0
Get Alert
Please Wait... Processing your request... Please Wait.
You must sign in to sign-up for alerts.

Please confirm that your email address is correct, so you can successfully receive this alert.

1
Letter   |    
Paroxetine Treatment in Alcohol Amnestic Disorder
U. W. Preuss, M.D.; M. Soyka, M.D.
The Journal of Neuropsychiatry and Clinical Neurosciences 1999;11:286a-287.
View Author and Article Information

SSRIsAlcoholAlcohol Amnestic Disorder

SIR: The medical treatment of alcohol amnestic disorder (AAD) is a challenge. AAD follows Wernicke encephalopathy in about 80% of cases.1 Typical psychiatric features of AAD are short-term memory loss and disorientation to time, place, and person, but there is no damage to ultrashort memory, consciousness, or cognitive functions.2 Confabulations are typical but not necessary for diagnosis of AAD.

Only a few studies have been conducted in medical treatment of AAD, and each had a study population of 10 or fewer.

The theoretical basis for the treatment of AAD with an SSRI comes from the suggestion that enhancing serotonergic neurotransmission might play a potentially therapeutic role in AAD.3 Controversial results were reported by two research groups publishing four studies within the last 10 years.

In one of the first studies in this research area, 8 patients with AAD were treated with fluvoxamine in doses between 200 and 400 mg/day vs. control subjects in a double-blind crossover study over a period of 6 weeks.3,4 A significant improvement of memory function was observed in the treated group. Similar results were reported from a later study by this group,5 of 10 patients treated with fluvoxamine in doses up to 200 mg/day in a 4-week interval. However, in another study,6 no such improvement of memory function or cognitive or verbal performance was reported in 8 AAD patients treated with fluvoxamine in doses up to 200 mg/day.

+

Case Report

A 51-year-old male patient had a history of chronic alcoholism for at least 20 years. He was admitted to our ward from an emergency unit with symptoms of Wernicke encephalopathy. He had severe disturbances of memory function and showed confabulations and disorientation to time and place. Psychomotor disturbances were seen, as well as neurologic symptoms, including ataxia and ophthalmoplegia. The patient's cranial computed tomography and nuclear magnetic resonance imaging showed cortical atrophy; basal brain structural damages, such as mammillary bodies; and enlargement of ventricles. With a thiamine treatment up to 400 mg/day iv, the neurological symptoms disappeared within days, but memory disturbances and disorientation in time and place persisted.

We started treatment with the SSRI paroxetine, with up to maximum dosage of 60 mg/day. Paroxetine instead of fluvoxamine was chosen for AAD treatment because of its shorter half-life, lack of active metabolites, and its supposedly fewer side effects compared with other SSRIs. A lower dosage can be administered, as well.7

A maximum paroxetine plasma-concentration of 387 ng/ml was found after 7 weeks of treatment. The plasma level was in the upper 5% of values from 1,302 inpatients from our hospital (level/dosage: 6.45; 95% confidence interval: level/dosage>5.54). The patient was tested before and retested with the same psychological tests after 7 weeks of medication. Improvement of memory function was observed; the patient recognized 5 pictures out of 12 (vs. l in the first testing); there was an improvement on the SKT (Syndrom Kurz Test8); and he showed a time improvement of 50% on the pathfinder test. However, despite improvement of memory function, disorientation persisted, and the patient was recommended for continued inpatient treatment.

In treatment studies, those patients with plasma fluvoxamine concentrations above 350 ng/ml showed the greatest improvements in memory function, whereas those with plasma concentrations below 150 ng/ml had negligible changes in memory function.4 The patient's paroxetine plasma levels observed in our case were higher than those of 95% of patients treated for depression in our hospital.

Paroxetine may contribute to improvement of memory function in AAD patients. However, larger studies with SSRIs in combination with memory training in AAD patients are needed to evaluate its use in alcohol-induced amnestic syndromes.

Masuhr KF, Neumann M: Neurologie, 2: Auflage. Stuttgart, Germany, Hippokrates-Verlag, 1992
 
Preuss UW, Soyka M: The Wernicke-Korsakoff-syndrome: clinical and pathophysiological characteristics. Fortschr Neurol Psychiatr  1997; 9:413—420
 
Martin PR, Adinoff B, Eckardt MJ, et al: Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine: preliminary findings. Arch Gen Psychiatry  1990; 46:617—621
 
Martin PR, Adinolf B, Lane E, et al: Fluvoxamine treatment of alcoholic amnestic disorder. Eur Neuropsychopharmacol  1995; 5:27—33
[CrossRef] | [PubMed]
 
Stapleton JM, Eckardt MJ, Martin P, et al: Treatment of alcoholic organic brain syndrome with the serotonin reuptake inhibitor fluvoxamine: a preliminary study. Adv Alcohol Subst Abuse  1994; 7:47—51
 
O'Carroll RE, Moffoot AP, Ebmeier KP, et al: Effects of fluvoxamine treatment on cognitive functioning in the alcoholic Korsakoff syndrome. Psychopharmacology (Berlin [Germany])  1994; 116:85—88
[CrossRef]
 
Feighner JP: Klinische Wirkungen von Serotonin-Wiederaufnahmehemmern: eine Übersicht. Fortschr Neurol Psychiatr 1994; 62(suppl 1):9—15
 
Overall JE, Schaltenbrand R: The SKT neuropsychological test battery. J Geriatr Psychiatry Neurol  1992; 5:220—227
[PubMed]
 
+

References

Masuhr KF, Neumann M: Neurologie, 2: Auflage. Stuttgart, Germany, Hippokrates-Verlag, 1992
 
Preuss UW, Soyka M: The Wernicke-Korsakoff-syndrome: clinical and pathophysiological characteristics. Fortschr Neurol Psychiatr  1997; 9:413—420
 
Martin PR, Adinoff B, Eckardt MJ, et al: Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine: preliminary findings. Arch Gen Psychiatry  1990; 46:617—621
 
Martin PR, Adinolf B, Lane E, et al: Fluvoxamine treatment of alcoholic amnestic disorder. Eur Neuropsychopharmacol  1995; 5:27—33
[CrossRef] | [PubMed]
 
Stapleton JM, Eckardt MJ, Martin P, et al: Treatment of alcoholic organic brain syndrome with the serotonin reuptake inhibitor fluvoxamine: a preliminary study. Adv Alcohol Subst Abuse  1994; 7:47—51
 
O'Carroll RE, Moffoot AP, Ebmeier KP, et al: Effects of fluvoxamine treatment on cognitive functioning in the alcoholic Korsakoff syndrome. Psychopharmacology (Berlin [Germany])  1994; 116:85—88
[CrossRef]
 
Feighner JP: Klinische Wirkungen von Serotonin-Wiederaufnahmehemmern: eine Übersicht. Fortschr Neurol Psychiatr 1994; 62(suppl 1):9—15
 
Overall JE, Schaltenbrand R: The SKT neuropsychological test battery. J Geriatr Psychiatry Neurol  1992; 5:220—227
[PubMed]
 
+
+

CME Activity

There is currently no quiz available for this resource. Please click here to go to the CME page to find another.
Submit a Comments
Please read the other comments before you post yours. Contributors must reveal any conflict of interest.
Comments are moderated and will appear on the site at the discertion of APA editorial staff.

* = Required Field
(if multiple authors, separate names by comma)
Example: John Doe



Related Content
Books
Manual of Clinical Psychopharmacology, 7th Edition > Chapter 3.  >
Manual of Clinical Psychopharmacology, 7th Edition > Chapter 1.  >
Manual of Clinical Psychopharmacology, 7th Edition > Chapter 12.  >
Gabbard's Treatments of Psychiatric Disorders, 4th Edition > Chapter 1.  >
The American Psychiatric Publishing Textbook of Geriatric Psychiatry, 4th Edition > Chapter 26.  >
Topic Collections
Psychiatric News
PubMed Articles