Can a patient with a history of substance abuse, currently experiencing withdrawal symptoms and being evaluated with the Clinical Institute Withdrawal Assessment (CIWA) scale, who is unsteady while walking, be considered to have an ataxic gait?

Unsteady Gait in CIWA Patients: Ataxia vs. Alcohol Withdrawal

An unsteady gait in a patient undergoing CIWA assessment is most likely due to alcohol withdrawal itself rather than true cerebellar ataxia, though both can coexist and must be distinguished through careful clinical examination.

Understanding the Clinical Context

The unsteady gait you're observing is probably a manifestation of alcohol withdrawal syndrome rather than ataxia. Here's why this distinction matters:

Alcohol Withdrawal as the Primary Cause

• Autonomic instability from alcohol withdrawal commonly causes gait unsteadiness through tremor, anxiety, and general motor dysfunction that develops 6-24 hours after cessation 1, 2
• Hand tremor and motor instability are cardinal features of AWS, appearing as part of the autonomic nervous system activation that characterizes withdrawal 1
• The CIWA-Ar scale specifically assesses tremor as one of its 10 core items, recognizing motor instability as a fundamental withdrawal symptom 1

True Ataxia: A Different Clinical Picture

Ataxia is defined as the inability to generate coordinated voluntary movement, manifesting as clumsiness, dysmetria, abnormal gait, and dyssynergia—not simply unsteadiness 3

Key distinguishing features of true cerebellar ataxia include 3, 4:

• Wide-based gait with lateral veering and irregular steps
• Unsteadiness that does NOT significantly worsen with eye closure (negative Romberg test)
• Associated cerebellar signs: dysmetria, dysdiadochokinesia, nystagmus, titubation
• Reduced step frequency with prolonged stance duration 4

Critical Differential Diagnosis

Proprioceptive (sensory) ataxia must be excluded, as it can mimic cerebellar ataxia but has a dramatically positive Romberg test (worsens with eye closure) 5

Wernicke encephalopathy is the most dangerous diagnosis to miss in this population 1, 2:

• Presents with confusion, disorientation, and ataxic gait in alcohol-dependent patients
• Can develop days to weeks after cessation if thiamine was inadequate 2
• Requires immediate high-dose thiamine 100-500 mg IV before any glucose administration 2

Immediate Clinical Assessment Algorithm

Step 1: Assess Withdrawal Severity

• Measure CIWA-Ar score immediately to quantify withdrawal symptoms 1
• Check vital signs for autonomic instability: tachycardia, hypertension, fever, sweating 1, 2
• Scores ≥8 indicate need for benzodiazepine therapy 1

Step 2: Perform Targeted Neurological Examination

• Test Romberg sign: If dramatically positive (patient falls with eyes closed), suspect proprioceptive ataxia or sensory neuropathy 5
• Assess for cerebellar signs: finger-to-nose testing, rapid alternating movements, heel-to-shin testing 3
• Evaluate gait pattern: True cerebellar ataxia shows wide-based, irregular steps with lateral veering 4
• Check for nystagmus and dysarthria, which suggest cerebellar involvement 3

Step 3: Rule Out Wernicke Encephalopathy

• Administer thiamine 100-500 mg IV immediately before any glucose-containing fluids 1, 2
• This is mandatory for ALL patients with alcohol withdrawal, regardless of whether Wernicke's is confirmed 1
• Look for the classic triad: confusion, ophthalmoplegia, ataxia (though only 10% have all three) 2

Step 4: Consider Hepatic Encephalopathy

• Evaluate for underlying liver disease, which can present with confusion and altered mental status 2
• This can be triggered by alcohol cessation, dehydration, or electrolyte imbalances 2

Management Based on Findings

If Withdrawal-Related Unsteadiness (Most Likely)

Benzodiazepines are the gold standard treatment 1, 2:

• Diazepam 10 mg orally every 3-4 hours for moderate withdrawal 1
• Lorazepam 6-12 mg/day if hepatic dysfunction, elderly, or respiratory compromise 1, 2
• Continue thiamine 100-300 mg/day throughout withdrawal and for 2-3 months after 1, 2

Monitor closely for progression 1:

• Frequent vital signs to detect autonomic instability
• Evaluate for dehydration, electrolyte imbalances (especially magnesium)
• Watch for infection, GI bleeding, pancreatitis

If True Cerebellar Ataxia Suspected

Obtain brain MRI without and with contrast to exclude cerebellar lesions, brainstem pathology, or structural abnormalities 5

Consider MRI of cervical/thoracic spine if proprioceptive deficits or spinal cord signs are present 5

Provide assistive devices (canes, walkers) to improve stability and reduce fall risk 5

If Wernicke Encephalopathy Confirmed or Suspected

Immediate high-dose thiamine 500 mg IV is crucial 2

Continue thiamine 100-300 mg/day for 2-3 months following resolution 1, 2

Common Pitfalls to Avoid

• Do NOT assume all unsteadiness in withdrawal patients is ataxia—most is simply withdrawal-related motor dysfunction 1
• Do NOT give glucose before thiamine—this can precipitate acute Wernicke encephalopathy 1, 2
• Do NOT use anticonvulsants for withdrawal seizures—benzodiazepines are the only proven treatment 1
• Do NOT continue benzodiazepines beyond 10-14 days due to abuse potential 1
• Do NOT discharge without psychiatric consultation for long-term abstinence planning 1, 2

Post-Acute Management

After withdrawal stabilization 1:

• Psychiatric consultation is mandatory for evaluation and long-term planning
• Offer relapse prevention: acamprosate, naltrexone (if no severe liver disease), disulfiram, or baclofen
• Encourage engagement with mutual help groups like Alcoholics Anonymous