DIAGNOSIS
APALLICO COMA caused be a deep haemorrhagic lesion INTRAPARENCHIMALE on the left side with a result of a ILEUM ISCHIUM PUBLIC fracture dx.
On the 05/07/1995 the patient due to an acute arizing of the heamatoma INTRAPARENCHIMALE TEMPORO insular on the left unside had a road accident and then suffered on ILEUM ISCHIUM PUBICA DX fracture.
After highlighting a deep heamatome on the left unside through a TACOGRAPH test, given because of a serius state of come, the patient was transfered to the neurological ward of TREVISO hospital and was submitted to anangiographic study which did not highlight vascular malformations.
No further surgery was undertoken. After somtime the state of come stabilized it self with an apparence of a main TETRAPARESI on dx.
Other TACOGRAPH tests are caried out for the progressive reabsorption of the heamatic CEREBRALE collection.
On the 19/07/1995 the patient was transfered to intensive care in FELTRE hospital: there had been a superficiality of the state of coma, but there was not an enviromental partecipation andan inability to verbal expression or to a static TETRAPARESI plus a dx with REFLECTIVITY from decortication.
From 18/08/1995 the patient has been hospitalized here at our department for the neurological reabilitation phase.
Even after a prolonged rehabilitative treatment the objective neurological picture and the stationariness state of conscience with PSYCHOSENSORIAL stimulation have directed the diagnosis to an APALLICA syndrome with severe cortic undercortical suffering in relation to the hemorrahagic injury and the suffering of the cortical structure because of the prolonged state of coma.
To confirm this syndrome on the 11/10/1995 we have proceded with a global celebral PET investigation. The evidence was a not reable global cortical hipometabolism, more evident in the left unside hemisphere, and the finding which lay put down for an extended cortical compromise, a TALAMICA DEAFFERENTAZIONE etc. are unfortunately PATOGNOMICI for the APALLICO come situation.
The neuroligical picture is at the moment stationary. The patient stays in a sitting position with help, there is not voluntary mobility of the limbs and the spastic TETRAPARESI dominant on the dx unside remains.
The attention is seriously limited and there is an absense of partecipation to the environment even with spoken affettive or PSYCHOSENSORIAL solicitation. We notice stereotype facial mime.
Nourishment is attended, with resumption of the swalling, there is not a controll of the sphincter. The latest check ups from the EMETOCHIMICI tests do not reveal particular altereations.
The pelvis fractures seems consolidated and the patient does not seem to suffer from the passive mobility.
During his stay the patient has undertaken a motory and PSYCHOSENSORIAL rihabilitative treatment and even if the neurological deficit are now stable, in these cases there is heed to continue an competent rehabilitative programme for a long time.
Astrome therapy we suggest:
GARDENALE 100 1cps in the evening
LIORESA 25 1c twice a day
ZANTAC 150 in the evening