert, 2018).
6. Describe three common manifestations that can be observed in a person with Parkinson’s disease. Why might these make it difficult for patients to maintain adequate nutrition and hydration? What potential complications may ensue?
Common manifestations that can be observed in a person with Parkinson’s disease (PD) include bradykinesia or slowness of movements, tremors in the hands at rest and a repetitive pill-rolling motion of the hands, difficulty chewing and swallowing food with prolonged eating time, and 20 % of affected persons develop dementia in the later stages (VanMeter & Hubert, 2018). Patients with PD have difficulty maintaining adequate nutrition and hydration due to several factors. According to Kim et al. (2016), malnutrition is recognized as an essential problem in PD patients. Kim et al. (2016) describe the first factor as related to motor symptoms. Bradykinesia, rigidity, tremors, and gait disturbances cause some patients to have trouble performing their activities of daily living (ADL) such as grocery shopping, preparing meals, and eating or swallowing food independently (Kim et al., 2016). These types of disabilities might also be linked to levodopa-related motor complications such as dyskinesia (Kim et al., 2016). Kim et al. (2016) identified that the second factor could be related to psychosocial and cognitive factors like depression, anxiety, and dementia, contributing to lowered food intake and weight loss in individuals suffering from PD. A final and vital factor to consider is related to the side effects observed with medications used to manage PD, including change of taste, nausea, vomiting, and loss of appetite (Kim et al., 2016). Adequate evaluation of the nutritional and hydration status of PD patients and determination of the factors that contribute to malnutrition in PD patients are particularly relevant when treating these individuals. Potential complications from inadequate food and fluid intake in patients with PD can lead to poorer quality of life, adverse health outcomes, higher mortality rates, and prolonged length of hospital stay (Kim et al., 2016). Adequate evaluation of the nutritional and hydration status of PD patients and determination of the factors that contribute to them are particularly relevant when treating these individuals.
References
Kim, S. R., Chung, S. J., & Yoo, S. (2016). Factors contributing to malnutrition in patients with Parkinson’s disease. International Journal of Nursing Practice (John Wiley & Sons, Inc.), 22(2), 129–137. https://doi.org/10.1111/ijn.12377
Laurent, V. A., Bernard, J. Y., & Chevignard, M. (2020). High Frequency of Previous Abuse and Missed Diagnoses Prior to Abusive Head Trauma: A Consecutive Case Series of 100 Forensic Examinations. Child Abuse Review, 29(3), 231–241. https://doi.org/10.1002/car.2638
VanMeter, K. C., & Hubert, R. J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders.
Wang, Y., Guo, Z., Fan, D., Lu, H., Xie, D., Zhang, D., Jiang, Y., Li, P., & Teng, H. (2018). A Meta-Analysis of the Influencing Factors for Tracheostomy after Cervical Spinal Cord Injury. BioMed Research International, 2018, 1–10. https://doi.org/10.1155/2018/5895830

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