Biomedical subjects

D Greitz

Publications and source records attributed to D Greitz.

27 records · Page 2Linked to original sources

PubMed1993

A theoretical study of amplitude modulation and time shifting in quantitative MR measurements of motion in brain tissue.

MR imaging pulse sequences can be made sensitive to motion by adding gradients with different strengths at different time intervals. In the well-known phase mapping method, such velocity encoding gradients are used to obtain phase information linear to the velocity of the studied object in the direction of the gradient. When very low velocities are studied, a long duration velocity-encoded gradient is required to obtain sufficient velocity sensitivity. In such cases, variation in the object velocity during the execution of the sequence may hamper the accuracy of the method. In this study, we have made a computer simulation of the performance of a phase mapping method sequence (TE = 46 msec) designed for quantitative studies of motion in brain tissue. Using a Gaussian-shaped velocity input function, the time shifting and the amplitude modulation properties of the sequence was studied for various values of the duration, defined as the full width of tenth of maximum (FWTM), of the input function. The time shift corresponded well to the center of the 180 degrees RF pulse, and the amplitude modulation was seen to decrease with increasing time duration of the velocity input function. Applied on in vivo data, where an approximately gaussian-shaped brain motion velocity pattern was assumed to have a duration of 150 msec, the amplitude modulation of the sequence was estimated to 2%.

Brain↗

PubMed1993

On the pulsatile nature of intracranial and spinal CSF-circulation demonstrated by MR imaging.

Cerebrospinal fluid (CSF) flow was studied in 24 healthy volunteers using gated MR phase imaging. The subarachnoid space (SAS) was divided into 5 compartments depending on the magnitude of the pulsatile CSF flows: a high velocity compartment in the area of the brain stem and spinal cord, 2 slow ones at the upper and lower extremes of the SAS, and finally 2 intermediate velocity compartments in between. The main pulsatile spinal flow channel had a meandering pattern. The extraventricular CSF-circulation can be explained by pulsatile CSF flow without the necessity of assuming existence of a net flow. A successive time offset during the cardiac cycle has been found in the fronto-occipital direction of the interplay between the arterial expansion, brain expansion, volume changes of the CSF spaces and of the veins. It is proposed to name this time offset the intracranial "volume wave" (VoW).

Adult↗

PubMed1993

Cerebrospinal fluid circulation and associated intracranial dynamics. A radiologic investigation using MR imaging and radionuclide cisternography.

UNLABELLED: AIMS OF THE PRESENT INVESTIGATION: Observations made in a preliminary study of pulsatile cerebrospinal fluid (CSF) and brain motions using MR imaging called for a reconsideration of the CSF flow model currently accepted. The following questions were addressed: 1) The nature of the CSF-circulation, e.g., the magnitude and pattern of pulsatile and bulk flow; 2) The driving forces of the CSF circulation and assessment of the role of associated hemodynamics and brain motions; 3) The major routes for the absorption of CSF. MATERIAL AND METHODS: CSF flow and associated hemodynamics were studied using gated MR imaging, in 26 healthy volunteers, 5 patients with communicating hydrocephalus and 10 with benign intracranial hypertension. Radionuclide cisternography was performed in 10 individuals with venous vasculitis. RESULTS AND CONCLUSIONS: 1) The CSF-circulation is propelled by a pulsating flow, which causes an effective mixing. This flow is produced by the alternating pressure gradient, which is a consequence of the systolic expansion of the intracranial arteries causing expulsion of CSF into the compliant and contractable spinal subarachnoid space. 2) No bulk flow is necessary to explain the transport of tracers in the subarachnoid space. 3) The main absorption of the CSF is not through the Pacchionian granulations, but a major part of the CSF transportation to the blood-stream is likely to occur via the paravascular and extracellular spaces of the central nervous system. 4) The intracranial dynamics may be regarded as the result of an interplay between the demands for space by the four components of the intracranial content, i.e. the arterial blood, brain volume, venous blood and the CSF. This interaction is shown to have a time offset within the cerebral hemispheres in a fronto-occipital direction during the cardiac cycle (the fronto-occipital "volume wave"). 5) The outflow from the cranial cavity to the cervical subarachnoid space (SAS) is dependent in size and timing on the intracranial arterial expansion during systole. Similarly, the outflow from the aqueduct mirrors the brain expansion. The brain expansion is typically very small as evident from the minute aqueductal flow observed in healthy individuals. This expansion occurs simultaneously with an inflow of CSF and will be directed inwards towards the ventricular system. The brain expansion is of decisive importance for the formation of the normal transcerebral pressure gradient. 6) The instantaneous increase of flow in the superior sagittal sinus at the beginning of the systole reflects a direct pressure transmission via the SAS from the expanding arteries to the cerebral veins. It is contended that this early increase in venous pressure together with the volume wave is most likely an important prerequisite for sustaining normal intracranial pressure (ICP) and normal cerebral blood flow. This counter pressure should be reduced in hydrocephalus due to the decreased arterial expansion and could explain the reduced blood flow as well as an increased transmantle pressure gradient causing the ventricular dilatation. An increased pressure in the venous system is likely to be the cause of increases in ICP, including the increased pressure observed in benign intracranial hypertension (BIH).

Adult↗

PubMed1992

Pulsatile brain movement and associated hydrodynamics studied by magnetic resonance phase imaging. The Monro-Kellie doctrine revisited.

Brain tissue movements were studied in axial, sagittal and coronal planes in 15 healthy volunteers, using a gated spin echo MRI sequence. All movements had characteristics different from those of perfusion and diffusion. The highest velocities occurred during systole in the basal ganglia (maximum 1.0 mm/s) and brain stem (maximum 1.5 mm/s). The movements were directed caudally, medially and posteriorly in the basal ganglia, and caudally-anteriorly in the pons. Caudad and anterior motion increased towards the foramen magnum and towards the midline. The resultant movement occurred in a funnel-shaped fashion as if the brain were pulled by the spinal cord. This may be explained by venting of brain and cerebrospinal fluid (CSF) through the tentorial notch and foramen magnum. The intracranial volume is assumed to be always constant by the Monro-Kellie doctrine. The intracranial dynamics can be viewed as an interplay between the spatial requirements of four main components: arterial blood, capillary blood (brain volume), venous blood and CSF. These components could be characterized, and the expansion of the arteries and the brain differentiated, by applying the Monro-Kellie doctrine to every moment of the cardiac cycle. The arterial expansion causes a re-moulding of the brain that enables its piston-like action. The arterial expansion creates the prerequisites for the expansion of the brain by venting CSF to the spinal canal. The expansion of the brain is, in turn, responsible for compression of the ventricular system and hence for the intraventricular flow of CSF.

Adult↗

PubMed1992

SUNCT may be another manifestation of orbital venous vasculitis.

A patient with more than 20 years of SUNCT, i.e., long lasting periods with frequent attacks of intense orbital pain with a duration of about one minute, associated with ipsilateral conjunctival injection, lacrimation, rhinorrhea and facial sweating is described. Some attacks were possibly related to increased cerebral blood flow but could also be triggered from the oral area. Orbital phlebography showed pathologic changes on the side of the pain, changes which were normalized when these attacks ceased to appear. Due to these findings in conjunction with serum evidence of inflammation, associated systemic symptoms and susceptibility to steroids and azathioprine, venous vasculitis is suggested to be the cause of SUNCT in this patient. Carbamazepine and sumatriptan decreased the frequency, intensity and duration of attacks, although not completely.

Headache↗

PubMed1992

Cerebrospinal fluid pressure and venous pressure in "dynamite headache" and cluster headache attacks.

Six patients with episodic cluster headache were investigated as to blood pressure, heart rate, cerebrospinal fluid pressure (Pcsf) and frontal vein pressure (Pvf) during five nitroglycerin (NG) provoked attacks and one spontaneous attack. In a seventh studied patient the NG failed to provoke an attack. The earlier reported decrease of systolic blood pressure and increase of diastolic blood pressure and heart rate after NG administration were also found in these patients. The "dynamite headache" was related to the start and duration of an increase of the cerebrospinal fluid pressure. There was no relationship between the start or the maximum pain of the cluster headache attack and changes in Pcsf or Pvf. On breathing oxygen during a cluster headache attack, there was a decrease of Pcsf but in some patients a temporary increase of Pvf was observed, which possibly indicates that oxygen simultaneously attains constriction of arteries and veins.

Adult↗

PubMed1992

MRI of intracranial arteries in nitroglycerin induced cluster headache attacks.

Eight patients with episodic cluster headache, five in active episode, three out of episode, were investigated as to diameters of intracranial arteries before and after nitroglycerin (NG) administration. The diameter of all intracranial carotids were increased about 10 minutes after NG, although more in the patients in episode than in patients out of episode. The dilatation remained for the next 60 minutes in the patients who did not get a cluster headache attack. There was a normalization of the diameters of the internal carotid arteries compared to the initial values, at maximum pain in all patients who got a cluster headache attack. Similar changes were also found in the basilar arteries. The findings support the hypothesis of a constriction of intracranial arteries at maximum pain in cluster headache attacks to stop the pain.

Cerebral Arteries↗

PubMedDate not supplied

Theoretical and experimental evaluation of phase-dispersion effects caused by brain motion in diffusion and perfusion MR imaging.

We investigated intravoxel phase dispersion caused by pulsatile brain motion in diffusion spin-echo pulse sequences. Mathematical models were used to describe the spatial and temporal velocity distributions of human brain motion. The spatial distribution of brain-tissue velocity introduces a phase spread over one voxel, leading to signal loss. This signal loss was estimated theoretically, and effects on observed diffusion coefficient and perfused capillary fraction were assessed. When parameters from a diffusion pulse sequence without motion compensation were used, and ECG triggering with inappropriate delay times was assumed, the maximal signal loss caused by brain-motion-induced phase dispersion was predicted to be 21%. This corresponds to a 95% overestimation of the diffusion coefficient, and the perfusion-fraction error was small. Corresponding calculations for motion-compensated pulse sequences predicted a 1% to 1.5% signal loss due to undesired phase dispersion, whereas experimental results indicated a signal loss related to brain motion of 4%.

Adult↗

PubMedDate not supplied

A method for MR quantification of flow velocities in blood and CSF using interleaved gradient-echo pulse sequences.

The aim of this study was to establish a rapid method for in vivo quantification of a large range of flow velocities using phase information. A basic gradient-echo sequence was constructed, in which flow was encoded along the slice selection direction by variation of the amplitude of a bipolar gradient without changes in sequence timings. The influence of field inhomogeneities and eddy currents was studied in a 1.5 T interleaved sequences for calibration and in vivo flow determination were constructed, and flow information was obtained by pairwise subtraction of velocity-encoded from velocity non-encoded phase images. Calibration was performed in a nongated mode using flow phantoms, and the results were compared with theoretically calculated encoding efficiencies. In vivo flow was studied in healthy volunteers in three different areas using cardiac gating; central blood flow in the great thoracic vessels, peripheral blood flow in the popliteal vessels, and flow of cerebrospinal fluid (CSF) in the cerebral aqueduct. The results show good agreement with results obtained with other techniques. The proposed method for flow determination was shown to be rapid and flexible, and we thus conclude that it seems well suited for routine clinical MR examinations.

Aorta↗