Cerebral Autoregulation in Alzheimer's Disease. Before and After Treatment with Galantamine: an Open-Label Pilot Study.

Cerebral Autoregulation in Alzheimer's Disease. Before and After Treatment with Galantamine: an Open-Label Pilot Study. - Cerebral Autoregulation in Alzheimer's Disease

Status

Active, not recruiting

Phases

Unknown

Study type

Observational

Source

NL-OMON

Registry ID

NL-OMON32291

Enrollment

Registered

2008-05-20

Start date

2007-11-01

Completion date

Unknown

Last updated

2024-05-13

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

dementia

Interventions

None listed

Eligibility

Age

18 Years to 99 Years

Inclusion criteria

Inclusion criteria: Meeting DMS-IV R criteria for dementia meeting NINCDS-ADRDA criteria for probable AD clinical dementia rating scale (CDR) 0.5 - 2

Exclusion criteria

Exclusion criteria: Contra-indication for or unwilling to receive treatment with cholinesterase inhibitors major cerebrovascular disease (stroke)

Design outcomes

Primary

Measure	Time frame
Primary Objective: to test the hypothesis that ChEIs augment cerebral autoregulation in patients with AD. To test this hypothesis, we will continuously monitor CBF together with BP before and during treatment with ChEIs in patients with AD. Primary outcome parameter: dynamic cerebral autoregulation, quantified by the parameter phase lead. Explanatory note on cerebral autoregulation and vasomotor reactivity Dynamic cerebral autoregulation will be quantified by transfer function analysis based on spectral analysis of induced oscillations in beat-to-beat changes in CBF-velocity, recorded by TCD, and beat-to-beat changes in blood pressure, recorded by Finapres. The transfer function between BP and CBF-velocity will be characterized by the parameters phase lead and gain. The gain quantifies the damping effect of dynamic CA on changes in BP and marks the efficiency of the response, whereas phase shifts can be considered surrogate measures for the time delay of the autoregulatory response. A positive phase shift indicates that oscillations in CBF-velocity lead oscillations in BP; changes in CBF-velocity recover faster than changes in BP and this is interpreted as intact dynamic CA. Cerebral vasomotor reactivity is defined as the cerebrovascular response to changes in arterial carbon dioxide (CO2), a potent cerebral vasodilator. Hypercapnia augments CBF, whereas hypocapnia reduces CBF. Hypocapnia is induced by hyperventilation, hypercapnia is induced by inhalation of room air, enriched with 7 % CO2. Vasomotor reactivity will be expressed as the percentage changes in CBF-velocity.	—

Measure

Time frame

Primary Objective: to test the hypothesis that ChEI*s augment cerebral autoregulation in patients with AD. To test this hypothesis, we will continuously monitor CBF together with BP before and during treatment with ChEI*s in patients with AD. Primary outcome parameter: dynamic cerebral autoregulation, quantified by the parameter *phase lead*. Explanatory note on cerebral autoregulation and vasomotor reactivity Dynamic cerebral autoregulation will be quantified by transfer function analysis based on spectral analysis of induced oscillations in beat-to-beat changes in CBF-velocity, recorded by TCD, and beat-to-beat changes in blood pressure, recorded by Finapres. The transfer function between BP and CBF-velocity will be characterized by the parameters phase lead and gain. The gain quantifies the damping effect of dynamic CA on changes in BP and marks the efficiency of the response, whereas phase shifts can be considered surrogate measures for the time delay of the autoregulatory response. A positive phase shift indicates that oscillations in CBF-velocity lead oscillations in BP; changes in CBF-velocity recover faster than changes in BP and this is interpreted as intact dynamic CA. Cerebral vasomotor reactivity is defined as the cerebrovascular response to changes in arterial carbon dioxide (CO2), a potent cerebral vasodilator. Hypercapnia augments CBF, whereas hypocapnia reduces CBF. Hypocapnia is induced by hyperventilation, hypercapnia is induced by inhalation of room air, enriched with 7 % CO2. Vasomotor reactivity will be expressed as the percentage changes in CBF-velocity.

—

Secondary

Measure	Time frame
-dynamic cerebral autoregulation, quantified by the parameter gain -vasomotor reactivity	—

Countries

Netherlands

Outcome results