Solanum erianthum Poisoning Causing Speech Disturbance: A Case Series

Abstract

The Solanaceae plant family (Solanum), such as capsicum, eggplant, potato, and tomato, is made up of common plants consumed by humans. Despite having medicinal benefits, these plants can produce toxic alkaloid compounds. We report 2 cases of uncommon Solanum erianthum poisoning after consuming the berries as a meal. Both patients presented with slurring of speech, which is easily mistaken for a stroke. Symptoms developed 19 h after consuming the wild berries and resolved spontaneously 12 h after onset. Both patients recovered with no neurologic deficit. No antidote was given in either case. The Solanaceae plant family is a common group of plants consumed by humans and is considered one of the largest genera. The phytochemical profile showed that the leaves and berries contain toxic glycoalkaloid levels, which can cause gastrointestinal and neurologic symptoms in poisoning cases. Reports have shown that the toxic glycoalkaloids can inhibit the cholinesterase enzyme, thus producing cholinergic effects. Theoretically, atropine is the choice of antidote, but no case report of atropine use has been documented. Treatment of S erianthum poisoning remains supportive care. These cases highlight the rare occurrence of poisoning from S erianthum and emphasize the necessity for considering toxicologic causes in nonlocalizing neurologic symptoms.

Introduction

The Solanaceae plant family (Solanum), such as capsicum, eggplant, potato, and tomato, are common plants consumed by humans. It is considered one of the largest genera and has >1500 species, some of which have pharmaceutical benefits. ¹ It is commonly used for alternative medicine purposes such as malaria, fever, gout, cancer, and abdominal pain.^2,3 Despite having beneficial compounds, Solanum spp produce toxic compounds, including glycoalkaloids and alkaloids, that can cause variable symptoms in poisoning cases. ⁴ Consumption of certain Solanum spp, such as Solanum torvum (commonly known as susumber or turkey berry) or Solanum erianthum, has been associated with gastrointestinal and neurologic symptoms. ⁵ We present a case series of uncommon S erianthum poisoning in patients who presented with slurring of speech.

Case Reports

Case 1

A 69-y-old female with no known medical illnesses was referred to our emergency department with sudden-onset slurring of speech associated with dizziness, myalgia, and 3 episodes of diarrhea. On further history, she revealed that she had consumed an estimated 20 wild berries (Figure 1) cooked with chili paste on 2 occasions ∼19 and 12 hours prior. The berries were from a wild plant that grew behind her housing area and was later identified as S erianthum after consultation with experts. On examination, the patient was alert with good perfusion, and her vital signs were within normal limits. Neurologic examination of the upper and lower limbs was normal. Cranial nerve examination showed no significant abnormalities and negative cerebellar signs. Other systemic examinations were unremarkable. Electrocardiography showed normal sinus rhythm with a heart rate of 80 beats/min. Her blood workup revealed hypochromic microcytic anemia, mild hypokalemia, hypomagnesemia, hypophosphatemia, raised creatine kinase (CK) concentration, mild transaminitis, and mild metabolic acidosis. A summary of her laboratory findings is provided in Table 1. The patient was given symptomatic treatment for her diarrhea and myalgia while her electrolyte abnormalities were corrected. Her speech disturbance resolved spontaneously 12 h after onset. She was admitted to hospital for further observation. During the admission, her CK level trend improved, and she remained asymptomatic.

Figure 1.

Solanum erianthum berries, which appear globose, around 1 cm long, with stellate-tomentose stems covered with fine hairs.

Table 1.

Summary of the blood investigations for Cases 1 and 2.

Lab value	Case 1			Case 2
	On admission	12 h	Day 2	On admission
Full blood count
Total white cell count (normal, 3.4–10 × 109/L)	10.2			8.0
Hemoglobin (normal, 11.6–15.1 × 1012/L)	10.7			10.6
MCV (normal, 70–86 fL)	66.5			69.0
MCHC (normal, 30–36 g/dL)	29.0			29.2
Platelets (normal, 158–410 × 109/L)	482			289
HCT (normal, 31.8–42.4%)	32.0			33.0
Renal profile
Urea (normal, 1.8–6.4 mmol/L)	3.1	1.8		3.5
Sodium (normal, 136–146 mmol/L)	136.0	140.0		137.0
Potassium (normal, 3.5–5.1 mmol/L)	3.0	3.29		4.0
Creatinine (normal, 45–84 μmol/L)	46	54		43
Liver function tests
ALT (normal, <35 U/L)	25	38		15
AST (normal, <35 U/L)	79	112		22
ALP (normal, 33–98 U/L)	111	109		73
Albumin (normal, 35–53 g/L)	41	40		43
Creatine kinase (normal, <145 U/L)	2247	1632	1032	266
Calcium (normal, 2.20–2.65 mmol/L)	2.31	2.23		2.12
Phosphate (normal, 0.81–1.45 mmol/L)	0.31	1.63		0.70
Magnesium (normal, 0.73–1.06 mmol/L)	0.53			0.52
Venous blood gases
pH (normal, 7.35–7.45)	7.289	7.34		7.344
HCO3 (normal, 22–28 mmol/L)	19.8	22.5		21.8
BE (normal, −3.2–1.8 mmol/L)		−0.7
Lactate (normal, 0.4–0.8 mmol/L)	0.8	0.8		0.7
Coagulation profile
PT (normal, 11.7–15.3 s)	9.9			10.2
International normalized ratio	0.92			0.95
aPTT (normal, 30.0–44.4 s)	22.3			27.7

MCV, mean corpuscular volume; MCHC, mean corpuscular hemoglobin concentration; HCT, hematocrit; ALT, alanine aminotransferase; AST, aspartate aminotransferase; ALP, alkaline phosphatase; BE, base excess; PT, prothrombin time; aPTT, activated partial thromboplastin time

Case 2

This patient was a 68-y-old female with chronic hypertension and type 2 diabetes mellitus. She presented with acute-onset slurring of speech, dizziness, and myalgia. Further questioning revealed that she was a relative of the patient in Case 1 described earlier, who had consumed the same wild berries cooked with chili paste. They had eaten approximately the same amount of berries on 2 separate occasions together. On review, the patient was comfortable, not in distress, and well perfused. Her vital signs showed a blood pressure of 160/81 mm Hg, pulse rate of 78 beats/min, respiratory rate of 16 breaths/min, saturation of 99% on room air, and normothermia. Physical examination showed no significant neurologic abnormalities, and her electrocardiography was normal. Blood investigation revealed hypochromic microcytic anemia, marginally raised CK level, mild metabolic acidosis, hypomagnesemia, and hypophosphatemia. A summary of her blood investigation is provided in Table 1. Her symptoms resolved 12 h after onset, and she remained asymptomatic. She was observed for 24 h and was discharged well.

Discussion

We identified the culprit plant as S erianthum (commonly known as potato tree) with the assistance of the Malaysia Remote Envenomation Consultation Service and a botanist after patient admission. S erianthum is a small tree with stellate tomentose, distinctive velvety leaves that are green on the upper side with fine hairs on the underside ⁶ (Figures 2 and 3). As with the other Solanum spp, the berries contain toxic glycoalkaloids.

Figure 2.

Solanum erianthum tree, which is commonly described as scrub (left), around 1.5 to 2.5 m tall, with stellate-tomentose stems and berries (right).

Figure 3.

Solanum erianthum, with distinctive velvety leaves that are green on the upper side (left) with fine hairs on the lower side (right).

A phytochemical profile showed that the leaves and berries contain the highest total alkaloid concentration. ³ The main glycoalkaloids identified are solamargine and solasonine, which contribute to the plant's bioactive properties, including antimicrobial, antioxidant, and enzyme inhibitory activities. ³ Exposure of the berries to elevated temperatures, storage duration, and light variation can increase the glycoalkaloid content up to 50-fold. ⁵ In this case series, the berries were cooked, and the high heat exposure likely multiplied the glycoalkaloid content. There is one reported case in the medical literature of S erianthum toxicity, and the patient presented with confusion, disorientation, and agitation. ⁷

Glycoalkaloid intoxication by Solanum spp is associated with predominantly gastrointestinal symptoms (ie, vomiting, diarrhea, or abdominal pain) lasting 2 to 20 h. ⁵ Besides this, neurologic symptoms (eg, dysarthria, slurred speech, dysphagia, ataxia, or blurry vision) also have been reported in Solaneous spp intoxications. ⁸ The symptoms result mainly from direct cholinergic receptor stimulation, producing nicotinic and muscarinic effects, as described in a susumber berries poisoning case report, but Solanum spp were not mentioned. ⁹ S erianthum has been reported to be able to inhibit acetylcholinesterase and plasma cholinesterase. ³

We have noted that in Case 1, the CK level was raised more than 5 times the upper limit. This has brought us to ponder that S erianthum intoxication can cause rhabdomyolysis and lead to metabolic acidosis and electrolyte disturbances in the patient. However, the patient in Case 2, who had consumed similar berries, did not exhibit the same CK profile. Because the patients were unable to quantify the amount of berries consumed, respectively, this could explain the reason why only Patient 1 developed rhabdomyolysis. Interestingly, no such anecdotal report of rhabdomyolysis by S erianthum intoxication has been reported so far.

Treatment for S erianthum poisoning is generally supportive care. In our patients, both had full recovery without any major intervention or antidote. Activated charcoal may be considered in severe ingestion or early presentation. Theoretically, atropine is the antidote of choice because Solanum poisoning can produce cholinergic effects. However, until recently, no anecdote or case report of managing such patients with atropine has been published.

It is also important to highlight that in instances where 2 patients exhibit the same symptoms, this can aid in narrowing down the causes to external factors such as food or toxic exposure. When strokelike signs and symptoms cannot be localized to a brain lesion, toxicology considerations become pertinent. By obtaining a detailed dietary and toxicologic history in such patients, the culprit plant, such as S erianthum, can be pinpointed.

Conclusion

In conclusion, these cases highlight the rare occurrence of poisoning from S erianthum and emphasize the need for considering toxicologic causes when a patient presents with nonlocalizing dysarthria.