We report the case of a 58-year-old man who was admitted to our rehabilitation unit from a subacute care unit with a diagnosis of Schizophrenic Disorder.
Its only antecedent up to 54 years old was a lumbar discal hernia surgery.
It is right for writing and needs optical correction for reading.
Treated in administration, he has worked well for over 30 years as head of management in a company.
She lives with her wife and two younger children.
At the age of 54, she suffered an episode of mutism and disconnection of the environment with hypotonia.
Epidermitis is suspected and referred to the neurology service, which after the study catalogues it as complex partial seizures.
The initial EEG (with photostimulation and sleep deprivation) does not reflect the paroxysms, there is only background activity with an alpha occipital rhythm at 9 Hz, without irritative signs or focality.
Treatment with valproate sodium is started (we do not know dose and duration) with a virtually null response and, upon repeated epsiodia, abandons the medication and follow-up.
The family describes the persistence of the clinic as recurrent episodes of mutism and disconnection, of increasing frequency.
At the age of 56, the patient was admitted to the neurology service due to a sudden episode of dysarthria, paresthesia in the right upper limb, and disconnection of the medium with masticatory movements and fixation of the mass.
A new EEG showed mild dysfunction in the left temporal region on a normal background activity.
Cranial CT, MRI and MR angiography showed no pathological changes.
At discharge the diagnosis was a probable migraine episode with visual aura and hypercholesterolemia, with treatment with sodium valproate (500 mg/day), atorvastatin/day) and acetylsalicylic acid (300 mg).
In subsequent outpatient follow-up, SPECT showed a minimal perfusion defect in the left temporoparietal region.
In the week after discharge, the patient disappears several hours from home.
They find him in his trough, caught in a harness, in a state of akinetic mutism and unresponsive to stimuli.
They study the case Internal Medicine and Neurology and found no pathological data justifying the complementary tests.
They do find a major conflict at work and relationship level, suspecting an episode of diversion.
Interconsultation with psychiatry is the first contact of the patient with this specialty.
The diagnosis of the first admission to the acute psychiatric unit is catatonia to be affiliated.
He presents mutism and lack of response to persistent stimuli after 7 days of treatment with diazepam (40 mg/day).
It was decided to administer ECT (7 sessions) and start antidepressant treatment with venlatine (150 mg/day).
Along the ECT sessions spontaneous speech is recovered, but there is still difficulty in expression (anomia and longilalia), a complete lacunar amnesia of the previous episode, and an incomplete amnesia of more events (of more weeks).
After hospital discharge, amnesia episodes persist, with motor and language block.
It has difficulties in making an autonomous life, including basic aspects of self-care, and appears a secondary picture of anxiety and low mood that motivates the second psychiatric admission, of several weeks.
Then, "episodes of absence with distinctive features and posterior amnesia" are described, which are labeled as recessive, with partial recovery of amnesia.
Antidepressant treatment is modified to escitalopram (20 mg/day), adding dipotassium clorazepate (15 mg/day) and trazodone (100 mg/day).
Diagnosis at discharge is congenital amnesia.
A month later, the patient required a third psychiatric admission due to intense anguish, despair, self-harm, persistence of amnestic symptoms, and severe impairment of global functioning.
Due to the high frequency of admissions and functional impairment, she is referred to the subacute care unit, where she is diagnosed with schizophrenic disorder.
They are based on torpid evolution, lack of response to medication and biographical disruption, despite the absence of positive psychotic symptoms.
The patient was prescribed olanzapine (20 mg/day) and partially anxiety and self-lytic ideation persisting episodes of amnesia and headache.
The important destructuring that the patient suffered in all vitals motivates the referral to the rehabilitation unit our center, where it proceeds to review the entire history considering that the diagnosis until then was impractical.
There was no family history of psychiatric or neurological diseases.
The patient is the fifth in the six brothers' ward, her pregnancy, delivery and maturational development were normal.
She was 4 years old and described a childhood "features and normal", with good academic performance and social functioning.
The patient describes episodes of bullying as moments of "fear of consciousness" lasting minutes without a triggering factor identified, with headache and a state of later dreaming.
There is amnesia of the episode.
The frequency is initially monthly or weekly, but with time it becomes daily.
It verifies failures in the autobiographical memory, including concrete and important facts in the upbringinging of their children, of the conjugal relationship and other events, which is a source of alarm for the family.
This confirms the existence of recurrent episodic amnesia.
According to them, there may be moments of stupor, often with masticatory motor automatisms, but they do not appreciate loss of consciousness and the rest of the cognitive functions seem normal.
They confirm the memory loss of episodes and previous self-reported data, as well as the difficulty in retaining memories generated in the days and weeks after admission (e.g. during hospitalization).
At psychopathological level only clinical features compatible with a major depressive episode are observed, which is interpreted as secondary to severe and progressive deterioration.
Neuropsychological assessment indicates difficulties in prospective memory, without problems in immediate and working memory.
It has difficulties in visual and verbal long-term memory, and difficulties to retrieve information from past episodes.
There is no global cognitive impairment (standard language, gnoses, and praxis).
There is a marked general slowness in tasks with and without motor component, which could be explained by its picture.
Nevertheless, long-term memory difficulties are not explained by motivational causes, since the patient made an effort to perform the tests.
The conclusion is that these findings are not explained only by the presence of psychiatric problems.
Based on the above, the diagnosis of transient epileptic amnesia is proposed, since we consider that the diagnostic criteria defined for this entity are fulfilled.
As an initial pharmacological measure, in order to rule out a functional origin of the clinic, treatment should be discontinued.
Antidepressant treatment was prescribed with venlatine (2.25 mg/day), mimicazapine (30 mg/day) and aripiprazole (as an antidepressant potentiator, at a dose of 5 mg/day), and significantly improved
As paroxysms persisted after resolution of the condition, and with suspected transient epileptic amnesia, levetiracetam was introduced at increasing doses (hasta 1500 mg/ 12).
During the first weeks of growth she presented isolated episodes of amnesia, which have not been recorded later for 4 months.
The patient, currently asymptomatic, continues in the psychosocial rehabilitation program to recover adequate personal functioning and return home.
