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LSD is a white powder or a clear, colorless liquid. Synonyms: d-lysergic
acid diethylamide; acid, animal, barrels, beast, blotter, ‘cid,
dots, kool aid, LSD-25, lysergide, microdots, panes, sandoz, tabs, trips,
white lightning, window panes.
Source: LSD is manufactured from lysergic
acid which occurs naturally in the ergot fungus that grows on wheat
and rye. It is a Schedule I controlled substance, available in liquid,
powder, tablet (microdots), and capsule form. The liquid is often applied
to blotter paper squares (frequently with colorful designs), stickers,
sugar cubes, candy, or soda crackers. LSD is also available in dropper
bottles or in the form of gelatin sheets/shapes (window panes).
Drug Class: Hallucinogen, psychedelic, psychotomimetic.
Medical and Recreational Uses: No medicinal
use. Recreationally used as a hallucinogen and for its ability to alter
human perception and mood.
Potency, Purity and Dose: The strength of illicit LSD nowadays
ranges from 20 to 80 m g per dose, which is considerably less than doses
reported during the 1960s and early 1970s, of 100-200 m g or higher
per unit. Experienced users typically administer 100-200 m g for a “good
high”. The potency of liquid LSD in dropper bottles may vary because
the liquid is water based.
Route of Administration: Primarily oral administration,
but can be inhaled, injected, and transdermally applied.
Pharmacodynamics: LSD is primarily a non-selective
5-HT agonist. LSD may exert its hallucinogenic effect by interacting
with 5-HT 2A receptors as a partial agonist and modulating the NMDA
receptor-mediated sensory, perceptual, affective and cognitive processes.
LSD mimics 5-HT at 5-HT 1A receptors, producing a marked slowing of
the firing rate of serotonergic neurons.
Pharmacokinetics: LSD has a plasma half-life of
2.5-4 hours. Metabolites of LSD include N-desmethyl-LSD, hydroxy-LSD,
2-oxo-LSD, and 2-oxo-3-hydroxy-LSD. These metabolites are all inactive.
Molecular Interactions / Receptor Chemistry: Metabolism
via cytochrome P450 isoenzymes has not been described.
Blood to Plasma Concentration Ratio: Data
not available.
Interpretation of Blood Concentrations: Threshold
toxic dose in humans has been reported with 100-200 mg with associated
blood concentrations of 2-30 ng/mL. Intravenous doses of 1-2 mg /kg
have been associated with blood concentrations of 1-5 ng/mL LSD. Single
oral doses of 160 mg resulted in peak plasma concentrations of up to
9 ng/mL LSD.
Interpretation of Urine Test Results: LSD use can typically
be detected in urine for periods of 2-5 days. In a reported case of
LSD intoxication, a concentration of 11 ng/mL of LSD was detected in
the urine. In subjects receiving 200-400 mg of LSD, concentrations
in urine ranged from 1-55 ng/mL.
Effects: Effects are unpredictable and will
depend on the dose ingested, the user’s personality and mood,
expectations and the surroundings.
Psychological: Hallucinations, increased color perception,
altered mental state, thought disorders, temporary psychosis, delusions,
body image changes, and impaired depth, time and space perceptions.
Users may feel several emotions at once or swing rapidly from one emotion
to another. “Bad trips” may consist of severe, terrifying
thoughts and feelings, fear of losing control, and despair.
Physiological: Tachycardia, hypertension, dilated pupils,
sweating, loss of appetite, sleeplessness, dry mouth, tremors, speech
difficulties, and piloerection.
Side Effect Profile: Rhabdomyolysis, renal
failure, prolonged mania, panic, impairment in color discrimination,
and residual visual effects have been described. LSD users may manifest
relatively long-lasting psychoses, such as schizophrenia or severe depression.
Duration of Effects: Onset of effects is
rapid following intravenous administration (10 minutes). Following oral
ingestion, onset of the first effects are experienced in 20-30 minutes,
peaking at 2-4 hours and gradually diminishing over 6-8 hours. Residual
effects may last longer. Flashbacks may occur suddenly, often without
warning, and may occur within a few days or more than a year after use.
Tolerance, Dependence and Withdrawal Effects: Frequent,
repeated doses of LSD are unusual and therefore tolerance is not commonly
seen. Tolerance does develop to the behavioral effects after 3-4 daily
doses, but no withdrawal syndrome has been described. LSD is not considered
an addictive drug since it does not produce compulsive drug-seeking
behavior.
Drug Interactions: C ross-tolerance with
mescaline and psilocybin has been demonstrated in animal models. LSD
blocks subjective alcohol effects in many subjects. Possible seizures
when concurrently taken with lithium or fluoxetine.
Performance Effects: LSD produces significant
psychedelic effects with doses as little as 25-50 mg. LSD impairs reaction
time (auditory and visual), choice reaction time, and visual acuity
for up to 4 hours. Impaired divided attention, ataxia, and grossly distorted
perception have also been reported following LSD use.
Effects on Driving: Epidemiology studies
suggest the incidence of LSD in driving under the influence cases is
extremely rare. In Denver, Colorado between Jan 1988 to June 1990, 242
drivers detained for driving while impaired were evaluated by drug recognition
examiners; only 1 case of LSD was confirmed following urine toxicology
screens.
DEC Category: Hallucinogen.
DEC Profile: Horizontal gaze nystagmus not
present; vertical gaze nystagmus not present; lack of convergence not
present; pupil size dilated; reaction to light normal; pulse rate elevated;
blood pressure elevated; body temperature elevated. Other characteristic
indicators may include extreme changes in behavior and mood, trance-like
state, sweating, body tremors, piloerection, hallucinations, paranoia,
and changes in sense of light, hearing, touch and smell.
Panel’s Assessment of Driving Risks: The
use of LSD is not compatible with the skills required for driving due
to its severe psychomotor, cognitive and residual effects.
References and Recommended Reading:
Abraham HD. A chronic impairment of colour vision in users of LSD. Br
J Psychiat 1982;140(5):518-20.
Aghajanian GK, Marek GJ. Serotonin and hallucinogens. Neuropsychopharm 1999;21(2
Supp):16S-23S.
Aranov VL, Liang X, Russo A, Wang RY. LSD and DOB: Interaction with
5-HT(2A) receptors to inhibit NMDA receptor-mediated transmission in
the rat prefrontal cortex. Eur J Neurosci 1999;11(9):3064-72.
Barrett SP, Archambault J, Engelberg JM, Pihl RO. Hallucinogenic drugs
attenuate the subjective response to alcohol in humans. Human Psychopharm 2000;15(7):559-65.
Baselt RC. Drug effects on psychomotor performance. Biomedical
Publications, Foster City, CA; pp 225-226;2001.
Burns M, Page T, Leikin J. Drug information handbook for the criminal
justice professional. Lexi-Comp Inc., Hudson, Ohio, USA;1998.
Kawasaki A, Purvin V. Persistent palinopsia following ingestion of
lysergic acid diethylamide (LSD). Arch Opthalm 1996;114(1):47-50.
Kulig K. LSD. Emerg Med Clin N Am 1990;8(3):551-8.
Lechowicz W. LSD determination using high-performance liquid chromatography
with fluorescence spectroscopy. Z Zaga Nauk Sadow 1999;39:54-64.
Madden JS. LSD and post-hallucinogen perceptual disorder. Addiction 1994;89:762-3.
McCarron MM, Walberg CB, Baselt RC. Confirmation of LSD intoxication
by analysis of serum and urine. J Analyt Tox 1990;14(3):165-7.
Smith DE, Seymour RB. Dream becomes nightmare. Adverse reactions to
LSD. J Psych Drugs 1985;17(4):297-303.
Taunton-Rigby A, Sher SE, Kelley PR. Lysergic acid diethylamide: radioimmunoassay. Science 1980;181:165-6.
Tomaszewski C, Kirk M, Bingham E, Saltzman B, Cook R, Kulig K. Urine
toxicology screens in drivers suspected of driving while impaired from
drugs. J Tox Clin Tox 1996;34(1):37-44.
Upshall DG, Wailling DG. The determination of LSD in human plasma
following oral administration. Clin Chim Acta 1972;36(1):67-73.
Vardy MM, Kay SR. LSD psychosis or LSD-induced schizophrenia? A multimethod
inquiry. Arch Gen Psychiat 1983;40(8):877-83.
Williams RH, Erickson T. Evaluating hallucinogenic or psychedelic drug
intoxication in an emergency setting. Lab Med 2000;31(7):394-401.
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