A 44-year-old single man who lives with his mother and works in a protected employment.
Diagnosis of Schizophrenia Recurrent (F20.5, CIE-10) (11) under follow-up at his Mental Health Center and psychopharmacological treatment with 400 mg of amisulpiazepam-ride, 10 mg.
Non-daily but maintained consumption of tramadol, cannabis, alcohol and cocaine.
As antecedent sound highlights a difficulty in psychotic gait, as a consequence of multiple traumatism in the context of an episode 14 years ago.
The patient is found by his mother in the unconscious home without response to stimuli and without being able to specify the time he had in that state.
Self-poisoning with a large undetermined amount of tramadol, benzodiazepines, alcohol and cocaine.
Approach in the Intensive Care Unit for 6 days.
Complications include acute kidney injury, kidney failure and pneumonia.
Normal skull CT.
Training and transfer to Internal Medicine ward, one week of admission, somatic episode.
He was transferred to the Psychiatry Department, with a voluntary admission.
During the first five days of admission to the Psychiatry Unit the patient remains psychopathologically stable.
Non-psychotic criticism of the episode defined as "collocon" and of which he points out not being able to remember concrete conditioners, but rather a previous discussion with the mother.
Adapted to the rhythm of the Unit, participates in activities of Therapy or Path.
Euthymic, within the previous defectuality, concrete plans for the future, solutions with the family with adequate response, possibility of discharge and follow-up in their Mental Health Center.
However, after these first asymptomatic days, the patient begins to present with a progressive temporal-spatial disorientation accompanied by marked bpsychia, ataxia (generalized motor deterioration) and slowing down (generalised motor development).
Failures caused by mental illness accompanied by a memory, aphasia and apraxia
Nevertheless, the patient feels like a placid attitude.
No distress, sustained sleep.
No changes in previous psychiatric treatment.
Despite the insistence of the family in pointing out "a psychotic sprout" (...) the picture is framed in a cognitive impairment of cortical characteristics with striking affectation of the attentional system, executive function, memory function.
EEG shows marked slowing and diffuse attenuation of background rhythm.
After evaluation by Internal Medicine and Neurology, the patient was transferred to the Neurology Department.
The initial cranial MRI shows that supratentorially there is a pattern of diffuse frontoparietal leukodystrophy predominantly hyperintense on T2-weighted sequences, with a discrete restriction component on diffusion sequences.
(T2-MRI, image 1; T2-FLAIR MRI, image 2).
1.
Ten days later, establishing a comparison with the previous MRI, a greater signal alteration was observed in diffusion sequences with progression of the clinical picture at T2 and T2-FLAIR at the bilateral frontal-occipital-frontal pole and T2-IR regression.
During the twenty days of admission to Neurology there is no clinical infectious or analytical alteration and the determination of serology and antibodies is normal.
We conclude that both clinical and neuroimaging alterations are compatible with a late hypoxic encephalopathy leaving the doubt of the possibility of previous leukodystrophic lesions in white matter.
However, there is no family history of interest and there is no previous history to suggest the presence of leukodystrophy.
During his stay in Neurology the patient slowly improves spontaneously, maintaining previous psychiatric treatment.
On admission he was only able to walk with a walker and needed to be directed.
Upon discharge, she moves with guns without difficulty, is able to make coins in the machine to take a coffee, has improved very importantly Psychiatry and Memory, but still has moments of disorientation.
She came daily to the Rehabilitation Service.
