Depresie severă post-accident vascular cerebral silenţios

 Severe depression after silent stroke

First published: 16 septembrie 2020

Editorial Group: MEDICHUB MEDIA

DOI: 10.26416/Psih.62.3.2020.3879


Depressive disorder of somatic etiology is termed organic depressive disorder or depressive disorder secondary to a general medical condition. The organic cause of affective manifestations should always be considered and excluded because there are many organic diseases (e.g., neurological, endocrinological) that can present with psychiatric symptoms. In this paper, we report the case of a 54-year-old female patient, without a history of mental diseases, admitted for symptoms of a severe depressive episode with psychotic symptomatology, in whom recent sequelae of a silent stroke were neurologically detected by imaging.

organic depression, post-stroke depression, stroke


Tulburarea depresivă având la bază o etiologie somatică poartă numele de tulburare depresivă organică sau tulburare depresivă secundară unei condiţii medicale generale. Cauza organică a manifestărilor afective trebuie mereu considerată şi exclusă, deoarece există numeroase patologii organice (de exemplu, neurologice sau endocrinologice) care pot prezenta simptome psihiatrice. În lucrarea de faţă, prezentăm cazul unei paciente de 54 de ani, fără antecedente psihiatrice, internată pentru simptomatologia unui episod depresiv sever cu simptome psihotice la care se decelează imagistic sechele recente ale unui accident vascular cerebral silenţios, din punct de vedere obiectiv neurologic.


Brain dysfunction associated with certain medical and neurological diseases can cause any psychiatric symptom. This means that the presentations considered to be “psychiatric” are always likely to be explained by an unexplored or unidentified underlying medical pathology. Missing the organic disease may have catastrophic consequences for the patient by delay of diagnosis, lack of specific and timely treatment, with a negative impact on evolution, costs and quality of life(1).

The following clinical case brings to the foreground a psychiatric picture as the unique manifestation of a silent stroke, the difficulty consisting of orienting towards a possible neurological involvement, despite the absence of objective neurological deficits.

It is known that depression is the most frequent psychiatric disorder associated with cerebrovascular diseases(2), some studies showing that at least 30-60% of patients who have suffered a stroke present depression symptoms. Currently, the mechanism of post-stroke depression remains unclear(3) and, although it was believed that the occurrence of depressive symptoms was largely the consequence of the sudden onset of physical handicap, awareness of cognitive deficits and loss of personal independence secondary to stroke, it was observed that depression also occurs in the case of hidden, “silent”, asymptomatic stroke, without obvious neurological deficits(4). Although the prevalence of silent stroke varies between 12.9%(5) and 38%(6), its real prevalence in the general population remains unknown. Also, it is unclear whether this is really asymptomatic(7). Fujikawa et al.(8) propose the possible presence of psychiatric symptoms as manifestations of silent stroke. In clinical practice, stroke in the frontal lobe most frequently causes depression, because it is involved in emotional processing, as well as in superior cognitive processes, memory, attention and executive function(9). The picture of clinical manifestations contains a broad spectrum: from impulsivity and disinhibition to apathy, abulia and amotivational syndrome(10).

The authors wish to evidence the importance of exploring organicity and the attention given to the patient and his/her reports, with the repetition of anamnesis and diagnostic hypotheses whenever necessary.

Case report

We present the case of the patient B.M.M., aged 54 years old, from an urban area, admitted to the Clinic of Psychiatry in the period 16 June 2020 – 3 July 2020.

The 54-year-old female patient, without a history of mental diseases, but with two known previous psychiatric examinations during the week prior to admission, noncompliant with the prescribed psychotropic treatment, was brought to emergency by her husband, for symptoms of a severe depressive episode with psychotic symptomatology: negative hyperthymia with sad mood, anhedonia, fatigue, micromanic delirious ideas, guilt, reduced useful and daily performance, inappetence with weight loss and mixed insomnia, symptoms starting about one month before, with progressive worsening. At presentation, the patient was calm, but with a passive attitude, with verbal negativity, and subsequently she answered the questions only by head movements. She did not even tell her name when asked, and she did not sign the informed consent for admission.

Patient’s history

The patient was known to have cardiovascular disease (essential hypertension and viral myocarditis at the age of 40 years old, under specific treatment, poorly controlled chronic tachycardia, grade II mitral insufficiency) and familial aggregation for cardiac disease (her father, paternal cousins, mother and sister). She came from a legally constituted family with two children, a supportive intrafamilial environment based on harmonious relationships. She attended higher education, subsequently working as a lawyer and dedicating a considerable amount of time to her career. She was married and had a daughter.

Objective examination at admission: BMI=23, BP=150/100 mmHg, VR=110 bpm, neurological examination within normal limits.

The psychic examination was performed heteroanamnestically at admission because the patient showed verbal negativity.

  • Clothing: adequate.

  • Hygiene: maintained.

  • Facies: sad, hypomobile.

  • Gestures: hypomobile.

  • Verbal contact and dialogue: not initiated, verbal negativity, approval or disapproval by head movements.

  • Attitude: partially cooperative, passive.

  • Perception: high perceptual threshold, no qualitative disorders could be evidenced at the time of examination.

  • Attention: concentration hypoprosexia with sectorial hyperprosexia focused on delirious themes.

  • Memory: cannot be evaluated.

  • Thinking: slow idea flow, delirious interpretation, micromanic helpless, guilt ideas, consistent with the mood, pessimism, catastrophic ideas.

  • Affectivity: negative hyperthymia with sad mood, anhedonia, apathy, freely floating anxiety.

  • Activity: psychomotor inhibition with psychomotor restlessness episodes, fatigue, adynamia, diminished daily and useful performance, social withdrawal, bradykinesia.

  • Volition: abulia.

  • Instincts: diminished eating instinct, conservation instinct present.

  • Nycthemeral rhythm: mixed insomnia.

  • Consciousness: cannot be evaluated, absence of disease awareness.

  • Personality: cannot be evaluated.

Paraclinically, a mild inflammatory syndrome was detected, as well as leukocytosis with neutrophilia, leukocyturia, urinary sediment with frequent leukocytes interpreted as urinary infection, and specific antibiotic treatment according to the antibiogram was administered. Thyroid function (TSH, FT4) was within normal limits. ECG detected sinus rhytm, tachycardia (VR=115 bpm), without terminal phase changes.

Drug therapy, in-hospital evolution and additional investigations

Given that the patient was not adequately hydrated and nourished before admission, hydroelectrolytic rebalancing therapy and vitamin group B therapy were added to the therapeutic scheme. The patient had high blood pressure values and tachycardia, despite the treatment for associated cardiac disease. Specific treatment (enalapril 5 mg, metoprolol 50 mg) was administered; BP and VR were monitored in order to stabilize values.

An SSRI antidepressant (sertraline) was chosen, which was initiated at a dose of 50 mg/day, with a progressive increase to 100 mg/day, and an atypical antipsychotic (olanzapine 5 mg/day) and an incisive antipsychotic (haloperidol as an oral solution initially in doses of 3 mg/day) were added to fight psychotic symptoms, with the monitoring of adverse effects. The patient had psychomotor inhibition, verbal negativity, and she refused medication. One vial of Zyprexa® i.m. injection was administered, and sertraline and haloperidol administration was progressively stopped. Venlafaxine 75 mg/day was added to the therapeutic scheme, the dose being increased up to 225 mg/day, along with aripiprazole 10 mg/day, increased up to 20 mg/day.

Somatically, tachycardia persisted, which is why the dose of bisoprolol was increased to 10 mg/day. Antibiotic therapy for UTI with ceftriaxone 1 g/day p.o. was also initiated, after previous testing for 7 days.

All symptoms present in the clinical picture were typical of a depressive episode. However, during admission, the patient had a favorable evolution from a psychiatric point of view, with the improvement of depressive symptoms, but evidencing marked focused attention and working memory deficits. History was retaken, with emphasis on cognitive deficits, and the patient reported that “I feel better, I feel that I have recovered, but I cannot focus and I didn’t use to be like that”. Subsequently, she reported that she had an episode on May 6, during which “I got stuck, I couldn’t speak, then I repeated the same words several times. Then I felt that something happened inside my body, that something didn’t work. I was like Stela Popescu during her last speech. I told this to my husband when I got home, but he didn’t believe me”. Correlated with the lack of psychiatric history, but with a personal and family history of cardiac involvement, a cerebrovascular pathology or cognitive impairment was suspected.

Brain computed tomography was performed, which evidenced a hypodensity with the disappearance of cortico-subcortical differentiation in the right middle frontal gyrus of 16/15/25 mm (AP/LL/CC), with an appearance of subacute ischemic stroke. The extensive objective neurological examination as part of the neurological examination performed detected no pathological changes. The patient also underwent internal and cardiological examination, with the modification of treatment for cardiac pathology, and echocardiography and carotid Doppler, which detected bilateral carotid atheromatosis. A subsequent brain MRI reconfirmed right frontal ischemic stroke, this time sequelar. After the detection of stroke, the therapeutic scheme was supplemented with a platelet antiaggregant (Aspenter® 75 mg/day), a hypolipidemic drug (Sortis® 20 mg/day), and the dose of Micardis Plus® (a combination of telmisartan+hydrochlorothiazide) was increased to 80/25 mg.

Psychological examination

The examination of the verbal memory capacity with the Rey test evidences a normal curve, as follows: an increase at each repetition, starting with eight memorized words, and an increase rate of two words at each repetition. The examination of the visual memory capacity with the complex figure test evidences the following aspects: during the copying phase, the patient uses an adequate strategy, which allows a good structuring of the perceptual field expressed in the execution of the 17/18 elements. In this phase, the graphic approach shows a good analysis and perceptual synthesis capacity, as well as an ability to establish relationships between them and integrate them in meaningful units. During the reproduction phase, the strategy is the same as in the copying phase, but a weakening of the perceptual field occurs, which is expressed in the execution of the 8/18 elements. Visual memory with diminished efficiency and the memorizing strategies used are not effective. Dependent disharmonic personality (SCID II), without conflictual contact with the environment. A good adaptation capacity. At the time of the examination, the psychopathological picture describes a tendency to perfectionism, depressive elements, and interpretive elements. Sudden fear in the context of increased susceptibility. The inhibited and projective ego takes awareness of actions at a low level. Judgements change under the influence of emotions. Significantly diminished assertiveness. Developed elaboration capacity and vivid interests.

The final therapeutic scheme, to which the best therapeutic response was obtained, was venlafaxine 225 mg/day, olanzapine 5 mg/day, aripiprazole 20 mg/day, and for the associated somatic disorders: Aspenter® 75 mg/day, Sortis® 20 mg/day, bisoprolol 10 mg/day, Micardis Plus® 80/25 mg 1tb/day and a course of 10 days with Cerebrolysin®.

The patient was discharged on 3.07.2020 with the diagnosis (according to ICD): organic depressive disorder. Dependent personality.

The depressive disorder is causally linked and manifests subsequently to stroke onset, brain dysfunction respectively, the diagnosis being supported by:

  • the evidence that stroke is associated with depression (clinical studies, literature data);

  • there is a temporal relationship (about two weeks) between the occurrence of stroke and the onset of depressive symptoms;

  • the absence of evidence suggesting an alternative etiology for depressive symptoms (lack of personal and family history of affective disorders).

Among recommendations at discharge, we mention the importance of adequate psychiatric as well as neurological and cardiac follow-up, compliance with specialized recommendations, secondary prevention of stroke and cognitive training. Regarding treatment, the drug doses required for stable remission with the minimum effective doses will be tested, and the duration of treatment will be correlated with evolution. The depressive symptoms as well as cognitive dysfunction will be periodically reevaluated, with the possibility of adding during evolution, in case of worsening of cognitive dysfunction, an antidementia drug. 


Even in the presence of a typical picture of depression, the psychiatrist should take into consideration and exclude a possible organic etiology. In practice, the exploratory approach can often be difficult and requires an opening and attention oriented towards the patient, as well as an effective multidisciplinary collaboration. The particularity of the case is the presence of psychiatric symptoms in the foreground, as a consequence of neurological involvement evidenced only by imaging and by secondary cognitive deficits.


Repeating history taking and diagnostic approach in case of the occurrence or observation of new or different elements compared to the initial hypothesis and paying attention to patient’s reports are important. It is said that “we see what we look for”, so it would be useful to train our mind to always explore and, despite the focus on psychiatric pathology, to investigate and exclude organicity. 


  1. Welch KA, Carson AJ. When psychiatric symptoms reflect medical conditions. Clin Med (Lond). 2018; 18(1):80-87. doi:10.7861/clinmedicine.18-1-80

  2. Ghoge H, Sharma S, Sonawalla S, Parikh R. Cerebrovascular diseases and depression. Curr Psychiatry Rep. 2003; 5(3):231-238. doi:10.1007/s11920-003-0048-7

  3. Shi Y, Zeng Y, Wu L, et al. A Study of the Brain Abnormalities of Post-Stroke Depression in Frontal Lobe Lesion. Sci Rep. 2017; 7(1):13203. Published 2017 Oct 16. doi:10.1038/s41598-017-13681-w

  4. Albert PR. Is poststroke depression the same as major depression? J Psychiatry Neurosci. 2018; 43(2):76-78. doi:10.1503/jpn.180015

  5. Shinkawa A, Ueda K, Kiyohara Y, et al. Silent cerebral infarction in a community-based autopsy series in Japan. The Hisayama Study. Stroke. 1995; 26(3): 380-385.

  6. Ricci S, Celani MG, La Rosa F, et al. Silent brain infarctions in patients with first-ever stroke. A community-based study in Umbria, Italy. Stroke. 1993; 24(5): 647-651.

  7. Nagaratnam N, Bou-Haidar P, Leung H. Confused and disturbed behaviour in the elderly following silent frontal lobe infarction. American Journal of Alzheimer’s Disease & Other Dementias. 2003; 333–339. 

  8. Fujikawa T, Yamawaki S, Touhouda Y. Silent cerebral infarctions in patients with late-onset mania. Stroke. 1995; 26(6): 946-949.

  9. Shi YZ, et al. The relationship between frontal lobe lesions, course of post-stroke depression, and 1-year prognosis in patients with first-ever ischemic stroke. PloS One. 2014; 9, e100456.

  10. García Carretero R, Beamonte-Vela B, Silvano-Cocinero J, et al. Behavioural changes as the first manifestation of a silent frontal lobe stroke. BMJ Case Reports CP. 2019; 12:bcr-2018-227617. 


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