Give an account of the layers that cover the brain and spinal cord. Include in your answer their composition, function and how they are involved in a NAMED disease.
(1510 words)
The brain and spinal cord are covered by three membranes called meninges, which when looked at from within outwards, are termed the pia, the arachnoid, and the dura mater. The pia is closely attached to the nervous tissue and follows the convolutions of the brain. The space between the pia and the arachnoid (the subarachnoid space) is filled with cerebrospinal fluid (CSF). This fluid is found in the ventricles of the cerebral hemispheres and the brain stem. Major cerebral arteries and veins run in the subarachnoid space. Small nutrient vessels pass into the cortex from the arteries. The arachnoid is a delicate membrane resembling a spider’s web and forming a continuous sheet in contact with the dura, which is the toughest and most fibrous of the three membranes.
The pia mater contains fibroblasts, collagenous fibres, and the processes of underlying astrocytes. Since the pia and the arachnoid are structurally continuous, they are often considered as a single unit, the pia-arachnoid or leptomeninges. Flattened mesothelial cells line the apposed surfaces of the pia and arachnoid layers and their interconnecting fibres. Mesothelium also covers the outer surface of the arachnoid mater.
Central nervous system (CNS) arteries and veins pass in the subarachnoid space loosely attached to the pia mater. Larger vessels extending into the nervous tissue are surrounded by a delicate layer of pia mater. Between the penetrating vessels and the pia there is a perivascular space which is continuous with the subarachnoid space.
The subdural space containing a minute amount of fluid separates the dura mater from the arachnoid layer. In the cranium, the dura mater merges with the periosteum of the skull whereas around the spinal cord the dura is suspended from the periosteum of the spinal canal by the denticulate ligaments. The intervening epidural space is filled with loose, fibro-fatty connective tissue and a venous plexus.
As the CNS contains no lymphatics, interstitial fluid is thought to drain outwards from the brain to join the subarachnoid CSF via the perivascular spaces. A blood-brain barrier has been postulated to explain the inability of many constituents of plasma to pass from the circulatory system into the CNS. This barrier probably consists of the brain capillary endothelial cells, which are bound by tight junctions, and their supporting basement membrane.
Pathological processes may involve the meninges and CSF. The dura mater may be stripped from the skull by haemorrhage secondary to the tearing of a blood vessel in a fracture. It could also be removed from the skull by exudation into the extradural space by infection of the adjacent bone, e.g. in mastoiditis (inflammation caused by an infection of the middle ear).
Micro-organisms and their toxins can spread in the subarachnoid space, filling it with inflammatory exudate. The inflammation may then spread into the brain around the nutrient blood vessels which become surrounded by collections of leucocytes. Blood, pus, and micro-organisms also reach the cerebral ventricles via the CSF because the ventricles communicate with the subarachnoid space. CSF examination is therefore very useful in the diagnosis and treatment of diseases of the nervous system. Specimens are normally obtained by lumbar puncture but ventricular or cisternal puncture may sometimes be required. An increase or decrease in the CSF pressure may be of diagnostic value. Laboratory tests involve microbiology, serology, cytology, and biochemistry. Normal CSF is clear and colourless, does not coagulate and has a specific gravity of 1.006. It contains about 0.15-0.45 g/l protein, 2.8-4.4 mmol/l glucose, 128 mmol/l sodium, and 128 mmol/l chloride. A few mononuclear cells may be found in normal CSF but rarely more than 4/ul.
Infections of the nervous system are not very common because the brain and spinal cord are well protected. However, as in meningitis (inflammation of the meninges), if a micro-organism gains access to the nervous system, the infection spreads rapidly via the CSF pathways. Many micro-organisms which are relatively non-pathogenic elsewhere in the body may cause serious and sometimes fatal infection of the nervous system.
Meningitis may involve the dura (pachymeningitis) or the pia and arachnoid (leptomeningitis), which is more common. In pachymeningitis, the underlying infection in the bones of the skull (as in chronic suppurative otitis media or mastoiditis) extends to the dura. Pyogenic organisms spread from the bone, causing suppuration in the dura which may lead to the formation of an extradural abscess. As the dura becomes swollen and softened, the infection may penetrate through it and spread over the cerebral hemisphere to form a subdural abscess. The organisms may also spread to the subarachnoid space, causing localised or general leptomeningitis.
In leptomeningitis, often simply referred to as meningitis, micro-organisms provoke an inflammatory reaction in the subarachnoid space. Exudate is added to the CSF, which is a good culture medium for many bacteria. There are many different causal organisms, both viral and bacterial. Acute purulent meningitis is caused by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (pneumococcus), and the haemophilus group. Escherichia coli is a fairly common cause of bacterial meningitis in infants. Some viral diseases of the nervous system, and also subarachnoid haemorrhage, can produce symptoms suggestive of acute bacterial meningitis. Meningitis may also be caused by Mycobacterium tuberculosis, pyogenic cocci, the bacilli of the coli-typhoid group, the anthrax bacillus, Treponema pallidum, leptospirae, and various fungi.
In most cases the route of infection is through the bloodstream. Meningococcal meningitis (cerebrospinal fever) is spread by droplets from people who harbour the infection in the nasopharynx. Poor hygienic conditions with overcrowding favour the spread of the disease, which tends to occur in epidemic form among recruits in overcrowded barracks and refugees in camps. The meningococci pass from the nasopharynx to the meninges via the blood. During epidemics, fatal meningococcal septicaemia can occur without meningitis, death sometimes occurring within a few hours of infection. A characteristic feature of meningococcal septicaemia is the occurrence of a haemorrhagic rash from which the old name “spotted fever” is derived.
Meningitis may result from spread of infections in the middle ear or in any of the air sinuses in the base of the skull. It can also be a consequence of an open depressed fracture. In fact, acute leptomeningitis is a fairly common complication of a fracture of the base of the skull as a result of direct spread of organisms from air sinuses or the nasopharynx.
Sometimes the infection is iatrogenic from the introduction of micro-organisms during surgery or lumbar puncture with non-sterile instruments to obtain CSF. In such cases the bacteria are introduced directly into the subarachnoid space, resulting in a rapidly ensuing generalised meningitis. Pathology reveals structural changes in the meninges during meningococcal infection. Exudate, which accumulates in the subarachnoid space, is most easily seen where the space is wide, i.e. within sulci (the grooves or furrows separating the convolutions of the cerebral cortex) and at the base of the brain, where it accumulates around the optic chiasma and in the adjacent cisterns. It varies markedly in appearance, even in the same type of infection. There may merely be excess of turbid fluid in the sulci, or the exudate may be abundant, yellowish and fibrinous or purulent. It may even interfere with the flow of CSF to cause a certain degree of hydrocephalus.
Inflammation caused by meningococcal infection may extend into the cerebral ventricles. They contain turbid CSF and a coating of fibrin is seen on their walls and on the choroid plexuses. Exudate is also abundant in the spinal subarachnoid space, particularly on the dorsal surface of the cord.
Meningitis is diagnosed by CSF examination. The CSF is usually turbid and may be distinctly purulent. Polymorphonuclear leucocytes are seen on microscopy. The protein content is raised and the glucose reduced or absent. The causal organisms are often apparent, although in some cases they can be obtained only by culture. Vigorous early treatment with antibiotics is normally effective in resolving the infection. Inadequate or delayed treatment may result in thickening and oedema of the meninges. The exudate may cause obstruction in the subarachnoid space, leading to hydrocephalus. Any involvement of the cranial nerves in this process could lead to paralysis.
In contrast to meningococcal meningitis, viral meningitis is usually not a very severe illness and it can be a common acute infection of the nervous system, particularly in children. Many different types of viruses can cause the disease. In Britain, the enteroviruses and the mumps virus are most frequently implicated. Enterovirus meningitis normally occurs in summer. It may be seen as an epidemic in which one or perhaps two enteroviruses predominate. The virus is spread by the faecal-oral route.
The layers that cover the brain and spinal cord play a very important part in their function and are adversely affected in many diseases of the nervous system such as meningitis.
BIBLIOGRAPHY
Green, J.H. (1978). An Introduction to Human Physiology, 3rd Ed., OUP.
Levison, D.A., Reid, R., Burt, A.D., Harrison, D.J., Fleming, S. (Eds.) (2008). Muir’s Textbook of Pathology, 14th Ed., Hodder Arnold.
Marieb, E.N. & Hoehn, K. (2006). Human Anatomy and Physiology, Benjamin-Cummings.
Young, B., Lowe, J.S., Stevens, A., Heath, J.W. (2006). Wheater’s Functional Histology, 5th Ed., Churchill Livingstone.