Tulburări neurocognitive la pacienţii cu dependenţă cronică alcoolică

 Neurocognitive disorders in patients with alcoholic dependence

First published: 20 noiembrie 2021

Editorial Group: MEDICHUB MEDIA

DOI: 10.26416/Psih.67.4.2021.5736


Progressive neurocognitive, affective and behavioural deterioration in the case of the patient with chronic alcoholic dependence leads to a deterioration in all spheres of functionality. Intellectual decline is often the trigger of degradation in terms of career, social and family path. A long-term, two-way therapeutic approach is required, through drug treatment and specific psychotherapeutic interventions.

chronic alcoholic dependence, intellectual deterioration, two-way therapeutic approach


Deteriorarea progresivă neurocognitivă, afectivă şi comportamentală, în cazul pacientului cu dependenţă cronică alcoolică, duce la o deteriorarea în toate sferele de funcţionalitate. Afectarea intelectuală reprezintă de multe ori triggerul degradării în ceea ce priveşte parcursului profesional, social şi familial. Se impune astfel o abordare terapeutică, pe termen lung, bidirecţională, prin tratament medicamentos şi intervenţii psihoterapeutice specifice.

We present the case of a man diagnosed with alcohol-induced amnestic syndrome (Wernicke-Korsakoff syndrome), symptoms based on ICD-10 diagnostic criteria. The patient had significant cognitive impairments, measured with the Mini-Mental State Examination (MMSE). A complex treatment was initiated, with parenteral neurotrophic factors, vitamins (thiamine/pyridoxine/ascorbic acid), oral psychotropic drugs, including antidepressants, and psychotherapy. After a few weeks, the cognitive symptoms have been improved as a result of the prescribed treatment. Antidepressants and psychotherapy allow the long-term approach of alcohol dependence in the future.

Patient description

The patient is a 55-year-old male, living in the city, university graduated, divorced and currently living with his parents.

Case history. The patient comes from a family of intellectuals with a high level of sociocultural status, being the first child of two (his brother being 3 years younger than him).

His school performance was good, as a results of the parent’s control, whose expectations of him were very high.

His confidence was high only when he had his pockets filled with money. As a consequence of the strict parents, the rigid atmosphere, the parents’ unrealistic expectations of him led to behaviour damage in the adolescent stage: alcohol, showing off, rebel attitude.

Admission symptoms (8.12.2020): temporospatial and self-orientation disorders (“Now I’m at the supermarket for shopping”); memory disorders, confabulations (The day before the admission he was present at work and in the evening he cooked a steak for his parents); sad mood, generalized hypobulia, sleeplessness, marked ineptitude.

Physical examination:

  • underweight patient (BMI 17.65)

  • hepatomegaly

  • cerebellar syndrome with ataxia (inability to move without support, lack of motor coordination)

  • lateral nystagmus

  • deficiency toxic polyneuropathy

  • pressure sores at bilateral sacral level – grade III (in the last period being bedridden due to motor disorders, he continued to consume alcohol; his mother brought him alcoholic drinks to bed, being pity of him).

Psychological examination

  • Consumption of alcohol (AUDIT) = 39 points (alcohol consumption, very damaging for his health).

  • Global cognitive damage: anterograde memory loss and retrograde type lacunar, confabulation, constructive dyspraxia (MMSE = 16).

  • Sad mood, generalised hypobulia, anxiety (BDI = 21 points, moderate intensity).

  • Personality test (SCID-II): passive-aggressive personality disorder.

Laboratory tests

  • ency anemia – FE-29.6 µg/dl;iron defici

  • Hb12.3g/dl; Ht 35.7%

  • low uric acid – 3.03 mg/dl

  • low magnesium – 1.02 mg/dl

  • ionogram – normal

  • EKG – sinus rhythm, axe going left

  • Cerebral CT – cortico-subcortical diffuse atrophy

  • PCR COVID-19 test – negative


From the anamnestic data, the physical and psychological examination, the laboratory examinations and imaging, it was established the main diagnosis: alcohol-induced amnestic syndrome (Wernicke-Korsakoff syndrome)(1).

Therapeutic plan

  • Correcting/improving the overall cognitive deficit with nutritional rebalancing (priority).

  • The treatment of depression (after the improvement of cognitive symptomatology) – drug treatment and psychotherapy, to allow the long-term approach of alcohol dependence in the future.

  • Treatment of bedsores.

Treatment instituted (initial stage – first five days)

  • in B1 (thiamine hydrochloride) –Vitam

  • 400 mg/day/i.v.

  • Vitamin B6 (pyridoxine hydrochloride) –

  • 250 mg/day/i.v.

  • Ferrous sulphate anhydrous – 320 mg (100 mg Fe2+)

  • Ascorbic acid – 60 mg.

  • Silymarin – 450 mg/day.

  • Pantoprazole – 40 mg, 1 tb/day.

  • Tonotil-N (combination of essential amino acids with hydroxocobalamin) – 2 flacons per day.

  • Treatment of bedsores: daily toileting and dressing with hydrocolloidal gel (Hydrosorb®), anti-bedsores mattress.

Assessment after the initial stage of treatment

The evolution (after the initial stage) was slightly favourable, with the improvement of cognitive disorders (MMSE=18), ataxia and coordination disorders, but the temporospatial disorientation and the sad mood with thoughts of guilt persisted (the patient was aware of the memory and concentration disorders which aggravated his depressive symptomatology; BDI=21).

Treatment (later stage)

Antidepressant treatment – tianeptinum 12.5 mg, 3 tablets per day.

Cerebrolysin® (purified brain proteins derived from swine brain) 10 ml/day, infused, for 20 days, was added in the treatment protocol, due to the presence of a moderate cognitive deterioration and an evident diffuse cortical atrophy (on cerebral CT), even after 10 days of treatment.

A psychotherapeutic intervention was started through short-term motivational psychotherapy in order to provide support to maintain the long-term abstinence.

Evolution after the later stage treatment (30 days after admission) 

The neurological symptoms have been improved; the significant cognitive deficit remitted (MMSE=24), maintaining the attention dysfunctionality; we observed an important improvement regarding mood, with a strong motivation for abstinence from alcohol.

Evolution after discharge

The patient had a favourable evolution after discharge. He returned to the monthly control, and continues the treatment with neurotrophic factors and psychotherapy. Also, he has restarted sports (swimming) and old hobbies (gardening), he has committed to handle the accounting of the family firm, but still does not have an active social life (the pandemic being also a cause).


The goal of this case presentation is to highlight the progressive decline of a patient with chronic alcoholic addiction who ends up losing everything and manages to be “reborn” when he realized the severity of physical and mental damage (especially cognitively).

Many of the studies in the specific literature describes the neurotrophic effect of treatment with Cerebrolisyn® regarding brain protection, as well as repair, in order to counteract pathologies of acute and chronic neurological disorders.

From the published data so far, I picked up the study of Vaghef et al. (2019)(2), described below, to illustrate the important role of Cerebrolysin® for brain regeneration, with concern to various organic, metabolic, as well as neurodegenerative brain dysfunctions associated with alcohol consumption: “Cerebrolysin® attenuates ethanol-induced spatial memory impairments through inhibition of hippocampal oxidative stress and apoptotic cell death in rats” (Vaghef et al., 2019)(2).

This study investigated the potential neuroprotective effect of Cerebrolysin® (CBL), a combination of neurotrophic factors, on the cognitive and biochemical alteration induced by chronic ethanol administration in rats.

The animals were divided into five groups, as follows: control, ethanol (4 g/kg, for 30 days), ethanol plus CBL 1 ml/kg, ethanol plus CBL 2.5 ml/kg, and ethanol plus 5 ml/kg.

Morris water maze (MWM) test was performed to assess the cognitive impairment.

The status of the lipid peroxidation marker (MDA), antioxidant capacity, as well as alteration of the apoptotic factors such as Bcl-2, BAX, and cleaved-caspase 9 and 3 were evaluated in hippocampus.

The results showed that CBL treatment not only normalized the increased MDA levels in the alcoholic rats and enhanced the antioxidant defense, but also reduced the BAX/Bcl-2 ratio and cleaved  caspase 9 and 3 in the hippocampus.

The spatial memory was improved.

The findings of this study provide evidence for the promising therapeutic effect of CBL in chronic ethanol consumption through counteracting oxidative stress and apoptosis markers.


This clinical case suggests the possibility that Cerebrolysin®, the only drug available for clinical use containing active fragments of important neurotrophic factors such as BDNF, GDNF, CNTF and NGF and others, may help in the treatment of the mental and behavioural disorders due to psychoactive substance abuse. Cerebrolysin® treatment seems to be safe when used in combination with thiamine and others vitamins and with antidepressant treatment.

The drug approach (the correction of the deficiency of thiamine mainly, neurotrophic factors and antidepressant medication) together with psychotherapy managed in relatively short time to repair what destroyed alcohol addiction in 40 years!  


1. Brämer GR. International statistical classification of diseases and related health problems. Tenth revision. World Health Stat Q. 1988;41(1):32-6.
 2. Vaghef L, Farajdokht F, Erfani M, Majdi A, Sadigh-Eteghad S, Karimi P, Sandoghchian Shotorbani S, Seyedi Vafaee M, Mahmoudi J. Cerebrolysin attenuates ethanol-induced spatial memory impairments through inhibition of hippocampal oxidative stress and apoptotic cell death in rats. Alcohol. 2019 Sep;79:127-135.