The brain is perfused by arterial inflow from both internal carotid arteries and both vertebral arteries. Venous drainage is mainly via the internal jugular veins, with a minor contribution from the vertebral veins and the epidural venous plexus.

Normal brain function requires a certain blood volume and normal intracranial pressure.

Possible signs of impaired cerebral perfusion include headache, seizures, memory loss, dizziness, syncope, migraine and vomiting.

When cerebral perfusion is suspected to be impaired, the arterial inflow is the primary area of investigation. This is often unrestricted, especially in younger patients.

The venous drainage branch of the cerebral circulation is rarely considered in clinical practice.

It is important to recognize that patients with abdominal vascular compression syndromes often have impaired venous outflow from the cranium.

Abdominal vascular problems are not usually considered in the context of cerebral dysfunction. However, the impact of abdominal compression syndromes on venous outflow from the brain can be readily understood by considering the underlying anatomy.

The central nervous system consists of the brain and the spinal cord. These structures converge at the level of the foramen magnum occipitalis. At the same level, the cerebrospinal fluid of the spine and the brain merge. In addition, the venous plexus of the spine – the epidural plexus – is connected to the intracranial veins.

In this way, increased pressure in the spinal compartment is transmitted directly to the intracranial compartment.

An early clinical sign of the situation is nocturnal nasal congestion, which disappears about 30-60 minutes after rising from sleep to an upright trunk position (sitting or standing). In such a posture gravitation shifts fluids caudally – cerebrospinal fluid towards the spine and venous blood towards the lower hemisphere of the body.

When the collateral circulation of abdominal venous compression syndromes – namely congestion of the left renal vein (so-called nutcracker syndrome) and/or congestion of the left common iliac vein (so-called May-Thurner syndrome) – involves the spinal cord, maintenance of normal intracranial pressure depends on the additional compensatory transport capacity of the other drainage routes, namely the internal jugular veins.

The vertebral veins have a limited capacity to adapt to larger volumes because they pass through bony rings – the lateral processes of the cervical vertebrae – the so-called transverse foramina of the upper six cervical vertebrae.

The internal jugular vein is the main primary route of cerebral drainage and has the greatest potential for functional adaptation if the other two routes fail to meet actual demand.

The need to accommodate the additional volume can increase enormously if large venous volumes enter the spinal veins if the spine becomes part of the collateral circulation of the compressed left renal vein and/or the compressed left common iliac vein.

There are several small connections from the area of the pelvic veins to the spine and a peculiar one connecting the left renal vein to the spine called the tronc réno-rachidièn.

The latter can transport very large volumes towards the spinal canal, as a severely compressed left renal vein can bypass large volumes via this route if the natural primary route towards the pelvis via the left ovarian/spermatic vein cannot take over in the presence of concomitant compression of the left common iliac vein. It should be remembered that both compression syndromes usually occur together, the so-called nutcracker syndrome and a possible May- Thurner syndrome. Then the spine has to receive large volumes from these compressed veins. In such a situation, the increase of the intraspinal pressure, and intracranial pressure, depends on the patient’s posture. In general, intracranial pressure increases when the patient is lying down and decreases when the trunk is upright and the head is the highest point of the body. In this case, all the fluids tend to run down, driven by the force of gravity, and the symptoms in the pelvis and legs increase, while the cranial and cerebral symptoms may decrease, at least to some extent.

This may still be well compensated for in terms of cerebral symptoms if the transport capacity of the vertebral veins but for the most part of the internal jugular veins is not exhausted.

However, if the jugular veins are also compressed, severe symptoms may occur, such as headache and dizziness at the beginning and convulsions as the disease progresses.

All compression syndromes are based on an increasing curvature of the spine. Since the path from the head to the feet must remain in the centre of gravity of all the weights around the spine, a curvature in one direction must be compensated for by a subsequent curvature of the adjacent spinal segment in the other direction.

It is therefore not surprising that increased lordotic curvature, which is the cause of many abdominal compression syndromes, is causally related to increased cervical lordotic curvature, since the bending of the lumbar segment is mirrored by an equally opposite kyphotic thoracic segment to increased cervical lordosis, which causes compression of the jugular veins. Their compression is most commonly found at the level of the third to fifth cervical vertebrae, as this is where the apex of the cervical lordotic curve is usually located.

All the cervical structures ventral to the spine then push the internal jugular vein ventrally, compressing this soft vessel and often causing significant narrowing. This narrowing can become almost complete if the jugular vein is positioned in front of the carotid artery, which then presses the vein against the thick sternocleidomastoid muscle.

In many patients, the compression is mainly on one side, but it is not uncommon for both sides to be significantly compressed, causing often unbearable cerebral symptoms, mainly headaches, nausea and convulsions, when the abdominal and pelvic veins are draining blood into the spinal compartment.

A case report illustrates these general considerations.