Monday, April 30, 2007

Lamotrigine Info - Medication Candidate for seizure relief

Lamotrigine Message boards-

http://www.bluelight.ru/vb/archive/index.php/t-208772.html

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.

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

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