Monro-Kellie 2.0: The Dynamic Vascular and Venous Pathophysiological Components of Intracranial Pressure

Metadata

• Author: Mark H Wilson
• Full Title: Monro-Kellie 2.0: The Dynamic Vascular and Venous Pathophysiological Components of Intracranial Pressure
• Category: #books
• Document Tags: neuro Neuro

Highlights

• additional mass results in a large volume of CSF then venous blood displacement (View Highlight)
• cerebral blood flow resulting from any given MAP will differ between individuals (amongst whom the range of ‘autoregulation’ of flow may vary), and with differences in the vasodilator PaCO2 (View Highlight)
• Cerebral venous drainage is significantly asymmetric in circa 50% of subjects.25 Transverse sinus drainage is predominantly right sided in approximately 40% of subjects and left sided in about 18% (View Highlight)
• Only a small minority of people have significant drainage through the cervical venous plexi28 which are of much greater significance in supine mammals such as swine that have not evolved to the gravitational effects of becoming bipeds. (View Highlight)
• Unlike the strong muscular arterial walls, those of the venous sinuses (being triangular dural reflections (Figure 2(b)) are susceptible to dilatation and compression. In the sitting position, the sagittal sinus has a negative pressure that can result in (potentially fatal) air embolism if opened. When supine, bleeding from the sinuses can be torrential. Likewise, when upright, human internal jugular veins tend to collapse under negative pressure, but engorge on lying (View Highlight)
• failure for venous efferent flow to precisely match arterial afferent flow (even when the failure results from intracranial venous compromise) will yield immediate and dramatic changes in intracranial volume and pressure (View Highlight)
• increasing central venous pressure (CVP) results in increasing ICP when compliance is lost,33 and this in turn results in the formation of brain oedema and swelling (View Highlight)
• They demonstrated that pressure on the sinuses (particularly tension at the margins) caused significant headache pain (View Highlight)
• As cerebral blood flow rises, so too must venous drainage. Venous distension will occur up to a limit, after which intravenous pressure (and that upstream, and thus ICP) will rise steeply (in a similar manner to when the limits of compliance are reached in the classic Monro-Kellie doctrine (View Highlight)
• The thin dural venous sinus walls make them prone to both focal and diffuse compression (View Highlight)
• Acute compression may result from a depressed skull fracture (Figure 4(a)) or, more commonly, from an expanding mass (e.g. extradural/periosteal haematoma) that may actually be the result of a damaged sinus (View Highlight)
• Compression may in turn lead to thrombosis and both may cause intracranial hypertension (View Highlight)
• Focal transverse sinus stenosis (graded as shown in Figure 4(c))41 is associated with idiopathic intracranial hypertension (IIH characterised by headache, loss of peripheral vision and nausea).42,43 Bilateral stenosis is found in up to 90% of sufferers.44–46 Moreover, endoluminal stenting of stenotic regions can dramatically improve symptoms.45,47–49 IIH tends to be a disease of young overweight women. The additional weight may be contributory to intra-cerebral venous hypertension (through mechanisms III, IV, and V outlined below), tipping a patient that would otherwise be asymptomatic into the decompensated category. (View Highlight)
• Diffuse brain swelling can also cause generalised venous compression creating an internal starling type resistor (View Highlight)
• A cycle of venous hypertension, cerebral swelling, further venous compression and therefore hypertension occurs. This cycle can be broken with CSF drainage although it is likely to recur again, not as CSF accumulates but as venous hypertension recurs (View Highlight)
• Raised CSF pressure partly obstructs venous sinus outflow, thereby increasing sinus pressure and then CSF pressure, et sequor. (View Highlight)
• The diffuse parenchymal volume increase that occurs with prolonged hypoxia (such as occurs at altitude) has recently also been demonstrated to cause venous compression which may in turn raise ICP (View Highlight)
• Queckenstedt’s35 test is now an outdated technique for investigating spinal stenosis. The test comprised jugular venous compression with concurrent lumbar puncture. Those with spinal stenosis have a slower lumbar pressure CSF rise than those without (View Highlight)
• Poor head position is often overlooked but is an incredibly important cause of raised ICP (View Highlight)
• Cervical collars can increase ICP from about 4.5 mmHg76–78 to as much as 14.5 mmHg,77 the rise being greater in those with baseline ICP > 15 mmHg (View Highlight)
• Other cervical causes of acute venous hypertension include near hanging and strangulation which can induce venous/haemorrhagic infarction.82 More chronic causes include jugular syndromes blocking outflow83 and superior vena cava obstruction (View Highlight)
• Abdominal compartment syndrome (raised intra-abdominal pressure causing organ dysfunction) raises ICP in brain-injured patients (View Highlight)
• In recent years a very significant number of astronauts have complained of loss of peripheral vision (so-called visual impairment-ICP),94 a symptom also occurring in IIH. The lack of gravity results in upper thoracic venous hypertension and hence a similar pathological process may underlie this condition (View Highlight)
• Hypobaric hypoxia increases cerebral blood flow to maintain brain oxygenation96,97 and limitations in cerebral venous drainage may underlie the pathogenesis of high-altitude headache through cerebral venous engorgement (View Highlight)
• While the traditional Monroe-Kellie doctrine holds, imbalances in arterial inflow and venous outflow also affect ICP. The venous outflow can be altered intracranially and extracranially (View Highlight)