Characteristics:	Associated features:
– generalised. – aggravated by bending or coughing. – worse in the morning on awakening; may awaken patient from sleep. – the severity of the headache gradually progresses.

– vomiting in later stages.

– transient loss of vision (obscuration) with sudden change in posture.

– eventual impairment of conscious level

Management:

further investigations are essential – CT or MRI

Low pressure headache

Low pressure headache occurs most commonly after lumbar puncture but can arise spontaneously (Spontaneous intracranial hypotension). Headache is worse on standing and improves lying flat. After LP no investigation is needed. If no cause is apparent MRI will show downward displacement cerebellar tonsils and meningeal enhancement with contrast (Gd). Spontaneous improvement is usual. Occasionally a dural ‘blood patch’ at the site of CSF leak (post LP or epidural anaesthesia) is necessary.

NON-NEUROLOGICAL CAUSES OF HEADACHE

Local causes:

Sinuses: Well localised. Worse in morning. Affected by posture, e.g. bending.

X-ray – sinus opacified. Treatment – decongestants or drainage.

Ocular: Refraction errors may result in ‘muscle contraction’ headaches

– resolves when corrected with glasses.

Acute glaucoma can produce headache but is accompanied by other symptoms, e.g. misting of vision, ‘haloes’.

Dental disease: Discomfort localised to teeth. Check for malocclusion.

Check temporomandibular joints.

Systemic causes:

Headache may accompany any febrile illness or may be the presenting feature of accelerated hypertension or metabolic disease, e.g. hypoglycaemia, hypercalcaemia.

Many drugs produce headache

– through vasodilatation, e.g. bronchodilators, antihistamines

– on withdrawal, e.g. amphetamines, benzodiazepines, caffeine.

MENINGISM

Evidence of meningeal irritation caused by infection or subarachnoid haemorrhage results in characteristic clinical features (though not all will necessarily be present):

RAISED INTRACRANIAL PRESSURE

The skull is basically a rigid structure. Since its contents – brain, blood and cerebrospinal fluid (CSF) – are incompressible, an increase in one constituent or an expanding mass within the skull results in an increase in intracranial pressure (ICP) – the ‘Monro-Kellie doctrine’.

Compensatory mechanisms for an expanding intracranial mass lesion:

CEREBROSPINAL FLUID (CSF)

Secreted at a rate of 500 ml per day from the choroid plexus, CSF flows through the ventricular system and enters the subarachnoid space via the 4th ventricular foramina of Magendie and Luschka.

Under normal conditions, CSF flows freely through the subarachnoid space and is absorbed into the venous system through the arachnoid villi. If flow is obstructed at any point in the pathway, hydrocephalus with an associated rise in intracranial pressure develops, as a result of continued CSF production. With an expanding intracranial mass lesion, normal pressure is initially maintained by CSF expulsion to the expandable lumbar theca. Further expansion and subsequent brain shift may obstruct the free flow of CSF not only to the lumbar theca but also to the arachnoid villi, causing an acute rise in intracranial pressure.

BRAIN WATER/OEDEMA

Cerebral oedema – an excess of brain water – may develop around an intrinsic lesion within the brain tissue, e.g. tumour or abscess or in relation to traumatic or ischaemic brain damage, and contribute to the space-occupying effect.

Different forms of cerebral oedema exist:

Vasogenic: excess fluid (protein rich) passes through damaged vessel walls to the extracellular space – especially in the white matter. The extracellular fluid gradually infiltrates throughout normal brain tissue towards the ventricular CSF and this drainage route may aid clearance. e.g. adjacent to tumour.

Cytotoxic: fluid accumulates within cells – neurons and glia i.e. intracellular, e.g. toxic or metabolic states.

Interstitial: when obstructive hydrocephalus develops, CSF is forced through to the extracellular space especially in the periventricular white matter.

With ischaemic damage, as cell metabolism fails, intracellular Na⁺ and Ca²⁺ increase and the cells swell i.e. cytotoxic oedema. Capillary damage follows and vasogenic oedema supervenes.

CEREBRAL BLOOD FLOW (CBF)/CEREBRAL BLOOD VOLUME (CBV)

Blood flow is dependent on blood pressure and the vascular resistance:

Inside the skull, intracranial pressure must be taken into account:

Under normal conditions the cerebral blood flow is coupled to the energy requirements of brain tissue. Various regulatory mechanisms acting on the arterioles maintain a cerebral blood flow sufficient to meet the metabolic demands.

FACTORS AFFECTING THE CEREBRAL VASCULATURE

Chemoregulation

– Change in extracellular pH or an accumulation of metabolic by-products directly affects the vessel calibre.

– Any change in arteriolar PCO₂ has a direct effect on cerebral vessels, but only a reduction of PO₂ to < 50 mmHg has a significant effect.

Autoregulation

– A change in the cerebral perfusion pressure results in a compensatory change in vessel calibre.

Any change in blood vessel diameter results in considerable variation in cerebral blood volume and this, in turn, directly affects intracranial pressure.

Energy requirements differ in different parts of the brain. To meet such needs in the white matter, flow is 20 ml/100 g/min, whereas in the grey matter flow is as high as 100ml/100g/min.

Autoregulation is a compensatory mechanism which permits fluctuation in the cerebral perfusion pressure within certain limits without significantly altering cerebral blood flow.

A drop in cerebral perfusion pressure produces vasodilation (probably due to a direct ‘myogenic’ effect on the vascular smooth muscle) thereby maintaining flow; a rise in the cerebral perfusion pressure causes vasoconstriction.

Neurogenic influences appear to have little direct effect on the cerebral vessels but they may alter the range of pressure changes over which autoregulation acts.

Autoregulation fails when the cerebral perfusion pressure falls below 60 mmHg or rises above 160 mmHg. At these extremes, cerebral blood flow is more directly related to the perfusion pressure.

In damaged brain (e.g. after head injury or subarachnoid haemorrhage), autoregulation is impaired; a drop in cerebral perfusion pressure is more likely to reduce cerebral blood flow and cause ischaemia. Conversely, a high cerebral perfusion may increase the cerebral blood flow, break down the blood–brain barrier and produce cerebral oedema as in hypertensive encephalopathy.

INTRACRANIAL PRESSURE (ICP)

Intracranial pressure, measured relative to the foramen of Monro, under normal conditions ranges from 0–135 mm CSF (0–10 mmHg) although very high pressure, e.g. 1000 mm CSF may occur transiently during coughing or straining.

When intracranial pressure is monitored with a ventricular catheter, regular waves due to pulse and respiratory effects are recorded (page 53). As an intracranial mass expands and as the compensatory reserves diminish, transient pressure elevations (pressure waves) are superimposed. These become more frequent and more prominent as the mean pressure rises.

Eventually the rise in intracranial pressure and resultant fall in cerebral perfusion pressure reach a critical level and a significant reduction in cerebral blood flow occurs. Electrical activity in the cortex fails at flow rates about 20 ml/100 g/min. If autoregulation is already impaired these effects develop even earlier. When intracranial pressure reaches the mean arterial blood pressure, cerebral blood flow ceases.