Neuroscience · Year 2 · from Neuroscience
Case 3: Alcoholic Cerebellar Degeneration
Patient Presentation
Demographics: 55-year-old male
Chief Complaint: Difficulty walking for several months
History of Present Illness: A 55-year-old man is brought in by his brother who reports progressive unsteadiness when walking over the past 6 months. The patient requires support to walk and has fallen multiple times. He also reports numbness and burning in his feet. His speech has become slightly slurred. The patient admits to drinking a pint of vodka daily for the past 20 years and has had poor nutritional intake. He was hospitalized twice for alcohol withdrawal. He denies arm clumsiness or visual problems.
Physical Examination:
- Vital signs: BP 145/88, HR 94
- General: Cachectic, poor hygiene, spider angiomata on chest
- Neurological:
- Mental status: Mild memory impairment (short-term); otherwise oriented
- Cranial nerves: Mild horizontal nystagmus; no ophthalmoplegia; no facial weakness
- Motor: Mild proximal weakness (4+/5) upper and lower extremities
- Sensory: Decreased sensation to pinprick and vibration in stocking distribution (distal legs)
- Reflexes: 2+ in upper extremities; 1+ at knees; absent ankle jerks
- Coordination: Legs markedly more ataxic than arms - severe heel-to-shin dysmetria; finger-to-nose relatively preserved
- Gait: Wide-based, ataxic gait with truncal instability; cannot tandem walk
- Speech: Mildly dysarthric
Workup:
- MRI brain: Superior cerebellar vermis atrophy; mild cerebral atrophy
- Vitamin levels: Thiamine (B1) low; B12 and folate low-normal
- Liver function tests: Elevated AST, ALT, GGT (alcoholic liver disease pattern)
- Nerve conduction studies: Length-dependent axonal sensorimotor polyneuropathy
- Blood glucose: 135 mg/dL (impaired fasting glucose)
Diagnosis: Alcoholic cerebellar degeneration with peripheral neuropathy
Treatment:
- Thiamine 500 mg IV three times daily for 3-5 days, then oral maintenance
- Multivitamin with folate and B12 supplementation
- Alcohol cessation counseling and referral to addiction services
- Nutritional rehabilitation
- Physical therapy for gait training
- Gabapentin for neuropathic symptoms
- Mild improvement with abstinence and nutrition; gait ataxia largely persistent
Clinical Pearl: Alcoholic cerebellar degeneration classically affects the superior vermis, causing a characteristic clinical pattern: gait and truncal ataxia is severe while arm coordination is relatively preserved. This contrasts with other cerebellar pathologies that often affect the hemispheres more prominently. The vermis controls midline/axial coordination (gait, trunk), while the hemispheres control appendicular coordination. The pathophysiology involves direct alcohol toxicity and thiamine deficiency. Unlike Wernicke encephalopathy (which can cause similar ataxia but acutely), alcoholic cerebellar degeneration develops insidiously and is often irreversible, though abstinence and thiamine may prevent further progression.
Clinical Image
Image Description: Sagittal T1-weighted MRI of the brain showing cerebellar vermis atrophy with widened folia and enlarged fourth ventricle, characteristic of superior vermian atrophy seen in alcoholic cerebellar degeneration.
Attribution: Image from Radiopaedia (https://radiopaedia.org/), Creative Commons Attribution-NonCommercial-ShareAlike 3.0 license.