A 29-year-old woman, single, lives with her parents, with no history of organic or psychiatric pathology or toxic abuse, was admitted to neurology due to behavioral changes, disorientation and lack of connection with the environment.
The family reported that it was the first of these characteristics, which for two weeks had seen the patient desanimating little communicative (not identifying any trigger), there was no mention of the biological aspect, support, lost rhythm, etc.
All this was the reason for great family distress, so they went to the family doctor, being treated as a depressive condition and being given sertraline 50 mg/day (1 week before admission).
The evolution was torpid, presenting episodes of psychomotor agitation and disorientation, reason why the family decides to take the patient to the emergency room.
There was no family history of significant psychiatric or organic disease.
On examination, apart from spatio-temporal disorientation and agitation, nothing remarkable was found, with no neurological focus.
Cerebral laboratory tests (blood count, coagulation, liver, kidney, thyroid, urine, folic acid and vitamin B12) and tomography were normal.
Urine toxicities were negative.
Lumbar puncture (LP) showed 26 leukocytes/mm3.
The patient presented a generalized tonic-clonic seizure in the emergency room. She was admitted with a presumptive diagnosis of viral encephalitis, and started treatment with beta-blocker and valproic acid.
During admission, she was evaluated by Psychiatry.
The family again reported that the patient had been apathetic for two weeks, repeating that she had "dry veins of the head".
It was classified as a psychotic depression and venlatine 75 mg/day was discontinued.
Serology for HIV, Brucella, Cytomegalovirus, Herpes Sifilis, Toxoplasmosis and Epstein were negative.
During the first week of hospitalization, the patient was confused, had unmotivated soliloquies and laughs.
LP was repeated (34 leukocytes/mm3, lymphocytes 100 %, serology and cerebrospinal fluid (CSF) culture for Brucella, Lúes and Borrellia were negative).
Brain MRI was normal.
The antidepressant was suspended and tiapride was paused.
During the second week, the electroencephalogram (EEG) showed signs of moderate diffuse slow encephalopathy.
The patient did not respond to simple orders, she was mute, stuporous, so tiapride was discontinued, leaving intramuscular haloperidol in case of agitation.
Due to the torpid evolution she was admitted to the ICU with the withdrawal of valproic acid and the initiation of levetirazepam.
The patient began to present involuntary movements and dystonias.
Transthoracic echocardiography was normal.
Megadoses of corticosteroids and hemin were added (suspected as acute intermittent porphyria).
Due to the most frequent complex tonic seizures, sedation and endotracheal intubation were decided.
Uroporphyrins were not detected, coproporphyrins and zinc were within normal limits (the hemine was suspended).
LP was repeated, showing normal mycobacterial and mycoplasma etiology.
Sedation was removed during the fourth week: the patient responded to simple orders, had facial myoclonus and buccolingual movements, and the patient was admitted for extubation.
EEG showed signs of diffuse encephalopathy.
Prion disease (protein-negative in CSF) was ruled out.
Gynecologic ultrasound showed a slightly enlarged ovary.
During the sixth week, ceruloplasmin, serum copper and abdominal ultrasound were normal.
The patient was more conscious and reactive.
The possibility of encephalitis in relation to non-objectified teratoma was raised.
LP was repeated for the presence of paraneoplastic antibodies (anti-Hu, anti-Yo, anti-Ri, anti-CV2, anti-physin, anti-NMDA), anti-NMDA and anti-canal antibodies.
Recipients were diagnosed with Alzheimers Disease (CD-R) due to agitation-psychotics and delusions of mental disorder (NAM), starting with ziprasidone 40 mg/day, up to 160 mg/day.
