Table of contents :

• types of action
• PNS-directed
• local anesthetics
• anti-muscle hyperactivity
• peripherally active antiemetics
• CNS-directed
• general anesthetics
• central analgesics
• anti-headache drugs
• anti-migraine drugs
• centrally active antitussive agents
• centrally active antiemetics
• anorexiants / anorectic drugs
• anti-pediatric anorexia
• anti-male and female sexual dysfunctions
• anti-CNS degenerative disorders
• psychoactive / psychotropic drugs / psychodrugs
• anxiolytics / minor tranquilizers / psycholeptics => myorelaxants/antiseizures => sedatives => hypnotics
• antipsychotics / major tranquilizers / neuroleptics / psycholeptics
• psychoanaleptics
• antidepressants / mood-elevating agents
• mood-stabilizing drugs
• anti-psychological dependence drugs
• psychotonic / nervous reconstituents
• psychostimulants
• cerumenolytics
• web resources

Types of action

• inhibition of neurotransmitter synthesis => depletion of neurotransmitter
• metabolic transformation by same pathway as precursor of transmitter => displacement of the true transmitter by false transmitters
• blockade of reuptake system at nerve terminal membrane => accumulation of neurotransmitter at receptors and depletion of neurotransmitter
• blockade of transport system of storage granule (vesicle) membrane => destruction of neutrotrasmitter by cytoplasmic enzymes and depletion from nerve terminals
• promotion of neuroexocytosis or displacement of transmitter from axonal terminal => initial mimetic action followed by depletion
• prevention of release of transmitter
• mimicry of transmitter at postsynaptic receptor
• blockade of endogenous transmitter at postsynaptic receptor
• mimicry of transmitter at presynaptic receptor
• blockade of endogenous transmitter at presynaptic receptor
• inhibition of enzymatic breakdown of transmitter

• local anesthetics induce loss of pain without loss of consciousness
• voltage-gated Na⁺ channel blockers : effectiveness ~ myelinization (drugs are lipophilic) ~ number of channels in the open configuration (drugs enter channels in the protonated form only and block them in the open configuration) ~ discharge rate ~ 1 / Ø_neuron. Administration routes : topical, infiltrations, regional IV injection, troncular (near nerves), spinal, epidural. Co-administer a vasoconstrictor (e.g. epinephrine) to slow down clearance and avoid side effects from systemic spread.

Web resources : The Virtual Library - Anesthesiology
• phentolamine mesylate / NV-101 (source : Novalar Pharmaceuticals, Inc.) : a vasodilator which acts a local dental anesthetic reversal agent
• anti-muscle hyperactivity
• s.c. / i.m. BoNT/A (Botox^®, originally Oculinum^®; source : Allergan Inc. of Irvine, Calif) is used in therapy of ...
• strabismus
• blepharospasm
• focal dystonias
• cervical dystonia causing tension headache / migraine
• laryngospasm
• writer's cramp
• hemifacial spasm
• tremors
• tics
• piriformis syndrome
• lumbalgias
• upper limb spasticity associated with stroke
• hyperhidrosis of the axilla
• wrinkles : glabellar lines associated with corrugator and/or procerus muscle activity
• achalasia
• myofascial pain syndrome
• detrusor hyperreflexia in spinal cord injury
Each vial of Botox contains 100 units of Clostridium botulinum neurotoxin A complex that is vacuum-dried to be reconstituted before use.
The purpose of the therapies is to actually produce "local" botulism of the musculature injected. If the cases of "systemic" botulism are due to Botox
injections, it may be that the material was incorrectly diluted, too large a volume of correctly diluted toxin was given, or a manufacturing error occurred. If the latter occurred, more cases may be found. Therapy must be continual since the effect of the toxin usually lasts for no more than 3 to 6 months. Side effects are rare.  A Florida woman died in 2003 after suffering an allergic reaction to Botox. But the company that makes the drug stresses its safety record -- saying just 7 people had serious side effects in the 1990s.
• BoNT/B (Myobloc^® or Neurobloc^®) was more recently licensed by the FDA for cervical dystonia.
• peripherally active antiemetics (see also centrally active antiemetics)
• GR agonists
• 5-HT₁ agonists
• k antagonists
• a₂ agonists
• SST₂ agonists
• CCK₁ antagonists
• GnRH-R agonists
• antivertiginous drugs
• cerebral CCB flunarizine is effective in the treatment of vestibular disorders. Side effects : somnolence, weight gain, and, in rare cases, extrapyramidal symptoms and depression. This putative antivertiginous property is really due to the anticalcic action of the drug and not to a more classical antagonistic effect on H₁ receptors
• vasodilators
• nicotinic acid
• b-pyridylcarbinol
• betahistine dihydrochloride (Serc^®, Betaserc^®, Vasomotal^®, Vertiserc^®, Vertin^®, Urutal^®, Agiserc^®) is an orally effective histamine-like drug. SERC® treats the underlying cause of vertigo by normalizing the flow of impulses and improving blood flow in the inner ear in the treatment of Ménière's disease and symptomatic treatment of vestibular vertigo
• nicotinyl alcohol (Roniacol^®)
• nylidrin (Arlidin^®, Arlidin Forte^®, PMS Nylidrin^®)

• general anesthetics (intravenous or inhalatory) induce loss of sensation and consciousness
• GABA_A agonists, including neurosteroids
• Gly agonists
• N_CNS antagonists
• NMDA-R antagonists
• a₂ agonists
• two-pore voltage-gated K⁺ channel activators
• syntaxin 1A-SNAP-25-synaptobrevin 1 / VAMP1 complex inhibitors
• neuromuscular blocking agents : N antagonists
Suppression of nerve cell activity, required to form connections and thrive in a baby's growing brain, leads to neuronal apoptosis.
• full-face mask : a device used in anesthesia to confine the gas to be delivered through the mask into the respiratory tract through the nose or mouth.
• needle-through-needle technique : a technique of anesthetic administration in which a narrow spinal needle is advanced through the lumen of a larger-gauge needle such as a Tuohy needle and past its tip to puncture the dura so that spinal and epidural anesthesia can be administered at the same time.
• central analgesics (vs. nociceptive pain)
• m opioid receptors agonists :
• systemic analgesic therapy (SAT)
• oral
• oral transmucosal
• parenteral
• patient-controlled analgesia (PCA)
• computer-assisted continuous infusion (CACI)
• peripheral
• rectal
• nebulizer
• transdermal
• iontophoretic
• intraspinal (epidural or intrathecal / "spinal") infusion
By combining m opioid receptors agonists with NMDA-R antagonists, tolerance is impaired and analgesia is enhanced without an increase in the dose of opioid.
1 mg i.m. of morphine equals 3 mg p.o.
Acute toxicity (resulting from clinical overdosage, accidental overdosage in addicts, or attempts at suicide) : miosis (pinpoint pupils; mydriasis when asphyxia intervenes), nausea and vomiting due to CTZ stimulation, pulmonary edema, muscular rigidity (in the chest wall => respiratory failure), catalepsy, circling, stereotypical behaviour, decreased propulsive GI tract motility, increased pressure in the biliary tract, pseudoimmunologic urticaria and asthma => anaphylactoid reactions, dizziness, mental clouding, dysphoria, urinary retention, orthostatic hypotension, respiratory depression (reduction in responsiveness of the brainstem respiratory centers to P_CO2 => apnea => respiratory arrest => cyanosis => death (greater risk if combined with general anesthetics, tranquilizers, alohol, or sedative-hypnotics)
Therapy for acute overdose : nasotracheal aspiration, ventilation, i.v. naloxone ("overshoot" phenomena : rebound tachypnea, secondary systemic arterial hypertension, tachycardia, and ventricular arrhythmias)
Chronic toxicity : GERD, constipation, immunosuppression
Treatment for chronic abuse :
• maintenance programs to treat opioid withdrawal syndrome
• stabilization with long-acting m opioid receptor agonists => not experience the ups and downs they experienced while on heroin, drug craving diminishes and may disappear, neuroendocrine rhythms eventually are restored.
• methadone : administered PO de visu, half-life = 15 hours, respiratory depression, no theratogenic effect => used in addicted pregnants and newborns. It doesn't cause mood instability, dysphoria, and craving. 80 mg for each g of heroin assumed / die. Ethanol, diphenylidantoine, phenobarbital, carbamazepine, tetracyclines, and rifampicin up-regulate methadone-catabolyzing cytochromes, while erythromycin, cimetidine, and ketoconazole down-regulate their expression.
• L-a-acetylmethadol (LAAM) / levomethadyl acetate : longer half-life (= 71-143 hours) => 60-140 mg every 2 days or 130+130+180 mg in a week. Theratogenic. Side effects : fatigue, insomnia, cough, irritability, constipation, secondary systemic arterial hypertension, bradycardia, hepatitis, exanthema, diplopia, sexual impotence.
• nor-LAAM
• dinor-LAAM
• buprenorphine : neither respiratory depression nor euphoria
• inhibitors of noradrenergic neurotransmission from the locus ceruleus (to replace loss of opioid suppression of the locus ceruleus systemm during the abstinence syndrome) alleviate many of the symptoms of opioid withdrawal,
• a_2A agonists (clonidine) cause arterial hypotension as a side effect
• I₁ agonists (lofexidine) don't cause arterial hypotension
• activation of the endogenous opioid system with acupuncture and several methods of CNS activation utilizing transcutaneous electrical stimulation.
• detoxification
• gradually decreasing doses of m opioid receptor agonists to prevent withdrawal symptoms : -5 mg / days for 3 days (from 100 to 20 mg / day) => - 2 mg / day till the end (usually therapy lasts for > 1 year). weekly control of opiate catabolytes in urine. If no catabolytes are found for 3 weeks, domiciliary therapy can be evaluated for Sundays => week-ends => no longer than a week. Adjuvant therapy :
• anxiolytics
• antiemetics
• rapid opiate detoxification (ROD)
• Waismann Method^sm of Accelerated Neuro-Regulation - formerly known as rapid detox : patients have a greater than 64% chance of maintaining an opiate-free life based on 1-year research.
• ultra-rapid opiate detoxification (UROD) lasts 24 hours and consists of ...
• 12 hours : guanfacine (to decrease blood pressure and heart rate prior, during and shortly after detoxification)
• 3 hours :
• naltrexone (p.o., to precipitate withdrawal)
• drugs to prevent peripheral side effects from opiate antagonists :
• antiemetics (ondansetron or metoclopramide)
• antidiarrhoics (loperamide)
• general anaesthetic (midazolam, IV for 4 hours) : the patient is unconscious and thus not experiencing withdrawal discomfort.
• naloxone (i.v., to test detoxification states about 4h after sleep induction),
• at awakening : guanfacine (continued administration in decreasing doses when patient begins to wake up from sedation)
• day after : naltrexone (p.o.) (for 3 months). A depot formulation of naltrexone which provides 30 days of medication after a single injection is in clinical trials.
It removes physical dependence but not psychological dependence.
• CB₁ agonists
• CB₂ agonists are promising candidates for the treatment of pain. CB₂ receptor activation inhibits acute, inflammatory, and neuropathic pain responses but does not cause CNS effects, consistent with the lack of CB₂ receptors in the normal CNS. Activation stimulates release from keratinocytes of the endogenous opioid b-endorphin, which then acts at opioid receptors on primary afferent neurons to inhibit nociception^ref.
• NK₁ antagonists works in animals but not in humans
• RET agonists
• adenylate cyclase inhibitors block coupling of NMDA-R to cAMP
• GABA_B agonists or GABA transaminase inhibitors in rostral agranular insular cortex (RAIC)^ref (both the anterior cingulate cortex and insular cortex receive pain messages and are thought to process motor and emotional responses to pain)
• anti-headache
• COX-1 inhibitors
• anti-migraine
• 5-HT_1D antagonists (triptans (p.o.; s.c. sumatriptan is the most effective))
• 5-HT_{2A / 2} antagonists
• 5-HT_{2C / 1C} antagonists
• anticonvulsant
• CGRP receptor antagonists are effective in treating migraine attacks up to 6 hours after onset^ref
• centrally active antitussive agents (see also peripherally active antitussive agents)
• opiate agonists
• hydroxycodone / dihydrocodeinone
• hydroxymorphone
• levorphanol
• dextromethorphan (DXM) hydrobromide
• levopropoxyphene napsylate
• noscapine, a non-addictive derivative of opium, has been used worldwide since the 1950's as an anti-cough medication. Noscapine was originally proposed as an anti-cancer agent in the early 1960's. However major studies of its broad anti-cancer effects were only done in recent years.
• H₁ antagonist
• diphenhydramine
• carbetapentane (Histatuss Pediatric^® in combination with chlorpheniramine, ephedrine, and phenylephrine)
• caramiphen (Parpanit^®, Taoryl^®)
• chlophedianol (Carafen Cough Syrup^®; Carafen Cough Tablets^®, Parpanit^®)
• glaucine (Glauvent^®)
• pholcodine / 3-O-(2-morpholinoethyl)morphine
• benzonatate (Tessalon^®)
• centrally active antiemetics (see also peripherally active antiemetics) (vs. nausea and vomiting)
• sedative H₁ antagonists
• 5-HT₃ antagonists

Side effects : headache (9%) and constipation (5%)
• D₂ antagonists
• M₁ antagonists
• NK1 antagonists
• CB₁ agonists
• symptomatic : anxiolytics
• anorexiants / appetite-suppressants / anorectic drugs (vs. obesity)
• anorexiant amphetamines
• diethylpropion (2-(diethylamino)propiophenone) hydrochloride (Tenuate^®, Dospan^®)
• anti-pediatric anorexia
• sedative H₁ antagonists
• anti-male and female sexual dysfunctions
• MC1R agonists (nasally administered peptides)
• anti-CNS neurodegenerative disorders
• anti-Parkinson's disease (PD)
• direct and indirect dopaminergic agonists
• dopamine doesn't cross the blood-brain barrier (BBB) and is used as a peripheral vasoconstrictor
• dopamine precursors
• levodopa / L-3,4-dihydroxyphenylalanine (L-DOPA^®, Larodopa^®, Dopar^®; Sinemet^® in combination with carbidopa) has t_1/2 = 100' (4-5 doses a day).
Side effects : in early PD, the duration of the beneficial effects of levodopa may exceed the plasma lifetime of the drug, suggesting that the nigrostriatal dopamione system retains some capacity to store and release dopamine. A principal limitation of the long-term use (3 years or so) of levodopa is that, with time, this apparent "buffering" capacity is lost, and the patient's motor state may fluctuate dramatically with each dose of levodopa.
• wearing off phenomenon : each dose of levodopa effectively improves mobility for a period of time, perhaps 1 to 2 hours, but rigidity and akinesia rapidly return at the end of the dosing interval. Increasing the dose and frequency of administration can improve this situation, but this often is limited by development of dyskinesias, observed most often when the plasma levodopa concentration is high, although, in some individuals, dyskinesias or dystonia may be triggered when the level is rising or falling. These movements can be uncomfortable and disabling as the rigidity and akinesia of PD. In the later stages of PD, patients may fluctuate rapidly between being "off", having no beneficial effects from their medications, and being "on" but with disabling dyskinesias, a situation called the on-off phenomenon
• psychoses, treated with atypical antipsychotics (conventional antipsychotics worsen parkinsonism)
Contraindications :
• MAO-A inhibitors
• vitamin B₆
Associations with :
• peripherally acting DOPA decarboxylase inhibitors (benserazide and carbiDOPA) : othwerwise peripherally produced dopamine would cross the blood-brain barrier on ly by 1% and would affect peripheral receptors causing nausea and vomiting
• peripherally acting COMT inhibitors
• centrally acting MAO-B inhibitors : delay disease progression by a few months
• centrally acting D₁ agonists
• centrally acting D₂ agonists (rapirinol, pramipexol, catergoline and lisuride)

Pergolide has t_1/2 = 20 hr, cavergoline = 60 hrs => no fluctuations in plasma levels, but poor potency (only s.c. apomorphine infusion (t_1/2 = 1 hour) is as effective as L-DOPA)
Side effects :
• orthostatic systemic arterial hypotension
• nausea and vomiting (only at the begininning of the therapy as peripheral dopamine receptors undergo tolerance rapidly : can be prevented with peripherally acting D₂ antagonists (e.g. domperidone))
• sleepiness
• psychoses, treated with atypical antipsychotics (conventional antipsychotics worsen parkinsonism)
Usually in patients with age < 60 years centrally acting D₂ agonists are used before L-DOPA, while in elderlies the contrary is practiced
• centrally acting cholinergic agonists
• M₁ antagonists
• M₂ antagonists
• M₃antagonists
• M₄ antagonists
• M₅ antagonists
• centrally acting NMDA-R antagonists (amantadine)
• centrally acting A_2A antagonists
• R.O.S. scavengers : vitamin E and coenzyme Q₁₀, iron chelators, zinc chelators
• safinamide (SAF) ((S)-(+)-2-(4-(3-fluorobenzyloxy) benzylamino)propanamide) was initially synthetized by Farmitalia Carlo Erba (Italy). Following initial anticonvulsant screening, safinamide was selected for its potency, broad spectrum of action, and good safety margin. Pharmacodynamic properties probably relevant to its antiepileptic activity are use- and frequency-dependent block of voltage sensitive Na+ channels, block of Ca++ channels, and glutamate release inhibition. Possibly contributing mechanism are also selective and reversible monoamide oxidase B inhibition and dopamine and noradrenaline uptake inhibition. The high selectivity for the sigma-1 receptor site does not entail psychotomimetic or behavioral changes. In several experimental in vitro and in vivo conditions, SAF exerts neurorescuing and neuroprotectant effects. Safinamide is water soluble and suitable for 1 times a day oral administration in humans. In a pilot phase II study in 38 refractory epilepsy patients affected by multiple types of seizures, 41% of subjects obtained > or =50% seizure reduction during a 12-week escalating dose up to 300 mg 1 times day compared with perspective baseline. Safinamide is being developed in phase III for treatment of Parkinson's disease, whereas the development in epilepsy relates to the industrial strategy of the company^ref.
• anti-Alzheimer's disease (AD)
• therapy of cognitive disorder
• direct and indirect cholinergic agonists
• choline chloride
• phosphatidylcholine / lecithin
• AChE inhibitors (rivastigmine, donepezil, and galantamine)
• both sage and lemon balm have previously been shown to improve memory and/or reduce agitation in Alzheimer’s patients : 4 compounds isolated from an extract of sage root are AChE inhibitors.
• M₁ antagonists
• M₂ antagonists
• M₃antagonists
• M₄ antagonists
• M₅ antagonists
• NMDA-R antagonists : patients with moderate to severe AD who switched to memantine treatment (20 mg daily) for 52 weeks from their previous placebo therapy experienced a significant benefit in all main efficacy assessments (functional, global, and cognitive) relative to their mean rate of decline with placebo treatment during the double-blind period (P<.05). The completion rate for the extension phase of the study was high (78%) and the favorable adverse event profile for memantine therapy was similar to that seen in the double-blind study^ref
• b-secretase inhibitors, i.e. b-site APP-cleaving enzyme (BACE) and BACE2 inhibitors
• g-secretase inhibitors
• Zn chelating agents
• HMG-CoA inhibitors can reduce the risk of AD by reducing the production of Ab: indeed the b-amyloid precursor protein (APP) / protease nexin-II contains a sphingolipid binding domain.
• GABA_B antagonists^ref
• NSAIDs : some (e.g. indomethacin), but not all, can reduce the risk of AD due to their ability to reduce Ab₄₂. Ab₄₂-lowering NSAIDs specifically affect the proximity between APP and presenilin 1 (PS1) and alter presenilin 1 conformation both in vitro and in vivo, suggesting a novel allosteric mechanism of action^ref
• Y-27632, a selective NSAID Rock inhibitor, can reduce Ab₄₂
• plaque busters : as it is believed that abnormal binding of a metal ligand in the metal-binding sites of the normal, soluble proteins is a major factor in the pathogenesis and continued pathology of the resulting diseases, chelators which cross the blood-brain barrier (BBB), have potential for therapy or as a recurring prophylactic treatment when administered at low doses
• picolinic acid blocks tangle formation in vitro and reverses it as well better than traditional chelators
• selective amyloid b₄₂ (Ab₄₂) lowering agents (SALAs) :
• MPC-7869 / R-flurbiprofen (Flurizan™; source : Myriad Genetics, Inc.). The Phase 2 study showed that patients with mild Alzheimer's disease who received the 800 mg twice-daily dose of flurizan achieved between 34% and 45% slowing in decline on the 3 primary endpoints (activities of daily living, overall function and cognitive ability). A > 20% slowing in decline is generally regarded as clinically significant^ref.
• 800 mg tarenflurbil twice per day was well tolerated for up to 24 months of treatment, with evidence of a dose-related effect on measures of daily activities and global function in patients with mild AD^ref
• NC-531 (Alzhemed™; source : Neurochem) is a sulfated glycosaminoglycan mimetic that inhibits amyloid plaque formation. Phase I clinical trials were ongoing in November 1999, and by October 2002 phase II trials were underway^ref.
• cyclohexanehexol stereoisomers : when given orally to a transgenic mouse model of AD, inhibit aggregation of amyloid b peptide (Ab) into high-molecular-weight oligomers in the brain and ameliorate several AD–like phenotypes in these mice, including impaired cognition, altered synaptic physiology, cerebral A pathology and accelerated mortality. These therapeutic effects, which occur regardless of whether the compounds are given before or well after the onset of the AD–like phenotype, support the idea that the accumulation of Ab oligomers has a central role in the pathogenesis of AD^ref
• amyloid-b antagonists : tramiprosate (Alzhemed^®, Cerebril^®; source : Neurochem, Inc.) is a glycosaminoglycan (GAG) mimetic designed to interfere with the actions of Ab early in the cascade of amyloidogenic events, also for the prevention of hemorrhagic stroke caused by cerebral amyloid angiopathy
• testosterone replacement therapy improved overall quality of life in patients with AD while having minimal effects on cognition^ref
• therapy of behavioral disorder
• atypical antipsychotics (clozapine, risperidone, olanzapine, quetiapine, ziprasidone, sertindole). Haloperidol may cause cholinergic impairment and parkinsonism in elderlies. Antipsychotic drugs do not seem to increase the risk of stroke or other adverse cerebrovascular events in agitated or psychotic people with AD
• 4% of elderlies with bipolar disorder taking lithium have Alzheimer's disease, compared with 21% of patients who are not taking the drug. When mice with NFT are treated with lithium for 5 months, brain tau levels decrease dramatically (cutting also the number of amyloid plaques) as inhibition of GSK-3 prevents phosphorylation-induced tangling
• anti-Huntington's disease (HD)
• NMDA-R antagonists
• symptomatic treatment
• antipsychotics (against dyskinesias)
• antidepressants
• anticonvulsants
• dopamine-depleting agents
• tetrabenazine
• reserpine
• anti-amyotrophic lateral sclerosis (ALS) / Lou Gehrig's disease
• NMDA-R antagonists (riluzole) improve survival from 3 to 6 months.
• kainate antagonists
• symptomatic therapy
• GABA_A antagonists
• GABA_B agonists
• a₂ agonists
• glatiramer acetate (GA)
• CNTF
• N-acetyl-L-aspartyl-L-glutamate (NAAG) peptidase inhibitors holds promise for a wide variety of diseases that involve glutamatergic transmission, and has implications for the diagnosis and therapy of cancer. This new class of compounds, of which at least one has entered clinical trials and proven to be well tolerated, has demonstrated efficacy in experimental models of pain, schizophrenia, amyotrophic lateral sclerosis, traumatic brain injury and, when appropriately functionalized, can image prostate cancer^ref
• psychotropic drugs / psychoactive drugs / psychodrugs
• psycholeptics
• anti-anxiety / anxiolytics / minor tranquilizers / psycholeptics (vs.anxiety disorders) => myorelaxants (vs. stroke, MS, ALS, spinal cord injuries, tetanus,strychnine poisoning, dystonias) => antiseizures (vs.seizures) => sedatives (vs. insomnia) => hypnotics / hypnogenics
• ethanol
• p.o. or i.v. GABA_A agonists
• thiocolchicoside (TCC) (Decontril^®, Miotens^®, Muscoril^®, Sciomir^®, Teraside^®, Tioside^®) i.m., a semi-synthetic derivative of the naturally occurring compound colchicoside,

Side effects : tonic-clonic seizures^ref
Contraindications : pregnancy, hepatopathies, elderly, cigarette smoking, platelet antiaggregants, and oral contraceptives
Side effects : excessive sedation, decrease of psychomotory performances, hang over, ataxia, paradoxal hyperactivity in babies
Tolerance to hypnotic effect occurs before than tolerance to anxiolytic effect.
Acute intoxication : fatigue, sleepiness, ataxia, systemic arterial hypotension, hypothermy, cognitive impairment (anterograde amnesia, attention deficit : they are used as experimental model of dementia), dysarthria.
Therapy : flumazenil and psychostimulants
Addiction risk relates on dose, lasting of treatment and patient's personality.
Symptoms of abstension crises may vary from anxiety, insomnia, irritability, nausea, headache, palpitations, tremors and sweats, to muscle pain, vomiting, lowering of sensitive thresholds, up to seizures and depersonalization.
• sedative H₁ antagonists

Side effects : paradoxical effect at high doses (euphoria => seizures), ataxia, diplopia, anorexia, nausea, vomiting, constipation or diarrhoea (reduced if administered during meals), partially parasympatholytics.
• K_Ca inhibitors
• voltage-gated KCNQ2-5 / K_V7.2-5 channel activators
• GABA_B agonists
• RYR1 antagonists
• bromide : any binary compound of bromine in which the bromine carries a negative charge (Br^–); specifically a salt (or organic ester) of hydrobromic acid (H⁺Br^–). Bromides produce depression of the central nervous system, and were once widely used for their sedative effect. Because overdosage (bromism) causes serious mental disturbances they are now seldom used, except occasionally in grand mal seizures
• cyclobenzaprine hydrochloride (Flexiban^®)
• tizanidine (TZ) (Mionidin^®, Sirdalud^®)
• pridinol mesylate (Lyseen^®)
• tolperisone hydrochloride (Mydocalm^®)
• antipsychotics / major tranquilizers / neuroleptics / psycholeptics (vs. psychoses and mania)
• lipophilic D₂ antagonists (low affinity)

Side effects :
• parasympatholytic (xerostomia, intraocular hypertension, arrhythmias, coronary artery diseases due to direct cardiotoxicity, secondary systemic arterial hypertension, constipation, urinary retention)
• extrapyramidal side effects (EPS) (expecially from classical neuroleptics, which are still used as more effective against acute psychoses ; thioridazine has poor extrapyramidal side effects as it is also a M₁ antagonist and so compensates dopaminergic block)
• reversible
• acute dystonia since first dose (neurodysleptic crises), expecially from metoclopramide : acute childhood encephalitis => rhythmic contraction of axial muscles; oculogirus crises ; neck extension ; glossoprotrusion ; opisthotonos.
• chronic
• apendolarim of upper limbs
• akathisia or more rarely hypertonic (not tremorigenous) akinesia
• neuroleptic malignant syndrome
• parkinsonism("neuroleptic impregnation").

Therapy : M₁ antagonists (neither D₂ agonists nor dopamine precursors can be used as they would worse psychosis !)
• perioral tremor ("rabbit syndrome")
• irreversible tardive dyskinesia (TD) stopping when sleeping => increased risk of suicide
• oral-facial dyskinesia ("sweet suckling") : this is due to excessive neurotrophin production by blocked dopaminergic neurons, which in turn leads to hyperinnervation of buccal muscles.
• widespread choreoathetosis or tardive dystonia
• sedation
• systemic arterial hypotension
• hyperprolactinemia (simulating a prolactinoma, hence contraindicated for females in fertile age, although no increased risk of prolactinoma or mammary carcinoma has been found)
• rash
• medullary aplasia
• cholestasis
• 5-HT_2A antagonists (high affinity) / atypical antipsychotics

 Side effects of clozapine and olanzapine :
• medullary aplasia (CBC each month)
• orthostatic systemic arterial hypotension
• decreased seizure threshold
• arrhythmias (tachycardia, ..)
• worsen OCD
• sialorrhoea
• insulin resistance^ref => obesity
• D₁ antagonists (?)
• D₃ agonists
• D₄ antagonists
• psychoanaleptics / analeptics :  exerting a stimulating effect upon the mind.
• 5-OH-Trp
• S-AdoMet
• antidepressants / mood-elevating agents / stimulants of mood (vs. depressions)
• thymoleptic / antidepressant : any drug that favorably modifies mood in serious affective disorders such as depression or mania; the main categories of thymoleptics include the tricyclics antidepressants, monoamine oxidase inhibitors, and lithium compounds
• thymeretics
• ethanol
• MAO-A inhibitors (IMAO) : due to irreversible actions of clinically used IMAO (not RIMA), up to 2 weeks may be required to regenerate fresh MAO enzyme and restore amine metabolism to normal after discontinuation of the drugs. Effective also against OCD and panic attacks.

Contraindications : assumption of food containing indirect sympathomimetic amines (e.g. tyramine in seasoned cheeses ("cheese effect"), red wines, smoked food (smoked ham, kippers, ...)), amphetamines or tricyclic antidepressants may cause secondary systemic arterial hypertension (not with RIMA).
Side effects from hydrazines : peripheral neuropathies, medullary aplasia, centrolobular hepatitis, weight gain, sexual dysfunction, edema.
• tricyclic antidepressants (TCA) : any of group of antidepressant drugs that contain 3 fused rings in their chemical structure and that potentiate the action of catecholamines; the tricyclic antidepressants include a number of compounds, which may be grouped into 4 classes on the basis of chemical structure:
• dibenzazepines
• dibenzocycloheptadienes
• dibenzoxazepines
• dibenzoxepines
Side effects :
• xerostomia
• constipation
• increased appetite
• hypertonia of detrusor muscle => prostatitis
• urinary retention in patients with BPH
• cardiac alterations (arrhtyhmias and dilated cardiomyopathy)
• noradrenaline reuptake inhibitors (NRI) / noradrenaline reuptake inhibitor (NARI / NaRI) : disinhibiting action
• selective noradrenalin reuptake inhibitors (SNRI)

Side effects : secondary systemic arterial hypertension
• selective serotonin reuptake inhibitors (SSRI) : sedative action. Only fluoxetine has been approved by the FDA to treat childhood depression : however, physicians regularly prescribe other medications 'off label' to treat depressed children. Almost half of patients with a unipolar and non-psychotic major depression will not respond to initial SSRI treatment. Patients who did not respond to SSRI treatment are significantly more depressed at baseline

Side effects :
• throat dryness => dry cough
• depression of libido
• increased craving for carbohydrates due to inhibition of 5-HT_2C => weight gain
• headache
• nausea and vomiting => weight loss
• diarrhea
• transaminitis
• sleepiness
• insomnia
• irritability
• hyperhidrosis
• suicide
• adult suicides linked to popular antidepressant^ref
• 2-3% of children taking SSRIs in controlled clinical trials experienced suicidal thoughts and behaviours because of the drugs. The MHRA has issued warnings about the risk of self harm and suicidal thoughts in young people taking the drugs^ref and the FDA in the USA has also heard reports of similar concerns^ref. FDA wants drug companies to post black-box warnings prominently in any television or magazine advertisements for their products and antidepressants should also be sold with a guide that tells parents to monitor children on the drugs for suicidal tendencies. Given the concern about the use of SSRIs by children and adolescents, it is important for doctors to monitor closely young adults up to the age of 30 starting or stopping the treatment^ref.
• little information is available on the frequency of SSRI treatment during pregnancy^ref : approximately 4 million live births occur in the USA each year, and about 92,000 of these infants are prenatally exposed to SSRIs^ref
• children or unborn babies exposed to fluoxetine could suffer from abnormal emotional development, animal studies suggest. Rats given the drug for the first few weeks of life perform poorly on tasks designed to test their confidence and ability to deal with stress (by placing them in a cross-shaped maze raised above the floor, a test that measures the willingness of the animals to explore an unusual environment). Adult rats dosed with Prozac early in life were less interested in venturing far from their starting point and spent less time moving around. Animal researchers take this behaviour as evidence of abnormal emotional development. Related tests revealed that rats given Prozac are also less willing to take risks to earn rewards such as food and take longer to escape unpleasant environments, a sign that they deal poorly with stress. Many pregnant women demand this treatment. They may otherwise have suicidal thoughts or a desire to kill their infants after birth. The rats were given a dose comparable to that which humans receive. The animals received the drugs a few days after birth, the stage of their development equivalent to the final third of a human pregnancy. The theory is backed up by studies of rats that have been genetically engineered to lack the molecules that recycle serotonin^ref. These rats have fewer serotonin-producing cells in the brainstem, an area that controls basic functions such as breathing and that connects widely to other areas of the brain. The serotonin cells that remain also fire less frequently than normal. Such rats exhibit behaviour similar to those in Gingrich's study.
• the risk of heart defects in babies whose mothers had taken Paxil early in pregnancy was about 2%, compared to a 1% risk in the whole population. In another study, the risk of heart defects in babies whose mothers had taken Paxil in the first 3 months of pregnancy was 1.5%, compared to 1% in babies whose mothers had taken other antidepressants in the first 3 months of pregnancy. Food and Drug Administration recently published a public health advisory concerning increased rates of congenital defects (and, specifically, heart defects) after the use of the SSRI paroxetine early in pregnancy^ref
• neonatal abstinence syndrome, a condition found in infants born with drug dependency^ref
• Kudos to Eliot Spitzer, New York state's attorney general, for championing a call for transparency in clinical trial results. In June 2004, Spitzer sued GlaxoSmithKline (GSK) for concealing negative data on the safety of its antidepressant Paxil in children. Related lawsuits cropped up elsewhere in the US and Europe. In August, GSK agreed to release the data on its website. Combined with the push for clinical trial registries from patient groups, governments and medical journal editors, GSK's settlement ushered in a new era of accountability in the pharmaceutical industry.
• persistent pulmonary hypertension of the newborn (PPHN) when used late in pregnancy^ref
• serotonin2-antagonists/serotonin reuptake inhibitors (SARI) / dual serotonergic antidepressants (DSA)

Side effects : priapism with tradozone
• selective serotonin noradrenalin reuptake inhibitors (SSNRI) / serotonin noradrenergic reuptake inhibitors (SNaRIs)
• noradrenergic and specific serotonergic antidepressants (NaSSA)
• noradrenaline and dopamine reuptake inhibitors (NDRI)

Side effects : active catabolites, activity unpredictable by serum levels, decreased catabolism of other drugs catabolized by CYP2D6 (35% of all current drugs), cholestasis, anti-H, anti-D (parkinsonism), parasympatholytic (xerostomia, intraocular hypertension, OCD, coronary artery diseases due to direct cardiotoxicity, secondary systemic arterial hypertension, constipation, urinary retention)
• ketamine may be the fastest-acting antidepressant ever tested. 71% f of 17 people with major depression who failed to respond to treatment with standard antidepressant drugs or more drastic methods, such as electroshock therapy, felt better the day after taking ketamine, and 35% still felt better a week later. None improved when dosed with a placebo^ref. Most striking was that some patients felt better < 2 hours after taking ketamine. Currently approved drugs can take weeks to remedy depression. Large doses of ketamine can cause brain damage in rodents, and its long-term health effects have not been studied in people. Scientists are currently testing a wide range of recreationally used-and-abused drugs, including ecstasy (MDMA) and psilocybin, the active ingredient of magic mushrooms, as potential therapeutics. Ketamine, invented in 1962 as an anaesthetic, is chemically related to phencyclidine (PCP), also known as angel dust. Both induce hallucinations and out-of-body experiences, hence their use as illegal psychedelics. Ketamine has milder psychotic effects than PCP and is therefore also used as a legal anesthetic and horse tranquillizer. Scientists are studying whether it can be used to treat alcoholism and chronic pain, as well as depression^ref. Ketamine targets NMDA receptor. Existing antidepressants target brain chemicals such as serotonin, but there is growing evidence that these drugs eventually affect NMDA receptors. Ketamine may work so quickly because it takes a short-cut straight to this part of the brain. The psychotic effects of ketamine, such as euphoria, wore off before the antidepressant effects kicked in, suggesting that the drug's psychotic and antidepressant effects are separate. One surprising aspect is that other drugs that induce euphoria, such as cocaine, usually lead to a depressive crash once the high wears off. Zarate's group is looking for substances with some of the chemical properties of ketamine, such as the ability to target NMDA, without the psychedelic effects. Other scientists have developed drugs that can be taken with ketamine to damp its side effects. Giving these drugs together might help patients feel better without getting high.
Tetracyclic antidepressants include both NaSSA and RIMA
Inhibition of the target proteins occurs rapidly, but clinical benefits are usually delayed for 2-4 weeks. The delay may reflect secondary adaptations, including downregulation of a₂- and b-adrenergic receptors. In the meanwhile anxiolytics can be co-administered.
Side effects :
• serotonin syndrome (SS) : a potentially fatal iatrogenic complication that occurs following concurrent administration of 2 or more serotonergic agents (e.g. extended-release venlafaxine and mirtazapine (agents that minimally inhibit the CYP2D6 system, which is responsible for tramadol metabolism; also mirtazepine monotherapy^ref) for depression and tramadol (an atypical analgesic that acts in part as a reuptake inhibitor of serotonin and norepinephrine) for chronic pain) consisting of sudden onset of 3 or more symptoms involving altered mental status, autonomic dysfunction, and neuromuscular abnormalities, resolved over a period of 36 hours after withdrawal. SS is a potentially life-threatening adverse drug reaction that results from therapeutic drug use, intentional self-poisoning, or inadvertent interactions between drugs. Three features of the serotonin syndrome are critical to an understanding of the disorder. First, the serotonin syndrome is not an idiopathic drug reaction; it is a predictable consequence of excess serotonergic agonism of central nervous system (CNS) receptors and peripheral serotonergic receptors. Second, excess serotonin produces a spectrum of clinical findings. Third, clinical manifestations of the serotonin syndrome range from barely perceptible to lethal^ref.
• cancer : possible effect of TCA and tetracyclic antidepressants on non-Hodgkin's lymphoma^ref. A modest association between 'ever' use of AD and breast cancer was found using the most parsimonious multivariate model. OR estimates did not change, but CI were widened and statistical significance lost, after adjustment for factors associated with breast cancer risk^ref. Preclinical studies found evidence for both tumor promotion and suppression, though the majority of studies predominantly examined TCA, with 1 report suggesting that TCAs with a nitrogen atom in the central ring are genotoxic. Of 13 clinical studies, 3 found a significant increase, 4 noted a trend increase, and 6 found no increase in risk for cancer with antidepressant (mostly TCA) use^ref.
• mood-stabilizing drugs are used to treat bipolar disorder (BPD)
• lithium carbonate (Li₂CO₃) or citrate (Eskalith^®, Lithobid^®, Carbolith^®, Carbolithium^®, Contemnol^®, Duralith^®, Hypnorex^®, Lentolith^®, Liskonum^®, Litarex^®, Lithane^®, Lithicarb^®, Lithizine^®, Maniprex^®, Milithin^®, Neurolepsin^®, Neurolithium^®, Phasal^®, Quilonorm^®, Teralithe^®) (at 0.5-0.8 mEq / L : 80% efficacy) acts as ..
• inducer of neurotensin expression in catecholaminergic neurons
• BPNT1 inhibitor
• inositole phosphate phosphatase inhibitor
• GSK-3b inhibitor. Phosphate molecules then attach to GSK-3, deactivating the enzyme further12. In turn, this affects the expression of the various genes influenced by GSK-3 levels. A month's treatment boosts the volume of total grey matter by an average of 3%. The drug may do this by prompting the production of new neurons, a process that some researchers believe involves GSK-3 : Li stimulates neural stem cells (NSC) in culture, causing them to multiply faster. But lithium boosts levels of N-acetyl aspartate, a marker for healthy cells in grey matter. This suggests that the drug could be protecting cells in patients with BPD, instead of, or as well as, prompting the growth of new neurons.
Biphasic clearance with fast (4-6 hours) and slow phases (monitor blood level during the latter one).
Contraindications : pregnancy
Side effects
• anticonvulsant agents / anti-epileptic drugs (AED) (p.o.) (vs. seizures) work by increasing GABAergic neurotransmission and decreasing glutamatergic neurotrasmission. Carbamazepine and valproate are teratogenic and should not be used in pregnants.
• GABA_A agonists (phenobarbital)
• indirect GABA agonists
• GABA transaminase inhibitors
• succinate semialdehyde dehydrogenase (SSAD) inhibitors
• GAT-1 inhibitors
• voltage-gated Na⁺ channel blockers (therapeutic range for carbamazepine is 4-12 mg/mL, obtained with 10-20 mg/kg/die in 3-4 doses)
• voltage-gated T-type Ca²⁺ channel
• voltage-gated KCNQ2-5 / K_V7.2-5 channel activators : also used for neuropathic pain, hyperalgesia and allodynia, and anxiety : therapeutic dose range (600-1200 mg/day). No tolerance, dependence or withdrawal potential has been reported, although adverse effects can include mild dizziness, headache, nausea and somnolence. Thus, retigabine may prove to be useful in the treatment of a diverse range of disease states in which neuronal hyperexcitability is a common underlying factor^ref.
• unknown mechanism blockers (CCB)
• felbamate (Felbatol^®)
• levetiracetam (Keppra^®)
AEDs are commonly prescribed for nonepileptic conditions, including migraine headache, chronic neuropathic pain, mood disorders, schizophrenia and various neuromuscular syndromes. In many of these conditions, as in epilepsy, the drugs act by modifying the excitability of nerve (or muscle) through effects on voltage-gated sodium and calcium channels or by promoting inhibition mediated by GABA_A receptors. In neuropathic pain, chronic nerve injury is associated with the redistribution and altered subunit compositions of sodium and calcium channels that predispose neurons in sensory pathways to fire spontaneously or at inappropriately high frequencies, often from ectopic sites. AEDs may counteract this abnormal activity by selectively affecting pain-specific firing; for example, many AEDs suppress high-frequency action potentials by blocking voltage-activated sodium channels in a use-dependent fashion. Alternatively, AEDs may specifically target pathological channels; for example, gabapentin is a ligand of a2d voltage-activated calcium channel subunits that are overexpressed in sensory neurons after nerve injury. Emerging evidence suggests that effects on signaling pathways that regulate neuronal plasticity and survival may be a factor in the delayed clinical efficacy of AEDs in some neuropsychiatric conditions, including bipolar affective disorder^ref.
Side effects :
• lamotrigine has been associated with labiopalatoschisis
• suppression of nerve cell activity, required to form connections and thrive in a baby's growing brain, leads to neuronal apoptosis. Experiments on immature rats' brains suggest that treating epileptic children with benzodiazepine drugs could do more harm than good. The neurotransmitters unlocked by these drugs cause changes in brain chemistry that actually promote epileptic activity. Anticonvulsant benzodiazepines are a last-ditch treatment used to stop seizures in both infants and adults. Some medical experts think that the electrical activity associated with seizures can change brain networks, making them more susceptible to future epileptic activity. Benzodiazepine drugs enhance the action of GABA in the immature hippocampus removed from baby rats, which triggers rapid electrical signalling in the immature hippocampus - a hallmark of epileptic seizures. Conversely, GABA_A antagonists seemed to prevent repeated seizures in the rats' brains. About a third of the 2.7 million epileptics in the USA are 17 or younger : a high-fat, low-carbohydrate diet reduces seizures in children with intractable epilepsy. 60-70% of kids with epilepsy don't have effective treatment options. Although benzodiazepine treatment is relatively rare, medics should still look more closely at the use of drugs that enhance GABA signalling : too much GABA signalling in the very young can make chloride ions build up in immature neurons, predisposing them to further epilepsy. The adult brain is probably very different : there, GABA inhibits the fast electrical signalling associated with adult epilepsy. This may be connected with changes in the way chloride ions are transported in and out of neurons as the brain grows older. Doctors should also investigate whether pregnant women taking benzodiazepines could be predisposing their children to epilepsy^ref
• several cutaneous and hematological adverse reactions have been observed during carbamazepine therapy. The various cutaneous eruptions caused by carbamazepine include morbilliform eruptions, urticaria, erythroderma, purpura, erythema multiforme,  Stevens-Johnson syndrome, toxic epidermal necrolysis, drug induced lupus, and photosensitivity. Various hematological side effects of carbamazepine include leukocytosis, persistent leucopenia, eosinophilia, agranulocytosis, aplastic anemia, and thrombocytopenia. The incidence of hematological reactions to carbamazepine has been estimated to range between 1:10,800 to 1:38,000 per year
• anti-psychological dependence drugs
• DAT inhibitors : a form of SLC6A3 and a variant of D₃appear to ease the difficulty of kicking the habit of tobacco smoking
• D₃ antagonists or partial agonists
• mecamylamine has been used since the 1950s to combat high blood pressure. But the drug also affects the brain - it reduces the release of a pleasure chemical called dopamine, which dulls the addictive effects and cravings associated with drugs such as nicotine and alcohol.
• psychotonic / nervous reconstituents
• psychostimulants / strimulants of alertness : they act by ...
• activating excitatory circuits : indirect orthosympathomimetics
• psychomotor drugs : pertaining to motor effects of cerebral or psychic activity.
• nootropic drugs : promoting the enhancement of cognition and memory and the facilitation of learning
• amphetamines
• ephedrine. Some athletes have advocated the use of ephedra-containing dietary supplements as performance-enhancing agents. On December 31, 2003, federal officials announced plans to ban ephedra immediately. Health and Human Services Secretary Tommy Thompson told reporters, "The time to stop using these products is now." This action followed several high-profile catastrophic outcomes linked to ephedra products, including the death of 23-year-old Baltimore Orioles pitcher Steve Bechler. Published studies reported that sales of ephedra-containing supplements represented < 1% of all dietary-supplement sales but that these products accounted for 64% of the serious adverse reactions to supplements reported to the Centers for Disease Control and Prevention^ref. Unfortunately, in April 2005, a federal court in Utah struck down the federal ban on ephedra. Many companies that make these products are located in Utah
• cocaine
• pemoline
• adrafinil (Olmifon^®)
• modafinil (Modiodal^®, Provigil^®, Alertec^®, Modiodal^®)
• inhibiting inhibitory circuits
• purinergic receptors antagonists
• GABA_A antagonists
• Gly receptor antagonists
• pipradol (Meratran^®)
• centrophenoxine (Cerutil^®, Helfergin^®, Lucidril^®)
• nikethamide (Coramine^®)
• doxapram (Dopram^®, Stimulexin^®)
• ethamivan (Emivan^®)
• pentylenetetrazol (Metrazol^®)
• bemegride (Megimide^®)
• mefexamide (Timodyne^®, Perneuron^®)
Therapeutic indications :
• for CNS diseases
• apnea neonatorum premature newborn
• hypersomnias
• Pickwick's disease
• lethargy
• narcolepsy
• ADHD
• for diseases not involving CNS
• obesity
Alertness drug arouses fears about 'lifestyle' misuse : 'Brain booster' found to reverse effects of sleep deprivation^ref
Dose-dependent side effects (related to individual sensitivity, environment (noises, temperature) and interaction with other drugs or current diseases) :
• acute overdose
• CNS : euphoric syndrome (hyperactivity) => dysphoric syndrome (anxiety, apathy, melancholy, anorexia, insomnia, hypersomnia, parasomnia)  => paranoideal psychosis (delirium, hallucinations, illusion of parasitoses, irritability) => cerebral edema, ischemic stroke, lobar cerebral parenchymatous hemorrhages, anosmia, acute neuropathy, extraotogenous tinnitus, epilepsy => death due to effects on...
• cardiovascular apparatus : secondary systemic arterial hypertension (+ 5 mmHg^ref) and secondary vascular pulmonary arterial hypertension => pulmonary edema, tachyarrhythmias => cardiac and respiratory standstill. On February 9, 2006, a Food and Drug Administration (FDA) advisory panel recommended that stimulant drugs prescribed for attention deficit–hyperactivity disorder (ADHD) carry warnings about the potential for an increased risk of sudden death and cardiovascular problems such as hypertension, cardiac arrest, arrhythmias, and stroke. Stimulant drugs are known to cause adverse cardiovascular effects^ref and 188 hospital admissions were reported in USA since Aug 1, 2003 to Dec 31, 2005^ref
Acute overdose therapy :
• osmotic diuretics
• i.v. NH₄⁺Cl^- to acidify urine (dissociated alkaloids are removed more easily)
• anxiolytics and sedatives
• neuroleptics / antipsychotic (risk to lower seizure threshold !)
• assisted respiration
• chronic abuse (due to reverse tolerance !)
• increase of basal metabolism due to orthosympathetic hypertone
• CNS : paranoideal psychoses, subarachnoid hemorrhages, rupture of brain aneurysms, epilepsy, hyperthermia, anorexia
• GI tract : decrease of gastric and intestinal secretions, liver steatosis => hepatitis
• respiratory apparatus : atrophic rhinitis, nasal septal perforation, chronic bronchitis
• cardiovascular apparatus : arrhythmias, AMI, toxic myocarditis, ascending aorta aneurysms and ruptures, vasculitis, intestinal ischemias
• madarosis from cocaine
Chronic abuse therapy :
• alternative psychostimulants
• antidepressants
• neuroleptics / antipsychotics
• psychiatric diagnosis
• psychodysleptics
• hallucinogens / psychedelic
• entheogenics (i.e. evoking religious visions)
• cerumenolytics : dispersion of impacted ear wax / cerumen^ref
• sodium bicarbonate and docusate sodium (Colace^®, Waxsol^®) disperse wax within 2 hours
• Arachis oil + p-dichlorobenzene + chlorbutol (Cerumol^®) is much slower
• olive oil has no effect
• urea hydrogen peroxide (Exterol^®)
• Otocerol^®)
• choline salicylate  + glycerin (Audax^®)
• almond oil + Arachis oil + camphor oil (Earex^®)
• triethanolamine polypeptide (Cerumenex^®)

• PDSP Drug Database at NIMH
• Psychiatric and Associated Drugs
• Psychiatric Drugs’ Active Ingredients and Trade Names by Peter Lehmann
• Associations
• American College of Neuropsychopharmacology (ACNP)

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