Let's Talk About Tha Belladonna Plant

[Randycigar]

I want to know about the Belladonna plant.. and i'm sure there are other ppl out there to, so if there is ANYONE out there that has the SLIGHTEST information on it.. plz tell us? Here are a couple of questions.. Is it really legal here in the US? Can I grow it or is it just for medical research? Also can i grow it where I live (I live up north in the US.. like WAY UP NORTH next to canada)? Is it deadly if take too much, and what is the amount(if you have take'n this plant and would like to out your weight and height down and how much was talk'n tha'd be great, that way we would know what a good amout for us would be)? How would someone spot this plant in your area? Where is a good place to buy the seeds to grow it? And last but not least, what are some of your experiences? now I dont' really want allll these questions asked, I'm just giving you a suggestion on what should be know. Thanks for your time..

(Note: I have heard this plant is VERY dangerous Hallucinagen Wise and should be take'n with SHITTTT LOADS of caution, if there is anyone out there that wants to try it.. plz read up on it 1st)

Randycigar Reviewed by Randycigar on 07-05-2005. Let's Talk About Tha Belladonna Plant I want to know about the Belladonna plant.. and i'm sure there are other ppl out there to, so if there is ANYONE out there that has the SLIGHTEST information on it.. plz tell us? Here are a couple of questions.. Is it really legal here in the US? Can I grow it or is it just for medical research? Also can i grow it where I live (I live up north in the US.. like WAY UP NORTH next to canada)? Is it deadly if take too much, and what is the amount(if you have take'n this plant and would like to out Rating: 5

[Dick Justice]

Erowid

But to save you time...

1. It is really legal. You can grow it, it grows naturally in a lot of places.
2. If you can grow weed in a refridgerator you can grow Belladonna in the northern US.
3. It is deadly to take too much, and the deadly amount is variable and hard to distinguish, especially since even Erowid refuses to give dosage information in the hopes of keeping people from trying it.
4. You would spot it by looking at pictures on Erowid, then remembering them when you see a plant that looks like em... I guess...
5. You can buy seeds anywhere online, just google em, you don't even need to grow it because eating the seeds can bring the same effect.
6. I don't have any experience with this, I doubt I'll ever try it.
7. Like you say, dangeroooooose. www.erowid.org

[MiddleburgsBum]

nah, I do want to try it, I love the idea of such an intence trip, something I'm lookin forward to trying in the future...prolly wont be a drug to party on, but I deff want to experience this for myself, yano? All you need to do is convince your sub-consious that your going to have a good trip and you'll be ok...but I do need info on dosage, so if anyone thats about 6'4'', 220 lbs lemme know how much u've tooken, I'd really be thankful...(by the way, thats pretty fucked up how erowid wont give info on this drug...I know its dangerous, but ppl are going to do it if they want to, so fuckin let em do it safely....bastards)

[Dick Justice]

Yeah that's not a wise move either I don't think, and you're entitled to try it, when you do post a full exp report, cause those reports on erowid always bug me out. Also erowid has the weight info box, so find an experience with 220 lbs.

[MiddleburgsBum]

Has anyone on these threads done this drug, or has everyone been scared away?

[Edgar]

I've done jimson weed; a closely related plant with a similar alkaloid content.

Here is my little report on it:
http://boards.cannabis.com/showthrea...119#post223119
Then scroll down to read of its availability, effects, and dangers.

and heres some more info on it: http://en.wikipedia.org/wiki/Jimson_weed

[Edgar]

and some info on belladonna:
http://en.wikipedia.org/wiki/Belladonna

[andruejaysin]

I've also done jimpson weed, don't know if it was a cool trip or not, just a blackout for a couple days. Just have someone hit you in the head with a hammer, same trip, and you don't have to worry about going to jail. Seriously, dude, I thought I was doing a small dose. Not small enough. Eat a ten strip, smoke crack, shoot herion, don't fuck with that shit!

[Delta9]

I woulden't, It looked cool to me at first, I almost did It, I had it in my hand, but I looked it up in an encycpopedia of herbal medicine, read about its toxicology, and cases of death from Teens trying it and threw the plant out. My guess is that it is not a happy experience, pissing on yourself and waking up 48 hours later with blood on your hands with no recollection of were you have been.

[Delta9]

Emergency Medicine (2003) 15, 376â??382
Blackwell Publishing Ltd. Toxicology
Presumed Angelâ??s trumpet poisoning
Presumed Angelâ??s trumpet (Brugmansia)
poisoning: Clinical effects and
epidemiology
Geoffrey K Isbister,1,3 Patrick Oakley,2 Andrew H Dawson3,1 and Ian M Whyte3,1
1Discipline of Clinical Pharmacology, University Of Newcastle, 2Department of Medicine,
John Hunter Hospital, 3Department of Clinical Toxicology and Pharmacology, Newcastle
Mater Misericordiae Hospital, Newcastle, New South Wales, Australia
Abstract
Objective: To investigate the pattern and epidemiology of anticholinergic plant poisoning, and to
characterize its time course and clinical features.
Methods: We reviewed all anticholinergic plant poisonings using a prospective database of all
poisonings admitted to a major toxicology unit in Australia. All patients that presented
with anticholinergic plant poisoning between July 1990 and June 2000 were included.
Patient demographics, details of poisoning, diagnostic clinical features, adverse effects
(seizures, arrhythmias, hypotension, accidental injury), and treatments required were
obtained. Important diagnostic features were analysed and compared to previous studies.
Results: Thirty-three patients were presumed to have ingested Brugmansia spp. (Angelâ??s
trumpet) based on their description of the plant; median age 18 years (interquartile
range 16â??20); 82% males. Thirty-one ingested a brewed tea or parts of the plant (flower).
Thirty-one used it recreationally. Common clinical features were: mydriasis (100%),
mean duration 29 h (SD 13) and delirium (88%) with a mean duration of 18 h (SD 12).
Tachycardia only occurred in 11 of the 33 patients (33%). In 24 patients where the time
of ingestion was certain, 7 of 8 (88%) patients presenting within 5 h had tachycardia
and only 5 out of 16 (31%) presenting after 5 h had tachycardia. There were no deaths,
seizures or arrhythmias (excepting tachycardia). One patient had hypotension and two
sustained accidental traumatic injuries. Nineteen patients required sedation, mainly with
benzodiazepines. Physostigmine was used diagnostically in eight cases.
Conclusions: Anticholinergic plant abuse is sporadic in nature. Most cases were moderate in severity,
requiring sedation only, and severe toxicity was rare. Mydriasis and delirium were the
commonest features, the later having important implications for management.
Key words: Angelâ??s trumpet, anticholinergic, brugmansia, datura, delirium, poisoning, toxicity.
Correspondence: Dr Geoffrey K Isbister, Discipline of Clinical Pharmacology, Level 5, Clinical Sciences Building, Newcastle Mater
Misericordiae Hospital, Waratah, NSW 2298, Australia. Email: [email protected]
Geoffrey K Isbister, BSc, MBBS, FACEM, Lecturer, Clinical Toxicologist and Emergency Physician; Patrick Oakley, MBBS, FRACP, Staff
Specialist; Andrew H Dawson, MBBS, FRCP (Ed), FRACP, Senior Staff Specialist; Ian M Whyte, MBBS, FRACP, FRCP (Ed), Director and
Associate Professor.
Presumed Angelâ??s trumpet poisoning
377
Introduction
Anticholinergic plant poisoning is a well recognized
cause of anticholinergic delirium, but is a relatively
uncommon presentation to hospital. Anticholinergic
plants contain a number of tropane alkaloids and
have been used in herbal medications, for religious ceremonies
and as poisons for many centuries.1â??4 A number
of plants from the family Solinaceae, including Atropa
belladonna (Deadly nightshade), Hensbane (Hyoscyamus
niger), Mandrake (Mandragora officinarum) and Datura
spp. have been used for centuries.1â??4 In modern times
the majority of anticholinergic plant poisonings have
resulted from Datura spp. or the closely related genus
Brugmansia, more commonly referred to as Angelâ??s
trumpet (Fig. 1).
Since the mid 1970s there has been increasing
recreational use of the anticholinergic plants Datura or
thornapple, and Angelâ??s trumpet or Brugmansia.3,5â??10
Prior to this, reports were often in children ingesting
the seeds accidentally11,12 or adolescents ingesting
over the counter asthma preparations, containing
stramonium and belladonna alkaloids, for recreational
use.13â??15 The seeds of Datura stramonium are ingested
or the flowers and leaves of Angelâ??s trumpet are
boiled to produce a tea that is ingested. These plants
are readily available hallucinogens, so are popular for
abuse by adolescents and young adults. A number of
tropane alkaloids are contained in these plants, the
major three being hyoscyamine, atropine and hyoscine.16
Unfortunately, the alkaloid content varies markedly
between plants, parts of the plants, season, hydration
of the plant and method of preparation.17 This means
it is almost impossible to accurately estimate the ingested
dose. Often the amount ingested causes potentially
harmful effects including anticholinergic delirium,
rather than the desired hallucinogenic effects.
There have been numerous reports of anticholinergic
plant poisoning over the last 30 years but the majority
have been case reports or small case series.2,4,9,10,18â??25
There are a few large series that have been reported to
poison centres or are data collected from non-medical
sources, such as coroners reports.7,14,26 There are only
two previous single centre series,8,12 both of Jimson
seed or Datura spp. There have been no studies over a
reasonable period of time examining the epidemiology
of recreational anticholinergic plant use.
We present 33 cases of anticholinergic plant poisoning
that occurred over a period of 10 years. There was a
sporadic occurrence of poisoning over the period. We
undertook an analysis of the clinical effects and their
time course, and compared this to previous studies.
Methods
All ED presentations and admissions to the Hunter
Area Toxicology Service (HATS) with poisoning are
prospectively entered into a clinical database.27 The unit
services the City of Newcastle with an approximate
population of 350 000. All presentations to emergency
departments in the region are either admitted to the
unit or notified to HATS and entered in the database.
Cases of anticholinergic plant poisoning were identified
by searching the HATS database.27 The cases included
consecutive anticholinergic plant poisoning presentations
to HATS between July 1990 and June 2000 where the
patient had stated they had ingested Angelâ??s trumpet
and/or accurately described the plant. The majority of
the data is collected prospectively, but the subjectsâ??
Figure 1. Angelâ??s trumpet or Brugmansia spp. (Botanical gardens,
Adelaide).
GK Isbister et al.
378
inpatient records were retrieved in some cases where
data was missing, and entered into the database.
The data collected prospectively included patient
demography (sex, age), details of the anticholinergic
plant use (intention, estimated time of administration,
route of administration, formulation, estimation of amount),
clinical features (heart rate [HR], blood pressure [BP], maximum
temperature, skin appearance, Glascow coma score
[GCS], pupillary dilation, duration, presence of a dry mouth,
bowel sounds, urinary retention, delirium and hallucinations),
investigations (ECG, blood tests), outcomes
(mortality, seizures, arrhythmias, hypotension), treatment
(decontamination, intravenous rehydration, cholinesterase
inhibitors, sedation, mechanical restraints).
In addition to the presence and absence of particular
clinical features, or a single measurement of a variable,
the time course of certain clinical features was examined,
including the timing of tachycardia, and the duration
of delirium and mydriasis. The frequency of seizures,
arrhythmias, hypotension, and accidental death or
injury resulting from delirium, were also examined.
For descriptive statistics, means and standard deviations
(SD) are quoted for normally distributed data,
while medians and interquartile ranges (IQR) are
used for non-parametric data. All statistical analysis
was done using GraphPad InStat (version 3.02 for
Windows 95, GraphPad Software, San Diego, CA, USA).
Results
Thirty-five patients presented with presumed Angelâ??s
trumpet poisoning between June 1990 and June 2000,
but there was only information available for 33
patients. All 33 patients stated they ingested Angelâ??s
trumpet, or gave a correct and recognizable description
of the plant (after the delirium had resolved). Patient
age ranged from 14 to 37 years, with a median of 18
years (IQR: 16â??20) and 27 of 33 were male. Thirty-one
of the cases were the result of ingestion of plant
derived material. Of these 31 patients, 18 persons
brewed a tea from the flowers of the plant, four ate the
flowers, eight ate an unspecified part of the plant and
one had the juice of the plant. The other two cases
were a result of inhalation of smoke produced by
burning the leaves.
Figure 2 shows the distribution of anticholinergic
plant poisoning over the 10 year period illustrating
the clustering of cases. Thirty-one of the subjects used
Angelâ??s trumpet recreationally and the other two took
it as a deliberate self poisoning.
The clinical effects of anticholinergic plant poisoning
are detailed in Table 1. Mydriasis occurred in 32 of 32
patients (100%) where it was recorded with a median
duration of 31 h (IQR 19â??36). Delirium occurred in
29 of 33 patients (88%) and was the main reason for
presentation to hospital. The median duration of anticholinergic
delirium was 16 h (IQR 10â??22). Tachycardia
only occurred in 11 of the 33 patients (33%) on
admission. In 24 patients where the time of ingestion
was certain, 7 of 8 patients (88%) presenting within
Figure 2. Frequency of Angelâ??s trumpet (Brugmansia spp.)
poisoning over the 10 year period.
Table 1. Clinical effects of anticholinergic plant poisoning in this
study
Clinical effects (%) Number of
cases with
the effect*
Mydriasis 100 32/32
Dry mouth 94 15/16
Delirium 88 29/33
Flushed skin 69 11/16
Agitation/aggressive 68 21/31
Reduced bowel sounds 63 15/24
Visual hallucinations 58 19/33
Tachycardia 33 11/33
Urinary retention 27 6/22
Fever 17 5/30
Increased systolic BP 15 5/33
GCS < 12 12 4/33
*The second number indicates the number of patients where
information was recorded for the clinical feature in question.
Tachycardia is defined as HR > 100 bpm and fever is defined as a
temperature > 37.2 °C.
Presumed Angelâ??s trumpet poisoning
379
5 h had tachycardia, but only 5 out of 16 (31%)
presenting after 5 h had tachycardia. In the seven
patients with tachycardia who presented within 5 h,
the initial tachycardia had resolved within 5 h of
ingestion. A low-grade fever occurred in five cases,
none above 38°C. There was less information on other
clinical effects including skin appearance, dry mouth,
bowel sounds and presence of urinary retention in
the notes, but the frequency in the cases recorded
is detailed in Table 1. The median length of stay in
hospital was 20 h (IQR 12â??34).
There were no deaths in this study, and no patients
had seizures, coma or arrhythmias (excepting sinus
tachycardia). There was an episode of hypotension in
one patient (BP 96/55) which responded rapidly to
intravenous fluids. Five patients were found wandering
and causing a disturbance and were brought in by police.
One patient sustained a calcaneal fracture following
a fall and another patient had soft-tissue injuries.
The main modalities of treatment included the administration
of cholinesterase inhibitors and sedative agents.
In eight patients physostigmine (2.5 mg) was used as a
diagnostic test, and in one neostigmine was used in
error reversing only the peripheral effects. In only one
patient was a dose (2.5 mg) of physostigmine repeated
and in most cases there was little information about
the response. Sedation was required in 19 of the 33
patients. Five patients received diazepam alone, 10
received diazepam and haloperidol, two received
diazepam and midazolam, one received diazepam and
thioridazine and one midazolam alone. The duration
of sedation required varied: seven for less than 6 h, nine
for 6â??12 h and three for 12â??24 h. The use of mechanical
restraints was recorded in only four patients.
Discussion
We present a consecutive single centre series of presumed
Angelâ??s trumpet poisonings. The longer duration of
the study gives a better indication of the clustering or
epidemic type presentations of these poisoning. All cases
presented to a single centre allowing better analysis of
clinical effects and correlation with previous studies.7,8,12
Angelâ??s trumpet poisoning occurred mainly in
young males in our study which is similar to three
other studies where the average ages were in the late
teens and the majority of patients were males.7,8,12 The
majority of cases were due to recreational use of the
plants, with only two cases of deliberate self-poisoning
in our study, and one case in the Klein-Schwartz
study.7 The majority of patients brewed the flowers
into a tea producing a rapidly absorbed formulation.
Details of such preparation techniques are readily
available, including recipes on the internet.
There is considerable confusion in the medical
literature about the common and scientific names of
this group of plants.4 Most of the larger series7,8,12
particularly in the United States, are of Jimsonweed
or Thornapple poisoning, which almost always refers
to Datura stramonium. This is a weed-like plant that
blossoms for 2â??3 months and produces a thorny pod
that contains numerous seeds (â??loco seedsâ??). The seeds
have the highest alkaloid content and are the part of
the plant most commonly ingested.7,8
Angelâ??s trumpet differs from Jimsonweed, and
although it was originally part of the genus Datura, it
has now been placed in a separate genus Brugmansia.28
The common name Angelâ??s trumpet refers to a number
of introduced species of Brugmansia in both Australia
and the United States19 with a readily recognizable
trumpet-like flower that grows up to 30 cm (Fig. 1).
The flowers of B. suaveleons are white, but the flowers
may be different colours in the other Brugmansia
species.28
In the region that our unit services D. stramonium
and Brugmansia spp. both occur. In no case was the
responsible plant brought in for identification, so
determining which species was involved was not
possible. However, there were no reports of seeds
ingested, making D. stramonium unlikely. It is likely
that in this study Angelâ??s trumpet was used in the
majority of cases because these plants are common,
have a recognizable flower, and are readily accessible
in the region. Most would have used B. suaveolens
which occurs throughout the region and has the large
white flowers (Fig. 1). The majority of patients brewed
a tea which is only possible from the flowers of
Brugmansia.
Some authors have suggested that there is an
increasing use of Datura spp. and Brugmansia spp.
because they are inexpensive, legal and readily
available.5,6,19 The only previous study over a long
enough period (5 years) was of Datura poisoning and
did not comment on the frequency of poisoning.7 There
is evidence to suggest that the reports of cases are
merely clusters being reported, and that there has
been no actual increase in the incidence since the late
1960s. Our study over a 10 year period supports this
(Fig. 2) with no increase in incidence, but rather
sporadic events or clusters of poisonings. The NSW
Poisons Information Centre reports a constant number
GK Isbister et al.
380
of calls regarding anticholinergic plant poisoning for
the period 1996â??2000.
Interestingly, there appears to be a somewhat
sporadic pattern of case reports in the literature with
at least two peaks in 1975â??775,8,10,12,19,21 and 1994â??
95,4,23,29 with reports in each peak from the United
States, Europe and Australasia. In this study the
majority of cases occurred between 1994 and 1995.
This overlaps with an unexplained increase in reports
of Angelâ??s trumpet poisonings to the Florida Poison
Control Centre from July to December in 19944 and
also in other parts of the United States23 and Europe.29
These all report clusters of poisonings, rather than
an increase in number of poisonings.
Although the clinical features of anticholinergic plant
poisoning have been previously reported,3,4,7,14,19,20,26
many of these series have been of clusters of severe cases,
retrospective studies done through poison centres7 or
from non-hospital sources.14 Except in four series of
anticholinergic plant poisoning, one of asthmador
powder14 and three with Jimsonweed,7,8,12 there is
considerable publication bias to severe cases as expected
with case reports. Our study gives a better picture of
the range of severity of anticholinergic poisoning and
is the only such study of presumed Angelâ??s trumpet
poisoning. Although delirium and agitation were common,
severe cases with fever, neurological manifestations
and coma did not occur. This is supported by the one
other study where there is information on a number of
cases over a period of time,7 and two single centre
studies with similar numbers.8,12
Most patients presented between 6 and 24 h after
ingestion, which is similar to other studies.12 The main
clinical features on presentation were delirium and
mydriasis. Other central anticholinergic effects included
agitation/aggression and visual hallucinations in more
than half of the patients. Peripheral features included
dry oral mucosa, flushed skin and reduced bowel sounds
in more than 60% of cases, but this only includes cases
where these were documented. This pattern of clinical
features is similar to two other single centre studies
(Table 1).8,12 In both these studies, and ours, mydriasis and
delirium were the commonest features, and the classical
peripheral signs occurred in over half of cases.
The main difference between our study and the
others was the much higher incidence of tachycardia
in the other studies (70â??80%).8,12 In this study, tachycardia
was only present in a third of patients at presentation,
and in those patients presenting early8 the
tachycardia resolved within 5 h. This is consistent with
there being an early and short period of tachycardia and
most patients presenting after 5 h. However, delirium
and mydriasis occurred in almost all patients with a
much longer duration. This may confuse the diagnosis
because tachycardia is a classic sign of anticholinergic
poisoning and a much higher incidence has been
reported in most other studies,8,12 although not in one
study.7 The reason for this discrepancy from other
studies is important and may relate to the continuing
absorption of Jimson seeds that potentially occurs and
was seen in one of these cases.12 This differs to the
rapid and complete absorption of a tea formulation of
Angelâ??s trumpet, the commonest ingested form in our
study. It could be further postulated that the longer
duration of the central nervous system effects
(delirium and mydriasis) are related to the slower
movement of these alkaloids in and out of the central
nervous system. This is supported by the fact that
atropine, a tropane alkaloid, has a much longer duration
of action on the eye than on HR.30
It is difficult to predict the severity of anticholinergic
plant poisoning because the ingested amount is
usually unknown and difficult to estimate because
there is no history from the patient or there is an
unclear amount of plant involved. Although in the
more severe cases the time course of anticholinergic
delirium and the duration of sedation were longer,
these could not be predicted from clinical features on
admission. In more severe anticholinergic poisonings
there is a decreased level of consciousness and coma
requiring medical intervention and supportive care9
although this did not occur in our series.
Mortality from anticholinergic plant poisoning is
uncommon and there were no deaths in this study. The
majority of deaths reported in association with anticholinergic
poisoning are a result of accidents associated
with the delirium.14,19,31 Drowning, exposure (hypothermia
or hyperthermia) and trauma are the commonest causes
of death. Two of the patients in our study suffered from
traumatic limb injury following a fall.
There has been much discussion in the literature
regarding the use of cholinesterase inhibitors in the
treatment of anticholinergic poisoning. Physostigmine
gained popularity in the late 1970s with a series of cases
suggesting its efficacy. Subsequently there were reports
of seizures with its use in tricyclic antidepressant
poisoning.32,33 A more recent retrospective study of 52
patients showed that physostigmine was more effective
than benzodiazepines in controlling agitation and reversing
delirium, and was associated with fewer complications.34
One of the major drawbacks of physostigmine has been
its short duration of action. There is some preliminary
Presumed Angelâ??s trumpet poisoning
381
evidence that repeat doses of another cholinesterase
inhibitor tacrine, which has a longer duration of
action, may be of benefit in the management of
these patients and appears to be safe (unpubl. data).
There are scattered reports of cholinesterase inhibitor
treatment of anticholinergic plant poisoning, including
the use of physostigmine,7,18 and tacrine.20,24 In this
study physostigmine was used in one quarter of cases,
but in all but one instance, only a single dose (2.5 mg)
was used, mainly for diagnostic purposes. There was
little information on patient response in most cases.
In this study diazepam was the most commonly used
agent for sedation, but in 10 cases haloperidol was used
in combination with it, and thioridazine in one. There
are theoretical problems with using antipsychotic agents
in anticholinergic poisoning due to their intrinsic
anticholinergic effects. Other authors have warned of this
risk19,35 and there is one reported case of Jimsonweed
poisoning where haloperidol worsened the patientâ??s
condition.18 Although in our series antipsychotics
did not appear to worsen the delirium, we would also
recommend benzodiazepines as first line agents for
sedation in anticholinergic delirium.2
Although this study suffers from being a retrospective
review of a clinical database, the majority of the information
in the database had been entered prospectively
in a standardized blinded manner.27,36 The routine
collection of all cases allowed a better characterization
of the clinical spectrum of effects. Information on the
treatment and comparison of different treatments was
not possible and limits the conclusions that can be
drawn regarding the safety and efficacy of cholinesterase
inhibitors and sedative agents.
Another limitation of the study was the inability to
have the ingested plants formally identified. However,
Angelâ??s trumpet is a readily recognizable plant because
of the large trumpet-like flowers (Fig. 1) making the
history from the patient reasonably reliable. Qualitative
or quantitative identification of tropane alkaloids in
urine or plasma is time consuming and expensive16
and because of variability in relative and total amounts
of these alkaloids in plants of the same species, this
would not allow identification of the plant species, and
would simply confirm that the person had ingested
tropane alkaloids.17
Conclusions
The sporadic and infrequent nature of recreational
anticholinergic plant poisoning makes diagnosis and
management difficult. There appears to be clusterings
of anticholinergic plant poisonings in the literature
which is supported in this study over 10 years. The
diagnosis may be delayed because of the unfamiliarity
of the treating physician with anticholinergic plants.
In young patients presenting with delirium, signs of
anticholinergic poisoning should be looked for. Our
study has shown that the time course and clinical
effects of anticholinergic plant poisoning in Australia,
where Angelâ??s trumpet is commonly used, differs to
that of Jimsonweed poisoning that has been more
commonly reported in studies from the United States.
This is due to the difference in the preparation ingested.
The rapid absorption of the commonly brewed formulation
of Angelâ??s trumpet, results in a shorter duration
of some features, most importantly tachycardia. However,
delirium and mydriasis last longer and may be the
principal features on presentation to hospital. Management
of anticholinergic poisoning continues to be
problematic. Cholinesterase inhibitors appear to be
the most effective treatment, but further studies
looking at safety and duration of action are required,
and availability problems in Australia need to be
addressed.
Acknowledgements
We would like to acknowledge Stuart Allen for
extracting the data from the database, and Deb Whyte
and Toni Nash for help retrieving the patient records
and entering the data into the database. We also thank
Corrine Balit for her comments on the manuscript.
Accepted 12 February 2003
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