Vittamed uses the ophthalmic artery (OA) as a natural ICP sensor. The OA is uniquely suited to this purpose because of its anatomical course.
The OA originates from the internal carotid artery inside the cranium, then traverses the optic canal with the optic nerve to enter the orbit where it supplies the optic nerve and the eye. It is subject to the ICP inside the cranium, but not in the orbit where the ambient pressure is equal to atmospheric pressure under normal circumstances.
The diameter of the OA inside the cranium is smaller than the orbit because of the influence of ICP. As a result, the blood flow velocity is higher intracranially than in the orbit. As pressure is added to the orbit, the diameter of the intraorbital segment of the OA diminishes, thereby elevating the blood flow velocity. Blood flow velocities in the distal and proximal (intracranial and intra-orbital) segments equilibrate when the external pressure added to the orbit approximates the ICP.
This point at which the external pressure added to the orbit equilibrates blood velocities in the intracranial and extracranial segment of the OA is called the balance point or equilibration point. The ICP can be derived from the amount of pressure required to reach the balance or equilibration point.
Because the OA is used as the ICP sensor, no external zero reference point is required. The use of the OA renders this method of ICP measurement entirely self-calibrating.
Blood flow velocities and other aspect of pulse dynamics are measured by means of image-guided transcranial and orbital Doppler ultrasound. Pressure is applied through the automated, computer-controlled inflation of an air cushion over the closed eye.
In practice, the patient is fitted with a frame similar to a swimming mask to which the ultrasound Doppler probe is fitted. The mask also contains a disposable inflatable air cushion.
Blood flow velocities in the proximal and distal OA are measured and displayed on a touchscreen-equipped computer. The automated, computer-controlled inflation module gently increases pressure in the air cushion stepwise until the balance point is reached. At that point, the ICP measuring device calculates the ICP and displays it on the screen.
Most of the process is automated. A number of additional controls are available for advanced clinical and research purposes.
A schematic of the noninvasive ICP measurement instrument
A special mask is positioned on the patient’s face. The mask holds an ultrasound transducer in contact with an inflatable cushion which is connected both to a computer regulated source of pressurized air. The air pump is used to increase the pressure against the closed eye. Simultaneously the ultrasound transducer measures compares the velocity of blood flow in the proximal and distal segments of the OA. The ICP is derived from the level of pressure required to equalize the pressure in the two segments.
Over 450 patients have been examined in the course of inpatient and outpatient mulitcenter trials in the EU and in the USA. There have been no adverse events.
- Accuracy (Systematic Bias) has of 0.5 mmHg
- Precision or Standard Deviation less than 2.5 mmHg
- Correlation with commercially available implanted monitoring devices R > 0.8
- Results statistically significant and clinically significant
- Results comparable to standard parenchymally implanted devices
Applications for ICP measurement in neurology and neurosurgery include the management of trauma, stroke, malignancy, hydrocephalus, shunt malfunction, craniofacial abnormalities, pseudotumor cerebri, migraine and other causes of chronic headache, and infection. Indications for non-invasive ICP measurement are the same, although non-invasive measurement should not be used when external CSF drainage might assist in the management of increased ICP.
Another application for ICP measurement is the diagnosis and management of glaucoma. Glaucoma is the second leading cause of blindness globally (World Health Organization, 2004. Global data on visual impairment in the year 2002. Bulletin of the World Health Organization, vol. 82, Number 11, November 2004, pp. 811–890; Quigley H.A. Number of people with glaucoma worldwide. British Journal of Ophthalmology. 1996;80(5):93–389. Cassard SD, Quigley HA, Gower EW, Friedman DS, Ramulu PY, Jampel HD. Regional variations and trends in the prevalence of diagnosed glaucoma in the Medicare population. Ophthalmology. 2012 Jul;119(7):1342-51. doi: 10.1016/j.ophtha.2012.01.032. Epub 2012 Apr 4 ).
Raised IOP is a risk factor for developing glaucoma, which is usually defined in terms of high IOP. Nevertheless, there is no definite threshold for intraocular pressure that causes glaucoma. One person may develop nerve damage at a relatively low-pressure, while another person may have high IOP for years and never develop nerve damages (Shields M.B. Normal-tension glaucoma: is it different from primary open-angle glaucoma? Current Opinion in ophthalmology. 2008;19(2):85–88.) Uncontrolled glaucoma progression leads to permanent damage of the optic nerve and visual field loss. These can result in blindness, which is why Glaucoma has been nicknamed “sneak thief of sight.” Damage may only be recognized at later stages of the disease. The same neuropathy can occur, however, even in the absence of elevated IOP. This syndrome has been called Normal Tension Glaucoma (NTG) or Low Tension Glaucoma (LTG).
NTG and LTG have the characteristics and visual-field loss of high tension glaucoma but show consistently normal IOP ( < 22 mm Hg). The number of patients with LTG and NTG may be equal to that of patients with high IOP. It is thought that as many patients may have LTG and NTG as have high tension glaucoma
Studies undertaken using Vittamed’s non-invasive intracranial pressure measurement instrument indicate that the normal gradient between IOP and ICP is reversed in NTG and LTG. Indeed, diagnosis depends on the ability to compare IOP and ICP (Berdahl John. Cerebrospinal pressure and glaucoma. 2009; Glaucoma Today. Available online at http://glaucomatoday.com/2009/10/GT1009_02.php.)
It is impractical to measure and follow ICP routinely using current, invasive ICP monitoring methods. The development of self-calibrating non-invasive ICP is offers a new and effective approach to the diagnosis and management of patients with LTG and NTG.
ICP is the abbreviation for intracranial pressure, the pressure within the skull.
The CSF is made in the ventricles (chambers) of the brain and circulates through the central nervous system (CNS) in the subarachnoid space. The CSF in the spine normally communicates with the CSF in the brain.
When the subarachnoid space in the lumbar spine is punctured, the pressure can be measured by means of a manometer, a transparent calibrated tube calibrated in millimeters of water. The pressure is expressed in terms of the height of the column of CSF in mm H2O.
Pressure can also be measured by cannulating the ventricles of the brain. This procedure is more invasive than a lumbar puncture, but also often produces more accurate measurements. It also allows for calibrated external drainage of CSF from the ventricle to reduce ICP.
Historically the ventricular cannula was attached to a manometer in the same way as the lumbar puncture needle. Ventricular pressure was similarly expressed in mm H2O.
More recently, pressure sensors were designed to be implanted intraparenchymally, within the substance of the brain, to simplify the surgical procedure. No column of CSF was involved. Following the convention in blood pressure measurement, these sensors were calibrated in millimeters of mercury (mm Hg) rather than in mm H2O,. One mm Hg is equal to 13.6 mm H2O.
Normal CSF pressure is generally cited as approximately 60–250 mm H20 (95% confidence intervals) with a population mean of 180mm in the usual clinical setting. There is considerable variability around this range, however, and a good deal of clinical judgement may be required to assess what value is acceptable for any individual patient. Pressure values must be interpreted in light of the clinical setting (Lee SC, Lueck CJ. Cerebrospinal Fluid Pressure in Adults. J Neuroophthalmology 2014. Sep; 34(3):278-83).
Abnormalities of ICP can result from many neurological and neurosurgical conditions, including trauma, tumors, hemorrhage, stroke, hydrocephalus, congenital abnormalities, infection, and other sources of altered CSF or intracranial blood flow dynamics. Elevated ICP (intracranial hypertension) may compromise cerebral perfusion or blood flow when the ICP exceeds mean arterial blood pressure. At that point, the brain may be starved of blood (ischaemia) and oxygen (hypoxia), resulting in neurological dysfunction which can progress to brain damage, visual loss and death. Elevated ICP requires careful monitoring and may require urgent intervention. Low ICP (intracranial hypotension) may also be abnormal and may also require treatment.