A 60-year-old patient with no relevant psychiatric history, history of left eye corneal transplantation and inguinal hernia surgery.
The patient contacts the emergency room to assess the presence of bilateral hearing loss of two weeks duration, referring a feeling of slippage similar to the feeling of rising to a great height, accompanied by speech and difficulty reading.
In recent months, the patient had started to have sleep problems related to work concerns and couple problems.
The patient was diagnosed with otorhinolaryngology for the study of hearing loss with normal results on examination and audiometry.
The examination showed no evidence of neurological focality, and CT without contrast showed no abnormal findings.
After consulting with Neurology, neurological symptoms were ruled out, estimating the possibility of presenting symptoms suggestive of stressful life events.
The patient is referred to primary care and psychiatric follow-up if necessary.
Two weeks after the first admission to the emergency department, the patient came for a new urgent evaluation due to the persistence of previous symptoms and increased difficulty sleeping.
It is cited for outpatient study by Neurology and Psychiatry.
The patient begins psychiatric follow-up in consultations with diagnostic orientation of possible additive disorder and start of treatment with Fluoxetine 20mg and Lormetazepám 1mg.
The patient was followed up in the Neurology Department, where a MRI study was requested, with no relevant findings and diagnostic orientation for congenital malformation.
One month later, the patient returned to the emergency department complaining of progressive worsening of gait disturbance, with improvement in sleep with benzodiazepines.
Once again valued by Neurology, paratonic rigidity stands out, with normal myocutaneous reflexes and no pyramidalism, confirming the idea of non-neurological condition.
Psychiatry valued this assistance, stressing in the exploration a mutism, global aphasia, that the patient tried to explain with gestures and a clumsiness in the ambulation of ataxia, without clear impressions.
It is proposed to the family that if the evolutionary picture and could not provide adequate care would propose admission to the Psychiatric Hospitalization Unit for study and treatment.
Olanzapine 5mg was prescribed.
One week after the last visit, the patient was admitted to the psychiatric ward with a clinical judgment of congenital disorder.
Upon admission, the patient remains mu, negativist, non-cooperative, unaware of his basic needs, with gait alteration, becoming impossible at times, although in a fluctuating and spontaneous way.
The evolution tends to mutism, maintenance of antigravity postures sometimes and in others without appreciating evident rigidity.
The observations of the nursing staff feed the confusion of the picture and the unlogical evolutionary pattern.
During one week, the evolution is aggravated with a tendency to precomatous murmur with the presence of generalized rigidity of paratonic characteristics, absence of visual reflex threat, urinary incontinence and fecal incontinence.
He was admitted to the neurology ward.
The result of the MRI that repeats approximately one month after the previous one shows a pattern compatible with spongiform encephalopathy, with bilateral and symmetrical lesions in caudal nuclei and anterior portion of the putamen lobe, with cortical alteration.
An EEG performed during wakefulness shows altered background activity, with slowing of background activity, composed of generalized theta frequencies. On this background frequency, there is no observed presence of moderate intermittent rIReptiform anomalies (delta activity).
The evolution of the patient is characterized by acute hepatitis and pneumonia possibly aspiration, precoma and finally coma.
The study and empirical treatment were completed to rule out Wilson's disease and immune-mediated encephalitis.
Serology for HIV, HBV and TP negative, tumour markers negative, heavy metals and toxic in urine negative, B12 normal and thyroid profile negative, Lumbar puncture sequence ruled out CD29 homozygous CT
The motor and cognitive deterioration was rapidly progressive from his first contact with the Emergency Department, in question of less than 5 months until the death of the patient.
