Dementia development during B vitamin therapy

The patient was a woman, born 1922, a retired cashier, a married non-smoker with migraine.

The present disease started with cataract in both eyes. Both lenses were subject to surgical intervention 1991.

The patient developed Parkinsonīs disease in 1992. The symptoms responded well to L-dopa treatment, T. Madopark 100 mg x 3. She had depressed monoamine metabolites in her cerebrospinal fluid and her somatostatin was 13 pg/mL, reference range 20-50.

A CT in 1993 suggested atrophy of substantia nigra and decreased density of the left corpus striatum. At the same time, it was noted that serum cobalamins (82-92 pmol/L) and serum folates (4-6 nmol/L) were depressed under their lower reference range. Oral high-dose cyanocobalamin (Behepan), 1 mg daily, and oral high-dose folic acid (Folacin), 10 mg daily, were added.

Subsequent monitoring mirrored satisfactory compliance and absorption of the patient, serum cobalamins 1,820 pmol/L, serum folates >50 nmol/L. However, the motility of the patient deteriorated successively in the period 1995-99.

An aphasia episode in 1998 left no marks in the CT picture. Prophylactic treatment with acetylsalicylic acid was started. The patient became more rigid and confused. She fainted repeatedly and developed dementia. An electroencephalogram in 1999 showed a slow basic rhythm, 6-7 Hz.

The conclusion of the clinician of the patient is that adequate treatment with B vitamins not always prevents the development of dementia.


Updated juli 15, 2000