HISTORY: TOO MUCH FOR TOO LONG
Mrs. B, age 73, has been alcohol-dependent for 20 years. Since her husband’s death 5 years ago, she has been drinking 1 to 2 liters of vodka a week. At her family’s insistence, she checks into a tertiary-care hospital for worsening alcohol use, memory problems, and increasing confusion.
Mrs. B’s family removed her car because of her alcohol and cognitive problems, but she walks half a mile to buy alcohol. She lives alone in an assisted-living facility and has been hospitalized for detoxification 3 times within 2 years.
At intake, her judgment and abstract thinking are impaired. She has poor insight into her condition. Physical examination reveals fine hand tremors. Lab test results and vital signs are normal. Mrs. B was previously diagnosed with bipolar disorder and takes divalproex, 250 each morning and 500 mg at bedtime, and paroxetine, 20 mg/d.
Mrs. B’s Folstein Mini-Mental State Examination (MMSE) score 1 week after admission was 5/30, indicating severe cognitive deficits. Her mood was euthymic, speech and motor activity were normal, and thought process was logical with intact associations. She exhibited no delusions or hallucinations but was disoriented, with a short attention span and poor concentration.
The authors’ observations
Mrs. B’s confusion has increased in recent weeks. Hand tremors could signal a neurologic problem triggered by a vascular event or alcohol use. Include dementia in the differential diagnosis.
Distinguishing between vascular dementia and alcohol-induced persisting dementia requires a thorough history, neurologic exam, and lab testing.
Vascular dementia. Cognition deteriorates step by step. Patients with this dementia have multiple vascular risk factors and display evidence of cerebrovascular events on physical examination or imaging studies. Watch for high blood pressure, high cholesterol, or obesity; history of diabetes, cardiac arrythmias, or strokes; or other vascular changes in the brain.
Alcohol-induced persisting dementia. Patients usually have abused alcohol for years, and memory slowly deteriorates. Vascular events that would explain cognitive deficits are not found. Such patients usually do not have vascular and cerebrovascular risk factors, but may exhibit worsening cognition in the context of alcohol use. Watch for mean corpuscular volume >100 femtoliters, gamma glutamyl transferase >50 U/L, and elevated liver function tests.
For Mrs. B, both dementia types were ruled out. Her memory problems were mild, and she had been functioning independently at the assisted-living facility. Dementia is not characterized by clouding of consciousness, and her disorder’s progression was fast. Mrs. B’s bipolar disorder was not a factor because she did not have significant depressive or manic symptoms.
Amnestic disorder. Mrs. B’s worsening mental status and neurologic signs after admission suggest amnestic disorder. Patients with amnestic disorder have trouble learning or recalling new information and forming new memories, although they can talk coherently and appropriately.
Injury to the diencephalic and medial temporal lobe structures triggers amnestic disorder. Head trauma, cerebral infections, and infarctions can damage these structures, but alcoholism is the most common cause.
ADMISSION: INCREASING CONFUSION
Mrs. B was admitted to the dual diagnosis unit for patients with substance use and psychiatric disorders. Although confused, she could eat and walk.
For 2 days, Mrs. B received chlordiazepoxide, 200 mg/d, for detoxification; a multivitamin tablet; and oral vitamin B1 (thiamine), 100 mg once daily. She also continued her divalproex/paroxetine regimen. Chlordiazepoxide was tapered and discontinued over 4 days. Vital signs remained normal.
Two days after starting detox, Mrs. B’s condition began to worsen. She became incontinent of urine and feces, had trouble eating, and required extensive assistance with activities of daily living.
On examination by the geriatric psychiatry team, Mrs. B appeared very confused. She was confabulating, had hand tremors, and was ataxic, with nystagmus on lateral gaze. Coordination was poor. Because she reported visual hallucinations and appeared delirious, divalproex sodium and paroxetine—which can worsen delirium—were stopped.
Head MRI with contrast revealed sulcal space prominence in the cerebral and cerebellar hemispheres, suggesting minimal volume loss, and nonspecific bilateral periventricular punctuate flairs and T2 hypodensities, indicating small-vessel ischemic disease. EEG showed moderate rhythm slowing. Blood and urine tests showed no infectious disease or metabolic abnormalities.
Lesions associated with Wernicke’s encephalopathy (WE) usually are found in the third ventricle, cerebral aqueduct, fourth ventricle, mamillary bodies, periaqueductal gray matter, dorsomedial thalamus, septal region, and oculomotor nuclei.
In approximately 50% of cases, damage to the cerebellum also occurs. Such damage is usually symmetrical and shows diffuse, patchy endothelial prominence, proliferation of microglia, and petechial hemorrhage.
In chronic cases, demyelination and gliosis occur. Neuronal loss is prominent in the medial thalamus. Atrophy of the mamillary bodies indicates chronic WE.
Source: References 8-10.