Ross & Wilson Anatomy and Physiology in Health and Illness (81 page)

Figure 7.51 
Typical posture of Parkinson’s disease.

Effects of poisons on the brain

Many chemicals, including drugs, environmental toxins and high levels of metabolites (see above) are damaging to the central nervous system. Neurone function may be disturbed either by damage to the neurone itself or be secondary to dysfunction of other organs, e.g. liver, kidneys. The outcome depends on the toxicity of the substance, the dose and the duration of exposure. This may range from minor short-term neurological disturbance, e.g. hypoglycaemia in diabetes mellitus (
p. 227
), to encephalopathy, which may cause coma and death as a consequence of liver failure (
p. 326
).

Infections of the central nervous system

Learning outcome

After studying this section you should be able to:

describe common infections of the nervous system and their effects on body function.

The brain and spinal cord are relatively well protected from microbial infection by the blood–brain barrier.

The micro-organisms usually involved are bacteria and viruses, occasionally protozoa and fungi. The infection may originate in the meninges (
meningitis
) or in the brain (
encephalitis
), then spread from one site to the other.

Bacterial infections

Entry of bacteria into the CNS may be:

•
direct – through a compound skull fracture or through the skull bones from, e.g., middle ear or paranasal sinus infections, mastoiditis

•
blood-borne – from infection elsewhere in the body, e.g. septicaemia, bacterial endocarditis (
p. 121
)

•
iatrogenic – introduced during an invasive procedure, e.g. lumbar puncture.

Bacterial meningitis

The term ‘meningitis’ usually refers to inflammation of the subarachnoid space and is most commonly transmitted through contact with an infected individual. Bacterial meningitis is usually preceded by a mild upper respiratory tract infection during which a few bacteria enter the bloodstream and are carried to the meninges. Common microbes include:

•
Haemophilus influenzae
in children between the ages of 2 and 5 years

•
Neisseria meningitidis
in those between 5 and 30 years, the most common type

•
Streptococcus pneumoniae
in people over 30 years.

Other pathogenic bacteria can also cause meningitis, e.g. those causing tuberculosis (
p. 261
) and syphilis.

Meningitis can also affect the dura mater, especially when spread is direct through a skull fracture or from a local infection. In this type, an extradural or subdural abscess may form and cause further spread if it ruptures.

The onset is usually sudden with severe headache, neck stiffness, photophobia (intolerance of bright light) and fever. This is sometimes accompanied by a petechial rash. CSF appears cloudy owing to the presence of many bacteria and neutrophils. Mortality and morbidity rates are considerable.

Viral infections

Entry of viruses into the CNS is usually blood-borne from viral infection elsewhere in the body and, less commonly, through the nervous system. In the latter situation,
neurotropic viruses
, i.e. those with an affinity for nervous tissue, travel along peripheral nerve from a site elsewhere, e.g. poliovirus. They enter the body via:

•
the alimentary tract, e.g. poliomyelitis

•
the respiratory tract, e.g. shingles

•
skin abrasions, e.g. rabies.

The effects of viral infections vary according to the site and the amount of tissue destroyed. Viruses may damage neurones by:

•
multiplying within them

•
stimulating an immune reaction which may explain why signs of some infections do not appear until there is a high antibody titre, 1 to 2 weeks after infection.

Viral meningitis

This is the most common form of meningitis and is usually a relatively mild infection followed by complete recovery.

Viral encephalitis

Viral encephalitis is rare and usually associated with a recent viral infection. Most cases are mild and recovery is usually complete. More serious cases are usually associated with rabies or
Herpes simplex
viruses. A wide variety of sites can be affected and, as neurones cannot be replaced, loss of function reflects the extent of damage. In severe infections neurones and neuroglia may be affected, followed by necrosis and gliosis. If the individual survives the initial acute phase there may be residual dysfunction, e.g. behavioural disturbances and dementia. If vital centres in the medulla are involved the condition can be fatal.

Herpes zoster (shingles)

Herpes zoster viruses cause chickenpox (varicella) mainly in children and shingles (zoster) in adults. Susceptible children may contract chickenpox from a person with shingles but not the reverse. Adults infected with the viruses may show no immediate signs of disease. The viruses may remain dormant in posterior root ganglia of the spinal nerves then become active years later, causing shingles. Reactivation may be either spontaneous or associated with intercurrent illness or depression of the immune system, e.g. by drugs, old age, AIDS.

The posterior root ganglion becomes acutely inflamed. From there the viruses travel along the sensory nerve to the surface tissues supplied, e.g. skin, cornea. The infection is usually unilateral and the most common sites are:

•
nerves supplying the trunk, sometimes two or three adjacent dermatomes (
Fig. 7.42
)

•
the ophthalmic division of the trigeminal nerve (
Fig. 7.44
), causing
trigeminal neuralgia
, and, if vesicles form on the cornea, there may be ulceration, scarring and residual interference with vision.

Affected tissues become inflamed and vesicles, containing serous fluid and viruses, develop along the course of the nerve. This is accompanied by persistent pain and hypersensitivity to touch (
hyperaesthesia
). Recovery is usually slow and there may be some loss of sensation, depending on the severity of the disease.

Poliomyelitis

This disease is usually caused by
polioviruses
and, occasionally, by other
enteroviruses
. The infection is spread by food contaminated by infected faecal matter and initially, viral multiplication occurs in the alimentary tract. The viruses are then blood-borne to the nervous system and invade anterior horn cells in the spinal cord. Usually there is a mild febrile illness with no indication of nerve damage. In mild cases there is complete recovery but there is permanent disability in many others. Irreversible damage to lower motor neurones (
p. 157
) causes muscle paralysis which, in the limbs, may lead to deformity because of the unopposed tonal contraction of antagonistic muscles. Death may occur owing to respiratory paralysis. Vaccination programmes have now almost eradicated this disease in developed countries.

Rabies

All warm-blooded animals are susceptible to the rabies virus, which is endemic in many countries but not in the UK. The main reservoirs of virus are wild animals, some of which may be carriers. These may infect domestic pets which then become the source of human infection. The viruses multiply in the salivary glands and are present in large numbers in saliva. They enter the body through skin abrasions and are believed to travel to the brain along peripheral nerves. The incubation period varies from about 2 weeks to several months, possibly reflecting the distance viruses travel between the site of entry and the brain. There is acute encephalomyelitis with extensive damage to the basal ganglia, midbrain and medulla oblongata. Involvement of the posterior root ganglia of the peripheral nerves causes meningeal irritation, extreme hyperaesthesia, muscle spasm and convulsions.
Hydrophobia
(hatred of water) and overflow of saliva from the mouth are due to painful spasm of the throat muscles that inhibits swallowing. In the advanced stages muscle spasm may alternate with flaccid paralysis and death is usually due to respiratory muscle spasm or paralysis.

Not all people exposed to the virus contract rabies, but in those who do, the mortality rate is high.

Human immunodeficiency virus (HIV)

The brain is often affected in individuals with AIDS (
p. 376
) resulting in opportunistic infection and dementia.

Creutzfeldt–Jakob disease

This infective condition may be caused by a ‘slow’ virus, the nature and transmission of which is poorly understood. It is thought to be via a heat-resistant transmissible particle known as a
prion protein
. It is a rapidly progressive form of dementia for which there is no known treatment so the condition is always fatal.

Myalgic encephalitis (ME)

This condition is also known as post-viral syndrome or chronic fatigue syndrome. It affects mostly teenagers and young adults and the aetiology is unknown. Sometimes the condition follows a viral illness. The effects include malaise, severe fatigue, poor concentration and myalgia. Recovery is usually spontaneous but sometimes results in chronic disability.

Demyelinating diseases

Learning outcome

After studying this section you should be able to:

explain how the signs and symptoms of demyelinating disease are related to pathological changes in the nervous system.