Post-traumatic hydrocephalus has been reported with an incidence of between 1.5 and 8% (French 1977; Koo 1977). It is common clinical experience that in survivors of severe traumatic brain injury (TBI) with prolonged coma or persistent vegetative state, the incidence of post-traumatic hydrocephalus seems to be higher than reported in the literature. The differential diagnosis between post-traumatic hydrocephalus and subcortical atrophy has not yet been resolved. The clinical symptoms which are diagnostic in normotensive hydrocephalus (cognitive deficits, ataxia, and sphyncter incontinence) are already common in the sequaele of severe TBI. In the last year we studied 5 patients with ventricular enlargement secondary to severe TBI (Glasgow Coma Scale <8), prolonged coma (duration of coma >15 days), and low tendency to neuromotor and neuropsychological recovery (Disability Rating Scale >16 for at least 60 days). We performed cerebral MR in all patients using a Philips Gyroscan (1 Tesla). In all patients we found an increased flow velocity at the level of the Sylvian aqueduct before ventricular peritoneal shunting. After shunting the T2 axial images showed a significant reduction in the flow velocity at the same level in 4 of the 5 patients operated on with a self-regulation valve; in 1 patient with a middle pressure valve, the aqueduct flow velocity did not show any significant modification. At the actual follow-up (8 months), the patients with a normalization of the Sylvian aqueductal flow velocity seem to achieve the best and quickest neuromotor and neuropsychological recovery.

Post-traumatic hydrocephalus: Possible neuroradiological markers as an indication for ventricular-peritoneal shunting

Sabatini U.;
2000-01-01

Abstract

Post-traumatic hydrocephalus has been reported with an incidence of between 1.5 and 8% (French 1977; Koo 1977). It is common clinical experience that in survivors of severe traumatic brain injury (TBI) with prolonged coma or persistent vegetative state, the incidence of post-traumatic hydrocephalus seems to be higher than reported in the literature. The differential diagnosis between post-traumatic hydrocephalus and subcortical atrophy has not yet been resolved. The clinical symptoms which are diagnostic in normotensive hydrocephalus (cognitive deficits, ataxia, and sphyncter incontinence) are already common in the sequaele of severe TBI. In the last year we studied 5 patients with ventricular enlargement secondary to severe TBI (Glasgow Coma Scale <8), prolonged coma (duration of coma >15 days), and low tendency to neuromotor and neuropsychological recovery (Disability Rating Scale >16 for at least 60 days). We performed cerebral MR in all patients using a Philips Gyroscan (1 Tesla). In all patients we found an increased flow velocity at the level of the Sylvian aqueduct before ventricular peritoneal shunting. After shunting the T2 axial images showed a significant reduction in the flow velocity at the same level in 4 of the 5 patients operated on with a self-regulation valve; in 1 patient with a middle pressure valve, the aqueduct flow velocity did not show any significant modification. At the actual follow-up (8 months), the patients with a normalization of the Sylvian aqueductal flow velocity seem to achieve the best and quickest neuromotor and neuropsychological recovery.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12317/109965
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