Meninges And Cerebrospinal Fluid
The brain is enclosed by three protective layers, which also extend down
the spinal cord.
• The dura mater is
a thick tough membrane lying close to the skull and vertebrae and innervated by
afferent fibres of the trigeminal and upper cervical nerves.
• Adjacent to the dura mater is
the arachnoid mater, a thin membrane with thread-like processes
that project into the subarachnoid space and making contact with the delicate
pia mater.
• The pia mater envelops
the spinal cord and contours of the brain surface and dips into the sulci.
The subarachnoid space is filled with cerebrospinal fluid (CSF) and also accommodates major arteries, branches of which project down through the pia into the central nervous system (CNS). At specific sites the size of the subarachnoid space increases to form cisterns. These are particularly prevalent in the region of the brain-stem and the largest is the cisterna magna found between the cerebellum and medulla.
The meninges extend caudally enclosing the spinal cord. Here the dura is
attached to the foramen magnum at its upper limit and projects down to the
second sacral vertebrae.
Cerebrospinal fluid (CSF) production and circulation
• CSF is secreted by the choroid plexuses,
which are found prima- rily in the ventricles.
• The rate of production varies between 300 and 500
mL/24 h and the ventricular volume is approximately 75 mL.
• CSF is similar to blood plasma although it contains
less albumin and glucose.
• After production, CSF flows from the lateral
ventricles into the third ventricle via the intraventricular
foramina of Monro and then passes into the fourth
ventricle through the central aqueduct of Sylvius and
into the subarachnoid space via the foramina of Luschka and Magendie.
From the subarachnoid space at the base of the brain, CSF flows rostrally over
the cerebral hemispheres or down into the spinal cord.
CSF reabsorption occurs within the superior sagittal and related venous
sinuses. Arachnoid granulations are minute pouches of the
arachnoid membrane projecting through the dura into the venous sinuses. The
exact mechanism by which CSF is reabsorbed is not clear but it does involve the
movement of all CSF constituents into the venous blood. As well as playing an
important part in main- taining a constant intracerebral chemical environment
(see below), the CSF also helps protect the brain from mechanical damage by
buffering the effects of impact.
Blood–brain barrier
The blood–brain barrier (BBB) used to be thought of as a single physical
barrier preventing the passage of molecules and cells into the brain. More
recently, however, it has been shown to be made up of a series of different
transport systems for facilitating or restricting the movement of molecules
across the blood–CSF inter- face. A characteristic of cerebral capillary
endothelial cells is the presence of tight junctions between such cells, which
are induced and maintained by astrocytic foot
processes (see Chapter 13). These unusually tight junctions reduce
opportunities for the movement of large molecules and cells, and thus require
the existence of specific transport systems for the passage of certain critical
molecules into the brain.
• Small molecules such as glucose pass readily into the
CSF despite not being lipid soluble.
• Larger protein molecules do not
enter the brain, but there are a number of carrier mechanisms that enable the
transport of other sugars and some amino acids.
The rôle of the barrier is to maintain a constant intracerebral chemical
environment and protect against osmotic challenges, while granting the CNS
relative immunological privilege by pre- venting cells from entering it (see
Chapter 62). However, from a therapeutic point of view the barrier reduces or
prevents the delivery of many large-molecular-weight drugs (e.g. antibiotics)
into the brain and represents a major problem in the treatment of many CNS
disorders.
Clinical disorders
Hydrocephalus
Hydrocephalus is defined as dilatation of the ventricular system and so
can be seen in cases of cerebral atrophy, e.g. dementia
(compensatory hydrocephalus). However, hydrocephalus can
also occur as a result of increased pressure within the ventricular system, secondary
to an obstruction in the flow of CSF (obstruc- tive hydrocephalus). This
typically occurs at the outlets from the fourth ventricle into the subarachnoid
space, where the obstruc- tion may be linked to the presence of a tumour,
congenital malformation or the sequelae of a previous infection (see below).
Alternatively, the flow of CSF from the third to the fourth ventri- cle may be
impaired as a result of the development of central aqueduct stenosis.
Hydrocephalus is also seen in rare conditions of oversecretion of CSF
(e.g. tumours of the choroid plexus) as well as in the common situation of
reduced absorption as is characteristically seen in spina bifida.
The symptomatology of hydrocephalus is varied but
classically the patient presents with features of raised intracranial pressure
(early morning headache, nausea, vomiting) and, in acute rises of pressure,
altered levels of consciousness with brief periods of visual loss. Overall,
probably the most common cause of raised intracra- nial pressure is a glioma
tumour (see Chapter 13) producing these effects by virtue of its
mass. Such tumours in the posterior fossa can also directly cause
hydrocephalus, which may contribute to the raised intracranial pressure.
In obstructive hydrocephalus the treatment
focuses on draining excess CSF using a variety of shunts linking the ventricles
to either the heart (atrium) or the peritoneal cavity.
Meningitis
Meningitis or inflammation within the meningeal membrane can be caused by
a number of different organisms. In acute infection there is the rapid spread
of inflammation throughout the entire subarachnoid space of the brain and
spinal cord, which produces the symptoms of headache, pyrexia, vomiting, neck
stiffness (meningism) and, in severe forms of the disease, reduced levels of
con- sciousness. The early administration of antibiotics is essential although
the type of antibiotic employed will depend on the nature of the organism
responsible for the inflammation.
In other cases the infection or inflammation may follow a more subacute
course, such as tuberculous meningitis or sarcoidosis.
In such cases, secondary hydrocephalus may ensue as a result of meningeal
thickening at the base of the brain obstructing CSF flow.
Rarely, tumours can spread up the meninges giving a malignant
meningitis. This characteristically presents as an evolving cranial
nerve or nerve root syndrome with pain. This is to be distinguished from
primary tumours of the meninges – meningiomas – which
are slow growing and benign, and typically present with epileptic seizures or
deficits secondary to compression of neighbouring CNS structures.
