User:Neurosoltisk/Proposal for Central Neurogenic Hyperventilation

Central Neurogenic Hyperventilation Project Proposal
General Background Information

Central Neurogenic Hyperventilation (CNH) is a rare neurological clinical disorder with relatively poorly understood pathophysiology. CNH is generally defined by an abnormal pattern of breathing characterized by deep and rapid breaths, though it is unrelated to other forms of hyperventilation associated with stress or panic attacks.

Proposed Project Outline

The project will tentatively be divided into six subcategories that will provide a thorough explanation of the history of the disorder, the current clinical information, and ongoing or future research that is being performed with CNH patients.

1. Background Information

This section will begin with the discovery of the syndrome in 1959 by Plum and Swandon using nine comatose patients. We will discuss how CNH was classified as a separate form of hyperventilation from other breathing disorders associated with Kussmaul's respirations, or panic attacks. Then we will discuss the generalities of what the disorder is, going into further detail and providing background information about the parts of the brainstem it affects (brainstem/pons). We will conclude this section with the relation of CNH to the respiratory centers of the brain. This will provide for the necessary background information needed to understand the causes and symptoms sections that would follow this introduction.

2. Causes

Causes of CNH include brainstem tumors, stroke, and head injuries. We will examine each of these causes individually and how and why each one results in CNH, particularly examining this through the neurophysiology.

3. Symptoms

CNH involves many different symptoms, some of which are not yet understood, and occur at different times depending on the progression of the onset of CNH. A list of symptoms we have so far found through research includes, but is not limited to, rapid breathing, which appears to not be able to be controlled by the patient, a low arterial partial pressure of carbon dioxide while maintaining a normal oxygen saturation, pH changes found mostly in the local areas of the affected brain areas in CNH (pH changes are not frequent in the cerebral spinal fluid), periods of confusion, lack of concentration that seems to increase as CNH progresses, unconsciousness in persons deeply progressed in CNH, weight loss, and the presence of hyperventilation even when the patient is asleep. These symptoms vary in all people. We will look for further research highlighting more specific details about the symptoms. We also propose finding any correlation between symptoms and why some are present and others are not, and any relationship between symptoms and the degree of progression of CNH. 4. Associations with other body systems

Researchers have attempted to find associations of other body systems with CNH. So far we have found that no associations are found with the cardiovascular system. The respiratory system has also been found to remain normal, with the lungs in normal condition and the hyperventilation stemming from the diaphragm. One research article did have a patient that resulted with edema in the lungs prior to death, and also developed pneumonia and bronchitis. We would like to further investigate more cases to find if there are any relationships between the respiratory system and CNH. Some relationships have been found with CNH and the renal system which affect urine production. Another association we have found is with the body's metabolism and CNH. We will perform more research and attempt to identify all body systems associated with CNH and how these systems relate.

5. Pathophysiology

The pathophysiology of central neurogenic hyperventilation is still very poorly understood, but in most patients it is characterized by tumorous growth infiltration into the pontine reticular formation. These lesions, however, are not strictly isolated to the pontine reticular formation and have been found to present themselves in the medulla and brainstem. The currently accepted mechanism proposed by Plum and Swandon in 1959 for this syndrome can be described as the interference of lesions with the brain to create unihibited stimulation of the expiratory and inhalatory centers.It has also been speculated that CNH may be caused by central nervous system lactate, which if presented in high concentrations could lead to an anaerobic metabolic environment for the brain. Other speculations of pathophysiology will be explored from case studies.

6. Treatment Treatment with morphine sulfate has been found to decrease respiratory rate, but treatment is commonly ineffective. Intravenous fentanyl, a short-acting narcotic, has also been used in patient cases that do not respond to morphine therapy. Aggressive treatment of the primary tumor is currently recommended, especially in children who present with more solid tumors. Treatment typically includes surgery, cranial radiation, and chemotherapy coupled with corticosteroids. Morphine sulfate functions by generally depressing the CNS system. Presentation of CNH in young children typically has high morbidity rates if the lesions are not responsive to chemotherapy.In adults, it is typically seen as deterioration sign before the final stages of medulla derangement leading to death.

7. Current, Ongoing, and Future Research

In this section we plan to include any and all research trials regarding CNH that are currently ongoing or planned for the future. Because CNH is, at this point in time, not widely understood and its pathophysiology remains unclear, it is important to consider advances that may be made in the future.