Lamotrigine Message boards-
http://www.bluelight.ru/vb/archive/index.php/t-208772.html
Monday, April 30, 2007
Patient Update
April 30, 2007
Patient is now home following the 8 day hospital stay.
It is evident that the doctors have decided to focus their attention on treating our family member as a psychiatric patient by perscribing a neuroleptic medication, Seroquel to control psychosis even though patient's EEG results show seizure activity in the temporal lobe.
Doctors we have dealt with in psychiatric field have been quick to medicate the behaivoral symptoms. Seizures could be causing the psychosis, but the psychiatrists are not addressing that. Patient was given seizure medication during hospital stay but we suspect it was discontinued toward the middle of hospital stay.
Patient was not sent home with any seizure medication even though Patient has experienced distinct symptoms that mirror those of temporal lobe epilepsy, including overwhelming/intense emotion connected to episodes of psychosis experienced from time to time, in this case emotion has consistently been fear. Periods of depression and lack of motivation have been common in between episodes of fear/psychosis.
Instead of leaving hospital with seizure medication, patient left with neuroleptic medication. Neuroleptics are known to induce seizure activity.
Patient is currently experiencing extreme inability to carry on a conversation, difficulty processing information quickly, much trouble with articulating thoughts. Patient's symptoms from Seroquel are strikinly similar to ones experienced in previous use of Respirdal. Overall cognitive functioning has decreased significantly to a pathetic level. Patient's cognitive problems are worse with Seroquel.
The neurologist with EEG results has been unable to come up with a diagnosis. We suspect patient is suffering from temporal lobe epilepsy with psychosis appearing symptoms. We feel patient should be treated for seizures, not psychosis. Patient experienced seizures as an infant and suffered from a head injury within the past 10-15 years and complained of undisclosed symptoms following that. Patient recently experienced episodes of passing out, blacking out, minor shaking and episodes of dizziness and tingling. Patient's psychosis symptoms consistently involve intense feeling of fear in every episode with periods of depression, lack of motivation, lack of energy experienced in between. Patient has mentioned a sensation of motion rising up from midsection (evidence of aura/partial seizure). Patient has experienced smells and tastes that were out of the ordinary.
Patient is now home following the 8 day hospital stay.
It is evident that the doctors have decided to focus their attention on treating our family member as a psychiatric patient by perscribing a neuroleptic medication, Seroquel to control psychosis even though patient's EEG results show seizure activity in the temporal lobe.
Doctors we have dealt with in psychiatric field have been quick to medicate the behaivoral symptoms. Seizures could be causing the psychosis, but the psychiatrists are not addressing that. Patient was given seizure medication during hospital stay but we suspect it was discontinued toward the middle of hospital stay.
Patient was not sent home with any seizure medication even though Patient has experienced distinct symptoms that mirror those of temporal lobe epilepsy, including overwhelming/intense emotion connected to episodes of psychosis experienced from time to time, in this case emotion has consistently been fear. Periods of depression and lack of motivation have been common in between episodes of fear/psychosis.
Instead of leaving hospital with seizure medication, patient left with neuroleptic medication. Neuroleptics are known to induce seizure activity.
Patient is currently experiencing extreme inability to carry on a conversation, difficulty processing information quickly, much trouble with articulating thoughts. Patient's symptoms from Seroquel are strikinly similar to ones experienced in previous use of Respirdal. Overall cognitive functioning has decreased significantly to a pathetic level. Patient's cognitive problems are worse with Seroquel.
The neurologist with EEG results has been unable to come up with a diagnosis. We suspect patient is suffering from temporal lobe epilepsy with psychosis appearing symptoms. We feel patient should be treated for seizures, not psychosis. Patient experienced seizures as an infant and suffered from a head injury within the past 10-15 years and complained of undisclosed symptoms following that. Patient recently experienced episodes of passing out, blacking out, minor shaking and episodes of dizziness and tingling. Patient's psychosis symptoms consistently involve intense feeling of fear in every episode with periods of depression, lack of motivation, lack of energy experienced in between. Patient has mentioned a sensation of motion rising up from midsection (evidence of aura/partial seizure). Patient has experienced smells and tastes that were out of the ordinary.
Thursday, April 26, 2007
Patient Update April 26, 2007
Prescribed meds update. This list was provided Thursday April 26 by the hospital. Most of this information is from the Wikipedia.
Ativan (Lorazepam) 1MG/6hrs possesses all five principal benzodiazepine actions (sedative/hypnotic, muscle relaxant, anxiolytic, amnestic and anticonvulsant), but to different extents. Lorazepam also has found use as an adjunct anti-nausea drug. Lorazepam is a potent drug and its unique pharmacological properties underlie both its drawbacks and its advantages. Lorazepam may be safer than many other benzodiazepines in patients with impaired liver function because it does not require hepatic oxidation, which means that, similar to oxazepam, it is less likely to
accumulate to an extent where it causes adverse reactions.[2] On regular use, lorazepam builds up to maximum serum levels after only 3 days and longer term use does not result in further accumulation. Similarly, on discontinuation of regular use, lorazepam serum levels become negligible after 3 days and undetectable after a week. Lorazepam is thought to bind more strongly to GABA receptors. Lorazepam is thus more predictable when used intravenously for status epilepticus, both in regard to its more prolonged anti-seizure effects and in less drug accumulation in the patient's body (causing prolonged sedation after effects), such as is seen when diazepam injections have needed to be repeated when their effects wore off. Lorazepam's inactive metabolite is another advantage over diazepam in this setting.
++Acute therapy of catatonic states either alone, or preferably together with haloperidol as lorazepam can have paradoxical effects). Long-term treatment of otherwise resistant forms of petit mal epilepsy. Short-term treatment of insomnia, particularly if associated with severe anxiety. Treatment of anxiety disorders (especially Panic Disorder)
--Benzodiazepines in general may sometimes unmask suicidal ideation in depressed patients (indirectly, through disinhibition or fear reduction, rather than through any known direct effect). Though relatively non-toxic, the concern is that benzodiazepines may inadvertently become facilitators of suicidal behaviour. Lorazepam should therefore not be prescribed alone in depression but only together with an appropriate antidepressant and at the minimal dose required. Long term therapy may lead to cognitive deficits, especially in the elderly, who may already be more prone to forgetfulness, but this is reversible after a period of discontinuation. The likelihood of abuse, dependence and withdrawal symptoms is thought to be substantially greater with lorazepam relative to other benzodiazepines because of its particular properties: (a) Lorazepam binds relatively strongly to the GABA receptor complex. (b) Lorazepam has a short serum half-life and its effects wear off quicker due to it having no active metabolite, in contrast to diazepam. (c) Lorazepam is highly potent, making even 0.5 mg a significant dose reduction. In the UK the smallest available tablet strength is 1 mg, accentuating this problem.
Addiction is not a unique problem to lorazepam but for the reasons given above lorazepam is best used short-term to minimise this risk. Coming off lorazepam is more realistically achieved by, first, gradually changing over to an equivalent dose of diazepam and, secondly, stabilizing the patient on diazepam before contemplating dose reductions. This stabilization period is important since lorazepam levels (and effects) fluctuate more than those of diazepam: anxiety symptoms are more noticeable when lorazepam wears off and symptom relief more drastic when taking another dose, which may reinforce psychological dependence. Diazepam is here best administered once daily to tackle this aspect of dependence. The dose is reduced gradually over a period of months or years, depending on prior dose and duration of use.
Seroquel (Quetiapine) 25MG/PM which acts antagonist on - D1 and D2 dopamine and 5-HT1A and 5-HT2 serotonin receptor. Also has an antagonistic effect on the histamine H1 receptor.
Quetiapine has the United States Food and Drug Administration (FDA) and international approvals for the treatment of schizophrenia, treatment as an adjunct to either Lithium or Divalproex, and acute mania in bipolar disorder. Additionally, in October 2006, Seroquel was approved by the FDA for the treatment of depressive episodes associated with Bipolar I (or Bipolar-II) Disorder.[1][2] Currently, Seroquel is the only agent approved for this indication—as a single agent monotherapy. It is also used off-label to treat other disorders, such as post-traumatic stress disorder, restless legs syndrome, autism, alcoholism, hallucinations in Parkinson's disease patients using ropinirole, Tourette syndrome,[3] and as a sedative for those with sleep disorders or anxiety disorders.
--may lower the seizure threshold,the development of diabetes, significant risk of development of the incurable neurological disorder tardive dyskinesia with any prolonged use. Constipation, headache, and mild weight gain. Less common side effects (less than 2% of patients) include: abnormal liver tests, dizziness, upset stomach, substantial weight gain, a stuffy nose, and increased paranoia. Of note is the somnolence/sedation that occurs with Seroquel - as this side effect is most pronounced within the first 7 days of treatment and decreases over time thereafter. There is a significant risk of development of the incurable neurological disorder tardive dyskinesia with any prolonged use of any neuroleptic drug. However, quetiapine is believed to be less likely to cause tardive dyskinesia[7][8] somewhat less often than typical antipsychotics based on the data sources which point to placebo-level incidence of extrapyramidal side effects (a claim that only Seroquel can make, based on current research). The rare, but life-threatening, neuroleptic malignant syndrome. Weight gain can be a problem for some patients using quetiapine, by causing the patient's appetite to persist even after meals. However, this effect may occur to a lesser degree compared to some other atypical antipsychotics such as olanzapine or clozapine. Like other atypical antipsychotics, there is some evidence suggesting a link to the development of diabetes, however this remains unclear and controversial.
Tegretol (Carbamazepine) 200MG/12hrs an anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy and bipolar disorder. It is also used to treat schizophrenia and trigeminal neuralgia.
Mechanism of action is relatively well understood. Voltage gated sodium channels are the molecular pores that allow brain cells (neurons) to generate action potentials, the electrical event that allows neurons to communicate over long distances. After the sodium channels open, to start the action potential, they inactivate, essentially closing the channel. Carbamazepine stabilizes the inactivated state of sodium channels, meaning that fewer sodium channels are available to open, making brain cells less excitable.
--drowsiness, motor-coordination impairment and/or upset stomach. cardiac arrythmias, blurry or double vision and/or the temporary or mild loss of blood cells or platelets. Underactivity of the thyroid gland may be provoked, so thyroid function tests are advisable every year or two. Small reductions in white cell count and serum sodium are common. reports of a bizarre auditory side effect, whereby patients perceive musical notes about a semitone lower than their actual pitch.
AND...
may aggravate juvenile myoclonic epilepsy, so it is important to mention any history of jerking, especially in the morning, before starting to take this drug.
Desyrel (Trazodone) 50MG/PM serotonin reuptake inhibitor and is also a 5-HT2 receptor antagonist.
--Episodes of complex partial seizures have been reported, possibility of discontinuation syndrome if the medication is stopped too quickly. Care must therefore be taken when coming off the medication, usually by a gradual process of tapering down the dose over a period of time. Elevated prolactin concentrations have been observed in patients taking trazodone. Skin rash, itching, edema, and, rarely, hemolytic anemia, methemoglobinemia, liver enzyme alterations, obstructive jaundice, leukocytoclastic vasculitis, purpuric maculopapular eruptions, photosensitivity and fever. Aching joints and muscles, peculiar taste, hypersalivation, chest pain, hematuria, red, tired and itchy eyes. Decrease and, more rarely, increase in libido, weight gain and loss, and rarely, menstrual irregularities, retrograde ejaculation and inhibition of ejaculation. Rare cases of idiosyncratic hepatotoxicity have been observed, possibly due to the formation of reactive metabolites. Nausea, vomiting, diarrhea, gastrointestinal discomfort, anorexia, increased appetite. Orthostatic hypotension, hypertension, tachycardia, palpitations, shortness of breath, apnea, syncope, arrhythmias, prolonged P-R interval, atrial fibrillation, bradycardia, ventricular ectopic activity (including ventricular tachycardia), myocardial infarction and cardiac arrest. Dry mouth, blurred vision, priapism, diplopia, miosis, nasal congestion, constipation, sweating, urinary retention, increased urinary frequency and incontinence. Drowsiness, fatigue, lethargy, psychomotor retardation, lightheadedness, dizziness, difficulty in concentration, confusion, sex drive increases.
OH, it gets better...
Tremor, headache, ataxia, akathisia, muscle stiffness, slurred speech, slowed speech, vertigo, tinnitus, tingling of extremities, paresthesia, weakness, complex partial seizures, and, rarely impaired speech, muscle twitching, numbness, dystonia and involuntary movements. Death by deliberate or accidental overdosage has been reported. There is no specific antidote for Trazodone.
thoughts...
We plan to contact the insurance company to discuss seeing a specialist which may actually cost them less than the current path. We have one lined up. Also, a discussion with the current assigned Dr. regarding why we are diagnosed Psychosis NOS when we have identified Drop Attacts, Seizures, Declining IQ that these neuroleptics are likely to further worsen the condition. And why Lamotrigine was not tested first when it is indicated for all the symptoms. Patient was visited today by sw/gwh at 7PM and was clearly in an Abilify-like state.
Patient experiencing emotion, but poor energy, poor social interaction, heavily druged. We suspect a new drug was introduced in the past 24 hours or began to take effect. Patient was responding much better the previous day via phone conversation and more in touch with feelings.
--gjh
Ativan (Lorazepam) 1MG/6hrs possesses all five principal benzodiazepine actions (sedative/hypnotic, muscle relaxant, anxiolytic, amnestic and anticonvulsant), but to different extents. Lorazepam also has found use as an adjunct anti-nausea drug. Lorazepam is a potent drug and its unique pharmacological properties underlie both its drawbacks and its advantages. Lorazepam may be safer than many other benzodiazepines in patients with impaired liver function because it does not require hepatic oxidation, which means that, similar to oxazepam, it is less likely to
accumulate to an extent where it causes adverse reactions.[2] On regular use, lorazepam builds up to maximum serum levels after only 3 days and longer term use does not result in further accumulation. Similarly, on discontinuation of regular use, lorazepam serum levels become negligible after 3 days and undetectable after a week. Lorazepam is thought to bind more strongly to GABA receptors. Lorazepam is thus more predictable when used intravenously for status epilepticus, both in regard to its more prolonged anti-seizure effects and in less drug accumulation in the patient's body (causing prolonged sedation after effects), such as is seen when diazepam injections have needed to be repeated when their effects wore off. Lorazepam's inactive metabolite is another advantage over diazepam in this setting.
++Acute therapy of catatonic states either alone, or preferably together with haloperidol as lorazepam can have paradoxical effects). Long-term treatment of otherwise resistant forms of petit mal epilepsy. Short-term treatment of insomnia, particularly if associated with severe anxiety. Treatment of anxiety disorders (especially Panic Disorder)
--Benzodiazepines in general may sometimes unmask suicidal ideation in depressed patients (indirectly, through disinhibition or fear reduction, rather than through any known direct effect). Though relatively non-toxic, the concern is that benzodiazepines may inadvertently become facilitators of suicidal behaviour. Lorazepam should therefore not be prescribed alone in depression but only together with an appropriate antidepressant and at the minimal dose required. Long term therapy may lead to cognitive deficits, especially in the elderly, who may already be more prone to forgetfulness, but this is reversible after a period of discontinuation. The likelihood of abuse, dependence and withdrawal symptoms is thought to be substantially greater with lorazepam relative to other benzodiazepines because of its particular properties: (a) Lorazepam binds relatively strongly to the GABA receptor complex. (b) Lorazepam has a short serum half-life and its effects wear off quicker due to it having no active metabolite, in contrast to diazepam. (c) Lorazepam is highly potent, making even 0.5 mg a significant dose reduction. In the UK the smallest available tablet strength is 1 mg, accentuating this problem.
Addiction is not a unique problem to lorazepam but for the reasons given above lorazepam is best used short-term to minimise this risk. Coming off lorazepam is more realistically achieved by, first, gradually changing over to an equivalent dose of diazepam and, secondly, stabilizing the patient on diazepam before contemplating dose reductions. This stabilization period is important since lorazepam levels (and effects) fluctuate more than those of diazepam: anxiety symptoms are more noticeable when lorazepam wears off and symptom relief more drastic when taking another dose, which may reinforce psychological dependence. Diazepam is here best administered once daily to tackle this aspect of dependence. The dose is reduced gradually over a period of months or years, depending on prior dose and duration of use.
Seroquel (Quetiapine) 25MG/PM which acts antagonist on - D1 and D2 dopamine and 5-HT1A and 5-HT2 serotonin receptor. Also has an antagonistic effect on the histamine H1 receptor.
Quetiapine has the United States Food and Drug Administration (FDA) and international approvals for the treatment of schizophrenia, treatment as an adjunct to either Lithium or Divalproex, and acute mania in bipolar disorder. Additionally, in October 2006, Seroquel was approved by the FDA for the treatment of depressive episodes associated with Bipolar I (or Bipolar-II) Disorder.[1][2] Currently, Seroquel is the only agent approved for this indication—as a single agent monotherapy. It is also used off-label to treat other disorders, such as post-traumatic stress disorder, restless legs syndrome, autism, alcoholism, hallucinations in Parkinson's disease patients using ropinirole, Tourette syndrome,[3] and as a sedative for those with sleep disorders or anxiety disorders.
--may lower the seizure threshold,the development of diabetes, significant risk of development of the incurable neurological disorder tardive dyskinesia with any prolonged use. Constipation, headache, and mild weight gain. Less common side effects (less than 2% of patients) include: abnormal liver tests, dizziness, upset stomach, substantial weight gain, a stuffy nose, and increased paranoia. Of note is the somnolence/sedation that occurs with Seroquel - as this side effect is most pronounced within the first 7 days of treatment and decreases over time thereafter. There is a significant risk of development of the incurable neurological disorder tardive dyskinesia with any prolonged use of any neuroleptic drug. However, quetiapine is believed to be less likely to cause tardive dyskinesia[7][8] somewhat less often than typical antipsychotics based on the data sources which point to placebo-level incidence of extrapyramidal side effects (a claim that only Seroquel can make, based on current research). The rare, but life-threatening, neuroleptic malignant syndrome. Weight gain can be a problem for some patients using quetiapine, by causing the patient's appetite to persist even after meals. However, this effect may occur to a lesser degree compared to some other atypical antipsychotics such as olanzapine or clozapine. Like other atypical antipsychotics, there is some evidence suggesting a link to the development of diabetes, however this remains unclear and controversial.
Tegretol (Carbamazepine) 200MG/12hrs an anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy and bipolar disorder. It is also used to treat schizophrenia and trigeminal neuralgia.
Mechanism of action is relatively well understood. Voltage gated sodium channels are the molecular pores that allow brain cells (neurons) to generate action potentials, the electrical event that allows neurons to communicate over long distances. After the sodium channels open, to start the action potential, they inactivate, essentially closing the channel. Carbamazepine stabilizes the inactivated state of sodium channels, meaning that fewer sodium channels are available to open, making brain cells less excitable.
--drowsiness, motor-coordination impairment and/or upset stomach. cardiac arrythmias, blurry or double vision and/or the temporary or mild loss of blood cells or platelets. Underactivity of the thyroid gland may be provoked, so thyroid function tests are advisable every year or two. Small reductions in white cell count and serum sodium are common. reports of a bizarre auditory side effect, whereby patients perceive musical notes about a semitone lower than their actual pitch.
AND...
may aggravate juvenile myoclonic epilepsy, so it is important to mention any history of jerking, especially in the morning, before starting to take this drug.
Desyrel (Trazodone) 50MG/PM serotonin reuptake inhibitor and is also a 5-HT2 receptor antagonist.
--Episodes of complex partial seizures have been reported, possibility of discontinuation syndrome if the medication is stopped too quickly. Care must therefore be taken when coming off the medication, usually by a gradual process of tapering down the dose over a period of time. Elevated prolactin concentrations have been observed in patients taking trazodone. Skin rash, itching, edema, and, rarely, hemolytic anemia, methemoglobinemia, liver enzyme alterations, obstructive jaundice, leukocytoclastic vasculitis, purpuric maculopapular eruptions, photosensitivity and fever. Aching joints and muscles, peculiar taste, hypersalivation, chest pain, hematuria, red, tired and itchy eyes. Decrease and, more rarely, increase in libido, weight gain and loss, and rarely, menstrual irregularities, retrograde ejaculation and inhibition of ejaculation. Rare cases of idiosyncratic hepatotoxicity have been observed, possibly due to the formation of reactive metabolites. Nausea, vomiting, diarrhea, gastrointestinal discomfort, anorexia, increased appetite. Orthostatic hypotension, hypertension, tachycardia, palpitations, shortness of breath, apnea, syncope, arrhythmias, prolonged P-R interval, atrial fibrillation, bradycardia, ventricular ectopic activity (including ventricular tachycardia), myocardial infarction and cardiac arrest. Dry mouth, blurred vision, priapism, diplopia, miosis, nasal congestion, constipation, sweating, urinary retention, increased urinary frequency and incontinence. Drowsiness, fatigue, lethargy, psychomotor retardation, lightheadedness, dizziness, difficulty in concentration, confusion, sex drive increases.
OH, it gets better...
Tremor, headache, ataxia, akathisia, muscle stiffness, slurred speech, slowed speech, vertigo, tinnitus, tingling of extremities, paresthesia, weakness, complex partial seizures, and, rarely impaired speech, muscle twitching, numbness, dystonia and involuntary movements. Death by deliberate or accidental overdosage has been reported. There is no specific antidote for Trazodone.
thoughts...
We plan to contact the insurance company to discuss seeing a specialist which may actually cost them less than the current path. We have one lined up. Also, a discussion with the current assigned Dr. regarding why we are diagnosed Psychosis NOS when we have identified Drop Attacts, Seizures, Declining IQ that these neuroleptics are likely to further worsen the condition. And why Lamotrigine was not tested first when it is indicated for all the symptoms. Patient was visited today by sw/gwh at 7PM and was clearly in an Abilify-like state.
Patient experiencing emotion, but poor energy, poor social interaction, heavily druged. We suspect a new drug was introduced in the past 24 hours or began to take effect. Patient was responding much better the previous day via phone conversation and more in touch with feelings.
--gjh
Sunday, April 22, 2007
Patient Update April 22, 2007
Patient spent 4 days in hospital as a result of calling police to the home for poisoning. Police realized this was 5th time visiting residence for psychosis. We had asked Patient to return to neurologist for checkup EEG and possible alternative meds for seizure. Patient was failing to make appointment. At this point I am livid. Here's why...
Dr. (original neurologist) had nothing to go on - although aware of seizures, no diagnosis. Had another EEG taken.
The Patient was delivered psych hospital last night at 11:00PM involuntary status.
The egotistical Dr. calls into question our desire to be involved with monitoring the quality of the Patient's care and does not comment on the faxed study or questions about prescribing Lamotrigine - ignored.
It now appears that a social worker at the hospital and a dr. at the psych hospital were involved in the transfer. Damaging meds are prescribed that took the patient three months to recover from. The family has provided the psych hospital system this warning - to HALT RISPERDAL IMMEDIATELY. They claim to have not seen the fax the next day. Three days later during a visit a member of the family sees the fax in a binder a RN is flipping through. Hmmm.
RN calls SW and says following this evening:
*Patient signed info release on paper to allow family status info.
*Patient is prescribed the following meds:
*Ativan (like Valium) anti-anxiety
*Tegretol (carbamazepine) Tegretol is an antiepileptic drug. Types of seizures treated with Tegretol include: grand mal, focal, psychomotor and mixed (seizures that include complex partial or grand mal seizures). Absence seizures (petit mal) do not respond to Tegretol.
*unknown antibiotic
*Risperdal at bed time! - caused Patients tardive and syptoms which included:
hallucinations audio and visual
had no dynamic conversation
had severe dizziness
had poor balance
had severely slowed motor movement
had severe tardive symptoms, eyes felt clamped shut, arms protruding in front of body
had no personality
had inability to discern emotion and social cues
had trouble making sentences
never started conversation
had inability to keep her eyes open
had nausea
and considering patients taking Risperdal are 50% risk for Diabetes - the family is demanding immediate halt of Risperdal. If the goal is to heal Patient, it must be stopped.
AND Patient presently being held involuntarily. Now ask yourself what happens to "second opinion"
-edited Friday 27th with updates
--gjh
Dr. (original neurologist) had nothing to go on - although aware of seizures, no diagnosis. Had another EEG taken.
The Patient was delivered psych hospital last night at 11:00PM involuntary status.
The egotistical Dr. calls into question our desire to be involved with monitoring the quality of the Patient's care and does not comment on the faxed study or questions about prescribing Lamotrigine - ignored.
It now appears that a social worker at the hospital and a dr. at the psych hospital were involved in the transfer. Damaging meds are prescribed that took the patient three months to recover from. The family has provided the psych hospital system this warning - to HALT RISPERDAL IMMEDIATELY. They claim to have not seen the fax the next day. Three days later during a visit a member of the family sees the fax in a binder a RN is flipping through. Hmmm.
RN calls SW and says following this evening:
*Patient signed info release on paper to allow family status info.
*Patient is prescribed the following meds:
*Ativan (like Valium) anti-anxiety
*Tegretol (carbamazepine) Tegretol is an antiepileptic drug. Types of seizures treated with Tegretol include: grand mal, focal, psychomotor and mixed (seizures that include complex partial or grand mal seizures). Absence seizures (petit mal) do not respond to Tegretol.
*unknown antibiotic
*Risperdal at bed time! - caused Patients tardive and syptoms which included:
hallucinations audio and visual
had no dynamic conversation
had severe dizziness
had poor balance
had severely slowed motor movement
had severe tardive symptoms, eyes felt clamped shut, arms protruding in front of body
had no personality
had inability to discern emotion and social cues
had trouble making sentences
never started conversation
had inability to keep her eyes open
had nausea
and considering patients taking Risperdal are 50% risk for Diabetes - the family is demanding immediate halt of Risperdal. If the goal is to heal Patient, it must be stopped.
AND Patient presently being held involuntarily. Now ask yourself what happens to "second opinion"
-edited Friday 27th with updates
--gjh
Saturday, February 24, 2007
DHEA, Melatonin, Seizures
I'm returning to the DHEA topic. Patient has taken a two week break from DHEA after taking for a couple months. One problem Patient has battled with lately is not having a regular sleep schedule, despite continuing Melatonin. Patient has typically been very tired around 7-8PM and gone to bed only to wake up at 1-2am.
While looking at possibilities to get the schedule under control I have decided to give DHEA a shot at it. Will request Patient take DHEA 2.5mg in late afternoon. Idea being that Patient will get a small burst of energy/activity boost to carry into evening hours for a target 10-11pm sleep time. Six to seven PM has also been typically when Patient has delusional thoughts so I want to see how DHEA affects this time of day.
I suggest you read the following links for a better understanding of the role of these hormones within the body.
"...It is this rebound response that is the large area of stimulated nerves
that cause the seizures. Once the brain has stimulated sufficient DHEA, then the seizure stops." (1)
(1) http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html
http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html
http://www.bio.net/hypermail/neuroscience/1998-January/030264.html
I've updated the protocol on right side of page with info about max levels of DHEA. I should add that it is estimated that males levels naturally are 10-15 mg daily, female levels are up to 20% less than male levels. Upregulation does not occur when DHEA is taken orally, so do not exceed the natural levels. Why on earth would anyone take 25, 50, 100mg ???
--gjh
While looking at possibilities to get the schedule under control I have decided to give DHEA a shot at it. Will request Patient take DHEA 2.5mg in late afternoon. Idea being that Patient will get a small burst of energy/activity boost to carry into evening hours for a target 10-11pm sleep time. Six to seven PM has also been typically when Patient has delusional thoughts so I want to see how DHEA affects this time of day.
I suggest you read the following links for a better understanding of the role of these hormones within the body.
"...It is this rebound response that is the large area of stimulated nerves
that cause the seizures. Once the brain has stimulated sufficient DHEA, then the seizure stops." (1)
(1) http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html
http://www.bio.net/bionet/mm/neur-sci/2000-April/043570.html
http://www.bio.net/hypermail/neuroscience/1998-January/030264.html
I've updated the protocol on right side of page with info about max levels of DHEA. I should add that it is estimated that males levels naturally are 10-15 mg daily, female levels are up to 20% less than male levels. Upregulation does not occur when DHEA is taken orally, so do not exceed the natural levels. Why on earth would anyone take 25, 50, 100mg ???
--gjh
Thursday, February 15, 2007
Phosphatidylserine (PS)
I found an excellent brief on Phosphatidylserine located at the link below. I did not find anything to suggest it would increase seizure activity, so I may introduce it for its list of benefits.
"PS is a fat-soluble nutrient and would be expected to require at least several days' dosing to build up in the nerve cell membranes." "PS appears in the blood at about 30 minutes. After a few more minutes uptake begins into the liver and, later, the brain." "Given orally, PS is rapidly absorbed and readily crosses the blood-brain barrier to reach the brain. There, its sites of action appear to be exclusively in cell membrane." "Structurally, PS protected the hippocampus (a major memory center) from the loss of dendrite connections that normally occurs with aging (see Nunzi et al, 1987)." "Nunzi and co-workers (1992) found that in the rat hippocampus, a fall-off in nerve growth factor receptor density occurs with aging. PS reversed this receptor density decline and seemed to enhance NGF production." "PS given to these athletes prior to starting exercise produced an impressive degree of down-regulation of the stress hormones"(1)
Regarding dosing: "A reasonable supplementation strategy with PS is to begin at 300 mg per day with meals for a month, then go into a maintenance mode at a lower level of intake (100 to 200 mg daily). There is no indication of potential problems from long-term supplementation with PS."(1)
"As a general rule, because PS is so safe the more severe the subject's problems the more aggressive can be the supplementation strategy. Patients with severe memory problems can be kept on all their other supplements and medications, and be given PS with their meals at 300 to 500 mg per day on an ongoing basis. Subjects afflicted with motor problems may respond better at 500 mg per day. Mood problems may require a starting dose of 400 mg per day. For age-related cognitive decline (ARCD), a daily intake of 300 mg may be appropriate. "(1)
(1) "Phosphatidylserine, A Remarkable Brain Cell Nutrient"
http://www.springboard4health.com/books_online/ps/phosphatidylserine.html
--gjh
"PS is a fat-soluble nutrient and would be expected to require at least several days' dosing to build up in the nerve cell membranes." "PS appears in the blood at about 30 minutes. After a few more minutes uptake begins into the liver and, later, the brain." "Given orally, PS is rapidly absorbed and readily crosses the blood-brain barrier to reach the brain. There, its sites of action appear to be exclusively in cell membrane." "Structurally, PS protected the hippocampus (a major memory center) from the loss of dendrite connections that normally occurs with aging (see Nunzi et al, 1987)." "Nunzi and co-workers (1992) found that in the rat hippocampus, a fall-off in nerve growth factor receptor density occurs with aging. PS reversed this receptor density decline and seemed to enhance NGF production." "PS given to these athletes prior to starting exercise produced an impressive degree of down-regulation of the stress hormones"(1)
Regarding dosing: "A reasonable supplementation strategy with PS is to begin at 300 mg per day with meals for a month, then go into a maintenance mode at a lower level of intake (100 to 200 mg daily). There is no indication of potential problems from long-term supplementation with PS."(1)
"As a general rule, because PS is so safe the more severe the subject's problems the more aggressive can be the supplementation strategy. Patients with severe memory problems can be kept on all their other supplements and medications, and be given PS with their meals at 300 to 500 mg per day on an ongoing basis. Subjects afflicted with motor problems may respond better at 500 mg per day. Mood problems may require a starting dose of 400 mg per day. For age-related cognitive decline (ARCD), a daily intake of 300 mg may be appropriate. "(1)
(1) "Phosphatidylserine, A Remarkable Brain Cell Nutrient"
http://www.springboard4health.com/books_online/ps/phosphatidylserine.html
--gjh
Friday, February 9, 2007
Patient Update February 9, 2007
Patient has not followed supplement protocol over the period of past week and reports from family about paranoia and psychosis have been relayed. Work schedule and vacation interferes with daily updates. I decided daily updates will not be necessary for blog at this time.
Had conversation with Patient about options: supplements or drugs. Since I am not seeing a significant reverse of paranoia or psychosis or memory deficit baseline behavior without heavy supplementation, I am ready to test a drug.
Based on the findings of the PRODH deficiency study, I have faxed a 24 page document to the Neurologist requesting a review and comment on the study as well as recommendation for a test period of Lamotrigine (drug.) I provided the study and info from wikipedia about the drug which I had been searching for over the past few weeks since finding the study details.
Here's my Letter to the Doctor:
I am providing information for your review and comment regarding prescribing Lamotrigine for Patient (blank). I have been keeping a blog (web journal http://orthosz.blogspot.com) of research and daily progress for Patient. Based on the findings of a study and what I have learned by controlling diet and supplements and monitoring daily, I would like to have you review the attached information for comment and possible prescription to target the regulation of glutamate. The findings of the study essentially report the following:
1. glutamate toxicity factor - loss of PRODH gene function directly causes hyperactivity of nerves that use glutamate to signal other nerves.
2. dopamine toxicity factor - loss of PRODH gene function causes upregulation of COMT gene responsible for encoding the enzyme that breaks down dopamine.
3. upregulation of COMT gene is not possible in patients with 22q11 microdeletion which causes toxic buildup of dopamine {and psychosis/paranoa in Patient.}
4. PRODH deficiency increases release of glutamate at synapses in hippocampus and inhibits LTP, important step in forming memories.
5. Lack of glutamate regulation due to loss of PRODH contributes to learning difficulties.
Over the period of time since our last visit I have learned that the supplement L-Theanine (apparently) has a direct boost effect on Dopamine and for this Patient, caused paranoia and psychosis. We have known for a long time that excess sugar in the diet has also triggered the psychosis and paranoia, just not as quickly as Theanine (a green tea extract.)
Lamotrigine would target the glutamate regulation, help to control the seizures, and control the drop attacks. I am hopeful that it may prevent the chain reaction of Dopamine toxicity as well. If the glutamate release at hippocampal neurons is presently toxic, this drug may help improve the memory which at is a steady, slow deficit currently.
Patient's mother suffered from seizures that eventually robbed her of memory. Patient has been experiencing daily morning dizziness. I am aware that for many people seizures occur in the twilight sleep just as they begin to wake up. We have used a GABA enhancing supplement called Kavinace (Phenibut, Taurine) which eliminated seizures and dizziness during the day. However, this is smoke and mirrors if what is broken has to do with regulating glutamate. Even with morning and evening doses of Kavinace we did not prevent the morning dizziness that occurred when first getting out of bed-possibly a partial seizure.
end of Letter
Had conversation with Patient about options: supplements or drugs. Since I am not seeing a significant reverse of paranoia or psychosis or memory deficit baseline behavior without heavy supplementation, I am ready to test a drug.
Based on the findings of the PRODH deficiency study, I have faxed a 24 page document to the Neurologist requesting a review and comment on the study as well as recommendation for a test period of Lamotrigine (drug.) I provided the study and info from wikipedia about the drug which I had been searching for over the past few weeks since finding the study details.
Here's my Letter to the Doctor:
I am providing information for your review and comment regarding prescribing Lamotrigine for Patient (blank). I have been keeping a blog (web journal http://orthosz.blogspot.com) of research and daily progress for Patient. Based on the findings of a study and what I have learned by controlling diet and supplements and monitoring daily, I would like to have you review the attached information for comment and possible prescription to target the regulation of glutamate. The findings of the study essentially report the following:
1. glutamate toxicity factor - loss of PRODH gene function directly causes hyperactivity of nerves that use glutamate to signal other nerves.
2. dopamine toxicity factor - loss of PRODH gene function causes upregulation of COMT gene responsible for encoding the enzyme that breaks down dopamine.
3. upregulation of COMT gene is not possible in patients with 22q11 microdeletion which causes toxic buildup of dopamine {and psychosis/paranoa in Patient.}
4. PRODH deficiency increases release of glutamate at synapses in hippocampus and inhibits LTP, important step in forming memories.
5. Lack of glutamate regulation due to loss of PRODH contributes to learning difficulties.
Over the period of time since our last visit I have learned that the supplement L-Theanine (apparently) has a direct boost effect on Dopamine and for this Patient, caused paranoia and psychosis. We have known for a long time that excess sugar in the diet has also triggered the psychosis and paranoia, just not as quickly as Theanine (a green tea extract.)
Lamotrigine would target the glutamate regulation, help to control the seizures, and control the drop attacks. I am hopeful that it may prevent the chain reaction of Dopamine toxicity as well. If the glutamate release at hippocampal neurons is presently toxic, this drug may help improve the memory which at is a steady, slow deficit currently.
Patient's mother suffered from seizures that eventually robbed her of memory. Patient has been experiencing daily morning dizziness. I am aware that for many people seizures occur in the twilight sleep just as they begin to wake up. We have used a GABA enhancing supplement called Kavinace (Phenibut, Taurine) which eliminated seizures and dizziness during the day. However, this is smoke and mirrors if what is broken has to do with regulating glutamate. Even with morning and evening doses of Kavinace we did not prevent the morning dizziness that occurred when first getting out of bed-possibly a partial seizure.
end of Letter
Friday, January 19, 2007
Patient Excitotoxins
This post (incomplete-to be updated) serves as a reminder for family meal planning, Patient supplement, environmental and diet NO-NOs:
_________BAD__________________________
Dopamine boosters
L-Theanine, Green Tea
Nicotine
_________BAD__________________________
Glutamate boosters
MSG - monosodium L-glutamate, (Seen as ingredient NATURAL FLAVORS in processed foods) Hydrolyzed Protein Sodium Caseinate or Calcium Caseinate, Autolyzed Yeast or Yeast Extract, Gelatin, Hydrolyzed Oat Flour
aspartame (nutrasweet),
candy, glutamic acid, glutamine, aspartate, and cysteine.
Mercury and aluminum trigger glutamate release.
hypoglycemia, or low calorie/starvation conditions stimulate release of glutamate and reduce the ability to remove excess levels of glutamate from the brain. Excess glutamate reduces glutathione levels - antioxidants found in the body which protect neurons from damage. Reduced Glutatione leads to the death of additional neurons.
(1.)
(1.)
(1.)
(1.) http://www.autismanswer.com/articles/yasko/approach_to_reversing.html
--gjh
_________BAD__________________________
Dopamine boosters
L-Theanine, Green Tea
Nicotine
_________BAD__________________________
Glutamate boosters
MSG - monosodium L-glutamate, (Seen as ingredient NATURAL FLAVORS in processed foods) Hydrolyzed Protein Sodium Caseinate or Calcium Caseinate, Autolyzed Yeast or Yeast Extract, Gelatin, Hydrolyzed Oat Flour
aspartame (nutrasweet),
candy, glutamic acid, glutamine, aspartate, and cysteine.
Mercury and aluminum trigger glutamate release.
hypoglycemia, or low calorie/starvation conditions stimulate release of glutamate and reduce the ability to remove excess levels of glutamate from the brain. Excess glutamate reduces glutathione levels - antioxidants found in the body which protect neurons from damage. Reduced Glutatione leads to the death of additional neurons.
Food Item | Free Glutamic (mg/100g) | Free Aspartic (mg/100g) |
Tomato | 140.0 | 35.0 |
Fresh tomato juice | 260.0 | 60.0 |
Processed tomato juice | 230.0 | 60.0 |
Grapefruit, white meat | 11.5 | 87.1 |
Grapefruit juice | 18.6 | 130.0 |
Orange juice | 21.0 | 89.0 |
Nectarine, fruit | 9.0 | 200.0 |
Peach juice | 32.0 | 212.0 |
Plum, yellow fruit | 7.9 | 185.0 |
Prunes (California) | 14.4 | 185.5 |
Prunes, dry | 18.6 | 518.4 |
Grape, red Malaga | 184.0 | 12 |
Grape juice | 258.0 | 16.8 |
Strawberry | 44.4 | 60.1 |
Potato | 102.0 | - |
Broccoli | 176.0 | 40.0 |
Parmesan Cheese | 1,200.0 | - |
Gruyere Cheese | 1,050.0 | 60.0 |
Mushroom (Psalliota campestris) | 180.0 | 30.0 |
Food Item | Bound Glutamate (mg/100g) |
| Parmesan Cheese | 9,847 |
| Eggs | 1,583 |
| Chicken | 3,309 |
| Duck | 3,636 |
| Beef | 2,846 |
| Pork | 2,325 |
| Cod | 2,101 |
| Mackerel | 2,382 |
| Salmon | 2,216 |
| Peas | 5,583 |
| Corn | 1,765 |
| Food Item | Glutamate (mg/g N) | Aspartate (mg/g N) |
Potato | 639 | 775 |
Sweet Potato | 541 | 825 |
Beet | 946 | 1,131 |
Apple | 700 | 1,300 |
Apricot | 372 | 1,300 |
Avocado | 769 | 1,413 |
Banana | 575 | 656 |
Fig | 600 | 1,500 |
Orange | 760 | 880 |
Pear | 540 | 2,800 |
Strawberry | 920 | 1,400 |
(1.) http://www.autismanswer.com/articles/yasko/approach_to_reversing.html
--gjh
Thursday, January 18, 2007
PRODH Deficiency
Patient had extra 100mg of L-Theanine today and within 90 minutes had elevated paranoia and panic. I've read that L-Theanine increases dopamine levels. Now when you read this genetic explanation, this entire blog/Patient history seems to parallel the information in the article.
The link below may be the genetic explanation for what may be happening with this Patient. The description of problematic neurotransmitters and the cause of the imbalance of glutamate and dopamine seems to match our findings with foods, supplements, drugs and behaviors of Patient history.
(1.) http://www.innovations-report.com/html/reports/life_sciences/report-52499.html
"Disruption of gene interaction linked to schizophrenia
Results of studies with laboratory model of PRODH deficiency demonstrate the role of COMT in compensating for overactive dopamine signaling, according to St. Jude
Disruption of the normal interaction between the genes PRODH and COMT contributes directly to major symptoms of schizophrenia by upsetting the balance of the brain chemicals glutamate and dopamine, according to a group of investigators that includes a scientist now at St. Jude Children’s Research Hospital.
The investigators developed a model of schizophrenia that provides a way to study and understand how the loss of both PRODH and COMT gene activity contributes to the symptoms of schizophrenia.
The insights they gained into the disease with this model are important because the loss of the PRODH gene causes the imbalance in the levels of both glutamate and dopamine; and this imbalance contributes directly to the symptoms of schizophrenia, according to Stanislav Zakharenko, MD, PhD, an assistant member of the Department of Developmental Neurobiology at St. Jude.
The team investigated the roles of PRODH and COMT because these genes are located in the q11 region of human chromosome 22. Previous work by other scientists showed that a mutation in this region--the 22q11 microdeletion--is one of the major risk factors for developing schizophrenia.
The study’s findings linked changes seen at the molecular level directly to symptoms of schizophrenia seen in humans, said Zakharenko, who is a co-author of a report on this work that appears in the November 15 issue of Nature Neuroscience. The work was completed by Zakharenko and his colleagues at Columbia University (New York), Rockefeller University (New York) and the University of Utrecht (the Netherlands). Zakharenko is continuing his work on the molecular causes of schizophrenia at St. Jude.
The key finding in the current study was that the models of PRODH deficiency had increased COMT activity in the frontal cortex of the brain. "This might reflect a response to the increased dopamine activity caused by PRODH deficiency," Zakharenko said. "And it shows that when PRODH is lost, the additional loss of COMT due to the 22q11 mutation may worsen the symptoms of schizophrenia by allowing dopamine levels to rise." The prefrontal cortex is the part of the brain involved in complex cognitive functioning (e.g., thinking and reasoning).
In the same issue of Nature Neuroscience, another group of investigators reports that their study of adolescents with the 22q11 deletion showed that low activity of COMT is a risk factor for loss of volume of the part of the brain called the prefrontal cortex; and that this same mutation also puts adolescents at risk for developing psychotic symptoms.
Using their model of schizophrenia, Zakharenko and collegues first discovered that the loss of PRODH function directly causes hyperactivity of nerves that use glutamate to signal other nerves in the brain. Next, they found that disruption of PRODH gene activity causes the upregulation of the COMT gene, which encodes for the enzyme that breaks down dopamine. Upregulation is the increase in the rate at which a gene is decoded so the protein it codes for can be manufactured by the cell.
Prior research had already shown that PRODH makes an enzyme that breaks down proline, an amino acid that mimics the action of glutamate on most nerves in the brain. When PRODH activity is low, proline levels are high, creating an excess of excitatory activity leading to overall hypersensitivity of nerve cells to stimulation that might contribute to some schizophrenia symptoms. "Our model of schizophrenia was particularly useful because it lacked only a part of PRODH gene, so the level of proline rose to approximately that seen in individuals with schizophrenia," Zakharenko said.
Although dopamine and glutamate systems were suspected to contribute separately to the development of schizophrenia, researchers had not found a clear connection between them, according to Zakharenko. However, the present study clearly shows this connection. Specifically, when PRODH activity is low, proline levels are high, and there is excess in dopamine activity, he said. The subsequent increase in COMT compensates for the increased release of this dopamine caused by PRODH deficiency. "This finding shows why loss of COMT activity is linked to symptoms of schizophrenia," Zakharenko said.
The study also showed why patients with schizophrenia who also have the 22q11 microdeletion are especially disadvantaged. "COMT upregulation appears to be a response that brings the level of dopamine signaling back to normal," Zakharenko said. "So patients with the 22q11 microdeletion are unable to compensate for their PRODH deficiency by upregulating COMT."
The team further showed that PRODH deficiency increased the release of glutamate at synapses formed by CA3 and CA1 neurons in the part of the brain called the hippocampus. These synapses are routinely used as models of specific types of brain activity responsible for learning and memory. A synapse is the gap between an incoming nerve and its target cell across that gap. Signals pass from one cell on one side of the gap to another cell on the other side. The increased release of excitatory chemicals glutamate and proline due to PRODH deficiency inhibited the ability of the synapse to undergo a change called long-term potentiation (LTP)--a long-lasting strengthening in the connection between two nerve cells. LTP is an important step in forming memories, and disruption of this process interferes with the ability to store information.
Another study using the PRODH-deficiency model showed that the drug D-amphetamine causes exaggerated movement similar to that caused by amphetamine in humans with schizophrenia, according to the researchers. A PRODH deficiency caused lab models to have problems remembering how to respond to an audible tone in a way that was previously learned.
"These observations showed that lack of regulation of glutamate levels due to loss of PRODH function contributed to learning difficulties similar to those found in schizophrenia," Zakharenko said.
Moreover, the researchers showed that PRODH deficiency caused a reduction in the levels of three proteins that, in combination, are associated with dopamine function in the frontal cortex. Because these proteins cooperate with COMT to regulate the overall dopamine activity, the microdeletion 22q11 is likely to contribute to schizophrenia symptoms by eliminating PRODH. "This finding is further evidence that PRODH and COMT interact to control dopamine levels and further explains why the 22q11 microdeletion is associated with schizophrenia," Zakharenko said.
Finally, the investigators used the drug D-amphetamine to stimulate release of dopamine, while blocking COMT activity with a drug called tolcapone. Blocking COMT activity significantly increased the effect of D-amphetamine in PRODH-deficient models, proving that disruption of COMT disrupts the brain’s ability to rein in dopamine activity.
"This genetic model offers a way to make additional predictions about how specific gene defects in addition to PRODH and COMT deletions contribute to the development of schizophrenia in patients with 22q11 microdeletions," said Zakharenko. "Further studies using this model will likely help to answer many more questions about this disease."
Other authors of the study include Joseph A. Gogos, Maria Karayiorgou, Marta Paterlini, Wen-Sung Lai, Jie Qin, Hui Zhang, Jun Mukai, David Sulzer, Paul Pavlidis and Steven A. Siegelbaum (Columbia University and Rockefeller University) and Koen G.C. Westphal and Berend Olivier (University of Utrecht)." (1.)
--gjh
The link below may be the genetic explanation for what may be happening with this Patient. The description of problematic neurotransmitters and the cause of the imbalance of glutamate and dopamine seems to match our findings with foods, supplements, drugs and behaviors of Patient history.
(1.) http://www.innovations-report.com/html/reports/life_sciences/report-52499.html
"Disruption of gene interaction linked to schizophrenia
Results of studies with laboratory model of PRODH deficiency demonstrate the role of COMT in compensating for overactive dopamine signaling, according to St. Jude
Disruption of the normal interaction between the genes PRODH and COMT contributes directly to major symptoms of schizophrenia by upsetting the balance of the brain chemicals glutamate and dopamine, according to a group of investigators that includes a scientist now at St. Jude Children’s Research Hospital.
The investigators developed a model of schizophrenia that provides a way to study and understand how the loss of both PRODH and COMT gene activity contributes to the symptoms of schizophrenia.
The insights they gained into the disease with this model are important because the loss of the PRODH gene causes the imbalance in the levels of both glutamate and dopamine; and this imbalance contributes directly to the symptoms of schizophrenia, according to Stanislav Zakharenko, MD, PhD, an assistant member of the Department of Developmental Neurobiology at St. Jude.
The team investigated the roles of PRODH and COMT because these genes are located in the q11 region of human chromosome 22. Previous work by other scientists showed that a mutation in this region--the 22q11 microdeletion--is one of the major risk factors for developing schizophrenia.
The study’s findings linked changes seen at the molecular level directly to symptoms of schizophrenia seen in humans, said Zakharenko, who is a co-author of a report on this work that appears in the November 15 issue of Nature Neuroscience. The work was completed by Zakharenko and his colleagues at Columbia University (New York), Rockefeller University (New York) and the University of Utrecht (the Netherlands). Zakharenko is continuing his work on the molecular causes of schizophrenia at St. Jude.
The key finding in the current study was that the models of PRODH deficiency had increased COMT activity in the frontal cortex of the brain. "This might reflect a response to the increased dopamine activity caused by PRODH deficiency," Zakharenko said. "And it shows that when PRODH is lost, the additional loss of COMT due to the 22q11 mutation may worsen the symptoms of schizophrenia by allowing dopamine levels to rise." The prefrontal cortex is the part of the brain involved in complex cognitive functioning (e.g., thinking and reasoning).
In the same issue of Nature Neuroscience, another group of investigators reports that their study of adolescents with the 22q11 deletion showed that low activity of COMT is a risk factor for loss of volume of the part of the brain called the prefrontal cortex; and that this same mutation also puts adolescents at risk for developing psychotic symptoms.
Using their model of schizophrenia, Zakharenko and collegues first discovered that the loss of PRODH function directly causes hyperactivity of nerves that use glutamate to signal other nerves in the brain. Next, they found that disruption of PRODH gene activity causes the upregulation of the COMT gene, which encodes for the enzyme that breaks down dopamine. Upregulation is the increase in the rate at which a gene is decoded so the protein it codes for can be manufactured by the cell.
Prior research had already shown that PRODH makes an enzyme that breaks down proline, an amino acid that mimics the action of glutamate on most nerves in the brain. When PRODH activity is low, proline levels are high, creating an excess of excitatory activity leading to overall hypersensitivity of nerve cells to stimulation that might contribute to some schizophrenia symptoms. "Our model of schizophrenia was particularly useful because it lacked only a part of PRODH gene, so the level of proline rose to approximately that seen in individuals with schizophrenia," Zakharenko said.
Although dopamine and glutamate systems were suspected to contribute separately to the development of schizophrenia, researchers had not found a clear connection between them, according to Zakharenko. However, the present study clearly shows this connection. Specifically, when PRODH activity is low, proline levels are high, and there is excess in dopamine activity, he said. The subsequent increase in COMT compensates for the increased release of this dopamine caused by PRODH deficiency. "This finding shows why loss of COMT activity is linked to symptoms of schizophrenia," Zakharenko said.
The study also showed why patients with schizophrenia who also have the 22q11 microdeletion are especially disadvantaged. "COMT upregulation appears to be a response that brings the level of dopamine signaling back to normal," Zakharenko said. "So patients with the 22q11 microdeletion are unable to compensate for their PRODH deficiency by upregulating COMT."
The team further showed that PRODH deficiency increased the release of glutamate at synapses formed by CA3 and CA1 neurons in the part of the brain called the hippocampus. These synapses are routinely used as models of specific types of brain activity responsible for learning and memory. A synapse is the gap between an incoming nerve and its target cell across that gap. Signals pass from one cell on one side of the gap to another cell on the other side. The increased release of excitatory chemicals glutamate and proline due to PRODH deficiency inhibited the ability of the synapse to undergo a change called long-term potentiation (LTP)--a long-lasting strengthening in the connection between two nerve cells. LTP is an important step in forming memories, and disruption of this process interferes with the ability to store information.
Another study using the PRODH-deficiency model showed that the drug D-amphetamine causes exaggerated movement similar to that caused by amphetamine in humans with schizophrenia, according to the researchers. A PRODH deficiency caused lab models to have problems remembering how to respond to an audible tone in a way that was previously learned.
"These observations showed that lack of regulation of glutamate levels due to loss of PRODH function contributed to learning difficulties similar to those found in schizophrenia," Zakharenko said.
Moreover, the researchers showed that PRODH deficiency caused a reduction in the levels of three proteins that, in combination, are associated with dopamine function in the frontal cortex. Because these proteins cooperate with COMT to regulate the overall dopamine activity, the microdeletion 22q11 is likely to contribute to schizophrenia symptoms by eliminating PRODH. "This finding is further evidence that PRODH and COMT interact to control dopamine levels and further explains why the 22q11 microdeletion is associated with schizophrenia," Zakharenko said.
Finally, the investigators used the drug D-amphetamine to stimulate release of dopamine, while blocking COMT activity with a drug called tolcapone. Blocking COMT activity significantly increased the effect of D-amphetamine in PRODH-deficient models, proving that disruption of COMT disrupts the brain’s ability to rein in dopamine activity.
"This genetic model offers a way to make additional predictions about how specific gene defects in addition to PRODH and COMT deletions contribute to the development of schizophrenia in patients with 22q11 microdeletions," said Zakharenko. "Further studies using this model will likely help to answer many more questions about this disease."
Other authors of the study include Joseph A. Gogos, Maria Karayiorgou, Marta Paterlini, Wen-Sung Lai, Jie Qin, Hui Zhang, Jun Mukai, David Sulzer, Paul Pavlidis and Steven A. Siegelbaum (Columbia University and Rockefeller University) and Koen G.C. Westphal and Berend Olivier (University of Utrecht)." (1.)
--gjh
Tuesday, January 16, 2007
Balancing mood with L-Theanine
L-Theanine information
Increasing L-Theanine from 100mg to 200mg today. Asked Patient to take one 100mg with AM meal and one 100mg with PM meal. The effects take approximately 30 minutes.
L-Theanine creates alert relaxation (non-drowsy) and stimulates production of Alpha brain waves, creating a deep state of relaxation similar to a massage or hot bath. Also plays a role in production of GABA.
(Updated 1-18-07) And unfortunately for this Patient it also appears to significantly increase Dopamine levels which elevates the SZ symptoms. Theanine is placed on hold in the supplement line up now.
CHANGED TO AVOID from ON HOLD 2-5-07
--gjh
Increasing L-Theanine from 100mg to 200mg today. Asked Patient to take one 100mg with AM meal and one 100mg with PM meal. The effects take approximately 30 minutes.
L-Theanine creates alert relaxation (non-drowsy) and stimulates production of Alpha brain waves, creating a deep state of relaxation similar to a massage or hot bath. Also plays a role in production of GABA.
(Updated 1-18-07) And unfortunately for this Patient it also appears to significantly increase Dopamine levels which elevates the SZ symptoms. Theanine is placed on hold in the supplement line up now.
CHANGED TO AVOID from ON HOLD 2-5-07
--gjh
Monday, January 15, 2007
Patient Update January 15, 2007
Patient reported January 14th that taste buds started working (normal flavors) the day the L-Carnosine was reduced to 250mg.
Additional L-Carnosine info:
Study that showed "Acceleration of metabolism of stress-related substances by L-carnosine."
--gjh
Additional L-Carnosine info:
Study that showed "Acceleration of metabolism of stress-related substances by L-carnosine."
--gjh
Wednesday, January 10, 2007
Patient Update January 10, 2007
Patient has been on Am and PM 475mg Kavinace daily for second week, first week PM only daily. Dizziness under control. Keeping the routine and the schedule on track is supportive for controlling the dizziness. Exercise on treadmill is daily for 10-15 minutes.
Minimum required exercise is 3 times a week for generating new brain cells. Challenging those cells with new learning and socialization helps integrate them permanently.
During the past week, 1,000 mg L-Carnosine (500mg am / 500mg pm) was taken and Patient had elevated levels of paranoia. L-Carnosine is said to have support affect on serotonin and dopamine. In the past, this Patient had elevated paranoia while on antidepressents. The 1,000mg has been reduced to 250mg once in AM for the next week. The intention was to have 500mg in AM, not 1,000mg which the Patient self administered. If paranoia reduces on the 250mg L-Carnosine, it will remain, otherwise it will be dropped to 100mg or eliminated. (update 1-13-07: Patient reported on 1-12-07 having difficulty exhaling, having tight chest - during the week long period of 1,000mg and this symptom is no longer present on 250mg after one day.)
L-Theanine 100mg has also been taken during the past week and will continue once in AM daily with regular supplements. (UPDATE 2-24-2007 Theanine caused elevated dopamine levels and paranoia so we have discontinued Theanine for this Patient.)
Sorry for the long delay in posting updates. Daily progress checks have been handled by phone over the period without posts. The progress has been consistent, slow, and positive. Mood appears to be improving. Still, there are good days and bad days for paranoia symptoms, but especially elevated over the past week on large 1,000 mg L-Carnosine-now reduced.
--gjh
Minimum required exercise is 3 times a week for generating new brain cells. Challenging those cells with new learning and socialization helps integrate them permanently.
During the past week, 1,000 mg L-Carnosine (500mg am / 500mg pm) was taken and Patient had elevated levels of paranoia. L-Carnosine is said to have support affect on serotonin and dopamine. In the past, this Patient had elevated paranoia while on antidepressents. The 1,000mg has been reduced to 250mg once in AM for the next week. The intention was to have 500mg in AM, not 1,000mg which the Patient self administered. If paranoia reduces on the 250mg L-Carnosine, it will remain, otherwise it will be dropped to 100mg or eliminated. (update 1-13-07: Patient reported on 1-12-07 having difficulty exhaling, having tight chest - during the week long period of 1,000mg and this symptom is no longer present on 250mg after one day.)
L-Theanine 100mg has also been taken during the past week and will continue once in AM daily with regular supplements. (UPDATE 2-24-2007 Theanine caused elevated dopamine levels and paranoia so we have discontinued Theanine for this Patient.)
Sorry for the long delay in posting updates. Daily progress checks have been handled by phone over the period without posts. The progress has been consistent, slow, and positive. Mood appears to be improving. Still, there are good days and bad days for paranoia symptoms, but especially elevated over the past week on large 1,000 mg L-Carnosine-now reduced.
--gjh
Sunday, December 24, 2006
Patient Update December 24, 2006
Exciting Information... Finally located a company that may be able to
help us at www.neurorelief.com. They seem to understand the need for
testing and addressing deficiencies and food allergies.
Food Allergy Testing Link http://www.neurorelief.com/index.php?option=com_content&task=view&id=241&Itemid=46
Basic Info http://www.neurorelief.com/index.php?option=com_content&task=section&id=7&Itemid=49
We will definitely be contacting them regarding getting Patient's levels tested and devising a more targeted therapy.
note: important supplements: L-Theanine, Taurine, L-Carnosine
--gjh - very excited!
help us at www.neurorelief.com. They seem to understand the need for
testing and addressing deficiencies and food allergies.
Food Allergy Testing Link http://www.neurorelief.com/index.php?option=com_content&task=view&id=241&Itemid=46
Basic Info http://www.neurorelief.com/index.php?option=com_content&task=section&id=7&Itemid=49
We will definitely be contacting them regarding getting Patient's levels tested and devising a more targeted therapy.
note: important supplements: L-Theanine, Taurine, L-Carnosine
--gjh - very excited!
Patient Update December 23, 2006
SW reported Patient doing well in AM.
Phone call with Patient at 6PM revealed morning dizziness, dizziness after lunch. 2 Neuro Optimizer pills taken at lunch, 1 at dinner, 1 before bed. (Discontinued, see below)
Family members living with Patient aren't interested in tracking progress and have decided to not contribute to the record, despite repeated
requests. Therefor, each update posted is information gathered as a
result of a phone call with Patient. Relying on the information provided by the Patient only is not providing an accurate record on some days.
Neuro Optimizer contains Acetyl L-Carnitine, which has warnings for seizure prone individuals. For this reason, we may need to halt Neuro Optimizer if the dizziness continues. (UPDATE 2-24-2007 Neuro Optimizer has been discontinued for this Patient due to elevated levels of paranoia AND seizure possibly caused by L-Carnatine in the combined supplement. Negative effects were seen within 48 hours or less, tested twice.)
I will likely introduce some testing of the Taurine blends found at neurorelief.com and I have new found hope we will eventually get something in the protocol that stabilizes the Patient.
--gjh
Phone call with Patient at 6PM revealed morning dizziness, dizziness after lunch. 2 Neuro Optimizer pills taken at lunch, 1 at dinner, 1 before bed. (Discontinued, see below)
Family members living with Patient aren't interested in tracking progress and have decided to not contribute to the record, despite repeated
requests. Therefor, each update posted is information gathered as a
result of a phone call with Patient. Relying on the information provided by the Patient only is not providing an accurate record on some days.
Neuro Optimizer contains Acetyl L-Carnitine, which has warnings for seizure prone individuals. For this reason, we may need to halt Neuro Optimizer if the dizziness continues. (UPDATE 2-24-2007 Neuro Optimizer has been discontinued for this Patient due to elevated levels of paranoia AND seizure possibly caused by L-Carnatine in the combined supplement. Negative effects were seen within 48 hours or less, tested twice.)
I will likely introduce some testing of the Taurine blends found at neurorelief.com and I have new found hope we will eventually get something in the protocol that stabilizes the Patient.
--gjh
Patient Update December 22, 2006
Patient started Dr. recommended Neuro Optimizer supplement. Took two with evening meal.
Tuesday, December 19, 2006
Patient Update December 19th 2006
Patient sounded alert and normal (7:40PM) and started conversation. Reported dizziness after getting out of bed. Exercised in AM. Turkey and Cheese sandwhich. Pumpkin pie today after lunch. Had spaghetti for dinner
--gjh.
--gjh.
Monday, December 18, 2006
Patient Update December 18th 2006
Spoke to at 9:00 PM, Patient sounded very tired, alertness increased slightly during 30 minute conversation. Family reported psychosis in the early evening which included voices and banging on something. Patient reported having cereal in morning, banana, spaghetti for dinner.
--gjh
--gjh
Sunday, December 17, 2006
Patient Update December 17th 2006
Patient felt light-headed shortly after consuming decaf coffee with a small amount of sugar.
Patient reported voices in walls, concern about some vehicles in the early evening.
Patient reported voices in walls, concern about some vehicles in the early evening.
Patient Update December 16th
Patient experienced minor paranoia at 4:45pm. Patient had not eaten anything since noon.
Saturday, December 16, 2006
Patient Update December 15, 2006
Patient experienced minor psychosis late afternoon and revealed that a candy bar had been eaten an hour before. Discussed with Patient the possibility of sugar metabolism problem and requested elimination of unnecessary, excessive sugar.
Neurologist conference called at 4PM. Decision was made to schedule Endocrinologist before starting any new seizure medication. Family has observed Patient has been seizure free, with no complaints of dizziness.
Decision was made to include DMG supplement in protocol. Patient has been visiting family, away from home for past 4 days in effort to reduce stress factors of psychosis.
Endocrinologist will be consulted Monday regarding appointment.
--gjh
Neurologist conference called at 4PM. Decision was made to schedule Endocrinologist before starting any new seizure medication. Family has observed Patient has been seizure free, with no complaints of dizziness.
Decision was made to include DMG supplement in protocol. Patient has been visiting family, away from home for past 4 days in effort to reduce stress factors of psychosis.
Endocrinologist will be consulted Monday regarding appointment.
--gjh
Friday, December 15, 2006
Hyperthyroidism
This link has information of what to look for in blood tests to see presence of hyperthyroidism:
http://www.emedicine.com/NEURO/topic371.htm
http://www.emedicine.com/NEURO/topic371.htm
Supplements and Epilepsy
Check this link out when more time is available.
Touches on supplements and nutrients recommended for seizures.
Also states the following:
"About 10 to 20% of epilepsy patients do not respond to drug therapy and may require surgery."
http://www.vitacost.com/science/hn/Concern/Epilepsy.htm#Condition-Symptoms
Touches on supplements and nutrients recommended for seizures.
Also states the following:
"About 10 to 20% of epilepsy patients do not respond to drug therapy and may require surgery."
http://www.vitacost.com/science/hn/Concern/Epilepsy.htm#Condition-Symptoms
Thursday, December 14, 2006
Magnesium and the Brain
"Magnesium Calms the Brain
People don't need to become severely deficient in magnesium for the brain to become hyperactive. A new study confirms earlier reports that a marginal magnesium intake overexcites the brain's neurons and results in less coherence--creating cacaphony rather than symphony--according to electroencephalogram (EEG) measurements. During half of the six-month study, 13 women consumed 115 milligrams of magnesium daily--or about 40 percent of the Recommended Dietary Allowance (RDA). During the other half, they got 315 mg daily--a little more than the 280 mg recommended for women. After only six weeks on the marginal intake, EEG readings showed significant differences in brain function.
"Magnesium is the fourth most abundant element in the brain and is essential in regulating central nervous system excitability. Clinical studies of people severely deficient in this essential element have reported epilepsy-type convulsions, dizziness and muscle tremors or twitching as well as many psychological symptoms, including irritability, anxiety, confusion, depression, apathy, loss of appetite and insomnia. While the marginal intake in this study did not produce such severe symptoms, it did hype brain activity.
"This is the first experimental study in which magnesium intakes were tightly controlled and EEG measurements were analyzed by computer so they could be statistically compared. Good sources of magnesium include whole grains, nuts, peanut butter, cottonseed, peanut and soybean flours, green leafy vegetables and spices. It's better to get magnesium from foods rather than supplements because high doses have a laxative effect--the body's way of preventing toxic levels."
http://www.ars.usda.gov/is/np/fnrb/fnrb1095.htm
People don't need to become severely deficient in magnesium for the brain to become hyperactive. A new study confirms earlier reports that a marginal magnesium intake overexcites the brain's neurons and results in less coherence--creating cacaphony rather than symphony--according to electroencephalogram (EEG) measurements. During half of the six-month study, 13 women consumed 115 milligrams of magnesium daily--or about 40 percent of the Recommended Dietary Allowance (RDA). During the other half, they got 315 mg daily--a little more than the 280 mg recommended for women. After only six weeks on the marginal intake, EEG readings showed significant differences in brain function.
"Magnesium is the fourth most abundant element in the brain and is essential in regulating central nervous system excitability. Clinical studies of people severely deficient in this essential element have reported epilepsy-type convulsions, dizziness and muscle tremors or twitching as well as many psychological symptoms, including irritability, anxiety, confusion, depression, apathy, loss of appetite and insomnia. While the marginal intake in this study did not produce such severe symptoms, it did hype brain activity.
"This is the first experimental study in which magnesium intakes were tightly controlled and EEG measurements were analyzed by computer so they could be statistically compared. Good sources of magnesium include whole grains, nuts, peanut butter, cottonseed, peanut and soybean flours, green leafy vegetables and spices. It's better to get magnesium from foods rather than supplements because high doses have a laxative effect--the body's way of preventing toxic levels."
http://www.ars.usda.gov/is/np/fnrb/fnrb1095.htm
Sugar Cravings
"When any carbohydrate is eaten, it is broken down into glucose by the body and is known as blood sugar. Insulin is a hormone secreted by the pancreas that takes the glucose from the blood and brings it into the body’s cells where it can be used for energy. However, if there is too much glucose in the blood from eating too many refined carbohydrates, then the body’s cells can stop responding to the insulin. This is called carbohydrate intolerance or insulin resistance.
"The problem does not stop there, because the glucose can not get into the cells for energy and the cells essentially starve. This has profound effects on the body, especially the brain, whose only source of energy is glucose. If the brain is not getting the necessary energy, it signals the body to crave more dietary carbohydrates. This begins a vicious cycle of low energy, sugar cravings, and increased consumption of dietary carbohydrates.
"But poor nutrition is not the only cause of this cycle. Chronic stress is also responsible. When the body is under continued stress, the stress hormone cortisol is continually produced. One of cortisol’s effects is to increase insulin production. This produces the same effect as eating too many carbohydrates.
"Carbohydrate intolerance can directly lead to obesity, diabetes, heart disease or stroke. But the good news is that the vicious cycle of carbohydrate intolerance can be broken through dietary and stress management."
http://carolinanewswire.com/news/News.cgi?database=columns.db&command=viewone&id=258&op=t
"The problem does not stop there, because the glucose can not get into the cells for energy and the cells essentially starve. This has profound effects on the body, especially the brain, whose only source of energy is glucose. If the brain is not getting the necessary energy, it signals the body to crave more dietary carbohydrates. This begins a vicious cycle of low energy, sugar cravings, and increased consumption of dietary carbohydrates.
"But poor nutrition is not the only cause of this cycle. Chronic stress is also responsible. When the body is under continued stress, the stress hormone cortisol is continually produced. One of cortisol’s effects is to increase insulin production. This produces the same effect as eating too many carbohydrates.
"Carbohydrate intolerance can directly lead to obesity, diabetes, heart disease or stroke. But the good news is that the vicious cycle of carbohydrate intolerance can be broken through dietary and stress management."
http://carolinanewswire.com/news/News.cgi?database=columns.db&command=viewone&id=258&op=t
Tuesday, December 12, 2006
Supplements for Seizure Control
Here's a post I found regarding Diet and Supplements for Seizure control. - (UPDATE) we HAVE changed our nutri-supplement protocol for dealing with seizures, we are still researching and making adjustments but, at this time we feel strongly that Kavinace was instrumental in controlling seizures for Patient.
The Post...
"
THE PROGRAM
Vitamins & Supplements prescribed by a Nutritionist MD
Eliminated Food Allergens (Grains, Dairy, Beans, Seeds, Peanuts, Sweeteners, Alcohols)
Along with the AEDs (Tegretol XR & Depakote ER), the anti-depressant (Prozac), and the anti-psychotic (Respirdal). {YIKES DRUGS!}
MY DIET
Eggs (hard boiled, scrambled, fried)
Fruit (raw)
Vegetables (raw & steemed)
Potatoes (mashed, boiled, baked, fried)
A Variety of Cooked Meats (Beef, Turkey, Chicken, Clams)
Juices (fresh squeezed)
Water (bottled or purified)
Prescribed Supplements & Medications
VITAMINS
B6 (Pyridoxal-5-Phospate)
Zinc
Evening Primrose Oil
Taurine w/p copper
Vitamin D3
Magnesium Gyconate
Vitamin C (ascorbic acid)
Folate
B12 (methylcobalamin)
Calcium Citrate
L-Tyrosine
L-Lysine
5-HTP
Potassium Iodide
Magnesium Citrate
Chromium Citrate
Molybdenum Citrate
Potassium Citrate
Boron Citrate
Vanadium Citrate
Digestive Enzymes
Multi-vitamin w/ lots of vegetables
As well as Chinese herbal & homeopathic remedies"(1.)
(1.) http://brain.hastypastry.net/forums/showthread.php?t=2727
The Post...
"
THE PROGRAM
Vitamins & Supplements prescribed by a Nutritionist MD
Eliminated Food Allergens (Grains, Dairy, Beans, Seeds, Peanuts, Sweeteners, Alcohols)
Along with the AEDs (Tegretol XR & Depakote ER), the anti-depressant (Prozac), and the anti-psychotic (Respirdal). {YIKES DRUGS!}
MY DIET
Eggs (hard boiled, scrambled, fried)
Fruit (raw)
Vegetables (raw & steemed)
Potatoes (mashed, boiled, baked, fried)
A Variety of Cooked Meats (Beef, Turkey, Chicken, Clams)
Juices (fresh squeezed)
Water (bottled or purified)
Prescribed Supplements & Medications
VITAMINS
B6 (Pyridoxal-5-Phospate)
Zinc
Evening Primrose Oil
Taurine w/p copper
Vitamin D3
Magnesium Gyconate
Vitamin C (ascorbic acid)
Folate
B12 (methylcobalamin)
Calcium Citrate
L-Tyrosine
L-Lysine
5-HTP
Potassium Iodide
Magnesium Citrate
Chromium Citrate
Molybdenum Citrate
Potassium Citrate
Boron Citrate
Vanadium Citrate
Digestive Enzymes
Multi-vitamin w/ lots of vegetables
As well as Chinese herbal & homeopathic remedies"(1.)
(1.) http://brain.hastypastry.net/forums/showthread.php?t=2727
L-Carnosine
One of the previous posts refers to L-Carnosine. This post will be updated with related info on L-Carnosine.
http://www.ethosplan.com/l-carnosine-information.asp
http://www.cherab.org/information/dietaryeffects/carnosine.html
http://cat.inist.fr/?aModele=afficheN&cpsidt=14508390
http://www.1stvitality.co.uk/az/carnosine/carnosine_an_antioxidant.htm
http://www.1stvitality.co.uk/az/carnosine/carnosine.htm
--gjh
http://www.ethosplan.com/l-carnosine-information.asp
http://www.cherab.org/information/dietaryeffects/carnosine.html
http://cat.inist.fr/?aModele=afficheN&cpsidt=14508390
http://www.1stvitality.co.uk/az/carnosine/carnosine_an_antioxidant.htm
http://www.1stvitality.co.uk/az/carnosine/carnosine.htm
--gjh
AMPAKINE Structures
I'll reaserch what I can find on AMPAKINE Structures as they relate to seizures (not SZ)
--gjh
--gjh
Patient Update December 11, 2006
Patient experienced "Keppra Anger" and psychosis side effects today. Patient was belligerent and almost violent. Made emergency call to Dr's office and spoke with neurologist. Result - Patient must stop Keppra today, evening dose was not taken. Side effects appeared about 4 days after starting medication (a couple pills were skipped due to poor memory and other emergencies attended by family. :( The dose was 250mg AM 250mg PM. Follow up call scheduled for Friday.
Patient had not had any seizures/dizziness since starting Keppra.
We think that we should see an endocrinologist and confirm we haven't missed something. Patient was said to have been hyperthyroid in the past.
--gjh
Patient had not had any seizures/dizziness since starting Keppra.
We think that we should see an endocrinologist and confirm we haven't missed something. Patient was said to have been hyperthyroid in the past.
--gjh
Saturday, December 9, 2006
Patient Update December 9, 2006
Patient had no dizzyness after lunch (rare), second day on drug Keppra. Noticed Patient speaking slower, perhaps both are indication that drug is already affecting GABA receptors.
No dizziness reported after evening meal.
--gjh
No dizziness reported after evening meal.
--gjh
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