The vast majority of chronic and recurrent headaches are believed, on no good evidence, to be due to ‘tension’ within the scalp muscles. What is certain is that they are, in terms of pathology, innocent. ‘Tight band’ sensations, pressure behind the eyes, and throbbing and bursting sensations are common.
depressed skull fracture or meningeal tear may be necessary.
Polyvalent vaccines are available against recurrent pneumococcal meningitis (e.g. when there is a CSF leak following skull fracture) and against some strains of meningococci (see p.23). In meningococcal outbreaks rifampicin prophylaxis should be given to contacts and family members as well as to the patient. Differential diagnosis of (SF pleocytosis Difficulties occur in meningitis when a raised, often mixed (lymphocyte and polymorph, i.e. pleocytic) picture is found but no infecting organism. This is sometimes called ‘aseptic meningitis’. The conditions should be considered.
Encephalitis is inflammation of brain parenchyma. It is caused by a wide variety of viruses and may also occur in bacterial and other infections. Acute viral encephalitis In many cases a viral aetiology is presumed but not confirmed serologically or by culture. The usual organisms cultured from cases of viral encephalitis in adults in the UK are Echo, Coxsackie, mumps and herpes simplex viruses.
Adenovirus, varicella zoster, influenza, measles and other viruses are rarer causes.
Many of these infections cause a mild self-limiting illnesswith headache and drowsiness. In a minority there is a more serious illness accompanied by focal signs, seizures and coma. Herpes simplex virus (HSV-1) accounts for many of these severe infections in Britain and has a mortality of around 20% even with treatment. In the Far East the Japanese B arbovirus is a more usual, and epidemic, cause of severe encephalitis, with a high mortality.
Partially treated bacterial meningitis
Tuberculosis or fungi
Parameningeal foci (e.g. paranasal sinus)
Cerebral venous or arterial infection
Following subarachnoid haemorrhage
Encephalitis, including AIDS
Rare causes (e.g. cerebral malaria, sarcoidosis, Behcet’s syndrome, Lyme disease)
• Bacterial meningitis complicated by cerebral oedema and/or cerebral venous thrombosis
• Cerebral abscess
• Acute disseminated encephalomyelitis
• Toxic confusional states in febrile illnesses and In septicaemia
Investigation in severe cases includes CT scanning (which characteristically shows areas of oedema), EEG (which shows slow-wave changes and/or ‘periodic complexes’) and viral serology of blood and CSF. Brain biopsy is now seldom performed in the UK.
Suspected herpes simplex encephalitis is immediatelytreated with intravenous acyclovir, the active form of which inhibits DNA synthesis. Phosphorylation of. this drug is dependent upon the presence of viral thymidine kinase; thus the drug is specific for herpesvirus infections. If the patient is in coma the outlook is poor whether or not drugs are given.Supportive measures are required for comatose patients. Seizures are treated with anticonvulsants. Prophylactic immunization is possible against Japanese B encephalitis and sometmes advised particularly for travellers to the Far East in endemic areas.
encephalomyelitis (AD E)
This follows many common viral infections (e.g. measles, varicella zoster, mumps and rubella) and rarely after immunization against rabies, influenza or pertussis. The clinical syndrome is often similar to acute viral encephalitis, with added focal brain stem and/or spinal cord lesions due to demyelination, but in which viral particlesare not usually present. The prognosis is variable. Mild cases recover completely but in severe cases (those in coma) mortality is around 25% and the survivors often have permanent brain damage. Treatment is supportive, with steroids and anticonvulsants.
Myelitis means inflammation of the spinal cord causing paraparesis or tetraparesis. It occurs with varicella zoster or as part of a postinfective encephalomyelitis. Poliomyelitis is a specific enterovirus infection of anterior horn cells.
HERPES ZOSTER (SHINGLES)
This is a recrudescence of infection with varicella zoster virus within the dorsal root ganglia, the original infection having been acquired in an attack of chickenpox many There may be obvious precipitating factors such as worry, noise, concentrated visual effort or fumes. Depression is also a frequent underlying cause. Tension headaches are often attributed to cervical spondylosis, refractive errors or high blood pressure; the evidence for these is poor. Similar headaches also follow head injuries,which may be minor.
There ar e no abnormal physical signs other than tenderness and tension in the nuchal and scalp muscles.
• Firm reassurance
• Avoiding the causes
• Physical treatments-massage, relaxation
• Antidepressants-when indicated
Investigation may be needed to confirm the benign nature of the problem.
Migraine means recurrent headaches associated with visual and gastrointestinal disturbance; despite the origin of the word, it does not invariably mean unilateral headache.
About 10% of any population sampled admit to these symptoms.
The cause of migraine is unknown. The headache, oftenthrobbing, is believed to be due to vasodilatation or oedema of blood vessels, with stimulation of nerve endings near affected extracranial and meningeal arteries. The release of vasoactive substances such as nitric oxide are thought to playa role. In addition, the serum level of 5- hydroxytryptamine rises at the onset of the prodromal symptoms and falls during the headache. Cerebral symptoms and signs (e.g. tingling of limbs, aphasia, weakness) are caused by ischaemia and/ordepression of cortical function. Definite precipitating factors are unusual. Somepatients complain of symptoms at times of relaxation(e.g. weekend migraine). Others find that chocolate (high in phenylethylamine) and cheese (high in tyramine) precipitate attacks. Migraine is common around puberty, at he menopause and premenstrually, and sometimes increases in severity or frequency with the contraceptivepill, in pregnancy and with the development of hypertension. There is no reason to suppose that migraine is associated with any major intracranial lesion. However, since migraine is such a common symptom complex, an intracranial mass lesion and migraine sometimes both occur in the same patient by coincidence. Rarely, migraine follows head injuries.
There are several types of migraine, the attacks varyingfrom intermittent headaches barely distinguishable from tension head aches to discrete episodes that mimic thromboembolic cerebral ischaemia. The distinction between the variants is somewhat artificial.
The attack itself may be divided into:
• Prodromal symptoms
• Headache and associated symptoms
Prior to the attack some patients experience a feeling of well-being.
Migraine with aura (classical)
Prodromal symptoms are usually visual and are related to ischaemia in the distribution of the intracranial arteries. There are unilateral patchy scotomata (when the retinal vessels are involved), unilateral blindness (involvement of the ophthalmic artery) and sometimes hemianopic field loss (involvement of the posterior cerebral artery). Teichopsia (flashes) and fortification spectra (jagged lines resembling battlements) are common. Transient aphasia sometimes occurs, together with tingling, numbness or vague weakness of one side. The patient feels nauseated.
The prodrome lasts for 15 min to 1 hour or more. Headache follows. This is occasionally hemicranial (‘splitting the head’) but often begins locally and becomes generalized. Nausea increases and vomiting follows. The patient is irritable and prefers to be in a darkened room. The superficial temporal artery (either or both) is engorged and pulsating.
After several hours the attack ceases. There is sometimes a diuresis towards the end of an attack. Sleep often follows.
Migraine without aura (common) This is the usual variety of migraine. Prodromal visual symptoms are vague. There is recurrent headache accompanied by nausea and malaise. Distinction from tension headache may be impossible.
The prodromal symptoms are due to ischaemia in theposterior cerebral circulation. Circumoral tingling, numbness of the tongue, vertigo, diplopia, transient blindness, syncope, dysarthria and ataxia occur.
This is a rarity in which classical migraine is accompanied by hemiparesis. Recovery occurs within 24 hours. Exceptionally, cerebral infarction follows.
This is a third (or exceptionally a sixth) nerve palsy occurring in a migraine attack. The condition is rare and is difficult to distinguish from other causes of a third nerve palsy (see p. 886) without investigation.
Facioplegic migraine This rarity is unilateral facial weakness occurring during a migraine attack.
The sudden onset of headache may be similar to meningitis or SAH.
The hemiplegic, visual and hemisensory symptoms must be distinguished from thromboembolic TIAs (see p. 906). In TIAs the maximum deficit is present immediately and headache is unusual.
Unilateral tingling or numbness should be distinguished from sensory epilepsy (partial seizures). In the latter a distinct ‘march’ of symptoms is usual.
REASSURANCE and relief of anxiety.
AVOIDANCE OF PRECIPITATING DIETARY FACTORS (rarely helpful).
PATIENTS ON ORAL CONTRACEPTIVEs-a change in brand or stopping of the drug may help. Severe hemiplegic symptoms are an indication for stopping these drugs.
During the attack
Paracetamol or other simple analgesics should be given, with antiemetics (e.g. metocloprarnide) if necessary. The 5-hydroxytryptamine (5HT1) agonist sumatiptan is of considerable value either by self-administered subcutaneous injection or orally in recurrent severe attacks. Itshould not be taken until 24 hours after ergotamine. Ergotamine tartrate (1-2 mg orally or rectally, 360 ILg by aerosol or 0.25-0.5 mg by injection) is sometimes, though not often, helpful if given early in attack. Ergotamine
should not be used in patients with a history of vascular disease.
It is particularly difficult to discern the true (as opposedto placebo) effects of prophylactic drugs in migraine. When drugs are necessary, the following are used: PIZOTIFEN (a 5-hydroxytryptamine antagonist) 0.5 mg at night for several days, increasing to 1.5 mg at night.Common side-effects are slight weight gain and drowsiness.
PROPRANOLOL 10 mg three times daily, increasing to 40-80 mg three times daily. METHYSERGIDE (a 5-hydroxytryptamine antagonist) 2- 6 mg daily. An occasional side-effect is retroperitoneal fibrosis, which precludes its use for longer than 6 months.