cancer

Clinical presentation and diagnosis of oral cancer
• Early diagnosis of oral cancer ishould lead to better  treatment results and, ideally, the Clinical diagnosis of oral cancer should be easy.
The tongue
• The majority of tongue cancers occurs on the  middle third of the lateral margins. extending early in the course of the disease on to the ventral aspect and floor of the mouth
• Approximately 25 per cent occur on the posterior thirdof the tongue, 20 per cent on the anterior third and rarely  on the dorsum.
 • Early tongue cancer may manifest in a variety of ways. Often the growth is exophytic with areas of ulceration. It may occur as an ulcer in the depths of a fissure or as an area of  superficial ulceration with unsuspected infiltration into the underlying muscle.
 • Leucoplakic patches may or may not be associated with the primary lesion. A minority of tongue cancers may be asympromatic, arising in an atrophic depapillated area  with an erythroplakic patch with peripheral streaks or areas of leucoplakia.
• Later in the course of the disease a more typical malignant ulcer will usually develop, often several centimetres in diameter.
• The ulcer is  hard in consistency with heaped.up and often everted edges. The floor is granular, indurated and bleeds readily. Often there are areas of necrosis.
• The growth infiltrates the tongue progressively causing increasing pain and difficulty with speech and swallowing.
• By this stage pain is often severe and constant, radiating to the neck and ears.
• Lymph node metastases at this stage are common - indeed 50 per cent may have palpable nodes at presentation.
• Because of the relatively early lymph node metastasis of tongue cancer, 12 per cent of patients may present with no symptoms other than 'a lump in theneck'.


The floor of the mouth
• The floor of the mouth is the second most common sire for oral cancer.
• It is defined as the U-shaped area between the lower alveolus and the ventral surface of the tongue; carcinomas arising at this sire involve adjacent structures very early in their natural history.
• Most tumours occur in the anterior segment of the floor of the mouth to one side of the midline.
• The lesion usually starts as an indurated mass which soon ulcerates.
• At an early stage the tongue and lingual aspect of the mandible become involved. This early involvement of the tongue leads to the characteristic slurring of the speech often noted in such patients.
• The infiltration is deceptive but may extend to reach the gingivae, tongue and


genioglossus muscle. Subperiosteal spread is rapid once the mandible is reached.
• Lymphatic metastasis, although early, is less common that with tongue cancer.spread is usually to the submandibular and jugulodigasrric nodes and may be bilateral. 
• Cancer in the floor of the mouth cancer is associated withe a pre-existing leucoplakia more commonly than at other sites.
The gingiva and alveolar ridge
• Carcinoma of the lower alveolar ridge occurs predominantly in the premolar and molar regions
• The patient usually presents with proliferative tissue at the gingival margins or superficial gingival ulceration. • Diagnosis is often delayed because there is a wide variety of inflammatory and reactive lesions which occur in this region in association with the teeth or dentures. indeed, there will often be a history of tooth extraction with subsequent failure of the socket to heal prior to definitive diagnosis.
The buccal mucosa
• The buccal mucosa extends from the upper alveolar ridge down to the lower alveolar ridge and from the commissure anteriorly to the mandibular ramus and retromolar region posteriorly
• Squamous cell carcinomas mostly arise either at the commissure or along the occlusal plane to the retromolar area, the majority being situated posteriorly. Exophyric, ulcero-infiltrative and verrucous types occur.
• The onset of the disease may be insidious, the patient sometimes presenting with trismus due to deep neoplastic infiltration into the buccinaror muscle.
• Extension posteriorly involves the anterior' pillar of the fauces and soft palate with consequent worsening of the prognosis.
• Ulcero-infiltrative lesions will often involve the le overlying skin of the cheek resulting in multiple sinuses. Lymph node spread is to the submental, submandibular, parotid and lateral pharyngeal nodes.
• Verrucous carcinoma occurs as a superficial proliferative exophytic lesion with minimal deep invasion and induration. Often the lesion' is densely keratinised and presents as a soft white velvety area mimicking benign hyperplasia.
• Lymph node metastasis is late and the tumour behaves as a low-grade squamous cell carcinoma.
The hard palate, maxillary alveolar ridge and floor of antrum
• These three sites are anatomically distinct, but a carcinoma arising from one site soon involves the others
• Consequently, it can be difficult to determine the exact site of origin. Except in countries where reverse smoking is practised, cancer of the plate is relatively uncommon.

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 sub-stance, the dose and the duration of exposure. This may: range from minor short-term neurological disturbance,, e.g. hypoglycaemia in diabetes mellitus  to, encephalopathy, which may cause coma and death as a consequence of liver failure . 

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, niastoiditis 
• blood-borne - from infection elsewhere in the body, e.g. septicaemia, bacterial endocarditis 
• 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 transmit-ted through contact with an infected individual. Bacte-rial 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. 

Viral infections 
Entry of viruses into the CNS is usually blood-borne from viral infection elsewhere in the body and, less com-monly, through the nervous system. In the latter situa-tion, 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 asso-ciated with rabies or Herpes simplex viruses. A wide vari-ety 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 individ-ual survives the initial acute phase there may be residual dysfunction, e.g. behavioural disturbances and demen-tia. If vital centres in the medulla are involved the condi-tion can be fatal.
Herpes zoster (shingles)
Herpes zoster viruses cause chickenpox (varicella) mainly in children and shingles (zoster) in adults. Sus-ceptible children may contract chickenpox from a per-son with shingles but not the reverse. Adults infected with the viruses may show no immediate signs of dis-ease. The viruses may remain dormant in posterior root ganglia of the spinal nerves then become active years later, causing shingles. Reactivation may be either spon-taneous 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:

Dementia

 Dementia is caused by progressive, irreversible degener-ation of the cerebral cortex and results in mental deterio-ration, usually over several years. There is gradual impairment of memory (especially short term), intellect and reasoning but consciousness is not affected. Emo-tional lability and personality change may also occur. 
Alzheimer's disease 
This condition is the commonest form of dementia in developed countries. The aetiology is unknown although genetic factors may be involved. Females are affected twice as often as males and it usually affects those over 60 years, the incidence increasing with age. There is pro-gressive atrophy of the cerebral cortex accompanied by deteriorating mental functioning. Death usually occurs between 2 and 8 years after onset. 
Huntington's disease
 This usually manifests itself between the ages of 30 and 50 years. It is inherited as an autosomal dominant disor-der  associated with deficient production of the neurotransmitter gamma aminobutyric acid (GABA). By the time of onset, the individual may have passed the genetic abnormality on to their children. Extrapyramidal changes cause chorea, rapid uncoordinated jerking movements of the limbs and involuntary twitching of the facial muscles. As the disease progresses, cortical atrophy causes personality changes and dementia. 
Secondary dementias 
Dementia may occur in association with other diseases:
 • cerebrovascular disease, e.g. multi-infarct dementia
 • infections, e.g. neurosyphilis, human immunodeficiency virus (HIV), Creutzfeldt-Jakob disease
 • cerebral trauma
 • alcoholism and some drugs
 • vitamin B deficiencies
 • metabolic disorders, e.g. hypothyroidism, uraemia, liver failure. 

Parkinson's disease 07.18 In this disease there is gradual degeneration of dopa.. mine releasing neurones in the extrapyramidal system, This leads to lack of control and coordination of muscle movement resulting in: 
• slowness of movement (bradykinesia) and difficulty initiating movements 
• fixed muscle tone causing expressionless facial features, rigidity of voluntary muscles causing the slow and characteristic stiff shuffling gait and stooping posture 
• muscle tremor of extremities that usually begins in one hand, e.g. 'pill rolling' movement of the fingers. Onset is usually between 45 and ki years. The cause is usu-ally unknown but some cases are associated with repeated trauma as in, e.g., 'punch drunk' boxers; tumours causing midbrain compression; drugs, e.g. phenothiazines; heavy: metal poisoning. There is progressive physical disability but the intellect is not impaired . 

Stroke (cerebrovascular disease)

Stroke (cerebrovascular disease)
 this condition is a common cause of death and disability, especially in older people. Predisposing factors elude: hypertension atheroma cigarette smoking diabetes mellitus. 
It occurs when blood flow to the brain is suddenly interrupted, causing hypoxia. The effects include paralysis of a limb or one side of the body and disturbances of speech and vision. The nature and extent of damage depend on the size and location of the affected blood vessels. The main causes are cerebral infarction (approx. 85%) and spontaneous intracranial haemorrhage (15%). 
Cerebral infarction 
 This is caused by atheroma complicated by thrombosis  or blockage of an artery by an embolus from e.g infective endocarditis. The cerebral hemispheres are usually affected. When complete recovery occurs within 24 hours, the event is called a transient ischaemic attack (TIA). Recurrence or completed stroke associated with permanent damage may follow. 
spontaneous intracranial haemorrhages 
the haemorrhage may be into the subarachnoid space or intracerebral . It is commonly associated with an aeurysm or hypertension. In each case the escaped blood may cause arterial spasm, leading to ischaemia, infarction, fibrosis (gliosis) and hypoxic brain damage. 

A severe haemorrhage may be instantly fatal while repeated small haemorrhages have a cumulative effect in extending brain damage (multi-infarct dementia). 
Intracerebral haemorrhage 
Prolonged hypertension leads to the formation of multi-ple microaneurysms in the walls of very small arteries in the brain. Rupture of one or more of these, due to continuing rise in blood pressure, is usually the cause of intracerebral haemorrhage. The most common sites are branches of the middle cerebral artery in the region of the internal capsule and the basal ganglia. Severe haemorrhage. This causes compression and destruction of tissue, a sudden increase in ICP and dis-tortion and herniation of the brain. Death follows when the vital centres in the medulla oblongata are dam-aged by haemorrhage or if there is coning due to increased ICP. 
Less severe haemorrhage. This causes paralysis and loss of sensation of varying severity, affecting the side of the body opposite the haemorrhage. If the bleeding stops and does not recur a fluid-filled cyst develops, i.e. the haematoma is walled off by gliosis, the blood clot is gradually absorbed and the cavity filled with tissue exudate. When the ICP returns to normal some function may be restored, e.g. speech and movement of limbs. 
Subarachnoid haemorrhage This is usually due to rupture of a berry aneurysm on one of the major cerebral arteries, or bleeding from a congenitally malformed blood vessel . The blood may remain localised but usually spreads in the subarachnoid space round the brain and spinal cord, causing a general increase in ICI' without distortion of the brain . The irritant effect of the blood may cause arterial spasm, leading to ischaemia, infarc-tion, gliosis and the effects of localised brain damage. It occurs most commonly in middle life, but occasionally in young people owing to rupture of a malformed blood vessel. This condition is often fatal or results in perma-nent disability.