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Hepatatic encepholaphapy
I have hepatic encephlopathy. Arter going to bed I feel a :neddle prick and then my leg jerks.
could be because of the encephlopathy?
could be because of the encephlopathy?
I dont think I will do the magnesium. You said, the downside was a mild laxititive. Got enough of taking the Lactulose. If you know what I mean.
I have compensated cirrhosis, so I can't add anything about the HE, but I did have some really bad problems with RLS during my recent treatment for the HCV. Don't try this without getting your doctor's approval first, but my RLS was helped a lot by just taking a magnesium supplement, 400mg at bedtime. The only downside that I'm aware of is that magnesium is also a mild laxative. I hope it helps you.
Update on the leg thing. Neuro says its RLL due to the fact of the hepC so what the heck will be the next hurdle, geez.
yeah Its a real drag isnt it. Hang in there. maybe they will come out with some more new meds..Having been in the med field for long. I dont know everything. Some times I think the doc see as some kinda hypocrondiac.
I also take lactlose for the liver. I slso have thyroid problems. Dont know much about thyroid and if it has any effect on cirrosis, as I have problems with concentration due to mental issues I also have memory loss, sometimes cant even wriite. I jusst lost my train of thought. I kont know too mush about anything. My doctors are lousy (they herd us through like cattle) I'm tired now so whatever you said I will have to look you up again. Oh yeh sense of humor(good one)
Your info was very helpful. how do you find all of this info. I have been all around on the PC but find so much more info in here. Being a Xmicrbiologist it was nice to see those "germ" words. They thought I got the HepC from the lab but then found out that I had several transfusions in the 70's when HepC was not discovered yet. Just my luck. ehhh. i am on a priobiotic which seems with the stats i saw is a very good thing. I am sure I continue to have more questions. And thanks for your continued info.
That is very interesting. I do have a history of DVT and PE. Plus platlets are always low. yes have some bruising on back of my legs. Will certainly check with doc. A very good thought, thanks alot.
If there is any bruising associated with the "needle prick" sensations it could b associated with the liver not producing clotting factors.
I am sorry that you are having all of these problems.
Here is an article in which you may be interested and you may want to discuss it with your hepatologist.
http://www.medhelp.org/posts/Cirrhosis-of-the-Liver/Probiotics-Cut-Risk-for-Hepatic-Encephalopathy-in-Half--/show/1943786
Here is an article in which you may be interested and you may want to discuss it with your hepatologist.
http://www.medhelp.org/posts/Cirrhosis-of-the-Liver/Probiotics-Cut-Risk-for-Hepatic-Encephalopathy-in-Half--/show/1943786
thanks will. shame that i have had hep c for over 30yrs before it was diagnosed. between the hep and neuro docs we are doing pretty as much as we can do. Heck even Johns Hopkins drs were a bust. will persieve geez sorry for the miss spelling. its that short term memory thing, math and spelling thing. thanks for your wonderful input
thanks pooh, yes am on lactulase,propanol for varies. have been having seizures and am on lactimal. Iwas diagnosed with hep c 13yrs ago that went unfouned for over 30yrs so you can imagine the amount of cirrosis i had.
the enceph has already spoiled my short term memory,math skills pretty much gone, sleep and you know the rest. did pegasus therapy but alot of money but did not help. liver functions are always high. we have had monitor the ammonia level frequnty. between the hep dr and neuro dr Ishall prove them all wrong and go on strongly. Heck, even hopkins could not help me.
Found that a good sense of humor works well with this disease.
excuse all spelling errors, just part of the enceph. i appreciated all your info
the enceph has already spoiled my short term memory,math skills pretty much gone, sleep and you know the rest. did pegasus therapy but alot of money but did not help. liver functions are always high. we have had monitor the ammonia level frequnty. between the hep dr and neuro dr Ishall prove them all wrong and go on strongly. Heck, even hopkins could not help me.
Found that a good sense of humor works well with this disease.
excuse all spelling errors, just part of the enceph. i appreciated all your info
Link to above article/data:
http://www.liver.ca/liver-disease/types/cirrhosis/hepatic-encephalopathy.aspx
http://www.liver.ca/liver-disease/types/cirrhosis/hepatic-encephalopathy.aspx
Just so it is clear about your question:
"Arter going to bed I feel a :neddle prick and then my leg jerks. could be because of the encephlopathy? "
-----------------------------
No, the needle pricks and leg jerks would NOT be CAUSED by encephalopathy. Encephalopathy does not cause needle pricks and leg jerks. You can have needle pricks and/or leg jerks from a variety of underlying diseases. You do not need to have Hep C or chronic liver disease to have them. What is important here is understanding what is an underlying cause and what is a symptom of an underlying cause/disease process. All three, encephalopathy, the needle pricks, and the leg jerks are symptoms of some underlying cause/underlying disease.
However, in your case, encephalopathy and the needle pricks and the leg jerks are most likely (but not definitely) being caused by the same underlying disorder/disease (chronic liver failure/Hep C) (I noticed in your profile that you are interested in Hepatitis C). So, while encephalopathy is NOT causing your needle pricks and leg jerks, chronic Hepatitis C and/or advancing liver disease are probably causing all three, encephalopathy, needle pricks, and leg jerks. You could have any of the three symptoms by themselves. None of the three symptoms is causing each other. But Hep C and/or chronic liver disease can cause all three of them.
Again, as I mentioned above, it is best to talk with your Hepatologist about all of your symptoms. He/she should know the best treatment for you and should refer you to other specialists as necessary. If you are not seeing a Hepatologist, then you need to make an appointment as soon as possible to see a Hepatologist. If you have hepatic encephalopathy then you need to be under the care of a qualified Hepatitlogist preferably at a large medical center/liver transplant center.
"Hepatic encephalopathy (HE) is a disorder of mental activity, neuromuscular function and consciousness that occurs as a result of either chronic or acute liver failure. This complex neuropsychiatric syndrome is primarily caused by metabolic abnormalities. The syndrome may occur spontaneously or be induced by some precipitating factor and may be reversible by improvement in liver function, correction of the precipitating factors or the administration of therapy. However, HE can eventually lead to coma, and may be fatal especially in acute liver failure.
Acute encephalopathy is generally rapidly progressive over a short course and is a complication of acute liver disease. This type of HE is a sign of terminal liver failure and most often occurs in patients with acute fulminant viral hepatitis, toxic hepatitis and Reye’s syndrome.
Chronic encephalopathy involves multiple recurrences of observable HE. It requires continuous therapy to decrease or prevent the development of symptoms during intervening periods. Usually, this type of HE is found in patients who have cirrhosis with extensive portal collateral circulation with surgically-created or spontaneously-evolving shunts. In between obvious episodes, HE can be subtle and low-grade such that it may not be noticeable. Chronic HE is a sign of significant decompensation from cirrhosis.
There are four different stages of symptoms of HE. The abnormalities that reflect mental and personality changes are distinguished from those reflecting neuromuscular functions.
In Stage 1, the symptoms include short attention span, nightmares and poor night time sleep with daytime sleepiness, restlessness, depression, aimless wandering, anxiety and irritability.
In Stage 2, the mental and personality changes include obvious drowsiness, obvious personality changes, gross impairment of ability to do mental tasks, slowed response, disobedience, sullenness, disorientation for time and place.
In Stage 3, the symptoms include bizarre behavior, occasional fits of rage, marked confusion, incomprehensible speech, paranoia and anger.
In Stage 4, coma is present and can be either responsive or unresponsive to painful stimuli.
HE can also be subtle and on-going. It may not be noticeable to anyone except close family members, or even the patient, who may notice mild forgetfulness, lack of concentration or that he or she is “not as sharp” as before.
The diagnosis of HE is made primarily by recognition of neuropsychiatric changes occurring in a patient with known liver disease. In a patient with cirrhosis, whose liver disease has been followed for some time, the diagnosis becomes readily apparent with development of several of the symptoms mentioned above. When confronted with a patient who presents with an encephalopathy or a patient known to have a history of previous or current liver disease and who has neurological impairment, it is very important that attention should be paid to neurological symptoms. Such symptoms include personality changes, hypersomnia, reversal of sleep pattern, presence of precipitating factors such as gastrointestinal bleeding, etc. The presence of a flapping tremor (in which hands cannot be held steady when the patient stretches out arms) is also an important physical sign in a patient with HE. A blood test may be performed to evaluate the ammonia level. There is no specific diagnostic test, but rather the improvement with treatment is the usual method of diagnosis.
The precise pathogenesis of HE still remains unknown. However, a number of substances and mechanisms have been implicated to cause HE. These substances include ammonia, mercaptans, free fatty acids, amino acid imbalance, altered GABA neurotransmission, other neurotransmitter changes, synaptic plasma membrane changes and false neurotransmitters. The disorders that occur when the liver fails are so complex that it is conceivable (and quite likely) that HE results from the complicated interplay of many of the factors mentioned above.
The most important aspect of patient management is the prompt recognition and correction of precipitating factors, when possible. Multiple precipitating factors are often present. These factors include dehydration, kidney failure, use of sedative or narcotics, GI bleeding, electrolyte abnormalities, dietary protein increase, infection, constipation and exacerbation of liver disease. The importance of recognizing and correcting any precipitating factors in patients with HE cannot be overemphasized. Infections, kidney failure and electrolyte abnormalities need to be treated and gastrointestinal bleeding must be stopped.
Patients with severe, repeated cases of encephalopathy may be told to reduce protein in the diet to lower ammonia production. The higher fiber content of a vegetable diet speeds up the passage of food through the intestine thereby altering the acidity in the intestines and helping to reduce the absorption of ammonia. However, dietary counselling is very important as too little protein in the diet can lead to malnutrition.
Lactulose is a non-absorbable synthetic sugar that is taken by mouth. It changes ammonia into ammonium in the colon which can then be excreted. Neomycin, Metronidazole and Rifaximin are antibiotics that may be used to control the growth of bacteria that produces ammonia in the colon. Sedatives, narcotics and any other medications that are broken down by the liver should be avoided if possible. Patients with alcoholic cirrhosis and HE should receive thiamine upon admission to hospital. Other medications and treatments may be recommended."
"Arter going to bed I feel a :neddle prick and then my leg jerks. could be because of the encephlopathy? "
-----------------------------
No, the needle pricks and leg jerks would NOT be CAUSED by encephalopathy. Encephalopathy does not cause needle pricks and leg jerks. You can have needle pricks and/or leg jerks from a variety of underlying diseases. You do not need to have Hep C or chronic liver disease to have them. What is important here is understanding what is an underlying cause and what is a symptom of an underlying cause/disease process. All three, encephalopathy, the needle pricks, and the leg jerks are symptoms of some underlying cause/underlying disease.
However, in your case, encephalopathy and the needle pricks and the leg jerks are most likely (but not definitely) being caused by the same underlying disorder/disease (chronic liver failure/Hep C) (I noticed in your profile that you are interested in Hepatitis C). So, while encephalopathy is NOT causing your needle pricks and leg jerks, chronic Hepatitis C and/or advancing liver disease are probably causing all three, encephalopathy, needle pricks, and leg jerks. You could have any of the three symptoms by themselves. None of the three symptoms is causing each other. But Hep C and/or chronic liver disease can cause all three of them.
Again, as I mentioned above, it is best to talk with your Hepatologist about all of your symptoms. He/she should know the best treatment for you and should refer you to other specialists as necessary. If you are not seeing a Hepatologist, then you need to make an appointment as soon as possible to see a Hepatologist. If you have hepatic encephalopathy then you need to be under the care of a qualified Hepatitlogist preferably at a large medical center/liver transplant center.
"Hepatic encephalopathy (HE) is a disorder of mental activity, neuromuscular function and consciousness that occurs as a result of either chronic or acute liver failure. This complex neuropsychiatric syndrome is primarily caused by metabolic abnormalities. The syndrome may occur spontaneously or be induced by some precipitating factor and may be reversible by improvement in liver function, correction of the precipitating factors or the administration of therapy. However, HE can eventually lead to coma, and may be fatal especially in acute liver failure.
Acute encephalopathy is generally rapidly progressive over a short course and is a complication of acute liver disease. This type of HE is a sign of terminal liver failure and most often occurs in patients with acute fulminant viral hepatitis, toxic hepatitis and Reye’s syndrome.
Chronic encephalopathy involves multiple recurrences of observable HE. It requires continuous therapy to decrease or prevent the development of symptoms during intervening periods. Usually, this type of HE is found in patients who have cirrhosis with extensive portal collateral circulation with surgically-created or spontaneously-evolving shunts. In between obvious episodes, HE can be subtle and low-grade such that it may not be noticeable. Chronic HE is a sign of significant decompensation from cirrhosis.
There are four different stages of symptoms of HE. The abnormalities that reflect mental and personality changes are distinguished from those reflecting neuromuscular functions.
In Stage 1, the symptoms include short attention span, nightmares and poor night time sleep with daytime sleepiness, restlessness, depression, aimless wandering, anxiety and irritability.
In Stage 2, the mental and personality changes include obvious drowsiness, obvious personality changes, gross impairment of ability to do mental tasks, slowed response, disobedience, sullenness, disorientation for time and place.
In Stage 3, the symptoms include bizarre behavior, occasional fits of rage, marked confusion, incomprehensible speech, paranoia and anger.
In Stage 4, coma is present and can be either responsive or unresponsive to painful stimuli.
HE can also be subtle and on-going. It may not be noticeable to anyone except close family members, or even the patient, who may notice mild forgetfulness, lack of concentration or that he or she is “not as sharp” as before.
The diagnosis of HE is made primarily by recognition of neuropsychiatric changes occurring in a patient with known liver disease. In a patient with cirrhosis, whose liver disease has been followed for some time, the diagnosis becomes readily apparent with development of several of the symptoms mentioned above. When confronted with a patient who presents with an encephalopathy or a patient known to have a history of previous or current liver disease and who has neurological impairment, it is very important that attention should be paid to neurological symptoms. Such symptoms include personality changes, hypersomnia, reversal of sleep pattern, presence of precipitating factors such as gastrointestinal bleeding, etc. The presence of a flapping tremor (in which hands cannot be held steady when the patient stretches out arms) is also an important physical sign in a patient with HE. A blood test may be performed to evaluate the ammonia level. There is no specific diagnostic test, but rather the improvement with treatment is the usual method of diagnosis.
The precise pathogenesis of HE still remains unknown. However, a number of substances and mechanisms have been implicated to cause HE. These substances include ammonia, mercaptans, free fatty acids, amino acid imbalance, altered GABA neurotransmission, other neurotransmitter changes, synaptic plasma membrane changes and false neurotransmitters. The disorders that occur when the liver fails are so complex that it is conceivable (and quite likely) that HE results from the complicated interplay of many of the factors mentioned above.
The most important aspect of patient management is the prompt recognition and correction of precipitating factors, when possible. Multiple precipitating factors are often present. These factors include dehydration, kidney failure, use of sedative or narcotics, GI bleeding, electrolyte abnormalities, dietary protein increase, infection, constipation and exacerbation of liver disease. The importance of recognizing and correcting any precipitating factors in patients with HE cannot be overemphasized. Infections, kidney failure and electrolyte abnormalities need to be treated and gastrointestinal bleeding must be stopped.
Patients with severe, repeated cases of encephalopathy may be told to reduce protein in the diet to lower ammonia production. The higher fiber content of a vegetable diet speeds up the passage of food through the intestine thereby altering the acidity in the intestines and helping to reduce the absorption of ammonia. However, dietary counselling is very important as too little protein in the diet can lead to malnutrition.
Lactulose is a non-absorbable synthetic sugar that is taken by mouth. It changes ammonia into ammonium in the colon which can then be excreted. Neomycin, Metronidazole and Rifaximin are antibiotics that may be used to control the growth of bacteria that produces ammonia in the colon. Sedatives, narcotics and any other medications that are broken down by the liver should be avoided if possible. Patients with alcoholic cirrhosis and HE should receive thiamine upon admission to hospital. Other medications and treatments may be recommended."
have hepatic encephlopathy. Arter going to bed I feel a :neddle prick and then my leg jerks.
-------------------------------------------
The manifestations of encephalopathy can be "many and varried" ( below)
http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm
Importantly however ,with HE are you under the care of a hepatologist and is the result of the HE from Hepatitis
Is there anything else we may be able to help you with as there are many here conversant with the condition of HE anf Hepatitis
best...
Will
-------------------------------------------
The manifestations of encephalopathy can be "many and varried" ( below)
http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm
Importantly however ,with HE are you under the care of a hepatologist and is the result of the HE from Hepatitis
Is there anything else we may be able to help you with as there are many here conversant with the condition of HE anf Hepatitis
best...
Will
"Arter going to bed I feel a :neddle prick and then my leg jerks.
Could be because of the encephlopathy? "
----------------------------------------
No, the needle pricks and the jerking leg are not from Hepatic Encephalopathy, per se. They are more likely due to either Peripheral Neuropathy or Restless Leg Syndrome or both. Or they could be from some other problem associated with Hep C and/or liver failure.
The Peripheral Neuropathy and Restless Leg Syndrome may be due to/associated with the liver failure and/or the Hepatitis C. Please discuss these symptoms with your Hepatologist (I hope you are seeing a Hepatologist/liver specialist) and perhaps he/she can help to alleviate some of these symptoms.
Hepatitis C has many extrahepatic manifestations. Peripheral Neuropathy is one of them.
"Peripheral Neuropathy (PN) is characterized by
numbness, burning, pins and needles sensations,
crawling skin, and itching that occurs most often in
the hands and feet, but can appear in other areas of the
body. People with HCV-related PN should be tested
for Cryoglobulinemia. In one study, it was found that
15.3% of people with HCV were diagnosed with PN.
Treatment consists of treating the underlying disease
(HCV) and avoiding any medications that cause or that
can make PN worse."
http://www.hcvadvocate.org/hepatitis/factsheets_pdf/Extrahepatic.pdf
http://www.ccjm.org/content/72/11/1005.full.pdf
"Restless legs syndrome (RLS) is a disorder of the part of the nervous system that affects the legs and causes an urge to move them. Because it usually interferes with sleep, it also is considered a sleep disorder.
Symptoms of Restless Legs Syndrome
People with restless legs syndrome have uncomfortable sensations in their legs (and sometimes arms or other parts of the body) and an irresistible urge to move their legs to relieve the sensations. The sensations are difficult to describe: they are an uncomfortable, "itchy," "pins and needles," or "creepy crawly" feeling in the legs. The sensations are usually worse at rest, especially when lying or sitting. The sensations can lead to sleep deprivation and stress.
The severity of RLS symptoms ranges from mild to intolerable. Symptoms can come and go and severity can also vary. The symptoms are generally worse in the evening and at night and less severe in the morning. For some people, symptoms may cause severe nightly sleep disruption that can significantly impair a person's quality of life.
Who Gets Restless Legs Syndrome?
Restless legs syndrome may affect up to 10% of the U.S. population. It affects both sexes but is more common in women and may begin at any age, even in young children. Most people who are affected severely are middle-aged or older.
RLS is often unrecognized or misdiagnosed. In many people it is not diagnosed until 10 to 20 years after symptoms begin. Once correctly diagnosed, RLS can often be treated successfully.
Causes of Restless Legs Syndrome
In most cases, doctors do not know the cause of restless leg syndrome; however, they suspect that genes play a role. About half of people with RLS also have a family member with the condition.
Other factors associated with the development or worsening of restless legs syndrome include:
Chronic diseases. Certain chronic diseases and medical conditions, including iron deficiency, Parkinson’s disease, kidney failure, diabetes, and peripheral neuropathy often include symptoms of RLS. Treating these conditions often gives some relief from restless legs symptoms.
Medications. Some types of medications, including antinausea drugs, antipsychotic drugs, some antidepressants, and cold and allergy medications containing antihistamines may worsen symptoms."
http://www.webmd.com/brain/restless-legs-syndrome/restless-legs-syndrome-rls
Best of luck going forward.
Could be because of the encephlopathy? "
----------------------------------------
No, the needle pricks and the jerking leg are not from Hepatic Encephalopathy, per se. They are more likely due to either Peripheral Neuropathy or Restless Leg Syndrome or both. Or they could be from some other problem associated with Hep C and/or liver failure.
The Peripheral Neuropathy and Restless Leg Syndrome may be due to/associated with the liver failure and/or the Hepatitis C. Please discuss these symptoms with your Hepatologist (I hope you are seeing a Hepatologist/liver specialist) and perhaps he/she can help to alleviate some of these symptoms.
Hepatitis C has many extrahepatic manifestations. Peripheral Neuropathy is one of them.
"Peripheral Neuropathy (PN) is characterized by
numbness, burning, pins and needles sensations,
crawling skin, and itching that occurs most often in
the hands and feet, but can appear in other areas of the
body. People with HCV-related PN should be tested
for Cryoglobulinemia. In one study, it was found that
15.3% of people with HCV were diagnosed with PN.
Treatment consists of treating the underlying disease
(HCV) and avoiding any medications that cause or that
can make PN worse."
http://www.hcvadvocate.org/hepatitis/factsheets_pdf/Extrahepatic.pdf
http://www.ccjm.org/content/72/11/1005.full.pdf
"Restless legs syndrome (RLS) is a disorder of the part of the nervous system that affects the legs and causes an urge to move them. Because it usually interferes with sleep, it also is considered a sleep disorder.
Symptoms of Restless Legs Syndrome
People with restless legs syndrome have uncomfortable sensations in their legs (and sometimes arms or other parts of the body) and an irresistible urge to move their legs to relieve the sensations. The sensations are difficult to describe: they are an uncomfortable, "itchy," "pins and needles," or "creepy crawly" feeling in the legs. The sensations are usually worse at rest, especially when lying or sitting. The sensations can lead to sleep deprivation and stress.
The severity of RLS symptoms ranges from mild to intolerable. Symptoms can come and go and severity can also vary. The symptoms are generally worse in the evening and at night and less severe in the morning. For some people, symptoms may cause severe nightly sleep disruption that can significantly impair a person's quality of life.
Who Gets Restless Legs Syndrome?
Restless legs syndrome may affect up to 10% of the U.S. population. It affects both sexes but is more common in women and may begin at any age, even in young children. Most people who are affected severely are middle-aged or older.
RLS is often unrecognized or misdiagnosed. In many people it is not diagnosed until 10 to 20 years after symptoms begin. Once correctly diagnosed, RLS can often be treated successfully.
Causes of Restless Legs Syndrome
In most cases, doctors do not know the cause of restless leg syndrome; however, they suspect that genes play a role. About half of people with RLS also have a family member with the condition.
Other factors associated with the development or worsening of restless legs syndrome include:
Chronic diseases. Certain chronic diseases and medical conditions, including iron deficiency, Parkinson’s disease, kidney failure, diabetes, and peripheral neuropathy often include symptoms of RLS. Treating these conditions often gives some relief from restless legs symptoms.
Medications. Some types of medications, including antinausea drugs, antipsychotic drugs, some antidepressants, and cold and allergy medications containing antihistamines may worsen symptoms."
http://www.webmd.com/brain/restless-legs-syndrome/restless-legs-syndrome-rls
Best of luck going forward.
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