Sažetak sa skupa

https://doi.org/10.24869/spsih.2026.214

Dementia-Like State Caused by Acute Intoxication and Chronic Polysubstance Abuse: A Case Report

Lea Kozina ; Klinika za psihijatriju Vrapče, Bolnička cesta 32, 10000 Zagreb, Hrvatska *
Mislav Gušćić ; Klinika za psihijatriju Vrapče, Bolnička cesta 32, 10000 Zagreb, Hrvatska
Zrnka Kovačić Petrović ; Klinika za psihijatriju Vrapče, Bolnička cesta 32, 10000 Zagreb, Hrvatska; Medicinski fakultet, Sveučilište u Zagrebu, Šalata 2, 10000 Zagreb, Hrvatska
Ivan Ćelić ; Klinika za psihijatriju Vrapče, Bolnička cesta 32, 10000 Zagreb, Hrvatska

* Dopisni autor.

Sažetak

Introduction: Acute intoxication with psychoactive
substances, their chronic abuse, and withdrawal
can cause harmful effects on the central
nervous system. The neurotoxic effects are numerous:
demyelinating changes, toxic leukoencephalopathy,
hypoxic‑ischemic brain injury, and
cerebral infarction. This paper presents a case of a
patient in whom a clinical picture of dementia developed
as a consequence of brain changes caused
by acute intoxication and chronic abuse of psychoactive
substances. Case report: A 30‑year‑old
female patient was treated in a somatic hospital
after a suicide attempt by intoxication with
pregabalin, buprenorphine, and diazepam. On
admission, she had impaired consciousness and
bradypnea. Brain CT was normal, while radiologic
workup verified bilateral pulmonary infiltrates with the development of sepsis. After stabilization
of her physical condition, she was transferred
to University Psychiatric Hospital Vrapče
for addiction treatment. On admission there, she
was taking quetiapine, pregabalin, levothyroxine,
and pantoprazole. She was clear in consciousness
and in contact, with psychomotor slowing, blunted
affect, organized thought flow, and no productive
psychopathology. It was learned that she had
been abusing cocaine, amphetamines, bupropion,
buprenorphine, pregabalin, and benzodiazepines.
After ten days of hospitalization, there was a
gradual development of confusion, ideational
apraxia, disorientation in time, amnesia with
confabulations, dysgraphia, dyscalculia, and loss
of independence in activities of daily living. EEG
showed diffuse dysrhythmic changes, and brain
MRI revealed bilaterally symmetric increased T2
signal of the deep and subcortical white matter
without mass effect, findings suspicious for toxic
demyelination associated with the use of adulterated
psychoactive substances. Treatment involved
reducing the dose of quetiapine, gradual
discontinuation of pregabalin, and introduction
of clonazepam. Vitamin B and D supplementation
was provided. A gradual recovery followed:
ideational apraxia resolved, the patient regained
independence in activities of daily living and
re‑established temporal orientation, with residual
partial amnesia for the period of deterioration.
Conclusion: Cognitive symptoms induced by the
abuse of psychoactive substances must be recognized
as early as possible so that treatment can
be initiated promptly, since recovery is possible.

Ključne riječi

psychoactive substances; dementia; demyelination; abuse

Hrčak ID:

352340

URI

https://hrcak.srce.hr/352340

Datum izdavanja:

15.6.2026.

Podaci na drugim jezicima: hrvatski

Posjeta: 0 *