Symptoms of Horteborts Syndrome - Term Paper Example

Title: Horteborts Syndrome Student’s Name: Instructor’s Name: Class Name: Date Assignment is due: Horteborts Syndrome Abstract The paper examines some of the symptoms of Horteborts syndrome. A brief introduction of the disease is given in the introduction. The paper then concentrates on a discussion of some of the symptoms that are associated with the condition. The symptoms tackled are seizures, severe headaches, muscle weakness and memory loss. Introduction There are two central systems that are involved in the circulation of fluids in the body (Walter 2002, p.143-45).The blood circulatory system is the more popular than the lymphatic system. It is a closed system. The lymphatic system is the other fluid circulatory system. Unlike the blood system, it is a closed system (Walter 2002, p.143-45). The two systems are related because the lymphatic system takes fluids from the tissues back to the blood (Walter 2002, p.143-45). In spite of the separation that is apparent in the two systems, sometimes blood has been observed to travel directly from the blood vessels to the lymphatic system (Walter 2002, p.143-45). This is through vascular malformations known as arteriovenous lymphatic shunts (Walter 2002, p.143-45). This brings about a condition known as Horteborts syndrome. It is a relatively rare condition, and in most cases, it is asymptomatic (Walter 2002, p.143-45). Horteborts syndrome is an anomalous gathering of blood vessels. In the normal setup, oxygenated blood is thrust by the heart via a scheme of branching tubing known as the arteries Walter 2002, p.143-45). It is pumped from the heart to the brain, where the oxygen- rich blood enters into the capillaries (Walter 2002, p.143-45). In the capillary beds, the blood, rich in oxygen, nourishes the body tissues. The deoxygenated blood goes back to the heart through thin walled branching tubes known as veins (Kumar 1999, p.122). Horteborts syndrome occurs when certain areas lack capillaries (Kumar 1999, p.122). This causes the blood to go back to the heart without nourishing the body tissues (Kumar 1999, p.122). In other words, the blood is short circuited from completing its normal route. In short, the food supply of the tissues is cut. Various conditions develop as a result of the interruption of the normal blood circulation (Kumar 1999, p.122). These include conditions like seizures, severe headaches, muscle weakness, vertigo, paralysis, dysarthria/aphasia and memory related problems such as dementia, confusion, and hallucinations (Kumar 1999, p.122). Seizures Epileptic seizures are some of the symptoms that come with Horteborts syndrome. Seizures are classified as some of the most general symptoms of this condition. Seizures are sometimes referred to as fits (Renkin 1994, p.159). They are defined as transient symptoms of excessive and synchronous neural activity in the human brain (Renkin 1994, p.159). They are manifested in wild thrashing movements for tonic-clonic class seizures, and in the mild category, a brief loss of memory. The purpose of this paper is to discuss the physiological connection of Horteborts syndrome to the occurrence. One of the conditions that cause seizures in people with Horteborts condition is Oedema. In ancient times, this condition was referred to as hydropsy, or dropsy. This is the abnormal accumulation of fluid below the skin, or in some cavity of the body (Renkin 1994, p.159). The balance of fluid homeostasis determines the interstitial fluids (Renkin 1994, p.159). Increasing the secretion of fluid into the interstitum causes Edema. Also, the impaired elimination of the said fluid causes Edema (Renkin 1994, p.159). Cutaneous Edema occurs when pressure is put on a small area (Michael 2008, p.48). a. The indentation caused by this pressure remains for a long time after the release of the fluidal strain (Michael 2008, p.48). This causes a condition known as pitting. Tangential pitting Oedema is the most common condition that comes about as a result of Horteborts syndrome (Michael 2008, p.48). A low plasma oncotic pressure comes about when significant amounts of proteins are found in body fluids. This is especially so with urine, and other fluids secreted by the kidney (Michael 2008, p.48). This happens when the shunts in the arteriovenous malformation area shuts the nourishment of the body tissue (Michael 2008, p.48). The result is that the protein in the plasma falls down (Michael 2008, p.48). The blood flowing back into the brain lacks the appropriate Amino acids and protenious contents available in plasma. A seizure then happens as there is no sufficient body power to drive the functions of the body (Michael 2008, p.48). This is due to the biochemical, and also structural alterations that occur in the subcutaneous membranes of capillaries, especially in the kidney glomerulae (Michael 2008, p.48).These alterations also occur to the blood vessels of other tissues in the body. This creates an increase in permeability in the body tissues (Michael 2008, p.48). The normal tissue turgidity is disturbed. There is a build up of pressure in the body tissues that offsets normal tissue functioning (Michael 2008, p.48). Fluid accumulation will occur in some specific organs because of inflammations, and tissue -specific mechanisms. This causes some tissue specific Edemas (Michael 2008, p.48). The physiological mechanisms that cause seizures in Horteborts syndrome are governed by six main factors. Chief among them is increased hydrostatic pressure and also minimized oncotic pressure within blood vessels (Kumar 1999, p.122). Blood vessel’s wall permeability and amplified tissue oncotic pressure are other factors that physiologically contribute to seizures in Horteborts syndrome. The other two factors are obstruction of fluid clearance through the lymphatic system, and alterations in the ability of the tissue to retain water(Michael 2008, p.48).This is due to increase hydrostatic pressure that causes retention of sodium and water by the kidneys (Kumar 1999, p.122). Production of interstitial fluid is governed by Starling equation forces. Hydrostatic force inside blood vessels causes water to filter outside to the body tissues (Kumar 1999, p.122). The result is that there is a difference in the concentration of protein between body tissue, and blood plasma (Kumar 1999, p.122). The oncotic strain of the higher level of protein in the plasma sucks water in reverse into the blood vessels from the body tissues (Kumar 1999, p.122). Starling’s equation posts that the speed, or rate of fluid seepage is set by the disparity between the two opposing forces, and by the wall vessel permeability water (Kumar 1999, p.122). Most seepage occurs in post capillaries venules, or in the capillaries. This is because they have semi permeable walls that let water to freely pass extra proteins (Kumar 1999, p.122). Memory loss Another symptom that is associated with Horteborts syndrome is memory loss. In discussing how memory loss occurs to Horteborts patients, it is good to understand the source and transmission of memories in the body. The human brain, together with the spinal cord, are immersed in a clear circulating fluid known scientifically as the cerebral spinal fluid (Evans, Wilberger &Bhatia 2007, p.1053). This fluid is abbreviated CSF. This cerebral spinal fluid is the transport mechanism of the central nervous system (Evans, Wilberger & Bhatia 2007, p.1053). This is because it transports nutrients to brain cells that are always at work. The cerebral spinal fluid also transports waste products from the brain cells (Evans, Wilberger & Bhatia 2007, p.1053). In addition, it serves to act as a shock absorber in order to shield the spinal cord and brain from traumatic shocks (Evans, Wilberger & Bhatia 2007, p.1053). The human brain has four cavities that are interconnected. These cavities are also known as ventricles. It is in these ventricles that the cerebral spinal fluid accumulates (Evans, Wilberger & Bhatia 2007, p.1053). The impairment of the capillaries in the brain causes the cerebral spinal fluid to accumulate (Evans, Wilberger & Bhatia 2007, and p.1053). This happens due to the blockage of the ventricles when there is a malformation of the arteriovenous junctions (Ling 2007, p.1532). Shunts form in the head, and the fluidal strain in the brain increases. Cerebral spinal fluid can accumulate in the brain due to blockage between ventricles (Evans, Wilberger & Bhatia 2007, p.1053). The accumulation of CFS in the brain can lead to overproduction, or under absorption of cerebral spinal fluid leading to a condition known as Hydrocephalus (Ling 2007, p.1532). The accumulation of excessive fluids in the brain and spinal cord pressures the brain tissues. The brain cells are extremely sensitive (Evans, Wilberger & Bhatia 2007, p.1053). This excessive pressure destroys the brain cells. This then leads to memory loss. It is imperative to understand that memory is associated to synapses in the brain (Ling 2007, p.1532). Synapses are the interfaces through which neural transmissions take place. The accumulation of tissue fluid in the brain disturbs the mechanism for synaptic plasticity (Tator 2008, p.78-83). This is because the blood plasma in the brain cells is reduced (Tator 2008, p.78-83). This in turn means that there is a lowering of post synaptic calcium concentration. This leads to protein kinase deactivation (Tator 2008, p.78-83). There occurs a strong polarization of the post synaptic cells. Magnesium ions are not displaced, and they constrain the calcium ions from entering the post synaptic cells. This implies that memory loss begins to occur (Tator 2008, p.78-83). As the pressure continues to mount on the brain tissue, the atrophy of brain cells continues. The synaptic pass becomes clouded and might break (Brown 1951, p.1585-87). Memory also works through a messenger transmission cascade. This works by the regulation of gene transcription and alterations of chief protein at synapses (Brown 1951, p.1585-87). Some of these key proteins include PKAII and CaMKII (Brown 1951, p.1585-87). Accumulation of tissue fluid leads to the deactivation of the messenger pathway due to decreased levels of CamKII and PKAII in the dendritic spine (Brown 1951, p.1585-87). There is also slowing of the growth of the dendritic spine volume. This leads to dephosphorylation of ion channels and inhibited permeability (Brown 1951, p.1585-87). This means that the memory channels are partially destroyed. The Horteborts syndrome patient experiences memory loss (Jes Olesen et al 2005, p.56). Muscle weakness Muscle weakness is another symptom of Horteborts syndrome. It is caused on one hand by nerve failure (Marx 2010, p.28). This is because nerves are the agents that control the contraction of muscles. Thus, muscles determine the sequence, force and number of muscular contractions (Marx 2010, p.28). Muscle failure and weakness occur when the lymphatic fluid accumulates in the tissues, especially in the brain tissues (Marx 2010, p.28). The neural centers that coordinate muscle strength and movement are pressed down by tissue fluid (Marx 2010, p.28). This causes them to send the wrong signal to the body muscles (Marx 2010, p.28). The lack of nutrients through shunting in the arteriovenous junctions affects metabolism. The amount of energy generated is thus reduced, and the muscles experience weakness (Enoka 1992, p.1639). The accumulation of tissue fluid also leads to the incapability of the body to supply adequate metabolites for the contraction of muscles (Marx 2010, p.28). This causes sub-optimal aerobic metabolism (Sahlin1986, p.86). This creates acidic anaerobic metabolic waste products that inhibit functioning of muscles. It also causes muscle derecruitment (Sahlin1986, p.86). This is caused by the inability of calcium ions to stimulate the muscle proteins actin and myosin to function (Sahlin1986, p.86). Because the waste products in the lymphatic system cannot be absorbed and filtered out of the body, the muscles encounter lactic acid accumulation (Sahlin1986, p.86). Lactic acid is produced as a waste product in the muscles. It causes intracellular acidity in the muscles. This acidity lowers the sensitivity of the contractile mechanism to calcium ions (Sahlin1986, p.86). Lactic acid accumulation also increases cytoplasmic calcium ions. This is through the inhibition of the body’s chemical pump (Sahlin1986, p.86). This is the pump that actively transmits calcium outside the cells. The result is that potassium is also inhibited from promoting muscular potential (Sahlin1986, p.86). Lactic acid also inhibits the chloride ions from helping in the contraction of muscles. This causes muscle weakness (Gandevia, 2001, p.1744). Severe headache Severe headache is another symptom of Horteborts symptom. A headache is pain that is located in the region of the neck and head (Jes Olesen et al 2005, p.56). In Horteborts syndrome, it is caused by the pressure that is applied on pain responsive structures’ surrounding the brain (Jes Olesen et al 2005, p.56) .The pain is not on the brain tissue because it is not sensitive to pain(Jes Olesen et al 2005, p.56). These pain receptive structures are grouped into two (Morris, Steven Baskin, Marcelo & Bigal 2008, p.178). There are the blood vessels, cranial, nerves and meninges that are within the cranium. There are also the muscles, nerves, arteries, vein, subcutaneous tissues, eyes, sinuses and mucous membranes among others that are situated outside the cranium (Jes Olesen et al 2005, p.56). Fluid accumulation in the brain results in traction of the blood vessels, and meninges (Morris, Steven Baskin, and Marcelo & Bigal 2008, p.178). The physiology is just like that of seizures, so the paper is not going to great depths. Conclusion In conclusion, it is useful to remember that Horteborts syndrome is a rare condition. The symptoms that are sampled in this paper are just some of the symptoms that the syndrome manifests. Information on the disease is not readily available. It is the hope of this author that the medical fraternity is going to start researching on the disease. 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