An anticonvulsant used for several types of seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. It is seldom effective in generalized tonic-clonic or partial seizures. The mechanism of action appears to involve the enhancement of GAMMA-AMINOBUTYRIC ACID receptor responses.
Substances that do not act as agonists or antagonists but do affect the GAMMA-AMINOBUTYRIC ACID receptor-ionophore complex. GABA-A receptors (RECEPTORS, GABA-A) appear to have at least three allosteric sites at which modulators act: a site at which BENZODIAZEPINES act by increasing the opening frequency of GAMMA-AMINOBUTYRIC ACID-activated chloride channels; a site at which BARBITURATES act to prolong the duration of channel opening; and a site at which some steroids may act. GENERAL ANESTHETICS probably act at least partly by potentiating GABAergic responses, but they are not included here.
Drugs used to prevent SEIZURES or reduce their severity.
A group of two-ring heterocyclic compounds consisting of a benzene ring fused to a diazepine ring.
An anticonvulsant especially useful in the treatment of absence seizures unaccompanied by other types of seizures.
A pharmaceutical agent that displays activity as a central nervous system and respiratory stimulant. It is considered a non-competitive GAMMA-AMINOBUTYRIC ACID antagonist. Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility.
A sedative and anticonvulsant often used in the treatment of alcohol withdrawal. Chlormethiazole has also been proposed as a neuroprotective agent. The mechanism of its therapeutic activity is not entirely clear, but it does potentiate GAMMA-AMINOBUTYRIC ACID receptors response and it may also affect glycine receptors.
Spasmodic swallowing of air.
A type of anxiety disorder characterized by unexpected panic attacks that last minutes or, rarely, hours. Panic attacks begin with intense apprehension, fear or terror and, often, a feeling of impending doom. Symptoms experienced during a panic attack include dyspnea or sensations of being smothered; dizziness, loss of balance or faintness; choking sensations; palpitations or accelerated heart rate; shakiness; sweating; nausea or other form of abdominal distress; depersonalization or derealization; paresthesias; hot flashes or chills; chest discomfort or pain; fear of dying and fear of not being in control of oneself or going crazy. Agoraphobia may also develop. Similar to other anxiety disorders, it may be inherited as an autosomal dominant trait.
A condition where seizures occur in association with ethanol abuse (ALCOHOLISM) without other identifiable causes. Seizures usually occur within the first 6-48 hours after the cessation of alcohol intake, but may occur during periods of alcohol intoxication. Single generalized tonic-clonic motor seizures are the most common subtype, however, STATUS EPILEPTICUS may occur. (Adams et al., Principles of Neurology, 6th ed, p1174)
An anticonvulsant used to control grand mal and psychomotor or focal seizures. Its mode of action is not fully understood, but some of its actions resemble those of PHENYTOIN; although there is little chemical resemblance between the two compounds, their three-dimensional structure is similar.
A clinically diverse group of epilepsy syndromes characterized either by myoclonic seizures or by myoclonus in association with other seizure types. Myoclonic epilepsy syndromes are divided into three subtypes based on etiology: familial, cryptogenic, and symptomatic (i.e., occurring secondary to known disease processes such as infections, hypoxic-ischemic injuries, trauma, etc.).
A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.
An anthelmintic with schistosomicidal activity against Schistosoma mansoni, but not against other Schistosoma spp. Oxamniquine causes worms to shift from the mesenteric veins to the liver where the male worms are retained; the female worms return to the mesentery, but can no longer release eggs. (From Martindale, The Extra Pharmacopoeia, 31st ed, p121)
Agents that alleviate ANXIETY, tension, and ANXIETY DISORDERS, promote sedation, and have a calming effect without affecting clarity of consciousness or neurologic conditions. ADRENERGIC BETA-ANTAGONISTS are commonly used in the symptomatic treatment of anxiety but are not included here.
Movements or behaviors associated with sleep, sleep stages, or partial arousals from sleep that may impair sleep maintenance. Parasomnias are generally divided into four groups: arousal disorders, sleep-wake transition disorders, parasomnias of REM sleep, and nonspecific parasomnias. (From Thorpy, Sleep Disorders Medicine, 1994, p191)
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."
A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of voltage dependent sodium channels.
Involuntary shock-like contractions, irregular in rhythm and amplitude, followed by relaxation, of a muscle or a group of muscles. This condition may be a feature of some CENTRAL NERVOUS SYSTEM DISEASES; (e.g., EPILEPSY, MYOCLONIC). Nocturnal myoclonus is the principal feature of the NOCTURNAL MYOCLONUS SYNDROME. (From Adams et al., Principles of Neurology, 6th ed, pp102-3).

The novel analgesic compound OT-7100 (5-n-butyl-7-(3,4,5-trimethoxybenzoylamino)pyrazolo[1,5-a]pyrimid ine) attenuates mechanical nociceptive responses in animal models of acute and peripheral neuropathic hyperalgesia. (1/180)

We investigated the effects of OT-7100, a novel analgesic compound (5-n-butyl-7-(3,4,5-trimethoxybenzoylamino)pyrazolo[1,5-a]pyrimidi ne), on prostaglandin E2 biosynthesis in vitro, acute hyperalgesia induced by yeast and substance P in rats and hyperalgesia in rats with a chronic constriction injury to the sciatic nerve (Bennett model), which is a model for peripheral neuropathic pain. OT-7100 did not inhibit prostaglandin E2 biosynthesis at 10(-8)-10(-4) M. Single oral doses of 3 and 10 mg/kg OT-7100 were effective on the hyperalgesia induced by yeast. Single oral doses of 0.1, 0.3, 1 and 3 mg/kg OT-7100 were effective on the hyperalgesia induced by substance P in which indomethacin had no effect. Repeated oral administration of OT-7100 (10 and 30 mg/kg) was effective in normalizing the mechanical nociceptive threshold in the injured paw without affecting the nociceptive threshold in the uninjured paw in the Bennett model. Indomethacin had no effect in this model. While amitriptyline (10 and 30 mg/kg) and clonazepam (3 and 10 mg/kg) significantly normalized the nociceptive threshold in the injured paw, they also increased the nociceptive threshold in the uninjured paw. These results suggest that OT-7100 is a new type of analgesic with the effect of normalizing the nociceptive threshold in peripheral neuropathic hyperalgesia.  (+info)

The effects of clonazepam on quality of life and work productivity in panic disorder. (2/180)

Although panic disorder has been associated with impaired quality of life (QOL) and financial dependence, no prior study has examined whether a clinical intervention will improve these outcomes. This study examines the effects of clinically titrated doses of clonazepam versus placebo on QOL and work productivity (WP) in patients with panic disorder. QOL and WP were measured in conjunction with a randomized, double-blind, placebo-controlled trial. The Medical Outcomes Study 36-Item Short Form Health Survey (SF-36) and Work Productivity and Impairment questionnaire were used to assess QOL and WP, respectively. Baseline assessments were obtained before randomizing patients to receive clinically titrated doses of clonazepam or placebo. Follow-up assessments were obtained after 6 weeks of therapy with the test drug or at premature termination from the study. Improvement on the SF-36 Mental Health Component Summary scale was more than twice as great with clonazepam than with placebo (P = 0.03). Clonazepam patients improved (P < 0.05) on all five measures of mental health-related QOL, and both measures of physical health-related QOL, and both measures of WP. Placebo patients improved on three of five measures of mental health-related QOL, but on no other measures. Patients with marked improvements on clinical measures of panic disorder severity, especially avoidance and fear of the main phobia, showed the greatest gains on the SF-36 Mental Health Component Summary scale. Clinically titrated doses of clonazepam significantly improved mental health-related QOL and WP in panic disorder patients. Lesser improvements were obtained with placebo.  (+info)

Reactive oxygen metabolites increase mitochondrial calcium in endothelial cells: implication of the Ca2+/Na+ exchanger. (3/180)

In endothelial cells, a bolus of hydrogen peroxide (H2O2) or oxygen metabolites generated by hypoxanthine-xanthine oxidase (HX-XO) increased the mitochondrial calcium concentration [Ca2+]m. Both agents caused a biphasic increase in [Ca2+]m which was preceded by a rise in cytosolic free calcium concentration [Ca2+]c (18 and 6 seconds for H2O2 and HX-XO, respectively). The peak and plateau elevations of [Ca2+] were consistently higher in the mitochondrial matrix than in the cytosol. In Ca2+-free/EGTA medium, the plateau phase of elevated [Ca2+] evoked by H2O2 due to capacitative Ca2+ influx was abolished in the cytosol, but was maintained in the mitochondria. In contrast to H2O2 and HX-XO, ATP which binds the P2Y purinoceptors induced an increase in [Ca2+]m that was similar to that of [Ca2+]c. When cells were first stimulated with inositol 1,4, 5-trisphosphate-generating agonists or the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA), subsequent addition of H2O2 did not affect [Ca2+]c, but still caused an elevation of [Ca2+]m. Moreover, the specific inhibitor of the mitochondrial Ca2+/Na+ exchanger, 7-chloro-3,5-dihydro-5-phenyl-1H-4.1-benzothiazepine-2-on (CGP37157), did not potentiate the effects of H2O2 and HX-XO on [Ca2+]m, while causing a marked increase in the peak [Ca2+]m and a significant attenuation of the rate of [Ca2+]m efflux upon addition of histamine or CPA. In permeabilized cells, H2O2 mimicked the effects of CGP37157 causing an increase in the basal level of matrix free Ca2+ and decreased efflux. Dissipation of the electrochemical proton gradient by carbonylcyanide p-(trifluoromethoxy) phenylhydrazone (FCCP), and blocade of the Ca2+ uptake by ruthenium red prevented [Ca2+]m increases evoked by H2O2. These results demonstrate that the H2O2-induced elevation in [Ca2+]m results from a transfer of Ca2+ secondary to increased [Ca2+]c, and an inhibition of the Ca2+/Na+ electroneutral exchanger of the mitochondria.  (+info)

Benzodiazepine receptor agonists modulate thymocyte apoptosis through reduction of the mitochondrial transmembrane potential. (4/180)

Peripheral-type benzodiazepines have been shown to exert immunological effects. In this study, we examined the effects of the peripheral-type benzodiazepines on murine thymocytes. Murine thymocytes that were incubated with the peripheral-type benzodiazepines underwent apoptosis associated with the collapse of mitochondrial transmembrane potential (delta psi(m)). The drugs stimulated dexamethasone- and etoposide-induced apoptosis with the enhanced collapse of delta psi(m). The central-type benzodiazepines had no effect on either the delta psi(m) or apoptosis. The reduction of delta psi(m) depended on protein synthesis and protein phosphorylation. These results suggest that the immunomodulating effect of benzodiazepines is in part due to the modulation of thymocyte apoptosis associated with the collapse of delta psi(m).  (+info)

Central and peripheral benzodiazepine ligands prevent mitochondrial damage induced by noise exposure in the rat myocardium: an ultrastructural study. (5/180)

Noise represents an environmental stress factor affecting several organs and apparatuses, including the cardiovascular system. In experimental animals undergoing noise exposure, subcellular myocardial changes have been reported, especially at the mitochondrial level. In previous studies we found that diazepam, acting at both central and peripheral benzodiazepine receptors, prevented the onset of this myocardial damage. In the present study, we investigated the specific role played by central and/or peripheral benzodiazepine receptors in preventing noise-induced myocardial alterations. In particular, the effect of clonazepam as a selective ligand for central sites, in comparison with the efficacy of ligands selective for peripheral sites, such as Ro 5-4864 and PK-11195, was evaluated. Rats were pretreated with the test drugs 30 min before exposure to noise for 6 or 12 hr and then sacrificed. After fixing, samples of right atrium and ventricle were taken and processed for either transmission or scanning electron microscopy. After 6 hr of noise exposure, only the atrium exhibited significant mitochondrial alterations, whereas after 12 hr both atrium and ventricle were damaged. As expected, diazepam prevented noise-induced mitochondrial injury at both 6 and 12 hr. By contrast, clonazepam was effective only after 6 hr. The peripheral ligand PK-11195 attenuated mitochondrial damage at both 6 and 12 hr, whereas Ro 5-4864 was effective only after 12 hr. In the present study, we confirm that noise exposure induces mitochondrial damage in the rat myocardium. Drugs acting at both central and peripheral benzodiazepine receptors significantly prevent this damage. Differences in the amount and in the duration of the protective effect might depend on variability in the potency and in the pharmacokinetics of the specific drugs.  (+info)

Mitochondrial clearance of cytosolic Ca(2+) in stimulated lizard motor nerve terminals proceeds without progressive elevation of mitochondrial matrix [Ca(2+)]. (6/180)

This study used fluorescent indicator dyes to measure changes in cytosolic and mitochondrial [Ca(2+)] produced by physiological stimulation of lizard motor nerve terminals. During repetitive action potential discharge at 10-50 Hz, the increase in average cytosolic [Ca(2+)] reached plateau at levels that increased with increasing stimulus frequency. This stabilization of cytosolic [Ca(2+)] was caused mainly by mitochondrial Ca(2+) uptake, because drugs that depolarize mitochondria greatly increased the stimulation-induced elevation of cytosolic [Ca(2+)], whereas blockers of other Ca(2+) clearance routes had little effect. Surprisingly, during this sustained Ca(2+) uptake the free [Ca(2+)] in the mitochondrial matrix never exceeded a plateau level of approximately 1 microM, regardless of stimulation frequency or pattern. When stimulation ceased, matrix [Ca(2+)] decreased over a slow ( approximately 10 min) time course consisting of an initial plateau followed by a return to baseline. These measurements demonstrate that sustained mitochondrial Ca(2+) uptake is not invariably accompanied by progressive elevation of matrix free [Ca(2+)]. Both the plateau of matrix free [Ca(2+)] during stimulation and its complex decay after stimulation could be accounted for by a model incorporating reversible formation of an insoluble Ca salt. This mechanism allows mitochondria to sequester large amounts of Ca(2+) while maintaining matrix free [Ca(2+)] at levels sufficient to activate Ca(2+)-dependent mitochondrial dehydrogenases, but below levels that activate the permeability transition pore.  (+info)

Human neuronal gamma-aminobutyric acid(A) receptors: coordinated subunit mRNA expression and functional correlates in individual dentate granule cells. (7/180)

gamma-Aminobutyric acid(A) receptors (GABARs) are heteromeric proteins composed of multiple subunits. Numerous subunit subtypes are expressed in individual neurons, which assemble in specific preferred GABAR configurations. Little is known, however, about the coordination of subunit expression within individual neurons or the impact this may have on GABAR function. To investigate this, it is necessary to profile quantitatively the expression of multiple subunit mRNAs within individual cells. In this study, single-cell antisense RNA amplification was used to examine the expression of 14 different GABAR subunit mRNAs simultaneously in individual human dentate granule cells (DGCs) harvested during hippocampectomy for intractable epilepsy. alpha4, beta2, and delta-mRNA levels were tightly correlated within individual DGCs, indicating that these subunits are expressed coordinately. Levels of alpha3- and beta2-mRNAs, as well as epsilon- and beta1-mRNAs, also were strongly correlated. No other subunit correlations were identified. Coordinated expression could not be explained by the chromosomal clustering of GABAR genes and was observed in control and epileptic rats as well as in humans, suggesting that it was not species-specific or secondary to epileptogenesis. Benzodiazepine augmentation of GABA-evoked currents also was examined to determine whether levels of subunit mRNA expression correlated with receptor pharmacology. This analysis delineated two distinct cell populations that differed in clonazepam modulation and patterns of alpha-subunit expression. Clonazepam augmentation correlated positively with the relative expression of alpha1- and gamma2-mRNAs and negatively with alpha4- and delta-mRNAs. These data demonstrate that specific GABAR subunit mRNAs exhibit coordinated control of expression in individual DGCs, which has significant impact on inhibitory function.  (+info)

A unique effect of clonazepam on frontal lobe seizure control. (8/180)

In a 16-year-old female, clonazepam (CZP) changed randomly occurring intractable tonic seizures of frontal lobe origin to a few sleep seizures when used as an adjunctive therapy. The significance of this change in the seizure pattern is discussed with an explanation of possible pathophysiologic mechanism.  (+info)

Aerophagy can be caused by a variety of factors such as eating too quickly or not chewing food properly, swallowing air while drinking carbonated beverages or eating with straws, or having a condition that affects the digestive system such as irritable bowel syndrome (IBS).

The symptoms of aerophagy can vary depending on the individual and the amount of air swallowed. Some common symptoms include abdominal pain, bloating, gas, discomfort, and difficulty burping or passing gas. In severe cases, aerophagy can lead to more serious complications such as bowel obstruction or perforation, which can be life-threatening.

Treatment for aerophagy usually involves avoiding activities that cause air swallowing, eating slowly and chewing food properly, and using over-the-counter medications to relieve symptoms such as antacids or gas relief medications. In severe cases, medical treatment may be necessary to manage complications such as bowel obstruction or perforation.

In conclusion, aerophagy is a rare condition that can cause abdominal pain and discomfort due to the accumulation of swallowed air in the stomach and intestines. Treatment usually involves avoiding activities that cause air swallowing and using over-the-counter medications to relieve symptoms, while severe cases may require medical treatment to manage complications.

The exact cause of PD is not known, but it is believed to involve a combination of biological, psychological, and environmental factors. Some research suggests that imbalances in neurotransmitters such as serotonin and gamma-aminobutyric acid (GABA) may play a role in the development of PD. Additionally, stressful life events, personality traits, and family history may also contribute to the onset of the disorder.

There are several treatments available for PD, including psychotherapy, medication, and lifestyle changes. Cognitive-behavioral therapy (CBT) is a common form of psychotherapy used to help individuals identify and change negative thought patterns and behaviors that contribute to their panic attacks. Antidepressant medications such as selective serotonin reuptake inhibitors (SSRIs) can also be effective in reducing the frequency and severity of panic attacks. Lifestyle changes such as regular exercise, stress management techniques, and avoiding stimulants like caffeine and nicotine can also help alleviate symptoms.

It's important to note that while PD is a treatable condition, it can be challenging to diagnose and treat, especially in individuals with comorbid conditions or those who are resistant to treatment. However, with proper diagnosis and treatment, many people with PD are able to manage their symptoms and improve their quality of life.

Alcohol withdrawal seizures can take several forms, including:

1. Generalized tonic-clonic seizures (GTCS): These are the most common type of alcohol withdrawal seizure and are characterized by a loss of consciousness, convulsions, and muscle stiffness.
2. Partial seizures: These seizures affect only part of the body, such as one arm or leg, and can be preceded by an aura (a warning sign) before the seizure begins.
3. Simple partial seizures: These seizures are characterized by a change in sensation, emotion, or consciousness without any loss of muscle control.
4. Complex partial seizures: These seizures involve a combination of simple partial seizures and can cause confusion, disorientation, and impaired awareness.
5. Absence seizures (petit mal seizures): These seizures are characterized by a brief loss of consciousness and can occur several times a day.

The risk of developing alcohol withdrawal seizures increases with the amount and frequency of alcohol consumption, as well as the duration of heavy drinking. Other factors that can contribute to the risk of AWS include:

1. Age: The risk of AWS increases with age, especially for individuals over the age of 40.
2. Gender: Women are more susceptible to AWS than men.
3. Nutritional deficiencies: Malnutrition and dehydration can exacerbate the risk of AWS.
4. Co-occurring medical conditions: Certain medical conditions, such as liver disease, heart disease, and sleep disorders, can increase the risk of AWS.
5. Family history: Individuals with a family history of alcoholism are more likely to develop AWS.

If you or someone you know is experiencing any of these symptoms, it is important to seek medical attention immediately. With prompt treatment, the likelihood of a successful outcome increases. Treatment for AWS typically involves a combination of supportive care, medication, and detoxification. In severe cases, hospitalization may be necessary to ensure the individual's safety and provide appropriate care.

Myoclonic epilepsy can be caused by a variety of factors, including genetic mutations, head injuries, and infections such as meningitis or encephalitis. It is typically diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalograms (EEGs) and imaging studies.

Treatment for myoclonic epilepsy typically involves anticonvulsant medications, which can help to reduce the frequency and severity of seizures. In some cases, surgery may be necessary to remove the area of the brain that is causing the seizures. Other treatments, such as vagus nerve stimulation or ketogenic diets, may also be considered for certain patients.

The prognosis for myoclonic epilepsy varies depending on the underlying cause of the condition and the effectiveness of treatment. In general, early diagnosis and appropriate management can improve the outlook for patients with this condition. However, some cases of myoclonic epilepsy may be more challenging to treat and may have a poorer prognosis.

Overall, myoclonic epilepsy is a specific type of epilepsy that is characterized by myoclonic seizures. It can be caused by a variety of factors and treated with anticonvulsant medications, surgery, or other therapies. The prognosis for this condition varies depending on the underlying cause and the effectiveness of treatment.

Some common types of parasomnias include:

1. Sleepwalking (somnambulism): Getting out of bed and walking around while asleep.
2. Sleep talking (talking in one's sleep).
3. Sleep eating (eating while asleep).
4. Sleep driving (driving while asleep).
5. Sexsomnia (engaging in sexual activities while asleep).
6. Night terrors (intense fear or anxiety while asleep).
7. Sleep paralysis (temporary inability to move or speak while falling asleep or waking up).
8. REM sleep behavior disorder (acting out dreams while asleep).

Parasomnias can be dangerous, as they can lead to injuries or accidents, and can also cause sleep disruption and daytime fatigue. Treatment options for parasomnias include medication, behavioral therapy, and lifestyle changes, such as establishing a regular sleep schedule and avoiding alcohol and sedatives before bedtime.

There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:

1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.

Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.

Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.

Myoclonus can be classified into several types based on its duration, frequency, and distribution. Some common types of myoclonus include:

1. Generalized myoclonus: This type affects the entire body and is often seen in conditions such as epilepsy, encephalitis, and multiple sclerosis.
2. Localized myoclonus: This type affects a specific area of the body, such as the arm or leg.
3. Progressive myoclonus: This type worsens over time and is often seen in conditions such as Parkinson's disease and Huntington's disease.
4. Periodic myoclonus: This type is characterized by recurring episodes of muscle contractions and releases, often triggered by specific stimuli such as noise or stress.
5. Task-specific myoclonus: This type is seen in individuals who perform repetitive tasks, such as typing or using a computer mouse.

Myoclonus can cause a range of symptoms, including muscle weakness, fatigue, and difficulty with coordination and balance. In some cases, myoclonus can also lead to falls or injuries. Treatment for myoclonus depends on the underlying cause and may include medications such as anticonvulsants, physical therapy, and lifestyle modifications.

Myoclonus is a relatively rare condition, but it can have a significant impact on an individual's quality of life. It can affect their ability to perform daily activities, participate in social events, and maintain their independence. If you or someone you know has been diagnosed with myoclonus, it is important to work closely with a healthcare provider to develop a personalized treatment plan and manage the condition effectively.

Poisons Information Monograph - Clonazepam Wikimedia Commons has media related to Clonazepam. "Clonazepam". Drug Information ... Because clonazepam is effective in low milligram doses (0.5 mg clonazepam = 10 mg diazepam), it is said to be among the class ... Clonazepam is mainly prescribed for the acute management of epilepsies. Clonazepam has been found to be effective in the acute ... If clonazepam is used during pregnancy or breastfeeding, it is recommended that serum levels of clonazepam are monitored and ...
Browne TR (May 1976). "Clonazepam. A review of a new anticonvulsant drug". Archives of Neurology. 33 (5): 326-332. doi:10.1001/ ...
"Clonazepam". MedlinePlus. 19 March 2020. Retrieved 28 March 2020. "Amitriptyline". MedlinePlus. 19 March 2020. Retrieved 28 ... Both Lhermitte's sign and painful dysesthesias usually respond to treatment with carbamazepine, clonazepam, or amitriptyline. ...
Clonazepam (1974). Clorazepate (1972). The following benzodiazepines are used to treat status epilepticus: Diazepam (1963). Can ... Browne TR (May 1976). "Clonazepam. A review of a new anticonvulsant drug". Arch Neurol. 33 (5): 326-32. doi:10.1001/archneur. ...
White MC, Silverman JJ, Harbison JW (February 1982). "Psychosis associated with clonazepam therapy for blepharospasm". The ... Jaffe R, Gibson E (June 1986). "Clonazepam withdrawal psychosis". Journal of Clinical Psychopharmacology. 6 (3): 193. doi: ... "Serious Psychological Symptoms Caused by Clonazepam". Läkartidningen. 73 (13): 1210-1211. PMID 1263638. Pétursson H (November ...
"Klonopin (clonazepam) Prescribing Guide" (PDF). Genetech USA, Inc. October 2017. Retrieved 20 January 2019. Asiri, Yousif A.; ...
Welch TR, Rumack BH, Hammond K (1977). "Clonazepam overdose resulting in cyclic coma". Clinical Toxicology. 10 (4): 433-6. doi: ...
However, clonazepam may be more effective. In any case, the quality of evidence for both treatments is very low and it is ... Melatonin is a safer alternative than clonazepam in the treatment of REM sleep behavior disorder - a condition associated with ...
Diazepam and clonazepam have been found to have long-lasting, but not permanent, immunotoxic effects in fetuses of rats. ... ISBN 978-0-19-852518-9. Cohen LS, Rosenbaum JF (October 1987). "Clonazepam: new uses and potential problems". The Journal of ...
Clonazepam is another treatment for RLS; like other benzodiazepines, it inhibits REM sleep by enhancing levels of GABA. This ... acute placebo-controlled sleep laboratory studies with clonazepam". European Neuropsychopharmacology. 11 (2): 153-161. doi: ... inhibition of REM sleep significantly decreases K-complex count, and unlike L-DOPA treatment, clonazepam studies report ...
Third-line medications are clonazepam and mirtazapine. Theophylline has been used by some practitioners to treat ET, though it ...
Crawley JN, Marangos PJ, Stivers J, Goodwin FK (January 1982). "Chronic clonazepam administration induces benzodiazepine ...
Raines, J. M.; Greenspan, D. (1987). "Clonazepam in the treatment of chronic schizophrenia". The American Journal of Psychiatry ...
RBD may be treated with melatonin or clonazepam. Melatonin may be more helpful in preventing injuries, and it offers a safer ... alternative, because clonazepam can produce deteriorating cognition, and worsen sleep apnea. Memantine is useful for some ...
Corrigan R, Derry S, Wiffen PJ, Moore RA (May 2012). "Clonazepam for neuropathic pain and fibromyalgia in adults". The Cochrane ... Corrigan R, Derry S, Wiffen PJ, Moore RA (May 2012). "Clonazepam for neuropathic pain and fibromyalgia in adults". The Cochrane ... Cochrane reviews from 2012 of clonazepam and phenytoin uncovered no evidence of sufficient quality to support their use in ... clonazepam, phenytoin, lacosamide, sodium valproate and carbamazepine). Opioid and opiate medications (such as buprenorphine, ...
It appears that benzodiazepines metabolized by nitro-reduction (clonazepam, nitrazepam) are unlikely to be affected by ... CYP2C19 (strongly) which metabolizes clonazepam, diazepam, phenytoin, etc. CYP2B6 (weakly) which metabolizes bupropion, ...
Clonazepam and high-dose piracetam can alleviate myoclonus. Phenytoin can worsen seizures and may speed up neurodegeneration; ...
Perlwitz R, Grimmberger E, Schmidtsdorf R (June 1980). "[Immediate effect of intravenous clonazepam on the EEG]". Psychiatrie, ...
Klonopin/Rivotril (clonazepam), for epilepsy and anxiety disorders. Kytril (granisetron), for chemotherapy-induced nausea and ...
Restless legs syndrome can be treated using clonazepam as a third line treatment option as the use of clonazepam is still ... Clonazepam, a benzodiazepine is used to treat many forms of parasomnia. Rapid eye movement behavior disorder responds well to ... In the UK, both clobazam and clonazepam are second-line choices for treating many forms of epilepsy. Clobazam also has a useful ... Lorazepam is most commonly used but clonazepam is sometimes prescribed for acute psychosis or mania; their long-term use is not ...
Stiripentol with clonazepam has mitigated seizures in some cases. Intravenous levetiracetam has shown to interrupt seizures in ...
Opioids may be used to help with pain, while clonazepam or sodium valproate may help with involuntary movements. CJD affects ... Myoclonic jerks can be handled with clonazepam or sodium valproate. Opiates can help in pain. Seizures are very uncommon but ...
In this case, Imipramine or low-dose Clonazepam is beneficial. The current prevalence of confusional arousals varies according ...
Others include diazepam, clonazepam, oxazepam, nitrazepam, flurazepam, bromazepam, and clorazepate. Lorazepam was first ... Sorel L, Mechler L, Harmant J (1981). "Comparative trial of intravenous lorazepam and clonazepam im status epilepticus". ...
In a double-blind placebo-controlled trial published in 1990 comparing it to clonazepam, 10 mg of clobazam was shown to be less ... "Respiratory and sedative effects of clobazam and clonazepam in volunteers". British Journal of Clinical Pharmacology. 29 (2): ... sedative than either 0.5 mg or 1 mg of clonazepam. The α1 subtype of the GABAA receptor, was shown to be responsible for the ...
Clonazepam functions by increasing GABA activity at the GABAA receptor. GABA is an inhibitory neurotransmitter, and therefore ... Clonazepam has been effective in minimising seizure activity, especially during puberty. Sodium valproate prevents the ... Seizure frequency can be regulated by the use of drugs such as clonazepam (or other benzodiazepines) and sodium valproate. ...
However, isoniazid and clonazepam have been used to treat dysmetria. Frenkel exercises treat dysmetria.[citation needed] ...
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  • Clonazepam is in a class of medications called benzodiazepines. (medlineplus.gov)
  • Clonazepam (clonazepan) belongs to a group of medicines called benzodiazepines. (drugs.com)
  • Benzodiazepines, such as clonazepam, given to the mother may cause neonatal sedation and breast feeding should be avoided. (pocketdrugguide.com)
  • For reference to extrapyramidal disorders associated with the use of benzodiazepines including clonazepam, see Effects on the Nervous System in Diazepam. (pocketdrugguide.com)
  • In humans, clonazepam is capable of suppressing the spike and wave discharge in absence seizures (petit mal) and decreasing the frequency, amplitude, duration and spread of discharge in minor motor seizures. (nih.gov)
  • Clonazepam is useful alone or as an adjunct in the treatment of the Lennox-Gastaut syndrome (petit mal variant), akinetic and myoclonic seizures. (nih.gov)
  • Clonazepam is used alone or in combination with other medications to control certain types of seizures. (medlineplus.gov)
  • Clonazepam (clonazepan) works by increasing the activity of a naturally occurring chemical in the brain that may become unbalanced and cause seizures or symptoms of panic disorder. (drugs.com)
  • Clonazepam is in the anticonvulsant class of drugs and is used to prevent seizures. (internetdrugcoupons.com)
  • Clonazepam, a benzodiazepine, enhances inhibition but is paradoxically useful for certain types of seizures. (yale.edu)
  • Withdrawal seizures and status might become an obstacle to the removal of useless or even deleterious therapy with clonazepam because the transient nature of these effects was not always recognised. (pocketdrugguide.com)
  • Clonazepam, a benzodiazepine, is used primarily as an anticonvulsant in the treatment of absence seizures, petit mal variant seizures (Lennox-Gastaut syndrome), akinetic and myoclonic seizures, and nocturnal myoclonus. (lgmpharma.com)
  • Clonazepam can be used to avoid and control seizures. (availablemeds.top)
  • If you have several various kinds of seizure disorders, you might experience a worsening of seizures when you initially start using clonazepam. (availablemeds.top)
  • Clonazepam pharmacokinetics are dose-independent throughout the dosing range. (nih.gov)
  • Study 1 was a 9-week, fixed-dose study involving clonazepam doses of 0.5, 1, 2, 3 or 4 mg/day or placebo. (nih.gov)
  • Study 2 was a 6-week, flexible-dose study involving clonazepam in a dose range of 0.5 to 4 mg/day or placebo. (nih.gov)
  • The mean clonazepam dose during the optimal dosing period was 2.3 mg/day. (nih.gov)
  • Your doctor probably will decrease your clonazepam dose gradually. (medlineplus.gov)
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  • A safety scoring system finds clonazepam possible to use cautiously during breastfeeding,[1] and an expert consensus guideline indicates that low-dose clonazepam is an acceptable choice for refractory restless leg syndrome during lactation. (nih.gov)
  • A woman taking oral clonazepam 1 mg daily donated milk samples between 3 and 6 days postpartum at 2 hours after a dose at the estimated peak serum concentration and just before a dose. (nih.gov)
  • The neonate was breastfed starting at 72 hours after delivery and her mother took clonazepam (dose not stated) during pregnancy and lactation. (nih.gov)
  • some improvement was noted when the dose was reduced but symptoms were still intolerable and clonazepam was withdrawn. (pocketdrugguide.com)
  • Clonazepam Loading Dose in Status Epilepticus: Is More Always Better? (bvsalud.org)
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  • There is no evidence that clonazepam induces its own metabolism or that of other drugs in humans. (nih.gov)
  • Drinking alcohol or using street drugs during your treatment with clonazepam also increases the risk that you will experience these serious, life-threatening side effects. (medlineplus.gov)
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  • Effects of clonazepam (1 mg for 1 day) and vigabatrin (1000 mg per day for 5 days) were investigated in a double-blind placebo-controlled cross-over study in 4 patients with hyperekplexia. (nih.gov)
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  • He was diagnosed with moderate depressive episode according to ICD-10 criteria and started on oral sertraline 50 mg/d, which was gradually increased to 100 mg/d over 1 month, and oral clonazepam 0.25 mg/d. (psychiatrist.com)
  • The principal adverse effect of clonazepam is drowsiness, which occurs in about 50% of all patients when starting therapy. (pocketdrugguide.com)
  • Chemically, clonazepam is 5-(2-chlorophenyl)-1,3-dihydro-7-nitro-2H-1,4-benzodiazepin-2-one. (nih.gov)
  • Clonazepam Tablets USP, a benzodiazepine, is available as scored tablets containing 0.5 mg of clonazepam and unscored tablets containing 1 mg or 2 mg of clonazepam. (nih.gov)
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  • On May 1, status epilepticus developed and was treated with clonazepam. (cdc.gov)
  • A study of the withdrawal of clonazepam therapy in 40 epileptic children found that 19 had withdrawal symptoms of increased seizure frequency, either alone or with other symptoms but that this effect was transient. (pocketdrugguide.com)
  • In the case of epileptic children and newborns, the doctor will determine whether Clonazepam therapy is appropriate. (offshorepharmacy.us)
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  • If you take clonazepam with any of these medications and you develop any of the following symptoms, call your doctor immediately or seek emergency medical care immediately: unusual dizziness, lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness. (medlineplus.gov)
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  • Treatment may include such medications as baclofen, diazepam, tizanidine or clonazepam. (nih.gov)
  • For a review of the effects of antiepileptic therapy, including clonazepam, on cognition and mood, including the risk of suicidal ideation. (pocketdrugguide.com)
  • A breastfed newborn infant whose mother was taking clonazepam during pregnancy and lactation (dosage not stated) had serum levels that increased from about 23 mcg/L at 24 hours of age to 43 mcg/L at 96 hours of age. (nih.gov)
  • The infant's serum clonazepam level was 2.9 mcg/L at 120 hours after birth, and 1 mcg/L at day 14. (nih.gov)
  • A pooled sample of infant serum from days 2 to 4 of age contained 4.7 mcg/L of clonazepam. (nih.gov)
  • Ten of 11 breastfed infants whose mothers were taking clonazepam in dosages of 0.25 to 2 mg daily had no detectable (assay limit varied from 5 to 14 mcg/L) clonazepam or metabolites in serum. (nih.gov)
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  • At endpoint, 74% of patients receiving clonazepam 1 mg/day were free of full panic attacks, compared to 56% of placebo-treated patients. (nih.gov)
  • Maternal clonazepam occasionally causes sedation in their breastfed infants, especially when given with other central nervous system depressants. (nih.gov)
  • The authors calculated that an exclusively breastfed infant would receive a maximum of 2.5% of the maternal weight-adjusted dosage of clonazepam. (nih.gov)
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  • In these studies, clonazepam was shown to be significantly more effective than placebo in treating panic disorder on change from baseline in panic attack frequency, the Clinician's Global Impression Severity of Illness Score and the Clinician's Global Impression Improvement Score. (nih.gov)
  • Clonazepam, but not vigabatrin, reduced startle activity significantly in both paradigms. (nih.gov)
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  • 4 Although a variety of cutaneous adverse effects have been reported with clonazepam, drug-induced itch as an isolated side effect has not yet been reported. (psychiatrist.com)
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  • The difference between clonazepam and placebo in reduction from baseline in the number of full panic attacks was approximately 1 panic attack per week. (nih.gov)
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