Electromyographic and laboratory findings in acute Solanum torvum poisoning.

CONTEXT: Solanum torvum berries, known as susumber or turkey berries, are prepared as part of traditional Jamaican dishes usually served with cod and rice. Poisoning is rare. Although toxic compounds have never been definitively isolated, previous reports suggest toxicity results from inhibition of acetylcholinesterases. We present a case of susumber berry poisoning with detailed electromyographic studies and laboratory analysis. CASE DETAILS: A 54-year-old woman presented to the Emergency Department (ED) complaining of vision, speech, and gait changes; emesis; and diffuse myalgias following consumption of susumber berries. The physical examination demonstrated an intact, lucid mental status, miosis, opsoclonus, severe dysarthria, dysmetria, mild extremity tenderness and weakness, and inability to ambulate. Her symptom constellation was interpreted as a stroke. DISCUSSION: Electromyography demonstrated a pattern of early full recruitment as well as myotonia during the period of acute toxicity. Additionally, solanaceous compounds, in particular solasonine and solanidine, were identified in leftover berries and the patient's serum. Store-bought commercial berries and subsequent serum samples were free of such toxic compounds. EMG studies, together with a laboratory analysis of berries or serum can assist in the differential diagnosis of stroke, and provide both a prognostic screening and confirmation of suspected glycoside toxicity.

Calbindin D28k expression and the absence of apoptosis in the cerebellum of Solanum bonariense L-intoxicated bovines.

Solanum bonariense intoxication is characterized by cerebellar neuronal vacuolation, degeneration, and necrosis. Cerebellar Purkinje cells seem especially susceptible, but more research is needed to determine the pathogenesis of neuronal necrosis and the mechanism of Purkinje cell susceptibility. Calbindin D28k (CbD28k) is highly expressed in Purkinje cells and has been used as a marker for normal and degenerative Purkinje cells. The goal of this study was to describe S bonariense-induced disease by ascertaining Purkinje cell-specific degenerative changes using CbD28k expression and to correlate this with apoptosis in Purkinje cells, as determined using TUNEL (transferase-mediated dUTP-biotin nick end-labeling) and ultrastructural changes. In all cases, an increase in both dose and duration of S bonariense intoxication resulted in a decrease in the number of Purkinje cells. CbD28k immunohistochemistry was an excellent marker for Purkinje cells because immunoreactivity did not change in normal or degenerative tissues. This finding suggests that excessive calcium excitatory stimulation does not induce rapid neuronal degeneration and death. As found in previous studies, TUNEL tests and electron microscopy suggest that Purkinje cell degeneration and death are not occurring via an apoptotic process. These findings suggest that S bonariense poisoning induces progressive Purkinje cell death that is not mediated by excitotoxicity or apoptotic activation.

Solanaceous steroidal glycoalkaloids and poisoning by Solanum torvum, the normally edible susumber berry.

Ingestion of immature, environmentally stressed, or cultivar-specific Solanum species (particularly the potato) has been previously associated with gastrointestinal and neurological symptoms caused by solanaceous steroidal glycoalkaloids (SGAs). We report on two geographically, temporally disparate outbreaks of poisoning by susumber berries (Solanum torvum- Solanaceae) and on detection of alkaloids not present in non-toxic berries. Five family members in New York City participated in a traditional evening meal containing Jamaican susumber berries. All those consuming berries were symptomatic the following morning with varying degrees of gastrointestinal distress, dizziness, slurred speech, cranial nerve deficits, and ataxia. The most seriously afflicted patient developed hypertension, confusion, proximal upper extremity weakness, and hypercapnic respiratory failure requiring prolonged mechanical ventilation. A separate cohort of six patients in Toronto ate unripe Jamaican susumber berries. They presented 14h post-ingestion with varying degrees of diarrhea, weakness, facial paralysis, slurred speech, ataxia, early hypertension, and proximal weakness. Two patients had ventilatory decompensation; one required intubation. Poisonous berries appeared indistinguishable from non-toxic varieties. We isolated solasonine, larger amounts of solamargine, and other steroidal glycoalkaloids in the toxic berry strains. S. torvum poisoning can produce significant neurological and gastrointestinal effects which appear to be mediated by SGAs present in the berries.

Central diabetes insipidus following digestion Solanum indicum L. concentrated solution.

In Taiwan, Solanum indicum L. has been used in folk medicine for the treatment of inflammation, toothache, ascites, edema, and wound infection. The plant is rich in solanine, an alkaloidal glycoside. We report a 43-year-old man who developed polyuria and polydipsia after taking seven doses of concentrated solution of Solanum indicum L. over two weeks. A water deprivation test and a low serum antidiuretic hormone level helped to confirm a diagnosis of central diabetes insipidus. We suggest that excessive doses of Solanum indicum L. may cause central diabetes insipidus.

A female with central anticholinergic syndrome responsive to neostigmine.

Central anticholinergic syndrome is a rarely observed condition in children. The occurrence of this syndrome after ingestion of Solanum pseudocapsicum is infrequent because findings tend to be milder and localized to the gastrointestinal system, without central nervous system involvement. Most patients do not present with diagnostic problems because their relatives can usually report any ingestion of poisonous agents; however, when drug poisoning or plant ingestion is uncertain, a differential diagnosis with encephalitis must be considered. Physostigmine salicylate is the specific antidote because it crosses the blood-brain barrier because of its tertiary ammonium group. Neostigmine methylsulfate has a quaternary ammonium group, which prevents its penetration through the blood-brain barrier; hence its primary influence is believed to be due to its action on the peripheral nervous system. We describe a female with central anticholinergic syndrome caused by ingestion of Solanum pseudocapsicum. A slow intravenous infusion of neostigmine methylsulfate (0.03 mg/kg) immediately resolved the clinical picture. To our knowledge, this case is the first reported of central anticholinergic syndrome occurring after ingestion of Solanum pseudocapsicum in a child and the first report of a complete and rapid remission after intravenous neostigmine methylsulfate administration.

[Solanine and chaconine: occurrence, properties, methods for determination]. / Solanina i chakonina--wystepowanie, wlasciwosci, metody oznaczania.

Glycoalkaloids are naturally occurring toxicants in plants that are members of the Solanaceae family. In this paper occurrence of glycoalkaloids, especially solanine and chaconine in potatoes and tomatoes, were reviewed. Basing on literature, toxicological properties and methods of determination were reported. Attention was paid to common content of glycoalkaloids in potatoes and tomatoes and their commercial products. Solanine and chaconine are usually present at low levels in large majority of current commercial varieties but they can accumulate to high levels in greened, stored, damaged potatoes. High concentration may cause acute poisoning, including gastro-intestinal and neurological disturbances, in man. The upper limit, recognized as a safe (non-toxic), was presented. According to WHO normal levels in potatoes 20-100 mg per kg of potatoes is not of toxicological concern.

Anticholinergic toxicity from nightshade berry poisoning responsive to physostigmine.

The woody nightshade, Solanum dulcamara, belongs to the genus Solanum and its primary toxin is solanine. We report a large nightshade ingestion in a 4-yr-old girl who presented to the emergency department in acute anticholinergic crisis. The child was given 0.2 mg of intravenous physostigmine (0.02 mg/kg). Within 50 min, the patient received two additional equal doses with complete resolution of symptoms. After 36 h of observation, the child was discharged. Our patient presented with symptoms more suggestive of the deadly nightshade species, Atropa belladonna, which is native to Europe; however, a detailed laboratory analysis of the suspect berries revealed no atropine or hyoscyamine. Analysis did reveal sterols consistent with solanine. This is a unique case presentation of woody nightshade, S. dulcamara, poisoning presenting with anticholinergic crisis and responding to physostigmine.