Article Text

Download PDFPDF

Coma with focal neurological signs caused by Datura stramonium intoxication in a young man
  1. S Oberndorfer1,
  2. W Grisold1,
  3. G Hinterholzer2,
  4. M Rosner2
  1. 1Department Neurology and LBI for Neurooncology, Kaiser Franz Josef Hospital, Kundratstrasse 3, 1100 Vienna, Austria
  2. 2Intensive Care Unit, Kaiser Franz Josef Hospital, Kundratstrasse 3, 1100 Vienna, Austria
  1. Correspondence to:
 Dr S Oberndorfer;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Intoxication with Datura stramonium, which contains a variety of tropine alkaloids, produces atropine-like effects. The seeds of D stramonium (semen stramonii) in particular contain hyoscyamine, scopolamine, and atropine. Symptoms include agitation, disorientation, hallucination, flushed skin, dilatation of pupils, urine retention, seizures, and respiratory depression.1 D stramonium is voluntarily used for its hallucinogenic properties.2 Its anticholinergic compounds are likely to produce delirium and stupor but rarely cause deep coma.3

A common diagnostic error is to mistake coma resulting from brainstem infarction, supratentorial mass lesions, metabolic disorders, or hypoxia for coma resulting from poisoning. The initial distinction of these conditions may be difficult.4 We report an unusual case of D stramonium intoxication in a patient who initially presented with deep coma, focal neurological signs, and decorticate posture.

A 30 year old male patient was admitted to an emergency unit for acute loss of consciousness. The accompanying person reported that the patient had had a few beers and then suddenly fell on his back. He was unconscious and awoke for a few seconds but shortly afterward lost consciousness again and remained in a stiff position and unconscious until admission.

The first neurological examination was performed one and a half hours after the sudden onset of symptoms. There was no evidence of trauma. Vital signs, such as cardiopulmonary function, body temperature, and blood oxygenation, were normal. Initial laboratory testing for electrolyte disorders, renal or hepatic failure, and hypoglycaemia or hyperglycaemia found no major pathology. Blood alcohol concentration was 1.1‰.

Neurologically, he presented in a decorticate posture. The upper limbs were in a paratonic flexor position with increase of flexion tonus to noxious stimuli, which was more pronounced on the right side. The lower extremities did not respond to noxious stimuli and remained in an extensor position, which was also slightly more pronounced on the right side. Both the upper and the lower extremities greatly resisted passive motion. The patient had no verbal responses. The eyes could not be opened with verbal or painful stimuli. Both pupils were completely dilated and not reactive to light. The eyeballs were divergent. Corneal responses were bilaterally absent.

The horizontal oculocephalic response, however, was intact, while the vertical response was minimal. Swallowing reflex was minimal but also intact. Respiratory patterns were regular. Deep tendon reflexes could not be evaluated because of the massive increased muscle tone. Plantar response was extensor, bilaterally, more prominent on the right side. Tachycardia and retention of urine were also present. Initially the patient scored four on the Glasgow coma scale.

Magnetic resonance imaging of the brain was performed to detect brainstem infarction or supratentorial mass lesions. There were no pathological findings. Common metabolic disorders such as hypoglycaemia or hyperglycaemia, hepatic or renal failure, electrolyte disorders, disorders of systemic acid-base balance, and hyperthyroidism were excluded by laboratory examinations. Urine samples for benzodiazepines and morphines were negative. Analysis of cerebrospinal fluid to exclude subarachnoidal haemorrhage or infectious disease showed normal cell count, protein concentration, and cytology. Possible status epilepticus was also considered. However, administration of 10 mg diazepam had no effect.

The next neurological examination was performed three hours later. Vital signs were stable. The upper limbs were still in a flexor position and the lower limbs were still extensor; however, the increased muscle tone began to decrease and was less resistant to passive motion. He withdrew abnormally from painful stimuli. Plantar response was extensor on the right side. The pupils were still dilated and not reactive to light but both corneal reflexes were intact. No verbal responses could be obtained. He now scored six on the Glasgow coma scale. Seven hours later he was sitting in his bed in a state of confusion. Over the next hours, the patient’s neurological signs subsided gradually.

Finally, we were informed about the intake of D stramonium seeds. Analysis of blood samples found increased concentrations of alkaloids. Treatment during the clinical course was supportive with cardiopulmonary monitoring. Thirty six hours after admission the patient was discharged in good clinical condition, without neurological deficits except amnesia regarding the acute toxic episode.

Coma from exogenous poisons or drugs is a common diagnostic problem, not only because of the variety of clinical symptoms but also because of incomplete medical histories and misguided efforts by families and friends to conceal facts. Even if a particular toxic agent is suspected, results of a chemical analysis may arrive too late. Therefore, an accurate and immediate diagnosis depends mostly on the clinical findings.

Our patient presented with coma in a decorticate posture. Initially a severe multifocal brainstem infarction or supratentorial mass lesions were suggested. However, the discrepancies of deep coma, absent brainstem reflexes such as corneal reflexes and non-reactive dilated pupils, and, on the other hand, the intact oculocephalic and swallowing reflex, and especially the regular respiratory patterns made the findings inconclusive and a toxicological cause probable. Moreover, vital signs were stable and magnetic resonance imaging of the brain, cerebrospinal fluid, and laboratory examinations showed no major pathological findings.

D stramonium is misused for its hallucinogenic effects. It can be obtained as a herb, as a powder, and as seeds. The typical anticholinergic effects of D stramonium are well known. Coma with focal neurological signs and decorticate posture is an unusual presentation of D stramonium intoxication. However, the presence of coma in our patient was linked to the atropine effect, described as the central anticholinergic syndrome, which has been reported in the literature.5

Physostigmine, which may reverse anticholinergic toxicity, was not administered because it can produce severe complications such as seizures and cardiac arrhythmia.1,4 Moreover, the patient’s neurological symptoms subsided gradually.

Regarding this uncommon clinical presentation, the pharmacological interaction between ethanol and D stramonium must also be taken into account. However, as far as we are aware, no clinical or pharmacological interactions between ethanol and D stramonium in humans have been described in the literature.

D stramonium intoxication with the clinical picture of coma, decorticate posture, and focal neurological signs is an important clinical observation, which must be taken into account in other comatose states.



  • Competing interests: none declared