Acute-Onset Dystonia Following Ashwagandha Supplementation

Ashwagandha (Withania somnifera) is a widely hyped herbal panacea that we have discussed several times previously, e.g.:

• Ashwagandha, an Ayurvedic wonder herb?
• Are herbal remedies the answer to hair loss?
• Ayurvedic medicine in the management of hypertension: how to kill millions with quackery and bullshit
• Why does the BBC mislead the public on matters related to so-called alternative medicine (SCAM)?

Although it is generally considered safe, rare adverse neurological effects may occur. This paper presents the case of a previously healthy adult male who developed acute-onset dystonia following the initiation of Ashwagandha supplementation.

A 40-year-old Asian male presented to the neurology outpatient clinic with a two-week history of intermittent abnormal neck movements, sustained conjugate ocular deviation to the left, and unsteady gait. His symptoms were characterized by painful involuntary neck muscle contractions, transient speech difficulty (aphonia), and episodes of sustained eye deviation. According to his wife, he also experienced intermittent delayed responsiveness and several near-falls, veering unpredictably while walking.

The onset of these symptoms had occurred approximately one week after initiating daily self-administration of a commercially available Ashwagandha (Withania somnifera) supplement. He had taken it for a total of 25 days prior to presentation, primarily to alleviate stress and improve sleep. He denied recent infections, fever, head trauma, seizures, alcohol or recreational drug use, or exposure to known neurotoxins. There was no history of psychiatric illness, and he was not on any chronic prescription medications except for intermittent use of diazepam 2.5 mg twice daily for anxiety, which he had started before initiating Ashwagandha and had not recently adjusted. His past medical history was significant for hyperlipidemia, for which he was not actively treated. Family history was notable for premature coronary artery disease. There was no personal or family history of movement disorders or neuropsychiatric conditions. Extensive diagnostic evaluation failed to identify an alternative etiology. Discontinuation of Ashwagandha and initiation of symptomatic treatment led to the resolution of symptoms.

The authors concluded that this case underscores the importance of considering herbal supplements as potential contributors to neurological presentations.

The active constituents of the plant, withanolides and alkaloids, have been shown to modulate gamma-aminobutyric acid (GABA) receptor activity, reduce cortisol levels, and exert antioxidative and anti-inflammatory actions. Whether these effects explain the present case seems doubtful. One might even doubt that a causal link exists at all. What is beyond doubt, however, is the fact that traditional herbal remedies can cause serious problems either because of their active ingredients, contaminations, adulteerations, or interactions with synthetic drugs.

My advice, therefore, is to be cautious and to disbelief the often-voiced notions that its long tradition of usage or its naturalness means that a treatment is risk-free.