Alcohol withdrawal can trigger a dramatic symptom shift in alcohol-related Parkinsonism, with potentially significant worsening disability, a case study reveals.
In a letter to the editor published in the Internal Medicine Journal [link here], Chinese neurologists described the case of a 62-year-old man with decades-long chronic alcoholism who presented with a one year history of progressive bilateral hand resting/kinetic tremor, bradykinesia, rigidity and gait instability.
Neurological examinations showed upper limb tremor, increased muscle tone, stooped posture, shuffling gait with reduced arm swing and mild trunk ataxia.
The man also had vitamin B deficiencies but no significant liver dysfunction.
During hospitalisation, the man experienced acute withdrawal syndrome – including hallucinations, confabulation, incoherent speech and nocturnal shouting – after discontinuing his drinking habits.
His condition improved following a small dose of ethanol and olanzapine.
While the man’s tremors lessened after ceasing alcohol, he experienced severe ‘lead-pipe’ rigidity and bradykinesia classified as stage 5 (advanced) on the Hoehn and Yahr scale. His condition included symptoms such as masked face and difficulty opening his mouth, chewing and swallowing, while he also became bedridden and required assistance with basic movement.
The patient was treated with Parkinson’s drugs levodopa and pramipexole.
Remarkably, the team noted his symptoms resolved almost completely after 40 days and by one-year follow-up the patient had self-discontinued the medications without any recurrence of tremor, rigidity and gait abnormalities.
“This case presents the transformation of Parkinsonian phenotype in alcoholic Parkinsonism: from tremor-dominant during chronic intoxication to bradykinesia rigidity-dominant following acute alcohol withdrawal,” the authors said.
“This suggests that chronic alcohol intoxication and acute alcohol withdrawal may trigger distinct types of Parkinsonism through different pathophysiological mechanisms.”
The doctors said their case highlighted the importance of recognising the dynamic clinical evolution of Parkinsonism in patients with chronic alcohol dependence, particularly the potential for a dramatic symptom transformation during withdrawal.
The symptom shift might be driven by significant reductions in striatal dopamine availability during extreme cases of withdrawal, together with relative cholinergic hyperactivity, which the researchers said was an established inducer of rigidity.
“Clinicians should be vigilant for this rare transformation when managing alcohol withdrawal in patients with pre-existing or emerging Parkinsonian features,” they said.